A Casebook of Twenty Surgical Cases

A CASEBOOK OF TWENTY SURGICAL CASES DR. SUNILDATH JUGOOL (MBBS,UWI)

The University of the West Indies Submitted in partial fulfillment of the requirements for the degree of DOCTOR OF MEDICINE (DM), GENERAL SURGERY

DR SUNILDATH JUGOOL (MBBS,UWI) 2013

Dedication

To my wife, Sherry and kids (Sarvesh and Shreya), my mother, my father, brothers and sisters.

Thank you for the encouragement, support and sacrifices you made towards my training.

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Acknowledgements The success of this project depended largely on the encouragement and guidelines of many persons. I would like to express my deepest appreciation and thanks to the following persons: ยง Professor Vijay Naraynsingh, who possesses the attitude and the substance of a genius. His clinical and surgical skills have continued to be impressive and he is an exemplary role model. He has continuously conveyed a spirit of adventure with regard to research and an excitement anent to teaching. He was always willing to assist and made himself available to the call of the residents. This was particularly inspiring to me in preparing this casebook. ยง The General Surgery Consultants at the San Fernando General Hospital: Dr. S. Budhooram, Dr. J. Shah, Dr. Y. Maraj, Dr. D Dan and Dr. T. Kuruvilla. The effort exerted to ensure availability of both professional and personal time to facilitate my learning is held in high esteem. It was indeed a pleasure to be a part of each of their teams during which time I was able to acquire both clinical and non-clinical skills. Most importantly, I am grateful for the opportunity afforded me to have access to their patients and to be involved in their surgical management. I would like to offer special thanks to Dr. Dilip Dan, who was both a great teacher and an admirable role model, and one whom I consider to be a modern surgeon.

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The compilation of these cases would not have been possible without the patients themselves. I thank them immensely. In addition, I would like to express appreciation to the other doctors in the surgical service at the General Hospital, San Fernando who helped to manage these patients and were also tolerant of my needs during this time. The efforts of the surgical and theatre nurses who helped to care for these patients are also appreciated and to them I am grateful. I would like to also thank the doctors in radiology for helping to educate me, facilitating the relevant investigations for these patients and assisting with acquiring images for the presentations.

I also express thanks to my fellow residents and interns for the support and continued encouragement during the preparation of this book. In particular, I would like to thank Dr Dave Harnanan for always willing to help, offering support and guidance in an objective manner. I would like to thank Ms Gemma Constantine and Alisha Constantine-Applewhite for assisting with the reviewing and correcting of my writing during the preparation of this case book. They offered support and advice unconditionally, and always had positive suggestions to make things work.

I would also like to thank my parents, my brothers and sisters. They were always supporting and encouraging me with their best wishes. Finally, I would like to thank my wife, Sherry, my rock, for standing with me and offering encouragement in such a profound way through the good times and the bad. My children, Sarvesh and Shreya, I thank them for their inspiration and motivation and I am sure when they are older they will understand just how much they too supported my efforts.

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Preface These twenty cases were identified during the DM residency at the General Hospital, San Fernando. They represent a combination of common surgical conditions and a few rare ones. The cases were selected to capture a wide spectrum of general surgical conditions that are common, likely to present a challenge to us in the Caribbean and based on clinical interest. Although I was involved in the management of these cases, it was under the guidance of the Consultant General Surgeons at the General Hospital San Fernando.

The discussion for each case was formulated on evidence based data as presented in the world literature. The information was used to identify the most appropriate treatment strategies, in particular the surgical aspects of management. The evidence was used to justify the management outlined for each case or identify areas for improvement in some and others. Others identified areas of controversy and these were outlined where relevant.

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You cannot teach a man anything; you can only help him to find it within himself. – Galileo

Table of Contents 1. Acute Sigmoid Diverticulitis

1

2. Laparoscopic Ventral Hernia Repair

19

3. Blunt Duodenal Injury

40

4. Flail Chest Injury 63 5. Gallstone Ileus 85 6. Hemorrhoids 106 7. Blunt Hepatic Trauma 133 8. Postoperative Ileus 150 9. Ductal Carcinoma in Situ

169

10. Obstructing Left Colon Cancer

186

11. Acute Appendicitis 199 12. Obturator hernia 212 13. Multinodular Goitre 227 14. Sentinel Lymph Node Biopsy in Breast Cancer

237

15. Rectal Cancer 263 16. The Colonic Esophageal Conduit

303

17. Perforated Duodenal Ulcer

322

18. Pancreaticoduodenectomy (PJ vs PG)

355

19. Crohn’s Disease of the Colon

383

20. Ruptured Abdominal Aortic Aneurysm

396

A CASEBOOK OF TWENTY SURGICAL CASES

1. ACUTE SIGMOID DIVERTICULITIS

Change in operative strategies/particular reference to young patients

INTRODUCTION Sigmoid diverticulitis is a common disease of the Western World and results in a significant number of hospital admissions with considerable societal costs due to loss of productivity. The prevalence of diverticulae in the sigmoid increases proportionally with ageing and only rarely results in the inflammation referred to as sigmoid diverticulitis. The spectrum of sigmoid diverticulitis ranges from a single episode of mild sigmoid inflammation amenable to outpatient treatment to a life-threatening generalized peritonitis caused by acute diverticular perforation which requires urgent surgical intervention. Recurrence has been shown to increase with subsequent episodes.

Previous case series and retrospective studies suggest that without surgical intervention, patients with recurrent diverticular disease are at risk of more severe complications. In particular, the younger patient has been described as being susceptible to more virulent disease with greater risk of recurrence and perforation than the older patients.

Therefore it seems quite plausible that early elective surgery will prevent future attacks and avoid complications. In fact, national societies, including the American Society of Colon and Rectal Surgery, have previously recommended elective colectomy in patients younger than 50 years who have experienced one episode of acute diverticulitis in an effort to prevent increased morbidity and mortality.

More recent data have provided evidence to the contrary. It appears that 1

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the natural history of sigmoid diverticulitis does not result in increased risk of complications and the behavior in younger adults, are no different.

A case of acute sigmoid diverticulitis managed medically is described. This is followed by a literature review regarding the controversies surrounding the role of elective sigmoid colectomy for such patients.

CASE History: A 41 year old gentleman presented with a 2 day history of lower abdominal pain. The pain was described as initially mild and cramp-like but eventually became constant. The discomfort began along the left abdomen and then across the lower abdomen. On the day of presentation, the patient reported the pain to be maximal in the sub-umbilical area and was aggravated on walking.

No analgesics or remedial actions were taken. His appetite had waned but there was no vomiting. The patient continued to pass flatus but had no bowel action since the onset of pain and he experienced no bloating or abdominal distention.

This was his first episode of such pain. His bowel actions were otherwise regular and not associated with per rectal bleeding.

Systematic enquiry was otherwise non contributory. This gentleman had no previous medical or surgical history and had no family history of gastrointestinal tract disease. This gentleman was married, lived with his wife and 10yr old child. His occupation was a scrap metal dealer.

Physical Examination: A medium built gentleman lying comfortably. His mucous membranes were pink and moist with vital signs: BP 132/90mmHg, P 102 min-1, RR 20min-1, T 37.2oC. Significant findings were confined to the abdomen which revealed that it moved 2

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with respiration and was soft. He was tender though across the lower abdomen with mild percussion tenderness, maximally on the right suprapubic area. There was no renal angle tenderness. His bowel sounds were normal.

The external genitalia were normal and there were no groin hernias. Digital rectal examination revealed no external abnormalities, his anal tone was normal, the prostate was not enlarged and the anorectum was palpably normal without any rectal bogginess or fever.

Investigations: CBC: Hb 13.3 mgdl-1, WCC 15.1 x 103 /µl, Plt 300 x 103/µl.

Renal function and amylase levels were normal, CRP 9 mg/dl.

Chest and Abdominal X-rays were normal.

CT Scan: The sigmoid colon appeared thickened with diverticulae and surrounding fat stranding.(see Fig 1,2)

Diagnosis: Acute Sigmoid Diverticulitis (Hinchey’s I) Treatment: 1.

Admitted to the surgical ward

2.

Allowed clear sips orally

3.

Analgesia: Paracetamol (1g q 6h) and Pethidine (50mg im q 8h prn)

4.

Antibiotics: Augmentin 1.2 g IV tds

5.

IVF: 2l/ 24hrs (RL, D5S)

His condition improved over 5 days when he was discharged and advised regarding adequate water in take and a high fibre diet. A gastroenterology request was made for colonoscopy in 6- weeks.

Three months later he was reviewed in the outpatient clinic. He remained as3

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ymptomatic and the colonoscopy confirmed diverticular disease with no other pathology. He was advised of the potential complications of diverticular disease and for review in a year.

Figure 1: Fat stranding in relation to the sigmoid colon

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Fig2.

Fig 2: No pelvic collection. Fat stranding and diverticulae of the sigmoid colon

DISCUSSION

Diverticular disease was first reported by Littre in the 1700s. These were felt to be pathologic curiosities and unlikely to cause symptons.(1) Considered rare in the early part of the 20th century, diverticulosis is one of the most common colonic conditions in Western populations. Diverticulosis is generally rare before age 30 years but is such that 40% of the population develops diverticulosis by age 60 years and 60% of those age 80 years.(2) In approximately 95% of cases, 5

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diverticular involve the sigmoid and left colon. An estimated 10%-25% of patients who develop diverticulosis will develop diverticulitis. Clinical data suggests that the incidence of diverticulitis is increasing: Ricciardi and colleagues examined the incidence of diverticulitis in the 1991 to 2005 period and noted an increase in discharges from 5.1 cases per 1000 inpatients in 1991, to 7.6 cases per 1000 inpatients in 2005 (p<0.0001).(3)

There are three main clinical presentations of diverticular disease related to inflammation. The most common clinical presentation of sigmoid diverticulitis is left sided abdominal pain with or without an associated mass, fever, and leukocytosis. Patients generally resolve with antibiotics and may experience recurrent attacks. This group of patients is regarded as uncomplicated diverticulitis but guidelines for their further management remain nebulous. Another manifestation is smoldering disease that only partially resolves with antibiotics and medical therapy. Such patients have recurrent symptoms that can manifest with ongoing low grade fever and left sided abdominal pain. These patients along with the third presentation, complicated diverticulitis require surgical intervention. Complicated diverticulitis includes patients presenting with obstruction, mass/abscess, fistula, perforation.

Computerised Axial Tomography (CT) is considered the imaging modality of choice for the diagnosis of sigmoid diverticulitis, with a sensitivity varying from 85% - 97% and specificity 77%.(4) CT scanning confirms a diagnosis of diverticular disease but is also helpful in excluding other intra-abdominal clinical entities. The differential diagnosis of suspected acute diverticulitis includes acute appendicitis, bowel obstruction, colorectal cancer, gynecologic disease, inflammatory bowel disease, irritable bowel syndrome, ischemic colitis and pyelonephritis. The most important diagnosis to exclude on initial presentation is colorectal cancer. After resolution of a presumed attack of diverticulitis an en6

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doscopic examination of the colon should be carried out to exclude the presence of malignancy or Crohnâ&#x20AC;&#x2122;s disease, as recommended by the American Society of colon and Rectal Surgeons published practice parameters for the management of sigmoid diverticulitis 2006.(5)

Ambrosetti and colleagues first proposed a system for classifying the severity of diverticulitis based on CT findings to guide clinical management. CT findings consistent with mild diverticulitis included localized wall thickening (>5mm) and inflammation of the pericolic fat. Severe CT findings were the combination of localized wall thickening and inflammation of the pericolic fat with abscess, extraluminal air or extraluminal contrast. They noted that patients with severe CT findings underwent operative intervention more frequently than those patients with mild findings (33% vs 15%). Patients younger than 50 years of age with severe findings on CT scan were also more likely to have recurrences or complications.(6)

The traditional Hinchey classification was based on the degree and extent of the abdominal and pelvic disease identified at the time of surgery and associated with perforated diverticular disease of the colon. CT findings that are relevant to clinical management were re-classified into a classification system based on the Hinchey classification system:

Modified Hinchey Classification System (7)

Stage 0

Mild clinical diverticulitis

Stage Ia

Confined pericolic inflammation â&#x20AC;&#x201C; phlegmon

Stage Ib

Confined pericolic abscess (within sigmoid mesocolon)

Stage II

Pelvic, distant intra-abdominal or intra-peritoneal abscess

Stage III

Generalised purulent peritonitis

Stage IV

Fecal peritonitis

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Kaiser and colleagues found that disease severity using the modified CT Hinchey classification system correlated with post-operative morbidity and mortality.

They also found that the CT stage correlated with recurrence when patients were managed non-operatively. The presence of a diverticulitis â&#x20AC;&#x201C; associated abscess was one particular factor that was highly associated with risk of failure of non-operative management. They suggested that patients who were admitted with a diverticular abscess should receive strong consideration of an elective resection.(8)

Uncomplicated acute sigmoid diverticulitis is subjected to non-operative management. Bowel rest and broad spectrum antibiotics are the main stays of non-operative management of acute diverticulitis. While antibiotic treatment is important the specific intensity and duration of treatment are relatively uncertain. The flora of the colon is polymicrobial, but predominantly anaerobic and gram negative. Therefore, a broad spectrum antibiotic with coverage of anaerobic bacteria is intuitively necessary. Relatively few studies have addressed which antibiotic regime is most prudent. Kellum et al compared cefoxitin to gentamicin/clindamycin and found similar efficacy in a study of 51 patients.(9) In another study by Ridgway et al oral ciprofloxacin was found to be non inferior when compared to intravenous metronidazole.(10) Most recently, Schug â&#x20AC;&#x201C; Pass et al analysed a 4 day vs a 7 day course of intravenous ertapenam in the inpatient treatment of acute diverticulitis and found them to be equivalent.(11) Given this relatively modest guidance from evidence the appropriate antibiotic course generally consists of intravenous antibiotics until discharged, then a 10-14 day course of an oral equivalent.(11)

Although bowel rest is widely practiced there is no randomized trial of the impact of bowel rest on the natural history of acute diverticulitis. It seems common sense to avoid passage of fecal matter across an inflamed colon (and necessarily micro 8

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perforated). Given this absence of evidence, the use of bowel rest is empiric.

The vast majority of patients hospitalized for acute non complicated acute diverticulitis will improve on medical therapy. A patientâ&#x20AC;&#x2122;s clinical course may deteriorate despite appropriate conservative measures. These patients are clear indications for repeat imaging to identify an abscess or consider surgical intervention.

The risk of recurrence in patients with uncomplicated acute diverticulitis treated non operatively is reported to be between 7-25% with the risk of recurrence increasing with each subsequent episode .(12,13) In one study by Parks, 25% of 317 patients admitted with a diagnosis of acute diverticulitis were readmitted with a second episode. Other findings were that with each recurrent attack the patient is less likely to respond to medical therapy (70% chance the patient will respond with the first episode as compared with 6% chance of responding with the third episode). On account of this, it is recommended that after two attacks of uncomplicated diverticulitis resectional surgery is recommended.(14) This has been the basis for the practice parameters outlined by the ASCRS in 2000. The same advice was given by Stollman et al in 2004 but with the conclusion of Parks as the only supporting evidence.(15)

Faramakis et al in a questionnaire survey of 120 patients, revealed that at 5 years following hospital admissions for complicated diverticulitis: 10 patients had died from further recurrent complicated diverticulitis, 40 of the remaining 110 were still symptomatic. Of 77 patients initially managed by sigmoid resection only 2 were symptomatic, while 37 of 43 patients managed conservatively were symptomatic.(16) These findings and those of Parks are the only evidence that has been used to support the oft repeated recommendations of elective sigmoid elective resection after acute sigmoid diverticulitis. The clinical relevance of this recommendation is that further attacks may result in complicated diverticulitis 9

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(abscess, fistula, obstruction, bleeding or perforation). Overall mortality rates associated with surgery for these complicated scenarios are high and range between 6% and 17% .(17) Prophylactic surgical resection would thus prevent serious complications including the need for emergent operations and a colostomy.

Current studies report slightly lower recurrent rates than previously published and dispute prior beliefs that patients with recurrent diverticulitis are at an increased risk of complicated disease and higher mortality rates. In a retrospective review by Eglinton et al, 503 patients with acute diverticulitis were followed for a median of 8.4 years. Uncomplicated diverticulitis was diagnosed in 337 patients in whom 95% were managed non- operatively. Patients managed non-operatively had an overall recurrence rate of 23.4% with only 18.8% of patients experiencing a single recurrent episode and less than 5% with more than one episode of recurrence. Complicated diverticulitis developed in 5% with 3.1% requiring surgical management and no deaths were recorded.(15)(18) Pittet et al performed a retrospective cohort study of 271 patients admitted with diverticulitis and confirmed by CT. Patients were divided into two groups comparing 202 patients with an initial episode of diverticulitis to 69 patients with recurrent diverticulitis, conservative management was equally successful in both groups (89.2% vs 90%). Patients in the recurrent group were also shown to have less risk of requiring operative intervention and no mortality.(19)

Based on data from retrospective studies and case series recurrent episodes were considered as less likely to respond to medical therapy, leading to complicated diverticulitis and high mortality.(20,21) These findings have been refuted by Anaya and Flum.(22) They reported a population based study that identified over 25,000 patients with an initial episode of diverticulitis using a state wide hospital discharge database. Of the 20,136 patients treated non-operatively only 5.5% required readmission for recurrence, followed by emergency colectomy or 10

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colostomy. Thirty day mortality for the emergency case group was 3.1%, significantly less than the percentage reported by previous studies. In accordance with the above noted reports, numerous studies support the conclusion that recurrence of diverticulitis is no longer associated with risk of medical failure, increased risk of complicated disease or higher mortality.(23,24,25)

Despite the concerns expressed in previous reports that recurrent episodes of acute diverticulitis may result in complicated diverticulitis and higher mortality, a growing body of evidence demonstrated that perforated diverticular disease most commonly occur in the initial episode of diverticulitis. In contrast, those patients who develop complicated disease during a recurrent episode tend to present with pericolic abscess or phlegmon rather than perforation.(26) A study by the Mayo clinic demonstrated that patients with no prior history of diverticulitis had a higher likelihood of presenting with perforation and a higher mortality and morbidity compared to patients with one or more prior episodes.

In

addition, those patients with multiple episodes of diverticulitis who developed complicated disease tended to have similar mortality rates compared to patients undergoing elective resection.(27) These recent findings have altered surgical practice such that sigmoid resection for acute diverticulitis is not routinely offered after the initial or following a second attack of acute diverticulitis. In fact, the guidelines for surgery have been revised and the ASCRS 2006 currently states that the number of attacks of uncomplicated diverticulitis is not necessarily an overriding factor in defining the appropriateness of surgery.(27) European communities have also had a similar view and these reports have changed the practice parameters there as well.(28)

If previous practice recommendations of elective sigmoid colectomy after two episodes of non complicated acute diverticulitis were true, the current recommendations would result in a higher incidence of complicated diverticular dis11

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ease. Ricciardi et al demonstrated that changing practice patterns reflected a decline in colectomies performed for uncomplicated diverticulitis from 17.9% in 1991 to 13.7% in 2005 and for complicated diverticulitis from 71% in 1991 to 55.5% in 2005. In contrast the proportion of free diverticular perforations remained stable.(3) Given that most patients with complicated diverticulitis are likely to present to hospital during their first episode of symptoms the stable rate of perforated diverticulitis is not surprising. This adds further evidence that prophylactic surgery for recurrent diverticulitis to prevent future diverticulitis complications is unsubstantiated. One of the major reasons cited for offering elective resection is to eliminate the risk of recurrent disease, however, elective resection does not eliminate the risk of recurrent disease as recurrence rates after elective surgery have been reported between 8 and 12%.(29,30)

In the case discussed here, on review after colonoscopy the patient was advised about lifestyle measures (ensure adequate roughage and fiber in his diet, and maintain an ideal body weight). No routine follow up was planned but an open review in the outpatients was allowed. However, this patient being 50 years of age belongs to a controversial group as far as further management of his diverticular disease is concerned. Several authors have proposed that patients younger than 50 years of age present with a more virulent form of diverticulitis.

In fact, previous recommendations have advocated elective sigmoid resection for young patients after one established attack of diverticulitis.(31)

Although younger men are proposed to have severe diverticulitis much more than older men, they require operative intervention less often.(32) In a more recent series, patients younger than 50 years of age were found to present more frequently with evidence of severe disease on abdominal CT. However, these results did not give insight into long term outcomes.(33)

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Although there is some evidence that young patients appear with a more virulent form of the disease, it is not clear that these patients would go on to have a recurrence. In a study by Guzzo and Hyman, one patient out of 196 young patients (less then 50 years) had a free perforation after medical management of diverticulitis after a median follow up of five years.(25) Chautems et al in a prospective study identified that younger patients were more likely to experience persistent or recurrent disease with increased severity of disease on CT.(34) Severe CT abnormalities such as abscess, stenosis, or fistula were factors of poor outcome. When stratified by severity of disease, age failed to reach significance as a predictor of outcome and most patients did not experience further complications nor did they require emergency surgery. Furthermore, mortality due to diverticular complications was reported as zero with a median follow up of 9.5 years. Whereas for older patients, death was related to previous co-morbidity and a severe degree of peritonitis, mostly related to their first episode of diverticulitis, mortality of younger patients was due to complications from the surgical procedure itself, that is, anastomotic leak.(35) The dictum that diverticulitis in young patients has a more virulent course has been further challenged: Vignati and colleagues noted that younger patients with diverticulitis had an identical clinical course compared with older patients .(36) Salem and Flum have noted that younger patients had no different rates of conservative management, need for emergency operation, or mortality.(37)

Despite conflicting evidence among various studies regarding the risk of recurrence in younger patients after non-operative treatment the rates of recurrence and complications appear small. Consequently, the evidence supporting that the more aggressive nature of acute diverticulitis requires more aggressive surgical care probably requires more convincing data.

Laparoscopic surgery is increasingly preferred in the elective surgical treatment 13

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of sigmoid diverticular disease. Several single institutional series have confirmed the feasibility and safety of the laparoscopic approach.(38) Further support for the laparoscopic approach for sigmoid colectomy was provided by a prospective randomized double blinded study. This study accrued 104 patients and patients were similar with respect to gender, age, body mass index, co-morbidities, indications for surgery and previous surgical procedures. The results indicated a conversion rate of 19% and mortality of 1%, significant reduction in pain and need for systemic analgesic requirements, decreased hospital stay, and improved quality of life on short term SF-36 questionnaires. There was a significant reduction of major complications defined as a composite inclusive of intra-abdominal abscess, anastomotic leakage, pulmonary embolism and myocardial infarction. Major complications combined for a 25% rate after open surgery versus 10% after laparoscopic procedures.(39) With increased exposure and training, further implementation of the laparoscopic approach to sigmoid colectomy is likely. Contemporary proponents of surgery after two attacks argue that earlier surgery favorably impacts patients symptoms and that an increased number of diverticulitis attacks proportionally increases the conversion rates at the time of elective laparoscopic sigmoid resection.(40,41)

Considering the available evidence by published articles, early elective surgery following recurrent non complicated diverticulitis would have a minimal effect on preventing diverticular perforations and emergency surgeries. No doubt some patients may have multiple episodes and continue to experience pain or seek medical attention. Salem et al conducted a study to evaluate lifetime risks of death and colectomy care and costs and quality of life associated with elective colectomy after subsequent episodes of diverticulitis. It appears that expectant management through three episodes of acute non complicated diverticulitis with elective colectomy after the fourth episode is associated with lower rates of death and colostomy and is cost saving for both younger and older patients.(42) 14

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It is commendable that the single report by Parks has influenced the treatment protocol for acute diverticulitis for such a long time. However, the diagnostic armamentarium has changed significantly since his report. The advent of CT, multiple antibiotics and better understanding of the disease patterns related to acute diverticulitis have changed modern practice.

CONCLUSION The number of attacks of uncomplicated diverticulitis is not necessarily an overriding factor in defining the appropriateness of surgery. The indication for surgery should be influenced by the age, and medical condition of the patient, the severity and frequency of the attacks and the presence of ongoing symptoms. The current evidence has demonstrated that most patients who present with complicated diverticulitis will have complicated disease on the first attack and that resection from uncomplicated diverticulitis does not prevent the development of complicated diverticulitis. Patients under the age of 50 years are at no greater risk of recurrent attacks of complicated or non complicated diverticulitis and should be treated as their older counterparts.. Thus the indications for elective sigmoid resection are determined by the severity of disease, the risk of subsequent attacks of diverticulitis and complications of the disease in addition to the age, and other co-morbidities of the patient.

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2. Jacobs DO. Clinical practice. Diverticulitis. N Engl J Med 2007; 357: 2057- 66.

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11. Schug-Pass C, Geers P, Hügel O, et al. Prospective randomized trial comparing short-term antibiotic therapy versus standard therapy for acute uncomplicated sigmoid diverticulitis. Int J Colorectal Dis 25:751-759, 2010 12. Janes SE, Meagher A, Frizelle FA. Management of diverticulitis. BMJ 2006; 332:271-275.

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15. Stollman N, Raskin JB. Diverticular disease of the colon. Lancet 2004; 363: 631–639.

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Seminars Colon Rectal Surg 2011; 22: 180-188.

18. Eglinton T, Nguyen T, Raniga S, et al. Patterns of recurrence in patients with acute diverticulitis. Br J Surg 2010; 97:952-957.

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A CASEBOOK OF TWENTY SURGICAL CASES 19. Pittet O, Kotzampassakis N, Schmidt S, et al. Recurrent left colonic diverticulitis episodes: More severe than the initial diverticulitis? World J Surg 2009;33:547-552.

20. Hackford AW, Schoetz DJ Jr, Coller JA, et al. Surgical management of complicated diverticulitis. The Lahey Clinic experience, 1967 to 1982. Dis Colon Rectum 1985; 28:317-321.

21. Moreaux J, Vons C. Elective resection for diverticular disease of the sigmoid colon. Br J Surg 1990; 77:1036-1038.

22. Anaya DA, Flum DR. Risk of emergency colectomy and colostomy in patients with diverticular disease. Arch Surg 2005; 140: 681-685.

23. Kotzampassakis N, Pittet O, Schmidt S, et al. Presentation and treatment outcome of diverticulitis in younger adults: A different disease than in older patients? Dis Colon Rectum 2010; 53:333-338.

24. Hjern F, Josephson T, Altman D, et al. Outcome of younger patients with acute diverticulitis.

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25. Guzzo J, Hyman N. Diverticulitis in young patients: Is resection after a single attack always warranted? Dis Colon Rectum 2004; 47:1187-1190.

26. Hall J, Hammerich K, Roberts P. New paradigms in the management of diverticular disease.

Curr Probl Surg 2010; 47(9): 680-735.

27. Rafferty J, Shellito P, Hyman NH, et al. Practice parameters for sigmoid diverticulitis. Dis Colon Rectum 2006; 49: 939-44.

28. Anderson JC, Bundgaard L, ELbrond H, et al. Danish national guidelines for treatment of diverticular disease. Dan Med J 2012; 59(5): C4453.

29. Thaler K, Baig MK, Berho M, et al. Determinants of recurrence after sigmoid resection for uncomplicated diverticulitis. Dis Colon Rectum 2003; 46:385-388.

30. Thörn M, Graf W, Stefànsson T, et al. Clinical and functional results after elective colonic resection in 75 consecutive patients with diverticular disease. Am J Surg 2002; 183:7-11.

31. Wong WD, Wexner SD, Lowry A, et al. Practice parameters for the treatment of sigmoid diverticulitis – supporting documentation. In: The Standards Task force. The American Society of Colon and Rectal Surgeons. Dis Colon Rectum 2000; 43: 290-7.

32. Ambrosetti P, Robert JH, Witzig JA, et al. Acute left colonic diverticulitis: a prospective analysis of 226 consecutive cases. Surgery 1994; 115(5): 546-50.

33. Hall JF, Roberts PL, Ricciardi R, et al. Colonic diverticulitis: Does age predict severity of disease on CT imaging? Dis Colon Rectum 2010; 53(2): 121-5.

34. Chautems RC, Ambrosetti P, Ludwig A, et al. Long-term follow-up after first acute episode of sigmoid diverticulitis: Is surgery mandatory? : A prospective study of 118 patients. Dis Colon Rectum 2002; 45:962-966.

35. Chapman JR, Dozois EJ, Wolff BG, et al. Diverticulitis: A progressive disease? Do multiple recurrences predict less favorable outcomes? Ann Surg 243:876-830, 2006 [discussion 880883] 36. Vignati PV, Welch JP, Cohen JL. Long- term management of diverticulitis in young patients.

Dis Colon Rectum 1995; 38: 627- 9.

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A CASEBOOK OF TWENTY SURGICAL CASES 37. Salem L, Flum DR. Primary anastomosis or Hartmannâ&#x20AC;&#x2122;s procedure for patients with diverticular peritonitis.? A systematic review. Dis Colon Rectum 2004; 47: 1953-1964.

38. Stocchi L . Current indications and role of surgery in the management of sigmoid diverticulitis. World J Gastroenterol 2010 February 21; 16(7): 804-817.

39. Klarenbeek BR, Veenhof AA, Bergamaschi R, et al. Laparoscopic sigmoid resection for diverticulitis decreases major morbidity rates: a randomized control trial: short-term results of the Sigma Trial. Ann Surg 2009; 249: 39-44.

40. Makela JT, Kiviniemi HO, Laitinen ST. Elective surgery for recurrent diverticulitis. Hepatogastroenterology 2007; 54: 1412-1416 41. Cole K, Fassler S, Suryadevara S, et al. Increasing the number of attacks increases the conversion rate in laparoscopic diverticulitis surgery. Surg Endosc 2009; 23: 1088-1092.

42. Salem L, Veenstra DL, Sullivan SD, et al. The timing of elective colectomy in diverticulitis: A decision analysis. J Am Coll Surg 2004; 199:904-912.

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2.

LAPAROSCOPIC VENTRAL HERNIA REPAIR Coming of age.

INTRODUCTION The repair of ventral hernias remains one of the most common operations performed by general surgeons. Despite the frequency with which this procedure is performed the ideal approach to repair is yet to be agreed upon. Generally ventral hernias are acquired, but the majority is accounted for by incisional hernias. Causation of incisional hernias is multifactorial and these hernias contribute importantly to the long term morbidity of conventional surgery. Until techniques for the prevention of hernias are established, repair of these defects will remain an important problem for all abdominal surgeons.

Many hernia repair methods have been described. Traditional primary repair entails a laparotomy with suture approximation of strong fascial tissue on each side of the defect. However, recurrent rates after this procedure range from 41-52% during long term studies. Herniorrhaphies in which large prosthetic meshes are implanted appear to have lower failure rates. The best results seem to be if the mesh is placed in a retro-rectus position: the Rives-Stoppa-Wantz Repair. While the use of prosthetic meshes has been rewarded by lower failure rates the required dissection of wide areas of soft tissue contributes to an increased incidence of wound infections and wound related complications. Laparoscopic Ventral Hernia Repair (LVHR) is a recent development that has been shown to be an effective way of treating ventral hernias. This minimally invasive approach is based on the same physical and surgical principles as the open underlay procedure of the Rives-Stoppa-Wantz repair. It offers shorter hospital stay, improved patient outcomes, and fewer complications than traditional open 19

A CASEBOOK OF TWENTY SURGICAL CASES

procedures.

Despite a trend in popularity acceptance by the surgical community has been challenging. The technique is itself evolving and as such has inherent controversies. Two cases of ventral hernia repairs are described, one laparoscopic and the other open. This is followed by a discussion on the challenges and related controversies associated with laparoscopic ventral hernia repair and its outcomes.

CASE 1 History: A 44 year old nuts vendor complained of intermittent sharp epigastric pain over 6-8 months. This pain was worse on physical exertion, particularly on lifting of heavy objects. He experienced no vomiting or constitutional symptoms. He reported feeling a lump on the upper midline area of the abdomen.

This lump he could reduce in a recumbent position.

Systematic enquiry was otherwise non-contributory. The patient reported no past medical or surgical history. He had no allergies and smoked 10-12 cigarettes per day for the past 20 years.

Physical examination: A well looking gentleman; Vital signs BP 124/64 mmHg, P 68min-1, RR 18min1.

Cardiorespiratory examination was normal. Abdominal examination revealed a doughy lump (5 x 4 cm) in the mid-epigastric area. The lump was irreducible and associated with mild tenderness on deep palpation. Otherwise the abdomen was soft with no organomegaly or other masses. Other hernia orifices were clinically normal. Bowel sounds were present and normal. Digital rectal examination revealed normal anal tone, light brown stool within and palpably normal mucosa.

20

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A clinical diagnosis of an epigastric hernia was made and the patient was prepared for a laparoscopic VH repair.

Investigations: Hb 14.2 gdl-1, WCC 10 x 103 /Âľl, Plt 302 x 103 /Âľl, HbA1C 4.9%, Normal renal function.

CXR: Normal cardiac silhouette and lung fields.

ECG: Normal sinus rhythm

Surgical Treatment: The patient was admitted electively and kept nil per oral the night before surgery. The abdomen was shaved on the morning of surgery.

After a general anaesthetic was administered a nasogastric tube was passed as well as a Foley catheter. The arms were tucked to the sides and the abdomen was cleaned and draped.

A pneumoperitoneum was created with the aid of a 12mm optical port inserted in the lateral left abdomen. Three further ports were inserted (left subcostal, left iliac fossa, right lateral).

Findings: a hernia defect was identified in relation to the clinical finding. This contained a knuckle of omentum. Other smaller divets were noted superior and inferior to the main defect.

The omentum was taken down and a Dual mesh placed to effect the repair. The size was determined by estimating the dimensions from the outside using needle markers. The mesh was introduced via the 12mm port and fixed in place with 2 rows of spiral staples (Covidien Protack Fixation device 5mm) and transfascial sutures (Goretex suture No. 5). After careful inspection for bleeding and any inadvertent injury the pneumoperitoneum was released under direct vision. (see 21

A CASEBOOK OF TWENTY SURGICAL CASES

Fig 1)

Post-operatively the Foleyâ&#x20AC;&#x2122;s catheter and nasogastric tube were removed. Once the patient was fully awake he was allowed to have diet, sit and ambulate.

He was discharged 5 days later and reviewed in the clinic 1 week following discharge. By this time the pain was much better and the skin incisions were healed.

After 6 months of follow up he reported no complaints and had started vending 1 month post operatively.

CASE 2 History: A 72 year old woman presented with an incisional hernia. This lady who is hypertensive had an open appendicectomy in her thirties. She had good exercise tolerance and her blood pressure was well controlled.

Physical examination: Vital signs: BP 144/80 mmHg, P 88, RR 18 min-1, T 36.50C Cardiorespiratory examination was normal.

Abdominal examination revealed a 6cm swelling along the midline scar. This was reducible and revealed a 3cm defect.

Pre-operative blood tests and ECG were normal. The patient was consented for an open repair of incisional hernia.

Surgical procedure: (Fig 2 & Fig 3) An incision was made along the previous scar and the hernia neck defined. Further dissection revealed smaller defects along the previous scar. The subcutaneous dissection was extended to a 10cm diameter to allow appropriate coverage 22

A CASEBOOK OF TWENTY SURGICAL CASES

with prolene mesh. The midline fascia was re-approximated with 1prolene in continuous fashion. The herniorhaphy was effected with onlay placement of prolene mesh fixed with 2/0 prolene sutures.

Postoperative course: The patient was discharged on day 5 on simple analgesics (Paracetamol). On review in the outpatient department 4 weeks later she presented with a seroma.

This required multiple aspirations over the next 4 weeks at which point it settled.

Fig 1: Dressings on port sites and transfascial suture sites. Minimal soft tissue injury compared to the extensive dissections done for open repairs

23

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Fig 2: Extensive dissection to define herniation and allow mesh placement

Fig 3: Onlay placement of Prolene mesh

24

A CASEBOOK OF TWENTY SURGICAL CASES

DISCUSSION The repair of ventral hernias (VH) remains one of the most common operations performed by general surgeons. Despite the frequency with which this procedure is performed, there is little agreement and extensive controversy regarding the cause of most of these hernias or the ideal method to repair these problems.

Ventral herniation is a common long term complication of abdominal surgery.

Certain patient risk factors such as malnutrition, obesity, steroid use, type 2 diabetes, COPD and radiation therapy results in a predictably high incidence of ventral herniation. Other molecular disorders and cellular derangements in hemostasis, inflammation, and remodelling can impair wound healing and predispose patients to incisional hernia formation.(1) The exact incidence of incisional hernia formation after laparotomy is unknown but is estimated to be as high as 50%.(2) The magnitude of this problem is reflected in a 3-20% incisional hernia rate necessitating repair of approximately 90,000 ventral hernias annually in the US.(3)

Traditional primary repair entails a laparotomy with suture approximation of strong fascial tissue on each side of the defect. However, recurrence rates after this procedure range from 41-52%.(4) Recognising these unsatisfactory results, the concept of tension free hernia repair using synthetic polypropylene mesh was introduced by Usher and colleagues in the 1950s.(5) Since then the principles of tension free mesh reinforcement is considered the gold standard of all hernia repairs. The prosthetic can be placed superficial to the fascial closure (onlay), as a bridge secured to the fascial edges, (inlay) or underneath the fascia (underlay) in either a retro-rectus, pre-peritoneal or intra-peritoneal position.

While there are proponents of each technique Rudmik and colleagues in a review article of primary versus prosthetic repair of VH demonstrated that prosthetic mesh placement was more durable than primary repair when the mesh 25

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was placed in the underlay position.(7) This retro-rectus repair is referred to as the Rives-Stoppa-Wantz repair. With this technique consistently low recurrence rates of 0-14% has been reported with long term follow up.(8)

Open techniques require dissection of wide areas of soft tissue which contributes to an increased incidence of wound infections and wound related complications (12% or higher).(6) The continued search for lower recurrence rates with decreased morbidity led to the development of the minimally invasive or laparoscopic approach to ventral hernia repair. In 1993, Le Blanc and Booth were the first to report laparoscopic repair of an incisional hernia.(9) This technique is based on the same principles of the Rives-Stoppa-Wantz repair, in which mesh is fixed deep to the fascial defect with wide coverage, to the healthy abdominal wall fascia. Intra-abdominal pressure now acts to fix the mesh in place as forces are dispersed over the entire abdominal wall. The laparoscopic repair differs in that mesh is placed inside the peritoneal cavity rather than in the rectro-rectus position, without the associated soft tissue dissection. This reduction in soft tissue trauma results in a predictable reduction in wound morbidity and mesh infections. Additionally, the laparoscopic approach provides a unique internal view of the entire abdominal wall, enabling the surgeon to identify smaller remote sub-clinical defects.

After induction of general anesthesia the patient was positioned supine on the operating room table with arms tucked at the sides. Prophylactic antibiotics (against skin flora) are routinely given and an orogastric tube is placed for gastric decompression, as well as a Foleyâ&#x20AC;&#x2122;s catheter for decompression of the bladder. Pneumatic calf compression was employed. The abdomen was shaved, prepped, and draped widely to allow for the lateral placement of ports (anterior axillary line).

26

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Pneumoperitoneum was created via a 12mm dilating optical port on the left lateral aspect at the umbilical level. Three further ports were inserted (left subcostal, left iliac fossa, and right lateral). Ports are placed in the lateral abdominal wall, far enough away from the edge of the hernia defect such that the mesh being used in the repair does not overlap them. Lateral abdominal wall adhesions must be removed prior to port placement to avoid inadvertent injuries.(1)

All adhesions to the abdominal wall are lysed using blunt and sharp dissection. If electrocautery is used it should be done sparingly to avoid inadvertent thermal injury to the visceral organs. Adhesiolysis in the case described was done using the harmonic scalpel. Typically, a plane is developed between the abdominal wall and the adherent abdominal contents, which allows for safe and gentle dissection. This dissection must be performed with the utmost care to avoid causing, or more importantly, missing an injury to the bowel. Following adhesiolysis, the hernia contents are reduced. This can be achieved with a combination of external manual pressure and gentle traction using atraumatic laparoscopic graspers. In some cases, it may be necessary to extend the fascial defect with sharp dissection to adequately reduce the hernia contents. The viability of incarcerated bowel must be assessed and necrotic or non viable bowel must be resected.(1)

After the hernia contents are reduced the edges of the defect are identified and measured. The mesh to be used is then sized such that a 5cm overlap is achieved.

In the case described, the mesh size was determined by using needle markers on the outside. The size measurements can also be made intracorporally using a sterile plastic ruler or suture. One has to be aware of a few issues in relation to mesh sizing. The pneumoperitoneum stretches the abdominal wall. Also the outer circumference of the stretched abdomen is greater than that of the peritoneal surface. While wide coverage is the aim overzealous mesh could result in 27

A CASEBOOK OF TWENTY SURGICAL CASES

crumpling which may affect the dynamism of the abdominal wall and encourage adhesions. (1)

A 15cm x 10 cm dual mesh (Gore) was selected. Four cardinal sutures were placed and the mesh was then rolled and introduced into the abdomen via the camera port. The mesh was then unfurled and oriented. Using a transfascial suture passer the cardinal sutures were brought externally via a 3mm skin incision at the said cardinal points. These were subsequently tied to keep the mesh in place. A Covidien Protack Fixation device (5mm) was used to fix the mesh to the abdominal wall by making an inner and outer row of staples. The rows were 2-3cm apart and each tack was 1-2cm along each row. Additionally, transfascial sutures were placed with the aid of the needle passer via 3mm skin incisions in a clock-face fashion. The abdomen was then examined for any untoward bleeding or iatrogenic bowel injury. The 5mm ports were removed under direct vision and the abdomen was desufflated during which the mesh was inspected. The 12mm telescope port was then removed and the skin incision closed with 3/0 prolene suture in subcuticular fashion.

Although the laparoscopic technique provides many intuitive advantages, it still has certain technical challenges and internal controversies regarding best practice techniques that must be overcome. Further refinements in techniques concentrate on appropriate methods of sizing the mesh and introduction of the mesh into the abdomen as large pieces of mesh may not be amenable to introduction via a laparoscopic port.

One of the most highly controversial areas of laparoscopic ventral hernias is the appropriate method of mesh fixation. The concern is whether spiral tact fixation is sufficient or whether transfascial fixation sutures are needed. Early experience with spiral tacks alone was associated with a high recurrence rate.

28

A CASEBOOK OF TWENTY SURGICAL CASES

This was remedied by transfascial sutures to prevent mesh migrations. As such, Le Blanc and Booth advocated the routine use of transfascial sutures for LVH repair

(10,11)

. Many surgeons have adopted the use of transfascial sutures as in

the case presented here. The 5mm spiral tack is typically only 3.8mm in depth when applied. Most meshes are approximately 1mm thick and an appropriately placed tack typically has a 1mm cuff on the visceral side, only 1.8mm of tack is available to obtain purchase into the abdominal wall. Although most surgeons would agree that transfascial sutures are necessary, the exact number remains unknown. Further study is required to determine the spacing and intervals that would benefit LVH repair without compromise to the dynamism of the abdominal wall. Despite the obvious benefits, these extra sutures result in and can be the cause of significant early and long term pain (1). In the case presented here the patient experienced significant pain which limited his mobility and delayed his discharge as he required opiate analgesia.

Placement of the mesh in an intra-peritoneal location results in the bowel being in direct contact with the mesh. Polypropylene mesh is the most commonly used mesh for abdominal hernias. As far as intraperitoneal placement is concerned an ethos has developed that polypropylene should not be used as it is associated with long term risk of bowel erosion, fistula formation, and small bowel obstruction.(8) The evidence for this lies in individual experiences and case reports.(12,13) Even so the available literature is quite contradictory. Halm et al reviewed 335 patients who had prosthetic incisional hernia repair. In this study, 66 patients underwent re-laparotomy: of these 39 had intraperitoneal placement of mesh. Small bowel resections were required in 8 patients. Surgical site infections occurred in 10 patients while enterocutaneous fistula was rare.(14) Conversely, Vrijland et al on review of 136 patients with polypropylene incisional repair observed a 6% wound infection rate, with wound sinus formation in 2 patients. No enterocutaneous fistulae were noted and no complications 29

A CASEBOOK OF TWENTY SURGICAL CASES

required mesh removal.(15) In recognition of the possibility of these complications there has been an explosion of meshes unto the market in search of the ideal mesh for intraperitoneal placement. Most synthetic meshes available for intraperitoneal usage contain one side that faces the viscera with some design to reduce adhesion formation and the other side to promote good tissue ingrowth into the abdominal wall. In the case presented Dual mesh (Gore) was used.

This is an expanded PTFE (ePTFE) prosthetic with rough (Fascial component) and smooth (Visceral component ). Other bilayer meshes include(16):

NAME

FASCIAL

VISCERAL

_______________________________________________________________ C-Qur

Lightweight propylene

Omega & fatty acid

Composix Polypropylene ePTFE (smooth) Composix Ex

Lightweight polypropylene

ePTFE (smooth)

Dualex

ePTFE (rough)

ePTFE (smooth)

Parietex composite

Polyester

Collagen

Proceed

Lightweight polypropylene

Oxidized Regenerated cellulose

Sepramesh

Lightweight polypropylene

Hydrogel

Expanded PTFE is a common choice for laparoscopic VH due to a lack of reported bowel obstruction or fistula formation. A study sponsored by a Society of American Gastrointestinal Endoscopic Surgeonâ&#x20AC;&#x2122;s Grant compared pure ePTFE grafts with products combined with polypropylene. The product with polypropylene had significantly more intestinal adhesions and no greater abdominal wall ingrowth than the pure ePTFE products.(17)

Although there are extensive comparative studies evaluating different meshes, these are based on animal models. These data are repeatedly quoted by several authors with little if any human data available comparing the long term outcomes of different meshes. Recent reviews of reported case series demonstrate 30

A CASEBOOK OF TWENTY SURGICAL CASES

no clinical advantages to select one mesh over the other.(18,19) The controversy over the appropriate mesh continues especially since the various meshes designed for intraperitoneal placement has increased cost compared to polypropylene. While largely condemned by others(1) there are recent reports of the use of polypropylene to good effect in an intraperitoneal position for VH repair.

Yildirim et al. reviewed 25 patients who had ventral/incisional hernia repair with prolene mesh in an intra-peritoneal location. There were 4 local wound complications but unrelated to mesh. Long-term follow up revealed no recurrence or mesh related issues.(20) Similarly, Quadri et al. reviewed 80 patients in whom ventral/incisional hernia repair was effected with intra-peritoneal placement of prolene mesh via laparoscopic and open techniques. They identified superior short term outcomes with the laparoscopic approach and long term follow up identified no mesh related problems. These authors concluded that the use of prolene mesh was effective and notably cheaper than the numerous composite meshes on the market.(21) This is a point of note which may be relevant to most third world settings where health care costs are a major challenge. As for the present it would appear that while several options are available, no mesh is currently ideal. Most mesh selection is based on personal experience and anecdotal evidence as a paucity of human data is available comparing the long term outcomes of different mesh use.

The results of reported series so far indicate that laparoscopic ventral hernia offers the expected benefits of laparoscopy â&#x20AC;&#x201C; earlier discharge from hospital and less wound related complications. More specifically, the hernia recurrence rates are similar to those of the open approach.(22) However, in one meta-analysis post operative pain was noted to be similar to the open retro-rectus repair.(23) A Cochrane database review identified no difference in recurrent rates between open and laparoscopic surgery, a general trend towards shorter hospital stay and in some cases higher in-hospital costs. The most significant and consistent 31

A CASEBOOK OF TWENTY SURGICAL CASES

result was that laparoscopic surgery reduced the risk of wound infections.(24).

A recent assessment of quality of life following LVH repair showed that this approach was independently associated with more frequent discomforts, movement limitation and overall symptoms when compared with open VH repair at one month. As noted previously they also identified shorter length of stay and fewer infections with equal recurrent rates. In the short term, it would appear that laparoscopic VH repair was associated with a decreased quality of life.(25)

Despite the advantages of decreased wound complications in LVH repair seroma formation is one of the most common postoperative findings in both laparoscopic and open incisional hernia repairs. In large open hernia repairs, the resultant dead space beneath the skin flaps often is treated prophylactically by the placement of closed suction drains so that the resultant seroma is aspirated as it forms. In laparoscopy, because drains are not routinely placed, seromas are seen more often.(1) The presence of seroma is so prevalent, in fact, that many surgeons do not consider the occurrence of routine self-limited seromas as pathologic, reserving that description for seromas that require intervention (eg, drainage), that become infected, or that persist beyond a defined amount of time, usually 6 to 8 weeks.(1) Common practices include placing the patient in an abdominal binder postoperatively, and research has indicated significant reduction in seroma and hematoma formation with this method. Patients should be informed of this possible post-operative development and that it spontaneously resolves in some cases (1).

One interesting potential problem which has been noted in relation to the laparoscopic VH repair is that of small bowel injury. This generally occurs with adhesiolysis and reduction of bowel contents from the hernia sack. In one study, a recognized enterotomy was associated with a mortality of 1.7%. However this rate increased to 7.7% when the enterotomy was missed.(26) Although the 32

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impact of an enterotomy is significant, the outcome of a missed enterotomy is one of the most devastating complications. This is a known complication of re-operative surgery and therefore calls for vigilance and due care during the procedure. In addition, the surgeon must be clear about the possible strategies when a bowel injury occurs as the resultant peritoneal contamination introduces the potential for mesh sepsis with further morbidity and generally precludes use of a synthetic mesh. These include, opening the abdomen, repairing the injury, and performing a primary suture repair, which may require a biological mesh as re-enforcement or in certain circumstances placement of a synthetic mesh. Another option is to repair the injury laparoscopically, complete the adhesiolysis, admit the patient to the hospital and return to the operating room in 2â&#x20AC;&#x201C;6 days for laparoscopic mesh placement.(8) This situation also requires for the attendant surgeon to be skilled in both the laparoscopic and open techniques to effect repair. Other options include native tissue replacement using tensor fascia lata, gracilis, vastus lateralis, rectus femoris or latissimus dorsi muscle flaps. These flaps have variable recurrence rates and donor site morbidity.(8)

The most popular autologous tissue flap used is the abdominal wall component separation technique. This technique was first described by Ramirez and colleagues in 1990.(27) There are several variations but basically it involves gaining access to the lateral abdominal wall musculature, transecting the external oblique aponeurosis 2cm lateral to its insertion into the linea semilunaris, and separating the external oblique muscle from the internal oblique muscle in its avascular plane. The rectus abdominus complex then is advanced medially, creating a vascularized and innervated myofascial flap to cover the hernia defect.

This technique allows for up to 10 cm of unilateral myofascial advancement at the umbilicus.

It has been shown, based on widely quoted comparative studies, that with lapa33

A CASEBOOK OF TWENTY SURGICAL CASES

roscopic VH repair, wound complication rates, patient discomfort, length of hospital stay, time to return to normal activities and recurrent rates (0-11%) are all reduced.(28) Despite this, whether laparoscopic VH repair is the better option compared to open remains controversial. There are still unanswered questions which for now lack level 1 evidence to fortify the positions regarding the appropriate mesh, the appropriate fixation method, and although most authors express the need for wide mesh coverage: how wide is wide? Several articles have been reported in regard to these issues but suffer from methodological flaws, these include, small sample size, short term follow up, and variability in practice.

The heterogeneity in the multiple published articles makes it difficult to make hard general recommendations. These issues have developed reluctance among some general surgeons to adapt the laparoscopic method of repair for ventral hernias.(29)

As experience has been gained the laparoscopic ventral hernia repair is becoming more commonly employed. The indication for this procedure in some patient groups is somewhat controversial. The use of carbon dioxide as the insufflation agent during laparoscopy is a contraindication to laparoscopic herniorrhaphy for patients who have severe chronic obstructive pulmonary disease. Because even a relatively modest increase in afterload or decrease in preload would prove problematic, patients who have extremely poor cardiac reserve may be better served by an open approach or watchful waiting. (30)

Although the laparoscopic ventral hernia repair has been shown to decrease the inflammatory response to surgery, many surgeons remain reluctant to perform laparoscopic ventral hernia repairs in patients who are elderly. This is partly because of the concern of tolerating the hemodynamic and ventilatory changes associated with laparoscopy, and the longer operative times and frequent steep Trendelenburg position used during laparoscopic surgery.(8) Studies indicate 34

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though that this procedure is feasible and prospective studies may help identify patients at greater risk. Tessier and colleagues evaluated 97 patients undergoing laparoscopic ventral hernia repair with 76% of patients being older than 60 years. Although the older patients group (greater than or equal to 60 years) had more comorbidities, this group demonstrated comparable postoperative length of hospital stay and complication rates when compared with the younger group (younger than 60 yrs).(31) Another report by Lee et al conducted a retrospective study comparing the clinical outcome of 117 patients undergoing laparoscopic ventral hernia repairs with mesh in two age groups (younger than 55 years versus greater than or equal to 55 yrs). The postoperative complications were higher in the elderly group (12.9% versus 4.8%), and the recurrence rate was also higher in the older group (3.7% versus 1.6%). These differences, however, were not statistically significant. Despite these apparent differences between the two groups, the overall outcomes in the elderly patients were encouraging.(32)

Obesity has long been considered a risk factor for hernia formation and hernia recurrence, as it predisposes the patient for postoperative wound complications.

The extensive tissue dissection required for most open ventral hernia repairs can lead to tissue ischemia and necrosis, resulting in increased incidence of wound infection. Laparoscopic VH repair is regarded as being a relative contraindication in patients who are obese because of the perceived technical challenges and surgeon inexperience with a developing technique. With the improvement in technology and greater surgeon insight with this technically challenging group of patients it appears that the laparoscopic approach is feasible and may even be superior. Novitsky and colleagues reported the results of a large group of patients, in which 109 (67%) patients had BMIs greater than 35 kg/m2. In this study, the mean operative time was 178 minutes, and five patients (3%) required conversion to an open repair secondary to dense adhesions, small bowel enterotomy , inability to reduce an incarcerated omentum/bowel , and a fistula in a 35

A CASEBOOK OF TWENTY SURGICAL CASES

previously placed mesh . No perioperative mortality was noted in this study.

Twenty patients (12.3%) experienced postoperative complications that included persistent abdominal discomfort, urinary tract infections, pulmonary complications, and mesh infections. Two patients required removal of the prosthetic meshes because of wound infections. Although most patients experienced early postoperative wound seromas, they were managed conservatively and resolved without any interventions. The hernia recurrence rate was 5.5% after a mean follow-up of 25 months. This study suggested that prior failed ventral hernia repairs appear to be a predictive factor for future hernia repair failure in both nonobese and obese populations. Novitsky noted a hernia recurrence rate of 1.4% in his obese patients undergoing their first hernia repair, much lower than the 5.5% reported in the overall population. Therefore, the author advocates the use of laparoscopic approach in obese patients undergoing their initial hernia repair to avoid future failures of multiple open procedures. This has the great potential of reducing future patient morbidities associated with multiple failed repairs (33). Novitskyâ&#x20AC;&#x2122;s study was followed by another large study in which 901 patients were stratified into two groups of BMI greater (n= 134) or less (n= 767) than 40 kg/m2. The morbidly obese group had longer operative time (154 versus 119 minutes, P< 0.01) and hospital stay (3.6 versus 2.4 days, P = 0.03). The peri-operative complication rates in the two groups were comparable (19.7% versus 15.3%, P = 0.46). For a mean follow-up of 19 months, the hernia recurrence rate was 8.3% in the morbidly obese group and 2.9% in the non-morbidly obese group (P=0.003) (34). These two large studies indicated that laparoscopic repairs did not result in more adverse events in patients who are obese compared with non-obese patients. Overall several studies have reported peri-operative morbidities in the range of 3% to 31% and hernia recurrence rate of 0% to 7.8% in the obese population.(8)

36

A CASEBOOK OF TWENTY SURGICAL CASES

CONCLUSION Laparoscopic procedures are now a common part of the armamentarium of most general surgeons (example laparoscopic cholecystectomy, laparoscopic appendectomy, laparoscopic inguinal hernia repair). As experience increases, so will the interest in new and different procedures. The popularity of laparoscopic VH repair has increased in the last decade and has been extended to include patients thought to be at greater risk (e.g. elderly, obese). While the answer regarding the appropriate prosthetic and refinement in the technical aspects of the procedure are being identified, so far LVHR is at least as effective, if not superior to, the open approach in a number of outcomes.

37

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REFERENCES 1.Turner PL, Park AE. Laparoscopic repair of ventral incisional hernias: pros and cons. Surg Clin N Am 2008; 88: 85-100.

2. Anthony T, Bergen PC, Kim LT, et al. Factors affecting recurrences following incisional herniorrhaphy. World J Surg 2000;24:95–100.

3. Read RC, Yoder G. Recent trends in the management of incisional herniation. Arch Surg.

1989;124: 485-488.

4. Larson GM. Ventral hernia repair by the laparoscopic approach. Surg Clin NorthAm 2000; 80:1329–40.

5. Usher FC, Ochsner J, Tuttle LL Jr. Use of marlex mesh in the repair of incisional hernias. Am Surg 1958; 24(12): 967–74.

6. Leber GE, Garb JL, Alexander AI, et al. Long-term complications associated with prosthetic repair of incisional hernias. Arch Surg. 1998; 133:378-382.

7. Rudmik LR, Schieman C, Dixon E, et al. Laparoscopic hernia repair: a review of the literature. Hernia 2006; 10:110–9.

8. Jin J, Rosen MJ. Laparoscopic versus open ventral hernia repair. Surg Clin N Am 2008; 88: 1083–1100.

9. LeBlanc KA, Booth WV. Laparoscopic repair of incisional abdominal hernia using expanded poly tetrafluoroethylene: preliminary findings. Surg Laparosc Endosc 1993;3: 39–41.

10. LeBlanc KA. The critical technical aspects of laparoscopic repair of ventral and incisional hernias. Am Surg 2001; 67: 809–12.

11. LeBlanc KA, Booth WV, Whitaker JM, et al. Laparoscopic incisional and ventral herniorrhaphy: our initial 100 patients. Hernia 2001; 5: 41–5.

12.Kaufman Z, Engelberg M, Zager M. Fecal fistula: a late complication of Marlex mesh repair.

Dis Colon Rectum 1981; 24(7): 543-4.

13. Park A, Birch DW, Lovrics P. Laparoscopic and open incisional hernia repair: a comparison study. Surgery. 1998; 124:816–821; discussion 821–822.

14. Halm JA, de Wall LL, Steyerberg EW, et al. Intraperitoneal polypropylene mesh hernia repair complicates subsequent abdominal surgery. World J Surg 2007;31(2): 423-9.

15. Vrijland WW, Jekeel J, Steyerberg EW, et al. Intraperitoneal polypropylene mesh repair of incisional hernia is not associated with enterocutaneous fistula. Br J Surg 2000;87(3): 348-52.

16. Le Blanc KA. Incisional, epigastric and umbilical hernias. In: Current Surgical Therapy,10th edition. Editors: JL Cameron , AM Cameron.2011, Elsevier, Saunders.Philadelphia. pp 498.

17. Mathews BD, Mostafa G, Carbonell AM, et al. Evaluation of adhesion formation and host tissue response to intra-abdominal polytetrafluoroethylene mesh and composite prosthetic mesh. J Surg Res 2005;123(2): 227-34.

18. Eriksen JR, Gogenur I, Rosenberg J. Choice of mesh for laparoscopic ventral hernia repair.

Hernia 2007;11(6): 481-92.

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19. Kapischke M, Schulz T, Schipper T, et al. Open versus laparoscopic incisional hernia repair: something different from a meta-analysis. Surg Endosc 2008; 22(10): 2251-60.

20. Yildirim M, Engin O, Karademir M, et al. Is repair of incisional hernias by polypropylene mesh a safe procedure? Med Princ Prac, 2010; 19(2): 129-32.

21. Quadri SJ, Khan M, Wani SN, et al. Laparoscoic and open incisional hernia repair using polypropelene mesh- a comparative single centre study. Int J Surg 2010; 8(6): 479-83.

22. Forbes SS, Eskicioglu C, McLeod RS, et al. Meta-analysis of randomised controlled trials comparing open and laparoscopic ventral and icisional hernia repair with mesh. Br J Surg 2009; 96(8): 851-8.

23. Sajid MS, Bokhari SA, Mallick AS, et al. Laparoscopic versus open repair of incisional / ventral hernia: a meta-analysis. Am J Surg 2009; 197(1): 64-72.

24. Sauerland S, Walgenbach M, Habermalz B, et al. Laparoscopic versus open surgical techniques for ventral or incisional hernia repair. Cochrane Database Systematic Review, 2011;16(3):CD007781.

25. Colavita PD, Tsirline VB, Belyansky I, et al. Prospective, long term comparison of quality of life in laparoscopic versus open ventral hernia repair. Ann Surg 2012; 256(5): 714-23.

26. LeBlanc KA, Elieson MJ, Corder JM III. Enterotomy and mortality rates of laparoscopic incisional and ventral hernia repair: a review of the literature.

JSLS 2007;11:408–14.

27. Ramirez OM, Ruas E, Dellan AL. Components separation method for closure of abdominal wall defects: an anatomic and clinical study. Plast Reconstr Surg 1990;86:519–26.

28. Heniford BT, Park A, Ramshaw BJ, et al. Laparoscopic repair of ventral hernias: nine years experience with 850 consecutive hernias. Ann Surg 2003; 238(3): 391-9.

29. Alder AC, Alder SC, Livingston EH, et al. Current opinions about laparoscopic incisional hernia repair: a survey of practicing surgeons. Am J Surg 2007;194: 659–62.

30. Henny CP, Hofland J. Laparoscopic surgery: pitfalls due to anesthesia, positioning, and pneumoperitoneum. Surg Endosc 2005; 19: 1163–71.

31. Tessier DJ, Swain JM, Harold KL. Safety of laparoscopic ventral hernia repair in older patients. Hernia 2006; 10: 53–7.

32.Lee YK, Iqbal A, Vitamvas M, et al. Is it safe to perform laparoscopic ventral hernia repair with mesh in elderly patients? Hernia 2007; 10: 53–7.

33. Novitsky YW, Cobb WS, Kercher KW, et al. Laparoscopic ventral hernia repair in obese patients, a new standard of care. Arch Surg 2006; 141: 57–61.

34.Tsereteli Z, Pryor BA, Heniford BT, et al. Laparoscopic ventral hernia repair (LVHR) in morbidly obese patients. Hernia 2007; 12: 233–8.

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3. BLUNT DUODENAL INJURY A potentially complex injury with potentially simple solutions

INTRODUCTION Duodenal perforation following blunt abdominal trauma is an uncommon and often overlooked injury leading to increased mortality and morbidity. Duodenal injuries are found in only 3.7% of all laparotomies for trauma. This trend is likely to change given the increase in road traffic accidents and violent crimes noted in our society today which includes liberal use of guns and knives.

The anatomical location of the duodenum presents a challenge in diagnosing these injuries but also involves injury to other nearby organs (eg: pancreas, liver, inferior vena cava ). Surgical management of these patients is a considerable challenge where failure to do so properly may have devastating results.

The overall mortality rate of duodenal injuries continues to be significant with several series reported a range of 5.3% to 30%, with an average of 17%.

The duodenal contents are a mixture of gastric juice and enzymes with the perfect solution to digestion. This together with the passage of at least 6 litres of fluid on a daily basis makes the prospect of dehiscence of the duodenal repair a real one, with increased morbidity and sometimes mortality. The great majority of duodenal perforations may be managed with single surgical procedures.

Some cases however, comprise high risk lesions thought to have a higher risk of dehiscence and fistula rates. These high risk injuries are related to pancreatic injury, blunt or missile injury, involvement of more than 75% of the duodenal wall, injury of the first or second part of the duodenum, time interval between injury and repair of more than 24 hours and associated common bile duct injury.

On account of this several adjunctive operative procedures have been proposed 40

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in an attempt to reduce the incidence of dehiscence of the duodenal suture line.

A case of duodenal injury following blunt abdominal trauma is described followed by a discussion regarding the methods of repair of this duodenal injury and the role of adjunctive procedures which may prevent dehiscence.

CASE History: A 30 year old man presented with marked abdominal pain following a fall. He fell while riding a bicycle downhill. He hit himself with the bicycle handle, end on, in the right abdomen. This occurred 17 hours earlier. There was no loss of consciousness or respiratory distress.

He reported no allergies, no past medical or surgical history and had drunk 4 beers immediately before the incident.

Physical examination: Vital signs: BP 108/70 mmHg, P110min-1, RR 26min-1, T 378 0C, GCS: 15/15 Respiratory: Chest expansion was equal and spring test was negative. There was no subcutaneous emphysema, the trachea was central and breath sounds were vesicular and equal bilaterally.

Cardiovascular: Peripheral pulses were present and equal bilaterally. The capillary refill was <2secs. His heart sounds were normal.

Abdomen: A circular imprint was noted on the skin of the right upper quadrant (Fig 1). Palpation revealed generalised rebound and guarding. This was maximal in the upper abdomen. DRE revealed no blood.

The pelvis was clinically stable and no injury to the upper or lower limbs was present.

Investigations: Hb 12.05 g/dl, WCC 13.2 x 103/Âľl, Plts 314 x 103 /Âľl Na 132 mmol-1, K 4.1 mmol-1, BUN 10 mg/dl, Cr 1.0 mg/dl, Amylase 88 u.

41

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CXR: Lung fields were clear, with no features of hemo- or pneumo- thorax.

There were no bony injuries.

CT (abdomen and pelvis): Free fluid and pneumoperitoneum were noted. The solid organs, aorta and inferior vena cava were all intact. The gallbladder, small and large bowel appeared uninjured. The patient was resuscitated, consented and prepared for an emergency laparotomy.

Surgical Findings and Procedure There was 1.5l of heavily bile stained fluid within the abdomen. A hole noted on the transverse mesocolon lead to an injury (Grade III) of the second part of the duodenum . There were two traumatic enterotomies with an intervening bridge of somewhat devitalised duodenal wall. Beneath this bridge was the ampulla, from which bile was seen to be flowing. The hepatoduodenal ligament and pancreas were visually uninjured.

Mobilisation of the right colon and Kocherisation of the duodenum revealed heavy bile staining of the retroperitoneum (Fig 2) extending to the pelvic brim on the right side.

The repair involved: -Debridement of the duodenal injury (>50%) and primary repair in two layers with 3/0 vicryl.

- Tube decompression: A T Tube (15Fr) was placed distal to the repair and exited from the lateral wall of the third part of the duodenum. (Fig 3) -Pyloric exclusion was performed using a TA 60mm instrument and gastrointestinal continuity restored via a gastrojejunostomy. (Fig 4,5) -The retroperitoeum was debrided. Peritoneal lavage with 4l of warmed saline was done and two drains placed. One alongside the duodenum and exited the right abdomen, the other in the vicinity of the gastrojejunostomy and exited the 42

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left abdomen.

Postoperative Course The patient spent 48hours on the HDU and was then discharged to the ward.

He made steady improvement and was discharged after 10days (the two abdominal drains and urinary catheter were removed). Interestingly, during this time there was no drainage from the duodenal T tube and it was kept in place.

A contrast study was done via the T tube on day 28 which showed free flow of contrast within the duodenum with no leakage. The T tube was gradually pulled over the next two weeks.

The patient progressively improved and has been doing well, tolerating diet and has since returned to work.

Fig 1: Circular imprint of handle bar on abdomen

43

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Fig 2: Bile staining of the retroperitoneum

Fig 3: Repaired duodenal injury with lateral T tube duodenostomy

44

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Fig 4: Application of the TA stapler across the pylorus

Fig 5: Stapled pyloric exclusion

45

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DISCUSSION Penetrating trauma is the leading cause of duodenal injury in countries with a high incidence if civilian violence such as the USA and South Africa, where 75-80% of this trauma is due to gunshot wounds.(1) Blunt injury of the duodenum is both less common and more difficult to diagnose than penetrating injury and may occur in isolation or with pancreatic injury. It usually occurs from crushing of the duodenum between spine and steering wheel, handlebar, or some other force applied to the anterior aspect of the abdomen. Such injury may be associated with flexion/distraction fracture of L1 - L2 vertebrae (The Chance fracture). Physical blows (punches, kicks) to the mid epigastrium are also common. Less commonly, deceleration may produce a tear at the junction of the third and fourth parts of the duodenum and tears of the first and second parts have occasionally been reported.(1) These injuries occur at the junction of free (intra peritoneal) parts of the duodenum with fixed (retro peritoneal) parts.

A high index of suspicion, based on mechanism of injury and physical examination, may lead to further diagnostic studies.

Injuries to the duodenum are uncommon, occurring in only 3-5% of all abdominal injuries with an increasing worldwide trend noted with increase in road traffic accidents and use of firearms.(1,2) The retroperitoneal location of the duodenum and its close proximity to a number of other viscera and major vascular structures means that isolated injury of the duodenum is itself rare, particularly following penetrating trauma. The second portion of the duodenum is injured most commonly in 35% of cases. The third and fourth portions are each injured in approximately 15% of the cases, and the first portion in only 10%, while multiple injuries are seen in the remaining.(3)

In penetrating injury the need for abdominal exploration is usually dictated by associated injuries and the diagnosis of duodenal injury is usually made at lapa46

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rotomy. Duodenal injuries from blunt trauma continue to pose a diagnostic challenge. The organâ&#x20AC;&#x2122;s retroperitoneal location may produce minimal and vague symptoms such as abdominal, back, or flank pain. Pain radiating to the neck or testicles have also been reported.(3) The importance of early diagnosis was underscored by Lucas and Ledgerwood in 1975. They reported a mortality of 11% in patients with blunt duodenal trauma treated within 24 hours compared with a rate of 40% if the treatment was delayed for more than 24 hours.(4)

The ability to measure serum amylase levels is attractive and this may be used as supportive evidence for a possible duodenal injury as the leakage of duodenal contents may increase serum levels of amylase. The duodenum is retroperitoneal, the concentration of amylase in the fluid that leaks is variable and amylase levels often takes hours to days to increase after injury. Although serial determination of serum amylase is better than a single, isolated assay on admission, sensitivity is still poor and serial determination involves necessary delays in treatment. (5,6) If the serum amylase level is raised on admission, a diligent search for duodenal rupture is warranted. The presence of a normal amylase level, however, does not exclude duodenal injury.(1)

Radiological studies may be helpful in the diagnosis. Plain radiographs of the abdomen are useful when gas bubbles are present in the retroperitoneum adjacent to the right psoas muscle, around the right kidney or anterior to the upper lumbar spine. They may also show free intraperitoneal gas and although rarely seen, gas in the biliary tree has also been described.(3) Obliteration of the right psoas muscle shadow or fracture of the transverse processes of the lumbar vertebrae are indicative of forceful retroperitoneal trauma and serve as a predictor of duodenal injury.(7)

An upper gastrointestinal series using water soluble contrast material provides 47

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positive results in 50% of patients with duodenal perforations.(8) Meglumine (gastrograffin) should be infused via a nasogastric tube rather than swallowed and the study should be done in the right lateral position. If no leakage is observed, the investigation continues with the patient in the supine and then in the left lateral position. If the gastrograffin study is negative, it should be followed by administration of a barium contrast agent since it allows detection of small perforations more readily.(9) Upper gastrointestinal studies with contrast media are also indicated in patients with a suspected hematoma of the duodenum, because they may demonstrate the classic â&#x20AC;&#x2DC;coiled springâ&#x20AC;&#x2122; appearance of complete obstruction by the hematoma. (1)

Computed tomography (CT) has been added to the diagnostic armamentarium for subtle duodenal injury. It is very sensitive to the presence of small amounts of retroperitoneal air, blood or contrast agent extravasated from the injured duodenum, especially in children. (10) Its reliability in adults is more controversial.

Ballard et al reviewed the diagnostic features and injury pattern of 206 cases of blunt duodenal injuries. When CT was used as the primary diagnostic investigation, only 11% of cases were associated with extravasation of contrast while 22% of cases were normal. (11) The presence of periduodenal wall thickening or hematomas without extravasation of contrast material should be investigated with a gastrointestinal study using gastrograffin. If normal, it should be followed by a barium contrast study if the patientâ&#x20AC;&#x2122;s condition allows.

Exploratory laparotomy remains the ultimate diagnostic test if a high degree of suspicion of duodenal injury continues in the face of absent or equivocal radiographic signs. In the case described, CT demonstrated free intraperitoneal air and demonstrated features consistent with peritonitis. All patients undergoing a laparotomy for abdominal trauma should be explored through a long midline incision. Upper midline retroperitoneal hematomas should be explored to rule 48

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out underlying duodenal, pancreatic or vascular injury. It is wise to ensure that proximal and distal control of the aorta and distal control of the inferior vena cava, are readily available before the hematoma is explored. Mobilisation of the whole duodenum is mandatory for exclusion of duodenal injury. Initially the Kocher manoeuvre is performed by dividing the lateral peritoneal attachment of the duodenum and mobilising both the second and third parts medially with a combination of sharp and blunt dissections. Entry into the lesser sac by way of the gastrocolic ligament provides exposure of the posterior aspect of the proximal position of the first part of the duodenum and the medial aspect of the second part. Better inspection of the third part and inspection of the fourth part of the duodenum may be achieved by mobilising the ligament of Treitz, and performing the Catell and Braasch manoeuvre. This manoeuvre requires the mobilisation of the right colon (including the hepatic flexure) from right to left so that the right colon and small intestine may be elevated. The small bowel mobilisation is undertaken by sharply incising its retroperitoneal attachments from the lower right quadrant to the ligament of Trietz. Severe oedema, crepitations or bile staining of the periduodenal tissues implies a duodenal injury until proven otherwise. If the exploration of the duodenum is negative but there is still a strong suspicion of duodenal injury, Bootman et al recommended instillation of methylene blue through a nasogastric tube.(12) Rapid staining of periduodenal tissues is unmistakable evidence of an intestinal leak in this area, and the lack of staining, in their hands, has proven reliable in ruling out full thickness duodenal injury.

Duodenal injury are graded by the commonly accepted Organ Injury Scale of the American Association for the Surgery of Trauma(13):

49

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Duodenal injury severity scale.

Grade

Injury

(1)

Hematoma involving single portion of wall Laceration: partial thickness, no perforation

(11)

(III)

Hematoma involving more than 1 portion

Laceration: <50% circumference distribution

Laceration: disruption 50%â&#x20AC;&#x201C;75% circumference of 2nd portion Disruption 50%â&#x20AC;&#x201C;100% circumference of 1st, 3rd, or 4th portions

(IV)

Laceration: disruption of >75% circumference of 2nd portion Involvement of ampulla or distal common bile duct

(V)

Laceration: massive disruption of duodenopancreatic complex Duodenal devascularization

While this simple tabular description of the injury provides a quick working knowledge of the injury and provides some kind of standardisation, it is important to be aware of simple and more important features of the injury. This includes the timing of injury. As previously noted, this mortality increases with delay in treatment, the anatomical relation of the injury to the ampulla of Vater, the characteristics of the injury (simple laceration versus duodenal wall destruction), the involved circumference of the duodenum and associated injury to the biliary tract, pancreas or major vascular injury.

Division of the duodenum into a proximal portion (1st and 2nd parts) and distal portion (3rd and 4th parts), provides a practical approach to assessing and dealing with these injuries. The lower portion may generally be treated like small bowel where the injuries can be managed by debridement and closure or resection and re- anastomosis. The more proximal position has complex anatomical structures within it (common bile duct and sphincter of Oddi) and the 50

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pylorus. It requires distinct manoeuvres to diagnose injury (e.g. cholangiogram) and complex techniques to repair them. The first and second parts of the duodenum are densely adherent and dependent for their blood supply on the head of the pancreas. This makes diagnosis and management of any injury complex and resection of the duodenum impossible, unless involving the entire C loop and pancreatic head.

Optimal management of duodenal injuries requires a complete assessment for any associated injury to the pancreas as well as the bile duct and the ampulla.

Therefore, an injury to the duodenal sweep in the second portion must prompt an evaluation of these structures. This can be accomplished by a careful visualisation of the pancreatic head for hematoma or laceration. In the case presented, there was no visual injury to the pancreas or the structures within the hepato - duodenal ligament with bile noted to be flowing through the ampulla. Bile extravasation with a laceration in the area of the head of the pancreas may suggest an injury to the intrapancreatic portion of the bile duct or the ampulla. If there is a laceration to the second portion of the duodenum, injury to the adjacent portion of the pancreas and questionable integrity of the major pancreatic duct, intraoperative pancreatography is recommended in this hemodynamically stable patient. This is important as the presence of pancreatic duct injury influences the need for more complex procedures during this repair. (14).

The great majority (70-80%) of duodenal perforations may be managed with simple surgical procedures- debridement and primary suture repair. This is particularly true of penetrating injuries where the time interval between injury and operation is usually short.(15,16) The remaining injuries comprise cases considered to be high risk lesions. These injuries are regarded as having a higher likelihood of repair dehiscence with increased morbidity and mortality. Though there is some controversy regarding which injuries are classified as high risk or 51

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complex, a review of the literature indicates that the following factors may lead surgeons to consider an injury as severe: blunt trauma or bullet wounds, delay to repair exceeding 24 hours, injury to the first or second parts of the duodenum, duodenal injuries of AAST - OIS grade â&#x2030;Ľ III, associated injuries to the pancreas or common bile duct (or both) and compromised blood supply to the duodenum.

(2, 7, 9, 15)

For such injuries several adjunctive procedures have been proposed in

an attempt to the reduce the incidence of dehiscence of the duodenal suture line.

Closure of the duodenal injury should be oriented transversely, if possible to avoid luminal compromise, at the same time avoiding excessive inversion. Longitudinal duodenotomies may usually be closed transversely if the length of the duodenal injury is less than 50% of the circumference of the duodenum. If primary closure would compromise the lumen of the duodenum or tension of the repair, several options are available.

In a canine model, Kobbold and Thal described the use of a jejunal serosal patch to close the duodenal defect, where the serosa of a loop of jejunum was sutured to the edges of the duodenal defect. The authors found that the serosa exposed to the lumen had undergone a complete mucosal resurfacing at 8 weeks. (17) The clinical application of this technique for duodenal trauma has been limited and suture line leaks have been reported. The serosal patch was also advocated by others to reinforce the duodenal suture line. Although the addition of such a jejunal serosal patch to duodenal repair is attractive, its superiority over simple repair alone has not been documented.(3).

In complete transection of the duodenum, the preferred method of repair is primary anastomosis of the two ends after appropriate debridement and mobilisation. It is frequently the case with injuries of the first, third and fourth part of the duodenum that mobilisation is technically not difficult. However, if a 52

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large amount of tissue is lost, approximation of the duodenal ends may not be possible without producing undue tension on the suture line. If this is the case and complete transection occurs in the first part of the duodenum, antrectomy should be performed with closure of the duodenal stump and a Billroth II gastrojejunostomy. When such injuries occur distal to the ampulla of Vater, closure of the distal duodenum and Roux-en-Y duodenal-jejenal anastomosis is appropriate (3). Mobilisation of the second part of the duodenum is limited by its shared blood supply with the head of the pancreas. A direct anastomosis to a Roux-en-Y loop sutured over the duodenal defect in an end to side fashion is the procedure of choice. This may also be applied as an alternative method of operative management for extensive defects of the other parts of the duodenum when primary anastomosis is not feasible. External drainage should always be provided because it affords early detection and control of duodenal fistula (1).

In the high risk duodenal injury, repair is followed by a potentially increased incidence of suture line dehiscence. To protect the repair the gastrointestinal contents with their proteolytic enzymes may be diverted. This technique may make the management of a duodenal fistula easier.

Tube decompression was the earliest technique used for decompression of the duodenum and diversion of its contents in an attempt to preserve the integrity of the duodenorraphy. The technique was introduced for trauma by Stone and Geroni as a triple ostomy. This consists of a gastrostomy tube to decompress the stomach, a retrograde jejunostomy to decompress the duodenum and an antegrade jejunostomy to feed the patient. The initially favourable reports on the ability of this technique to decrease the incidence of dehiscence of the duodenorraphy has not been supported by more recent work (18,19). The drawbacks of the technique include several new perforations being made in the gastrointestinal tract, the inefficiency of the jejunostomy tube in decompressing properly the duodenum and the common scenario of the drain falling out or being removed 53

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by the patient.(9) In the case described, the T tube placed in the second part of the duodenum drained minimal for about 10 days.

Duodenal diverticulisation is another diversion procedure first described by Berne and associates in 1968 for the treatment of combined extensive injury to the duodenum and pancreas or severe injury of the duodenum alone. The operation consists of suture closure of the duodenal injury, gastric antrectomy with end to side gastrojejunostomy, tube duodenostomy and generous drainage in the region of the duodenal repair. Berne and associates reported in 50 patients with this procedure in 2 series. The duodenal fistula rate was 14% and overall mortality 16%. (3) In a more recent report from the same institution by Shorr et al, duodenal diverticulisation was used in 12 of 105 patients. Two of these patients developed duodenal fistulas and subsequently succumbed to septic complications, a mortality rate of 17%.

(20)

The main problem with duodenal diverticu-

lisation is that it is time consuming, ill advised in a hemodynamically unstable patient or when multiple injuries are present. Furthermore resection of a normal distal stomach cannot be beneficial and should not be considered unless there is a large amount of destruction and tissue loss and no other cause is possible.

Pyloric exclusion was devised as an alternative to diverticulisation to shorten the operative time and make the procedure reversible. After primary repair of the duodenal wound is achieved, a gastrotomy incision is made on the greater curvature over the antrum over its most dependent position, at a site suitable for a gastrojejunostomy. The pyloric ring is identified and grasped from inside the gastrotomy. It is then closed with a running suture of a nonabsorbable material such as polypropylene. As in the case described, an alternative is placing a staple line across the pylorus. A gastrojejunostomy is performed at the gastrotomy site. Irrespective of the method used to close the pylorus, care must be taken to avoid closure of the prepyloric antrum, as this causes increased gastrin secre54

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tions and elevated gastric acid output. The procedure was originally described

by Summers in 1903 and was first used clinically in the 1970â&#x20AC;&#x2122;s.(3)

The first large series of this procedure was reported by Vaughan and colleagues from Ben Taub Hospital : pyloric exclusion was used on 75% of 175 patients presenting with duodenal trauma and had a mortality rate of 19% and fistula formation rate of 5%. (21) This procedure has gained popularity and is regarded by many authors to offer the best combination of limited surgery in cases of severely injured patients, with effective exclusion of the duodenum until after healing has occurred. Several authors advocate the use of pyloric exclusion and consider it to be the procedure of choice for patients with severe duodenal trauma.(21,22,23,24) Martin et al managed 313 patients with duodenal trauma of which 128 with severe duodenal injuries were treated with pyloric exclusion and the duodenal fistula rate was 5.5% (two deaths due to fistulas occurred). (22).

Degiannis et al studied pyloric exclusion for treating severe penetrating injuries of the duodenum with a postoperative fistula rate of 43% among patients who received only primary repair and 12% among patients for whom pyloric exclusion was added to the surgical treatment. The authors concluded that Grade III duodenal injures due to gunshot wounds should always be treated with pyloric exclusion.(24) Cogbill et al reported on 27 patients managed with pyloric exclusion following duodenal injuries. In this study only 2 patients died secondary to duodenal complications (repair dehiscence and sepsis), thus suggesting that pyloric exclusion is a useful adjunct for more complex injuries.(19)

Despite the general acceptance of this procedure, there are still some internal controversies that are yet to be settled and some modifications of the technique have been described.

Vagotomy is not usually part of this surgical procedure. Some authors have ad55

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vocated for its addition as marginal ulceration as high as 10% have been noted.

(22,23)

In one authorâ&#x20AC;&#x2122;s experience, two patients without vagotomy presented with

either perforation or bleeding (23).

Ginzburg et al performed pyloric exclusion without gastrojejunostomy on four patients, in order to avoid the extensive surgical repair required so that they could focus on all the other associated injuries. They observed that spontaneous opening of the pylorus occurred and that the mean hospital stay was 29 days thus concluding that gastrojejunostomy should not be used routinely on patients undergoing pyloric exclusion (25).

The rate or timing of recanalisation of the closed pylorus is still not known. In addition, early or late complications are still not yet clearly defined. An experimental study was done on 30 rats subjected to pyloric exclusion with different occlusion suture materials and gastrojejunostomy with or without vagotomy. It was observed that non absorbable sutures maintained the pyloric closure for a longer duration (36.3 Âą 11.6 days) and that vagotomy reduced gastric inflammation without influencing the time when the pylorus should be re-opened. (26) In another study, Pierro et al compared the results from primary repair versus repair associated with pyloric exclusion and gastrojejunostomy to treat complex duodenal injuries in 24 dogs. They did not observe any differences in the incidence of duodenal stenosis, fistula formation, intra abdominal abscess or death between the two groups, but pyloric exclusion was a longer and more traumatic procedure, and it resulted in greater weight loss and increased incidence of vomiting among the animals. (27)

The foregoing discussion clearly refers to the situation where the patient is relatively stable and has either isolated injury or minimal surrounding injuries. The anatomical location of the duodenum and pancreas and the mechanism so in56

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volved in causing injury is associated with a high prevalence of vascular and solid organ injury which dictates damage control techniques. Arrest of active haemorrhage must be the primary concern for these patients, to prevent the development of the downward spiral of acidosis, hypothermia and progressive coagulopathy. Avoiding lengthy complex procedures during the initial operation is most important. For those with duodenal injury requiring a damage control procedure, the damaged duodenum in debrided, the ends sutured or tied off with surgical tape and dealt with at a planned re-operation. A feeding jejunostomy should be placed as early as possible to provide enteral nutrition. (3). More destructive injuries including the pancreas or biliary system indicates more complex procedures, which are not discussed here.

The most serious complication following the treatment of duodenal injury is the development of a duodenal fistula from suture line dehiscence. In a collective review of 15 series of 1408 patients with duodenal injuries, Asensio and colleagues noted a 0-17% incidence of duodenal fistula. Other complications reported with duodenal trauma include intra- abdominal abscess (10.9-18.4%), pancreatitis (2.5-14.9%), duodenal obstruction (1.1-1.8%), and bile duct fistula (1.3%). (15) The advent of pyloric exclusion has limited the duodenal fistula rate to an average of 5%.(16). These results seemed to have quelled the controversy regarding the most appropriate diversion procedure.

However, for all the comfort provided by the pyloric exclusion procedure, more recent literature may have once again raised new questions and concerns about the need for pyloric exclusion. A recent study by Seamon et al examined patients with penetrating duodenal injuries of grade â&#x2030;Ľ II and pancreaticoduodenal injuries, excluding patients who died within 48 hours due to massive associated injuries. Fifteen of 29 patients were treated without pyloric exclusion and 14 with exclusion, and the groups were similar with regard to sex, age, mecha57

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nism of injury, hemodynamic stability, injury grade (a trend toward greater injury severity was noted in the pyloric exclusion group), injury severity score associated abdominal injuries and mortality rate. None of these patients suffered a duodenal fistula. The results indicated a trend towards a higher overall complication rate in the pyloric exclusion group (71% vs. 33%) although this difference was not statistically significant. The same pattern was observed for the pancreatic fistula rate (40% vs. 0%) and the length of hospital stay (24.3 days vs. 13.5 days) and the in hospital mortality was similar in the two populations (21 vs. 17%). The authors concluded that simple repair without pyloric exclusion was both adequate and safe for most penetrating duodenal injuries and suggested abandonment of pyloric exclusion. There were several obvious significant study limitations here though. Most notably the small retrospective nature of the group, patients were not randomised and pyloric exclusion may have been offered to the higher risk patients as adjudged by the surgeon (28).

An earlier study by Rickard et al, demonstrated management of 30 duodenal injuries without recourse to any diversion procedures. As far as was possible in stable patients, duodenal injuries were debrided and treated by primary repair, resection and anastomosis or over sewn as part of a damage control procedures.

Four patients died a as result of multiple other injuries and required damage control procedures. There were 4 abscesses but no duodenal fistula and there was one case of duodenal stenosis. Theses authors advised against the use of pyloric exclusion and argued that the procedure probably offers little advantage over adequate nasogastric drainage when primary duodenal repair is carried out and is associated with increased operative time an additional intestinal anastomosis and increased risk of marginal ulcers. (29)

In a 2008 study from the US, the American College of Surgeons National Trauma Data bank evaluated adult patients with severe duodenal injuries (AAST â&#x2030;Ľ3) 58

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undergoing primary repair only or repair with pyloric exclusion within 24 hours of admission. Despite similar demographics pyloric exclusion was associated with a longer mean hospital stay (32.2 vs. 22.2 days p =0.003) and was not associated with a mortality benefit. In addition, a non-significant trend towards increased development of septic abdominal complications (intra-abdominal abscess, wound infection, dehiscence) was observed with pyloric exclusion. (30)

Velmahos et al demonstrated that for a total of 50 patients with severe duodenal injuries (AAST III, IV, V), (34 patients treated with simple duodenorrhaphy or resection and primary anastomosis versus 16 patients treated with pyloric exclusion) that there were no differences in morbidity (including complications specific to duodenal repair), mortality and intensive care unit and hospital length of stay between the two groups. There were more patients with pancreatic injuries and injuries involving the first and second parts of the duodenum in the pylorus exclusion group.(31)

It appears that the current trend of repair of duodenal injuries is to offer primary repair and resection with primary anastomosis as far as is possible with wide drainage .Numerous authors have indicated the need to keep surgical intervention for these patients simple even without the use of diversion of duodenal contents. It is possible that the improved outcomes currently observed by some authors reflect better resuscitation and intensive care support. It is also possible that in the era of developing the duodenal diversion techniques there was a lower threshold to perform these procedures with the intention of proving their worth. The literature repeatedly opines that there is an inherent fear of duodenal injuries due to an increase risk of wound dehiscence. This has possibly become a cultural concern amongst surgeons and possibly not warranted. These lesions are not common enough to expose them to randomised controlled trials and many of the case series are quite small (19, 23, 24).

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CONCLUSION Blunt injury of the duodenum is both less common and more difficult to diagnose than penetrating injury and may occur in isolation or with pancreatic injury. Diagnosis requires a high index of suspicion, based on mechanism of injury and physical examination. Delayed treatment exceeding 24 hours results in high mortality. The main concern following repair of these injuries are suture line dehiscence (as high as 30%). Decompression and diversion techniques have helped to decrease the mortality and morbidity (5%). These observations are being challenged. The current literature reflects that when dealing with duodenal injuries, some surgeons now prefer to avoid complex reconstructive procedures and are advocating necessary debridement, adequate drainage and primary repair. Improvements in resuscitative and intensive care support have probably contributed to the improved results. Despite the various definitions of severe or complex duodenal injuries and grading systems, the degree of oedema, contusion, or friability of the injured duodenum require judgement calls which can only be made on an individual basis: condition of the patient and experience of the surgeon. The secret probably lies in careful handling of the tissues and a meticulous repair along with good resuscitation and after care. The ultimate procedure lies with the experience and comfort of the surgeon.

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REFERENCES 1Degiannis E, Boffard K. Duodenal injuries. Br J Surg 2000; 87: 1473-1479.

2.Weigelt JA. Duodenal injuries. Surg Clin North Am. 1990;70(3):529-39.

3.Ivatury RR, Nassoura ZE, Simon RJ, et al. Complex duodenal injuries. Surg Clin North Am. 1996; 76(4): 797-812.

4. Lucas CE, Ledgerwood AM. Factors influencing outcome after blunt duodenal injury. J Trauma 1975; 15:839.

5.Olsen WR. The serum amylase in blunt abdominal trauma. J Trauma 1973; 13: 200-4.

6. Flint LM Jr, McCoy M, Richardson JM, et al. Duodenal injury. Analysis of common misconceptions in diagnosis and treatment. Ann Surg 1979; 191: 697-702.

7.Snyder WH III, Weigelt JA, Watkins WL, et al. The surgical management of duodenal trauma.

Precepts based on a review of 247 cases. Arch Surg 1980; 115: 422-9.

8. Adkins RB Jr, Keyser JE III. Recent experiences with duodenal trauma. Am Surg 1985; 51: 121-131.

9.Carillo EH, Richardson JD, Miller FB. Evolution in the management of duodenal injuries. J Trauma 1996; 40: 1037-46.

10.Kunin JR, Korobkin M, Ellis JH, et al. Duodenal injuries caused by blunt abdominal trauma: value of CT in differentiating perforation from hematoma. Am J Roentgenol 1993; 163: 1221-3.

11.Ballard RB, Badellino MM, Eynon CA, et al. Blunt duodenal rupture: a 6 year statewide experience. J Trauma 1997; 43: 229-32.

12.Brotman S, Cisternino S, Myers RA, et al. A test to help diagnosis of rupture in the injured duodenum. Injury 1981; 12:464-5.

13.Moore EE, Cogbill TH, Malangoni MA, et al. Organ injury scaling II: pancreas, duodenum, small bowel, colon and rectum. J Trauma 1990; 30: 1427-9.

14. Ivatury RR, Nallathambi MN, Rao PM, et al: Penetrating pancreatic injuries. Am Surg 1990; 2: 90-5.

15. Asensio JA, Feliciano DV, Britt LD, Kerstein MD. Management of duodenal injuries. Curr Probl Surg. 1993; 30(11):1023-93.

16. Fraga GP,Biazotto G, Bortoto JB, et al. The use of pyloric exclusion for treating duodenal trauma: case series.Sao Paulo Med J. 2008; 126(6):337-41.

17. Kobbold EE, Thal AP: A simple method for the management of experimental wounds of the duodenum. Surg Gynecol Obstet 1963; 116:340-4.

18.Ivatury RR, Nallathambi MN, Gaudino J, et al. Penetrating duodenal injuries. Analysis of 100 consecutive cases. Ann Surg 1985; 202: 153-8.

19. Cogbill TH, Moore EE, Feliciano DV, et al. Conservative management of duodenal trauma: a multi center perspective. J Trauma 1990; 30: 1469-75.

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A CASEBOOK OF TWENTY SURGICAL CASES 20. Shorr RM, Greaney GC, Donovan AJ: Injuries of the duodenum. Am J Surg 1987; 154(1): 93-8.

21. Vaughan GD 3rd, Frazier OH, Graham DY, et al. The use of pyloric exclusion in the management of severe duodenal injuries. Am J Surg. 1977; 134(6): 785-90.

22. Martin TD, Feliciano DV, Mattox KL, et al. Severe duodenal injuries. Treatment with pyloric exclusion and gastrojejunostomy. Arch Surg. 1983;118(5):631-5.

23. Buck JR, Sorensen VJ, Fath JJ, et al. Severe pancreatico-duodenal injuries: the effectiveness of pyloric exclusion with vagotomy. Am Surg. 1992; 58(9): 557-60.

24. Degiannis E, Krawczykowski D, Velmahos GC, et al. Pyloric exclusion in severe penetrating injuries of the duodenum. World J Surg. 1993; 17(6):751-4.

25. Ginzburg E, Carrillo EH, Sosa JL, et al. Pyloric exclusion in the management of duodenal trauma: is concomitant gastrojejunostomy necessary? Am Surg. 1997;63(11):964-6.

26. CĂŠsar JMS, Petroianu A, GouvĂŞa AP, et al. Reopening of pylorus after its closure, in rats.

Rev Col Bras Cir. 2005; 32(6): 328-31.

27. Pierro AC, Mantovani M, Reis NS,et al. Treatment of complex duodenal lesions: comparison between simple repair and repair associated to pyloric exclusion and gastrojejunostomy in dogs. Acta Cir Bras. 2005; 20(1):28-38.

28.Seamon MJ, Pieri PG, Fisher CA, et al. A ten-year retrospective review does pyloric exclusion improve clinical outcome after penetrating duodenal and combined pancreatico-duodenal injuries? J Trauma 2007; 62(4): 829-33.

29. Rickard MJ, Brohi K, Bautz PC. Pancreatic and duodenal injuries: keep it simple. ANZ J Surg 2005; 75(7): 581-6.

30.DuBose JJ, Inaba K, Teixeira PG, et al. Pyloric exclusion in the treatment of severe duodenal injuries: results from the National Trauma Data Bank. Am Surg 2008; 74(10): 925-9.

31. Velmahos GC, Constantinou C, Kasotakis G. Safety of repair for severe duodenal injuries.

World J Surg 2008; 32(1): 7-12.

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4.

FLAIL CHEST INJURY To fix or not to fix?

INTRODUCTION Thoracic trauma is common and causes a variety of injuries, ranging from minor abrasions and contusions to life threatening insults to the thoracic viscera.

Thoracic trauma is also associated with a high morbidity and mortality. Thoracic trauma accounts for 20% of all trauma deaths making it second only to head and spinal cord injuries. Fortunately most thoracic injuries do not require major surgical intervention. Most chest wall and intra-thoracic injuries can be managed with simple tube thoracostomy, mechanical ventilation, aggressive pain control and other supportive care. The cause of thoracic trauma includes motor vehicular accidents, assaults, falls, occupational related crush injuries and sport injuries. Most thoracic injuries sustained in motor vehicle accident are blunt in nature. Flail chest is a known consequence of blunt trauma and can carry a high morbidity and mortality. The majority of these patients can be managed successfully with adequate analgesia, pulmonary toileting and oxygenation. In recent times there has been renewed interest in the operative fixation of the chest wall for some patients with flail chest injuries. A case of flail chest injury is described here. The management trends and outcomes for patients with flail chest injuries are outlined; in particular the evidence for operative fixation is discussed.

CASE History: A 44 year old man presented to the emergency department 2 hours after sustaining a crush injury to the left chest. He was accidentally pinned by a reversing truck against a metal cylinder. Initially treatment was done at the District Health Facility and then referred to the General Hospital. He reported no previous medical or surgical history but has been smoking 1 pack of cigarettes/ day for the last 30 years.

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Resuscitation was done as per ATLS protocol. On examination: BP 89/35, P 100, RR 30/min with oxygen saturations 100%. There was gross paradoxical movement of the left lateral chest wall with subcutaneous emphysema. The chest tube initially placed had to be replaced as it was malpositioned. His vital signs normalized and the X-ray trauma series was performed. A flail segment was seen involving left ribs 3-6.

A CT scan of the chest and abdomen was done. Contusions were noted in the left lung base and the previously noted rib fractures were seen. The patient was transferred to the HDU where an epidural catheter was placed for analgesia (12.5ml Bupivacaine + 2mg Fentanyl in 35.5ml of normal saline at 5ml/hour) to allow for proper ventilation and pulmonary toilet. Despite this his respiratory rate increased to 40 bpm overnight. His breathing became more laboured and required intubation and ventilator support. A tracheostomy was done on day 5 in anticipation of prolonged ventilation. The following measures were also instituted: feeding via nasogastric tube, prophylaxis for DVT was commenced (clexane 40 mg) along with chest and limb physiotherapy. Ventilatory support was gradually weaned off over 13 days. He was discharged from hospital on day 18.

Review in the outpatient clinic revealed persistent chest pain which limited his physical activities. He was also experiencing shortness of breath. Clinically he was able to converse in full sentences and no visible chest wall deformity could be detected. A request was made for a lung function test but the service was not currently available. After 6 months his symptoms were subjectively better. He was unable to return to work though and the lung function tests are awaited.

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DISCUSSION Thoracic trauma is associated with a high morbidity and mortality. Thoracic trauma accounts for 20% of all trauma deaths making it second only to head and spinal cord injuries.(1) Fortunately most thoracic injuries do not require major surgical intervention. Flail chest is a known consequence of blunt trauma and can carry a high morbidity and mortality. The majority of these patients can be managed successfully with adequate analgesia, pulmonary toileting and oxygenation. In recent times there has been renewed interest in the operative fixation of the chest wall for some patients with flail chest injuries.

The flail chest as we know it today was described as early as 1955 by Cohen.(2) The synonym ‘‘stove in chest’’ was used earlier, and was first described in 1945 by Hagen.(2) A specific type of flail chest called the ‘steering wheel’ injury was described in 1949 by Heroy.(2) Flail chest is variably defined in the literature. The most commonly cited definition is unilateral fracture of four or more consecutive ribs in at least two places. This results in paradoxical movement of the flail segment in respiration. The injury generally results from compressive forces with frontal and lateral impact. Severe anterior compressive forces may cause sternochondral disruption and a subsequent sternal flail. Flail chest can be sub divided into anterior and posterior depending on the presence of fractures along the anterior and posterior rib angles respectively. Flail chest occurs in ten percent of thoracic trauma cases and has a reported mortality rate between ten and fifteen percent.(3,4,5)

The diagnosis of flail chest is clinical and requires an index of suspicion. The injury mechanism is important and therefore this information must be carefully ascertained from the emergency medical personnel. These patients should undergo a standard initial trauma resuscitation including airway, breathing and circulation assessment. Physical examination generally reveals a paradoxical motion of the chest wall segment.

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Fig 1: Flail segment paradoxically indrawn on inspiration

Fig 2: Flail segment paradoxically blown out in expiration

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Fig 3: Chest X-ray illustrating the left flail segment

Fig 4: CT images illustrating the deformed chest wall

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Fig 4a: CT images illustrating the deformed chest wall

Fig 4b: CT images illustrating the deformed chest wall

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The awake patient usually complains of severe chest wall pain and may manifest signs of respiratory insufficiency including tachypnea and splinting. Decreased breath sounds may indicate a pneumothorax, pulmonary contusion or hemothorax. Radiographic evaluation begins with a portable antero-posterior chest radiograph. This may not reveal the posterolateral rib fractures and among seriously injured patients is not exceptionally sensitive for rib fractures.(6,7,8)

Of course these patients should have a complete trauma series x-ray examination but specifically many trauma surgeons are recommending chest CT angiography as a screening tool for occult intrathoracic injury in patients with significant blunt chest trauma. Irrespective of chest radiographic findings 8% of patients brought to a trauma center following a high speed motor vehicular accident, a fall greater than 4.5 m or having been struck by an automobile and thrown more than three meters had aortic injury revealed by chest CT angiography. In addition 65% of patients with significant blunt trauma who have an admission chest CT will have significant intrathoracic injuries that are missed by chest radiograph alone.(9,10)

The management strategies and challenges in treating flail chest injuries are related to the following five issues: 1. The problem of ventilation perfusion mismatch 2. Maintaining adequate pulmonary toilet 3. Adequate but not excessive fluid resuscitation 4. Pain control 5. A decision regarding possible surgical chest wall fixation

Younger patients with isolated flail chest injury may ventilate adequately with 69

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good pain relief. However, the patient’s comorbidities and age greatly influence the clinical outcome. Beyond age 55 years, the likelihood of death in cases of flail chest increases 132% for every ten year increase in age and 30% for each unit increase in injury severity score.(11) In non intubated patients the disruption of chest wall mechanics will dramatically decrease tidal volumes and effective coughing with a corresponding predisposition to sputum retention, atelectasis and pneumonia.

Early mechanical ventilatory assistance should be provided to patients with severe concomitant injuries. An injury severity score greater than twenty three, head or truncal organ injury, shock on admission and blood transfusions within the first twenty four hours have all been associated with the need for mechanical ventilation. The mortality rate of patients with severe associated injuries may be decreased by 50% to 60% if mechanical ventilation is instituted within twenty four hours of injury. The mortality rate can exceed 90% however for patients with flail chest and hypotension who develop hypoxia for a period of more than twenty four hours. A low threshold for intubation of patients with flail chest especially those with comorbidities and the elderly, is warranted.(12) Intermittent positive pressure ventilation was first successfully used to manage flail chest in the 1950’s .(13) Cullen and colleagues further supported the use of intermittent mechanical ventilation in the treatment of flail chest injury.(14) During the 1960’s and early 1970’s, flail chest was managed with early tracheostomy and mechanical ventilation. It was believed that the hypoxia, decreased compliance and increased work of breathing and decline in pulmonary function testing were solely caused by the flail segment. Williams in 1948 described a typical clinical triad related to flail chest: intrabronchial hemorrhage, ineffectual cough and typical anoxia.(15) However, attention to the underlying contused lung was not drawn until 1975 when Trinkle and co workers demonstrated conclusively that the respiratory insufficiency associated with flail chest was related 70

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to pulmonary contusion and not the paradoxical chest wall movement. They recommended primary treatment of the underlying injury with a combination of fluid restriction, corticosteroids, aggressive pulmonary toilet and pain control.

They reported a decrease in mortality rate from 21% to 0%, a 5 fold decrease in morbidity and a nearly 3.5 fold decrease in hospital stay in these patients when compared with those undergoing tracheostomy and mechanical ventilation.(16)

Pulmonary contusion should be anticipated in any patient who sustains significant high-energy blunt chest impact. A history of the inciting event and physical findings of chest wall trauma, especially the presence of fractures or a flail segment increase the odds of having and underlying lung contusion. The absence of rib fractures however does not eliminate the possibilities of pulmonary contusion. Focal or diffuse homogenous opacification on chest radiograph is the mainstay of diagnosis. Unlike aspiration pneumonitis, the opacification seen with pulmonary contusion is irregular and does not conform to segments or lobes within the lung. Pulmonary contusion is not always immediately apparent radiographically; one third of patients fail to demonstrate a lesion consistent with this diagnosis on the initial chest xray. Although the mean time to opacification is six hours, it may take up to forty eight hours for pulmonary contusion to be established.(17)

Computerized tomography scans have been advocated as a more accurate means of detecting and quantifying pulmonary contusion. Schild et al identified 100% detection rate for pulmonary contusion using CT compared to 38% with plain xray.(18) The degree of contusion has implications for worsening respiratory function and need for ventilation: 82% of patients with a contusion of at least 20% developed Acute Respiratory Distress Syndrome (ARDS) versus only 22% of patients with a contusion less than 20%. There was also an increase trend in the development of pneumonia in cases of greater areas of contusion and all 71

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patients with contusion greater than 28% required intubation compared with no patients with less than 18% contusion.(19)

Ideally patients with flail chest and pulmonary contusion should be admitted to at least a high dependency unit for supportive care: adequate analgesia with a view to early mobilization to allow or encourage coughing and deep breathing. Supplemental oxygen to treat hypoxia is administered and placement of thoracostomy tubes to relieve hemopneumothorax as necessary. Epidural analgesia has proved extremely effective in managing the acute pain from chest wall injury. Splinting and paradoxical chest wall motions are improved to near normal levels. Epidural use improves pulmonary toilet by enabling the patient to breathe deeply, cough effectively and actively participate in chest physiotherapy. Adverse effects such as hypotension in the under-resuscitated patient, respiratory depression and epidural infection can limit its effectiveness. In addition, epidural analgesia can hinder diagnosis of intra-abdominal injuries in critically ill trauma patients. Despite these potential problems, epidural analgesia remains central in the management of flail chest injury.(20,21,22,23)

At present it is widely accepted that respiratory impairment in flail chest patients is only partially due to inefficient ventilation related to the paradoxical movement of the chest wall, but is significantly influenced by other associated thoracic injuries, in particular pulmonary contusion and atelectasis. As such selected ventilation and tracheostomy have become standard treatment for patients with flail chest. It is well known that patients with severe flail chest still require prolonged ventilation and may develop post traumatic pneumonia.

Long term disability has also been reported in cases with conservative treatment and patients managed with internal pneumatic stabilization.

Controversy has surrounded the issue of fluid management in relation to pulmo72

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nary contusion. Although the overzealous use of crystalloid solution has been blamed for exacerbation of the hypoxia of pulmonary contusion, prospective studies have failed to substantiate this claim.(24) Standard resuscitation with crystalloids and blood products as indicated to obtaine euvolemia is probably the ideal.(24) The use of steroids has been shown to be of no benefit and may impair bacterial clearance within the pulmonary tissue.(24,25)

Patients with larger contusions and those associated with more severe injuries expressed fairly consistent symptoms: dyspnea, decreased exercise tolerance and chest pain on the side of the injury. Landercasper et al reviewed 62 patients who sustained a flail chest injury including 42 who had a concomitant pulmonary contusion. Thirty two patients were available for follow up for a mean of five years: 25% complained of chest tightness, 49% thoracic pain and 63% dyspnea. On examination 46% were unable to expand their chest circumference by greater than 5cm and 57% had abnormal spirometry.(26) Similar data were presented by Beal and Oreskovich, showing 64% of patients sustaining a flail chest injury had long term morbidity of persistent chest wall pain exacerbated by activity, chest wall deformity and dyspnea on exertion.(27) Kishikawa et al prospectively followed 18 patients with severe blunt chest trauma. Patients without a pulmonary contusion had normal pulmonary function test with six months of the injury, while patients with pulmonary contusions and a group of patients from one to four years earlier showed CT evidence of fibrosis, persistently decreased functional residual capacity and arterial oxygen partial pressure.(28) These data has provided the impetus for reconsideration of rib fixation for patients with flail chest injury in the last decade.

The 1950â&#x20AC;&#x2122;s saw increase attention to flail chest injuries due to the ever growing use of automobiles, with mortality rates up to 80% reported.(29,30) In an attempt to improve the mortality rates numerous novel ideas and techniques emerged 73

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largely aimed at controlling the paradoxical chest wall movement associated with flail chest injuries.

The methods of chest wall support can be divided into non-operative and operative strategies. The simplest reported non-operative measure is strapping the chest with adhesive tape, described by Berry et al.(31) Hagen was the first to describe a form of respiratory support using an apparatus called the drinker respirator (also known as the â&#x20AC;&#x153;iron lungâ&#x20AC;?).(32) This technique used external splinting based on a repetitive cycle of creating a vacuum in a metal cylinder and subsequently this negative pressure was transferred to the chest wall of the patient creating inspiratory cycles. Schrire described a large suction device referred to as the Cape Town Limpet that was analogous to a sink plunger. This suction cup was applied to the flail segment and subsequently put under traction.(33)

Further ideas for external support saw the adoption of percutaneous techniques to stabilize the sternum or lateral flail segment. The traction devices included towel clips, bullet forceps, metal wires around ribs and even placement of a cork screw with traction on the sternum .(2)

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The Drinker Respirator (Iron Lung) (2)

The Capetown Limpet (2)

Corkscrew for traction on a sternal flail (2)

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Invasive techniques for rib fracture and flail chest stabilization developed in parallel with the percutaneous techniques. Common surgical techniques included simple wire suture fixation of the fracture ends, rush rod fixation of the flail segment and many designs of plates for fixation. While there were several reports on surgical stabilization of flail chest injury with these various techniques they provided little or no details on complications, needless to say none of them became widely popular. Interest in these probably waned further with the use of pneumatic internal stabilization.

With discovery of positive pressure ventilation pneumatic internal stabilization became the preferred method of chest wall stabilization for the latter half of the last century to present. However, the last decade has seen resurgence in interests for operative stabilization of flail chest injuries. The evidence for this renewed interest comes from two prospective randomized trials. Tanaka et al selected 37 patients out of 148 with flail chest injuries who met strict inclusion criteria for a prospective randomized study of surgical versus internal pneumatic stabilization. All patients we initially treated with positive pressure ventilation. At five days post injury 18 patients were randomized to operative fixation with Judet Struts and 19 patients with positive pressure ventilation.

Patients in each group had identical extubation criteria. They found significant differences in the number of days requiring mechanical ventilation (10.8 versus 18.3), number of days ICU (16.5 versus 26.8) and pneumonia (22% versus 90%) between surgical and non-surgical groups respectively. In addition they also found a difference in the rate of return to work at 6 months (61% versus 5%) and the total cost of care. Patients in the non-surgical group had greater complaints of chest tightness, thoracic pain and dyspnea at 6 to 12 months following surgery.(34) A second randomized prospective study by Granetzny et al compared outcomes in 20 patients treated using surgical fixation with intra76

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medullary k wires and 20 patients treated non-surgically with adhesive plaster strapping. They too found a significant difference in the number of days of ventilator use (2 versus 12), the number of days in the ICU (9.6 versus 14.6), residual chest wall deformities (1 versus 9), pneumonia (10% versus 50%) and wound infection rates (10% versus 0%) between the operative and the nonoperative groups respectively. They also noted significantly improved pulmonary function tests performed at 2 months post injury in the operative group.(35)

Lardinois et al prospectively evaluated 66 of 732 patients with a flail chest injury. Indications for fixation included respiratory failure (n=28), progressive displacement of the flail segment (n=15), failure to wean for pulmonary reasons (n=21) and thoracotomy for associated thoracic injuries (n=2). Pulmonary contusions involving, on average 30% of the lung volume was present in 80% of the patients. They found that immediate extubation was possible in 47% of patients and the mean ventilator time was 2.1 days. They also found a return to work rate at 2 months post surgery of 100%. Plate removal was required in 11% of patients because of hardware related pains.(36)

An interesting report was made by Voggenreiter et al following a retrospective study of surgical fixation for flail chest in patients with pulmonary contusion. Many experts believe that the underlying lung injury, rather than the bony injury is the major contributor to the morbidity and mortality following flail chest injuries. They studied the outcomes of surgical fixation in 10 patients with and 10 patients without pulmonary contusion. They also evaluated 18 matched patients without pulmonary contusion treated non-surgically. Significant differences were identified in the number of ventilator days (30.8 versus 6.5) and rates of pneumonia (40% versus 10%) and mortality (30% versus 0%) between the surgical patients with and without pulmonary contusion respectively. They also found significant differences in ventilation days (6.5 77

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versus 26.7) and pneumonia (10% versus 27%) between the surgical and nonsurgical patients without pulmonary contusion. They concluded that patients with flail chest and no contusion had better outcomes if surgical stabilization is performed early, while patients with flail chest and pulmonary contusion should be fixed only if paradoxical motion or progressive collapse is noted.(37)

Nirula et al retrospectively compared 30 patients treated surgically with 30 non-surgically treated patients matched based on age, injury severity score and chest abbreviated injury score. Indications for surgery included severe flail chest, pain, bleeding and failure to wean. The primary outcome measures of ICU days and total hospital days did not show a statistically significant difference between the groups. However, the number of ventilator days measured from the time of surgery to extubation was significantly lower in the operative group (2.9 days) relative to the non-operative group (9.4 days).(38)

Ahmed and Mohyuddin compared 26 patients treated surgically with k-wire fixation of one rib of the flail segment with 38 patients treated non-surgically using positive pressure ventilation. The rib was stabilized â&#x20AC;&#x153;on retreatâ&#x20AC;? after other surgical interventions including treatment of a hemothorax, treatment of a major air leak or associated abdominal and orthopaedic injuries. No statistical analysis was performed and the groups were not matched or randomised.

However, they reported improved outcomes in the number of ICU days (21 versus 9), the number of ventilator days (15 versus 3.9), the number of patients requiring tracheostomy (37% versus 11%), the rate of chest infection (50% versus 15%), sepsis rate (24% versus 4%) and the mortality rate (29% versus 8%)between the non-operative and operative groups respectively.(39)

On studying these four comparative and two prospective studies, in general there is a decrease in the number of days requiring mechani78

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cal ventilation, number of days in ICU and the rate of chest infection all favoring operative fixation of the flail segment.

In addition, a

number of case series have also reported similar trends as noted here.

Of course with surgical intervention, despite the benefits noted the possibility of complication exists. In order to assess this, a study was conducted by Nirula et al to determine the complication rates associated with surgical fixation of flail chest injuries. Of 650 rib fractures reported the complications included 8 superficial wound infections (1.2%), 4 draining wound without infection, 2 pleural empyemas, 1 wound hematoma, 1 persistent pleural effusion and 1 case of osteomyelitis. They noted 8 hardware failures and 9 patients requiring hardware removal. These results indicate an acceptable rate of complications and also lend support to the operative fixation of the chest wall for flail chest injury.(40)

Despite the data in support of, operative management of chest wall injuries is a controversial topic. This was highlighted by the recent report by Mayberry et al: in a questionnaire survey the majority of respondents (82% of general surgeons, 66% of orthopaedic surgeons and 71% of thoracic surgeons responded that operative repair of rib fractures was indicated in selected patients. Fewer (17% of general surgeons, 32% of orthopaedic surgeon and 23% of thoracic surgeons) responded that operative repair of rib fractures was rarely or never indicated. Only 21% of trauma surgeons and 52% of thoracic surgeons indicated they had ever performed or assisted in open reduction and internal fixation of rib fractures. Furthermore 22% of all 405 respondents indicated that they were familiar with a randomised study of surgical repair for flail chest injury.(41)

Non-operative management, consisting of pulmonary toilet, pain control, and selective ventilatory support is the standard treatment of flail chest injuries at most institutions. The data reviewed indicates the interest in the operative fixa79

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tion of rib fractures in chest wall injury syndromes such as flail chest is in renaissance due to:

路 Recognition that many patients with flail chest treated non-operatively do no liberate from the ventilator in as timely a fashion as desired with increased rates of nosocomial pneumonia and tracheostomy. 路 Recognition that many of these patients develop long term pain and disability. 路 Development of sophisticated fracture fixation techniques e.g. locked plate fixation and rib specific prostheses.

Contemporary reports now indicate that rib fracture fixation can be performed with low morbidity and virtually no mortality with improved outcomes when compared to non-operative controls. In fact, the National Institute for Health and Clinical Excellence of the United Kingdom recently issued a guidance stating that stabilizing flail chest with metal implants may be applied routinely.(42)

Despite the consideration for operative fixation, in order for optimal procedures to be performed with acceptable complication rates surgeons advocating chest wall repairs will need to further refine operative techniques and operative indications and provide adequate training for colleagues. At present some fixation devices include: metal plates, absorbable plates, intramedullary struts, Judet struts and U plates. On the basis of the current literature no formal recommendation can be made for one prosthetic over the other.(43)

CONCLUSION While operative stabilization of a flail chest is increasingly recognized and a valid approach to improve pulmonary mechanics in selected trauma patients, it is still somewhat controversial with current debate focusing on patient selec80

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tion and the timing of operative intervention. Based on the available evidence indications for surgical fixation could be rationalized as follows: 路 Patients who require a thoracotomy because of associated thoracic injuries. 路 Patients with deteriorating pulmonary function despite aggressive clearance of bronchial secretions and adequate analgesia, requiring internal pneumatic stabilization and without pulmonary contusion (these patients should be considered for early stabilization. 路 Intubated patients with previous severe pulmonary contusion and cerebral injuries in order to reduce the duration of internal pneumatic stabilization when the patient fails to wean from the ventilator. 路 Patients with extensive antero-lateral flail chest and progressive dislocation of the fractured ribs in order to prevent late chest wall deformity and a consequent restrictive pulmonary disorder.

In the case described, the patient did have pulmonary contusion. Consideration for rib fixation could have been given at the time of his tracheostomy.

However, he was weaned off the ventilator in a reasonable time (5 days).

Three months following his discharge though, he continued to have physically limiting chest wall pain. This patient is a heavy smoker and did demonstrate displacement of the flail segment on CT. Chest wall fixation may have been helpful in preventing any restrictive compromise of his respiratory mechanics that may affect him in the future. Unfortunately, neither the expertise nor the fixation devices were available at the institution at this time.

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REFERENCES 1.LoCicero J, Mattox K. Epidemiology of chest trauma. Surg Clin North Am. 1989;69(1):15–19.

2. Bimelman M, Poeze M, Blokhius TJ, et al. Historic overview of treatment techniques for rib fractures and flail chest. Eur J Trauma Emerg Surg. 2010; 36:407-15.

3. Clark G, Schecter W, Trunkey D. Variables affecting outcome in blunt chest trauma: flail chest vs. pulmonary contusion. J Trauma. 1988;28:298–304 4. Ciraulo D, Elliott D, Mitchell K, et al. Flail chest as a marker for significant injuries. J Am Coll Surg. 1994;178:466–470 5. Glinz W. Problems caused by the unstable thoracic wall and by cardiac injury due to blunt injury. Injury. 1986;17:322–326 6. Ziegler DW, Agarwal NN. The morbidity and mortality of rib fractures. J Trauma.

1994;37(6):975–979 7. Lee RB, Bass SM, Morris JA, et al. Three or more rib fractures as an indicator for transfer to a level I trauma center: a population study. J Trauma. 1990;30(6):689–694 8. Roux P, Fisher RM. Chest injuries in children: an analysis of 100 cases of blunt chest trauma from motor vehicle accidents. J Pediatr Surg. 1992;27(5):551–555 9. Trupka A, Waydhas C, Hallfeldt KKJ, et al.Value of thoracic computed tomography in the first assessment of severely injured patients with blunt chest trauma: results of a prospective study. J Trauma. 1997;43(3):405–412 10. Demetriades D, Gomez H, Velmahos GC, et al. Routine helical computed tomographic evaluation of the mediastinum in high-risk blunt trauma patients. Arch Surg. 1998;133:1084–1088 11. Albaugh G, Kann B, Puc MM, et al.Age-adjusted outcomes in traumatic flail chest injuries in the elderly. Am Surg. 2000;66(10):978–981 12. Sankaran S, Wilson RF. Factors affecting prognosis in patients with flail chest. J Thorac Cardiovasc Surg. 1970;60(3):402–410 13. Avery E, Morch E, Benson D. Critically crushed chests: a new method of treatment with continuous mechanical hyperventilation to produce alkalotic apnea and internal pneumatic stabilization. J Thorac Surg. 1956;32:291–311 14. Cullen P, Modell J, Dirby R. Treatment of flail chest: use of intermittent mandatory ventilation and positive end-expiratory pressure. Arch Surg. 1975;110:1099–1103.

15. Williams M. Severe crushing injury to the chest. Ann Surg. 1948;128(5):1006–11.

16. Trinkle J, Richardson J, Franz J, et al. Management of flail chest without mechanical ventilation. Ann Thorac Surg. 1975;19(4):355–363 17. Miller PR, Croce MA, Bee TK, et al. ARDS after pulmonary contusion: accurate measurement of contusion volume identifies high risk patients. J Trauma. 2001;51(2):223–230 18. Schild HH, Strunk H, Weber W, et al. Pulmonary contusion: CT vs. plain radiograms. J Comput Assist Tomogr. 1989;13(3):417–420 19. Wagner RB, Crawford WO, Schimpf PP, et al. Quantitation and pattern of parenchymal

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1988;12(4):270–281 20. Mackersie R, Karagianes T, Hoyt DB, et al. Prospective evaluation of epidural and intravenous administration of fentanyl for pain control and restoration of ventilatory function following multiple ribs fractures. J Trauma. 1991;31:443–449 21. Worthley L. Thoracic epidural in the management of chest trauma: a study of 161 cases. Intensive Care Med. 1985;11:312–315 22. Dittman M, Ferstl A, Wolff G. Epidural analgesia for the treatment of multiple rib fractures.

Eur J Intensive Care Med. 1975;1:71–75 23. Ward A, Gillatt D. Delayed diagnosis of traumatic rupture of the spleen: a warning of the use of thoracic epidural analgesia in chest trauma. Injury. 1989;20:178–179 24. Bongard FS, Lewis FR. Crystalloid resuscitation of patients with pulmonary contusion. Am J Surg. 1984;148:145–151 25. Richardson JD, Woods D, Johanson WG, et al. Lung bacterial clearance following pulmonary contusion. Surgery. 1979;86 26. Landercasper J, Cogbill TH, Lindesmith LA. Long-term disability after flail chest injury. J Trauma. 1984;24(5):410–414 27. Beal SL, Oreskovich MR. Long-term disability associated with flail chest injury. Am J Surg.

1985;150:324–326 28. Kishikawa M, Yoshioka T, Shimazu T, et al. Pulmonary Contusion causes long-term respiratory dysfunction with decreased functional residual capacity. J Trauma. 1991;31(9):1203–1210 29.Ginsberg R, Kostin R.5 New approaches to the management of flail chest. Can Med Assoc J. 1977;116(6):613-5.

30. Relihan M, Litwin M. Morbidity and mortality associated with flail chest injury: a review of 85 cases. J Trauma. 1973; 13(8): 663-71.

31. Berry F. Treatment of injuries to the chest. Am J Surg.1941; 54:280.

32.Hagen K. Multiple rib fractures treated with a Drinker respirator: a case report. JBJS Am. 1945; 27(2):330-4.

33. Schrire T. Control of the crushed chest: the use of the ‘‘CapeTown Limpet.’’ Dis Chest. 1963; 44:141–5.

34. Tanaka H, Yukioka T, Yamaguti Y, et al. Surgical stabilization of internal pneumatic stabilization? A prospective randomized study of the management of severe flail chest patients. J Trauma.

2002;52(4):727–32.

35. Granetzny A, Abd M, Emam E, et al. Surgical versus conservative treatment of flail chest.

Evaluation of the pulmonary status. Interact Cardivasc Thoracic Surg. 2005;4(6): 583-7.

36. Lardinois D, Krueger T, Dusmet M, et al. Pulmonary function tests after operative stabilisation of the chest wall for flail chest. Eur J Cardiothoracic Surg. 2001;20(3):496-501.

37. Voggenreiter G, Neudeck F, Aufmkolk M, et al. Operative chest wall stabilization in flail chestoutcomes of patients with or without pulmonary contusion. J Am Coll Surg.

1998;187(2):130–8.

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38. Nirula R, Allen B, Layman R, et al. Rib fracture stabilization in patients sustaining blunt chest injury. Am Surg. 2006;72(4):307–9.

39. Ahmed Z, Mohyuddin Z. Management of flail chest injury: internal fixation versus endotracheal intubation and ventilation. J Thorac Cardiovasc Surg. 1995;110(6):1676–80.

40. Nirula R, Diaz JJ Jr, Trunkey DD, et al. Rib fracture repair: indications, technical issues, and future directions. World J Surg. 2009;33(1):14–22.

41. Mayberry JC, Ham LB, Schipper PH, et al. Surveyed opinion of American trauma, orthopedic, and thoracic surgeons on rib and sternal fracture repair. J Trauma. 2009;66:875-9.

42. Insertion of metal rib reinforcements to stabilise a flail chest wall (IPG361). National Institute for Health and Clinical Excellence (NICE), 2010.

43.Lafferty PM, Anavian J, Will RE, Cole PA. Operative treatment of chest wall injuries: Indications, techniques and outcomes. J Bone Joint Surg Am. 2011;93:97-110.

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5. GALLSTONE

ILEUS

A case of rolling stones

INTRODUCTION Intestinal obstruction from gallstones is a surgical emergency that presents in the elderly. Peri-operative mortality rates for gallstone ileus remain high at 1217%. Although this is an improvement, the high rates could be attributed to the delay in diagnosis in an elderly group of patients with multiple co-morbidities.

Despite being described more than 400 years previously, there is still debate regarding the appropriate surgical therapy for emergency treatment of gallstone ileus (GSI). The pinnacle of operative intervention is enterotomy and retrieval of the obstructing calculus or calculi. However, leaving the biliary-enteric fistula intact predisposes to complications: recurrent gallstone ileus, cholecystitis and recurrent cholangitis. This has prompted some surgeons to undertake in addition to enterolithotomy, a cholecystectomy and fistula closure (one stage procedure). This however is at the risk of prolonged operating time and a higher mortality. Others opine for a staged procedure (two stage), to allow for dealing with the bilio-enteric fistula and gallbladder, if symptoms recur. This is a topic of ongoing controversy with proponents for both the one stage and the two stage approach. Endoscopic and laparoscopic extraction of the obstructing gallstone has been popularized in recent times. Improvement in technology has provided other adjuncts to aid in relieving the obstruction.

A case of gallstone ileus resulting in large bowel obstruction is described. The different presentations of an obstructing gallstone are outlined along with the relevant therapeutic options and the evidence for a one stage procedure.

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CASE History: A 75 year old woman presented as an emergency with supra-pubic and left lower abdominal pain. The pain began 8 days prior, and waxed and wane until the day before presentation. It was now constant but intermittently worse.

The patient identified no aggravating or relieving factors and there was no particular radiation.

The patient passed no stool for the duration of her symptoms but attested to normal passage of flatus. During the last week a mucoid discharge was seen on a few occasions with the passage of flatus.

Her appetite was maintained and there were no constitutional symptoms. Of note she gave no history of right upper quadrant pain or fatty food intolerance.

Her bowel actions occurred daily and there was no change in frequency or consistency in the previous 6 months. She never experienced per rectal bleeding.

This woman did not have any chronic illnesses. While in her 20â&#x20AC;&#x2122;s, she had surgery for a pelvic abscess which included drainage and left salpingectomy.

This lady lived on her own, attended church and enjoyed dancing.

Physical Examination: This patient walked into the examination room. Her reported age was 75 years.

However, her appearance was closer to a 60 year old. Her vital signs were: BP 150/70 mmHg, P 86 min-1, RR 18min-1, T 360C.

Her Cardiorespiratory examination was normal. The previously placed nasogastric tube drained 200mls of light green fluid. The abdominal examination revealed a slightly distended abdomen which was globally soft. The Pfannensteil scar resulting from the drainage of the pelvis abscess was now non-existent.

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There was mild tenderness in the left lower abdomen and suprapubic area. This was associated with guarding but no rebound phenomenon. The abdomen was hyper-resonant to percussion and bowel sounds were high pitched. The patient passed flatus during the examination. There was no evidence of any inguinal or femoral hernias. Digital rectal examination was normal. The urinary catheter drained 400 mls.

Investigations: Hb 11.5 g/dl, WCC 12 x103 /Âľl, Plts 334 x 103 /Âľl. Na 134 mmol-1, K 3.2 mmol-1, BUN 22 mg/dl, Cr 1.1 mg/dl.

Amylase 25 u, AST 18 u, ALT 21 u, Total Bilirubin levels1.8 mg/dls.

CXR: normal AXR: The large bowel was dilated (up to 8cm) with a cut off at the sigmoid colon. Interestingly an air cholangiogram was seen. (Fig 1)

*

Fig1: Abdominal Xray indicating an obstructed left colon. Note the air cholangiogram (boxed area) in the right upper quadrant

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This suggested an obstructing gallstone. Given her age and the related large bowel obstruction a CT scan was arranged. This confirmed pneumobilia and 2.5cm, ovoid, radio dense mass obstructing the distal sigmoid colon. The findings (Riglerâ&#x20AC;&#x2122;s sign) were in keeping with an obstructing gallstone. (Fig 2, Fig 3)

Fig. 2: Air within the biliary tree

Fig 3: Gallstone within the distal sigmoid colon. Note the surrounding fat stranding

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The patient was resuscitated with intravenous fluids, kept nil by mouth and antibiotics administered. Because she did not have absolute constipation, conservative management continued overnight. The next day an urgent colonoscopy was performed. This showed that a gallstone was in fact lodged at 25 cm. (Fig 4) It was not possible to negotiate the scope past the stone. Attempts to fragment the stone with a grasper proved futile. The largest retrieval basket available did not allow sufficient purchase on the stone to attempt withdrawal. The mucosa appeared inflamed and a few diverticulae were noted in the vicinity.

Surgical Treatment: A midline incision was made. The point of obstruction was at the pelvic brim.

Here the bowel wall was ischemic due to pressure necrosis. Distal to this the rectum was covered with dense pelvic adhesions probably related to the current acute diverticulitis and previous pelvic abscess/ salpingectomy.

The sigmoid colon was mobilized and resected with the stone (3 x 2.5 cm) extruding the eroded bowel wall. (Fig 5) A very short cuff of bowel distally allowed for the lumen to be sutured close. The pelvic inflammation and adhesions precluded a safe anastomosis.

The cholecystocolonic fistula was identified and allowed safe dissection of the gallbladder. The fistula allowed a finger tip. It was thought big enough to allow fecal contents to enter and therefore place the patient at risk of repeated cholangitis. A cholecystectomy was performed. The cystic duct was transfixed with a 2/0 vicryl suture and the freshened colotomy repaired in 2 layers with 2/0 vicryl.

An end colostomy was fashioned in the left abdomen.

Her recovery was uneventful. The patient was discharged 8 days later. The gall89

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bladder histology was available 3 weeks later and showed features consistent with chronic cholecystitis.

Fig 4: Endoscopic view of the impacted stone

Fig 5: The retrieved 3 x 2.5 cm gallstone

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DISCUSSION Intestinal obstruction from gallstones is a surgical emergency that presents in the elderly. Peri-operative mortality rates related to gallstone ileus remain high at 12-17% (1). Bartholin first described a cholecystointestinal fistula with a gallstone within the gastrointestinal (GI) tract in 1654.(2) Courvoisier published the first series of 131 cases of gallstone ileus in 1890 with a mortality of 44% from 125 operations.(2) This clinical entity predominantly affects elderly females.

In patients aged 65 years or older, GSI accounts for 25% of all small bowel obstructions. The medical co-morbidities affecting the elderly population contribute to the high morbidity and mortality that is associated with gallstone ileus. Initial reports described a mortality of 40-70% but this has decreased to approximately 15% in recent years.(1,3) The significant mortality associated with this condition requires timely diagnosis and appropriate management.

GSI is frequently preceded by an episode of acute cholecystitis. The resulting inflammation and adhesions facilitate the erosion of the offending gallstone via the gall bladder wall forming a cholecystoenteric fistula. The gallstone subsequently passes into the gut. Impacted gallstone range in size from 2-10 cm, however stones greater than 2-2.5cm usually presents as an obstruction.(3) Less commonly there may be a fistulous connection between the common bile duct and the gut. GSI may develop in the absence of a bilio-enteric fistula. The explanation resides in the migration of a stone through the Vater papilla spontaneously or following sphincterotomy followed by the ‘in situ’ growth, particularly if there is distal stenosis or diverticulae of the small bowel.(4)

The point of obstruction is most often the terminal ileum (84%) because of its smaller diameter, but it can occur throughout the GI tract.(5) These patients often report symptoms consistent with small bowel obstruction. Bouveret’s Syndrome, described in 1896, represents obstruction due to a stone lodged in 91

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the proximal duodenum following a cholecystoduodenal fistula and accounts for 3-10 % of cases of GSI.(5) In a recent systematic review, Cappell and Davis described the most common symptoms of patients with Bouveret’s syndrome as nausea and vomiting (86%), and abdominal pain (71%); less commonly, patients present with hematemesis, weight loss, and anorexia.(6) Similarly, a cholecystocolonic fistula (as in this case) may allow passage of a stone into the colon with resultant obstruction, most commonly at the sigmoid. Reisner and Cohen reported that only 4% of cases of GSI was impacted in the colon.(7) Most of these patients present with symptoms of large bowel obstruction. Other even rarer presentations include obstruction of the appendix and the entrance to a Meckel’s diverticulum.(8,9)

While symptoms vary depending on the site of obstruction, nausea, vomiting, pain and constipation are commonly present. These can be intermittent in nature, caused by a tumbling phenomenon – the result of a stone intermittently obstructing, then, traveling through until it passes out or becomes impacted in the intestine. The diagnosis of GSI is a challenge with delayed presentations and diagnosis being made on average 3-8 days after onset of symptoms.(10) While half of all patients who present with gallstone ileus have a prior history of biliary symptoms, such symptoms immediately preceding gallstone ileus are rare.

(11)

This patient had no previous biliary or bowel symptoms.

Cholecystocolonic fistula (CF) may remain asymptomatic for a prolonged period but may present variations of the following symptoms: fever, nausea, vomiting, attack of right upper quadrant pain and jaundice. These symptoms cannot be directly attributable to the CF but rather to the main etiologic factor, gallstones.

This constellation of symptoms may also indicate possible cholecystitis, cholangitis or pancreatitis. A more specific symptom complex has been described which includes diarrhea and Vitamin K mal-absorption. The CF facilitates flow 92

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of bile into the colon which induces a bile-acid diarrhea. Bypass of the terminal ileum reduces re-absorption which may affect absorption of fat and fat soluble vitamins.(12) The blood results of the patient described indicated hypokalemia.

Non-specific symptoms can make pre-operative diagnosis quite a challenge.

A correct pre-operative diagnosis is infrequent with reports ranging from 2050%. (13) Three clinical types of presentations may be encountered: acute (corresponding to the classic gallstone ileus), subacute (corresponding to partial obstruction) and a more chronic variety ( repeated bouts of pain due to passage of the stone within the bowel).(1) Hildebrandt described three clinical types: blocked (50%), remittent (30%) and peritonitis (20%).(14) The clinical preoperative diagnosis may be established on the Mordor Triad: history of gallstones, clinical signs of cholecystitis and bowel obstruction suddenly installed, with an interrupted progress.(4)

A positive diagnosis is usually based on clinical examination (small bowel obstruction), plain abdominal radiography and abdominal CT scan. Historically, the plain abdominal radiograph was the gold standard diagnostic test. Rigler, Borman, and Noble in 1941 described the classic radiologic findings of gallstone ileus, known as Riglerâ&#x20AC;&#x2122;s triad: (1) partial or complete intestinal obstruction, (2) pneumobilia, and (3) aberrant gallstone in the intestine. The presence of all three findings, however, is only reported among 17% to 35% in the literature.(3) The plain X-ray in the case described did not demonstrate the obstructing calculus.

Ultrasound techniques are more sensitive at detecting pneumobilia and ectopic gallstones. Combining the two modalities has increased the sensitivity of diagnosis of gallstone ileus to 74%. Several studies advocate the use of ultrasound in combination with abdominal films to increase the sensitivity of diagnosis.(15)

More recent studies report CT findings of gallstone ileus to be more sensitive 93

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than plain abdominal films or ultrasound. Rigler’s triad is detected more frequently using CT examinations.(16,17.18) Sensitivity of diagnosing gallstone ileus using CT is reportedly up to 93% . Approximately 15–25% of gallstones are isoattenuating and not well visualized on CT. (17) CT examinations can be useful for detecting ectopic gallstones and the presence of pneumobilia, and for aiding the assessment of the degree of inflammation around the site of the cholecystointestinal fistula .(18) In addition, it may demonstrate co-existent pathology relevant to the clinical presentation. Despite the clinical suspicion raised on plain abdominal x-ray, the CT was performed to exclude a left colonic malignancy in the case described earlier. The CT demonstrated features of acute diverticulitis. CT examination allows an earlier diagnosis which may prevent bowel wall injury (ulceration, ischemia, perforation) resulting from the impacted calculus.

Information can also be gained regarding the condition of the gallbladder and bilio-enteric fistula. This can be useful in planning or deciding an undertaking of a cholecystectomy during the surgery to relieve the intestinal obstruction. Although symptoms are nonspecific, one should have a higher index of suspicion in elderly patients without a prior surgical history or other obvious cause for a mechanical obstruction. The radiographic studies can augment clinical findings to make the correct preoperative diagnosis of gallstone ileus.

The diagnosis of Bouveret’s syndrome is usually made via endoscopy. Grove, in 1976, was the first to describe a case of pyloric obstruction due to a gallstone as diagnosed by gastroscopy.(19) On endoscopy, visualization of a stone causing obstruction is seen in about 69% of patients and obstruction in the absence of a visualized stone or fistula is seen in 31% of cases. In the remaining cases, the stone may not actually be visualized because it is compressing the lumen and only partially visualized through the duodenal wall. Other findings described include excessive retained food or fluid in the stomach and inflammation, edema, or ulcer at the impacted site.(6) 94

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The principal goal of management of gallstone ileus is relief of mechanical bowel obstruction. This is generally attained by exploratory laparotomy and enterolithotomy. A longitudinal incision is made proximal to the impacted gallstone, the stone is extracted and the enterotomy repaired transversely in two (2) layers. The procedure is completed with examination of the entire length of bowel to exclude other calculi which may cause further symptoms.(3)

Whilst open surgery has been the mainstay of treatment, more recently other approaches have been employed. The endoscopic approach is appealing in cases of Bouveret’s syndrome, particularly when open surgery historically portends a significant morbidity and mortality.(1,2,7) The first successful endoscopic extraction for Bouveret’s syndrome was described in 1985 by Bedogni et al.(20) Subsequently, a number of case reports have been published describing successful endoscopic management of Bouveret’s syndrome. Endoscopic management often necessitates the use of different sized and shaped snares, grasping forceps, retrieval baskets and nets, biliary balloons, and sometimes even a side-viewing endoscope; it can be technically challenging, time-consuming, and success rates in case series have been previously reported to be less than10% .(21) Endoscopic extraction, endoscopic laser lithotripsy (ILL) and intracorporeal electrohydraulic lithotripsy (IEHL) have all been reported as alternatives to surgery for more proximal gallstone obstruction whereas surgery is routinely recommended for individuals with impaction of the gallstone more distally (gallstone ileus).(22,23)

Extracorporeal shockwave lithotripsy (ESWL) has also been used with success in treating patients with Bouveret’s syndrome. Limitations of using ESWL include the need for several return sessions, in addition to eventual endoscopy.

Also, ESWL may be difficult to perform in obese patients or if there are gas95

A CASEBOOK OF TWENTY SURGICAL CASES

containing bowel loops interposed between the gallstone and the abdominal wall.(5)

In general, the success rate of endoscopic extraction is dependent on stone size.

Stones, that are larger than 2.5 cm are more difficult to extract endoscopically, although extractions of stones up to 3cm, have been reported.(21) Larger stones can cause ischemic ulceration of the adjacent duodenal wall. Moreover, these stones tend to have a hard outer shell and soft inner core making mechanical fragmentation with endoscopic forceps or laser more difficult. A particular risk with the endoscopic approaches is converting a proximal gallstone ileus into a distal gallstone ileus. In a handful of cases, surgery was needed subsequent to upper endoscopy due to stricture, sepsis, and a second stone in the duodenum .(24)

Endoscopic therapies also offer a less invasive approach to relieve obstructing gallstones in the colon. Zaretsky in 1977 described the colonoscopic diagnosis and relief of large bowel obstruction caused by an impacted gallstone.(25) Nonsurgical treatment of gallstone(s) impacted in the colon has been described using extracorporeal lithotripsy, dormia baskets and polypectomy snares.(26,27,28) These techniques, while successful in situations where the gallstone is small enough to be endoscopically extracted or where it yields enough to be broken with less radical endoscopic methods, can be inadequate for management of large stones. Zielinski et al described the use of EHL to fragment a large stone impacted in the sigmoid colon.(29) Colonoscopy was performed in the case described to exclude any associated large bowel pathology (neoplasm) as well as attempt retrieval of the calculus. The available retrieval baskets were too small.

The inflamed colon was also not yielding sufficiently to aid maneuverability of the stone or the scope. There were no energy sources available to fragment the stone.

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Gallstone ileus is a rare entity but the evolution of laparoscopy has prompted some surgeons to attempt enterolithotomy laparoscopically. The enterolithotomy may be performed laparoscopically or laparoscopically assisted, when, after finding the gallstone, the bowel segment is pulled out through a small laparotomy, the gallstone is mobilized backward and the enterolithotomy is performed.(30,31,32) In a retrospective study (32 patients with gallstone ileus treated with laparoscopic enterolithotomy or classic surgery, between 1992 and 2004; 19 laparoscopic; 2 conversions), Moberg and Montgomery conclude that laparoscopically assisted enterolithotomy may be recommended for both diagnosis or treatment.(33) For the present the laparoscopic approach does not represent the therapeutic gold standard because of the difficult examination of the distended bowel, finding the gallstone, increased time of the surgery and the need for specialized trained surgeons in advanced and emergency laparoscopy.(10)

The gold standard procedure is exploratory laparotomy and enterolithotomy.

Surgical treatment encompasses three options: 1) management of the bowel obstruction only, 2) treating the obstruction and taking down the fistula and cholecystectomy, and 3) relieving the obstruction and treating the gallbladder and fistula as a second stage procedure if clinically warranted.

The high mortality rates associated with gallstone ileus, often secondary to the comorbidities of the affected population, historically prompted surgeons to solely address removal of the obstructing stone. There was no attempt at the initial operation to treat the cholecystoenteric fistula or remove the gallbladder.

In the most common situation, ileal obstruction requires an enterotomy oriented longitudinally on the antimesenteric border of the bowel (most frequently of 1520 cm proximally to the obstruction site). The gallstone is mobilized upstream and delivered via the enterotomy. This is followed by a repair of the bowel wall 97

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transversely in one or two layers. Proximal mobilisation of the stone allows the enterotomy to be performed in a safe zone where there are no mucosal lesions or threat to the microcirculation from the impacted stone. The entire bowel is subsequently palpated to exclude other calculi. The Kopel maneuver (pushing the gallstone through the Bauhin (ileo-cecal) valve with the help of a clamp) is forbidden, due to the possibility of causing damage to the bowel wall.(4) Usually it is not possible to “milk” the stone in either direction in Bouveret’s Syndrome.

However, if the stone can be “milked” proximally, the enterotomy should be made in normal bowel with closure perpendicular to the opening to avoid stricture formation. It may be necessary on occasion to perform a gastrojejunostomy and leave the duodenal stone in place. Stones lodged in the colon may require temporary colostomy and impacted small bowel stones may require resection.

(34)

In the case described there was pressure induced ischemia on the distal sig-

moid colon wall. The concomitant diverticulitis made pelvic dissection unsafe and a Hartmann’s procedure was performed.

This clinical problem generally affects the elderly. The elderly population has a greater chance of having other co-morbidities, namely diabetes, hypertension and ischemic heart disease. Earlier reports indicate that a high mortality is seen in elderly patients with gallstone ileus. There was therefore no attempt at the initial operation to treat the cholecystoenteric fistula or remove the gallbladder.

Holz in 1929 and Welch in 1957, described a one-stage procedure consisting of enterolithotomy, closure of the cholecystoenteric fistula and cholecystectomy, to prevent future recurrence of gallstone ileus or cholangitis.(3). This has been the topic of debate in the management of gallstone ileus in the ensuing years.

Proponents of the enterolithotomy alone approach argue that the fistula will usually close when the obstruction is relieved, and any residual stones in the gallbladder will pass via the fistula. Also, most patients will not suffer any re98

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sidual symptoms from either the fistula or the gallbladder.

Enterotomy and stone extraction will resolve the intestinal obstruction, but leave the patient at risk of further symptoms. These may include obstruction ( if there are residual stones within the gallbladder), persistent symptoms from an inflamed gallbladder, a possible increased risk of developing gallbladder cancer and the risk of malabsorption form a cholecysto-colonic fistula.(7,11,12) For these reasons, alternative approaches include enterolithotomy, cholecystectomy and fistula repair as a one-stage procedure, or enterolithotomy and interval cholecystectomy with fistula repair when the patient has recovered from the acute episode.

In the largest review of the literature involving 1001 cases the one stage procedure had a 16.9% mortality rate compared with 11.7% for enterolithotomy alone (not statistically significant). Eighty percent of these patients were treated with enterolithotomy alone. The recurrence rate of gallstone ileus in those treated with enterolithotomy alone was less than 5%. This is not dissimilar to the 6 of 113 patients who experienced recurrent gallstone ileus after a one-stage procedure as a result of residual common bile stones or unrecognised enteric stones.

Additionally, only 10% of patients required re-operation for persistent biliary symptoms.(7) Although this study included a large number of patients, this series was collated by pooling patients from 70 published series spanning 40 years, with widely differing lengths of follow-up and evolving surgical technique during this time period. Furthermore, none of these studies were randomised and the reasons for selecting one operative strategy over another are not detailed but are likely to be influenced by surgical bias.

Doko and colleagues conducted a retrospective review of 30 cases of GI treated by enterolithotomy or one stage procedure (enterolithotomy with cholecystectomy and fistula repair). There was a statistically significant difference in the 99

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operating time with the duration of surgery 100 minutes longer in the one stage group. The in-hospital mortality was 9% for the enterolithotomy group and 11% for the one stage group. The one stage procedure had a higher complication rate. However, the study was not randomised and the selection process for each operative approach was not detailed; it is likely that there was selection bias for the two operative approaches. These authors made a recommendation for the one stage procedure in cases where patients had acute cholecystitis, gangrenous gallbladder or residual gallstone stones at the time of operation.(35)

Similar findings were reported by Rodriguez-Sanjuan et al in a series of 25patients. Morbidity after enterolithotomy was 50% compared to 66% following a one-stage procedure. Mortality was 19% after an enterolithotomy alone and 33% in patients undergoing a one-stage procedure. In this study, the surgical approach was selected by the surgeon at the time of operation without randomization. Follow-up varied widely from 4 months to 8 years.(36) Clavien et al. advocated a one-stage procedure where feasible. In their study of 37 patients, there was a 17% incidence of recurrent gallstone ileus in the 23 patients treated with enterolithotomy alone, higher than the 5â&#x20AC;&#x201C;10% reported in other series.(37)

Tan and colleagues reviewed a series of 19 patients who had the one stage procedure versus enterolithotomy alone. The one stage procedure was performed in those patients who had lower ASA (American Society of Anaesthiesiologists) class and operative times were significantly longer (â&#x2030;Ľ 100 minutes) in the one stage group. There was no significant difference in morbidity between the groups and they had no mortality in either group. They were able to recommend the one-stage procedure in fit low risk patients and those who were not haemodynamically unstable pre-operatively. For patients with higher ASA grades and co-morbidities, enterolithotomy alone should be performed. In addition, to avoid recurrent biliary symptoms they also recommended fistula repair for 100

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patients with cholecystocolonic fistula.(38) More recently, others have published data supporting a one-stage procedure where mortality rates as low as 6% were reported.(37,39) A review of the literature thus defends the one-stage procedure in the ideal patient, however with potentially significant morbidity and mortality. For those patients who are hemodynamically unstable or have significant inflammation or dense adhesions, enterolithotomy alone should be performed. In the case described, pelvic inflammation presented more problems than the cholecystocolonic fistula. Further support of the one stage procedure is conferred by the advent of laparoscopic intervention. Sica et al. reported, in 2005, the first case of uneventful stone removal and cholecystectomy by laparoscopy.(40)

The final treatment option is a two stage procedure, where the enterolithotomy is performed as the initial emergency procedure and subsequent cholecystectomy and fistula disconnection performed 4-6 weeks later. The results of recent literature reveal the low recurrence rates of gallstone ileus and few complications in patients managed expectantly after enterolithotomy. The two stage procedure with scheduled follow-up biliary surgery is not common.(7,10,38)

CONCLUSION The incidence of gallstone ileus is low but may increase due to aging of the population and better more widely available investigative tools such as CT. The uniform management of this surgical emergency has not been clearly defined.

Endoscopic techniques have been well described to be effective in retrieving the stone and relieving the obstruction. These techniques are limited by the availability of equipment and expertise.

There are advocates for both enterolithotomy alone to relieve obstruction with biliary tract surgery either simultaneously (one stage procedure) or at a later 101

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date (two stage procedure). For the most part following enterolithotomy alone, the remaining fistula can close spontaneously once the obstruction has been resolved and complications related to persistent fistula are uncommon. More recent literature have noted recurrent biliary symptoms that may require surgery and have published data supporting a one stage procedure where mortality rates are low (<6%) when compared to historical rates (40%). Despite these rewarding figures and the progress noted with laparoscopic intervention surgeons must exercise a selective approach for the one stage procedure. The one stage procedure may be considered specifically for the younger, fitter patients who are well pre-optimised and when the surgical field indicates its feasibility.

The laparoscopic approach is not to be routinely recommended as experience is limited and will require advanced laparoscopic skills. Cholecystocolonic fistula is one situation where fistula disconnection should be considered.

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REFERENCES 1. Rodríguez Hermosa JI, Codina Cazador A, Gironès Vilà J, et al. Gallstone Ileus: results of analysis of a series of 40 patients. Gastroenterol Hepatol 2001; 24: 489-494.

2. Deckoff SL. Gallstone ileus: a report of 12 cases. Ann Surg 1955;142(1):52–65.

3. Zaliekas J, Munson L. Complications of gallstones: the Mirizzi syndrome, gallstone ileus, gallstone pancreatitis, complications of ‘lost gallstones’. Surg Clin N Am 2008; 88: 1345-1368.

4. Beuran M, Ivanov I, Venter MD. Gallstone ileus- Clinical and therapeutic aspects. J Med & Life 2010; 3(4): 365-371.

5. Doycheva I, Limaye A, Suman A, et al. Bouveret’s Syndrome: case report and review of the literature. Gastr Res Prac 2009; 1-4.

6. Cappell MS, Davis M. Characterization of Bouveret’s syndrome: a comprehensive review of 128 cases, Am J Gastroenterol, 2006; 101(9): 139–2146.

7. Reisner RM, Cohen JR. Gallstone ileus. A review of 1001 cases. Am.Surg. 1994; 60: 441446.

8. Muthukumarasamy G, Venkata S, Shaikh IA, et al. Gallstone ileus: surgical strategies and clinical outcome. J Dig Dis 2008; 9: 156-161.

9. Nakamoto Y, Saga T, Fujishiro S, et al. Gallstone ileus with impaction at the neck of a Meckel’s diverticulum. Br J Radiol 1998; 71: 1320-1322.

10. Ayantunde AA, Agrawal A. Gallstone ileus: diagnosis and management. World J Surg 2007;31:1292–7.

11. Cooperman AM, Dickson ER, ReMine WH. Changing concepts in the surgical treatment of gallstone ileus. Ann Surg 1968;167(3):377–83.

12. Savvidou S, Goulis J, Gantzarou A, et al. Pneumobilia, chronic diarrhea, vitamin K malabsorption. A pathognomonic traid for cholecystocolonic fistulas. World J Gastroenterol 2009; 15(32): 4077-4082.

13. Chou JW, Hsu CH, Liao KF, et al. Gallstone ileus: report of two cases and review of the literature. World J Gastroenterol 2007;13(8):1295–8.

14. Hildebrandt J, Herrman U, Diettrich H. Gallstone ileus. A report of 104 cases. Chirurg.

1990; 61: 392-395.

15. Ripolles T, Miguel-Dasit A, Errando J, et al. Gallstone ileus: increased diagnostic sensitivity by combining plain film and ultrasound. Abdom Imaging 2001;26:401–5.

16.Lassandro F, Gagliardi N, Scuderi M, et al. Gallstone ileus analysis of radiological findings in 27 patients. Eur J Radiol 2004;50:23–9.

17 Yu CY, Lin CC, Shyu RY, et al. Value of CT in the diagnosis and management of gallstone ileus. World J Gastroenterol 2005;11(14):2142–7.

18. Lassandro F, Romano S, Ragozzino A, et al. Role of helical CT in diagnosis of gallstone ileus and related conditions. AJR Am J Roentgenol 2005;185:1159–65.

103

A CASEBOOK OF TWENTY SURGICAL CASES 19. Grove O. Acute pyloric obstruction by gallstone: report of a case diagnosed by gastroscopy.

Gastrointestinal Endoscopy 1976; 22(4): 212–213.

20.Bedogni G, Continin S, Meinero M, et al. Pyloroduodenal obstruction due to a biliary stone (Bouveret’s syndrome) managed by endoscopic extraction. Gastrointestinal Endoscopy 1985; 31 (1): 36-38.

21. Lowe AS, Stephenson S, Kay CL, et al.Duodenal obstruction by gallstone (Bouveret’s syndrome): a review of the literature. Endoscopy 2005; 37(1): 82–87.

22.Maiss J, Hochberger J,Muehldorfer S, et al. Successful treatment of Bouveret’s syndrome by endoscopic laser lithotripsy. Endoscopy 1999;(31(2):S4–S5.

23.Moriai T, Hasegawa T, Fuzita M, et al. Successful removal of massive intragastric gallstones by endoscopic electrohydraulic lithotripsy and mechanical lithotripsy. Am J Gastroenterol 1991; 86(5): 627–629.

24.Moschos J, Pilpilidis I, Antonopoulos Z, et al. Complicated endoscopic management of Bouveret’s syndrome. A case report and review, Rom J Gastroenterol 2005; 14 (1): 75–77.

25. Zaretzky B, Kodsi BE, Iswara K. Colonoscopic diagnosis and relief of large bowel obstruction caused by impacted gallstone. Gastrointest Endosc 1977; 23: 210-211.

26. Meyenberger C, Michel C, Metzger U, et al. Gallstone ileus treated by extracorporeal shockwave lithotripsy. Gastrointest Endosc 1996; 43: 508-511.

27. Garcia-López S, Sebastián JJ, Uribarrena R, et al. Successful endoscopic relief of large bowel obstruction in a case of a sigmoid colon gallstone ileus. J Clin Gastroenterol 1997; 24: 291-292.

28 Roberts SR, Chang C, Chapman T, et al. Colonoscopic removal of a gallstone obstructing the sigmoid colon. J Tenn Med Assoc 1990; 83: 18-19.

29.Zielinski MD, Ferreira LE, Baron TH. Successful endoscopic treatment of colonic gallstone ileus using electrohydraulic lithotripsy. World J Gastroenterol 2010 ; 16(12): 1533-1536 30. Montgomery A. Laparoscope guided enterolithotomy for gallstone ileus. Surg. Laparosc.

Endosc. 1993; 3: 310-314.

31. Franklin ME Jr., Dorman JP, Schuessler WW. Laparoscopic treatment of gallstone ileus: a case report and review of the literature. J Laparoendosc. Surg. 1994;4: 265- 272.

32. Sarli L, Pietra N, Costi R, et al. Gallstone ileus: laparoscopic assisted enterolithotomy.

J.Am. Coll.Surg. 1998;186: 370-371.

33. Moberg AC, Montgomery A. Laparoscopically assisted or open enterolithotomy for gallstone ileus. British Journal of Surgery 2007;94: 53-57.

34.Dan D, Collure DW, Hoover EL. Bouveret’s syndrome: revisiting gallstone obstruction of the duodenum. J Natl Med Assoc. 2003; 95: 969-973.

35. Doko M, Zovak N, Kopljar M, et al. Comparison of surgical treatments of gallstone ileus: a preliminary report. World J Surg 2003; 27: 400–4.

36. Rodriguez-Sanjuan JC, Casado F, Fernandez MJ, et al. Cholecystectomy and fistula closure versus entero-lithotomy alone in gallstone ileus. Br J Surg 1997; 84: 634–7.

37. Clavien PA, Richon J, Burgan S, et al. Gallstone ileus. Br J Surg 1990; 77: 737–42.

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38. Tan YM, Wong WK, Ooi LL. A comparison of two surgical strategies for the emergency treatment of gallstone ileus. Singapore Med J 2004;45(2):69–72.

39. Zuegal N, Hehl A, Lindemann F, et al. Advantages of one-stage repair in case of gallstone ileus. Hepato-Gastroenterol 1997; 44:59-62.

40. Sica GS, Sileri P, Gaspari AL. Laparoscopic treatment of Bouveret’s syndrome presenting as acute pancreatitis. J Soc Laparoendosc Surg 2005;9(4): 472–475.

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6. HEMORRHOIDS INTRODUCTION: Hemorrhoids are a very common anorectal condition defined as the symptomatic enlargement and distal displacement of the normal anal cushions. They affect millions of people around the world, and represent a major medical and socioeconomic problem. Multiple factors have been claimed to be the etiologies of hemorrhoidal development, including constipation and prolonged straining.

The abnormal dilatation and distortion of the vascular channel, together with destructive changes in the supporting connective tissue within the anal cushion, is a paramount finding of hemorrhoidal disease.

Despite hemorrhoid disease being a benign condition, it has been studied extensively. Improvements in our understanding of the anatomy of hemorrhoids have prompted the development of new and innovative methods of treatment.

The most common symptom of hemorrhoids is rectal bleeding associated with bowel movement. Numerous surgical treatment options have been outlined, including office based procedures that allow for treatment without anaesthesia.

Two cases of per rectal bleeding relating to hemorrhoids are presented here, each managed differently. The various treatment modalities for hemorrhoids are outlined in relation to the current literature.

CASE 1 History: A 45 year old man, referred via the A&E, reported bright red per rectal bleeding every day for the past 3weeks. This was not associated with pain and occurred with each bowel action (twice daily). There was no change to the frequency or consistency of his stool. He explained that the per rectal bleeding has been present for the past year but to a much lesser extent and less frequently.

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The patient did not experience tenesmus or symptoms of anemia. His appetite was maintained and his weight he described as stable.

Systematic enquiry was otherwise non-contributory. He reported no past medical or surgical history.

This man was a taxi driver and had no family history of gastrointestinal disease (benign or malignant).

Physical examination: He had pallor of the mucus membranes and vital signs were: BP 144/92 mmHg, P 88 min-1, RR 18 min-1, T 372 0C. There was no evidence of weight loss. There was no palpable lymphadenopathy and cardiac and respiratory examination was otherwise normal.

The abdomen had no abnormal findings and digital rectal examination was normal. There was no blood at this time.

Proctoscopy revealed secondary hemorrhoids at the 3,7 and 11 o’clock positions. Rigid sigmoidoscopy was possible to 18cm and the mucosa was normal.

There were some stool lumps present but they were green.

Investigations: Hb 7.8 g/dl, MCV 72 fl, MCH 22.8, WCC 8.4 x 103 µl-1, Plt 399 x 103 µl-1. Normal renal and liver function tests including PT, PTT. CXR: normal.

A nasogastric tube was placed on admission and the aspirate was bile tinged.

In view of the microcytic hypochromic anemia an urgent gastroscopy and colonoscopy was performed. The esophagus, stomach and duodenum were normal.

The colonoscope passed to the cecum and this was normal.

A diagnosis of anemia secondary to hemorrhoidal bleeding was made and this was treated with rubber band ligation. Rubber bands (x2) were placed on the 107

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base of the hemorrhoids at 3 and 7 oâ&#x20AC;&#x2122;clock positions.

His symptoms improved and at 6 months his hemoglobin level was 12.8 g/dl.

CASE 2 History: A 55 year old man was referred to the surgical outpatient clinic for per rectal bleeding. He explained that this has been present for about three years. The bleeding generally occurred with bowel actions. It was a bright red nature and painless, mainly on wiping himself but on occasion would be seen dripping into the toilet bowl. His bowel actions were twice daily and he attested that at times he would have to strain at stool. There was no change in frequency or consistency of his stool and he reported no constitutional symptoms. Despite using topical agents, including Preparation H, during the last year he developed a fleshy protrusion which he now had to replace.

Systematic

enquiry

was

otherwise

non-contributory.

This

gentle-

man, a construction worker, was an asthmatic and had a previous appendicectomy. He had no family history of gastrointestinal tract disease.

Physical examination: A well looking gentleman with vital signs: BP 128/88mmHg, P 76min-1, RR 18min-1, T 365 0C. His mucous membranes were pink and cardiorespiratory examination was normal.

His abdomen bore a scar in the right iliac fossa in keeping with his previous appendicectomy. Otherwise the abdomen was normal. On inspection of the anus the anoderm at the verge appeared redundant. Digital rectal examination identified a palpably normal anorectum with normal tone.

Proctoscopy revealed large third degree hemorrhoids at the 3, 7, 11 oâ&#x20AC;&#x2122;clock positions. Rigid sigmoidoscopy was normal at 20cm.

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Investigations: Hb 9.4 g/ dl, MCV 70 fl, MCH 24, WCC 5 x 103 µ/l ,Plt 121 x 103 µ/l.

A barium enema was performed to image the large bowel. There was no evidence of polyps, diverticular disease or a cancer. The patient was informed of his diagnosis, third degree hemorrhoids, consented and given a date for hemorrhoidectomy. This was performed a few weeks later via Milligan-Morgan technique. The hemorrhoids at the 3 and 11 o’clock positions were excised.

This was done with the aid of diathermy dissection and the apical pedicles were suture ligated. He reported minimal pain post operatively and was discharged home the following day with advice on adequate water intake, adequate dietary fibre, sitz bath and a prescription for paracetamol, arcoxia, and metronidazole for 1 week.

At 2 weeks post operatively the wounds are almost completely healed and he has not had any bleeding. The remaining hemorrhoid at 7 o’clock appears smaller.

(Fig 4,5,6).

Fig1 Proctoscopy demonstrating 2nd degree hemorrhoids at 3, 7, 11 o’ clock positions.

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Fig2 Operating proctoscope: allows the hemorrhoid to prolapse into view.

Fig 3 Apparatus for rubber band ligation: rubber bands, pointed tip spigot to facilitate mounting of the rubber band (black), applicator.

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Fig 4, 5: 3rd degree hemorrhoids

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Fig 6: Anus 2 weeks after Milligan-Morgan Hemorrhoidectomy (almost healed wound; note how much smaller the residual hemorrhoid at 7 oâ&#x20AC;&#x2122;clock has become).

DISCUSSION Hemorrhoids are cushions of highly vascular tissue found within the submucosal space and are considered part of the normal anatomy of the anal canal. The anal canal contains 3 main cushions that are found in the left lateral, right anterior, and right posterior positions. Within these hemorrhoidal cushions, blood vessels, elastic tissue, connective tissue, and smooth muscle are found. Together, these tissues contribute to 15% to 20% of the resting pressure within the anal canal. Each cushion surrounds arteriovenous communications between the terminal branches of the superior and middle rectal arteries and the superior, middle, and inferior rectal veins.(1)

Hemorrhoidal cushions have several important functions within the anal canal.

By engorging with blood and causing closure of the anal canal, they contribute to the maintenance of anal continence and prevention of stool leakage during cough112

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ing, straining, or sneezing. When engorged with blood, these cushions also serve as protection for the underlying anal sphincters during the act of defecation. This tissue also plays a key role in sensory function, which is central to the differentiation between liquid, solid, and gas and the subsequent decision to evacuate.(1,2)

The exact pathophysiology of hemorrhoidal development is poorly understood.

For years the theory of varicose veins, which postulated that hemorrhoids were caused by varicose veins in the anal canal, had been popular but now it is obsolete because hemorrhoids and anorectal varices are proven to be distinct entities.

Today, the theory of sliding anal canal lining is widely accepted. This proposes that hemorrhoids develop when the supporting tissues of the anal cushions disintegrate or deteriorate. Hemorrhoids are therefore the pathological term to describe the abnormal downward displacement of the anal cushions causing venous dilatation.

(3)

The anal cushions of patients with hemorrhoids show significant pathological

changes. These changes include abnormal venous dilatation, vascular thrombosis, degenerative process in the collagen fibers and fibroelastic tissues (Parks ligament), distortion and rupture of the anal subepithelial muscle (of Treitz). In addition to these findings, a severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia and thrombosis.(4)

Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. In 2004, Chung et al reported that endoglin (CD105), which is one of the binding sites of TGF-β and is a proliferative marker for neovascularization, was expressed in more than half of hemorrhoidal tissue specimens compared to none taken from the normal anorectal mucosa. This marker was prominently found in venules larger than 100 Οm. Moreover, these workers found that 113

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microvascular density increased in hemorrhoidal tissue especially when thrombosis and stromal vascular endothelial growth factors (VEGF) were present.(5)

The muscular fibroelastic supportive tissue of the hemorrhoidal plexus degenerates with a patientâ&#x20AC;&#x2122;s age. As a result, the mobility of the plexus increases in relation to the intrarectal pressure. At the same time, the vessels of this plexus become enlarged. This plus the increased mobility caused by insufficient supportive structures are the reason for prolapsing piles. The mucosa becomes more fragile, and bleeding occurs. Arteriovenous shunts are usually closed, thus enabling capillary blood exchange. Specific irritation can cause such shunts to open. As a result, spasms of the precapillary sphincters occur, and flow through the shunts increases. This leads to high interior pressure and dilation of the hemorrhoidal venous plexus. It also explains the bright red color of the blood presented by bleeding hemorrhoids.(6)

Many factors contribute to the development of pathologic changes within the hemorrhoidal cushions, including constipation, prolonged straining, exercise, gravity, nutrition (low-fiber diet), pregnancy, increased intra-abdominal pressure, irregular bowel habits (constipation/diarrhea), genetics, absence of valves within the hemorrhoidal veins, and aging. These factors lead to increased pressure within the submucosal arteriovenous plexus and ultimately contribute to swelling of the cushions, laxity of the supporting connective tissue, and protrusion into and through the anal canal.(7)

Hemorrhoids are a very common anorectal condition affecting millions of people around the world, and represent a major medical and socioeconomic problem. There is some confusion though among lay people and doctors, who misuse the terms hemorrhoids and piles to cover a variety of complaints.

This has led to estimates of prevalence varying from 4.4% among adults in 114

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the United States to 36.4% in general practice in London.(8) The true epidemiology of this disease is unknown because patients have a tendency to use self-medication rather than to seek proper medical attention. An epidemiologic study by Johanson et al in 1990 showed that 10 million people in the United States complained of hemorrhoids, corresponding to a prevalence rate of 4.4%.

In both sexes, peak prevalence occurred between age 45-65 years and the development of hemorrhoids before the age of 20 years was unusual. Whites and higher socioeconomic status individuals were affected more frequently than blacks and those of lower socioeconomic status. However, this association may reflect differences in healthseeking behavior rather than true prevalence.(9)

The most common manifestation of hemorrhoids is painless rectal bleeding associated with bowel movement, described by patients as blood dripping into the toilet bowl. The blood is typically bright red as hemorrhoidal tissue has direct arteriovenous communication.(10) Prolapse occurs with a bowel movement and is associated with an uncomfortable sensation of fullness and incomplete evacuation; patients complain of a lump at the anal verge. Soiling may occur in third and fourth degree hemorrhoids as a result of impaired continence or production of mucus discharge. Discharge can cause perianal irritation and itching. Fourth degree hemorrhoids may become “strangulated” and present with acute severe pain. Progressive venous engorgement and incarceration of the acutely inflamed hemorrhoid leads to thrombosis and infarction.

Assessment should include anoscopy and a digital examination in the left lateral position. The perianal area should be inspected for the presence of skin tags, fissures, fistulae, polyps, or tumours. Prolapsing hemorrhoids may appear at the anal verge on straining. The hemorrhoidal cushions can be viewed by using the anoscope in the left lateral, right anterior, and right posterior positions (3 o’clock, 7 o’clock, 11 o’clock positions). Hemorrhoidal size, 115

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severity of inflammation, bleeding and importantly, sphincter tone should be assessed. Treatment will be guided by degree and severity of symptoms.

Positive fecal occult blood or anemia should not be attributed to hemorrhoids until the colon is adequately evaluated especially when the bleeding is atypical for hemorrhoids, when no source of bleeding is evident on anorectal examination, or when the patient has significant risk factors for colorectal neoplasia.(11)

Often, patients are referred to a surgeon already diagnosed with hemorrhoids or ‘‘piles’’, but it is still important to rule out other causes of similar symptoms. The differential diagnosis of hemorrhoids includes anal fissure, perirectal abscess, anal fistula, anal stenosis, malignancy, inflammatory bowel disease ( Crohn’s disease and ulcerative colitis), anal condyloma, pruritus ani, rectal prolapse, hypertrophied anal papilla, and skin tags.(1) Although not all-inclusive, this list does emphasize that many other conditions may be concomitantly present or cause similar symptoms.

A hemorrhoid classification system is useful not only to help in choosing between treatments, but also to allow the comparison of therapeutic outcomes among them. Hemorrhoids are generally classified on the basis of their location and degree of prolapse. Internal hemorrhoids originate from the inferior hemorrhoidal venous plexus above the dentate line and are covered by mucosa, while external hemorrhoids are dilated venules of this plexus located below the dentate line and are covered with squamous epithelium. Mixed (interno-external) hemorrhoids arise both above and below the dentate line. Internal hemorrhoids are further graded based on their appearance and degree of prolapse, known as Goligher’s classification:(11) (1)First degree hemorrhoids (grade I): The anal cushions bleed but do not prolapse , 116

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(2) Second-degree hemorrhoids (grade II): The anal cushions prolapse through the anus on straining but reduce spontaneously, (3) Third-degree hemorrhoids (grade III): The anal cushions prolapse through the anus on straining or exertion and require manual replacement into the anal canal, (4) Fourthdegree hemorrhoids (grade IV): The prolapse stays out at all times and is irreducible. Acutely thrombosed, incarcerated internal hemorrhoids and incarcerated, thrombosed hemorrhoids involving circumferential rectal mucosal prolapse are also fourth-degree hemorrhoids.

The treatment of symptomatic hemorrhoids varies and ranges from conservative therapy involving dietary and lifestyle changes to use of various pharmacological agents and creams, office-based nonoperative procedures, and operative hemorrhoidectomy.

The shearing action of passing hard stool on the anal mucosa is generally accepted by all to cause damage to the anal cushions and lead to symptomatic hemorrhoids. Therefore increasing intake of fiber or providing added bulk in the diet might help eliminate straining during defecation. In clinical studies of hemorrhoids, fiber supplement reduced the risk of persisting symptoms and bleeding by approximately 50%, but did not improve the symptoms of prolapse, pain, and itching . Fiber supplement is therefore regarded as an effective treatment in non-prolapsing hemorrhoids.(12) It may take take up to 6 wk for a significant improvement to be manifest. As fiber supplements are safe and cheap, they remain an integral part of both initial treatment and of a regimen following other therapeutic modalities of hemorrhoids.

Lifestyle modification should also be advised to any patients with any degree of hemorrhoids as a part of treatment and as a preventive mea117

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sure. These changes include increasing the intake of dietary fiber and oral fluids, reducing consumption of fat, having regular exercise, improving anal hygiene, abstaining from both straining and reading on the toilet, and avoiding medication that causes constipation or diarrhea.(13)

A number of topical preparations are available including creams and suppositories, and most of them can be bought without a prescription. Strong evidence supporting the true efficacy of these drugs is lacking. These topical medications can contain various ingredients such as local anesthesia, corticosteroids, antibiotics and anti-inflammatory drugs. Topical treatment may be effective in selected groups of hemorrhoidal patients. For instance, Tjandra et al showed a good result with topical glyceryl trinitrate 0.2% ointment for relieving hemorrhoidal symptoms in patients with low-grade hemorrhoids and high resting anal canal pressures. However, 43% of the patients experienced headache during the treatment.(14) Perrotti et al reported the good efficacy of local application of nifedipine ointment in treatment of acute thrombosed external hemorrhoids.(15) It is worth noting that the effect of topical application of nitrite and calcium channel blocker on the symptomatic relief of hemorrhoids may be a consequence of their relaxation effect on the internal anal sphincter, rather than on the hemorrhoid tissue, where one might anticipate a predominantly vasodilator effect.

Some topical treatment targets vasoconstriction of the vascular channels within hemorrhoids such as Preparation-H, an agent commonly associated with the treatment of symptomatic haemorrhoids. It contains 0.25% phenylephrine, petrolatum, light mineral oil, and shark liver oil. Phenylephrine is a vasoconstrictor having preferential vasopressor effect on the arterial site of circulation, whereas the other ingredients are considered protectants. Preparation-H is available in many forms, including ointment, cream, gel, suppositories, and medicated and portable wipes.(7) It provides temporary relief 118

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of acute symptoms of hemorrhoids, such as bleeding and pain on defecation.

Oral medications have been used to address the symptoms of hemorrhoids. Of these the oral flavonoids seems most relevant. These venotonic agents were first described in the treatment of chronic venous insufficiency and edema. They appeared to be capable of increasing vascular tone, reducing venous capacity, decreasing capillary permeability, and facilitating lymphatic drainage as well as having anti-inflammatory effects. Although their precise mechanism of action remains unclear, they are used as an oral medication for hemorrhoidal treatment, particularly in Europe and Asia.(16) The micronization of the drug to particles of less than 2 Îźm not only improved its solubility and absorption, but also shortened the onset of action. A recent meta-analysis of flavonoids for hemorrhoidal treatment, including 14 randomized trials and 1514 patients, suggested that flavonoids decreased risk of bleeding by 67%, persistent pain by 65% and itching by 35%, and also reduced the recurrence rate by 47%.(17) Some investigators reported that micronized purified flavonoid fraction can reduce rectal discomfort, pain and secondary hemorrhage following hemorrhoidectomy.(18)

Oral calcium dobesilate is another venotonic drug commonly used in diabetic retinopathy and chronic venous insufficiency as well as in the treatment of acute symptoms of hemorrhoids. It was demonstrated that calcium dobesilate decreased capillary permeability, inhibited platelet aggregation and improved blood viscosity; thus resulting in reduction of tissue edema.(19) A clinical trial of hemorrhoid treatment showed that calcium dobesilate, in conjunction with fiber supplement, provided an effective symptomatic relief from acute bleeding, and it was associated with a significant improvement in the inflammation of hemorrhoids.(20)

Cultural practices influence the treatment of hemorrhoids. Several other preparations are available including herbal remedies. Indeed a Cochrane review in119

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dicated that traditional Chinese medicinal herbs significantly improved overall symptoms and bleeding as well as decreased the inflammation of perianal mucosa.(21)

These agents may be used to provide short term relief from discomfort, but there is a lack of evidence to support their widespread use. They do not affect the underlying pathological changes in the anal cushions. As a result interventional procedures may be required to treat the persistence of symptoms or the progression of the grade. Interventional procedures are classified as non-operative and operative. The non-operative measures are appealing since they can be performed on an outpatient basis.

They are generally well tolerated but may require repeated applications.

Rubber band ligation (RBL) is a simple, quick, and effective means of treating first- and second-degree hemorrhoids and selected patients with thirddegree hemorrhoids. Ligation of the hemorrhoidal tissue with a rubber band causes ischemic necrosis and scarring, leading to fixation of the connective tissue to the rectal wall. The technique was originally described by Barron in 1963 and is the most commonly used outpatient treatment.(22)

Anoscopy is performed to identify the hemorrhoidâ&#x20AC;&#x2122;s origin, which is grasped by using a forceps or suction device. A band is then applied at its base. The strangulated hemorrhoid becomes necrotic and sloughs off, while the underlying tissue undergoes fixation by fibrotic wound healing. If the procedure is well tolerated, up to three piles can be banded at one visit. This increases the risk of discomfort (29% in multiple banding versus 4.5% in single banding), vasovagal symptoms (5.2% in multiple bandings versus 0% in single bandings), and urinary symptoms (12.3% in multiple bandings versus 0% in single bandings).(23) Multiple banding does not increase the risk 120

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of major complications. Injection of a local anaesthetic does not reduce the discomfort associated with multiple banding. If application of the first band causes discomfort then repeat sessions of single banding are advised.(24)

In a study of 512 patients, major complications including urinary retention, rectal bleeding, pelvic sepsis, and perianal abscess occurred in 2.5% (13 patients) of procedures and required admission to hospital. Minor complications including hemorrhoid thrombosis, band displacement, mild bleeding, and formation of mucosal ulcers occurred in 4.6% (24 patients).(25) Band ligation is the most effective outpatient procedure for hemorrhoids. RBL has a success rate varying from 50% to 100%, depending on the length of time between procedure and follow-up and the degree of hemorrhoids ligated (first- and second-degree hemorrhoids have higher success rates).(2,26) Several studies have suggested that approximately 68% of patients experience recurrence of symptoms at 4 to 5 years follow-up, although these symptoms often resolve with repeat RBL; only 10% of patients progress to needing surgical hemorrhoidectomy.(2,27,28)

An absolute contraindication to RBL is the use of sodium warfarin (Coumadin) or heparin because of the risk of hematoma formation and bleeding, particularly when the tissue sloughs off 5 to 7 days after the procedure. Similarly, patients taking aspirin or platelet-altering drugs, such as clopidogrel bisulfate (Plavix), should be advised to avoid these drugs for a period of 5 to 7 days before and after the banding procedure, to minimize the risk of bleeding. Patients who are unable to stop taking sodium warfarin, heparin, or platelet-altering drugs, may be better candidates for a procedure, such as sclerotherapy, which has a theoretically lower risk of postprocedure bleeding.(2)

Sclerotherapy is currently recommended as a treatment option for first- and second-degree hemorrhoids. The rationale of injecting chemical agents is to create 121

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a fixation of mucosa to the underlying muscle by fibrosis. The solutions used are 5% phenol in oil, vegetable oil, quinine, and urea hydrochloride or hypertonic salt solution.(29) It is important that the injection be made into submucosa at the base of the hemorrhoidal tissue and not into the hemorrhoids themselves. Failure to do so can cause immediate transient precordial and upper abdominal pain.(30) Misplacement of the injection may also result in mucosal ulceration or necrosis, and rare septic complications such as prostatic abscess and retroperitoneal sepsis.(31) Antibiotic prophylaxis is indicated for patients with predisposing valvular heart disease or immunodeficiency because of the possibility of bacteremia after sclerotherapy.(32) Recurrence of symptoms occurs in approximately 30% of patients 4 years after the initial injection of a sclerosing agent.(2) Although commonly used the its role for bleeding hemorrhoids is somewhat controversial. Senapti reported on a prospective randomised trial of injection sclerotherapy versus bulk laxatives in the treatment of bleeding hemorrhoids; no significant difference in bleeding at 6 months after either injection sclerotherapy with bulk laxative or bulk laxatives alone was found.(33) With this in mind and the potential complications as outlined above extreme caution is advised when using sclerotherapy.

The infrared coagulator produces infrared radiation which coagulates tissue and evaporizes water in the cell, causing shrinkage of the hemorrhoid mass.

A probe is applied to the base of the hemorrhoid through the anoscope and the recommended contact time is between 1.0-1.5 s, depending on the intensity and wavelength of the coagulator.(34) The necrotic tissue is seen as a white spot after the procedure and eventually heals with fibrosis. Compared with sclerotherapy, infrared coagulation (IRC) is less technique-dependent and avoids the potential complications of misplaced sclerosing injection.(29) Although IRC is a safe and rapid procedure, it may not be suitable for large, prolapsing hemorrhoids.

There are two meta-analyses comparing outcomes among the three com122

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mon non-operative treatments of hemorrhoids (sclerotherapy, RBL and IRC).(35,36) These two studies demonstrated that RBL resulted in the fewest recurrent symptoms of hemorrhoids and the lowest rate of retreatment, but that it led to a significantly higher incidence of pain following the procedure. Hence, RBL could be recommended as the initial non-operative modality for treatment of grade I-III hemorrhoids. In a British survey of almost 900 general and colorectal surgeons, RBL was the most common procedure performed, following by sclerotherapy and hemorrhoidectomy.(37)

Other non operative therapies include cryotherapy and radiofrequency ablation. Cryotherapy ablates the hemorrhoidal tissue with a freezing cryoprobe. It has been claimed to cause less pain because sensory nerve endings are destroyed at very low temperature. However, its use has been associated with prolonged pain, foul-smelling discharge and a high rate of persistent hemorrhoidal mass.(38) It is therefore rarely used.

Radiofrequency ablation (RFA) is a relatively new modality of hemorrhoidal treatment. A ball electrode connected to a radiofrequency generator is placed on the hemorrhoidal tissue and causes the contacting tissue to be coagulated and evaporized. By this method, vascular components of hemorrhoids are reduced and hemorrhoidal mass will be fixed to the underlying tissue by subsequent fibrosis. RFA can be performed on an outpatient basis and via an anoscope similar to sclerotherapy. Its complications include acute urinary retention, wound infection, and perianal thrombosis. Although RFA is a virtually painless procedure, it is associated with a higher rate of recurrent bleeding and prolapse.(39)

Operative hemorrhoidectomy is indicated in the treatment of combined internal and external hemorrhoids or third- and fourth degree hemorrhoids, especially in patients who are unresponsive to other methods of treatment or those with 123

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extensive disease.(40) Less than 10% of patients referred for specialist treatment will require surgery.(41) Only symptomatic haemorrhoidal tissue should be excised (â&#x20AC;&#x153;limited haemorrhoidectomyâ&#x20AC;?).(42) This conserves the sensory anoderm for continence and decreases postoperative pain and anal stenosis.

Historically, numerous procedures have been described for the surgical treatment of symptomatic hemorrhoids, including those by Buie, Fansler, Ferguson, Milligan-Morgan, Parks, Salmon, and Whitehead.(7) The open hemorrhoidectomy, otherwise known as the Milligan-Morgan hemorrhoidectomy (MMH), is most commonly performed in the United Kingdom. This technique involves excision of the internal and external components of the hemorrhoid, with suture ligation of the hemorrhoidal pedicles. The vascular pedicle is ligated, and the wounds are left open to granulate, separated by bridges of skin and mucosa.(8) In the United States the Ferguson hemorrhoidectomy is more popular. The hemorrhoid is exposed in the anoscope, and excision and ligation are performed in its anatomical position. The wound is closed with a continuous suture. Both methods are effective forms of treatment; in theory wound closure should offer faster healing, but this has not been shown consistently.

Wound dehiscence after excision of three piles prolongs healing after closed surgery (6.9 weeks in closed operation versus 4.9 weeks in open operation).(43)

Although open and closed hemorrhoidectomy result in extremely high success rates, significant postoperative pain remains a major obstacle. Unlike the office-based procedures where patients are able to return to their normal activities fairly quickly, patients who undergo operative hemorrhoidectomy are not able to return to their normal routine for approximately 2 to 4 weeks. Severe pain can be successfully managed using a combination of narcotic analgesics, NSAIDs, muscle relaxants, and local treatments, such as sitz baths and ice packs.(7) The addition of prophylactic metronidazole reduces pain 124

A CASEBOOK OF TWENTY SURGICAL CASES

and convalescence after day surgery and increases patientsâ&#x20AC;&#x2122; satisfaction.(44)

Gencosmanoglu and colleagues performed a study evaluating the open and closed technique to determine any difference, comparing operating time, analgesic requirement, hospital stay, morbidity rate, duration of inability to work, and healing time. The investigators found operative time to be significantly shorter when the open technique was performed (35 +/- 7 minutes) compared with the closed technique (45 +/- 8 minutes). There was also no significant difference observed in the duration of hospital stay or the duration of inability to work. The average healing time was significantly shorter in the closed hemorrhoidectomy group, 2.8 +/- 0.6 weeks, compared with 3.5 +/- 0.5 weeks for open hemorrhoidectomy.

The patients who had undergone hemorrhoidectomy with the Ferguson technique were more likely to require pain medication initially, and they were also more likely to develop complications, such as urinary retention and anal stenosis.(45)

Excisional hemorrhoidectomy is the most effective treatment for hemorrhoids with the lowest rate of recurrence compared to other modalities.(36) It can be performed using scissors, diathermy or vascular- sealing devices such as Ligasure (Covidien, United States) and Harmonic scalpel (Ethicon Endosurgery, United States).(16)

Excisional hemorrhoidectomy can be performed safely under perianal anesthetic infiltration as an ambulatory surgery. Studies have shown that day case haemorrhoidectomy is feasible in 82% of selected patients and resulted in a high degree of satisfaction among patients.(17) Laxatives will reduce pain during the first postoperative motion, and restricting perioperative intravenous fluid will minimize the risk of urinary retention.

(46)

Other than pain significant postoperative complications include acute urinary retention (2%-36%), postoperative bleeding (0.03%-6%), bacteremia and sep125

A CASEBOOK OF TWENTY SURGICAL CASES

tic complications (0.5%-5.5%), wound breakdown, unhealed wound, loss of anal sensation, mucosa prolapse, anal stricture (0%-6%), and even fecal incontinence (2%-12%).(1,47)

A new technique based on doppler-guided ligation of the terminal branches of the superior hemorrhoidal artery was introduced in 1995 as an alternative to hemorrhoidectomy. Doppler-guided hemorrhoidal artery ligation (DGHAL) has become increasingly popular in Europe. A Doppler transducer can be inserted into the anal canal and rotated to identify the terminal branches of the superior hemorrhoidal arteries for ligation. The arterial sound emitted from the transducer demarcates the location of the hemorrhoidal artery, which can then be suture ligated.(48) Complications include bleeding, thrombosis, pain, and fissure. Postprocedure pain has been shown to be less than that experienced with other procedures. (49,50) A recent case series of 100 patients followed for 3 years resulted in a 12% recurrence rate and low complication rate (6%).(49) This technique has gone through several iterations of instrumentation since its release, and although not widely used, has consistent literature demonstrating less pain at the cost of slightly higher recurrence when compared with operative excision.

Stapled hemorrhoidopexy (SH) has been introduced since 1998.(51) A circular stapling device is used to excise a ring of redundant rectal mucosa proximal to hemorrhoids and resuspend the hemorrhoids back within the anal canal.

Apart from lifting the prolapsing hemorrhoids, blood supply to hemorrhoidal tissue is also interrupted. A recent meta-analysis comparing surgical outcomes between SH and hemorrhoidectomy, which included 27 randomized, controlled trials with 2279 procedures, showed that SH was associated with less pain, earlier return of bowel function, shorter hospital stay, earlier return to normal activities, and better wound healing, as well as higher degree of patient satisfaction.(52) However, in the longer term, SH was associated with a higher 126

A CASEBOOK OF TWENTY SURGICAL CASES

rate of prolapse.(52,53,54) Considering the recurrence rate, cost of stapling device and potential serious complications including rectovaginal fistula(55) and rectal stricture(56,57), SH is generally reserved for patients with circumferential prolapsing hemorrhoids and having â&#x2030;Ľ 3 lesions of advanced internal hemorrhoids.

DGHAL and SH, both aim to correct the pathophysiology of hemorrhoids by reducing blood flow to the anal canal (dearterialization) and eliminating anorectal mucosal prolapse (reposition), respectively. A recent retrospective study of 18-month outcomes of DGHAL (n = 51) and SH (n = 63) for grade III hemorrhoids revealed that both procedures were safe and effective.

DGHAL had less pain, shorter hospital stay, and faster functional recovery; however, it was associated with higher recurrence rate and lower patient satisfaction rating.(58) Lately, a smaller prospective trial comparing DGHAL to SH for grade II-III hemorrhoids showed similar short-term and long-term outcomes of the two procedures.(59) Nevertheless, patients undergoing DGHAL returned to work quicker, and had fewer complication rates than those receiving SH.

CONCLUSION Symptomatic hemorrhoids are very common. Improved understanding of the pathophysiology of hemorrhoids has sparked innovative ideas for addressing this condition. On reviewing the data as outlined above the following recommendations can be made:

-Dietary modification consisting of adequate fluid and fiber intake is the primary first-line nonoperative therapy for patients with symptomatic hemorrhoid disease.

-Most patients with grade I, II, and III hemorrhoid disease in whom medical

treatment

fails

may

be

effectively

treated

with

office-

based procedures, such as banding, sclerotherapy and infrared coagulation. Hemorrhoid banding is typically the most effective option.

-Surgical hemorrhoidectomy should be reserved for patients who are refrac127

A CASEBOOK OF TWENTY SURGICAL CASES

tory to office procedures, who are unable to tolerate office procedures, who have large external hemorrhoids, or who have combined internal and external hemorrhoids with significant prolapse (grades III to IV). DHAL and SH are good alternatives but are expensive and have higher recurrence rates.

In counseling patients regarding hemorrhoid procedures, surgical and non surgical, it remains essential to set expectations at the time of consultation, detailing expected postoperative recovery, potential complications, and functional result. With all available options on hand, the surgeon can confidently select the proper treatment for each individual patientâ&#x20AC;&#x2122;s distressing, and often longstanding, symptoms.

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A CASEBOOK OF TWENTY SURGICAL CASES

REFERENCES 1. Cintron J, Abcarian H. Benign anorectal: hemorrhoids. In: Wolff BG, Fleshman JW, Beck DE, et al, editors. The ASCRS textbook of colon and rectal surgery. New York: Springer-Verlag, Inc; 2007. p. 156–77.

2. Fleshman J, Madoff R. Hemorrhoids. In: Cameron J, editor. Current surgical therapy. 8th edition. Philadelphia: Elsevier; 2004. p. 245–52.

3. Thomson WH. The nature of haemorrhoids. Br J Surg 1975; 62: 542-552.

4. Morgado PJ, Suárez JA, Gómez LG, et al. Histoclinical basis for a new classification of hemorrhoidal disease. Dis Colon Rectum 1988; 31: 474-480.

5. Chung YC, Hou YC, Pan AC. Endoglin (CD105) expression in the development of haemorrhoids. Eur J Clin Invest 2004; 34: 107-112.

6. Scheyer M, Antonietti E, Rollinger G, et al. Doppler-guided hemorrhoidal artery ligation. Am J Surg 2006; 191:89-93.

7. Sneider EB, Maykel JA. Diagnosis and management of symptomatic hemorrhoids. Surg Clin N Am 2010;90: (2010) 17–32.

8.Nishar PJ, Scholefield JH. Managing haemorrhoids. BMJ 2003; 327:847–51.

9. Johanson JF, Sonnenberg A. The prevalence of hemorrhoids and chronic constipation. An epidemiologic study. Gastroenterology 1990; 98: 380-386.

10. Aigner F, Gruber H, Conrad F, et al. Revised morphology and hemodynamics of the anorectal vascular plexus: impact on the course of hemorrhoidal disease. Int J Colorectal Dis 2009; 24: 105-113.

11. American Gastroenterological Association medical position statement: Diagnosis and treatment of hemorrhoids. Gastroenterology 2004; 126: 1461-1462.

12. Alonso-Coello P, Mills E, Heels-Ansdell D, et al. Fiber for the treatment of hemorrhoids complications: a systematic review and metaanalysis. Am J Gastroenterol 2006; 101: 181-188.

13. Welton ML, Chang GJ, Shelton AA. Hemorrhoids. In: Doherty GM, editor. Current surgical diagnosis and treatment. 12th edition. New York: Lange; 2006. p. 738–64.

14. Tjandra JJ, Tan JJ, Lim JF, et al. Rectogesic (glyceryl trinitrate 0.2%) ointment relieves symptoms of haemorrhoids associated with high resting anal canal pressures. Colorectal Dis 2007; 9: 457-463.

15. Perrotti P, Antropoli C, Molino D, et al. Conservative treatment of acute thrombosed external hemorrhoids with topical nifedipine. Dis Colon Rectum 2001; 44: 405-409.

16. Lohsiriwat V. Hemorrhoids: from basic pathophysiology to clinical management. World J Gastroenterol 2012 ; 18(17): 2009-2017.

17. Alonso-Coello P, Zhou Q, Martinez-Zapata MJ, et al. Meta-analysis of flavonoids for the treatment of haemorrhoids. Br J Surg 2006; 93: 909-920.

18. La Torre F, Nicolai AP. Clinical use of micronized purified flavonoid fraction for treatment

129

A CASEBOOK OF TWENTY SURGICAL CASES of symptoms after hemorrhoidectomy: results of a randomized, controlled, clinical trial. Dis Colon Rectum 2004; 47: 704-710.

19. Misra MC. Drug treatment of haemorrhoids. Drugs 2005; 65: 1481-1491.

20. Menteş BB, Görgül A, Tatlicioğlu E, et al. Efficacy of calcium dobesilate in treating acute attacks of hemorrhoidal disease. Dis Colon Rectum 2001; 44: 1489-1495.

21. Gan T, Liu YD, Wang Y, et al. Traditional Chinese Medicine herbs for stopping bleeding from haemorrhoids. Cochrane Database Syst Rev 2010: CD006791.

22. Barron J. Office ligation treatment of hemorrhoids. Dis Colon Rectum 1963;6: 109–13.

23. Lee HH, Spencer RJ, Beart RW, Jr. Multiple hemorrhoidal bandings in a single session. Dis Colon Rectum 1994; 37:37-41.

24. Law WL, Chu KW. Triple rubber band ligation for hemorrhoids: prospective, randomized trial of use of local anesthetic injection. Dis Colon Rectum 1999; 42: 363-6.

25. Bat L, Melzer E, Koler M, et al. Complications of rubber band ligation of symptomatic internal hemorrhoids. Dis Colon Rectum 1993; 36:287-90.

26. Beck DE. Benign rectal, anal, and perineal problems. In: Barie PS, Cance WG, Jerkovich JG, et al, editors. ACS surgery: principles and practice. New York:WebMD; 2005. p. 739–51.

27. Savioz D, Roche B, Glauser T, et al. Rubber band ligation of hemorrhoids: relapse as a function of time. Int J Colorectal Dis 1998;13:154–6.

28. Walker AJ, Leicester RJ, Nicholls RJ, et al. A prospective study of infrared coagulation, injection and rubber band ligation in the treatment of haemorrhoids. Int J Colorectal Dis 1990;5:113–6.

29. Kaidar-Person O, Person B, Wexner SD. Hemorrhoidal disease: A comprehensive review. J Am Coll Surg 2007; 204: 102-117.

30.Mann CV, Motson R, Clifton M. The immediate response to injection therapy for first-degree haemorrhoids. J R Soc Med 1988; 81: 146-148.

31. Guy RJ, Seow-Choen F. Septic complications after treatment of haemorrhoids. Br J Surg 2003; 90: 147-156.

32. Adami B, Eckardt VF, Suermann RB, et al. Bacteremia after proctoscopy and hemorrhoidal injection sclerotherapy. Dis Colon Rectum 1981; 24: 373-374.

33.Senapati A, Nicholls RJ. A randomised trial to compare the results of injection sclerotherapy with a bulk laxative alone in the treatment of bleeding haemorrhoids. Int J Colorectal Dis 1988 ;3(2):124-6.

34. Ricci MP, Matos D, Saad SS. Rubber band ligation and infrared photocoagulation for the outpatient treatment of hemorrhoidal disease. Acta Cir Bras 2008; 23: 102-106.

35. Johanson JF, Rimm A. Optimal nonsurgical treatment of hemorrhoids: a comparative analysis of infrared coagulation, rubber band ligation, and injection sclerotherapy. Am J Gastroenterol 1992; 87: 1600-1606.

36. MacRae HM, McLeod RS. Comparison of hemorrhoidal treatment modalities. A meta-analysis. Dis Colon Rectum 1995; 38: 687-694.

130

A CASEBOOK OF TWENTY SURGICAL CASES 37. Beattie GC, Wilson RG, Loudon MA. The contemporary management of haemorrhoids.

Colorectal Dis 2002; 4: 450-454.

38. Smith LE, Goodreau JJ, Fouty WJ. Operative hemorrhoidectomy versus cryodestruction.

Dis Colon Rectum 1979; 22: 10-16.

39. Gupta PJ. Radiofrequency coagulation versus rubber band ligation in early hemorrhoids: pain versus gain. Medicina (Kaunas) 2004; 40: 232-237.

40. MacRae HM, McLeod RS. Comparison of hemorrhoidal treatments: a meta-analysis. Can J Surg 1997;40:14-7.

41. Bleday R, Pena JP, Rothenberger DA, et al. Symptomatic hemorrhoids: current incidence and complications of operative therapy. Dis Colon Rectum 1992;35:477-81.

42. Hayssen TK, Luchtefeld MA, Senagore AJ. Limited hemorrhoidectomy: results and longterm follow-up. Dis Colon Rectum 1999;42:909-14;discussion 914-5.

43. Ho YH, Seow-Choen F, Tan M, et al. Randomized controlled trial of open and closed haemorrhoidectomy. Br J Surg 1997; 84:1729-30.

44. Carapeti EA, Kamm MA, McDonald PJ, et al. Double-blind randomised controlled trial of effect of metronidazole on pain after daycase haemorrhoidectomy. Lancet 1998;351:169-72.

45. Gencosmanoglu R, Orhan S, Demet K, et al. Hemorrhoidectomy: open or closed technique?

Dis Colon Rectum 2002;45(1):70–5.

46. Hunt L, Luck AJ, Rudkin G, et al. Day-case haemorrhoidectomy. Br J Surg 1999;86:255-8.

47. Pattana-arun J, Wesarachawit W, Tantiphlachiva K, et al. A comparison of early postoperative results between urgent closed hemorrhoidectomy for prolapsed thrombosed hemorrhoids and elective closed hemorrhoidectomy. J Med Assoc Thai 2009; 92: 1610-1615.

48. Morinaga K, Hasuda K, Ikeda T. A novel therapy for internal hemorrhoids: ligation of the hemorrhoidal artery with a newly devised instrument (Moricorn) in conjunction with a Doppler flowmeter. Am J Gastroenterol 1995; 90: 610-613 49. Faucheron JL, Gangner Y. Doppler-guided hemorrhoidal artery ligation for the treatment of symptomatic hemorrhoids: early and three year follow-up results in 100 consecutive patients.

Dis Colon Rectum 2008;51:945–9.

50. Conaghan P, Farouk R. Doppler-guided hemorrhoid artery ligation reduces the need for conventional hemorrhoid surgery in patients who fail rubber band ligation treatment. Dis Colon Rectum 2009;52:127–30.

51. Longo A. Treatment of hemorrhoids disease by reduction of mucosa and haemorrhoidal prolapse with a circular suturing device: A new procedure. Proceedings of the 6th World Congress of Endoscopic Surgery; 1998 June 3-6; Rome, Italy.

52. Burch J, Epstein D, Sari AB, et al. Stapled haemorrhoidopexy for the treatment of haemorrhoids: a systematic review. Colorectal Dis 2009; 11: 233-243; discussion 243.

53. Giordano P, Gravante G, Sorge R, et al. Longterm outcomes of stapled hemorrhoidopexy vs conventional hemorrhoidectomy: a meta-analysis of randomized controlled trials. Arch Surg 2009; 144: 266-272.

54. Shao WJ, Li GC, Zhang ZH, et al. Systematic review and meta-analysis of randomized controlled trials comparing stapled haemorrhoidopexy with conventional haemorrhoidectomy.

131

A CASEBOOK OF TWENTY SURGICAL CASES Br J Surg 2008; 95: 147-160.

55. Angelone G, Giardiello C, Prota C. Stapled hemorrhoidopexy. Complications and 2-year follow-up. Chir Ital 2006; 58:753-760.

56. Dowden JE, Stanley JD, Moore RA. Obstructed defecation after stapled hemorrhoidopexy: a report of four cases. Am Surg 2010; 76: 622-625.

57. Ravo B, Amato A, Bianco V, et al. Complications after stapled hemorrhoidectomy: can they be prevented? Tech Coloproctol 2002; 6:83-88.

58. Avital S, Itah R, Skornick Y, et al. Outcome of stapled hemorrhoidopexy versus dopplerguided hemorrhoidal artery ligation for grade III hemorrhoids. Tech Coloproctol 2011; 15: 267271.

59. Giordano P, Nastro P, Davies A, et al. Prospective evaluation of stapled haemorrhoidopexy versus transanal haemorrhoidal dearterialisation for stage II and III haemorrhoids:three-year outcomes. Tech Coloproctol 2011; 15: 67-73.

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7.

BLUNT HEPATIC TRAUMA The role of nonoperative management.

INTRODUCTION During the last 30 years, treatment of blunt hepatic injuries has dramatically changed. A shift occurred from operative management emphasizing non-resectional techniques and packing in the 1980s to selective non-operative management in the 1990s and now to non-operative management with selective operative management.

Non-operative management (NOM) of blunt liver injuries has become the standard of care in hemo-dynamically stable patients. NOM has been shown to be safe, even in patients with high grade injuries, with overall success rate in the 85-98% range. With the success of NOM, increasingly complex and severe liver injuries are being managed non-operatively.

Concomitant with this has been an increase in hepatic related complications, such as, delayed hemorrhage, prolonged bile leak, biloma, bile peritonitis, abscess, haemobilia, and hepatic necrosis. This has made NOM of high grade liver injuries somewhat controversial. Despite the success of NOM some researchers have identified that for some patients these complications could be avoided by liver resection.

A case is described here of a Grade IV liver injury managed non-operatively.

The discussion which follows describes the NOM of blunt liver injury and its outcomes and the views of those that challenge this concept.

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A CASEBOOK OF TWENTY SURGICAL CASES

CASE History: A 20 year old female was involved in a motor vehicle accident. This occurred 4hours prior to her presentation to the A&E. This accident claimed the lives of the 3 other occupants (mother, father, aunt). She was a rear seat passenger in a car which met head on with a 4x4 van. Her main complaint was central chest pain. The patient did not have any loss of consciousness.

Her

initial

assessment

was

done

as

per

the

ATLS

protocol.

Physical Examination: The patient was obviously anxious and appeared tachypneic. Her vital signs were: BP 132/78mmHg, P 120 min-1, RR 32 min-1, T 378 0C, GCS 15/15. Minimal facial bruising was present with no evidence of CSF rhinorrhea or ottorrhea.

Respiratory: Shallow breaths were noted. There was no external bruising

present,

no

subcutaneous

emphysema

palpated

but

tenderness

was noted along the sternal body. The trachea appeared central. Her breath sounds were vesicular but decreased in the bases bilaterally.

Cardiovascular: All peripheral pulses were present and demonstrated equal volumes. Of note, her JVP was not elevated and heart sounds appeared normal.

Abdominal: The abdomen (obese) moved with respiration. Palpation revealed upper abdominal tenderness. Bowel sounds were present. DRE was normal.

Pelvic spring test was negative and both the upper and lower limbs were normal apart from a laceration at the lower, lateral aspect of the right thigh.

Investigations: Hb: 10.8 g/dl, WCC 13.09 x 103/Âľl, plts 144 x 103/Âľl U&E: Na 144 mmol-1, K 4.6 mmol-1, Cl 115 mmol-1, BUN 10 mgdl-1, Cr 0.7 mgdl-1, Amylase 28 u.

ECG: sinus tachycardia 134

A CASEBOOK OF TWENTY SURGICAL CASES

CXR: pneumo ic

Inadequate thorax.

angles.

There

for There were

expansion was no

mild rib

but

no

blunting fractures

evidence of or

the

of

hemo/

costo-phren-

pneumoperitoneum.

CT (abdomen and pelvis): Fractures of Coinaudâ&#x20AC;&#x2122;s segments 5,6 and 7 of the liver with minimal perihepatic free fluid. The other solid organs were normal. A small amount of free fluid was noted in the pelvis and there was no intra-peritoneal air. The bony pelvis was also normal. (see Fig 1)

Figure 1: Selected CT scan images illustrating fractures of Coinaudâ&#x20AC;&#x2122;s segments 5, 6 and 7.

135

A CASEBOOK OF TWENTY SURGICAL CASES

A FAST scan done 2 hours later revealed no increase in intra-peritoneal free fluid. A repeat Hb at this time was 10.5 mg/dl. The patient was transferred to the ICU thereafter (BP 130/70 mmHg, P 128 min-1, RR 28min-1).

During the first 24 hours, serial (4hourly) Hb were stable (10.02 â&#x20AC;&#x201C; 10.5 g/dl).

The patient was placed on morphine im injections 4 hourly and clinically examined before each dose.

Her arterial blood gas indicated: pH 7.4, pCO2 31.3, pO2 152.9, BEB -0.2. Her urine output was maintained at 35- 40 mls/ hour and her clinical condition remained stable. After the first 24 hours her Hb had dropped by 1.5g and one unit of blood transfused. Her vital signs indicated a persistent tachycardia and respiratory rate of 26- 30 min-1. An echocardiogram demonstrated a normal functioning heart. A repeat CT scan demonstrated a stable injury with no increase in intra-abdominal free fluid to suggest further/ ongoing hemorrhage.

A diagnosis of grade IV liver injury with SIRS (Systemic Inflammatory Response Syndrome) was made. Thromboprophylaxis was commenced with clexane (40mg sc od) and chest physiotherapy administered.

Her condition improved over the next 4 days at which point she was transferred to the ward. Diet and mobility was initiated and her catheter removed.

At this point the patient was informed of the death of her parents, in the presence of relatives. A psychiatric referral was made. A planned CT was done on day 10 post admission. This did not demonstrate any further bleeding, aneurysm development or suggestion of collections developing. The patient was discharged on day 12. On review in the outpatients 6 weeks later she was doing well with no sequelae to the injury.

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A CASEBOOK OF TWENTY SURGICAL CASES

DISCUSSION The liver is the largest solid organ in the body. It is the most commonly injured abdominal organ. NOM of blunt liver injury is attractive as it avoids the additional morbidity/stress of an anesthetic and further surgery.

The pre World War II era was defined by a fear of operating on the liver for trauma. In a report of operative intervention from that time, the overall mortality of the group studied was 44% while the operative mortality was 40%.

The author sited that while non-operative management was recommended by many, the mortality suffered by some patients may result from oversight of intestinal perforation or insufficient drainage of liver wounds.(1)

Interest in liver surgery for trauma was entertained thereafter but was met with difficulty in controlling hemorrhage. There did not appear to be any significant difference in mortality whether the patient had an operation or not: it was 53.6% if an operation was performed and 60% when there was no operation. To control hemorrhage from the liver, the surgeons used the Pringle maneuver, cautery, packing with various materials such as gauze or muscle, omentum, and ligature carried on a blunt, non-cutting, supple needle. Liver injuries in the first 40 years of the twentieth century were characterized by high mortality, and resection of liver tissue was rarely done.(2)

During the second World War a paradigm shift was noted. In 1942 and 1943, the Second Auxiliary Surgical Group managed liver injuries the same way. The authors noted that as time passed, serious complications were noted frequently following this method of treatment: disastrous hemorrhage followed the removal of gauze packs. Abscesses occurred within the liver or within the perihepatic spaces, and hepatic necrosis was observed in areas that had been packed. Peritonitis, hepatitis, fistulas and numerous other complications followed this form of 137

A CASEBOOK OF TWENTY SURGICAL CASES

treatment. By draining most liver injuries and abandoning the use of gauze packs, the mortality rate dropped from 30% to 17% in the next two years. The authors concluded that superficial liver wounds that were not bleeding could be drained only. Larger wounds that were bleeding at the time of exploration required suturing as well as drainage. For a small group of patients (fewer than 10%) who had severe bursting, crushing, or high-velocity bullet wounds, it was necessary to do resectional debridement and possibly lobectomy. They also advocated formal lobectomy for retrohepatic caval injuries or major hepatic vein injuries.(3)

Following World War II, reports from large hospitals showed an increase in the number of patients presenting with liver injuries. By exercising a selective approach to non-operative and operative approaches with selective drainage and resectional techniques, there was a corresponding decrease in operative mortality. A study undertaken at Southwestern Medical School in Dallas, Texas (time period January 1953 to January 1963) was reported. Two hundred fiftynine injuries are reported: 31 patients sustained blunt injuries, 111 had gunshot wounds, and 117 had stab wounds. Of the patients with blunt injuries, 64.5% presented in shock. The treatment in these patients included 8.9% who had no suture but were drained; 71.1% had suture and drains. Gauze packs were used in only 1 patient and resection was performed in 9.6% of the patients. Overall mortality in this series was 11.2%; 20% for those 25 patients who had resections.(4)

In 1965, Root et al introduced diagnostic peritoneal lavage, and one of their recommendations was that it be used in diagnosing intraperitoneal bleeding following blunt trauma.(5) Before 1965, it is estimated conservatively in multiple clinical series, intraperitoneal blood was not diagnosed in up to 50% of all patients with blunt abdominal injury. DPL turned out to be very sensitive at picking up peritoneal blood and initially all of these patients were operat138

A CASEBOOK OF TWENTY SURGICAL CASES

ed on. It soon became clear that diagnostic peritoneal lavage was too sensitive and resulted in non-therapeutic laparotomies in up to 30% of patients.(6)

The year 1981 marked the introduction of computed tomography for diagnosing visceral injuries following blunt trauma .(7) Shortly after introduction of CT, the concept of non operative management of liver injuries was also reintroduced, albeit in a small percentage of cases.(8) Through increased use of CT, it was appreciated that many liver injuries, particularly Grade I and II, did not require operative management. CT was also extremely valuable in picking up associated injuries that might require operation, and also in diagnosing retroperitoneal injuries that might require surgical intervention. Diagnostic peritoneal lavage is incapable of this differentiation. In essence, nonoperative management of liver injuries and CT are inextricably linked. It is also important to recognize that CT is not only qualitative and allows the surgeon to make a decision whether the patient needs an operation or not, but it also picks up other injuries that are missed by diagnostic peritoneal lavage.(9) An equally important contribution of CT to our understanding of liver injuries is the diagnosis of late complications.(10,11)

During the last 30 years, treatment of blunt hepatic injuries has dramatically changed. A shift occurred from operative management emphasizing non-resectional techniques and packing in the 1980s to selective non-operative management in the 1990s and now to non-operative management with selective operative management.

The enthusiasm for NOM has been rewarded with overall success rates of 85% - 98% including patients with high grade injury.(12,13,14) As such, NOM of blunt liver injuries has become the standard of care in hemo-dynamically stable patients. This is fortified by: realization that more than 50% of liver injuries stop bleeding spontaneously, the precedent of successful non-operative management 139

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in pediatric patients, knowledge that the liver has tremendous capacity to heal after injury and improvements in liver imaging with CT scan.(15)

The liver is suspended by superior attachments to the diaphragm and anterior attachments of the coronary ligaments, triangular ligaments and the falciform ligament. It is also attached to the lesser curve of the stomach. Deceleration injuries result in tears at these sites of fixation. A common deceleration injury creates a fracture between the posterior segments and the anterior segments of the right lobe. A crushing mechanism or a focused blunt injury to the right upper quadrant of the abdomen compresses the ribs into the liver causing a stellate-type laceration across the dome and anterior surface of the right lobe, often termed a â&#x20AC;&#x153;bearclaw injuryâ&#x20AC;?. Anterior-posterior forces can produce a split liver, often through the line of Cantlie. In general, blunt trauma more commonly affects the right hepatic lobe.(16)

Criteria for non-operative management include foremost hemo-dynamic stability, absence of other abdominal injuries that require laparotomy, immediate availability of resources including a fully staffed operating room, and a vigilant surgeon. The stable patient should undergo a rapid physical examination and chest radiography. Although outward signs of injury are non-specific and the absence of such findings do not exclude injury, seatbelt signs or other marks, regions of tenderness, and obvious penetrating wounds must be noted. Patients with a seatbelt sign have a 3 fold higher incidence of liver injury than those patients presenting without a seatbelt sign.(17) Right-sided rib fractures or pulmonary contusion should also raise suspicion for hepatic injury.

Computerised Tomography (CT) is the standard diagnostic modality for stable trauma patients with a suspected abdominal injury. CT has a reported sensitivity of 92% to 97% and a specificity of 98.7% for detection of liver injury.(18) 140

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The type and grade of liver injury, the volume of hemoperitoneum and differentiation between clotted blood and active bleeding can be identified. CT scan also allows diagnosis of associated intra-peritoneal and retroperitoneal injuries, including splenic, renal, bowel, and chest trauma, and pelvic fractures. As such, CT has been instrumental in formulating the liver organ injury scale, as per the American Association for Surgery and Trauma: LIVER ORGAN INJURY SCALE(19)

GRADE

DESCRIPTION

I

Hematoma

Subcapsular, < 10% surface area

Laceration

Capsular tear, <1 cm parenchymaldepth

III

Hematoma

Subcapsular, 10-50% surface area; intraparenchymal, <10cm diameter

Laceration

1-3m parenchymal depth, <10cm in length

III

Hematoma

Subcapsular >50% surface area or expanding; ruptured subcapsular or

parenchymal hematoma

Laceration

>3cm parenchymal depth

IV

Hematoma

Parenchymal disruption involving 25-75% of hepatic lobe or 1-3 Couinaud

segments within a lobe

V

Parenchymal disruption of >75% of hepatic lobe or >3 Couinaud segments

Laceration

within a single lobe

Juxtahepatic venous injuries; i.e. retrohepatic vena cava/ central major

Vascular

Hepatic vein VI Hepatic avulsion

Provided that the patient has no other source of bleeding or hollow viscus injury and also assuming physiologic stability Grade I and II injuries can be managed non-operatively. It is the Grade III, IV, and V injuries that are potentially more problematic and require care and diligence.

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One of the initial challenges in identifying patients for NOM is determining the presence of hemo-dynamic instability. The traditionally accepted value is ≤ 90 mmHg, however, there is no well accepted definition. Recent studies demonstrate that patients are at risk for hemorrhage and death with a blood pressure ≤110mmhg and a base deficit of 4.(20,21)

Interpretation of the CT findings is also very important in determining the need for surgical or radiological intervention. The finding of a “blush” or pooling of intravenous contrast material within the liver parenchyma on CT scanning is indicative of active hemorrhage. Fang and colleagues confirmed that intraperitoneal extravasation was the most specific sign to predict the need for surgery.(22) Although data is limited, it would be logical to suggest that hemo-dynamically stable patients with free intraperitoneal extravasation undergo immediate angiography if readily available. In our setting this is not the case and with limited supply of blood and blood products these patients will require surgery. A patient in whom there is hemodynamic stability with intraparenchymal contrast pooling presents a dilemma. At present, it is not clear from available data whether immediate angiographic embolisation is required. Close observation alone with planned angiographic embolisation for signs of ongoing bleeding, such as, a drop in hematocrit or need for transfusion may be an option.(23)

The non-operative strategies involved for these patients involve: serial hemoglobin levels every 6 hours, monitoring of vital signs and serial abdominal examination. The possibility of bowel injury still exists as is further bleeding.(24)

In the case presented, morphine 5 mg was administered every 6 hours for analgesia. The physical examination was performed just prior to each dose. This was to try and eliminate any masking of early signs of peritonitis by opiate analgesia. Grade I and II liver injuries may be managed on a ward setting, however, 142

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Grade III, IV and V injuries are better off on the intensive care.

Over the next 24-48 hours, diet and gentle ambulation are reintroduced, within the confines of other injuries. During this time, a diligent search for failure of NOM is carried out. In this respect, patient selection is important and factors that may predict failure of NOM has been identified. These include: hypotension on admission, high CT grades of injury and the need for blood transfusion.

Fang and colleagues regard hemo-dynamically stable patients with intraperitoneal contrast extravasation and hemoperitoneum in 6 compartments on CT at high risk for the need of surgical intervention after blunt hepatic trauma. In addition, the risk for failure of non-operative management approaches 96% in the presence of: 1. a splenic or renal injury with a positive FAST (focused abdominal sonography in trauma) result 2. an estimated amount of free fluid on CT of greater than 300ml 3. the requirement for blood transfusion

If all these factors are absent, the risk of failure of non-operative management is only 2%.(22)

The NOM of blunt hepatic injuries includes addressing the resulting complications. This extended arm of NOM requires the availability of equipment and expertise to provide adjunctive therapeutic measures, such as, interventional radiology and ERCP. Twenty-five percent (25%) of patients with blunt hepatic injury managed non-operatively, 92% of whom have Grade IV or V injury, will require an intervention for complications (25,26)

Bile leaks are a frequent complication in the NOM of liver injuries, occurring in 6-20% of cases. Biliary complications are variable in their time of presentation 143

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and may require multiple treatment strategies. Ultrasound and CT scan are used to diagnose a biloma, whereas a hepatobiliary iminodiacetic acid scan is used to show an active bile leak. Most collections can be managed by ultrasound or CT guided percutaneous drainage. Carillo and colleagues determined that one third of patients diagnosed with a biloma required ERCP and stent placement in addition to radiological drainage to manage the bile leak.(25)

A less common complication is hemobilia, caused by an abnormal communication between an intrahepatic blood vessel, usually an artery, and the biliary tree.

The incidence after trauma is less than 3% and is more often associated with blunt trauma than with penetrating injuries. Hemobilia presents as gastrointestinal bleeding with or without abdominal pain and jaundice caused by bile ducts occluded with blood products. This complication has been reported immediately after the initial trauma or up to 4 months later.(27) Croce and colleagues noted that 80% of patients with hemobilia also had bile leaks detected on hepatobiliary scans.(28) Angiography permits precise identification and selective embolisation of the appropriate branch vessel as opposed to the surgical alternative of ligation of a main hepatic artery or hepatic resection thereby preserving more functional liver tissue.(27) These patients may proceed to development of hepatic or perihepatic abscesses due to damaged or devitalized parenchyma. These appear on CT as a focal collection with gas bubbles or a fluid collection with an air fluid level. The incidence is low and these can usually be managed by percutaneous catheter drainage with radiological guidance, though operative drainage may still be needed for failures.(12)

Despite the successes of many, of NOM of blunt hepatic injuries there is concern that too many (particularly Grades III, IV and V) are managed without debridement or resection. This has resulted in a worrying trend in liver related morbidity in the literature. In light of this, Strong and colleagues have chal144

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lenged the trauma surgery community. They contend that there are patients whose livers have been so shattered that survival is dependent on eradication of this diseased/devitalized portion of liver by resection. In their experience, for 37 patients with Grade III, IV and V injuries that required hepatic resection, there were three deaths (mortality rate 8%). With their good results they questioned whether the reported numerous successes of NOM is misleading as there may be failure to mention associated intra-abdominal trauma that required operative intervention and that complications are too high. They further argue that authors reporting few or no resections for severe liver injuries may reflect lack of experience in gaining rapid control of liver bleeding and lack of ability to carry out an anatomic resection, which may have implications for training.(29)

Currently, non-operative management is being used with increasing frequency in complex liver injuries.(30) While non-operative management clearly reduces hepatic related mortality, current attention needs to be focused on hepatic related morbidity.

In a retrospective review of 453 complex blunt liver injuries (Grade III â&#x20AC;&#x201C; V) a hepatic morbidity rate of 13% was noted. Patients with high grade injuries and need for transfusion within 24 hours may be predictors of further morbidity.(31) These investigators concluded that such patients may be selected for a semielective liver resection or screened with CT. Both of these recommendations will obviously only hold true if complications could be accurately identified and treated early and subsequent morbidity and mortality are decreased and avoided. The answers to these questions therefore lie in a prospective study.

Some investigators recommend routine CT for all NOM blunt hepatic injury patients 4 to 7 days following injury as this will diagnose bilomas and hepatic necrosis and may also show arterial aneurysms and fistula.(3) Currently no con145

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sensus as to whether routine CT scans are justified exists, with data suggesting that they are of limited value.(32,33) A recent article provides further evidence for this: 530 patients of which 45% were complex hepatic injuries had NOM follow up scans revealed that most injuries were either unchanged or improved.

Only 3 patients underwent intervention based on their follow up scans. Each of these patients had clinical signs or symptoms that were indicative of hepatic abnormalities.(34)

The case described here had a repeat CT scan on day 4. This was in relation to an elevated white cell count (22,000), a persistent tachycardia and a temperature of 38.50C, her abdomen remained clinically normal. The CT revealed that the initial findings were quite stable. A diagnosis of Systemic Inflammatory Response Syndrome (SIRS) was made. In the early phase of NOM extreme vigilance is required to detect clinical changes that may indicate a missed hollow viscus injury or bile peritonititis. However, knowledge of the natural history of NOM is important as it is not unusual for these patients to have abdominal discomfort and SIRS. This was noted by Cogbill et al who also noted that 64% of patients with complex liver injuries were hyperpyrexic for the first three post injury days, presumably from devitalized hepatic tissue.(35)

CONCLUSION Despite the concerns of Strong et al, there is a plethora of evidence which favour NOM of blunt hepatic injuries. The NOM pathway requires access to several adjunctive procedures and skills for example interventional radiology and a skilled endoscopist. In the absence of these additional tools, the surgeon needs to exercise good clinical judgment and must be extremely vigilant to detect hepatic related morbidity or missed injuries. By extension, the surgeon must be adept at controlling and dealing with ongoing hemorrhage that requires surgical intervention. As NOM continues to evolve acquiring this skill may prove 146

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difficult for trainees in our setting. Further work needs to be done in order to predict patients likely to benefit from surgical intervention in order to avoid delayed complications. NOM clearly is possible in patients with higher grade liver injuries and would help to avoid unnecessary surgical morbidity in a group of patients who may not tolerate further physiological insults.

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REFERENCES 1.Tilton BJ. Considerations regarding wounds of the livers. Ann Surg 1905;61:20–30.

2. Lamb CA. Rupture of the liver. N Engl J Med 1939;221:855–9.

3. Trunkey DD. Hepatic trauma: contemporary management. Surg Clin North Am 2004;84:437– 50.

4. McClellan RN, Shires T. Management of liver trauma in 259 consecutive patients. Ann Surg 1965;161:48–57.

5. Root HD, Howser CW, McKinley CR, et al. Diagnostic peritoneal lavage. Surgery 1965; 57:633–7.

6. Olsen WR, Redman HC, Hildreth DC. Quantitative peritoneal lavage in blunt abdominal trauma. Arch Surg 1972;104:536–43.

7. Federle MP, Goldberg HI, Kaiser KA, et al. Evaluation of abdominal trauma by computed tomography. Radiology 1981;138:637–44.

8. Meyer AA, Crass RA, Lim RC, et al. Selective non-operative management of blunt liver injury using computed tomography. Arch Surg 1985;120:550–4.

9. Goldstein AS, Sclafani S, Kuppferstein NH, et al. The diagnostic superiority of computed tomography. Journal of Trauma 1985;25:938–46.

10. Geis WP, Schulz KA, Giacchino JL, et al. The fate of unruptured intrahepatic hematomas.

Surgery 1991;90:689–97.

11. Inoguchi H, Mii S, Sakata H, et al. Intrahepatic pseudoaneurysm after surgical hemostasis for a delayed hemorrhage due to blunt liver injury: report of case. Surg Today 2001;31: 367–70.

12. Kozar RA, Moore FA, Moore EE, et al. Western trauma association critical decisions in trauma: nonoperative management of adult blunt hepatic trauma. J Trauma. 2009;67:1144 –1149.

13. Malhotra AK, Fabian TC, Croce MA, et al. Blunt hepatic injury: a paradigm shift from operative to nonoperative management in the 1990s. Ann Surg. 2000;231:804–813.

14. Meredith JW, Young JS, Bowling J, et al. Nonoperative management of blunt hepatic trauma: the exception or the rule? J Trauma. 1994;36:529 –535.

15.Badger SA, Barclay R, Diamond T, et al. Management of liver trauma. World J Surg 2009;33:2522–37.

16.Piper GL, Peitzman AB. Current management of hepatic trauma. Surg Clin N Am 2010; 90: 775- 785.

17. Sharma OP, Oswanski MF, Kaminski BP, et al. Clinical implications of the seat belt sign in blunt trauma. Am Surg 2009;75(9):822–7.

18. Hoff WS, Holevar M, Nagy KK, et al. Practice management guidelines for the evaluation of blunt abdominal trauma: the EAST practice management guidelines work group. J Trauma 2002;53:602–15.

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19.Moore EE, Shackford SR , Pachter HL. Organ injury scaling: spleen, liver and kidney. J Trauma 1995; 38: 323-4.

20. Eastridge BJ, Scalino J, McManus JG, et al. Hypotension begins at 110mm Hg: redefining “hypotension” with data. J Trauma. 2007;63:291–297; discussion 297–299.

21. Davis JW, Parks SN, Kaups KL, et al. Admission base deficit predicts transfusion requirements and risk of complications. J Trauma. 1996;41:769 –774.

22. Fang JF, Wong YC, Lin BC, et al. The CT risk factors for the need of operative treatment in initially stable patients after blunt hepatic trauma. J Trauma. 2006;61:547–553; discussion 553–554.

23. Kozar RA, Moore JB, Niles SE, et al. Complications of nonoperative management of highgrade blunt hepatic injuries. J Trauma. 2005;59:1066–1071.

24. Velmahos GC, Toutouzas KG, Radin R, et al. Nonoperative treatment of blunt injury to solid abdominal organs: a prospective study. Arch Surg 2003;138(8): 844–51.

25.Carillo EH, Spain DA, Wohltmann CD, et al. Interventional techniques are useful adjuncts in nonoperative management of hepatic injuries. J Trauma 1999;46:619–22.

26.Trunkey DD. Hepatic trauma: contemporary management. Surg Clin North Am 2004;84:437– 50.

27. Forlee MV, Krige JE, Welman CJ, et al. Haemobilia after penetrating and blunt liver injury: treatment with selective hepatic artery embolisation. Injury 2004;35(1):23–8.

28. Croce MA, Fabian TC, Spiers AP, et al. Traumatic hepatic artery pseudoaneurysm with hemobilia. Am J Surg 1994;138:235–8.

29. Strong RW. The management of blunt liver injuries. Aust N Z J Surg. 1999;69:609-616.

30. Strong RW, Lynch SV, Wall DR, Liu CL. Anatomic resection for severe liver trauma. Surgery. 1998;123:251-57.

31. Kozar RA, Moore FA, Cothren C , et al. Risk factors for hepatic morbidity following nonoperative management. Arch Surg 2006; 141: 451-459.

32. Allins A, Ho T, Nguyen TH, et al. Limited value of routine follow-up CT scans in nonoperative management of blunt liver and splenic injuries. Am Surg. 1996;62:883-886.

33. Cuff RF, Cogbill TH, Lambert PJ. Nonoperative management of blunt liver trauma: the value of follow-up abdominal computed tomography scans. Am Surg. 2000; 66:332-336.

34. Cox JC, Fabian TC, Maish III GO, et al. Routine follow-up imaging is unnecessary in the management of blunt hepatic injury. J Trauma 2005; 59: 1175-1180.

35. Cogbill TH, Moore EE, Feliciano DV, et al. Hepatic enzyme response and hyperpyrexia alter severe liver injuries. Am Surg. 1992; 58:395-399.

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8. POSTOPERATIVE

ILEUS

Developing strategies to deal with an old foe.

INTRODUCTION Despite the advancements in surgical techniques and pre-operative care, post operative ileus (POI) continues to be the most common complication of abdominal surgery. In essence, post operative ileus can be described as the deceleration or arrest of intestinal motility following abdominal surgery or intra-abdominal trauma. Initially presenting with abdominal distention and cessation of defecation, POI progresses with nausea, vomiting and abdominal discomfort. This condition, which delays resumption of normal nutrition and mobilization, is one of the most significant causes of extended hospitalization following surgery.

Traditional treatment strategies included bowel rest and nasogastric decompression along with fluid and electrolyte balance. The general thinking is that these measures hasten recovery from POI by reducing the incidence of complications such as infection and anastomotic dehiscence. While still a common practice, recent data have called this into question. Better understanding of the pathophysiology of POI have encouraged changes in time honored practices and introduced other measures which may help in the resolution of POI.

A case of POI following laparotomy for an appendix abscess is described and this is followed by a discussion which includes the pathophysiology of POI and current treatment strategies.

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CASE History: A 61 year old woman presented with a 4 day history of right lower quadrant abdominal pain. During the previous 2 days it became worse notably aggravated by movement and she began vomiting (6 episodes). The vomitus consisted of dark green fluid. Her appetite had waned but she continued to pass flatus. The patient felt a slight fever on the day of presentation.

Systematic enquiry identified no urinary symptoms, no history of trauma or previous large bowel symptoms.

This patient was a known hypertensive and this was well controlled with enalapril (20 mg once daily). She had no previous surgical procedures. The patient did not smoke or consume alcohol and worked as an attendant at the hospital.

Physical examination: An ill looking woman with vital signs: RR 20min-1, P 124 min-1, BP 133/90 mmHg, T 38.20C. Respiratory and cardiac examination was normal. Per abdominal examination revealed tenderness in the right lower quadrant of the abdomen with an underlying mass. The mass was tender and dull to percussion. In addition there was no organomegaly and on auscultation bowel sounds were present but normal.

Digital rectal examination revealed that her sphincter tone was normal. There was no mucosal abnormality and the stool was brown and pasty with no evidence of blood or mucus. No pelvic masses or bogginess were detected with the examining finger.

Investigations: Blood: Hb 12.8 mg/dl, WCC 17.5 x 103 /Âľl, Plt 383 x 103 /Âľl. Na 136 mmol-1, K 3 .9mmol-1, BUN 28 mgdl-1, Cr 1.1 mgdl-1, CRP 28 mgdl-1, Amylase 119 u/dl.

Total Bilirubin 1.8 mgdl-1, AST 23 u, ALT 18 u, Albumin 4.2 g/dl 151

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CXR: normal AXR: No features of intestinal obstruction. The lower abdomen demonstrated a ground glass appearance.

CT: An inflammatory mass was noted in the right iliac fossa in relation to the appendix. There were internal fluid collections consistent with an abscess. (Fig 1) The assistance of the radiologist was requested to consider ultrasound guided drainage of the abscess, however this was a Saturday and the logistics of accessing the appropriate drain and expertise was not possible.

A diagnosis of appendix mass abscess was made. The patient was resuscitated with the aim of performing a laparotomy.

The patient was admitted to the surgical ward. Intravenous fluids were administered (Normal saline 1L over 2 hours followed by 3L in 24 hours of Ringerâ&#x20AC;&#x2122;s lactate alternating with Dextrose 5% Saline). Intra-venous antibiotics were commenced (Zinacef 1.5g IV tds, Flagyl 500mg IV tds). The patient was catheterized and thrombo-embolic deterent stockings placed.

Informed consent was taken and the patient taken to the operating theatre 4 hours later.

Surgical Findings and procedure: Through a midline incision an abscess was identified in relation to the Ileocecum, within which the appendix was perforated. The base of the appendix, located in a retrocecal position and close to the ileocecal junction, was blown open and the adjacent cecum was unhealthy. The abscess was drained and the cavity debrided. An ileo-cecectomy was performed and an ileo-colic anastomosis fashioned with the aid of a 55mm GIA stapler. A 15fr intraperitoneal suction drain was placed along the right paracolic gutter into the pelvis and the abdomen closed en mass with 1Prolene suture. The skin incision was approximated with 2 interrupted stitches.

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Post-Operative course: Her clinical parameters improved over the next two days. The urine output was maintained at 40-50mls per hour and her WCC had decreased to 11 x 103 /Âľl. The contents of the suction drain was initially serosanguinous and eventually serous.

The patient continued to improve, but although her vital signs were normal and her mobility constantly improving, she did not pass flatus nor had a bowel movement. Of note her nasogastric drainage averaged 500 mls per day (light green) and her abdomen was now distended and uncomfortable.

Physical examination revealed a few basal crepitations on respiratory assessment. Her abdomen was distended and although tender in relation to her incision demonstrated no peritonism. The wound was healing with no evidence of cellulitis or deeper infection. Her bowel sounds were present but sparse and digital rectal examination was normal.

Serial blood investigations revealed her WCC 9 x 103, Hb 10.8 mg/ dl, CRP 5 mg/dl, K 4.2 mmol-1, Na 135 mmol-1, Corrected Ca 9.2 mmol-1, Mg 2.2 mmol-1.

A CT scan was arranged to exclude a mechanical obstruction and/or an abscess.

The CT revealed no ascites or abscess. There was no intestinal obstruction with the intestinal gas pattern followed through to the rectum and no transition zone demonstrated. The patient was diagnosed with a postoperative ileus. (Fig 2,3)

This was managed by maintaining her fluid and electrolyte balance, and DVT thromboprophylaxis while encouraging mobility and ambulation. The urinary catheter, abdominal drains and nasogastric tube were all removed. The patient was asked to chew gum, which she did, and to sip on fluids she wanted to taste.

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Fig 1: Appendix mass abscess in the right lower abdomen

Fig 2: No evidence of intra-abdominal collections or intestinal obstruction.

The ileus persisted and resolved on day 10. This was marked by the onset of propulsive gut activity (passage of flatus and stool). The patient was discharged on day 12 once her appetite had improved and confidence was restored.

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Fig 3: No evidence of intra-abdominal collections or intestinal obstruction.

DISCUSSION POI, described as a transient impairment of bowel motility that may occur after major surgery, continues to be the most common complication of abdominal surgery.(1) An initial delay of bowel motility appears to be an obligatory part of the normal surgical recovery process. Studies in which bowel motility is measured in real time suggest that the small bowel returns to normal peristaltic function within 12-24 hours, the stomach within 24-48 hours and the colon 3-5 days.(2) As colonic motility is the last to recover it is usually the limiting factor in resolving POI.

Gastrointestinal motility is expected to return to normal within 3-4 days post surgery. Failure to occur should lead one to suspect POI. Clinically, POI is characterized by abdominal distention and lack of bowel sounds, flatus, and bowel movements. In addition patients may experience nausea, vomiting and abdominal discomfort. Other potentially adverse effects of POI include increased post 155

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operative pain, delayed oral intake, poor wound healing, delayed post operative mobilization, increased risk of pulmonary complications, including pneumonia, pulmonary embolism and atelectasis, prolonged hospitalization, decreased patient satisfaction, and increased health care costs.(3)

On occasion it may become necessary to exclude a mechanical obstruction.

When an ileus fails to resolve by approximately the 5th-6th day, it may be important to identify a specific cause such as intra-abdominal abscess or anastomotic leak and to exclude an early post operative bowel obstruction due to adhesions, inflammation or intussusception.

The mechanisms involved in POI and the disorganized electrical activity following surgery are not well defined and are likely multifactorial. Recent experimental studies have demonstrated that the pathogenesis of POI consists of endogenous and pharmacological characteristics. The endogenous component can grossly be divided into two phases. The first phase (neural), results from activation of mechano-receptors and nociceptors by stimuli, such as incision of the skin and more importantly by direct manipulation of the intestine. Activation of these receptors initiates a neural reflex which is dependent on release of mediators (hormonal, neuro transmitters, etc) which inhibit GI motility and result in generalized intestinal hypomotility. The second more protracted phase (inflammatory), is caused by formation of an inflammatory infiltrate in the muscle layers of the intestines. Manipulation of the intestine initiates an inflammatory cascade which begins with activation and degranulation of macrophages. The eventual invasion by neutrophils which release nitric oxide and prostaglandins impairs intestinal smooth muscle contractility.(4) Opiates, which are used universally as analgesic agents following various surgical procedures also have a major importance in the pathogenesis of POI due to the depressive effects on GI transit.(5) 156

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Surgical injury can be followed by pain, nausea, vomiting and ileus, stress induced catabolism, impaired pulmonary function, increased cardiac demands and risk of thromboembolism. These problems can lead to complications, need for treatment in hospital, postoperative fatigue and delayed convalescence. Within the last decade numerous reports in the literature reflect a paradigm shift from traditional surgical philosophies including minimally invasive methods, use of fewer drains, and earlier introduction of nutrition. These enhanced recoveries after surgery or fast track pathways are designed to streamline peri-operative care using multi-modal strategies. These new strategies encourage early mobilization to augment the rapid return to functional recovery. (6,7) Some of these strategies are directly related to preventing and managing POI:

â&#x2013;Ą The routine use of preoperative mechanical bowel preparation has long been a tradition in colorectal surgery. One of the largest randomized controlled trials from Denmark in 2007 indicated that there was no benefit to bowel preparation in terms of anastomotic leakage, septic complication, fascial dehiscence or mortality.(8) In fact, others have noted that mechanical bowel preparation is likely associated with an increased risk of anastomotic leakage.(9). Shaffi et al evaluated 86 patients undergoing cystectomy and urinary diversion and reported that bowel preparation significantly increased incidence of POI and length of hospital stay.(10) In the case described here this was an emergency and so bowel preparation was not relevant.

â&#x2013;Ą The use of pre-operative carbohydrate loading, attenuates post operative insulin resistance, reduce nitrogen and protein losses, preserves skeletal muscle mass and reduces preoperative thirst, hunger and anxiety. Allowing carbohydrate drinks up to 2 hours preoperatively negated these metabolic effects and facilitates accelerated recovery 157

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through early return of bowel function and shorter hospital stay. Based on these observations some researchers have recommended that carbohydrate loading should replace overnight fasting pre-operatively.(11)

□ Several inhibitory reflexes in the GI tract have been proposed to play a role in POI, including activation of inhibitory reflexes due to sympathetic activation and bowel handling. Researchers have hypothesized that epidural local anesthetics may decrease POI by blocking these afferent sympathetic inhibitory reflexes. Indeed this has been demonstrated in a recent meta-analysis of 16 trials where there was a significant decrease in POI by 1.5 days when epidural local anesthesia was administered in patients having colorectal surgery.(12)

□ Non steroidal anti-inflammatory drugs (NSAIDS) may be beneficial in two ways: decreased need for opioid analgesia and decreased prostaglandin synthesis. Sim et al introduced an NSAID for analgesia along with morphine (administered via a patient controlled analgesia pump).

They demonstrated both an opioid sparing effect and reduced ileus after colorectal resection when an NSAID was included for analgesia.(13) The morphine requirement was reduced by almost 50% at 12 and 24 hours and bowel sounds and passage of flatus also occurred earlier (by 12 hours). (13)

□ Surgical trauma and direct manipulation of the intestine are major factors in the occurrence of POI. The introduction of minimally invasive techniques such as laparoscopy, significantly reduced the duration of POI and length of stay.(14) These improvements were noted in concert with decreased postoperative pain, decreased blood loss and improved pulmonary function. In the patient described earlier, the procedure 158

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was undertaken at night and the expertise was not available to undertake a laparoscopic procedure. The benefit noted with laparoscopic techniques is most probably due to minimization of trauma resulting in less pain and a diminished release of neurotransmitters and inflammatory mediators.

â&#x2013;Ą There was concern that high volume perioperative fluid therapy with resulting over-hydration might be detrimental in a number of respects, including impairment of cardiac and pulmonary function and the development of gut edema which would worsen POI. However, two recent randomized double blinded studies did not validate this concern finding no increases in either ileus or length of hospital stay related to the volume (restrictive or liberal) of perioperative fluid administration (15,16).

Some but not all of these measures are applicable to emergency bowel surgery.

These patients are often dehydrated because of the underlying pathology such as intestinal obstruction or in this case an appendix mass abscess. Administering oral liquids would be paradoxical since these patients need nasogastric decompression. They may in fact need large volumes of intravenous fluid to be adequately resuscitated for surgical undertaking.

Post operative analgesia is universal in all post operative treatment plans following abdominal surgery. Both endogenous opioids released in response to noxious stimuli and exogenous opioids are notorious for their inhibitory effect on gastrointestinal motility which may aggravate post-operative ileus. Therefore limiting opioid use postoperatively has been associated with a significant decrease in POI and remains a main stay of POI prevention and treatment strategies.(17) This is quite pertinent in our setting as epidural anesthesia/analgesia 159

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is not readily available. In an attempt to decrease the opioid load though IV Diclofenac was included in the analgesic regime for post operative care.

Nasogastric decompression and the practice of advancing postoperative feeding only after the presence of bowel sounds and/or flatus has been a routine in surgery for decades. Cheatham et al published a meta-analysis of all clinical trials comparing selective versus routine nasogastric (NG) decompression after laparotomy and found that routine insertion of an NG tube (NGT) resulted in increased adverse effects including fever, pneumonia and atelectasis.(18) They concluded that only 5% of patients stood to benefit from NGT decompression and it should therefore be used selectively. This study was conducted on elective surgical patients though. The patient described underwent an emergency laparotomy and a POI was somewhat expected because of peritonitis and bowel handling. However, the 2007 Cochrane report reviewed the role of nasogastric tube decompression after both emergency and elective abdominal operations.

In this review 5240 patients were randomised into two groups, one with and the other without routine nasogastric decompression. The results indicated earlier return of bowel function, and a decrease in pulmonary complications in patients without routine nasogastric tube drainage. In addition anastomotic leak was comparable between both groups.(19) They too recommended selective use of NGT.

Another age old practice that has been regarded in recent times as being futile is the placement of abdominal drains. Many surgeons find comfort in placement of these drains, but these may be a source of wound infection, and can lead to increased hospital stay. Several studies have demonstrated no benefit of drains to deterring anastomotic leak. Kumar et al randomized 180 patients undergoing subtotal gastrectomy into two groups, drains and no drains. There was no significant difference between the groups in regard to time to return to normal GI 160

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motility, length of hospital stay or overall mortality.(20) While avoiding drains may not directly avoid POI it may in principle, at least, decrease patient discomfort and encourage ambulation.

Early enteral nutrition after abdominal surgery is another new strategy which challenges traditional practice. There is a growing popularity of early feeling as a potential strategy to avert POI. In a report by Stewart et al, when early enteral nutrition was introduced following colorectal resection, patients passed flatus and stool much sooner than the control group. There was also a reduction in the duration of POI and hospital stay.(21) Anderson et al in a review of 13 randomized controlled trials, demonstrated that earlier feeding resulted in decreased post surgical complications, but there was no advantage to keeping patients nil by mouth.(22) A more physiological way to address POI may be by introduction of enteral nutrition enriched with lipids. The enteral presence of lipids activates the autonomic nervous system via cholecystokinin receptors. This may help POI in two ways; one is that vagal innervation has an anti-inflammatory effect on the gut wall, and the other, the direct stimulation of peristalsis. Enteral administration of lipid rich nutrition was demonstrated to reduce postoperative ileus in a rodent model of intestinal manipulation.(23) Enteral nutrition enriched with lipids may reduce POI by activation of a nutritional anti-inflammatory pathway. It was shown to have prevented degranulation of mast cells, inhibited release of macrophage derived tumor necrosis factor-Îą and IL-6, and prevented influx of neutrophils into the intestinal muscularis to a greater extent than the control, low-lipid, nutrition.(23)

Interestingly, sham feeding is another physiological technique that activates the cephalic vagal axis by mimicking food intake, thereby stimulating bowel motility Cephalic-vagal stimulation from chewing alone gives rise to propulsive and hormonal gastrointestinal activity similar to that seen with normal eating.

161

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. Furthermore, activation of the cephalic phase elicits digestive functions

via vagovagal cholinergic reflexes.(26) Sham feeding by chewing gum has been shown to improve bowel movement and reduce time to first flatus (by 12.6 hours) and first defecation (23.11 hours) after open gastrointestinal surgery, and demonstrates a trend towards a reduced hospital stay.(27,28) This practice should be highly recommended as other advantages include being well tolerated, widely available and inexpensive. However, the exact mode of action remains to be investigated.

POI has plagued surgical abdominal recovery for well over a century. Not surprisingly pharmacological methods have been employed with a view to improving propulsive bowel activity. Despite stimulation of the motilin receptor and the migrating motor complex, erythromycin failed to improve postoperative bowel motility in multiple placebo-controlled, randomized studies.(29,30,31) Metoclopramide, a dopamine antagonist, also failed to improve postoperative bowel function in multiple trials.

(32)

Randomized studies have yielded contradictory

results on the effects of propranol on postoperative ileus.(33,34) Among nine studies of cisapride, four studies showed that cisapride significantly reduced postoperative ileus, one study noted an increase in the percentage of subjects passing flatus at 4 hours after surgery, and four studies were negative.

Three of the four positive studies used intravenous cisapride, whereas three of the four negative studies used intrarectal cisapride. The effect of cisapride on ileus may therefore depend on the route of administration.(32) Cisapride was, however, recently withdrawn from the market because of rare, but severe, cardiac toxicity.

Neostigmine, an acetylcholinesterase inhibitor, is beneficial in acute colonic pseudo obstruction and studies have suggested that it is also beneficial in ileus.(35) Traut et

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al examined 39 randomized control trials that included the use of erythromycin, cholecystokinin, intravenous lidocaine, neostigmine and other prokinetic agents to evaluate their benefits postoperatively. They found that the use of most agents were not supported in the postoperative period due to their lack of effect.(36) In uncontrolled studies, administration of laxatives resulted in early return of bowel motility and early discharge after gynecologic surgery.(37) These effects were confirmed in a randomized, double-blind, placebo-controlled study.(38)

However better understanding of the pathophysiology of POI has led researchers to a pharmacologic treatment option. The GI hypomotility noted with opioid drugs is due to its direct effect on peripheral Âľ receptors. Alvimopan is a peripherally acting Âľ receptor antagonist. This drug allows the analgesic effect of opioids due to their centrally acting properties and help restore GI motility by blocking the peripheral Âľ receptors.(39) The beneficial effect was demonstrated in 4 North American phase 3 trials and a single European phase 3 trial. In patients who were administered Alvimopan, GI recovery was 10-20 hours sooner for passage of flatus and stool and 13-26 hours sooner for tolerating solid food and first bowel movement.(39) Alvimopan obtained FDA approval for use in POI in 2008. It is to be used in a dose of 12mg (oral) given 30 minutes to 5 hours before surgery and subsequently twice daily for a maximum of 7 days post-operatively. The drug is generally well tolerated and is associated with increased risk of myocardial infarction when used on a long term basis. Therefore it is recommended for short term use only.(39)

In view of the multifactorial nature of the enigmatic POI clearly a multi-modal approach to its avoidance and treatment seems most fruitful. The ability to risk stratify patients would be helpful in instituting prophylactic and therapeutic measures in a timely fashion. Compelling data which permit the accurate prediction of patients most at risk for POI are lacking; however, several studies have ex163

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amined this issue. In a study of 666 patients with nonruptured abdominal aortic aneurysms, logistic regression analysis showed POI to be related to aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and preoperative history of angina.(40) A recent retrospective study of 88 abdominal surgery patients found that the duration of POI correlates with total surgery time, blood loss and total opiate dose.(41) Gervaz et al studied 124 patients undergoing laparotomy for colectomy (median age, 68 years) and found the duration of ileus significantly reduced in those cases performed by a colorectal surgeon and when opioid analgesia lasted for less than 2 days.(42)

Though POI is most often associated with abdominal surgery, it is also seen in cardiothoracic surgery, hip fracture repair, spine procedures, neurosurgical procedures, arthroscopic surgery, gynecologic surgery, genitourinary surgery, and abdominal wall herniorraphy among others.(43,44,45) Notably, POI is a complication of up to 4% of both total hip and total knee arthroplasties and abdominal hysterectomies.(43,46)

As outlined previously some of the current treatment strategies have created some controversy and others challenge traditional practice. This is evident in a survey of clinical practice following colon operations in 295 hospitals throughout Europe and the USA. NGTs tubes were left in situ in 40-66% of cases and pre-operative mechanical bowel preps were used in more than 85% of patients.

Ileus persisted for more than 5 days in nearly half of these patients and hospital stay was 7-10 days.(47) The indication is that, despite the proven effectiveness of some measures in ameliorating POI, there is reluctance to fully implement them and calls for further education.

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CONCLUSION POI is the commonest complication following abdominal surgery. However, it may affect patients undergoing various other procedures unrelated to the abdomen. POI may negatively impact on the convalescence of patients and contribute to increased health care costs. All clinicians should be educated about its pathophysiology and therapeutic strategies to minimize POI.

Various strategies to prevent POI and decrease the time needed for postoperative GI motility to return to normal function have been employed and/or are currently being investigated. The use of epidural local anesthetics for postoperative analgesia, when used in conjunction with fast-track perioperative care, has significantly shortened the time to return of normal bowel sounds and bowel movements. There is also clinical evidence that the use of anti-inflammatory drugs (NSAIDs and COX 2-inhibitors) may help to increase GI motility after abdominal surgery. Finally, new drugs such as alvimopan show promise for preventing POI. Though many of these strategies have been shown to be partially beneficial on their own, when used in combination as part of a fast-track protocol, a significant decrease in time to return of normal bowel function and shorten length of hospital stay can be expected.

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REFERENCES 1. Lubawski J, Saclarides T. Postoperative ileus: strategies for reduction. Ther Clin Risk Manag 2008;4:913-7.

2. Livingston EH, Passaro EP Jr. Postoperative ileus. Dig Dis Sci 1990;35(1):121–132.

3. Behm B, Stollman N: Postoperative ileus: etiologies and interventions. Clin Gastroenterol Hepatol 2003; 1: 71–80.

4. Lubbers T , Buurman W, Luyer M. Controlling postoperative ileus by vagal activation. World J Gastroenterol 2010 ; 16(14): 1683-1687.

5. Holte K, Kehlet H: Postoperative ileus: progress towards effective management. Drugs.

2002; 62: 2603–2615.

6. Kehlet H, Dahl JB. Anaesthesia, surgery and challenges in postoperative recovery. Lancet 2003; 362: 1921-1928.

7. Lassen K, Soop M, Nygren J et al. Consensus review of optimal perioperative care in colorectal surgery: Enhanced Recovery After Surgery (ERAS) group recommendations. Arch Surg 2009; 144:961-969.

8. Contant CM, Hop WC, van’t Sant HP, et al. Mechanical bowel preparation for elective colorectal surgery:a multicentre randomised trial. Lancet 2007;370:2112-7.

9. Bucher P, Gervaz P, Soravia C, et al. Randomized clinical trial of mechanical bowel preparation versus no preparation before elective left-sided colorectal surgery. Br J Surg 2005; 92:40914.

10. Shafii M, Murphy DM, Donovan MG, Hickey DP: Is mechanical bowel preparation necessary in patients undergoing cystectomy and urinary diversion? BJU Int 2002; 89: 879–881.

11.Melnyk M ,Casey RG, Black P, et al. Enhanced recovery after surgery (ERAS) protocols: Time to change practice? Can Urol Assoc J 2011; 5(5): 342-8.

12. Marret E, Remy C, Bonnet F: Meta-analysis of epidural analgesia versus parenteral opioid analgesia after colorectal surgery. Br J Surg 2007; 94: 665–673.

13. Sim R, Cheong DM, Wong KS, et al. Prospective randomized, double-blind, placebo-controlled study of pre- and postoperative administration of a COX-2-specific inhibitor as opioidsparing analgesia in major colorectal surgery. Colorectal Dis 2007; 9: 52–60.

14. Schwenk W, Haase O, Neudecker J, et al. Short term benefits for laparoscopic colorectal resection. Cochrane Database Syst Rev 2008.

15. Holte K, Foss NB, Andersen J, et al: Liberal or restrictive fluid administration in fast track colonic surgery: a randomized, double-blind study. Br J Anaesth 2007; 99: 500–508.

16. Holte K, Kristensen BB, Valentiner L, et al. Liberal versus restrictive fluid management in knee arthroplasty: a randomized, double-blind study. Anesth Analg 2007; 105: 465–474.

17. Ferraz AA, Cowles VE, Condon RE, et al. Non opioid analgesics shorten the duration of postoperative ileus. Am Surg 1995; 61:1079–1083.

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A CASEBOOK OF TWENTY SURGICAL CASES 18. Cheatham ML, Chapman WC, Key SP, et al. A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy. Ann Surg 1995; 221: 469–476.

19. Nelson R, Edwards S, Tse B. Prophylactic nasogastric decompression after abdominal surgery. Cochrane Database Sys Rev 2007, 18;(3).

20. Kumar M, Yang S, Jaiswal V, et al. Is prophylactic placement of drains necessary after subtotal gastrectomy? World J Gastroenterol 2007;13: 3738–3741.

21. Stewart BT, Woods RJ, Collopy BT, et al: Early feeding after elective open colorectal resections: a prospective randomized trial. Aust NZ J Surg.1998; 68:125–128.

22. Anderson HK, Lewis SJ, Thomas S: Early enteral nutrition within 24hr of colorectal surgery versus later commencement of feeding for postoperative complications. Cochrane Database Syst Rev 2006, 18:(6).

23. Lubbers T, Luyer MD, de Haan JJ, et al. Lipid- rich enteral nutrition reduces postoperative ileus in rats via activation of cholecystokinnin receptors. Ann Surg 2009; 249: 481-487.

24. Helman CA, Chewing gum is as effective as food in stimulating cephalic phase gastric secretion. Am J Gastroenterol 1988; 83: 640-642.

25. Person B, Wexner SD. The management of postoperative ileus. Curr Probl Surg 2006; 43: 6-65.

26. Vasquez W, Hernandez AV, Garcia-Sabrido JL. Is gum chewing useful for ileus after elective colorectal surgery? A systematic review and met-analysis of randomisec clinical trials. J Gastrointest Surg 2009; 13: 649-656.

27. Lunding JA, Nordstrom LM, Haukelid AO, et al. Vagal activation by sham feeding improves gastric motility in functional dyspepsia. Neurogastroenterol Motil 2008; 20: 618-624.

28. Fitzgerald JE, Ahmed I. Systematic review and meta-analysis of chewing-gum therapy in the reduction of postoperative paralytic ileus following gastrointestinal surgery. World J Surg 2009; 33: 2557-2566.

29. Bonacini M, Quiason S, Reynolds M, et al. Effect of intravenous erythromycin on postoperative ileus. Am J Gastroenterol 1993; 88(2): 208-211.

30. Lightfoot AJ, Eno M, Kreder KJ, et al. Treatment of postoperative ileus after bowel surgery with low-dose intravenous erythromycin. Urology 2007; 69(4): 611-615.

31.Smith AJ, Nissan A, Lanouette NM, et al. Prokinetic effect of erythromycin after colorectal surgery: randomized, placebo-controlled, double-blinded study. Dis Col Rectum.

2000;43(3):333–337.

32. Holte K, Kehlet H. Postoperative ileus: a preventable event. Br J Surg 2000; 87 (11): 14801493.

33. Hallerback B, Carlsen E, Carlsson K, et al. Beta-adrenoreceptor blockade in the treatment of postoperative adynamic ileus. Scand J Gastroenterol 1987; 22(2): 149-155.

34. Cheape JD, Wexner SD, James K, et al. Does metoclopramide reduce the length of ileus after colorectal surgery? A prospective randomized trial. Dis Colon Rectum 1991; 34(6): 437-441.

35. Orlando E, Finelli F, Colla M, et al. A double –blinded study of neostigmine versus placebo in paralytic ileus as a result of surgical interventions. Minerva Chir 1994; 49(5): 451-455.

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A CASEBOOK OF TWENTY SURGICAL CASES 36. Traut U, Brügger L, Kunz R, et al. Systemic prokinetic pharmacologic treatment for postoperative adynamic ileus following abdominal surgery in adults. Cochrane Database Syst Rev 2008; Issue 1, article No. CD004930.

37. Kraus K, Fanning J. Prospective trial of early feeding and bowel stimulation after radical hysterectomy. Am J Obstet Gynecol 2000; 182 (5): 996-998.

38. Hansen CT, Sorensen M, Moller C, et al. Effect of laxatives on gastrointestinal function recovery in fast-track hysterectomy: a double –blind, placebo controlled randomized study. Am J Obstet Gynecol 2007; 196(4): 311 e1-e7.

39. Kraft M, McLaren R, Du W, et al. Alvimopan (Entereg) for the management of post operative ileus in patient undergoing bowel resection. P & Te 2010; 1.

40. Johnston KW. Multicenter prospective study of nonruptured abdominal aortic aneurysm II. Variables predicting morbidity and mortality. J Vasc Surg 1989; 9: 437-447.

41. Artinyan A, Nunoo-Mensah JW, Balasubramaniam S, et al. Prolonged postoperative ileus: definition, risk factors and predictors after surgery. World J Surg, DOI: 10.1007/ s0026800894912.

42. Gervaz P, Bucher P, Scheiwiller A, Mugnier-Konrad B, et al. The duration of postoperative ileus after elective colectomy is correlated to surgical specialization. Int J Colorectal Dis 2006; 21: 542-546.

43. Berend KR, Lombardi AV Jr, Mallory TH, et al. Ileus following total hip or knee arthroplasty is associated with increased risk of deep venous thrombosis and pulmonary embolism. J Arthroplasty 2004; 19: 82–86.

44. Bianchi C, Ballard JL, Abou-Zamzam AM, et al. Anterior retroperitoneal lumbosacral spine exposure: operative technique and results. Ann Vasc Surg 2003; 17: 137-142.

45. Shapiro G, Green DW, Fatica NS, et al. Medical complications in scoliosis surgery. Curr Opin Pediatr 2001; 13: 36-41.

46. Story SK, Chamberlain RS. A comprehensive review of evidence based strategies to prevent and treat postoperative ileus. Dig Surg 2009;26:265–275.

47. Kehlet H, Buchler MW, Beart RW Jr, et al. Care after colonic operation- is it evidence based? Results from a multinational survey in Europe and the United States. J Am Coll Surg 2006; 202:45-54.

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9.DUCTAL CARCINOMA IN SITU (DCIS) Management Strategies.

INTRODUCTION The incidence of Ductal Carcinoma In Situ (DCIS) has seen a rapid increase in the last two decades. This has resulted in clinicians having to treat many more women with DCIS, a pre-invasive form of neoplasia. During the 1960s and 1970s the standard of care remained mastectomy. It was presumed that despite the absence of invasion in the histological specimens progression to invasive cancer inevitably occurred.

A better understanding of the nature of DCIS changed the treatment paradigm.

It became accepted that untreated DCIS did not always progress to invasive cancer. The inevitable progression of DCIS to invasive carcinoma has been challenged and the identification of DCIS at an early stage in its natural history that does not require treatment of the entire breast (whether by mastectomy or irradiation) has become an area of great interest with contentious issues.

The goal of therapy for patients with DCIS became prevention of invasive cancer by excising the affected tissue with a cosmetically acceptable result. Mastectomy is a curative treatment for approximately 98% of patients who have DCIS. However, no evidence exist which shows a survival benefit for mastectomy versus breast conservative surgery (BCS). Multiple prospective randomized trials comparing mastectomy and BCS in invasive carcinoma have shown no survival differences between these procedures therefore, mastectomy may be over treatment for patients with localized DCIS.

The literature reflects a 50% invasive relapse following BCS for DCIS. In order 169

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to nullify the possibility of morbidity related to breast cancer, adjuvant radiotherapy is employed along with BCS. However there are those who are reluctant to use radiotherapy (RT) for DCIS as a primary treatment. This is because a substantial proportion of lesions behave in a benign fashion and is unlikely to transform into carcinoma. While there is a sub group of patients who can avoid the morbidity and inconvenience of RT, identification of these patients is difficult. The Van Nuys Prognostic Index (VNPI) has been used to stratify patients into different groups that may reflect different degrees of risk of local failure and therefore identify those who may benefit from radiotherapy. While its simplicity is attractive there are questions regarding its validity. Tamoxifen has also shown to be beneficial as an adjunctive measure to reduce local failure rates in patients who demonstrates estrogen receptor positivity. Its exact role is still to be determined.

The cause specific survival of patients with DCIS is very high regardless of the type of local therapy. However, there is wide variation in recurrence rates which is the crux in the process of developing therapeutic strategies to prevent patients with DCIS from developing invasive cancer.

The case of a 49 year old woman with DCIS is described. A discussion follows which outlines the evidence for risk stratification and the role of adjunctive therapy (radiation, tamoxifen) in the management of DCIS.

CASE History: A 49 year old woman presented with a 2 month history of a left breast lump (painless). There were no changes over this time. She experienced no nipple discharge. The patient had her menarche at age 14yrs and was P3+2.

In her past history a total abdominal hysterectomy was performed for symptomatic fibroids 3 years previously. She was not placed on hormone replace170

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ment therapy and neither did she use any oral contraception previously. Significantly, her sister (aged 30 years) died of breast cancer.

Physical Examination: The right breast was clinically normal. The left breast revealed a 1.5cm firm lump in the upper outer quadrant of the left breast. There were no associated skin changes. There was no palpable lymphadenopathy.

Investigations: Mammograms were done and there was no asymmetry or microcalcifications noted. Trucut biopsy of the lump was performed and this showed: atypical lobular and ductal hyperplasia with no evidence of carcinoma.

Surgical treatment: Wide local excision of this lump was performed and the histology revealed the following: fibrocystic change and proliferative changes including severe sclerosing adenosis and duct epitheliosis. A 6mm focus of Ductal Carcinoma In-Situ (non comedo) was noted 1cm from the superior margin.

Follow up: An MRI was done subsequently to screen the right breast. There were many areas of mild and gradual enhancement seen scattered throughout, consistent with fibrocystic disease.

Her Van Nuys Prognostic Index was 5/12. After discussion at the breast multidisciplinary team meeting the patient was placed on Tamoxifen (20 mg per oral once daily for 5 years). There was no need for radiotherapy.

The patient was advised to perform 2 weekly self breast examinations and to 171

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attend the outpatient clinic for annual surveillance. After 2 years of follow up there have been no breast events.

DISCUSSION DCIS was first described by Foote and Stewart in 1946. (1) Before the widespread use of screening mammography, only 3-5% of mammary cancers were DCIS, most being palpable masses. (2) The incidence of DCIS increased significantly in the last two decades due to the widespread adoption of screening mammography.(3) Several studies report that DCIS accounts for 15-30% of all screened detected tumors in women participating in large organized screening programs. This accounts for a significant number of women who present for treatment to the surgical service.

In the early years following the description of DCIS, it was presumed that progression to invasive cancer inevitably occurred, largely due to the observation of co-existence of DCIS with invasive carcinoma. For this time period the standard of care was mastectomy. Subsequently, it became evident in the 1970s that not all DCIS progressed to invasive disease. In addition, autopsy studies also indicated that the incidence of DCIS in asymptomatic women ranges from 0.2% to 18.2%.(4,5,6) The inevitable progression to invasive carcinoma has been challenged and the identification of DCIS at an early stage in its natural history that may not require treatment of the entire breast (whether by mastectomy or irradiation) has become a topic of controversy.

Several studies have shown that total mastectomy for DCIS is superior to breast conservation surgery plus adjuvant radiotherapy, in terms of disease free survival (DFS). In a meta-analysis reported by Boyages et al the recurrence rate was 1.4% for mastectomy compared with 8.9% for BCR plus RT and 22.5% for BCS alone.(7) Similarly, Tunon-de-Lara et al in a study of 676 patients with 172

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DCIS, noted the local recurrence rate was 2.6% for the mastectomy group, 7.5% for the BCS plus RT group, and 14.5% for BCS alone group.(8) Clearly, mastectomy is an extremely effective therapy for DCIS, for which all patients are eligible. However, many argue that this is over treatment. This is because multiple prospective randomized trials comparing mastectomy and BCS in invasive carcinoma have shown no survival differences between these procedures. Nevertheless, mastectomy may be indicated for multi centric DCIS, large lesions (more than 4 cm), centrally located disease, inadequate margins after BCS in patients who prefer to have mastectomy and if adjuvant radiotherapy is thought to be contraindicated.(9)

This realization has encouraged a lot of attention on BCS for DCIS. The aim of BCS for localized DCIS is complete excision with clear margins and a cosmetically acceptable result. When breast conservation is elected rather than mastectomy, radiation therapy statistically decreases the likelihood of local recurrence when compared with excision alone, although radiation therapy like mastectomy may also represent over treatment for a significant number of patients who elect breast preservation.(10,11,12) Three prospective randomized controlled trials investigated the role of adjuvant radiotherapy after local excision of DCIS: the NSABP-B17 trial, the EORTC 10853 trial, and the UK/ANZ DCIS trial.

In the NSABP-B17 trial, 818 patients with localized DCIS were randomized to excision alone or excision plus adjuvant radiotherapy. After a mean follow up of 90 months, the investigators observed a significant reduction in both invasive (from 13.4% to 3.9%, p<0.0001) and non-invasive (from 13.4% to 8.2% p<0.0007) ipsilateral breast tumor recurrence (IBTR) associated with the use of adjuvant RT. Although all patient sub groups benefited from the addition of RT, the benefit was maximal in patients with comedo necrosis. These authors observed no significant difference in regional and distant recurrence or mortal173

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ity between the two study arms. This study has been criticized for its definition of clear margins, lack of requirement of specimen radiography, indetermination of tumor size and incomplete tissue processing of DCIS specimens. In this trial margins were considered to be free when “the tumor was not transected.” Assessments indicating lesions to be “close” or “too close” were not considered to represent margin involvement.(10) In the EORTC trial, 1010 patients with localized DCIS were randomized. After a median follow up of 4.25 years, the investigators observed that adjuvant RT had achieved significant reductions in all IBTR (p=0.005) and invasive recurrence rates, however, the reduction in DCIS recurrence failed to reach a statistical significance. Furthermore, the authors reported an unexpected significant increase in contra-lateral breast cancer in the irradiated group, though this may represent a spurious finding. The authors of the EORTC study found involved margins to be the most significant risk factor for local recurrence. Other risk factors included young age, poor differentiation, and symptomatic detection.

Although the risk of invasive recurrence was similar for high, intermediate, and low grade lesions, the incidence of subsequent metastatic disease was different: 41%, 15% and 5% respectively in these sub groups (11).

In the UK/ANZ DCIS trial which has a factorial 2x2 design, 1701 patients were randomized to RT and tamoxifen. After a median follow up of approximately 52.6 months, the authors observed that adjuvant RT was associated with a significant reduction in all IBTR events (invasive or DCIS). RT reduced the risk of ipsilateral DCIS by 64% (p=0.0004) and ipsilateral invasive cancer by 55% (p=0.01). The reduction in relative risks observed in this study were greater than those reported by the EORTC trial (35% and 40% respectively), but the reduction in the relative risk of ipsilateral invasive recurrence is smaller than that reported by the NSABP-B17 (71%). This difference might be explained by the difference in age distribution between the two trials. Patients entered into 174

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the UK/ANZ DCIS trial were older and more likely to be screen detected than those recruited for the NSABP-B17 trial.(12) An updated analysis of the results of the UK/ANZ trial confirmed the beneficial effect of RT for women with DCIS treated by complete local excision. After a median follow up of 12.7 years, 376 breast cancers were diagnosed (163 invasive, 197 DCIS, and 16 of unknown invasiveness). RT reduced the incidence of all new breast events (p<0.0001) reducing the incidence of ipsilateral invasive disease as well as ipsilateral DCIS but expectedly having no effect on contralateral breast cancer.(13) The results of these studies have led to the broad recommendation that RT is appropriate for all patients with DCIS who are treated with breast preservation.

However, several authors have reported on different subsets of patients within a population with DCIS, indicating that some patients may not require radiotherapy. This reflects the heterogeneous nature of DCIS and has generated ideas to identify patients of lesser potential risk of recurrence who may avoid RT. RT is not without side effects. It changes the texture of the breast, makes subsequent mammography more difficult to interpret, and its use precludes additional RT and breast conservation should a metachronous invasive breast cancer develop. RT should only be offered to those patients with DCIS likely to obtain a substantial benefit. Some authors have identified subsets of patients that may avoid RT: low grade lesions (Lagios et al) (14,15), small non-comedo lesions with uninvolved margins (Schwartz et al)(16), or well differentiated lesions (Zafrani et al)(17). Various studies have indicated that such patients may account for more than 30% of the total number of patients diagnosed with DCIS.(18) Subsets of patients who do not benefit from RT however have not been reproducibly identified. In a non randomized study Silverstein and colleagues compared outcomes of patients who had DCIS treated with and without RT and suggested that if a negative margin width of >1 cm was obtained, RT was 175

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not beneficial in reducing local recurrences, an issue not addressed in the three randomized trials described above. The probability of recurrence at 8 years was 0.04 among 133 patients with margin width >1 cm.(19) There was also no statistically significant benefit from post operative RT among patients with margin widths of 1-9mm. In an attempt to duplicate these findings Wong et al conducted a prospective study that hypothesized excision to a margin of > 1 cm results in a low rate of local recurrence in the absence of RT. In this study 158 patients with a mean age of 51 years and with predominantly grade 1 and 2 DCIS underwent excision of DCIS to a negative margin of >1 cm. The trial was prematurely stopped after the pre-defined boundaries for what was deemed as an acceptable recurrence rate was overstepped. The estimated 5 year ipsilateral recurrence rate accrued was 12% which is a value similar to the surgery only arms of the UK ANZ, EORTC and NSABP-B17 trials noted previously, and as such appeared to support the conclusion that there is in fact not a sub group of patients with DCIS for whom RT should not be offered.(20) In order to identify a subgroup of patients who can be safely spared adjuvant RT and its potential complications using a prospective database of 706 women who had BCS for pure DCIS and 12 year follow up, Silverstein designed a prognostic index known as the University of Southern California â&#x20AC;&#x201C; Van Nuys Prognostic Index (USC-VNPI).(21) The initial index was introduced in 1996 and combined tumor size, margin width, nuclear grade and the presence/absence of necrosis. Age was subsequently included in a modified version of the index (<40 years, 40-60 years, > 60 years) in order to improve the accuracy of the index in predicting local failure. There was no statistical difference in the 12 year local recurrence free survival in patients with VNPI scores of 4, 5, 6 regardless of whether or not RT was used (p>0.05). Patients with VNPI scores of 7, 8 or 9 received a statistically significant average 12-15% local recurrence free survival benefit when treated with RT (p=0.03). Patients with scores of 10, 11, 12, although showing the greatest absolute benefit from RT, experienced local 176

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recurrence rates of almost 50% at five years. These observations suggest that RT can be omitted after local excision in patients with scores 4, 5 and 6 and that mastectomy with or without immediate breast reconstruction should be considered in patients with scores 10, 11, 12. Patients with intermediate scores 7, 8, and 9 should be considered for treatment with RT or be re-excised if margin width is <10 mm and cosmetically feasible.(18) TABLE VNPI: PARAMETER

1

2

Size (mm)

≤ 15

15.1 – 40

>40

Margins (mm)

≥ 10

1 – 9

<1

Pathology

non high grade,

Age (years)

3________

non high grade,

high grade,

no necrosis

with necrosis

with necrosis

> 60

40 – 60

< 40

_______________________________________________________________ Silverstein and colleagues provided further evidence for the importance of the margin width in the treatment of DCIS. They retrospectively examined data for 469 patients with DCIS: 256 treated by excision alone, 213 received adjuvant RT after local excision. After a mean follow up of 81 months, the authors observed that with a margin width of 10mm or more the incidence of IBTR was only 2.3% and there was no significant benefit from adding adjuvant RT.(19) Some controversial aspects were noted though: □ The group of patients with a 10mm margin who did not have RT had significantly smaller lesions □ With excision margins of 1-9 mm the risk of IBTR after local excision alone was non significant. The tumor size was significantly higher in 177

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the RT arm (4.5mm vs 8mm) â&#x2013;Ą The group of patients who had margin width of <1mm, the relative risk of IBTR was significantly increased when RT was omitted. However this group of patients had larger cancers and a higher incidence of comedo necrosis than any of the other groups.(19)

The importance of margin width in determining local control after BCS for DCIS is controversial. Neuschatz and colleagues recently showed that a tumor margin width of >1mm is associated with a low recurrence rate at 5 years, for BCS alone or BCS plus RT (10.9% vs 4.6%). This was a statistically nonsignificant finding, however it was noted that lesion size > 15mm and margin width â&#x2030;¤ 1mm were associated with increased local recurrence.(21) Chan et al also reported that the cut off in terms of involved margins was <1mm and that there was no significant difference in the rates of local recurrence in patients treated by local excision with margins between 1-5mm, 5-10mm or >10mm.

The issue of margin width is further complicated by the fact that different measures of assessing surgical margins have been used: selected tangential sections, the margin shaving and cavity peel methods.(22) Therefore future clinical trials should adopt uniform criteria for margin evaluation. These retrospective studies by Chan and Neuschatz indicate that adjuvant RT could be safely omitted in patients with adequately excised (margin width >1mm), small (<15mm), non high grade DCIS not associated with significant necrosis. However the effect of these parameters and especially margin width on local recurrence should be evaluated in prospective randomized controlled trials that adopt uniform and practical methods in estimating the size of DCIS and margin widths. It is to be noted that margin width represents one parameter for which no standardized data was provided by the 3 randomized trials outlined previously (NSABP-B17, EORTC, UK/ANZ DCIS trial.

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Another important finding from Silverstein stratification of data according to margin width comes from the group with clearance of <1mm. Although adjuvant RT significantly decreased the incidence of IBTR from 58% to 30%(19); this recurrence rate would still be unacceptably high, suggesting that excision plus RT is not the optimal treatment for this subgroup of patients. Rather, further local excision or total mastectomy with or without reconstruction will be preferred.

The value of the VNPI in prediction of recurrence of DCIS after breast conserving surgery is somewhat controversial. In an attempt to validate the use of VNPI in a UK population by Boland et al, the clinic-pathological data including VNPI subgroups for 237 patients who had breast conserving operations for DCIS was examined. There were 37 ipsilateral local recurrences. Excision margin width (p<0.001) and tumor grade or simple nuclear grading (p=0.004) were the only independent risk factors for local recurrence. Excision margin width had three times more power than grade in predicting local recurrence. They concluded that the VNPI lacked discriminatory power for guiding further management.(23) More recently Macausaland et al reported that although trends were observed using the VNPI stratification system and local recurrence none reached statistical significance. They concluded that VNPI may not be a valid tool with which to assist with stratification of patients after excision alone for risk of IBTR.(24)

The variable acceptance of the VNPI (at least in the UK) is demonstrated by the interim findings of the Sloane Project. There was a very wide variation in the use of adjuvant RT by individual breast units, with some referring all patients treated by BCS for adjuvant RT and some referring none. A higher percentage of cases of unknown VNPI (16.8%) compared to its components (1% for grade, 4.6% for size, and 12.3% for margin width) was noted. In the multi-variate analysis of data derived, after adjustment for size and grade, the VNPI score 179

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was an artifact of it being included in the model along with the factors from which it is derived. Of note VNPI scores were seen to affect the chances of getting planned adjuvant RT, suggesting that clinicians may be starting to use this scoring system in routine practice in decision making.(24)

The VNPI, like most if not all scoring systems, is likely to not always be precise. While its use is variable it is the start of a process of standardization on which treatment can be based. Prospective trials would certainly help in the long term to assist in the validity of this scoring system. The VNPI is attractive as a simple, reproducible scoring system by which to risk stratify patients with DCIS and aid in guiding treatment options. In the case described here the patient had a modified VNPI of 5, despite the recommendation of NSABP-B17 trial RT was withheld. Based on the risk stratification by Silvertsteinâ&#x20AC;&#x2122;s VNPI radiotherapy was not indicated.

In view of her young age and family history of breast cancer, the patient was placed on tamoxifen. It was thought the systemic treatment may be instrumental in the prevention of local recurrence and also provide prophylaxis for the contralateral breast.

Two trials have studied the use of tamoxifen directly in women who have DCIS. The NSABP-24 trial randomized 1804 patients with DCIS who were treated with excision and RT to 20 mg tamoxifen daily or a placebo for five years. At a median follow up of 74 months in 1798 patients, the patients in the tamoxifen arm had an 8.2% incidence of breast cancer events compared with 13.4% in the placebo group (p=.0009). Tamoxifen reduced the rate of ipsilateral invasive recurrences by 44% but did not significantly reduce the risk of recurrent DCIS in the ipsilateral breast. Although the incidence of contralateral breast cancers were low (3.4% invasive and non invasive in the placebo group) a 52% reduc180

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tion was noted in the tamoxifen group. Tamoxifen was observed to reduce breast cancer events in those over and under aged 50 years with or without positive margins and in patients with comedo necrosis.(25)

The initial results of the UK-ANZ trial previously outlined were somewhat controversial. With a median follow up of 52.6 months there was no significant benefit from tamoxifen in preventing invasive ipsilateral or contralateral events after BCS. The only advantage of tamoxifen was a 3.4% reduction in ipsilateral in situ recurrence. Updated results after long term follow up (median 12.7 years), identified a reduction in new breast events that was significant.(13) No effect was identified on ipsilateral invasive new breast events and the largest events was on contralateral new breast events. The tamoxifen effect seem to be apparent only in patients who did not receive RT; however only 523 patients who received RT were in the tamoxifen randomization and a test for interaction between treatments was not significant. More specifically it is clear that the benefit from tamoxifen is restricted to women with estrogen receptor (ER) positive DCIS. Allred and colleagues determined the ER status in 732 patients with DCIS. ER was positive in 76% of patients: patients with ER positive DCIS treated with tamoxifen showed significant decreases in breast cancer at 10 years and overall follow up (median 14.5 years).(26) In addition, a Cochrane review of the role of tamoxifen after surgery for DCIS demonstrated a reduced recurrence of both ipsilateral and contralateral DCIS while a trend was noted towards decreased ipsilateral and contralateral invasive cancer. While tamoxifen after local excision for DCIS (with or without adjuvant RT) reduce the risk of recurrent DCIS it did not reduce the risk of overall mortality.(81)

In the case described here the patient was placed on tamoxifen for prophylaxis.

Unfortunately, hormone receptor testing was not available at the hospital and the patient could not afford this test privately. Having discussed the risk of 181

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tamoxifen therapy mainly with regards to endometrial carcinoma and venous thrombosis, the patient accepted chemoprevention. This patient already had a hysterectomy and in view of her family history, valued risk reduction with tamoxifen for her otherwise normal right breast.

AS for now the range of treatment options for patients with DCIS include: mastectomy, excision alone (BCS), excision plus RT. To date, no study of DCIS patients has shown a statistically significant difference in mortality when these three available treatments are compared. However as noted in the discussion above, there are clear differences in local recurrence rates and these can be extremely important. Long term > 10 years survival of patients treated for DCIS is >95% regardless of mode of therapy.(28) Local recurrences in patients who have struggled to save their breasts are both demoralizing and theoretically if invasive, a threat to life. Several reports indicate that on average half of recurrences are invasive. Some authors have reported in those patients who develop invasive recurrence the risk of developing distant metastases ranges from 11% - 27%.(29,30)

The varied behavior of DCIS makes it a heterogeneous entity. The greatest challenge is to work out which cases will not progress, which cases will progress to invasive carcinoma, and which cases will recur after excision. Han et al demonstrated in a study of 190 cases of DCIS with a median follow up of 8.7 years that patients with Her2neu Receptor positivity had a 40% recurrence compared to 21% in patients who were Her2neu negative. They concluded that Her2neu expression in DCIS is a significant predictor of local recurrence.

(31)

Further identification of genetic and molecular markers may help to select

patients for adjuvant therapy.

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CONCLUSION There is still uncertainty about the natural history of DCIS. The VNPI for now is a simple reproducible system that helps to guide decisions regarding therapeutic strategies which aim to prevent invasive breast cancer. Radiotherapy should be offered to patients with VNPI scores of 7-9, while mastectomy should be reserved for VNPI scores of 10-12. While studies with greater predictability for recurrent DCIS or invasive disease are awaited, clinicians should be aware of the long term risks and benefits of available therapy and include the preferences of the patient into the decision making process.

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REFERENCES 1. Schwartz GF, Terribile D. The treatment of ductal carcinoma in situ of the breast. Obstet Gynecol Clin N Am 2002;29(1): 189-200.

2. Rosner D, Bedwani RN, Vana J, et al. Noninvasive breast carcinoma: results of a national survey by the American College of Surgeons. Ann Surg 1980;192(2):139–47.

3. Ernster VL, Barclay J, Kerlikowske K et al: Incidence of and treatment for ductal carcinoma in situ of the breast. JAMA, 1996; 275: 913–18.

4. Wellings SR, Jensen HM. On the origin and progression of ductal carcinoma in the human breast. J Natl Cancer Inst 1973;50(5):1111–8.

5. Nielsen M, Jensen J, Anderson J. Precancerous and cancerous breast lesions during lifetime and at autopsy: a study of 83 women. Cancer 1984;54(4):612–5.

6. Alpers C, Wellings S. The prevalence of carcinoma in situ in normal and cancer-associated breast. Hum Pathol 1985;16(8):796–807.

7. Boyages J, Delaney G, Taylor R: Predictors of local recurrence after treatment of ductal carcinoma in situ: a meta-analysis. Cancer, 1999;85: 616–28.

8. Tunon-de-Lara C, de-Mascarel I, Mac-Grogan G et al: Analysis of 676 cases of ductal carcinoma in situ of the breast from 1971 to 1995: diagnosis and treatment-the experience of one institute. Am J Clin Oncol, 2001; 24: 531–36.

9. Schwartz GF, Solin LJ, Olivotto IA et al: The Consensus Conference on the Treatment of In Situ Ductal Carcinoma of the Breast, April 22-25,1999. The Breast Journal, 2000; 6: 4–13.

10. Fisher B, Dignam J, Wolmark N et al: Lumpectomy and Radiation Therapy for the Treatment of Intraductal Breast Cancer: Findings From National Surgical Adjuvant Breast and Bowel Project B-17. J Clin Oncol, 1998;16: 441–52.

11. Julien J-P, Bijker N, Fentiman S et al: Radiotherapy in breast-conserving treatment for ductal carcinoma in situ: first results of the EORTC randomized phase III trial 10853. Lancet, 2000; 355: 528–33.

12. Houghton J, George WD, Cuzick J, et al. Radiotherapy and tamoxifen in women with completely excised ductal carcinoma in situ of the breast in the UK, Australia, and New Zealand: randomised controlled trial. Lancet 2003;362:95–103.

13. Cuzick J, Ivana S, Pinder SE. Effect of tamoxifen and radiotherapy in women with locally excised ductal carcinoma in situ: long term results from the UK/ANZ DCIS Trial. Lancet Oncol.

2010; 12(1): 21-29.

14. Lagios M. Duct carcinoma in situ: pathology and treatment. Surg Clin North Am 1990;70:853–71.

15. Lagios M, Westdahl P, Margolin F, et al. Duct carcinoma in situ: relationship of extent of noninvasive disease to the frequency of occult invasion, multicentricity, lymph node metastases, and short term treatment failures. Cancer 1982;50:1309–14.

16. Schwartz G. The role of excision and surveillance alone in subclinical DCIS of the breast.

184

A CASEBOOK OF TWENTY SURGICAL CASES Oncology 1994;8:21–6.

17. Zafrani B, Leroyer A, Fourquet A, et al. Mammographically-detected ductal in situ carcinoma of the breast anaylyzed with a new classification. A study of 127 cases: correlation with estrogen and progesterone receptors, p53 and c-erbB-2 proteins, and proliferative activity. Semin Diagnost Pathol 1994;11:208–14.

18. Silverstein MJ. The University of Southern California/ Van Nuys prognostic index for ductal carcinoma in situ of the breast. Am J Surg 2003; 186: 337-343.

19. Silverstein MJ, LagiosMD, Groshen S, et al. The influence of margin width on local control of ductal carcinoma in situ of the breast. N Engl J Med 1999;340(19):1455–61.

20. Wong JS, Kaelin CM, Troyan SL, Gadd MA, Gelman R, Lester SC,Schnitt SJ, Sgroi DC, Silver BJ, Harris JR, Smith BL: Prospective study of wide excision alone for ductal carcinoma in situ of the breast. J Clin Oncol 2006, 24:1031-1036.

21. Neuschatz AC, DiPetrillo T, Safaii H et al: Margin width as a determinant of local control with and without radiation therapy for ductal carcinoma in situ (DCIS) of the breast. Int J Cancer, 2001; 96: 97–104.

22. Chan KC, Knox WF, Sinha G et al: Extent of excision margin width required in breast conserving surgery for ductal carcinoma in situ. Cancer, 2001;91:9-16.

23. Boland GP, Chan KC, Knox WF. Value of the Van Nuys Prognostic Index in prediction of recurrence of ductal carcinoma in situ after breast-conserving surgery. Br J Surg,2003;90(4): 426-32.

24. Dodwell D, Clemants K, Lawrence G et al: Radiotherapy following breast-conserving surgery for screen-detected ductal carcinoma in situ: indications and utilisation in the UK. Interim findings from the Sloane Project. Br J Cancer 2007, 97:725-729.

25. Fisher B, Dignam J, Wolmark N, et al. Tamoxifen in treatment of intraductal breast cancer: National Surgical Adjuvant Breast and Bowel Project B-24 randomised controlled trial. Lancet 999;353(9169):1993–2000.

26. Allred DC, Anderson SJ, Paik S et al. Adjuvant tamoxifen reduces subsequent breast cancer in women with estrogen receptor-positive ductal carcinoma in situ: a study based on NSABP protocol B-24. J Clin Oncol 2012; 20(12): 1268-73.

27. Staley H, McCallum I, Bruce J. Postoperative tamoxifen for ductal carcinoma in situ. Cochrane Database Syst Rev 2012;10: CD007847.

28. O’Sullivan MJ, Morrow M. Ductal carcinoma in situ- Current management. Surg Clin N Am 2007;87: 333-351.

29. Silverstein MJ, Lagios MD, Martino S, et al. Outcome after invasive local recurrence in patients with ductal carcinoma in situ of the breast. J Clin Oncol 1998;16(4):1367–73.

30. Solin LJ, Fourquet A, Vicini FA, et al. Salvage treatment for local recurrence after breast conserving surgery and radiation as initial treatment for mammographically detected ductal carcinoma in situ of the breast. Cancer 2001;91(6):1090–7.

31. Han K, Nofech-Mozes S, Narod S, et al. Expression of HER2neu in ductal carcinoma in situ is associated with local recurrence. Clin Oncol (R Coll Radiol) 2012; 24(3): 183-9.

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10. OBSTRUCTING LEFT COLON CANCER Towards lowering the rates of colostomy.

INTRODUCTION The majority of cases of acute colonic obstruction are secondary to colorectal cancer. Up to 20% of patients with colonic cancer present with symptoms of acute obstruction. Emergency surgery for acute colonic obstruction is associated with a significant risk of mortality and morbidity. Immediate resection and anastomosis in a massively distended and unprepared colon carries a high complication rate.

Traditionally, left-sided acute bowel obstruction is treated by a staged procedure. The treatment consisted of a three-stage operation: formation of a colostomy followed later by resection with a further admission to hospital for closure of the colostomy; this approach was gradually superseded by a two-stage operation consisting of primary excision of the tumor with an end colostomy (Hartmannâ&#x20AC;&#x2122;s procedure) and subsequent restoration of bowel continuity.

The surgical management of left-sided malignant large bowel obstruction has evolved considerably in the past few decades. Early fears of anastomotic dehiscence has been challenged and resulted in an increasing trend towards primary resection and anastomosis.

The case of a 65 year old woman who presented with an obstructing left colon cancer is presented. The evidence for primary resection and anastomosis in this condition is outlined including the factors that influence the surgical decision.

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CASE History: A 65 year old woman presented with a 2week history of progressive abdominal distention. This was associated with left sided abdominal pain and constipation. The pain she explained was of a colicky nature and the intensity became worse in the last 2 days. Her bowel actions were normally 1-2 motions per day. However for the last month the frequency had changed to once every 2-3 days and was not associated with per rectal bleeding or mucoid stools. Her last bowel action was 3 days previously and she did not pass any flatus in the last 24 hours. The patient had no vomiting.

Systematic enquiry revealed that she had no weight loss. Although she had not eaten properly in the last week due to her pain, her appetite was generally maintained. She experienced no symptoms of anemia.

Her past medical history included psoriasis. This patient had no previous surgery. She lived with her husband and had no family history of colonic polyps or colon cancer.

Physical examination: Vital signs: BP 167/94 mmHg, P100min-1, RR 22 min-1, T 370C. Her mucus membranes were pink and there was no palpable lymphadenopathy.

Cardio-respiratory examination was normal. Her abdomen was distended and resonant to percussion. There was tenderness but no rebound or guarding phenomenon. The bowel sounds were high pitched. DRE revealed normal tone and the rectum was empty. The previously placed nasogastric tube indicated a dark green aspirate (800mls). This she reported had improved her symptoms. A urinary catheter placed earlier had 500mls of concentrated urine.

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Investigations: Hb 12.2 g/dl, WCC 14 x 103/µl , Plt 240 x 103 µ/l. Her renal function and liver function tests were normal; the albumin level was 3.6 g/dl.

CXR: clear lung fields with a cardiothoracic ratio of 0.5.

AXR: The large bowel was distended and indicated a cut off in the sigmoid colon. The cecal diameter was 9cm. (Fig 1)

CT (abdomen and pelvis): The large bowel as previously noted was distended and the cut off was due to a soft tissue mass in the sigmoid colon. No diverticulae were seen. The liver appeared normal as were the other solid organs. There was no indication of enlarged lymph nodes and there was no ascites but a small amount of pelvic free fluid was seen.

Rigid sigmoidoscopy: up to 18cm the mucosa appeared normal; further endoscopic evaluation was not available at this time.

A diagnosis of large bowel obstruction secondary to a tumor was made. The patient was admitted to the ward and resuscitated. Informed consent was taken and the patient taken to the operating theatre for a laparotomy.

Surgical Findings and Procedure: A midline laparotomy was performed with the patient in Lloyd Davies position.

An obstructing tumor was identified in the distal sigmoid to rectosigmoid junction (Fig 2). The proximal colon was dilated but bore no evidence of bowel wall ischemia or serosal tears.

Decompression of the proximal colon was performed with the aid of a Savage’s decompressor Fig 3). A purse string (2/0 silk) suture was placed about 5cm proximal to the tumor. Through this the Savage’s decompressor was placed, the 188

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trocar removed and gas (mainly) and liquid stool was aspirated. The instrument was removed and the purse string tied. There was no fecal spillage.

This was followed by segmental excision of the tumour with adequate proximal and distal clearance. Bowel continuity was restored via side to end colorectal anastomosis with the aid of a 29mm ILS (intra luminal stapler) device.

A 15 Fr vacuum drain was placed in the pelvis and exited the left iliac fossa. En mass closure of the laparotomy incision (1 prolene suture) was performed and the skin closed with a 3/0 prolene suture in subcuticular fashion.

Her post-operative course was uneventful. Passage of flatus and stool resumed on postoperative day 5 and the patient was discharged on postoperative day 8.

The histopathology report was available 4 weeks later and indicated an adenocarcinoma which infiltrated the pericolic fascia and 4 of 12 lymph nodes were metastatic (pT3N2M0).

The patient successfully completed her adjuvant chemotherapy. Serial carcinoembryonic antigen levels were < 5 ng/ml. Follow up CT scan showed no evidence of metastatic disease and completion colonoscopy demonstrated normal mucosa from anus to cecum. At two years follow up the patient has had no worrying symptoms and continues annual review in the outpatient clinic.

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Fig 1: Abdominal X-ray illustrating features of leftsided large bowel obstruction.

Fig 2: Obstructing tumour in the distal sigmoid colon.

Fig 3: A Savageâ&#x20AC;&#x2122;s decompressor in use.

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DISCUSSION Colorectal cancer is common in developed countries and about 15%â&#x20AC;&#x201C;20% of patients present with an intestinal obstruction needing emergency surgery.(1) Obstructing tumors are generally more advanced, with a higher incidence of local extension and distant metastasis than non obstructing neoplasms. Furthermore, emergency surgery on a distended and unprepared bowel in high risk patients results in high morbidity and mortality rates.(2)

Until recently, the obstructing left-sided colonic lesions were traditionally managed by either three-stage surgery, consisting of diverting colostomy, colonic resection, and colostomy closure,(3) or two-stage surgery, consisting of resection with proximal colostomy or Hartmannâ&#x20AC;&#x2122;s procedure (HP) followed by later reconstruction.(4)

Several benefits might be associated with creation of a loop colostomy: it provides colonic decompression, minimizes surgical trauma, reduces the risk of contamination from unprepared bowel, allow staging and multidisciplinary evaluation prior to definitive treatment. There is only one RCT study, by Kronborg et al in 1995, comparing emergency colostomy with three stages procedure (58 patients) versus HP (63 patients) for OLCC. The authors showed no difference in terms of mortality (8/58 vs. 8/63 patients) and morbidity rate, recurrence rate and cancer specific survival. The overall length of hospital stay was shorter in the resection group.(5) In addition a Cochrane systematic review in 2008 by De Salvo et al, compared staged procedure vs. primary resection, and found similar mortality with either strategy.(6) The HP superseded the staged procedures which are no longer used, mainly due to prolonged hospitalisation and the need for multiple operations.

Surgical treatment of acute left-sided colonic obstruction is a major procedure.

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The proximal colon is distended and filled with liquid feces, and its wall is often of dubious viability with signs of impending ceacal perforation. Bowel contents are easily spilled through tears that are caused by distension or produced during mobilization. Primary anastomosis in left colonic obstruction bears the increased risk of breakdown because the unprepared colon is filled with large amounts of liquid fecal residue. Primary resection with immediate anastomosis has therefore been associated with a high anastomotic leak rate and mortality.(7,8)

Consequently, the absence of anastomosis makes HP a technically easier operation and obviously eliminates the risk of colon dehiscence in an already complex scenario such as occurs in high grade obstruction: thus HP still remains an option also suitable by less experienced and non specialist surgeons. The main disadvantage of HP is clearly the need for a second major operation to reverse the colostomy, which will be also associated with a risk of anastomotic dehiscence. Furthermore, it is somewhat disappointing to observe that the stoma reversal rate is only 20% in those patients with colon cancer.(9,10)

Hartmannâ&#x20AC;&#x2122;s procedure is generally regarded as the safest option in these scenarios. In 2004 Meyer et al by a prospective non randomized multicenter study compared, in emergency scenario, 213patients undergoing HP to 340 patients undergoing primary resection and anastomosis (PRA) for OLCC. The mortality rate in the case of palliation for HP and PRA respectively was 33% vs. 39% and in case of curative intent for HP and PRA respectively 7.5% vs. 9.2%, however both of them without statistical difference; also the morbidity rate was not significantly different among groups. The HP was the most frequent surgical option.(11) Finally among prospective non randomized and retrospective studies the rates of anastomotic leak in patients with OLCC treated with PRA range from 2.2% to 12%(3,9,12,13), which are similar to those reported for elective surgery ranging from 1.9% to 8% .(14,15,16) 192

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The safety of a primary colonic anastomosis can be increased by removing the feces during the surgical procedure. Primary resection and anastomosis has an advantage since it is a definite procedure that does not require further surgery.

The main disadvantages are that it requires a more experienced surgeon and there is a risk of anastomotic leakage from an unprepared bowel in an already very ill patient. There are no randomised controlled trials comparing HP and PRA. Various non-randomised studies have not shown HP to have any benefit in mortality.(3,9,11,12) Indeed, most studies have shown HP to be associated with a poorer prognosis which is most likely related to selection bias as anastomosis is avoided in high risk patients.(9,13) Although primary resection and anastomosis is generally preferred in selected patients, there is some debate as to the type of resection. One option is to do a total or subtotal colectomy.(17) This procedure avoids the problem of an unprepared bowel and also protects against any future malignancy of the right colon.

This is a more extensive operation with many patients complaining of diarrhea afterwards.(17,18) In the 1980s, segmental colectomy with intra-operative colonic irrigation (ICI) was suggested as an alternative operation.(18) It has the benefit of making an anastomosis on a prepared bowel and preserving the normal colon.

The main concerns are the prolonged operative time, the risk of spillage and contamination, and the need for increased expertise. There is only one RCT from the SCOTIA group that compared the two techniques. It concluded that segmental resection following ICI is the preferred treatment, due to fewer problems with bowel function. However, it did not show any difference in mortality or morbidity.(18) Another non-randomised study comparing the two techniques did not show any difference in mortality but showed significantly more surgical postoperative complications in the ICI group and in particular wound infections.(19) The main problem with ICI is that it was time consuming, having to allow up to an extra hour, although this is known to improve with experience.

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Absolute indications for subtotal colectomy in OLCC are right colon ischemia, cecal serosa tears or perforation, and synchronous proximal malignant tumours which occur in 3 to 10% of cases.(20) Total colectomy for OLCC (without cecal perforation or evidence of synchronous right colonic cancers) should no longer be preferred to segmental resection with ICI, since the two procedures are associated with same mortality/ morbidity, while total colectomy is associated with higher rates of impaired bowel function.

In a recent study with decision analysis indicated that unless surveillance results improve, subtotal colectomy still seems the preferred treatment for primary colorectal carcinoma in hereditary nonpolyposis colorectal cancer in view of the difference in life expectancy.(21) In the recent literature, there is no argument for the use of subtotal colectomy to avoid metachronous carcinomas, outside hereditary tumor syndromes.

On average, the ICI increases duration of surgery by an hour, although this time can improve with increasing experience. To overcome the problems of ICI, various studies suggested segmental resection and primary anastomosis with manual decompression only, as a safe alternative.(22,23,24) This idea was supported by various RCTs comparing mechanical bowel preparation, with no preparation in elective open colonic surgery. The results were separately examined in a Cochrane systematic review of 9 RCTs and in a meta-analysis of 7 RCTs .(25,26) Both studies concluded that there is no convincing evidence that mechanical bowel preparation is associated with reduced rates of anastomotic leakage after elective colorectal surgery.

Lim et al in 2005 published the only RCT comparing ICI (24 patients) with manual decompression (25 patients) in OLCC. They concluded that manual decompression is a shorter and simpler procedure than ICI, and offers similar results in terms of mortality, morbidity or anastomotic leak rates, but the study 194

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was underpowered.(27) In order to identify the more appropriate method reducing the fecal load, Kam et al published a systematic review on ICI vs. manual decompression in left-sided colorectal emergencies. They included 1 RCT, 1 prospective comparative trial and 5 prospective descriptive case series and concluded that, although the power of studies is poor and large-scale prospective randomized trial is desirable, no statistical significance could be shown between the two procedures.(28) At present either procedure could be performed, depending of the experience/preference of the surgeon.

A one-stage resection and anastomosis is a most welcomed option in OLCC. This may not be the case for all patients though and other parameters should be examined before choosing the operation.(9,12,13)The Association of Coloproctology of Great Britain and Ireland (ACPGBI) study of large bowel obstruction caused by colorectal cancer identified four important predictors of outcome – age, ASA grade, operative urgency, and Dukes stage.(12) Similar results have been echoed by other studies.(9,13) It would be considered appropriate to choose a simpler and safer procedure such as Hartmann’s operation or even a diverting colostomy for patients deemed to be at high risk. This consensus is reflected in a questionnaire survey of American gastrointestinal surgeons in 2001 who responded that 67% would perform Hartmann’s operation and 26% a simple colostomy in the high-risk patient.(29)

The experience and subspecialty of surgeon seems to be a primary factor in the choice of anastomosis or end colostomy. It has been shown that primary anastomosis is more likely to be performed by colorectal consultants than general surgeons, and consultants generally than unsupervised trainees.(30) The ACPGBI study has shown that the mortality rate following surgery was similar between ACPGBI and non-ACPGBI members.(12) This result can be challenged as the study was done on a voluntary basis. The Large Bowel Cancer Project showed 195

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that registrars had a higher mortality rate than consultants after primary resection for obstruction in the late 1970s, and this result has remained unchanged 20 years later in the Zorcolo study.(31,30) Other studies have also shown that unsupervised trainees had significantly greater morbidity, mortality and anastomotic dehiscence rates.(32,33)

CONCLUSION The surgical management of acute left-sided colonic obstruction still remains a challenge despite significant progress. The surgical options available to manage these patients are still regarded as controversial. This is largely because the literature power is relatively poor and the existing RCT are often not sufficiently robust in design. At present though, the evidence is sufficient to suggest that the majority of patients can be treated safely with one-stage resection and anastomosis. For the management of malignant left sided colonic obstruction, single-stage surgical techniques achieve good short- and long-term results, with similar or better morbidity and mortality rates and less sequelae than the more conservative two- or three-stage strategies, since most of the stomas will be permanent.

Segmental colectomy with anastomosis after intra-operative colonic irrigation or manual decompression is an effective and efficient practice, combining safety, low morbidity and mortality, and less consumption of resources. Subtotal colectomy, although associated with poor functional outcomes is still very useful in case of synchronous tumours or proximal bowel damage. Hartmannâ&#x20AC;&#x2122;s procedure should be reserved for high-risk patients. Simple colostomy has no role other than for palliation or use in very ill patients who would not survive any other procedure.

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REFERENCES 1.Lee YM, Law WL, Chu KW, et al. Emergency surgery for obstructing colorectal cancers: a comparison between right-sided and left-sided lesions. J Am Coll Surg 2001;192:719–25.

2. Runkel NS, Hinz U, Lehnert T, et al. Improved outcome after emergency surgery for cancer of the large intestine.Br J Surg 1998;85:1260–5.

3. Villar JM, Martinez AP, Villegas MT, et al. Surgical options for malignant left-sided colonic obstruction. Surg Today 2005, 35:275-281.

4. Chua CL. Surgical considerations in the Hartmann’s procedure. Aust N Z J Surg 1996;66:676– 9.

5. Kronborg O: Acute obstruction from tumour in the left colon without spread. A randomised trial of emergency colostomy versus resection. Int J Colorectal Dis 1995, 10:1-5.

6. De Salvo GL, Gava C, Lise M, et al. Curative surgery for obstruction from primary left colorectal carcinoma: Primary or staged resection? Cochrane Database Syst Rev 2004, 2:CD002101.

7. Carson SN, Poticha SM, Shields TW. Carcinoma obstructing the left side of the colon. Arch Surg 1977; 122: 23–526.

8. Phillips RKS, Hittinger R, Fry JS, et al. Malignant large bowel obstruction. Br J Surg 1985; 72 :296–302.

9. Zorcolo L, Covotta L, Carlomagno N, et al. Safety of primary anastomosis in emergency colo-rectal surgery. Colorectal Dis 2003, 5:262-269.

10. Desai DC, Brennan EJ, Reilly JF, et al. The utility of the Hartmann procedure. Am J Surg 1998, 175:152-154.

11. Meyer F, Marusch F, Coch A, et al. The German Study Group ‘Colorectal Carcinoma (Primary Tumor)’: Emergency operation in carcinomas of the left colon: value of Hartmann’s procedure. Tech Coloproctol 2004, 8(Suppl 1):S226-S229.

12. Tekkis PP, Kinsman R, Thompson MR, et al. The Association of Coloproctology of Great Britain and Ireland study of large bowel obstruction caused by colorectal cancer. Ann Surg 2004, 204:76-81.

13.Biondo S, Pares D, Frago R, et al. Large bowel obstruction: predictive factors for postoperative mortality. Dis Colon Rectum 2004, 47:1889-1897.

14. Zmora O, Mahajna A, Bar-Zakai B, et al. Is mechanical bowel preparation mandatory for left-sided colonic anastomosis? Results of a prospective randomize trial. Tech Coloproctol 2006, 10:131-135.

15. Kim J, Mittal R, Konyalian V, et al. Outcome analysis of patients undergoing colorectal resection for emergent and elective indications. Am Surg 2007, 73:991-993.

16. Bellows CF, Webber LS, Albo D, et al. Early predictors of anastomotic leaks after colectomy. Tech Coloproctol 2009, 13:41-47.

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A CASEBOOK OF TWENTY SURGICAL CASES 17. Deen KI, Madoff RD, Goldberg SM, et al. Surgical management of left colon obstruction: the University of Minnesota experience. J Am Coll Surg 1998; 187: 573–6.

18. The SCOTIA Study Group. Single-stage treatment for malignant left-sided colonic obstruction: a prospective randomized clinical trial comparing subtotalcolectomy with segmental resection following intraoperative irrigation. Br J Surg 1995; 82: 1622–7.

19. Torralba JA, Robles R, Parrilla P, et al. Subtotal colectomy vs. intraoperative colonic irrigation in the management of obstructed left colon carcinoma. Dis Colon Rectum 1998; 41: 18–22.

20. Hennekinne-Mucci S, Tuech JJ, Brehant O, et al: Emergency subtotal/total colectomy in the management of obstructed left colon carcinoma. Int J Colorectal Dis 2006, 21:538-541.

21. De vos tot Nederveen Cappel WH, Buskens E, Van Duijvendijk P, et al. Decision analysis in the surgical treatment of colorectal cancer due to a mismatch repair gene defect. Gut 2003; 52:1752–175.

22. Naraynsigh V, Rampaul R, Maharaj D, et al. Prospective study of primary anastomosis without colonic lavage for patients with an obstructed left colon. Br J Surg 1999, 86:1341-1344.

23. Turan M, Ok E, Sen M, et al. A simplified operative technique for single-staged resection of left sided colon obstructions: report of a 9-year experience. Surg Today 2002, 32:959-964 24. Patriti A, Contine A, Carbone E, et al. One-stage resection without colonic lavage in emergency surgery of the left colon. Colorectal Dis 2005, 7:332-338.

25. Guenaga K, Atallah AN, Castro AA, et al. Mechanical bowel preparation for elective colorectal surgery. Cochrane Database Syst Rev 2009, 1:CD001944.

26. Slim K, Vicaut E, Panis Y, et al. Meta-analysis of randomized clinical trials of colorectal surgery with or without mechanical bowel preparation. Br J Surg 2004, 91:1125-1130.

27. Lim JF, Tang CL, Seow-Choen F, et al. Prospective, randomized trial comparing intraoperative colonic irrigation with manual decompression only for obstructed left-sided colorectal cancer. Dis Colon Rectum 2005, 48:205-209.

28. Kam MH, Tang CL, Chan E, et al. Systematic review of intraoperative colonic irrigation vs. manual decompression in obstructed left-sided colorectal emergencies. Int J Colorectal Dis 2009, 24:1031-1037.

29. Goyal A, Schein M. Current practices in left-sided colonic emergencies. A survey of US gastrointestinal surgeons. Dig Surg 2001; 18: 399–402.

30. Zorcolo L, Covotta L, Carlomagno N, et al. Toward lowering morbidity, mortality and stoma formation in emergency colorectal surgery: the role of specialization. Dis Colon Rectum 2003; 46: 1461–8.

31. Phillips RK, Hittinger R, Fry JS, et al. Malignant large bowel obstruction. Br J Surg 1985; 72: 296–302.

32. Fielding LP, Stewart-Brown S, Blesovsky L. Large bowel obstruction caused by cancer: a prospective study. BMJ 1979; 2: 517–9.

33. Darby CR, Berry AR, Mortensen N. Management variability in surgery for colorectal emergencies. Br J Surg 1992; 79: 206–10.

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11. ACUTE APPENDICITIS Whatâ&#x20AC;&#x2122;s the role of laparoscopic appendicectomy?

INTRODUCTION Although more than a century has elapsed since McBurney first performed open appendicectomy this procedure remains the treatment of choice for acute appendicitis for most surgeons. In 1983 Semm performed the first laparoscopic appendicectomy. Ever since this, the efficiency and superiority of the laparoscopic approach compared to the open technique has been the subject of much debate. The idea of minimal surgical trauma resulting in significantly shorter hospital stay less post operative pain, faster return to daily activities, and better cosmetic outcomes, has made laparoscopic surgery for acute appendicitis very attractive. Concomitant with the use of laparoscopy for several other abdominal operations, there have been numerous reports of the use of laparoscopy for acute appendicitis. Despite this, the role of laparoscopic appendectomy for acute appendicitis remains contentious.

The following are two cases which were managed, one with open appendicectomy and the other laparoscopic, the outcomes of which were comparable. A discussion regarding the current views on the role of laparoscopic appendicectomy follows.

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CASE 1 History: A 28 year old woman presented with a 3 day history of right lower abdominal pain. This was initially intermittent for the first few hours but then became constant and progressively got worse. On the day of presentation she had vomited twice (bilious) and reported the pain being worse on walking. The patient was now anorexic and had no other gastro-intestinal symptoms. This patient had no urinary symptoms and her last normal menstrual period was 10 days previously. Systematic enquiry was otherwise non-contributory and she had no past medical or surgical history. This mother of 2 was also a school teacher.

Physical Examination: Ill looking woman with BP 120/80 mmHg, P 90 per min, RR 20 per min., Afebrile to touch (T 37oC), with mucus membranes pink and moist.

Significant findings were confined to the abdomen which revealed Right lower quadrant tenderness with marked guarding and local peritonism. Digital rectal and per vaginal examination was normal.

Investigations: Hb 11.8 mg/dl, WCC 14 x 103, Plts 283, Renal function and Amylase levels were normal. Urine pregnancy was negative.

Chest and Abdominal X rays were normal.

A clinical diagnosis of acute appendicitis was made. Resuscitative measures were instituted and informed consent was taken with a view to an open appendicectomy.

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Surgical Intervention: Under general anaesthetic an open appendicectomy was done via a Lanz incision. The para-cecal appendix was inflamed but not perforated.

Post-operatively: Antibiotics were continued to allow 2 further doses (Zinacef 750mg, Metronidazole 500mg) and the patient was allowed to ambulate as tolerated. Oral fluids were commenced later that day and she was discharged the following morning (Day 2). As per normal unit policy outpatient review was planned for 8 days time for removal of sutures and then 8 weeks later for review with histology.

There were no post operative complications and this patient returned to work on postoperative day 10.

CASE 2 History: A 24 year old woman presented with a 2 day history of right iliac fossa pain. This pain was initially peri-umbilical and migrated by the next morning. It was constant and got worse. There were no other related symptoms. This patient was a house wife who was nulliparous. Her last normal menstrual period was 2 weeks previously.

Physical examination: A young woman in no obvious distress. Vital signs were normal. The significant clinical finding was tenderness and guarding over McBurneyâ&#x20AC;&#x2122;s point on the abdomen.

Investigations: Hb 13 mg/dl, WCC 13.5 x 103, Plts 296, Renal function and Amylase levels were normal.

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Urine dipstick was negative for blood or white cells. Urine pregnancy test was negative.

Chest and Abdominal X rays were normal. An ultrasound scan of the abdomen was done which failed to visualise the appendix but there was no evidence of free fluid or pelvic pathology.

A diagnosis of acute appendicitis was made and the patient consented for a laparoscopic appendicectomy.

Surgical Intervention: A 3 port technique was used (subumbilical, suprapubic, left iliac fossa). The inflamed appendix over the pelvic brim was mobilized and the mesoappendix divided with the aid of harmonic scalpel. The base of the appendix was stapled using the Endo GIA (Ethicon) with blue cartridge and the appendix removed in a bag. The sub umbilical port was closed at the level of the linea alba with 1 prolene.

Post-operatively: The patient was allowed to ambulate once fully awake and also to commence oral fluids.Antibiotic was continued for 2 further doses (Zinacef 750mgs, Metronidazole 500mg). The patient was discharged the following morning and outpatient review planned for removal of sutures on postoperative day 10 and subsequent review in 8 weeks to review histology.

There were no post-operative complications.

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DISCUSSION Acute appendicitis is the commonest emergency abdominal problem requiring surgery. The first reports of appendicitis occurred in the early 1700s and Claudius Amyand performed the first known appendicectomy in 1735. He identified the appendix perforated by a pin within the scrotom.(1) Despite several reports regarding appendicitis and the need for appendicectomy, it was not until 1889 McBurney described a specific operation for acute appendicitis. A muscle splitting incision that bears his name and is commonly used today.(2) Since the days of McBurney who devised muscle splitting incision for appendicectomy, other incisions have been described (Rocky Davies, Rutherford Morrison, Battles, Lanz) but few have caught on.(3) The Lanz incision (transverse, curvilinear) incision 2cm superomedial to the anterior superior iliac spine is the other commonly used incision for open appendicectomy (OA) today. The cosmetic result of the scar makes it more appealing to surgeons and patients which is why it was used on case 1.

The strong desire by patients to avoid an abdominal scar (especially young women) and the wave of minimally invasive/laparoscopic surgery in the last decade together fuels the choice for laparoscopic appendicectomy (LA). There are medical factors that may also lend support to the laparoscopic approach.

Acute appendicitis while common can be a challenging surgical emergency, which if diagnosis is delayed may result in perforation and peritonitis, concomitant with a high mortality and morbidity.(4) Making the decision for appendicectomy based only on patients signs and symptoms result in removing normal appendices (negative appendicectomy) in 15-30% of cases.(5) Employing a laparoscopic approach may help to reduce this rate and avoid unnecessary appendicectomy.

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Fig 1: Open appendicectomy scar

Fig 2: Laparoscopic appendicectomy scars

The typical presentation of acute appendicitis is that of a young teenager â&#x20AC;&#x201C; young adult with right lower abdominal pain, tenderness and migration of the pain from the periumbilical area to the right iliac fossa which worsens over twelve to twenty-four hours. However, up to 25% of all patients with acute appendicitis present with atypical signs and symptoms. In these cases, the presence of common signs and symptoms and their progression are variable. The obvious risk is delay in diagnosis resulting in perforation and the necessity for operation in the face of a toxic patient with an acute abdomen.There are three situations that 204

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are associated with most atypical presentations (6,7) :

□ Extremes of age □ Variable appendiceal position within the abdomen □ Associated conditions: pregnancy, crohn’s disease, prior administration of antibiotics, steroids or other immunocompromised states, patients recovering from previous surgery

A laparoscopic approach in this setting of course helps with the diagnosis, may facilitate the procedure via a minimally invasive approach or help plan an appropriate incision.

Laparoscopic appendicectomy was first reported by Kurt Semm, a German gynecologist in 1983 but it was not until the early 1990s that this approach gained acceptance.(8). Over the last fifteen years, there has been a definite increase in the implementation of this procedure in the literature but there still exists contention regarding any added benefits or advantage.

In the case described, a 3-port technique was employed: 10mm port at the umbilicus (camera), 5mm port medial to the left anterior superior iliac spine, 12mm port in the suprapubic midline position. The patient was catheterized following the anesthetic. The inflamed appendix was mobilized into view and the mesoappendix with appendicular artery was divided with the aid of the harmonic scalpel. The appendicectomy was facilitated with an Endo GIA 45mm stapler (blue cartridge) via the suprapubic port and subsequently removed within an endobag to minimize contamination to the port site. After inspection to ensure no bleeding, the ports were removed under direct vision and the pneumoperitoneum desufflated. The umbilical port was closed with 1 prolene suture to the linear alba and 3/0 prolene to the skin wounds.

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Several publications in support of the laparoscopic approach to appendicectomy exist in the literature. The recurrent theme though is that of increased cost. Sporn et al identified an increased use of LA from 32.2% to 58% between 2000 â&#x20AC;&#x201C; 2005. They identified the cost associated with LA to be 22% and 9% higher for uncomplicated and complicated appendicitis when compared to OA.(9)

More recently Masoomi et al reported similarly an exorbitant cost to

manage acute appendicitis via the LA in the US with minimal clinical benefit.(10) Despite these findings, there is a point of view that the actual cost may improve with improvement in laparoscopic equipment and surgical expertise. Moore and coworkers have demonstrated an economic benefit of LA from a social perspective since shorter hospital stay and earlier return to daily activities is very important especially for patients who are young and lead a productive life. . Case 1 (open appendicectomy) was quite independent early after discharge

(11)

and actually returned to work after removal of sutures on day 10. Case 2 (laparoscopic) was also quite independent and resumed house chores within a week.

LA has also been noted to take longer. It was thought initially that this might be due to inexperience associated with a new procedure. However two recent meta-analysis have shown this to be a consistent finding.(12,13)

LA have repeatedly been associated with a higher rate of intra-abdominal abscess. Numerous articles have highlighted this occurrence and indeed it was a finding of the Cochrane Review 2010, where among 46 studies that contributed to this data intra-abdominal abscess were increased nearly three-fold after LA.(14) It was thought that this occurrence is related to cases of complicated (perforated) appendicitis. While no randomized controlled trials to demonstrate this exist, Tiwari et al found LA to be comparable or superior to OA for both complicated and uncomplicated disease.(15)

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The highest percentage of misdiagnosis in patients who appear to have appendicitis occurs in women of child bearing age. Gynecologic problems are frequently mistaken for appendicitis and the negative appendicectomy rate in young women ranges from 14%-40%.(16) As such, young women belong to a group of patients where laparoscopic appendicectomy may be preferred. Agresta and colleagues reviewed their findings at laparoscopy in patients with histologically proven appendicitis and normal appendices. Other diagnoses included adhesions, graafian follicle cysts, endometriosis, bleeding luteal cysts, ectopic pregnancy, perforated diverticulitis, perforated duodenal ulcer, ileitis and omental necrosis.(17) Thus the laparoscopic approach may be more beneficial to this group of patients (young females). The cosmetic element may be most desired by the younger female but for the two cases described, there was no cosmetic mismatch. The clinically relevant outcomes though would be to arrive at a diagnosis and treat appropriately and decrease recurrent admissions for missed diagnoses.

This argument lends support to the role of diagnostic laparoscopy in the investigation of abdominal pain and not necessarily to laparoscopic appendectomy.

It however leads to another controversial issue in the management of suspected acute appendicitis. For OA the external scar represents a life long expectation that the appendix has been removed and so if a normal appendix is encountered at OA, it should be removed. There is variability in this practice when it comes to laparoscopy though. Agresta et al adopted a position of always removing the appendix when it appears macroscopically normal. In their experience with laparoscopic appendectomy 24.6% of patients with grossly normal appendix demonstrated inflammation within the appendix wall on histological examination.(17)

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The benefits of removing a normal looking appendix include, early diagnosis of neoplastic lesions, diagnosis and cure of neurogenic appendix prevention of appendicitis in later life and most importantly, to decrease diagnostic confusion in further episodes of abdominal pain. A German group employed a strategy of always removing a normal looking appendix at laparoscopy for suspected acute appendicitis and over seven years this conferred no additional morbidity.(18) Van Dalen et al demonstrated no long term sequelae in patients (young women) whose appendix were found to be normal and were not removed at laparoscopy for suspected acute appendicitis.(19) Over time surgeons will have to make individual decisions about this practice but by removing the grossly normal appendix it prolongs the procedure, increases cost, and contributes to the negative appendicectomy rate. It also begs the obvious question of whether to remove organs with potential for future clinical presentations of right sided abdominal pain, for example, the gall bladder, the right colon, right fallopian tube and ovary.

CONCLUSION In conclusion, the collective results of appendicectomy indicate that regardless of the surgical approach (OA vs LA) it is associated with negligible mortality, an overall complication rate of less than 10% and wound infection rate of less than 2% with an average hospital length of stay of 2-3 days. In patients where there is doubt regarding the diagnosis particularly in women of child bearing age the laparoscopic approach may be better suited. Although LA is associated with an increased cost, in the analysis of data some researchers include patients who had diagnostic laparoscopy as investigation of pelvic pain and the appendix was removed at this procedure. This is a moot point, but may contribute to the overall cost of appendicectomy. If these cases are excluded the actual cost of treating acute by LA may be more comparable. On a broader scale though, once 208

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the expertise and equipment is available the laparoscopic approach should be incorporated in training of residents as a bridge to more advanced laparoscopic procedures.

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References 1. Shepherd JA. Acute appendicitis: a historical survey. Lancet 1954;2:299-302.

2. McBurney C. The incision made in the abdominal wall in cases of appendicitis,with a description of a new method of operation. Ann Surg 1894; 20:38-43.

3.Rintoul RF. Operation on the appendix. In: Farquharson’s(editor),Text Book of Operative Surery. 8th Edition ChurchillLivingstone (London)1995; pp 452-54.

4.Binnebösel M, Otto J, Stumpf M, et al. Acute appendicitis. Modern diagnostics–surgical ultrasound. Chirurg. 2009;80(7):579–587.

5. Nasiri S, Mohebbi F, Sodagari N, et al. Diagnostic value of ultrasound and the Modified Alvarado scoring system in acute appendicitis. Int J Emerg Med 2012; 5: 26.

6. Schwartz S and Ellis H. Appendix. In: Schwartz S and Ellis H, editors. Norwalk,Connecticut: Maingot’s Abdominal Operations. 9th ed. Norwalk, CT: Appleton &Lange; 1990, pp 953-77.

7. Sinanan M. Acute Abdomen and Appendix. In: Greenfield LJ, Mulholland MW,Oldham KT, Zelenock GB, editors. Surgery: Scientific Principles and Practice.Philadelphia: JB Lippincott; 1993, pp 1120-42.

8. Semm K. Endoscopic appendectomy. Endoscopy 1983;15: 59-64.

9. Sporn E, Petroski GF, Mancini GJ, et al. Laparoscopic appendectomy--is it worth the cost?

Trend analysis in the US from 2000 to 2005. J Am Coll Surg, 2009; 208(2): 179-85.e2.

10. Masoomi H, Mills S, Dolich MO, et al. Comparison of outcomes of laparoscopic ve rsus open appendectomy in children: data from the Nationwide Inpatient Sample (NIS), 20062008. World J Surg, 2012 Mar; 36(3):573-8.

11. Moore DE, Speroff T, Grogan E, et al. Cost perspectives of laparoscopic and open appendectomy. Surg Endosc 2005; 19: 374-378 12. Wei B, Qi CL, Chen TF, et al. Laparoscopic versus open appendectomy for acute appendicitis: a meta-analysis. Surg Endosc 2011; 25: 1199-208.

13. Liu Z, Zhang P, Ma Y, et al. Laparoscopy or not: a meta-analysis of the surgical effects of laparoscopic versus open appendicectomy. Surg Laparosc Endosc Percutan Tech 2010; 20: 36270.

14.Sauerland S, Jaschinki T, Neugebauer EA. Laparoscopic versus open surgery for suspected appendicitis. Cochrane Database Syst Rev. 2010 ; 6: (10) CD001546.

15. Tiwari MM, Reynoso JF, Tsang AW, et al. Comparison of outcomes of laparoscopic and open appendectomy in management of uncomplicated and complicated appendicitis. Ann Surg, 2011 ; 254(6): 927-32.

16. Prystowsky JB, Pugh CM, Nagle AP. Appendicitis. Curr Probl Surg 2005; 42: 694-742.

17. Agresta F, De Simone P, Michelet I,Bedin N. Laparoscopic Appendectomy: Why It Should Be Done? JSLS (2003)7:347-352 18. Garlipp B, Arlt G. Laparoscopy for suspected appendicitis: should an appendix that appears

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19. van Dalen R, Bagshaw PF, Dobbs BR, et al. The utility of laparoscopy in the diagnosis of acute appendicitis in women of reproductive age. Surg Endosc. 2003;17(8):1311-3

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12. OBTURATOR HERNIA Surgical anatomy and methods of repair.

INTRODUCTION Obturator hernia is a rare pelvic hernia with relatively high morbidity and mortality. Though certain characteristics define at-risk patients, symptoms of obturator hernia can be vague making pre-operative diagnosis challenging. Obturator hernia is an uncommon but important cause of intestinal obstruction.

The prevalence of these hernias is probably higher than previously thought. The widespread use of CT and increasing use of laparoscopy are diagnosing these hernias more frequently. Obturator hernia complicated by intestinal obstruction and bowel strangulation is associated with a high mortality (13-40%). Itâ&#x20AC;&#x2122;s general rarity and unique anatomical relations present a challenge to both diagnose and repair. Surgeons and emergency care physicians should therefore be aware of and include this in the differential diagnosis of intestinal obstruction.

A typical case of an obstructed obturator hernia is described followed by a discussion on diagnosis, the surgical anatomy and surgical approaches.

CASE History: A 67 year old woman presented with a two day history of worsening colicky abdominal pains associated with vomiting (multiple episodes), abdominal distention and inability to pass flatus or stool. She added that 5 days previously she felt similar pains and vomited twice, but this subsequently resolved.

On review of systems she reported no constitutional symptoms. Her bowel action occurred daily and the consistency and frequency was maintained 212

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until the onset of her symptoms. Her appetite was also maintained and although she appeared quite slim, this had been her body habitus for years.

In her previous medical history this patient was hypertensive for which she used preterax. In her past surgical history an open cholecystectomy was done 25 years previously for symptomatic gallstones. Of note she had bilateral inguinal hernia repairs done 5 years previously in the US.

Physical Examination: A elderly looking, slim woman with parched lips. Her vital signs were: P 102 min-1, BP 148/ 98 mmHg, RR 22 min-1, T 37oC. Her skin turgor was decreased.

Cardiorespiratory

examination

was

otherwise

normal.

The previously placed nasogastric tube drained green fluid. A Kocher’s incision was noted in the right upper quadrant of the abdomen. Her groin scars were not that obvious and there were no inguino-femoral swellings. Her abdomen was distended (but now smaller according to her). There was no tenderness or guarding. The bowel sounds were hyperactive. There were no palpable groin masses or cough impulses. Digital rectal examination revealed normal sphincter tone and no mucosal abnormalities. There were no palpable masses. A urinary catheter was in place and contained 300 mls of concentrated looking urine.

Investigations: Hb 11.1 g/dl, WCC 14 x 103 /µl , Plts 322 x 103 /µl, Na 134 mmol-1, K 3.1mmol-1, BUN 44 mg/dl, Cr 1.3 mg/dl.

CXR: normal AXR: Multiple loops of dilated small bowel were present. The air filled loops seem to lead into the pelvis.

CT (abdomen and pelvis): The obstruction was due to a right obturator hernia.

A femoral hernia was also noted but was not complicated.

It was noted retrospectively that the patient was having knee pains. The How213

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ship-Romberg test was positive.

The patient was resuscitated with crystalloids and her potassium corrected. Informed consent was obtained and the patient taken for laparotomy and repair of the obturator hernia.

Surgical treatment: A midline lower abdominal laparotomy was done. The findings at laparotomy were: 1.A plug mesh at the deep ring of the left inguinal canal.

2.Two plug meshes were noted on the right: one at the deep ring and the other more medially covering a previous direct hernia.

3.The right femoral hernia defect was noted and found to be empty; there was no left femoral hernia 4. A loop of ileum was caught in the obturator hernia.

The obturator canal was widened by incising the inferior aspect to release the trapped bowel. The peritoneum was dissected sufficiently to safeguard any anomalous vessels and to clearly see the necks of both the femoral and obturator hernias.

The femoral hernia was repaired by placing 3 interupted 2/0 prolene sutures opposing the inguinal ligament to the pectineal ligament.The obturator hernia was repaired by creating a plug with prolene mesh. This was placed within the neck and fixed at 3 points with 2/0 prolene suture.

The overlying peritoneum was repaired. The loop of bowel had recovered and no resection was necessary. Her recovery was uneventful. The patient was discharged 5 days later and was seen 6 weeks later in the outpatient clinic. She had no complaints and was discharged.

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DISCUSSION Arnaud de Ronsil in 1724 first described the obturator hernia and Henry Obre first successfully repaired it in 1851.

(1)

Obturator hernia occurs through the

obturator canal, which is 2-3 cm long and 1 cm wide, and contains the obturator nerve and vessels. Obturator hernia is nine times more common in females due to their wider pelvis, more triangular obturator canal opening and greater transverse diameter. The incidence rates of obturator hernia vary widely throughout different regions but generally accounts for 0.07% - 1.0% of all hernias and 0.2 – 1.6% of all cases of mechanical obstruction of the small bowel. Although a rare form of abdominal hernia, its mortality rate is highest among all abdominal wall hernias (range 13-40%).(2)

With the nickname, “little old lady’s hernia”, it usually occurs in multiparous and elderly emaciated women due to a wider pelvis and enlarged obturator canal. The loss of protective preperitoneal fat and lymphatic tissue (corpus adiposum) around the obturator vessels and nerves facilitates the formation of hernia.

The clinical presentation may be vague with symptoms of bowel obstruction (dull, crampy abdominal pain, nausea and vomiting) and these symptoms are present in >80% of patients. Although the cardinal clinical symptoms are those of intestinal obstruction it is usually partial due to a high frequency of Richter’s herniation (41% - 100%) of small bowel into the obturator canal. Obstruction can be acute or intermittent, which is an important clue to the diagnosis.

The clinical signs are those of small bowel obstruction. An external hernia is uncommon. Most other signs are due to compression of the obturator nerve by the hernia sac. The Howship-Romberg sign is characterized by pain in the medial thigh and less often the hip when the ipsilateral hip is abducted, extended and internally rotated and relieved by flexion. This sign is present in 15-50% of cases and based on it, a correct preoperative diagnosis can be made in only 20215

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38% of cases.(3) It is often overlooked or misinterpreted due to associated disorders of the hip like osteoarthritis. The Hannington-Kiff sign is a clinical sign in Fig 1: Abdominal X ray : multiple dilated loops of small bowel ending in the right pelvis

Fig 2: CT image: a femoral hernia is noted medial to the femoral vein. An obstructed obturator hernia is also noted between the obturator externus and pectineus muscles on the right

Fig 3: Artery forceps within the recess of the femoral hernia (Note the trapped loop within the obturator hernia )

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Fig 4: The prolene plug

Fig 5: The previous mesh plugs, femoral hernia repair and prolene plug repair of obturator hernia

Fig 6: The peritoneum repaired concealing the repair. Note the 2 previous mesh plugs

Fig 7: The previously trapped segment of ileum

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which there is an absent adductor reflex in the thigh in the presence of a positive patellar reflex. It is elicited by tapping over either the medial epicondyle of the femur or the medial condyle of the tibia, which should cause the adductor muscles of the hip to contract, moving the leg inwards. This test is more specific than the Howship-Romberg sign.(4) Per rectal and per vaginal examination can reveal a mass and adds clinical suspicion.

Various modalities have been used in the diagnosis of obturator hernia. Herniography, plain radiography of the abdomen, ultrasonography of the inguinal region and inner aspect of the thigh, small bowel follow through study, barium enema and magnetic resonance imaging have been reported in the literature.(5)

CT scan of the abdomen and pelvis is most relevant to a confirmatory diagnosis of obturator hernia. Recent series have reported that definite and early diagnosis of the obturator hernia can be made in 100% of cases with CT and represents the gold standard.(6,7) CT is minimally invasive, readily available, and requires a short time. Early diagnosis translates into immediate operative intervention which may prevent bowel resection and improve outcomes in a group of patients with generally advanced age.

The Obturator or adductor region lies in the medial portion of the upper third of the thigh between the extensor and the flexor muscle groups. This region includes the obturator canal and the origins of the adductor muscles from the margins of the obturator foramen and the obturator membrane. The obturator foramen is the largest foramen in the body and is formed by rami of the ischium and pubis. It lies on the antero lateral pelvic wall, inferior to the acetabulum. All but a small area of this huge foramen is closed by the obturator membrane, the fibers of which are continuous with the periosteum of the enclosing bones and 218

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with the tendinous attachments of the internal and external obturator muscles.

More specifically the obturator foramen is formed superiorly by the superior pubic ramus, medially by the pubic body and its inferior ramus, inferiorly by the ischial ramus and the anterior border of ischial body with participation of the margins of the acetabular notch.

The obturator canal is a tunnel 2-3 cm in length that begins in the pelvis at the defect in the obturator membrane and passes obliquely downward to end outside of the pelvis in the obturator region of the thigh. It is bounded superiorly and laterally by the wall of the obturator membrane and the internal and external obturator muscles. The obturator nerve, artery and vein and the fat body of the obturator canal pass through the canal.

The obturator nerve, formed by the ventral rami of lumbar nerves 2, 3 and 4, emerges from the medial border of the psoas muscle just behind the iliac vessels, where it travels with the obturator vessels. The obturator nerve usually enters the obturator canal superior to the artery and vein. Immediately on emerging from the canal, it divides into anterior and posterior divisions. The anterior division passes between the adductor longus and adductor brevis muscles, whereas the posterior division travels between the adductor brevis and adductor magnus muscles. Afferent fibres arise from the hip and knee joints and skin of the medial surface of the thigh.

The origin of the obturator artery varies, but in most cases, it arises from the internal iliac artery. The obturator artery travels downward on the obturator fascia and passes into the obturator canal, where it passes with the obturator vein below the obturator nerve. Within the pelvis, the obturator artery provides a retropubic branch to the posterior side of the pubic bone and often a branch 219

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to the bladder. As soon as it has passed through the canal, it divides into anterior and posterior branches. These branches anastomose to form a ring around the obturator foramen, from which twigs pass to the obturator externus, pectineus and adductor muscles. The anterior division typically anastomoses richly with the medial femoral circumflex branch of the femoral artery. In addition to supplying the adductor muscles, the posterior division provides a branch that passes to the head of the femur and others that enter nutrient foramina within the acetabular fossa.

The obturator artery and vein are often subject to variations in their origin and termination, respectively, being derived from the external iliac system rather than the internal iliac vasculature. Because such vessels cross the superior pubic ramus and Cooperâ&#x20AC;&#x2122;s ligaments near the femoral ring, their unexpected presence can become a matter or great concern to urologists, gynecologists and general surgeons. They are of obvious importance in the repair of inguinofemoral and obturator hernias.

The aberrant obturator artery is present in 30-69% of cases.(8) In approximately 40% of cases, the obturator artery is replaced by the aberrant obturator artery which arises most commonly from the inferior epigastric artery and less commonly from the external iliac artery. From its origin, the aberrant artery may pass medial to, lateral to, or directly across the femoral ring and Cooperâ&#x20AC;&#x2122;s ligament, thereafter descending into the pelvis. Such vessels are usually concealed by fat, loose connective tissue and lymphatic elements. These can be readily injured by sutures or staples applied in inguinal or femoral hernioplasty. Typically the artery gives rise to suprapubic and retropubic branches, supplies variably large branches to the bladder, and anastomoses with a normal obturator artery in the vicinity of the canal. The aberrant obturator vein has not been so well studied as its arterial counterparts. In some cases, the aberrant vein is quite 220

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large. Inadvertent injury during surgery can result in significant blood loss.

If both the aberrant and normal obturator arteries are present and anastomose, they form a corona mortis or â&#x20AC;&#x153;circle of deathâ&#x20AC;?, so called because bleeding from an injured vessel involves the combined vascular pressures of the internal and external iliac vessels and the medial femoral circumflex. Also, a severed artery or vein can retract into a position where it may be exceedingly difficult to secure the bleeder and achieve hemostasis. Anastomosing obturator arteries were found in 16% of cases and anastomosing obturator veins in 73% of cases in the study by Gilroy et al.(9)

Gray et al described three anatomical stages of the formation of obturator hernia. The first stage begins with the entrance of preperitoneal fat into the pelvic orifice of the obturator canal, forming a pilot fat plug. During the second stage, a peritoneal dimple forms and progresses to form a peritoneal sac. During the third stage, symptoms are produced by herniation of the viscera into the sac.(10)

A variety of surgical approaches to repair of obturator hernias have been suggested by several authors, but because of the rarity of the problem, no one investigator has adequate experience to advocate resoundingly any single surgical approach.

When the diagnosis of obturator hernia is known preoperatively and strangulation is not suspected the posterior preperitoneal approach is preferred and provides direct access to the hernia. This can be achieved either through an open approach using a lower midline or Pfannensteil incision (Cheatle â&#x20AC;&#x201C; Henry operation (11)) or laparoscopically. In the open prep-peritoneal approach the rectus abdominis muscles are separated in the midline and retracted laterally. The preperitoneal space is then developed which gives adequate access to the femoral 221

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and obturator defects. If petechiae or dark bowel suggest necrotic bowel, the peritoneal cavity can be easily entered for bowel resection.

Reduction of the hernia may occasionally require incision of the obturator membrane with care to avoid injury to the obturator nerve and vessels. If necessary, an incision should be made in the inferior aspect of the canal. Direct primary suture repair of the hernia defect is difficult because the foramen is bordered by bone and spanned by tough, immobile obturator membrane. Repair may be effected with a plug mesh or some surgeons prefer placing a large flat polypropylene mesh in the preperitoneal space to cover the obturator orifice as well as the femoral and inguinal areas.(12)

When the diagnosis is unclear or when strangulation is suspected the abdomen approached by open laparotomy is most favored, as in the case described. The hernia may then be repaired as described above, after opening the parietal peritoneum. In cases of strangulated or perforated bowel, gross contamination and/ or bowel resection, there is reluctance in using synthetic mesh. A biologic mesh may be placed or nearby tissue such as periosteal flaps, bladder wall, or uterine fundus or ligaments may be used.(13)

In the presence of a palpable mass, an obturator approach has been described.

The thigh should be flexed and abducted and a generous incision made over the mass. After the fascia lata is divided two muscles are exposed: the adductor longus medially and the pectineus, laterally. This approach may be physically difficult and dealing with strangulated bowel quite challenging. Inversion of the sac and suturing of the pectineus muscle to the periosteum are advised.(8) An inguinal approach has been described as early as the beginning of the 20th century (Milligan).(8) An inguinal hernia incision and pre-peritoneal dissection through the opening of the deep inguinal ring are made. The obturator hernia 222

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can be easily found 2 cm dorsally from the Cooperâ&#x20AC;&#x2122;s ligament extraperitoneally.

A small incision is made at medial sharp edge of the hernia defect. The hernia sac and its content can then be reduced. If the incarcerated bowel is viable, a prosthetic mesh is placed as a patch. If the bowel is necrotic, the damaged bowel loop is withdrawn through the wound and easily reconstructed extra-abdominally. This may be a suitable method in the frail and elderly high risk patient.(14)

The use of laparoscopy for repair of groin hernias has been extended to repair of obturator hernia. The first report in 1993 came from Germany and there has since been several case reports.(15)

With the advent of CT cases of obturator hernia are being diagnosed pre-operatively and can be repaired electively by a laparoscopic approach.(16, 17) Other instances of elective laparoscopic repair include incidental findings during laparoscopy for other conditions or inguinal hernias.(18,19) This is expected since the technique follows the same principles as for an inguinal hernia repair with mesh. Both TEP (Totally Extra Peritoneal) and TAPP (Transabdominal PrePeritoneal) approaches have been employed. The TAPP approach is more appropriate for emergency presentations as it allows for assessment of the bowel for viability. The laparoscopic repair of obturator hernia thus far is feasible with reasonable and safe results.(20)

The case presented here was of a patient with previous bilateral inguinal hernia repairs. In addition to the obstructed right obturator hernia she was also noted to have a right femoral hernia. A patient such as this if subjected to laparoscopic herniorrhaphy could benefit from laparoscopic examination for an occult obturator hernia. The laparoscopic inguinal hernia repair approach allows viewing of the entire mypopectineal orifice facilitating repair of any unexpected hernia and thereby reducing the chance of future complications thereof. Laparoscopic 223

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examination of both groins during laparoscopic unilateral inguinal hernia repair is an area of current interest/controversy. Bilateral examination of the inguinal regions during unilateral laparoscopic inguinal hernia repair is not routinely performed and scarcely reported. Exploration of the asymptomatic area may invite complications (bleeding, neuralgia) and defies basic surgical logic. Recent reports describe the routine exploration of both inguinal regions at laparoscopy.

The diagnosis of ipsilateral and contralateral occult hernias (femoral, inguinal, obturator) were made and these were also repaired with no significant increase in morbidity or patient dissatisfaction. (21,22)

CONCLUSION Obturator hernia is a rare clinical entity. In most cases it produces small bowel obstruction with high morbidity and mortality. The true prevalence is likely to increase due to an aging population, increased use of CT to investigate recurrent symptoms or other abdominal complaints, and also increased use of laparoscopic repair of groin hernias. It is important to be aware of the variable anatomy of the arteries and veins in the vicinity of the obturator canal. Inadvertent injuries to these structures may result in catastrophic hemorrhage. Several approaches and methods of herniorrhaphy are recognized. A prolene mesh plug is a suitable method. In the emergency presentation a laparotomy is a highly recommended. Intentional exploration of asymptomatic hernia orifices during elective laparoscopic inguinal hernia repair is worth considering. Prophylactic repair of occult hernias so discovered may help decrease the complications associated with obturator hernia.

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REFERENCES 1. Hsu CH, Wang CC, Jeng LB, et al. Obturator hernia: a case report of eight cases. Am Surg 1993; 59: 709-7011.

2. Mantoo SK, Mak K, Tan TJ. Obturator hernia: diagnosis and treatment in the modern era.

Singapore Med J 2009; 50(9): 866- 870.

3. Chung CC, Mok CO, Kwong KH, et al. Obturator hernia revisited: a review of 12 cases in 7 years. J R Coll Surg Edinb 1997; 42: 82-4.

4. Hannington-Kiff JG. â&#x20AC;&#x153;Absent thigh adductor reflex in obturator herniaâ&#x20AC;? Lancet 1980; 1 (8161): 180.

5. Li SS, Thi VKK. Two different surgical approaches for strangulated obturator hernias. Malys J Med Sci. 2012; 19(1): 69-72.)

6. Yokoyama Y, Yamaguchi A, Isogai M, et al. Thirty-six cases of obturator hernia: does computed tomography contribute to postoperative outcome? World J Surg 1999; 23: 214- 216.

7. Dundamadappa SK, Tsou IY, Goh JS. Clinics in diagnostic imaging (107). Singapore Med J 2006; 47: 88-94.

8. Skandalakis LJ, Androulakis J, Colburn GL. Obturator hernia: embryology, anatomy and surgical applications. Surg Clin N Am 2000 (80);1: 71-84.

9. Gilroy AM, Hermey DC, Dibendetto LM, et al. Variability of the obturator vessels. Clin Anat 1997;10: 328.

10. Gray SW, Skandalakis JE, Soria RE, et al. Strangulated obturator hernia. Surgery 1974; 75: 20-7.

11. Cervantes-Castro J, Rojas-Reyna G, Cicero-Lebrija A, et al. Experience with the CheatleHenry operation for femoral hernia repair. Cir Cir 2011; 79: 220-223.

12. Bergstein JM, Condon RE. Obturator hernia: current diagnosis and treatment . Surgery 1996; 119(2) :133-136.

13. Salameh JR. Primary and Unusual abdominal wall hernias. Surg Clin N Am 2008; 88: 4560.

14. Togawa Y, Murunoi T, Kawaguchi T, et al. Minimal incision transinguinal repair of obturator hernia. Hernia May 2013 Epub.

15. Tschudi J, Wagner M, Klaiber C. Laparoscopic operation of incarcerated obturator hernia with assisted intestinal resection. Chirurg 1993; 64: 827-8.

16. Chang SS, Shan YS, Lin YJ, et al. A review of obturator hernia and a proposed algorithm for its diagnosis and treatment. World J Surg 2005; 29: 450-4.

17. Hunt L, Morrison C, Lengyel J, et al. Laparoscopic management of of an obstructed obturator hernia: Should laparoscopic assessment be the default option? Hernia 2009; 13: 313-315.

18. Chowbey PK, Bandyopadhay SK, Khullar R, et al. Endoscopic Totally Extra-peritoneal re-

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A CASEBOOK OF TWENTY SURGICAL CASES pair for occult bilateral obturator hernias and multiple groin hernias. J Laparoendosc Adv Surg Tech A 2004; 14: 313-316.

19. Haith LR, Simeone MR, Reilly KJ, et al. Obturator Hernia: Laparoscopic diagnosis and repair. JSLS 1998; 2: 19-193.

20. Deeba S, Purkayastha S, Darzi A, et al. Obturator Hernias: a review of the laparoscopic approach. J Minim Access Surg. 2011; 7(4): 201-204.

21. Lal P, Philips P, Chander J, et al. Is unilateral laparoscopic TEP inguinal hernia repair a job half done? The case for bilateral repair. Surg Endosc. 2010; 24(7): 1737-45.

22. Dulucq JL, Wintringer P, Mahajna A. Occult hernias detected by laparoscopic totally extraperitoneal inguinal hernia repair: a prospective study. Hernia 2011; 15(4): 399-402.

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13.

MULTINODULAR GOITRE Going â&#x20AC;&#x2DC;Tâ&#x20AC;&#x2122; (thyroidectomy) Total

INTRODUCTION Benign nontoxic multinodular goiter (MNG) is among the most common endocrine disorders. The size and symptoms of these MNG are quite variable and may present from an incidental cervical swelling to a MNG with substernal extension and compressive aero digestive symptoms. The mainstay of treatment by most authorities is surgery. The surgical procedures reported for treatment of non toxic MNG range from some variant of subtotal thyroidectomy to total thyroidectomy. Recurrence rates are reportedly as high as 40% and recurrent surgery portends a much higher rate of RLN injury and hypocalcemia On the other hand, near total or total thyroidectomy requires the necessary surgical skill and installs the need for life long thyroid replacement therapy. While not free from recurrent laryngeal nerve injury or hypoparathyroidism, the literature reflects a sweeping trend towards total thyroidectomy for non toxic MNG. However, the extent of resection for MNG remains controversial.

A case of MNG is described which required re-operative surgery due to recurrence. This is followed by a discussion on the current surgical strategies for MNG.

CASE History: A 49 year old woman presented to the outpatient clinic with a recurrent swelling in the neck. The patient explained that a similar swelling was noted 8 years previously. This was diagnosed as a goiter for which she had surgery.

The current swelling grew gradually over the previous 4 years. This did not cause any compressive symptoms and her voice did not change (confirmed by 227

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her daughter). She reported no symptoms of hyper/ hypo- thyroidism. This lady was otherwise well and had no family history of thyroid related disease or any endocrinopathy.

Physical examination: A well looking lady with no stigmata of chronic disease, with a swelling noted in the anterior triangle of the neck. This moved with swallowing. The trachea was central and both lobes of the thyroid were palpably enlarged. The texture of the gland was firm and non-tender with the left slightly larger than the right, but there was no retrosternal extension. There was no palpable lymphadenopathy.

An ultrasound of the neck described that both lobes of the thyroid were enlarged and multiple nodules noted in both lobes. There were no calcifications.

The cardio-respiratory and gastrointestinal examinations were normal.

Blood investigations revealed normal complete blood counts, renal function, serum calcium levels and thyroid function tests.

On review of her past hospital records, a subtotal thyroidectomy was confirmed and the histology of the specimen described a multinodular goitre.

The patient was informed of a recurrent multinodular goitre. The patient requested surgical treatment. Following a discussion regarding the risks and benefits the patient was consented and booked for a total thyroidectomy.

A pre-operative indirect laryngoscopy described normal vocal cords. Her sugery was performed 7 weeks later.

Surgical treatment: A collar incision was made 2 finger breadths above the sternal notch (along the previous scar). The strap muscles were densely adherent to the thyroid gland and the dissection was notably challenging more so on the left side. The recurrent laryngeal nerve was not clearly visualised in the cephalad aspect on the left side.

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Both lobes were eventually mobilized and dissected off the trachea. The wound was closed in layers and a Penrose drain (1cm width) was placed within.

Outcome: No early post-operative complications were noted and the drain was removed the next morning. Serial serum calcium measurements were normal (9.2 , 9.4).

The patient was discharged with L-thyroxine 100mcg once daily.

On review in outpatient clinic 10 days later, the wound was satisfactory and the 3/0 subcutaneous prolene suture was removed. Of note her voice was hoarse.

This was thought to be related to a neuropraxia of the recurrent laryngeal nerve.

At 6 month review the patient was clinically and biochemically euthyroid but her hoarseness persisted. Laryngoscopy confirmed left vocal cord palsy.

DISCUSSION MNG refers to an enlarged thyroid gland with multiple areas of nodularity resulting from hyperplasia within the gland. Worldwide, MNG is the most common endocrine disorder affecting 500- 600 million people, where iodine deficiency is often the culprit. The prevalence worldwide is widely variable and directly related to iodine intake in regional populations. More current thinking indicates that MNG may result from the product of an interaction between genetically susceptible patients and indirect triggers (low iodine, smoking, and goitrogens).(1)

The natural history of MNG includes an increase in tissue with an annual growth potential of up to 20%.(2) Areas of increased functioning may progress to hyperthyroidism or toxic MNG (Plummerâ&#x20AC;&#x2122;s disease) which occurs in 5-10% of MNG in a five year period.(3) In addition, MNG may harbor occult malignancy at a rate of 4% although some investigators suggest a higher incidence in cases of substernal extension. (4,5) 229

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Patients with MNG are commonly unaware of any problem until diagnosed by a physician during evaluation for another problem. However, with long standing MNG some individuals develop compressive symptoms: globus sensation, dysphagia, or recumbent dyspnea. Tracheal deviation or narrowing may cause respiratory symptoms and hoarseness may develop as a result of laryngeal nerve pressure. Compression at the thoracic inlet with development of flushing, neck vein compression and shortness of breath may occur with Pembertonâ&#x20AC;&#x2122;s maneuver of raising the arms above oneâ&#x20AC;&#x2122;s head. Patients with a long history of MNG are more likely to develop clinical or sub clinical thyrotoxicosis which should be fully evaluated and treated if present. The cosmetic deformity of the neck is another reason for presentation in a number of individuals.(6)

For patients who are symptomatic or who accept treatment, surgery is the mainstay of treatment in most countries. Surgical resection is associated with reasonable success, provides pathologic confirmation, avoidance of radiation and offers one stage treatment. However, controversy remains regarding the extent of thyroid requiring removal to prevent recurrent MNG. The surgical technique utilized by the surgeon should allow for the best chance for removal of the abnormal thyroid tissue with the least morbidity.

Early concerns regarding surgery of the thyroid glands stem from the fact that operative management of goiter carried not only a high degree of morbidity, but also mortality. Before the 1860s hemorrhage and infection were common place and the mortality rate for thyriodectomy exceeded 40%.(7) With the use of aseptic technique, general anesthesia and meticulous hemostasis pioneers such as Kocher and Billroth brought about a dramatic reduction in mortality rates associated with thyroidectomy. By the dawn of the 20th Century these numbers had fallen to less than 1%.(7) Thereafter, there was little debate as to whether thyroidectomy could be performed without significant risk to the life of the pa230

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tient. The focus of thyroidectomy subsequently changed from trying to decrease mortality to limiting iatrogenic morbidity. Most notable was the potential for recurrent laryngeal nerve (RLN) injury. Kocher and colleagues regarded by many as the fathers of modern day thyriodectomy believed that the best way to avoid injury was to avoid the nerve entirely thus it became dogmatic among thyroid surgeons that any RLN seen during thyriodectomy was very likely to have been injured. This practice was challenged by Lahey in the 1920s and 1930s. Lahey reported his experience with deliberate exposure and identification of the RLN during over 10,000 thyroidectomies. He was rewarded with a RLN injury rate of less than 1% that was significantly lower than any previously published series.(8) As such, contemporary thyroid surgery aims at eradicating disease while preserving parathyroid gland function, RLN integrity and minimizing overall patient morbidity (RLN injury, tracheal injury and parathyroid insufficiency).

To minimize these post operative risks, all patients requiring surgery especially those with substernal goiter should be referred to experienced thyroid surgeons in high volume centres.(9) However in many settings thyroid surgeons may not be easily available and general surgeons are indicated for MNG surgery. As in the case described, a subtotal thyroidectomy is often performed.

Proponents of subtotal thyroidectomy identify preservation of the euthyroid state and protection of both the RLN and the parathyroid glands as advantages to this standpoint.

(8,10)

The long term risk of hypothyroidism after subtotal

resection of nontoxic MNG is insufficiently described but it is probably not significantly different from the 10-20% reported for toxic MNG.(11) Recurrence of the nontoxic MNG is seen in 15-40% of patients with long term follow up.

This increased risk is inversely correlated with the volume of the post operative remnant, whereas possible factors such as age, duration of goiter, and serum 231

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TSH levels during follow up do not seem to be of importance .(12, 13) With this high probability of goiter recurrence prophylactic levothyroxine therapy has been implemented as a preventative measure. This is a controversial practice. Surveys in both the US and Europe have demonstrated that 50% of clinicians prefer prophylactic post operative therapy.(14,15) . However, of four randomized trials, only Miccoli et al demonstrated a beneficial effect of this practice. At this time, evidence to support prophylactic post operative levothyroxine is lacking. (12,16,17,18) In the case described the patient was not on suppressive levothyroxine therapy and was euthyroid on her second presentation.

A reoperation for recurrent MNG accounts for approximately 10-15% of thyroidectomies. This is associated with a 3-10 fold increase in risk of surgical complications.(19) On account of this, a variety of thyroid resections have been undertaken to minimize the recurrence/reoperative rate and therefore minimize the chance of RLN injury. Although total thyroidectomy is the procedure of choice in patients with thyroid carcinoma the literature has seen a sweeping trend towards use of this procedure for MNG. Though seen by some as an overly hazardous procedure because of the risks of RLN injury and damage to parathyroid function, total thyroidectomy has been more frequently implemented in the surgical treatment of benign MNG in the recent past. On the contrary, numerous publications have demonstrated that the risk of recurrent MNG can be eliminated without an accompanying increased risk of permanent hypothyroidism or RLN injury. In fact, interestingly the reported rate of RLN injury is in the accepted less than 2%.(20,21,22)

Incidental finding of thyroid carcinoma is noted in 3-16% of cases. These also account for re-operative cases as these patients generally require completion thyroidectomy. Gila et al demonstrated a decrease in re-operative cases for oc232

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cult cancer with the benefits of acceptable rates of RLN injuries and transient hypocalcemia.(24) Less radical procedures have been performed for MNG. Erbil et al identified that near total thyriodectomy conferred similar benefits to total thyriodectomy.

By comparing total thyroidectomy vs near total thyroidectomy they commented that both approaches obviates the need for completion thyroidectomy in incidentally found cancer and while there is no difference in the rate of RLN palsy between the two methods near total thyroidectomy (9.8% vs 26%) causes a significantly lower rate or hypoparathyroidism.(25) In view of the good results with total thyroidectomy for MNG some clinicians have already noted a diminished need for re-operative surgery. In a recent review of 12,000 cases of thyroid surgery a gradual decline in re-operative cases was noted. Only 0.5% of cases required re-operative surgery in the last year of the study.(26) In an interesting report from Australia, Snook et al identified 10 of 3,044 patients who developed recurrent MNG following total thyroidectomy.

Only one was a true recurrence in the thyroid bed while the other nine involved elements of the embryological remnants (pyramidal tract, thyrothymic tract).

With the increasing trend in total resection for MNG, clinicians will need to be more aware of this possibility.(27)

CONCLUSION While surgical resection is the main therapeutic measure in individuals with symptomatic or large MNG, the extent of thyroid resection remains debatable.

Refinement of the surgical techniques and skill has decreased RLN injury to a mere 1-2% and rightly so, the focus of efforts of current surgical therapy is aimed at achieving a rate of zero. An experienced surgeon in the different surgical approaches to the thyroid is a definite asset. Most of the literature 233

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report series in hundreds and in some cases thousands. Our setting in Trinidad unfortunately is not visited by these large numbers of patients, nonetheless, particular attention during residency and training may help to improve the necessary surgical skill needed for thyroid surgery. In addition, this was my first case of a recurrent MNG and although uncommon, the surgical findings were sufficient to stimulate ideas on avoiding re-operative surgery.

It seems that when Lahey in the early 20th century was able to safely dissect and preserve the RLN, a single operation, total thyroidectomy, was described for both benign and malignant thyroid disease. Although surgeon preference would ultimately lie beneath the scar, the patient should be adequately counseled on the risks of recurrence and possible re-operative procedures with an associated increased risk of RLN and transient/permanent hypocalcemia if a sub total procedure is undertaken. While these may be attenuated by a total thyroidectomy, lifelong thyroid replacement therapy is required. This of course eliminates the bodyâ&#x20AC;&#x2122;s natural ability to regulate thyroid hormones during different climatic conditions (foreign travel or migration,) or different physiological states (eg mental stress, pregnancy). In addition, iodine deficiency is not endemic to Trinidad. In keeping with the current trends total thyroidectomy should be made the procedure of choice in patients desirous of surgery for multinodular goiter with the option for near total thyroidectomy or subtotal thyroidectomy if the surgical field demands it. This situation, and others like it, requires a level of judicious intra-operative surgical decision-making that comes only with experience.

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REFERENCES 1. Matovinovic J. Endemic goiter and cretinism at the dawn of the third millennium. Annu Rev Nutr 1983;3:341–412.

2. Berghout A, Wiersinga WM, Drexhage HA, et al. Comparison of placebo with L-thyroxine alone or with carbimazole for treatment of sporadic non-toxic goitre. Lancet 1990;336:193–7.

3. Elte J, Bussemaker JK, Haak A. The natural history of euthyroid multinodular goiter. Postgrad Med J 1990;66:186–90.

4. Tollin SR, Mery GM, Jelveh N, et al. The use of fine-needle aspiration biopsy under ultrasound guidance to assess the risk of malignancy in patients with a multinodular goiter. Thyroid 2000;10:235–41.

5. Netterville JC, Coleman SC, Smith JC, et al. Management of substernal goiter. Laryngoscope 1998;108:1611–7.

6. Day TA, Chu A, Hoang KG. Multinodular goiter. Otolaryngol Clin N Am,2003;36:35-54.

7. Becker WF. Presidential address: pioneers in thyroid surgery. Ann Surg 1977;185(5):493– 504.

8. Miller MC, Spiegel JR, Identification and monitoring of the Recurrent Laryngeal Nerve during thyroidectomy. Surg Oncol Clin N Am 2008;17: 121-144.

9. Bahn RS, Castro MR. Approach to the patient with non-toxic multinodular goiter.J Clin Endocrinol Metab 2011;96:1202–12.

10. Jensen MD, Gharib H, Naessens JM, et al. Treatment of toxic multinodular goiter (Plummer’s disease): surgery or radioiodine? World J Surg 1986;10:673–80.

11. Hermus AR, Huysmans DA. Treatment of benign nodular thyroid disease. N Engl J Med ,1998;338:1438–1447.

12. Hegedu’s L, Nygaard B, Hansen JM. Is routine thyroxine treatment to hinder postoperative recurrence of nontoxic goiter justified? J Clin Endocrinol Metab 1999;84:756–760.

13. Berghout A, Wiersinga WM, Drexhage HA, et al. The long-term outcome of thyroidectomy for sporadic non-toxic goitre. Clin Endocrinol,(Oxf) 1989; 31:193–199.

14. Bonnema SJ, Bennedbæk FN, Wiersinga WM, et al. Management of the nontoxic multinodular goitre: a European questionnaire study. Clin Endocrinol (Oxf) 2000; 53:5–12.

15. Bonnema SJ, Bennedbæk FN, Ladenson PW, et al. Management of the nontoxic multinodular goiter: a North American survey. J Clin Endocrinol Metab 2002; 87:112–117.

16. Geerdsen JP, Frølund L . Thyroid function after surgical treatment of nontoxic goitre. A randomized study of postoperative thyroxine administration. Acta Med Scand 1986; 220:341–345.

17. Bistrup C, Nielsen JD, Gregersen G, et al. Preventive effect of levothyroxine in patients operated for non-toxic goitre: a randomized trial of one hundred patients with nine years followup.

Clin Endocrinol (Oxf) 1994; 40:323–327.

18. Miccoli P, Antonelli A, Iacconi P, et al. Prospective, randomized, double-blind study about effectiveness of levothyroxine suppressive therapy in prevention of recurrence after operation:

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A CASEBOOK OF TWENTY SURGICAL CASES result at the third year of follow-up. Surgery 1993; 114:1097–1101.

19. Hegedus L, Bonnema SJ, Bennedbaek FN. Management of simple nodular goiter: current status and future perspectives. Endocr Rev 2003;24:102–32.

20. Moalem J, Suh I, Duh QY. Treatment and prevention of recurrence of multinodular goiter: an evidence based review of the literature. World J Surg 2008;32(7): 1301-12.

21. Tezelman S, Borucu I, Senyurek-Giles Y, et al. The change in surgical practice from subtotal to near total or total thyroidectomy in the treatment of patients with benign multinodular goiter.

World J Surg 2009; 33(3): 400-5.

22. Albayrak Y, Demiryilmaz I, Kaya Z, et al. Comparison of total thyroidectomy, bilateral subtotal thyroidectomy and Dunhill operations in the treatment of benign thyroid disorders.

Minerva Chir 2011; 66(3): 189-95.

23. Agarwal G, Aggarwal V. Is total thyroidectomy the surgical procedure of choice for benign multinodular goiter? An evidence- based review. World J Surg 2008; 32(7): 1313-24.

24. Giles Y, Boztepe H, TerziogluT, et al. The advantage of total thyroidectomy to avoid reoperation for incidental thyroid cancer in multinodular goiter. Arch of Surg 2004;139(2): 179-82.

25. Erbil Y, Barbaros U, Salmaslioglu A, et al. The advantage of near-total thyroidectomy to avoid post-operative hypoparathyroidism in benign multinodular goiter. Langenbecks Arch Surg,2006;391(6):567-73.

26. Vasica G, O’Neill CJ, Sidhu SB, et al. Reoperative surgery for bilateral multinodular goiter in the era of total thyroidectomy. Br J Surg 2012; 99(5): 688-92.

27. Snook KL, Stalberg PL, Sidhu SB, et al. Recurrence after total thyroidectomy for benign multinodular goiter. World J Surg. 2007; 31(3): 593- 8.

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14. SENTINEL LYPMH NODE BIOPSY IN BREAST CANCER

Adequate axillary staging with minimal morbidity in early stage breast cancer

INTRODUCTION The historic rationale for axillary lymph node dissection (ALND) in breast cancer has been three fold: prognostication, the prevention of axillary recurrence and the possibility of a survival benefit from the removal of positive (metastatic) axillary nodes. ALND is also well known to be associated with added co-morbidities, such as, seroma, chronic lymphedema, and numbness and paresthesia related to the ipsilateral upper limb.

Sentinel lymph node biopsy (SLNB) was adapted to the surgical treatment of breast cancer in the 1990s. Following this, several reports in the literature confirmed its validity and it has evolved to become the standard axillary staging procedure for patients with breast cancer.

With increased awareness by patients and health professionals some researchers have noted an increase in detection of early stage breast cancers. On account of this and current recommendations, the implementation of SLNB began at our hospital. The technique involved the use of methylene blue as the marker to aid in identification of the SLN. Most authorities agree that a learning curve exists to become competent at this technique to minimize false negative rates with some recommending at least twenty (20) cases. Others consider that with wider practice, by experienced clinicians may reduce this number to single digits.

To improve the treatment of women with breast cancer, SLNB was undertaken 237

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to improve our experience. The case of a forty-four (44) year old woman with breast cancer is described in which SLNB was performed followed by ALND. An account is given on the role of SLNB in the management of early stage breast cancer.

CASE History: A 44 year old woman presented with a 3 month history of a left breast lump. This had gradually increased in size, initially the size of a marble it was now the size of a plum, and also occasionally felt painful. This lump was not associated with any nipple discharge and the patient noticed no overlying skin changes. This woman had no previous breast symptoms or screening procedures.

The patient used the oral contraceptive pill in her early 20s. The patient experienced her menarche at 12 years of age and currently her menstrual cycles were regular occurring every 30 days and lasting 4 days. This patient was P1+1. Her daughter now age 9 years was breast fed.

This patient was otherwise well and reported no previous medical or surgical history. Of note her sister, now aged 52 years, was diagnosed with breast cancer 2 years previously.

Physical Examination: A 4 x 4cm lump was palpated in the left breast lateral to the nipple-areolar complex. This lump was firm and mobile with no skin tethering or fixation to the chest wall structures. There were no palpable lymph nodes in the axilla or supraclavicular fossa. The right breast and axilla was palpably normal.

Examination of the cardiovascular, respiratory and gastrointestinal systems was all normal.

USS of the breast: A 3.5cm lump was noted in the area of clinical interest with 238

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areas of hypoechoic signals.

Mammogram: A radio dense area in the left breast at 3 o clock position. There were no associated microcalcifications but the borders were irregular. The right breast mammogram was normal. Trucut biopsy was performed and this reported an invasive ductal carcinoma. (cT2N0M0)

The patient and her husband was informed of the diagnosis and after discussing her treatment options opted to have a modified radical mastectomy. In view of her clinically negative axilla, consent was also taken to perform a sentinel lymph node biopsy before proceeding to axillary nodal dissection. A staging CT scan of the chest abdomen and pelvis excluded any evidence of metastatic disease.

Surgical treatment: Under general anaesthetic 3ml of methylene blue was injected in a subdermal, periareolar location laterally (Fig 1). After massaging the area for 5 minutes, an incision was made just below the axillary hair line and adjacent to the pectoralis major border. The blue lymphatic tract was identified and followed by blunt dissection to the sentinel lymph node (Fig 2). The node was dissected free and labeled separately. No other tracts or nodes were identified.

The procedure continued with the mastectomy and a level 2 axillary dissection.

A 15fr suction drain was left in situ and the wound closed with 3/0 sc prolene.

The patient was discharged on the first postoperative day with instructions on caring for the drain including measuring the volume and resetting the vacuum.

On day 7 the drainage decreased to 20 mls per day at which point the drain was removed. After removal of the sutures on day 10 the patient did well and did not develop a seroma.

The histology report was available two weeks later and confirmed an invasive 239

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ductal carcinoma. The tumour measured 3cm in maximal diameter with grade 2 nuclear features and the closest resection margin was 1cm. There was no lymphovascular invasion. Hormone receptor and her2neu receptor testing was not available at this time.

The sentinel lymph node was negative for tumor and the formal axillary dissection indicated 12 nodes were retrieved and these were all free of tumor. (pT2N0M0) This patient did well and was referred on to the Oncologist for consideration of adjuvant chemotherapy.

DISCUSSION Metastasis of breast cancer to the axillary lymph nodes is an important prognostic factor in early breast cancer and also in the choice of adjuvant therapy.

The historic rationale for ALND in breast cancer has been three fold: prognostication the prevention of axillary recurrence and the possibility of a survival benefit from the removal of positive (metastatic) axillary nodes. The risks of ALND include seroma, wound infection, damage to nerves, reduced shoulder mobility and lymphedema. As a result of screening and increased awareness, lymph node metastasis has become less common such that a significant proportion of women may have an axillary clearance of normal nodes.

Removal of those lymph nodes that drain the primary tumor sites by sentinel lymph node biopsy can allow lymph node metastasis to be detected less invasively. SLNB is based on the hypothesis that the first node draining the primary tumor reflects the tumor status of the regional lymph node basin and this technique was adapted to breast cancer by Giuliano and colleagues.(1)

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Fig 1: Blue staining on lateral aspect of the areolar following subdermal injection of methylene blue.

Fig 2: The blue stained sentinel lymph node in the left axilla

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Although SLNB has been widely accepted it is worth noting a few technical aspects. Lymphatic mapping may be achieved with vital blue dye and/or radioactive tracer. Methylene blue is available at our hospital and 3mls were injected in the subareolar area between 2 oâ&#x20AC;&#x2122;clock and 5 oâ&#x20AC;&#x2122;clock and massaged for five minutes before the axillary dissection was undertaken. Several studies have evaluated the proportion of successful SLNB with blue dye, radiocolloid or combination of dye with isotope with respect to sentinel node identification rate, accuracy, and/or false negative rate. Morrow and colleagues performed a randomized trial comparing the use of blue dye alone with that of combined dye and isotope. The success rate of SLNB was higher with combined mapping than with blue dye alone (100% vs 86%, P=0.002). The accuracy and false negative rates were similar. An accuracy of 100% for combined mapping versus 98% for blue dye and a false-negative rate of 0% for combined mapping versus 5% for blue dye were observed.(2) In a study by Meyer-Rochow and colleagues similar identification rates, accuracies and sensitivities were reported with blue dye alone and triple modality consisting of pre-operative lymphoscintigraphy, intra-operative gamma probe and intra-operative blue dye.(3) In the American College of Surgeons Oncology Group (ACOSOG) Z0010 trial 5237 patients underwent SLNB. Blue dye alone was used in 14.8%, radiocolloid in 5.7%, and the combination of dye with isotope in 79.4%. No statistically significant difference in sentinel node identification or failure rate was seen (1.7%, 2.3%, 1.2%) for the blue dye, radiocolloid and the combination of dye with isotope respectively.(4)

Grube and Giuliano reviewed early published studies with 100 or more subjects reporting the identification and accuracy of SLNB using vital dye, gamma probe guided surgery or a combined technique. The overall false negative sentinel node identification rate ranged from 0-14.3% and the accuracy ranged from 93100%. The factors contributing to failure to identify the sentinel node includes 242

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variable lymphatic drainage pattern, patient or tumor characteristics, surgical technique, surgeon training, and pathologist experience.(5)

The primary site of lymphatic drainage from the breast is the axilla. However, 1.3% - 9.9% isolated internal mammary drainage has been reported. At present there is no consensus regarding the ideal sites for dye or radioactive colloid injection. In practice, peritumoral, intradermal or subareolar injections seem equally effective to identify axillary nodes. It is well documented that when blue dye and radiocolloid are injected in different quadrants of the same breast, both tracers drained to the same SLN in 93% of cases.(6) Two prospective randomized trials(7,8) and one multicentric study of 3961 patients(9) have demonstrated that an intradermal or periareolar injection allows a higher incidence of localization of SLN than a peritumoral injection while decreasing time to identification of the SLN. The periareolar route has the additional advantage of simplicity because it can be used for non-palpable and multicentric tumors. Intradermal injection, however, has been associated with an increase number of SLNs harvested and with a greater possibility of retrieving four or more SLNs.(10)

Giuliano noted that the accuracy of SLNB improves with experience. In his initial experience, the ability to identify the SLN and false negative rates improved in the latter half of the study.(3) Most surgeons agree that a learning curve exists.

The American Society of Breast Surgeons guidelines suggests that 20 cases of SLNB with back up ALND with an identification rate of 85% and a false negative rate of less than 5% are recommended before abandoning ALND.(11)

Studies have shown that increasing the number of sentinel nodes removed may increase accuracy and decrease false negative rates. In the National Surgical Adjuvant Breast and Bowel Project (NSABP) B32 trial, the false negative rate was 17% for removal of 1 sentinel node, 10% for 2 nodes removed, 6.9% 243

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for 3 nodes removed, 5.5% for 4 nodes removed, and 1% for removal of 5 or more nodes.(12) Zakaria and colleagues evaluated how many sentinel nodes are enough in SLNB for breast cancer and found that 98% of patients with lymph node metastasis were identified by the third node and 100% by the fourth node.

They concluded that by terminating the procedure at the fourth node improved accuracy but also reduced the morbidity of the procedure(13). Chagpar and colleagues evaluated whether removing 3 sentinel nodes is sufficient. When SLNB was limited to 3 nodes, the false negative rate was 10.3% and therefore cannot be recommended.(14) While experienced surgeons would need to remove only one node for a successful SLNB, in general it is best advised that all blue nodes or nodes at the end of blue lymphatic channels, hot nodes or nodes with radioactive counts >10% of the hottest node and any palpably suspicious nodes should be removed.

SLNB has repeatedly been shown to be reproducible and feasible. The overall accuracy of SLNB from multiple studies is 97% - 98% with a false negative rate from 5.5% - 9.8%. SLNB has been shown to be safe with an incidence of serious allergy (to isosulfan blue) of <1% and 1.25% incidence of skin necrosis (with methylene blue).(15) The significance of SLNB for early stage breast cancer is directed by the histological diagnosis of the SLN which could either be negative, in keeping with the clinical assessment, or positive for harboring metastasis.

In patients with sentinel node-negative cancer, the obvious concern for the patient is whether they will suffer the risk of axillary recurrence having not had ALND. Giuliano and colleagues were the first to report a prospective study to evaluate the safety and feasibility of SLNB as a replacement for ALND in women with histopathologically node-negative cancer. A total of 133 women with breast cancer 4 cm or less and clinically negative nodes were entered into 244

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a trial of SLNB with vital blue dye. In 67 patients with histopathologically tumor free SLN, the SLNB was the only axillary procedure. Adjuvant systemic therapy was administered to 33 patients (49%). No axillary radiation was given. At a 39 month follow-up no local or axillary recurrence was noted. If non sentinel nodes harbored metastatic disease a higher rate of axillary recurrence rate should have been observed.(16) This conclusion is extrapolated from the landmark NSABP-04 study where the axillary recurrence rate after total mastectomy without radiation therapy was 18% with more than three-quarters developing axillary recurrence within the first twenty-one months.(17) This was the first study to evaluate SLNB as the only axillary procedure in patients with histopathologically node-negative cancer. It provided evidence that suggests that ALND is not required in these patients and that SLNB provided accurate staging without sacrificing axillary control.

Subsequent to this finding numerous studies indicated that SLNB provided excellent axillary staging and regional control in patients with early node-negative breast cancer. Veronesi and colleagues published a single institution phase 3 study with a ten year follow-up. A set of 516 patients with tumor up to 2cm were randomized to SLNB followed by ALND or SLNB only if SN is negative.

Only 2 cases of axillary recurrence were reported. Both cases occurred in the SLNB group (0.77%). There were a total of 49 breast cancer related events, 23 in the SLNB group, and 26 in the ALND group (P=0.52). There was no difference between the two groups with respect to disease free survival (89.9% in the SLNB group vs 88.8% in the ALND group). The overall survival was slightly greater in the SLNB arm (93.5%) compared with the ALND arm (89.7%) but this was not statistically significant.(18)

Zavagno and colleagues reported on 479 patients from five institutions with early stage breast cancer and negative sentinel nodes who had SLNB alone. No 245

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clinical axillary recurrence was found at a median follow-up of 35.8 months.

Interestingly a mean of 1.4 sentinel nodes were removed and about 90% of the patients received systemic therapy.(19)

In a Swedish Multicenter Cohort study by Bergkvist and colleagues 3534 patients with breast cancer less than 3 cm were prospectively studied. It was reported that 2246 patients had tumor free sentinel node and underwent SLNB alone. At a median follow-up of 37 months, 27 patients (1.2%) had axillary recurrence. Of these 27 patients, 13 had isolated axillary recurrence, 7 had axillary and local recurrence in the breast, and 7 had axillary and distant metastases.

An overall survival 92.1% and a disease free survival of 91.6% were reported.(20)

Researchers at the Memorial Sloan Kettering Cancer Center (MSKCC) reported their experience with 4008 consecutive SLNB. There were 326 patients with tumor free sentinel nodes who had ALND and 2340 patients with tumor free sentinel nodes who had SLNB only. At a median follow-up on 31 months, 0.12% axillary recurrence was reported in the SLNB group.(21)

A systematic review and meta-analysis of 48 studies with 14959 patients who were sentinel node negative and did not undergo ALND was reported by Van der Ploeg and colleagues. At a median follow-up of 34 months, 0.3% axillary failure rate was reported.(22)

The ACOSOG Z0010 trial is one of the largest trials of SLNB involving 5237 patients with clinically node-negative breast cancer. This is a prospective multicenter observational study to determine the clinical significance of sentinel node and bone marrow metastases. Patients underwent lumpectomy and sentinel node biopsy with bilateral iliac crest bone marrow aspiration. At a median follow-up of 31 months, axillary recurrence occurred in only 0.2% of the pa246

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tients with sentinel node negative cancer. SLNB alone provided regional nodal control when the sentinel node is histopathologically tumor free.(4). Potential explanations for fewer then expected axillary relapses may be because of incidentally received radiation therapy during whole breast irradiation and effect of systemic therapy.

The less extensive dissection of the axilla using the SLNB technique is appealing from the point of view of avoiding or decreasing the much reported postoperative complications of ALND. These include paresthesia, lymphedema, and decreased shoulder abduction. The purpose of the NSABP B-32 trial was to establish whether SLNB can achieve the same therapeutic goals as conventional ALND but with less morbidity. A total of 5611 women with clinically nodenegative operable breast cancer were randomized to SLNB followed by ALND or to observation if the sentinel node was tumor free. The overall survival, disease-free survival, and regional control were statistically equivalent between the groups. When the sentinel node is histologically tumor free, SLNB alone with no further ALND is an appropriate, safe and effective therapy for patients with clinically node-negative breast cancer. The shoulder abduction

deficit

greater than 10% peaked at 1 week for the ALND (75%) and SLNB (41%) groups. Arm volume difference of greater than 10% was seen at 36 months for the ALND (14%) and SLNB (8%) groups. The rate of numbness peaked at 6 months for the ALND (49%) and SLNB (15%) groups. These results indicate the superiority of SLNB with respect to surgical morbidity outcomes over a 3 year follow up period.(12)

Multiple other studies indicate the improved morbidity rates associated with SLNB compared with ALND (Table 1). It is important to note that while rates are decreased these complications do occur after SLNB and may significantly impact on the quality of life for some patients.

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TABLE 1

Veronesi et al22 ALMANAC23

ACOSOG Z001024 NSABP B-3212

Morbidity

SLNB ALND

SLNB ALND

SLNB ALND

Wound Infection

NR

NR

11%

15%

1%

Seroma

NR

NR

NR

NR

Parasthesias

1%

68%

11%

Lymphedema

0%

12%

5%

SLNB ALND

8%

NR

NR

7.1%

14%

NR

NR

31%

9%

44%

10%

36%

13%

7%

11%

8%

14%

Overall the trials outlined previously indicate that SLNB are as effective as level I and level II axillary dissection in providing local regional control for clinical stage 1 and stage 2 breast cancers. This together with decreased morbidity has been rewarded by recommendation by the 2012 NCCN guidelines as appropriate axillary treatment once an experienced SLNB team is available. For this subset of patients sentinel lymph node mapping and excision is sufficient for axillary treatment once the SN is histopathologically negative.(25)

The finding of the SLN which is positive for metastasis has not met with a simple treatment plan as the histologically negative node. In fact, this is currently a point of ongoing controversy. The traditional treatment following a positive SLNB is ALND. In patients with clinically node-negative disease, the SLN is the only involved node in 40-60% of patients, which raises the question as to whether ALND offers additional therapeutic benefits for all patients.(16)

Several studies have reported short term outcomes in patients with sentinel node positive cancer who did not undergo completion ALND. Park and colleagues evaluated 287 patients with SLN positive disease who did not undergo ALND at the MSKCC. This was an observational non-randomized study. Patients in the SLN positive with no ALND group were older (59 yrs vs 52 yrs, P<0.071) had more favorable tumors, were more likely to have breast conservation (68% 248

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vs 55%, P<0.001), and had marginally higher rates of axillary local recurrence (2% vs 4%, P=0.004) at 23 and 30 months follow-up when compared with the SLN positive and ALND group. In both groups half of all axillary recurrences occurred as the only site of disease recurrence, whereas the remainder of axillary recurrences was coincident with ipsilateral breast recurrence or with distant relapse.(26)

Naik and colleagues reported a 1.4% axillary recurrence rate at a median follow-up of 31 months in 210 patients with SLN positive cancer who declined ALND. In these patients the axillary recurrence was infrequent in those who had completion ALND and those who did not, 0.35% and 1.4% respectively.(21)

There are reports of the subset of patients with SLN positive cancer who were older, had smaller tumors, less frequent lymphovascular invasion and lower volume SLN metastases who did not undergo completion ALND and had a 0% axillary recurrence. Fant and colleagues performed a retrospective review of 31 patients with SLN positive cancer who declined ALND. Most primary tumors were T1. A total of 27 patients had microscopic (<2 mm) metastasis and 4 patients had macroscopic metastasis found in the sentinel nodes. No axillary recurrences were detected at a 30 month follow-up.(27) Gunther and colleagues studies 46 women with SLN metastases who did not undergo ALND. The mean age was 61.6 years, mean tumor size was 1.65 cm, and 87% of that patients had estrogen receptor positive tumor. Seven patients (15%) had macro-metastases (>2mm), 16 (35%) had micro-metastases and 23 (50%) had cellular metastases.

No axillary recurrence was observed and one patient developed distant metastases during a 32 month follow-up.(28)

The International Breast Cancer Study Group (IBCSG) 10-93 randomized 473 patients, 60 years or older with clinically node-negative cancer into primary 249

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surgery and ALND or surgery without ALND. Tamoxifen was given for five years in both groups. The median age was 74 years: 80% had estrogen receptor positive disease. The primary end point was quality of life reported by the patient and physician assessment. At a median follow-up of 6.6 years, ALND and no ALND groups yielded similar disease free survival (67 vs 66%) and similar overall survival (75 vs 73%). About 28% of patients in the ALND group had involved nodes. Axillary recurrence was seen in 1% of the ALND group and 3% of the no ALND group. This randomized study examined the option of avoiding axillary surgery altogether and demonstrated in older women with clinically node-negative breast cancer who received adjuvant tamoxifen, the quality of life can be improved without compromising disease free survival or overall survival29.

The ACOSOG Z0011 trial opened in 1999 with a plan to randomize 1900 patients with breast conservation treatment and 1-2 positive SLN. This study closed early and failed to meet targeted accrual. This was partly due to low event rate and reluctance to randomize SLN positive patients to ALND in the early 2000s. In this prospective study, all patients were required to have negative margins in the breast excision and went on to have whole breast irradiation.

Adjuvant treatment was per the primary team with 96% receiving chemotherapy and 47% endocrine therapy. The trial closed early because of low accrual reaching only 47% of its accrual goals (891 patients). Median follow up for the evaluable patients was 6.3 years. At 5 years the local recurrence rate was 1.6% in the SLNB group compared with 3.1% in the ALND arm. There was also no difference in 5 year disease-free survival (89.9% vs 88.8%). The authors concluded that for selected patients with node-positive breast cancer, and low volume axillary disease, and SLNB alone does not result in inferior survival or inadequate local control.(30) Differences in survival between the two groups seem unlikely to emerge. Of 250

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note the Z0011 trial did not include patients undergoing mastectomy without radiation treatment, accelerated partial breast irradiation or whole breast radiation in the prone position, which would exclude low axillary treatment. Also patients receiving neoadjuvant therapy were excluded from the study. Further randomized studies are needed to confirm and expand the findings of the Z0011 trial. Of note ER negative status, age less then 50, and lack of adjuvant systematic therapy were associated with decreased overall survival. Therefore based on these results, following sentinel node mapping and excision, if a patient has a T1 or T2 tumor, has 1-2 positive SLN, was not treated with neoadjuvant therapy, is undergoing breast conservation therapy, and whole irradiation is planned, the current NCCN guidelines suggest considering no further axillary surgery.(25)

While treatment pathways, following a positive or negative lymph node has been outlined previously, pathological evaluation of retrieved SLN has created some controversy. Various differences have been observed among national and international guidelines on handling SLNs published in the literature. A survey by the European Working Group for Breast Screening Pathology reported that 240 pathologists replying to a questionnaire described 123 different pathology protocols.(31) The enhanced pathologic assessment associated with the SLN has resulted in the identification of increasingly small deposits of metastatic disease and subsequent upstaging of cancer. Giulano et al demonstrated a 13% increase in node-positive cases in the SLN group compared with matched historical controls staged by axillary dissection. Thereafter several large studies have confirmed this finding. The American Joint Committee on Cancer Staging Systems has changed to reflect this and include three categories of nodal metastases:

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1)

Isolated tumor cells (no cluster greater than 0.2mm, pNO(i+))

2)

Micro-metastases (0.2 â&#x20AC;&#x201C; 2 mm, pNI(mi)

3)

Macro-metastases (p>2mm)

However, the clinical significance of these very small metastatic deposits is uncertain. In a retrospective study conducted by the International Breast Cancer Study Group, 9% of 921 patients who had negative axillary lymph nodes on routine H&E single-section analysis were found to be node positive on serial sectioning. In some but not all groups these women had significantly poorer 5 year disease-free and overall survival (33). In a review of the published literature 1997, Dowlatshahi analysed all large and long-term studies and confirmed a statistically significant decrement in survival associated with the presence of axillary node micro metastases.(34) In addition, the group at MSKCC has used serial sections and immunohistochemistry to re-evaluate all axillary lymph nodes from 373 patients operated in the 1970s who were deemed to be node-negative by routine histopathology. The presence of any detectable micro metastatic disease was associated with worse disease free and overall survival.(35) In a review of 1959 cases treated at the European Institute of Oncology from 1997 to 2000, Colleoni and colleagues have found that minimal involvement (micro metastases or isolated tumor cells) of a single lymph node correlated with decreased disease-free survival and doubled the risk of distant metastases.(36)

The Dutch Micrometastases and Isolated Tumor Cells: Relevant and Robust or Rubbish (MIRROR) trial was a retrospective analysis of 2756 patients who underwent a SLNB before 2006 and were found to have isolated tumor cells or micro-metastases in the regional lymph nodes. They compared outcomes for 856 patients with node-negative disease and no systemic therapy with patients with isolated tumor cells or micro-metastases who did (N=995) and did 252

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not (N=856) receive systemic therapy. Disease free survival was poorer in patients with either isolated tumor cells or micro-metastases in the SLN (76.5% vs 85.7%; p<0.001), suggesting these small tumor deposits have some prognostic significance. However, this study included contra-lateral breast cancer in the definition of a disease “event” (accounting for 29% of events). Because the development of contra-lateral breast cancer is unlikely to be related to the presence of micro-metastatic axillary disease, this definition makes these findings difficult to interpret.(37)

This situation has been addressed prospectively in the ACOSOG Z0010 trial and the NSABP B32 trial. In ACOSOG Z0010, routine immunohistochemistry (IHC) was performed on SLN specimens to increase identification of isolated tumor cells and micro-metastases. In this study, no difference in 5 year overall (95.7% vs 95.1%) or disease free (92.2% vs 90.4%) survival was observed between patients with node-negative vs IHC positive SLNs.(38) Similarly, NSABP B32 performed IHC staining in all SLNs found to be negative on initial processing. No difference in overall of disease free survival was observed in patients with IHC detected metastases vs true negative SLNs.(39) Based on these recent findings the NCCN panel does not recommend routing cytokeratin IHC to define node involvement and believes that current treatment decisions should be based solely on H&E staining.(25)

While there is better guidance and wider acceptance for SLNB in T1-3 tumors, there are several clinical situations that warrant special consideration.

□ Inflammatory breast cancer is a relative contraindication to SLNB. Subdermal lymphatic invasion may inhibit migration of lymphatic mapping substrate, decreasing the accuracy in a patient population that has a 55-85% incidence of clinical positive node-positive disease.

253

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. Stearns and colleagues in their study of SLNB in locally advanced

and inflammatory breast cancers reported an identification rate of 75% with a false negative rate of 25% in the inflammatory breast cancer subgroup(41). Given the higher false negative rates, and lower identification rate consensus guidelines do not recommend SLNB in this group of patients.(15) â&#x2013;Ą Neoadjuvant chemotherapy is an accepted initial treatment of patients with large breast cancers who wish to undergo breast conservative surgery and for those with locally advanced breast cancer. Downstaging of the tumor occurs in most patients with 26% to 50% achieving a pathologic complete response to neoadjuvant chemotherapy.(42,43) Because this response occurs in the primary tumor and the nodal basin, it makes the timing of SLN mapping for patients undergoing neoadjuvant chemotherapy controversial.

The greatest benefit to performing SLNB before neoadjuvant chemotherapy is to allow for accurate staging of the axilla at the time of diagnosis. This information provides not only prognostic information but can be used to inform decisions for adjuvant radiation. However this approach requires patients to undergo two separate surgical procedures and if the pre-treatment SLN is found to be positive, commits them to an ALND regardless of the response to neoadjuvant therapy. In contrast, post neoadjuvant SLN biopsy accounts for patient response to chemotherapy and theoretically can spare patients with a good response an ALND. However, lower rates of SLN identification and increased false negative rates make the accuracy of post neoadjuvant therapy SLN biopsy uncertain.(44) â&#x2013;Ą It is estimated that 10% to 20% of patients diagnosed with DCIS are found to have occult invasive disease. Routine axillary staging is not required for pure DCIS unless a total mastectomy or an excision that 254

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may compromise future performance of SLNB is planned. Some researchers advocate SLNB with high grade, high volume disease or micro-invasion seen on core biopsy. If metastatic disease is found on SLNB in what was presumed to be pure DCIS, the disease is upstaged to reflect the nodal involvement and treated accordingly.(25) â&#x2013;Ą Prior axillary surgery is a relative contraindication to SLN biopsy because lymphatic drainage may be disrupted, possibly leading to an inability to identify an SLN or an increased false negative rate. The largest study examining this has been published from the MSKCC, looking at their experience with 117 patients with breast cancer undergoing re-operative SLN after a prior SLN biopsy or an ALND. The SLN was successfully identified in 55% of patients. Likelihood of successful mapping was higher after a previous SLN biopsy (74%) than after an ALND (38%). Of the 63 patients with successful mapping, 30% (N=19) had a non-axillary draining site identified: 8 had ipsilateral axillary drainage in addition to a second site, whereas 11 had only non axillary drainage. At a median 2.2 years of follow-up no axillary recurrences were observed. The conclusion drawn was that an SLN can be identified in most patients who have had prior axillary surgery, albeit in a lower rate than for initial SLN biopsies.(45) The effect of previous breast or axillary surgery on the accuracy of SLNB remains unclear and there is insufficient data to make any recommendations for or against SLNB in these patients. â&#x2013;Ą Multicentric breast disease is another controversial entity. The obvious concern regarding multicentric breast disease is that multiple tumors within the breast may drain to different SLNs, making an SLNB unreliable. Several retrospective studies have addressed this question and found the SLN identification rate to exceed 95%. False negative rate (confirmed by backup ALND) was 8.8% in a retrospective re255

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view of the ALMANAC trial and 8% in a large single institution study by the MSKCC.(46,47) An axillary recurrence rate of 0% was reported in a study of 142 patients of a median follow up of 28.8 months.(48).

Although these retrospective studies suggest that SLN could be an alternative to ALND in patients with multicentric breast cancer, larger prospective patient studies with longer follow up are needed to confirm the efficacy of SLN biopsy in this setting.

Much like the shift away from radical mastectomy procedures for all patients with breast cancer clearly the current trends are to perform less radical procedures in the axilla. The NSABP 04 trial indicated that tumor biology was different for some patients and that less extensive surgery with or without radiation therapy was as effective as radical (Halsted) mastectomy. A total of 1079 women with clinically negative axillary nodes underwent radical mastectomy, total mastectomy, without axillary dissection but with post operation irradiation, or total mastectomy with axillary dissection only if their nodes became positive.

Interestingly, no significant differences were observed among the three groups of women with respect to disease free survival, relapse-free survival, distantdisease-free survival, or overall survival, even after 25 years of follow up.(49)

The evidence as outlined previously indicates that SLNB can avoid formal ALND in a subgroup of patients with a clinically negative axilla. In particular, even patients with metastatic SLN may be spared the morbidity of ALND after the ACOSOG Z-0011, which is as yet still a point of debate. To determine which patients may benefit from further axillary surgery after the identification of a positive SLN some researchers at several institutions have developed normograms to calculate the likelihood of additional non SLNs being positive. The most recent normogram from the MD Anderson Cancer Center includes clinicopathological data: age, tumor size, histology, grade, presence of multifocal 256

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disease, ER, PR, and HER2-neu status, presence of lymphovascular invasion, number of SLN identified, number of positive SLN, maximum SLN metastasis size, and the presence of extra nodal extension. The following factors were predictive of positive non SLNs: the number of SLN identified, number of positive SLN, SLN metastasis size, extra nodal extension, tumor size, lymphovascular invasion and histology. Based on this research, normograms can be used to inform patient discussion on whether to consider completion ALND or not.(50)

Axillary node sampling is another potentially less morbid procedure than ALND which may allow for axillary staging. Axillary nodal sampling is the removal of an axillary node/s from the lower axilla without defining precise anatomic boundaries. Kissen et al showed that sampling failed to identify 8% of patients with lymph node metastases and failed to obtain a specimen with identifiable lymph nodes in another 10% of patients. Forrest et al removed pectoral nodes near the tail of the breast and reported metastases detection rates similar to those in radical mastectomy specimens. However, 25% of the sampling procedures did not yield lymph nodes and 10.5% of patients whose pectoral nodes were not identified or were identified as involved with tumor developed regionally recurrent disease.(52) These unguided methods clearly are suboptimal as a means of axillary staging.

CONCLUSION: The SLNB technique helps to identify specific lymph nodes draining primary breast cancer. Excision of these lymph nodes is associated with low morbidity and has been shown by several researchers to be accurate in staging the axilla.

It is now accepted that for early stage breast cancer (cT1-T3, NOMO) if the SLN is tumor free then formal ALND could be avoided. This approach may be extended for a highly selective group (T1-2, 1-2 positive SLN, was not treated with neoadjuvant therapy, is undergoing breast conservation therapy and whole 257

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breast radiation is planned) when the SLN is positive for tumor. As improved breast cancer screening allows identification of early-stage disease localized to the breast and because treatment plans are more often made on the basis of tumor biology, the role of completion ALND may be less critical.

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REFERENCES 1. Giuliano AE, Kirgan DM, Guenther JM, et al. Lymphatic mapping and sentinel lymphadenectomy for breast cancer. Ann Surg 1994; 220:391–401.

2. Morrow M, Rademaker AW, Bethke KP, et al. Learning sentinel node biopsy: results of a prospective randomized trial of two techniques. Surgery 1999; 126: 714–20.

3. Meyer-Rochow GY, Martin RC, Harman CR. Sentinel node biopsy in breast cancer: validation study and comparison of blue dye alone with triple modality localization. ANZ J Surg 2003; 73: 815–8.

4. Posther K, McCall LM, Blumencranz PW, et al. Sentinel node skills verification and surgeon performance data from a multicenter clinical trial for early-stage breast cancer. Ann Surg 2005;242:593–602.

5. Grube BJ, Giuliano AE. Sentinel lymph node dissection. In: Harris JR, Lippman ME,Morrow M, et al, editors. Disease of the breast. 4th edition. Philadelphia: Lippincott Williams &Wilkins; 2010. p. 547.

6. Nathanson SD, Wachna DL, Gilman D, et al. Pathways of lymphatic drainage from the breast.

Ann Surg Oncol 2001;8:837–43.

7. Povoski SP, Olsen JO, Young DC, et al. Prospective randomized clinical trial comparing intradermal, intraparenchymal, and subareolar injection routes for sentinel lymph node mapping and biopsy in breast cancer. Ann Surg Oncol 2006;13:1412–21.

8. Rodier JF, Velten M, Wilt M, et al. Prospective multicentric randomized study comparing periareolar and peritumoral injection of radiotracer and blue dye for the detection of sentinel lymph node in breast sparing procedure: FRANSENODE trial. J Clin Oncol 2007; 25: 3664–9.

9. Chagpar A, Martin RC, Chao C, et al. Validation of subareolar and periareolar injection techniques for breast sentinel lymph node biopsy. Arch Surg 2004; 139:614–20.

10. Chagpar AB, Carlson DJ, Laidley AL, et al. Factors influencing the number of sentinel lymph nodes identified in patients with breast cancer. Am J Surg 2007;194:860–4.

11. Lyman G, Giuliano AE, Somerfield M, et al. American Society of Clinical Oncology Guideline recommendations for sentinel lymph node biopsy in early-stage breast cancer. J Clin Oncol 2005; 23: 7703–20.

12. Krag DN, Anderson SJ, Julian TB, et al. Technical outcomes of sentinel-lymph-node dissection in patients with clinically node-negative breast cancer: results from the NSABP B-32 randomized phase III trial. Lancet Oncol 2007;8:881–8.

13. Zakaria S, Degnim AC, Kleer CG, et al. Sentinel lymph node biopsy for breast: how many nodes are enough? J Surg Oncol 2007; 96: 554–9.

14. Chagpar AB, Scoggins CR, Martin RC 2nd, et al. Are 3 sentinel nodes sufficient? Arch Surg 2007; 142: 456–60.

15. Williams RT, Winchester DP, Yao K, et al. Who should have or not have an axillary node dissection with breast cancer? Advances in Surgery 2012; 46: 1-18.

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16. Giuliano AE, Haigh PI, Brennan MB, et al. Prospective observational study of sentinel lymphadenectomy without further axillary dissection in patients with sentinel node-negative breast cancer. J Clin Oncol 2000; 18: 2553–9.

17. Fisher B, Jeong JH, Anderson S, et al. Twenty-five-year follow-up of a randomized trial comparing radical mastectomy, total mastectomy, and total mastectomy followed by irradiation.

N Engl J Med 2002; 347(8): 567–75.

18. Veronesi U, Viale G, Paganelli G, et al. Sentinel lymph node biopsy in breast cancer: ten year results of a randomized controlled study. Ann Surg 2010; 251(4): 595–600.

19. Zavagno G, Carcoforo P, Franchini Z, et al. Axillary recurrence after negative sentinel lymph node biopsy without axillary dissection: a study of 479 breast cancer patients. Eur J Surg Oncol 2005; 31: 715–20.

20. Bergkvist L, de Boniface J, Jonsson P-E, et al. Axillary recurrence rate after negative sentinel node biopsy in breast cancer. Three-year follow-up of the Swedish multicenter cohort study.

Ann Surg 2008; 247(1): 150–6.

21. Naik AM, Fey IV, Gemagnani M, et al. The risk of axillary relapse after sentinel lymph node biopsy for breast cancer is comparable with that of axillary lymph node dissection: a follow up of 4,008 procedures. Ann Surg 2004; 240: 462–71.

22. Veronesi U, Paganelli G, Viale G, et al. A randomized comparison of sentinelnode biopsy with routine axillary dissection in breast cancer. N Engl J Med 2003; 349: 546–53.

23. Mansel RE, Fallowfield L, Kissin M, et al. Randomized multicenter trial of sentinel node biopsy versus standard axillary treatment in operable breast cancer: the ALMANAC Trial.

J Natl Cancer Inst 2006;98:599–609.

24. Lucci A, McCall LM, Beitsch PD, et al. Surgical complications associated with sentinel lymph node dissection (SLND) plus axillary lymph node dissection compared with SLND alone in the American College of Surgeons Oncology Group Trial Z0011. J Clin Oncol 2007; 25: 3657–63.

25. National Comprehensive Cancer Network practice guidelines in oncology–V.1.2012.

Available at: http://www.nccn.org/professionals/physician_gls/PDF/breast.pdf. Accessed February 1, 2012.

26. Park J, Fey JV, Naik AM, et al. A declining rate of completion axillary dissection in sentinel lymph node-positive breast cancer patients is associated with the use of a multivariate nomogram. Ann Surg 2007; 245:462–8.

27. Fant JS, Grant MD, Knox SM, et al. Preliminary outcome analysis in patients with breast cancer and a positive sentinel lymph node who declined axillary dissection. Ann Surg Oncol 2003; 10:126–30.

28. Guenther JM, Hansen NM, DiFronzo LA, et al. Axillary dissection is not required for all patients with breast cancer and positive sentinel nodes. Arch Surg 2003; 138:52–6.

29. International Breast Cancer Study Group. Randomized trial comparing axillary clearance versus no axillary clearance in older patients with breast cancer: first results of international breast cancer study group trial 10–93. J Clin Oncol 2006; 24(3): 337–44.

30. Giuliano AE, McCall L, Beitsch P, et al. Locoregional recurrence after sentinel lymph node

260

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31. Cserni G, Amendoeira I, Apostolikas N, et al. Discrepancies in current practice of pathological evaluation of sentinel lymph nodes in breast cancer. Results of a questionnaire based survey by the European Working Group for Breast Screening Pathology. J Clin Pathol 2005; 57: 695–701.

32. Giuliano AE, Dale PS, Turner RR, et al. Improved axillary staging of breast cancer with sentinel lymphadenectomy. Ann Surg 1995; 180:700–4.

33. International (Ludwig) Breast Cancer Study Group. Prognostic importance of occult axillary lymph node micrometastases from breast cancers. Lancet 1990; 335: 1565–8.

34. Dowlatshahi K, Fan M, Snider HC, et al. Lymph node micrometastases from breast carcinoma: reviewing the dilemma. Cancer 1997; 80: 1188–97.

35. Tan LK, Giri D, Panageas K, et al. Occult micrometastases in axillary lymph nodes of breast cancer patients are significant: a retrospective study with long-term follow-up (abstract). Proc Am Soc Clin Oncol 2002;21:37.

36. Colleoni M, Rotmensz N, Peruzzotti G, et al. Size of breast cancer metastases in axillary lymph nodes: clinical relevance of minimal lymph node involvement. J Clin Oncol 2005;23: 1379–89.

37. de Boer M, van Deurzen CH, van Dijck JA, et al. Micrometastases or isolated tumor cells and the outcome of breast cancer. N Engl J Med 2009;361: 653–63.

38. Giuliano AE, Hawes D, Ballman KV, et al. Association of occult metastases in sentinel lymph nodes and bone marrow with survival among women with earlystage invasive breast cancer. JAMA 2011; 306:385–93.

39. Weaver DL, Ashikaga T, Krag DN, et al. Effect of occult metastases on survival in nodenegative breast cancer. N Engl J Med 2011; 364: 412–21.

40. Singletary SE. Surgical management of inflammatory breast cancer. Semin Oncol 2008; 35(1):72–7.

41. Stearns V, Ewing CA, Slack R, et al. Sentinel lymphadenectomy after neoadjuvant chemotherapy for breast cancer may reliably represent the axilla except for inflammatory breast cancer. Ann Surg Oncol 2002; 9(3): 235–42.

42. Gianni L, Eiermann W, Semiglazov V, et al. Neoadjuvant chemotherapy with trastuzumab followed by adjuvant trastuzumab versus neoadjuvant chemotherapy alone, in patients with HER2-positive locally advanced breast cancer (the NOAH trial): a randomised controlled superiority trial with a parallel HER2-negative cohort. Lancet 2010; 375:377–84.

43. Mauri D, Pavlidis N, Ioannidis JP. Neoadjuvant versus adjuvant systemic treatment in breast cancer: a meta-analysis. J Natl Cancer Inst 2005; 97: 188–94.

44. Mamounas EP, Brown A, Anderson S, et al. Sentinel node biopsy after neoadjuvant chemotherapy in breast cancer: results from National Surgical Adjuvant Breast and Bowel Project Protocol B-27. J Clin Oncol 2005; 23: 2694–702.

45. Port ER, Garcia-Etienne CA, Park J, et al. Reoperative sentinel lymph node biopsy: a new frontier in the management of ipsilateral breast tumor recurrence. Ann Surg Oncol 2007; 14: 2209–14.

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46. Port ER, Garcia-Etienne CA, Park J, et al. Reoperative sentinel lymph node biopsy: a new frontier in the management of ipsilateral breast tumor recurrence. Ann Surg Oncol 2007;14:2209–14.

47. Tousimis E, Van Zee KJ, Fey JV, et al. The accuracy of sentinel lymph node biopsy in multicentric and multifocal invasive breast cancers. J Am Coll Surg 2003;197: 529–35.

48.Knauer M, Konstantiniuk P, Haid A, et al. Multicentric breast cancer: a new indication for sentinel node biopsy: a multi-institutional validation study. J Clin Oncol 2006;24:3374–80.

49. Fisher B, Jeong JH, Anderson S, Bryant J, et al. Twenty-five-year follow up of a randomised trial comparing radical mastectomy, total mastectomy and total mastectomy followed by irradiation. N Engl J Med 2002; 347(8): 567-575.

50. Mittendorf EA, Hunt KK, Boughey JC, et al. Incorporation of sentinel lymph node metastasis size into a nomogram predicting nonsentinel lymph node involvement in breast cancer patients with a positive sentinel lymph node. Ann Surg 2012;255: 109–15.

51. Kissin MW, Thompson EM, Price AB, et al. The inadequacy of axillary sampling in breast cancer. Lancet 1982; 1:1210-1212.

52. Forrest A, Roberts M, Cant E, Shivas A. Simple mastectomy and pectoral node biopsy. Br J Surg 1976; 63:569-575.

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15. RECTAL CANCER

Development of neoadjuvant radiation and the challenge of recurrence in low rectal cancer.

INTRODUCTION Colorectal cancer is a major cause of morbidity and mortality throughout the world. It is the third most common cancer worldwide and the fourth most common cause of cancer related deaths. Of these cancers, 70% will arise in the colon whereas 30% will occur in the rectum. At diagnosis, approximately 25% of colon cancers are noted to have local extensions through the muscularis of the bowel wall. In contrast, 50% of cancers in the rectum exhibit this progression, with lymph node metastases seen in approximately two thirds of these cases.

The main stay of treatment for patients who have rectal cancer has been curative surgical resection with emphasis on minimizing morbidity and mortality.

Achieving local control of the disease and improving overall survival has been the challenge of rectal cancer. Refinement in surgical techniques i.e. TME (total mesorectal excision) has allowed improvement in outcomes in patients with resectable cancer.

Research has provided a greater understanding of the natural history of rectal cancer and pattern of recurrence. More precise histopathologic reporting have helped to define patients who have a high risk for local recurrence and disease progression after attempted curative resection.

The importance of identifying this group of patients is that, it allows for the selection of treatment options such as adjuvant therapy (radiation and/or chemotherapy) and neoadjuvant therapy.

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Several researchers have identified that for preoperatively identified locally advanced rectal cancer, neoadjuvant therapy is more beneficial. Further research has invested in defining the most appropriate sequence and composition of chemotherapy or radiation therapy regimes. Both short course preoperative and long course preoperative therapy have demonstrated benefits in improving resectability and local recurrence rates. However, there is continuing debate regarding which of these two approaches is more appropriate.

Multimodal therapy is now common place for the treatment of rectal cancer.

The benefits of adjuvant and neoadjuvant treatment strategies have now become better defined and afford more options for the treatment of these patients. Three cases of rectal cancers are described, each requiring an abdominoperineal resection of the rectum.

A discussion follows which explores the development of surgical and radiation therapies in the treatment of rectal cancer. It also includes a comment on the challenge of local recurrence in relation to low rectal cancer and abdominoperineal resection in the current era.

CASE 1 History: A 71 year old woman presented with a 3 month history of bright red per rectal bleeding. This occurred with defecation and was painless. The blood was noted in the toilet bowl and on wiping, but there was no dripping or squirting. Her normal bowel actions were once daily but the patient noted an increase frequency of 3 motions per day in recent weeks.

Otherwise she had no symptoms of anemia or constitutional symptoms. This patient was a devout Muslim, and was never married or had children. She ran a cafĂŠ with her sister.

In her previous history she had a lumpectomy on the right breast 20 years ago 264

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and this was benign. There was no family history of cancer.

Physical examination: A healthy looking lady with normal vital signs. Her mucous membranes were pink and moist. Abdominal examination was normal but DRE revealed an ulcerated 3-4cm lesion in a postero-lateral location 4-5cm from the anal verge.

This was confirmed on rigid sigmoidoscopy and biopsies were taken.

The histology revealed a moderately differentiated adenocarcinoma.

Investigations: Hb 11 g/dl, WCC 6 x 103/Âľl, Plts 238 x 103/Âľl. Renal function and liver function tests were normal. CEA 3 ng/ml Colonoscopy revealed a normal proximal colon.

Staging CT: No distant metastases were noted.

MRI (pelvis and anorectum): There was irregular circumferential thickening of the wall of the distal third of rectum. The mesorectal fascia was breached at left posterolateral aspect. Elsewhere the fascial planes were maintained. The tumor appeared up to fascial level. (Fig 1)

Following the recommendations of the MDT this patient had Neoadjuvant therapy (XELOX x 6 cycles, Radiotherapy 25cycles of 1.8Gy).

Repeat staging revealed no distant metastases on CT and a complete radiological response to therapy on MRI (see Fig 2). On examination 2 pea sized nodules were noted at 5cm from the anal verge in a postero-lateral location (ycT2NOMO).

An abdominoperineal resection of the anorectum was performed. The patient did well postoperatively and was discharged on day 13.

The histology of the resected specimen was described as moderately differen265

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tiated adenocarcinoma with invasion to pericolic fat. One satellite nodule in pericolic fat. Maximum tumour dimension of 1.7cm. No definite LN identified. (ypT3N0M0) After 2 years of follow up the patient continues to do well, her CEA 1.19ng/ml and surveillance CT showed no metastatic or recurrent disease.

CASE 2 History: A 48 year old man was admitted as an emergency with a history of peri-anal pain and anal discharge. This was present for the past 5 days. He reported no previous history of anal/rectal problems. Of note he had noticed blood admixed with his stool for about 3 months.

Systematic enquiry revealed weight loss of about 13kgs. He felt tired on most days and his diet was normal. He smoked a pack of cigarettes/ day for the past 20 years. He had no chronic illnesses and had no known history of colorectal cancer.

Physical examination: This gentleman appeared cachectic. His mucus membranes were pale. His pulse was 110 min-1 and temperature 378 0C. He had no clinically palpable lymph nodes. Cardiorespiratory systems were otherwise normal. The abdomen appeared scaphoid and the umbilicus normal. There was no organomegaly or ascites. DRE revealed perianal induration and bilateral fluctuation. A mass was palpable internally at 4cm.

Investigations: Hb 7.8g/dl, WCC 15 x 103/ l, Plts 340 x 103 /Âľl, BUN 32 mg/dl, Cr 1.4 mg/dl, Na 132 mmol-1, K 5.1 mmol-1, HIV negative.

CXR: normal.

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The patient was resuscitated and consented for an examination under anesthesia, rectal biopsy and sigmoid loop colostomy. At surgery a horseshoe perianal abscess was incised and drained. The previously palpated tumor occupied the right half of the rectal circumference 4cm from the anal verge and appeared fixed. Rigid sigmoidoscopy revealed the proximal extent to be 8cm but the mucosa was otherwise normal to 19cm. A sigmoid loop colostomy was fashioned.

Histology confirmed a rectal adenocarcinoma. His CEA level was 26.9 ng/ml.

CT scan of the abdomen and pelvis showed no distant metastases. An MRI done for local staging described an intermediate signal intensity mass noted 1.5cm from the anal verge. There was extension of tumor through the posterior and right lateral rectal muscularis mucosa. The levator muscles on the right appeared invaded by tumor which extended into the right ischio-anal fossa. (cT4N0M0) Following the MDT he was sent for neoadjuvant chemoradiotherapy (XELOX x 2cycles and then concurrent Xeloda with radiotherapy 1.8 Gy x 25 fractions).

Therapy was completed 9 months later and the patient reassessed. His CEA level was 5.5 ng/ml. On DRE a tumor was palpated 4 cm from the anal verge.

The deeper tissues gave the impression of increased density and coarse texture.

Post-neoadjuvant staging showed no distant metastases on CT. MRI revealed thickening of the walls of the mid to lower rectum with extension into the upper one third of the anal canal. There was still abnormal signal noted on the right side posteriorly which appeared beyond the muscularis propria and serosa with thickening of the levator ani muscle. (cT4N0M0) A sinus tract extended through the sphincter on the right leading to the right ischioanal fossa.

An extended APR was performed with a VRAM (vertical rectus abdominus muscle) flap for perineal coverage. (see Fig 3,4,5) He did well postoperatively and was discharged after 3 weeks. He suffered no complications.

The gross resected specimen revealed that the lower rectum showed a constrict267

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ing ulcerating tumor approximately 4cm with bowel wall invasion. Microscopic examination showed a moderately differentiated adenocarcinoma which penetrates to the muscularis propria. The circumferential margins were clear. There was no lymphovascular permeation and 0 of 6 lymph nodes were negative for tumor. (pT2N0M0)

This gentleman continued with XELOX x 4 cycles postoperatively and after 1 year has been doing well with no evidence of local or distant disease.

CASE 3 History: A 53 year old woman presented with a seven week history of per rectal bleeding. The bleeding was bright red and accompanied each bowel action. She also developed an increased stool frequency, pencil shaped stool, tenesmus and pain on defecation. Systematic enquiry was otherwise non-contributory. She suffered no chronic illnesses and had two caesarean sections. She had no family history of gastrointestinal cancers.

Physical examination: A comfortable, but anxious lady; her vital signs were normal, her mucus membranes pink.

Her cardiorespiratory systems were clinically normal. Examination of her abdomen revealed no abnormalities. However on DRE a sessile lesion was palpated along the right lower rectum about 2cm from the anal verge. It extended from 6 oâ&#x20AC;&#x2122;clock to 10 oâ&#x20AC;&#x2122;clock along the bowel circumference. Vaginal examination was normal.

Rigid sigmoidoscopy was possible to 20cm. There was no other pathology and biopsies were taken. The histology of the biopsy specimen reported an invasive 268

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adenocarcinoma.

Colonoscopy was possible to the caecum and no synchronous lesions were present. A staging CT showed no metastatic disease but of particular importance was that there was no distortion of pelvic tissue or perirectal fascia. There was no evidence of lymphadenopathy.

MRI was not available and the patient could not afford at this time. Based on the clinical examination and CT the stage was probably T 2 or T3.She was advised to consider neoadjuvant radiotherapy in light of this. The patient declined and preferred to have surgery and then decide on the need for adjuvant therapy.

An APR was performed and the patient did well. Histology described a moderatley differentiated invasive adenocarcinoma. The greatest dimension of the tumor was 4 cm. The tumor extended into the muscularis propria. Proximal, distal and deep margins were all negative for tumor. There was no lymphovascular invasion and 0 of 12 nodes were involved. (pT2N0M0). As this was stage 1 disease no adjuvant therapy was required. After 4 months of follow up she was well. (see Fig 6)

Fig 1: Irregular circumferential thickening of lower rectum with tumor: note the posterolateral extension

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Fig 2: MRI post neoadjuvant therapy: fascial planes undisturbed with clear rectal margins.

Fig 3: The perineal excision marked to include the fistulous track and wide perianal excision

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Fig 4: The pelvic dissection was taken up through the ischiorectal fossa to the levator ani origins; the levators were excised with the specimen. Note the wide defect created. This was closed with a VRAM.

Fig 5: The APR specimen; note the cylindrical shape of the perineal aspect of the specimen.

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Fig 6:Tumour in the lower third of the rectum (pT2)

DISCUSSION Colorectal cancer is a major cause of morbidity and mortality throughout the world. It accounts for 9% of all cancers, representing the third most common cancer and the fourth most common cause for cancer related deaths. Globally, over one million new cases were recorded in 2002. The countries noted to have the highest rates were Australia, New Zealand, Canada, the United States of America and parts of Europe. The countries with the lowest risks include China, India and parts of Africa and South America.(1) Data produced by the National Cancer Registry of Trinidad and Tobago in 2002, indicated colorectal cancer was the third common site of cancer with an incidence of 8.5% and mortality rate of 16.4%.(2)

Rectal cancer accounts for 30% of colorectal cancer.(3) At diagnosis, 25% of colon cancers are noted to have local extension through the muscularis of the 272

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bowel wall. In contrast, 50% of cancers in the rectum exhibit this progression, with lymph node metastases seen in approximately two thirds of these cases.(4) There exist some variability in defining the junction between the colon and rectum. A National Cancer Institute consensus panel recommended that the colon be defined as greater than 12cm and the rectum as 12cm or less from the anal verge, using rigid proctoscopy. This allows for assigning of patients to different treatment pathways. It has been observed that cancers located above 12cm behave like colon cancers with respect to recurrence patterns and prognosis.(5)

Several anatomic considerations also distinguish rectal cancer from those that occur in the colon. The extraperitoneal rectum resides within the narrow and bony confines of the pelvis. This makes surgical resection more difficult. Additionally, the absence of serosa below the peritoneal reflection facilitates deeper tumor growth in the perirectal fat. This may contribute to higher rates of locoregional failure.(6)

During the nineteenth century, rectal cancer was largely treated by perineal excision and a preliminary sigmoid colostomy. At the beginning of the twentieth century, W. Ernest Miles introduced the concept that the high local recurrence rate of 95% was related to the inability of the surgeon to completely excise the involved mesorectal nodes. He indicated that these were proximal to the primary tumor, and therefore beyond the surgeonâ&#x20AC;&#x2122;s reach. The abdominal perineal excision (APER) was designed to achieve the en bloc resection of the primary tumor, its direct extensions and the proximal or regional spread to lymph nodes residing in the mesorectum or the mesentery of the pelvic colon. Gabriel et al demonstrated that the pathologic premise of Mr Milesâ&#x20AC;&#x2122; APER was clinically correct with reported five year survival figures being 30% for lymph nodes positive resections versus only 17.9% for the perineal excisions.(7)

In 1939, Claude Dixon of the Mayo Clinic introduced the anterior resection for 273

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cancers of the rectum and recto sigmoid.(8) Experience with sphincter preservation grew and many others have contributed both cancer related and technical advances and refinements, striving for improved cancer results with fewer post operative complications or consequences. They also advocated for blunt or manual presacral pelvic dissection as the technique of choice for the resection of rectal cancer. The major cancer related risk of such dissection is violation of the mesorectum along undefined anatomic planes. This results in the residual mesorectum containing cancer within the pelvis. Worldwide local recurrence rates (LRR) of 30-40% were the norm and distant metastases affected 60-65% of node positive patients. (9) Impotence due to pelvic autonomic nerve damage was reported in 50-85% of male patients.

(10)

Neither from an oncologic nor

from a functional or a quality of life standpoint were these rewarding outcomes.

In 1986, Quirke and colleagues identified the cause of most local recurrences as the result of inadequate resection, particularly of tumor involving the circumferential margins of resection (CRM). They examined the specimens of 52 cases of primary rectal cancer undergoing conventional resection. These patients were thought to have undergone curative resections. Unsuspected CRM involvement was noted in 14 (27%) of specimens with visible gouges or carved out areas also present. This resulted from manual violation of the mesorectum caused by blunt dissection. During follow up, 12/14 (85%) went on to develop local pelvic recurrences.(11) Birbeck et al reported on 568 cases, the CRM was involved in 165/568 resected specimens. Overall LRR was 17.9%, but when the CRM was positive, 63/165 patients (38.2%) developed a local recurrence. However, when the CRM was negative, only 42/421 patients (9.98%) developed a local recurrence. (12) Ng and associates reported that histologically proven CRM status was also found to be a significant predictor of survival. Follow up of the patients studied by Quirke et al, revealed that 5 year survival and local recurrence free survival was 72% and 84% for CRM negative patients.

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For CRM positive patients, the results were 29% and 38% respectively.

(13)

Several studies have confirmed that inadequate circumferential margins of resection are responsible for local recurrences. In addition, negative circumferential margins of resection are essential to the prevention of local or pelvic recurrences. On account of this evidence and several studies on patterns of lymph node distribution in rectal cancer, several researchers investigated the role of sharp pelvic dissections along anatomic planes. They specifically addressed oncologic clearance and autonomic nerve function and this resulted in the surgical procedure called Total Mesorectal Excision (TME).

In 1993, Mc Farlane and colleagues published their land mark paper on the outcomes of TME in 171 high risk patients who would have qualified for postoperative adjuvant radiotherapy after conventional surgery at a cooperative group based at the Mayo clinic. In a retrospective analysis, Mc Farlane studied their consecutive patients with stages ≥ pT3, N0, or N1/N2 disease from 0 to 15cm from the anal verge, undergoing TME without radiation. The LRR for these patients was 5% and the rate of distant metastases was 22%. When compared with the results of patients undergoing conventional surgery, the LRR was 25% and distant metastasis was 62.7% with adjuvant radiation.

(14)

TME has independently evolved along more or less parallel pathways in the UK and the USA. The concept of TME was first introduced by Heald at the North Hampshire hospital in Basingstoke in 1979. By using sharp dissection under direct vision, a relatively bloodless plane is followed along the outer surface of the rectum. This technique ensures a specimen with intact mesorectum with negative tumor margins in the majority of resectable (mobile) rectal cancers.(15) Heald’s first series of 122 curative anterior resections showed a cumulative risk of local recurrence at five years of 2.7% and overall survival of 87.5% at five years.(16) These excellent results were matched in Enker’s personal series of 246 curable 275

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Dukes’ stage B and C patients of which only 18 developed a local recurrence. The actuarial cancer specific 5 year survival was 74.2%. (17) Aitken published a study on a series of 64 patients. These patients underwent a curative TME procedure and only one patient (1.6%) developed a local recurrence.

(18)

Standardization

of the techniques and its subsequent implementations has globally revealed low recurrence rates after TME of resectable tumors of the rectum. In the 3 cases described APR was performed with dissection according to TME using diathermy.

Local recurrence is a serious problem in the treatment of rectal cancer. It causes severe disabling symptoms that are difficult to treat and often kills the patient.

Prior to the TME era, radiotherapy (RT) for rectal cancer was introduced in the 1980’s in an attempt to decrease rates of local recurrence. Locoregional recurrence was notably high in locally advanced rectal cancer which led to the development of randomized trials exploring the possible benefit of post operative chemotherapy and radiotherapy in this subset of high risk patients.

In 1975, the Gastrointestinal Tumor Study Group (GITSG) GI – 7175 trial began randomizing patients to a four-arm trial after a curative resection for rectal adenocarcinoma. This trial randomized 227 patients to: no further therapy, radiation (40-80Gy/ 5 weeks), chemotherapy alone (flourouracil and semustine or methyl (CCNU)), or a combination of chemotherapy and radiotherapy. Patients undergoing the combined radiation therapy and chemotherapy regimen showed a statistically significant advantage in disease free and overall survival compared with the surgery alone group.

(19)

The NSABP R-01 adjuvant therapy trial randomized 500 patients with pathologic T3, T4, or node-positive disease. They were randomized to surgery alone versus adjuvant 5 flourouracil, semustine and vincrinstine versus adjuvant pelvic radiation. The trial showed improved disease free and overall survival in 276

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the chemotherapy group compared with surgery alone group. The adjuvant radiation group experienced a reduction in locoregional recurrence from 25% to 16% compared with the surgery alone group without a survival benefit.

(20)

Efforts aimed at improving local control and long term survival stimulated experimentation which gave rise to the concept of neoadjuvant RT in the 1990â&#x20AC;&#x2122;s. Initial reports from small studies suggested that efficacy with neoadjuvant RT was comparable or improved compared to adjuvant RT, and toxicity was less severe.

Specifically two different regimens of neoadjuvant RT, were being assessed: (1) Long course RT, used mainly in the US, (2) short course RT, used mainly in Europe.

The European Organization for Research and Treatment of Cancer (EORTC) designed a study to evaluate the efficacy and toxicity profile of neoadjuvant RT (long course). In this trial 466 patients were enrolled: 175 were ultimately randomized to surgery alone, 166 randomized to neoadjuvant RT followed by surgery. Patients in the neoadjuvant arm tolerated the treatment adequately, had significantly decreased local recurrence rates (15% versus 30%, p=0.003), but had no improvement in overall survival.

(21)

The Swedish Rectal Cancer Trial was the first major trial to demonstrate significant improvement in local control with short course RT (25 Gy in 5 consecutive daily fractions) followed by surgery, compared with surgery alone (11% versus 27%, p <0.001). In addition, the Swedish trial was the only trial to demonstrate improved five year survival rates for patients in the neoadjuvant arm (58% with versus 48% without RT, p =0.004). The patient population included those with stage one rectal cancer as well as locally advanced disease, but notably the standardize TME technique was not implemented which may have influenced the high mortality rate of the surgery only arm of this study. (22) The Dutch Colorectal Group performed a similar investigation, with the no277

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table exception of standardizing surgery to TME. Patients were randomized to either short course neoadjuvant RT followed by surgery in one week (n=695) or surgery alone (n=719). A significant decrease in local recurrence rates was found at two years in the neoadjuvant RT arm (2.4% versus 8.2%, p < 0.001), but no difference in overall survival (82% versus 81.8%, p=0.84).

(23)

These impressive results lead to the publication of several reports. Subsequently, two meta-analyses were published. Camma et al in their analysis of 14 randomized controlled trials identified that neoadjuvant RT significantly improved the five year survival rates (p=0.03), the cancer related mortality rates (p<0.001) and the local recurrence rates (p<0.001) when compared to adjuvant RT. (24) The Colorectal Cancer Collaborative group evaluated 22 randomized control trials (involving a total of 8507 patients) to determine whether adjuvant or neoadjuvant RT was superior in improving survival and decreasing local recurrence rates. The randomized controlled trials compared neoadjuvant therapy, adjuvant therapy or surgery alone and included both short course and long course RT. A significant improvement in the yearly local recurrence rates in the neoadjuvant RT arm (46% decrease versus surgery alone, p=0.00001) and in the adjuvant RT arm (a 37% decrease versus surgery alone, p=0.002). But the five year survival rate (45% with RT versus 42.1% with surgery alone) and the overall survival rate (62% with RT versus 63% with surgery alone, p=0.06) did not differ significantly. (25)

Historically, the combination of postoperative RT and flourouracil chemotherapy has been associated with reduced local recurrence and improved survival for locally advanced rectal cancer. Such regimens have been incorporated into neoadjuvant schedules designed to optimize the sequence of treatment modalities. In 2004 the German Rectal Cancer Group compared neoadjuvant combined modality treatment (CMT) with adjuvant, in patients with locally advanced rectal cancer. Patients were randomly assigned to two arms: (1) Neoadjuvant CMT (n=421) and (2) adjuvant CMT (n=402). All patients received long course RT and 5 FU 278

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based chemotherapy. The five year survival rates (76% with neoadjuvant CMT versus 74% with adjuvant CMT, p=0.8) did not differ significantly. The local recurrence rates significantly improved in the neoadjuvant arm (6% with neoadjuvant CMT versus 13% with adjuvant CMT, p=0.0006). The adjuvant arm had high rates of acute and long term toxicity (acute: 27% with neoadjuvant CMT versus 40% with adjuvant CMT, p=0.001; long term: 14% versus 24%, p=0.01).(26)

While neoadjuvant therapy was defined as standard of care for preoperatively staged greater than T3 or node positive disease, this was still a controversial issue. Opponents of neoadjuvant therapy argued that more patients are needlessly treated by neoadjuvant therapy administered on the basis of less than optimal preoperative imaging. As a result long term consequences of diminished sexual function and of bowel dysfunction associated with neoadjuvant therapy may attend a larger number of patients. They recommended that only appropriate patients be treated on the basis of pathologic or pTNM stage.

(27)

There are several theoretical advantages to the administration of preoperative therapy in the management of rectal cancer. The preoperative setting usually offers a well defined target with the tumor in place, and with intact tumor oxygen supply that may minimize tumor response rates. The absence of adhesions and postoperative changes minimizes small bowel toxicity. Patients with bulky or low lying rectal cancers may become candidates for sphincter preservation if they have an adequate response to therapy. Also, the ability to measure response to treatment may enable the identification of subgroups of patients with better clinical prognosis.

Most significantly the addition of neoadjuvant radiation has resulted in significant downsizing and down staging of low locally advanced rectal cancers making sphincter preservation procedures feasible and with good oncologic outcomes. Weiser et al performed a retrospective analysis of 148 patients with locally advanced rectal cancer (within 6cm the anal verge), 279

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who were treated with neoadjuvant CMT (long course) and selective adjuvant chemotherapy. The decision to perform sphincter preservation surgery was made intra-operatively.

The likelihood of sphincter preserv-

ing surgery was associated with significant tumor down staging.

They

concluded that neoadjuvant CMT facilitated sphincter preserving surgery.

(28)

However, short course neoadjuvant radiation does not seem to offer the same results. Sauer et al did not find a significant difference in the rate of sphincter preservation between the neoadjuvant and adjuvant treatment arms. However they did note that, within the subgroup of patients deemed to require APR preoperatively (n=194), this number of APR actually performed was significantly lower in the neoadjuvant arm (p=0.004).

(26)

Bujko et al specifically looked at whether neoadjuvant short course RT offered a benefit for sphincter preservation over neoadjuvant CMT in 316 patients and found no significant difference: 61% of patients in the RT arm and 58% in the CMT arm underwent sphincter preserving surgery (p=0.57).

They demonstrated that although short course RT improves local control, no strong evidence exists that it also improves rates of sphincter preserving surgery. This finding indicated that short course neoadjuvant RT does not have a significant effect in preoperative tumor downsizing or down staging.

(29)

A significant benefit of neoadjuvant RT is patientâ&#x20AC;&#x2122;s compliance with treatment.

Adjuvant RT has been associated with high rates of treatment interruptions. Lebwohl et al assessed for principal factors associated with treatment interruptions in 113 RT patients. Patients in the adjuvant arm had a significantly increased chance of RT interruption, as compared with the neoadjuvant RT. Development of an adverse event was also significantly correlated with RT interruption.

280

(30)

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Apart from the effects of oncologic control of disease, chemoradiation and surgical techniques both affect bowel function and sexual function. The Dutch colorectal group assessed anorectal functional outcomes after short course preoperative RT and TME and found significant differences between patients who did not undergo RT. RT patients had higher rate of fecal incontinence (62% with RT versus 38% without, p<0.001), pad wearing as a result of incontinence (56% versus 33%, p<0.001), and anal blood loss (11% versus 3%, p=0.004).

RT patients also reported significantly lower satisfaction in bowel function.

In addition to bowel and sexual dysfunction, RT patients may experience acute and late RT toxicity, including nausea/vomiting, post operative hernia femoral neck fracture, skin problems (none healing perineal wounds), ileus, anastomotic stricture and fistula. The Dutch colorectal group studied RT toxicity, intraoperative and postoperative complications, in patients who underwent short course neoadjvant RT and TME alone. No differences were found in operative time, intraoperative complications or hospital stay; however the amount of intraoperative blood loss was higher in the RT arm (p<0.001). Rates of perineal complications were also higher (29% with RT versus 18% with TME alone, p=0.008). There were no significant differences found in the rates of abdominal wound complications or in the overall postoperative mortality rates.

(31)

Frykholm looked at long term complications after either neoadjuvant short course RT or adjuvant long course RT as compared with surgery alone. Long term complications included recurrent abdominal pain, diarrhea, fecal incontinence, ileus, cystitis, paresthesias, delayed wound healing and any neurologic dysfunctions. In the adjuvant RT group the risk of developing a small bowel obstruction was significantly higher (p<0.01). Overall, the frequency of complications possibly related to RT in the neoadjuvant group was 20%; in the adjuvant group 41%.(32) Minsky et al. also demonstrated significantly lower rates 281

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of adverse events and improved compliance in patients treated with neoadjuvant CMT compared to patients treated with adjuvant CMT. Despite receiving higher doses of chemotherapy, the neoadjuvant arm experienced a 13% incidence of acute grade 3 and 4 toxicity compared to a 48% incidence in the adjuvant arm.(33)

Overall, patients with locally advanced rectal cancer clearly benefit in terms of locoregional control, from both neoadjuvant RT and the adjuvant RT: but patient compliance is better with neoadjuvant RT. The current standard treatment for patients with locally advanced rectal cancer in the US consists of neoadjuvant radiation (45-55 Gy, over five to six weeks), followed by neoadjuvant chemotherapy (five FU based infusion + leucovorin), surgery six to eight weeks after completion of chemotherapy, and additional adjuvant chemotherapy after surgery. In contrast the standard in most of Europe is now neoadjuvant short course RT. At present no definitive evidence demonstrates the superiority of using short versus long course RT and this is an area of ongoing debate in the treatment of rectal cancer.

The progress made with the implementation of neoadjuvant RT for locally advanced rectal cancer reflects the improvement in preoperative staging. Pathologic stage represents the most important prognostic factor for patients who have rectal cancer. The tumor-node-metastasis (TNM) system, as defined by the AJCC, is the most commonly used staging system and is based on depth of local invasion, extent of regional lymph node involvement and presence of distant metastasis. As the AJCC stage increases from stage I to stage IV, five year overall survival declines from greater than 90% to less than 10%.(34) (See Box 1 and 2) Synchronous polyps or cancers may be present in 4% to 15% of patients, therefore complete endoscopic evaluation of the entire colon is essential not only for visualization, location and biopsy of the primary rectal tumor but also to exclude additional lesions.(35)

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BOX 1

Tumor-node-metastasis (TNM) staging system for rectal cancer

Primary tumor (T) Tx-Primary tumor cannot be assessed Tis-Tumor insitu T1-Tumor invades submucosal T2-Tumor invades the muscularis propria T3-Tumor invades through the muscularis propria into the subserosa T4-Tumor invades other organs or structures, or perforates visceral peritoneum

Regional lymph nodes Nx-Regional lymph nodes cannot be assessed N0-No regional lymph node metastasis N1-Metastasis in one to three regional lymph nodes N2-Metastasis in four or more regional lymph nodes

Distant metastasis Mx-Presence or absence of distant disease cannot be determined M0-No distant metastasis detected M1-Distant metastasis detected Data AJCC Cancer Staging Manual, Seventh Edition, New York, 2010, Springer.

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BOX 2

Stage-specific 5 year survival Stage

Grouping Five-Year

Survival I

T1-2, N0, M0

>90%

IIA

T3, N0, M0

60%–85%

IIB

T4, N0, M0

60%–85%

IIIA

T1-2, N1, M0

55%–60%

IIIB

T3-4, N1, M0

35%–42%

IIIC

T-1-4, N1, M0

25%–27%

IV

T1-4, N0-2, M1

0-16%

Establishing the extent of local and locoregional involvement is imperative for patients who have rectal cancer, particularly those with locally advanced disease who is at higher risk of recurrence and disease progression. They can then be selected for neoadjuvant therapy.

History and physical examination may yield some clues as to the extent of local progression. Although many patients with early rectal cancer are asymptomatic and detected by screening, more advanced tumor in the rectum is often associated with a group of common symptoms such as rectal bleeding, change in the caliber of stools and tenesmus. Rectal pain may indicate more distal involvement of the anal canal or possibly of the sacral bones or nerves.

Digital Rectal Examination (DRE) is particularly important in determining the likelihood of sphincter preservation and can identify fixation and involvement of the sphincter complex, the distance from the anorectal ring and the size of the tumor. The overall accuracy of DRE in local staging is only approximately 65%.(36) To assess locoregional disease, other modalities are required.

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CT scanning is widely used for staging of colorectal cancer but its role is mainly to identify distant disease. While it can be useful for the local relationships of high rectal tumors to pelvic structures, its ability to distinguish the layers of the rectal wall and the inherent soft tissue planes is suboptimal. The sensitivity of CT in the local tumor staging of rectal cancer is 79%, only somewhat better than that reported for DRE. (37) In this respect, transrectal ultrasound (TRUS) and MRI have emerged as acceptable methods of determining local staging of rectal cancer.

The most common technique for assessing the depth of rectal wall invasion is transrectal ultrasound (TRUS); 360 degrees viewing transducers are available for use with either a flexible or rigid assembly. An integrated water-filled balloon enables close transducer contact and distension of the rectal wall.

Meta-analysis of ninety articles describing TRUS in staging of rectal cancer yielded a sensitivity and specificity of 94% and 86% respectively for muscularis invasion and 94% and 69%, respectively for perirectal tissue invasion.

Therefore, TRUS is ideal for staging of T1 /T2 tumors being considered for local, non radical surgery.(38) However, caution must be exercised in interpreting imaging for large, locally invasive or desmoplastic tumors, which make true tumor infiltration from tissue reactions difficult to discern and may result in overstaging. Other limitations of TRUS include the staging of stenotic circumferential rectal tumors that are unable to be traversed by endoscope and of lesions treated by preoperative radiotherapy, which decreases the accuracy of T staging secondary to increased echogenecity of the rectal wall. The overall accuracy of TRUS for T staging is reported to range from 80% to 95%.( 39) Nodal staging using TRUS is more challenging because metastasis is difficult to detect within a lymph node, and consequently sensitivity and specificity are approximately 55% and 78% respectively.(38) Sonographic lymph node changes associated with malignant involvement include a hypoechoic appearance, round nodal shape, and nodal diameter of 1cm or greater. Lymph 285

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nodes greater than 0.5cm in diameter have a 50% to 70% possibility of being metastatic, whereas those smaller than 4mm have a less than 20% likelihood of harboring metastasis. The overall accuracy of TRUS in determining metastatic perirectal nodal involvement is approximately 70% to 75%.(40)

The use of MRI for the local staging of rectal cancer, particularly with and endorectal coil technique is well described and offers several theoretic advantages compared with TRUS: it permits a larger field of view, tends to be less operator and technique-dependant and allows for the study of stenotic tumors.(41) A meta-analysis of 90 articles between 1995 and 2002 comparing the use of MRI, TRUS and CT for staging with histopathologic findings as the reference standard came to the following conclusions: for T1/T2 lesions TRUS and MRI had similar sensitivity but specificity was higher in TRUS (86 vs. 69%) and for T3 tumors, the sensitivity of TRUS was significantly higher than that of MRI or CT.

MRI can also be used to evaluate mesorectal nodal involvement. Rather than size criteria alone, lymph nodes can be characterized by imaging features. In their study of MRI with histological correlation, Brown and colleagues identified an irregular contour and an homogenous signal to be the most reliable MRI criteria for lymph node metastasis.(42) However as with TRUS, MRI has shown less accuracy in predicting perirectal nodal involvement. Sensitivity and specificity are approximately 64% and 58% respectively with an overall accuracy in nodal staging ranging from 60% to 70%.(43) Newer techniques such as high resolution, thin section MRI are better able to differentiate malignant tissue from the muscularis propria and define tumor infiltration of the mesorectal fascia (circumferential margin). The Magnetic Resonance Imaging and Rectal Cancer European Equivalence study (MERCURY) prospectively evaluated the depth of extramural tumor invasion in patients who had rectal cancer while comparing it with the histopathologic results as the gold standard. MRI assessment of tumor 286

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invasion was considered equivalent to conventional histopathologic evaluation to within 0.5mm.(44) Therefore, either high resolution MRI or TRUS is an acceptable method to determine preoperative tumor stage. Both MRI and TRUS are performed preoperatively to evaluate not only T-stage but also the likelihood of achieving a negative circumferential margin. This decision is based on data illustrating that distance from the primary tumor to the mesorectal fascia on MRI before neoadjuvant therapy accurately predicted surgical margin and mesorectal status and subsequently correlated with survival and local recurrence patterns.(45)

MRI and CT are variably available to us at our hospital. Case I and 2 benefited from MRI for local staging. Case 3 did not have local staging by MRI and by using DRE and CT was overstaged as T3 (actually pT2). MRI was not available at the time and the patient could not afford.

Further advances in these technologies will enhance the cliniciansâ&#x20AC;&#x2122; ability to structure treatment plans in a better way and help select patients for neoadjuvant therapy. Neoadjuvant therapy is now the standard of practice for locally advanced rectal cancer but there is debate regarding the dosage of radiation and the duration interval to surgery. There are two broad approaches to preoperative pelvic radiation therapy for resectable rectal cancer: short course radiation and long course chemoradiotherapy. Although the radiation techniques are similar, the fractionation and timing of surgery differ. In general short course radiation delivers 25 Gy units (5Gy in 5 fractions) of radiation followed by surgery one week later.

Long course chemotherapy delivers 50.4 Gy (1.8 Gy in 28 fractions) of radiation concurrently with chemotherapy followed by surgery four to eight weeks later.

Bujko et al. performed the first randomized control study on 312 patients with locally advanced T3-T4 resectable rectal cancer. The aim of the study was to compare survival, local control and late toxicity of patients who received short 287

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course preoperative radiation therapy versus similar outcomes in patients who received long course preoperative radiation and chemotherapy. The authors demonstrated that early radiation toxicity was higher in the chemoradiation group (18.2% versus 3.2%, p<0.001). The actuarial 4 year overall survival was 67.2% in the short course group and 66.2% in the chemoradiation group (p=0.960).

The crude incidence of local recurrence was 9.0% versus 14.2% (p=0.17) and severe late toxicity was 10.1% versus 7.1% (p=0.36) respectively. The results of the study were comparable. This study suffered from a few limitations. The study was unlikely to detect small differences as it was to detect a 15% difference. Post operative chemotherapy was administered more often in the short course group than in the preoperative chemoradiation group. The preoperative group probably achieved greater downstaging effect decreasing the number of patients for whom this treatment was considered beneficial. Interestingly although the preoperative protocol indicated that only patients with cT3, T4 disease were eligible, 39.5% of patients in the short course group actually had pT1/ T2 disease. This may have resulted partly from a downstaging effect in the short course radiotherapy observed if the time to surgery is more than ten days.(29)

The randomized trial of Federation Francophone Cancerologie Digestive 9203 was performed in order to compare preoperative radiotherapy with chemo radiotherapy in patients who presented a resectable T3-T4, Nx, M0 rectal adenocarcinoma assessable to DRE. Surgery was planned three weeks to ten weeks after the end of radiotherapy. All patients have received adjuvant chemotherapy with the same FU/leucovorin regimen. The primary end point of the trial was overall survival. In this trial 733 patients were eligible to participate and the results have shown that grade 3 or 4 acute toxicity was more frequent with chemo radiotherapy (14.6% versus 2.7%, p<0.05). There was no difference in sphincter preservation. Complete sterilization of the operative specimen was more frequent with chemo radiotherapy (11.4% versus 3.6%, p<0.05). The five year incidence 288

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of local recurrence was lower with chemo radiotherapy (8.1% versus 16.5%, p<0.05). The authors have concluded that preoperative chemoradiotherapy despite a moderate increase in acute toxicity and no impact on overall survival significantly improves local control of middle and distal rectal adenocarcinoma.(46)

The EORTC Radiotherapy Group Trial 22921 enrolled a randomized phase III trial in order to evaluate the addition of chemotherapy to preoperative radiotherapy and the use of postoperative chemotherapy in the treatment of patients with clinical stage T3 or T4 resectable rectal cancer. A total of 1011 patients were enrolled.

There were no significant differences in overall survival between the groups that received chemotherapy preoperatively and those that received it postoperatively.

The 5 year cumulative incidence rates for local recurrence were 8.7%, 9.6% and 7.6% in the groups that received chemotherapy preoperatively, postoperatively or both, respectively and 17.1% in the group that did not receive chemotherapy.

Notably the rate of adherence to preoperative chemotherapy was 42.9%. They concluded that chemotherapy regardless of whether it is administered before and after surgery confirm a significant benefit with respect to local control.(47)

Latkauskas et al. conducted a randomized controlled trial in eighty three patients with resectable stage II and III rectal adenocarcinoma. The aim was to compare the down staging achieved after long course chemo radiotherapy and short term radiotherapy followed by delayed surgery (6 weeks) in both groups. They found that the Ro (negative margins at resection) resection rate was 91.3% in the chemo radiation therapy and 86.5% in the short course radiotherapy group (p= 0.734). Sphincter preservation rates were 69.6% vs.

70.3% (p= 0.34) and postoperative complication rates were 26.1% vs. 40.5% (p= 0.22). There were more patients with ypT0 (complete pathological response) in the chemoradiation group (21% vs. 2.7%. p= 0.03) and more patients with pT3 disease in the short term radiotherapy group (75.7% vs. 52.2%, 289

A CASEBOOK OF TWENTY SURGICAL CASES

p= 0.36). Pathological down staging was observed in 21.6% in the short term radiotherapy group and in 39.1% in the chemoradiation group (p= 0.07). Tumors were smaller after pre operative chemoradiation (2.5cm vs. 3.3cm, p= 0.04). This study revealed significant downsizing and down staging in patients receiving long course pre operative chemo radiation compared with short course radiation but there was no difference in the Ro resection rates.(48)

The long term follow up data suggests that preoperative CMT affords durable oncologic outcomes in properly selected patients with T3, T4 and or node positive disease. There is however some debate as to whether all patients with locally advanced rectal cancer require preoperative CRT in particular regarding cT3N0M0 lesions. In an analysis of 95 pT3N0 patients treated with TME surgery alone, the five year actuarial recurrence rate was 12%, with five year disease specific and overall survival rate reported as 86.6% and 75% respectively, leaving some experts to suggest that adjuvant chemo radiation may be omitted in select patients with T3N0 rectal cancer.

(49)

In a recent evaluation of 188 patients who had cT3NO rectal cancer treated with preoperative chemoradiation, Guillem and colleagues showed that on final pathologic analysis 22% of patients harboured residual, undetected mesorectal lymph node involvement. Because preoperative CRT may reduce the total number of lymph nodes and may also sterilize mesorectal lymph nodes, the true rate of patients clinically stayed as T3N0 who actually have node positive disease may even be higher, perhaps as high as 45%.(50) Although the risks of overstaging T3 rectal cancer have been recognized (18% of patients with cT3N0 actually had pT2N0 disease according to the German Rectal Cancer Group

(26)

) it is possible that twice as many are understaged

based on the above findings. These data would support preoperative CRT for patients with cT3N0 rectal cancer staged by ERUS and MRI as under290

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staged patients could otherwise require post operative CRT, which is associated with inferior local control, higher toxicity and poor functional outcomes.

The overall results of these trials indicate similar long term survival, local control and late morbidity for short course RT and long course RT. The benefits of the short course RT are lower rates of early toxicity compared with chemoradiation, more economical and more convenient. On the other hand, the use of high dose per fraction raises concern about late toxicity.

Long course RT in chemoradiation might be better than the short course RT schedules at reducing local recurrences. Long course RT seems to be better at sphincter preservation because the tumor bulk is reduced before surgery.

However the debate is ongoing with different researchers trying to identify the correct combination of chemotherapeutic agents. Despite the transatlantic difference of opinion regarding these two approaches to neoadjuvant therapy a change is noted on the US front. Consideration is being given to the use of short course RT in order to better stratify patients who may benefit from adjuvant therapy because of the low probability of downstaging and therefore â&#x20AC;&#x153;unchangedâ&#x20AC;? initial TN staging.(51) It is hoped that the dilemma regarding the fractionation of radiotherapy and timing of surgery for rectal cancer will be decided by the ongoing Stockholm III trial. This multicenter trial has randomized patients to preoperative short course radiotherapy and surgery within one week or after four to eight weeks, or long course RT and surgery after four to eight weeks.

(52)

Other areas of active clinical investigations should include developing more

accurate imaging techniques and molecular markers, to identify patients with positive pelvic nodes to reduce overtreatment with preoperative chemotherapy.

Patients with cancer of the low rectum (0-5cm) suffer from a higher incidence of local recurrence and a poorer survival than patients with midrectal 291

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cancer.(53,54,55) Hida and others have demonstrated that low rectal cancers harbor rates of positive mesorectal nodes and a larger number of lateral pelvic sidewall nodes.(56 ,57) In addition Weiser et al. identified that rectal tumors in patients who undergo APR are often more locally advanced, more poorly differentiated and show a lesser response to neoadjuvant chemo radiotherapy.(58)

The knowledge that a distal margin of 1cm will safely allow complete tumor removal affords an even greater proportion of patients the opportunity of sphincter preserving surgery for low rectal cancer.(59) In addition, CMT has enabled an increased rate of sphincter preservation in patients with low lying tumors.(26) On account of this, patients have new options that may facilitate sphincter preservation (e.g. intersphincteric resection) and may also avoid the morbidity of TME (e.g Trans anal Endoscopic micro surgery) or non-operative treatment following complete response to the neoadjuvant treatment.

Intersphincteric resection represents the most extreme form of sphincter preserving surgery in which part or all of the internal sphincter is resected. This approach may be applied to tumors within 2cm of the sphincter complex and is made feasible by the recognition that distal intramural tumors spreading beyond 1cm is uncommon. Thus, intersphincteric resection becomes an option for patients with tumors within 2cm of the sphincter complex, in whom preoperative continence is intact and for whom the tumor, at least in its distal part is confined to the rectal wall. Follow up suggests that local (6.6%) and distant (8.8%) recurrence rates are comparable to those in published series of APR.(60) Patients with locally advanced (T3-T4) tumors may be candidates for intersphincteric resection if a favorable downstaging response to neoadjuvant CRT is demonstrated.(58) Transanal (TA) surgery for rectal cancer represents an attractive approach that may allow the morbidity and functional sequelae of TME to be avoided. Better surgical results with lower margin positivity are achieved following transanal endoscopic micro surgery (TEMS) than conventional transanal excision (2% 292

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versus 16%),(61) however outcomes are generally inferior to those following radical resection with a 3-5 fold increased local recurrence risks.(62) TEMS appears to be a reasonable option (LRR<5%) in selected patients with favorable pathological features (pT1, superficial submucosal penetration, well or moderately differentiated; <3cm diameter, no lymphovascular invasion). For tumors with less favorable features, the oncologic result following TEMS is inferior to that seen after TME. Difficulty in reliably predicting the T stage preoperatively remains an obstacle to patient selection. Likewise, predictions of N stage is problematic as up to 18% of T1 tumors will have associated nodal disease.(63)

One fifth to one quarter of patients following neoadjuvant CRT will show a complete pathological response. Predicting those likely to respond and those who have had a complete pathological response remains challenging. Up to 40% of patients who appear to have had a complete clinical response have residual disease following resection; conversely, approximately 10% of patients who have an incomplete clinical response will show a complete pathological response.(64, 65)

Habr-Gamma et al. have suggested that observation alone may be a viable alternative in selected patients who show a complete clinical response to neoadjuvant therapy. Local recurrence has been reported in 11% of those who had a complete clinical response. It appears that these patients are amenable to salvage therapy without adverse oncological outcomes in the event of local recurrence.(66)

The high local recurrence related to low rectal cancer as outlined previously makes implementations of these less aggressive surgical approaches controversial. Thus careful patient selection and counseling is important. While these measures offer the chance of sphincter preservation which is more welcomed by patients, they require specialized equipment and surgical expertise. Abdominoperineal resection is still a common operation for patients with tumors less than 293

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6cm from the anal verge. Several studies have identified increased rates of CRM involvement after APR and consequently increased rates of local recurrence when compared to anterior resection with TME. A 2 year audit performed by the Association of Coloprotcology of Great Britain and Ireland reported positive CRM in 16.7% of patients undergoing APR, compared to 7.5% undergoing anterior resection,(67) and recently, the MERCURY group reported a CRM involvement rate rate of 28.6% after APR, compared with 7.6% after anterior resection.(68)

Despite the biological nature of low rectal tumors as noted before, others have suggested that surgical techniques of APR may play a meaningful role in oncologic control. The APR is associated with a higher rate of inadvertent intra-operative perforation (8-26%), an important prognostic indicator of local recurrence with rates approximating 30%.(69) However, with meticulous surgery and the avoidance of tumor perforation and margin positivity, results following APR can be similar to those after AR.(55) These findings have influenced the call for a standardization of the technique of APR similar to what has been achieved for TME. TME has resulted in increase rates of low anterior resection of the rectum and significantly improved local disease control. It is felt that similar efforts on the operative technique of APR may help to improve oncological results. In the 3 cases described case 2 had an extended APR, the other 2 had conventional dissection.

During the conventional APR the surgeon commonly follows the plane outside the mesorectum down to the pelvic floor and the top of the anal canal. The mesorectum is mobilized from the levator muscles. This result in a high risk of inadvertent bowel perforation, the resulting specimen frequently having a waist at the lower end of the mesorectum and the CRM is often close to the rectal muscle tube.

Surgeons in Stockholm have described a more radical approach to APR which results in a cylindrical specimen. The procedure involves careful mobilization 294

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of the mesorectum only as far down as the origin of the levator muscles. After fashioning the end colostomy, the extended perineal dissection is performed with the patient now placed prone. This includes the sphincter complex and follows the inferior surface of the levators to a point laterally where they originate on the pelvic side wall. This point should be just inferior to the level where the abdominal procedure was terminated. The coccyx is often removed in continuity with the main specimen to improve direct visualization of the dissection.

In the case of anterior tumors in which the CRM is frequently threatened, a portion of prostate or vaginal wall may be removed as well. If the resulting pelvic floor defect is too large for primary closure, a gluteus maximus flap reconstruction or insertion of a prosthetic mesh may be performed. This modified procedure has two distinct advantages. The first is that a more cylindrical specimen is created which should increase the amount of tissue removed around the tumor and therefore reduce the CRM positivity. Secondly, it offers better visualization which should reduce chances of perforating the specimen.(70)

Increasing numbers of surgeons are now using these techniques with early evidence of improved local recurrence and survival. In a multicenter study from Europe 176 extra levator APR procedures from 11 colorectal surgeons were compared to 124 standard excisions from one UK center. Extra levator APR resulted in a reduction in CRM involvement (from 49.6% to 20.3%: p<0.001) and intraoperative perforation (from 28.2% to 8.2%: p<0.001) compared with standard surgery.(71) The only randomized clinical trial of conventional (n=32) versus cylindrical APR (n=35) APR for locally advanced cancer revealed: patients who received cylindrical APR had less operative time for the perineal portion (p<0.001), larger perineal defect (p<0.001) less intra-operative blood loss (p=0.001), similar total operative time (p=0.096) and more incidence of perineal pain (p<0.001).

There was a statistically significant improvement of local recurrence.(72)

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West et al. reviewed their experience with a standardized cylindrical APR dissection (n=128). Greater distance was observed from the muscularis propria or internal sphincter to the anterior, posterior and the lateral resection margins (all p<0.001). This was associated with a lower CRM involvement (14.8% versus 40.6%: p=0.13) and intra-operative perforation (3.7% versus 22.8%: p=0.255)73. Thus the cylindrical technique has the potential to improve patient outcomes substantially if appropriate surgical programmes are delivered.

One factor that could contribute to local recurrence which is outside the plane of APR is the involvement of the internal iliac nodes. Data from Japan has highlighted the correlation between the depths of tumor invasion and involved lateral pelvic wall lymph nodes. Fujita et al. demonstrated using multivariate analysis, that lateral pelvic lymph node dissection was a statistically significant prediction of outcome.(74) Dissection of the internal iliac nodes has not been popularized in the west due to considerable morbidity associated with it.

The low local recurrence rates achieved by the reports of cylindrical APR/extra levator APR do not support a routine role for lateral pelvic nodal dissection. Lateral pelvic nodal dissection was not performed in any of the 3 cases.

CONCLUSION A complete surgical resection of the primary tumor with its draining lymphatics is the mainstay of treatment for patients with adenocarcinoma of the rectum and TME and has become the standard of care for mid and distal rectal cancer. Local recurrences of rectal cancers however are still associated with significant morbidity and directly affect patients overall survival. Post operative chemoradiation has demonstrated an improvement in local control with stage 2 and 3 rectal cancer. Continued research and improvement in imaging modalities may allow for preoperative identification of patients that may benefit from neoadjuvant therapy.

Several studies support the use of either preoperative short course radio296

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therapy or long course combined chemo radiation to improve local control in locally advanced mid and low rectal cancers. Although studies to elucidate the advantages of one over the other are awaited, there is consensus that preoperative combined modality therapy and adequate surgical resection with TME currently provide the treatment standard for rectal cancer patients with T3, T4, N0 or any T 4 stage with N1 N2 disease.

Low rectal cancers are a particular challenge as they continue to demonstrate high local recurrence rates. Although an oncologic cure remains the main goal in the care of rectal cancer patients, sparing of the anal sphincter function as well as the preservation of normal urinary and sexual physiology are also major factors to be considered. The advent of TME has allowed for decrease rates of APR and greater sphincter preservation and also autonomic nerve preservation.

Low rectal tumors are accessible from the anal canal and may be treated by less aggressive surgery. This requires caution though, as even for early stage (T1) lesions the risk of lymph node metastasis can be significant. The APR is still necessary for some patients despite the success of TME and neoadjuvant therapy particularly for low rectal cancer. The efforts to achieve a cylindrical dissection in order to decrease CRM involvement seems warranted based on the decreased lower recurrence rates demonstrated by recent reports. Refinement of the surgical techniques and training for APR should be encouraged along the lines of TME.

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15. Heald RJ. A new approach to rectal cancer. Br J Hosp Med 1979;22:277-281.

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17.Enker WE, Thaler HT, Cranor ML, et al. Total mesorectal excision in the operative treatment of carcinoma of the rectum. J Am Coll Surg 1995;181:335-346.

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18. Aitken RJ. Mesorectal excision for rectal cancer. Br J Surg 1996;83:214-216.

19. Thomas PR, Lindblad AS. Adjuvant postoperative radiotherapy and chemotherapy in rectal carcinoma: a review of the Gastrointestinal Tumor Study Group experience. Radiother Oncol 1988;13(4):245–52.

20. Fisher B, Wolmark N, Rockette H, et al. Postoperative adjuvant chemotherapy or radiation therapy for rectal cancer: results from NSABP protocol R-01. J Natl Cancer Inst 1988;80(1):21– 9.

21. Gérard A, Buyse M, Nordlinger B, et al. Preoperative radiotherapy as adjuvant treatment in rectal cancer. Final results of a randomized study of the European Organization for Research and Treatment of Cancer (EORTC) Ann Surg. 1988;208:606–614.

22. Improved survival with preoperative radiotherapy in resectable rectal cancer. Swedish Rectal Cancer Trial. N Engl J Med. 1997;336:980–987.

23. Kapiteijn E, Marijnen CA, Nagtegaal ID, et al. Preoperative radiotherapy combined with total mesorectal excision for resectable rectal cancer. N Engl J Med. 2001; 345:638–646.

24. Cammà C, Giunta M, Fiorica F, et al.Preoperative radiotherapy for resectable rectal cancer: A meta-analysis. JAMA. 2000; 284:1008–1015.

25. Colorectal Cancer Collaborative Group. Adjuvant radiotherapy for rectal cancer: a systematic overview of 8,507 patients from 22 randomised trials. Lancet.2001; 358:1291–1304.

26. Sauer R, Becker H, Hohenberger W,et al. Preoperative versus postoperative chemoradiotherapy for rectal cancer. N Engl J Med. 2004;351:1731–1740.

27. Law WL, Ho JW, Chan R, Au G, Chu KW. Outcome of anterior resection for stage II rectal cancer without radiation: the role of adjuvant chemotherapy. Dis Colon Rectum. 2005;48:218– 226.

28. Weiser MR, Quah HM, Shia J, et al. Sphincter preservation in low rectal cancer is facilitated by preoperative chemoradiation and intersphincteric dissection. Ann Surg. 2009;249:236–242.

29. Bujko K, Nowacki MP, Nasierowska-Guttmejer A, et al. Long-term results of a randomized trial comparing preoperative short-course radiotherapy with preoperative conventionally fractionated chemoradiation for rectal cancer. Br J Surg. 2006; 93:1215–1223.

30. Lebwohl B, Ballas L, Cao Y, et al.Treatment interruption and discontinuation in radiotherapy for rectal cancer. Cancer Invest. 2010;28:289–294.

31. Peeters KC, van de Velde CJ, Leer JW, et al. Late side effects of short-course preoperative radiotherapy combined with total mesorectal excision for rectal cancer: increased bowel dysfunction in irradiated patients--a Dutch colorectal cancer group study. J Clin Oncol.

2005;23:6199–6206.

32. Frykholm GJ, Glimelius B, Påhlman L. Preoperative or postoperative irradiation in adenocarcinoma of the rectum: final treatment results of a randomized trial and an evaluation of late secondary effects. Dis Colon Rectum. 1993;36:564–572.

33. Minsky BD, Cohen AM, Kemeny N,et al. Combined modality therapy of rectal cancer: decreased acute toxicity with the preoperative approach. J Clin Oncol. 1992;10:1218–1224.

34.Asgeirsson T, Senagore AJ. Colon Cancer. In: Current Surgical Therapy , 10th Edition.Editors: Cameron JL, Cameron AM. 2011; Elsevier, Saunders. Philadelphia.pp.186.

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35. Hideya T, Tomohiro T, Nagasaki S, et al. Synchronous multiple colorectal adenocarcinomas.

Journal of Surgical Oncology 1997;64:304–7.

36. Brown G, Davies S, Williams GT, et al. Effectiveness of preoperative staging in rectal cancer: digital rectal examination, endoluminal ultrasound or magnetic resonance imaging? Br J Cancer 2004;91(1):23–9.

37.Meredith KL, Hoffe SE, Shibata D. The Multidisciplinary Management of Rectal Cancer.

Surg Clin N Am 2009; 89: 177-215.

38.Bipat S, Glas AS, Slors FJ, et al. Rectal cancer: local staging and assessment of lymph node involvement with endoluminal US, CT, and MR imaging—a metaanalysis. Radiology 2004; 232(3):773–83.

39. Siddiqui A, Fayiga Y, Huerta S. The role of endoscopic ultrasound in the evaluation of rectal cancer. Int Semin Surg Oncol 2006;3(36):1–7.

40. Beynon J, Mortensen NJ, Foy DM, et al. Pre-operative assessment of local invasion in rectal cancer: digital examination, endoluminal sonography or computed tomography? Br J Surg 1986;73(12):1015–7.

41. Orrom WJ, Wong WD, Rothenberger DA, et al. Endorectal ultrasound in the preoperative staging of rectal tumors. A learning experience. Dis Colon Rectum 1990;33(8):654–9.

42. Brown G, Richards CJ, Bourne MW. Morphologic predictors of lymph node status in rectal cancer with use of high-spatial-resolution MR imaging with histopathologic comparison. Radiology 2003;227(2):371–7.

43. Chun HK, Choi D, Kim MJ, et al. Preoperative staging of rectal cancer: comparison of 3-T high-field MRI and endorectal sonography. AJR Am J Roentgenol 2006;187(6):1557–62.

44. Mercury Study Group. Extramural depth of tumor invasion at thin-section MR in patients with rectal cancer: results of the MERCURY study. Radiology 2007; 243(1):132–9.

45. Wieder HA, Rosenberg R, Lordick F, et al. Rectal cancer: MR imaging before neoadjuvant chemotherapy and radiation therapy for prediction of tumor-free circumferential resection margins and long-term survival. Radiology 2007;243(3): 744–51.

46. Dejardin MT, Untereiner M, Leduc B, et al. Preoperative radiotherapy with or without concurrent fluorouracil and leucovorin in T3-4 rectal cancers: results of FFCD 9203. J Clin Oncol 2006; 24: 4620-4625.

47. Bosset JF, Collette L, Calais G, et al. Chemotherapy with preoperative radiotherapy in rectal cancer. N Engl J Med 2006; 355: 1114-1123.

48. Latkauskas T, Pauzas H, Gineikiene I,et al. Initial results of a randomized controlled trial comparing clinical and pathological downstaging of rectal cancer after preoperative shortcourse radiotherapy or long-term chemoradiotherapy, both with delayed surgery. Colorectal Dis 2012; 14: 294-298.

49. Merchant NB, Guillem JG, Paty PB, et al. T3N0 rectal cancer: results following sharp mesorectal excision and no adjuvant therapy. J Gastrointest Surg 1999; 3(6):642–7.

50. Guillem JG, Diaz-Gonzalez JA, Minsky BD, et al. cT3N0 rectal cancer: potential overtreatment with preoperative chemoradiotherapy is warranted. J Clin Oncol 2008;26(3):368–73.

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A CASEBOOK OF TWENTY SURGICAL CASES 51. Kachnic LA, Hong TS, Ryan DP: Rectal cancer at the crossroads: the dilemma of clinically staged T3, N0, M0 disease. J Clin Oncol 2008, 26:350-351.

52. Pettersson D, Cedermark B, Holm T, et al. Interim analysis of the Stockholm III trial of preoperative radiotherapy regimens for rectal cancer. Br J Surg 2010; 97: 580-587.

53. West NP, Finan PJ, Anderin C, et al. Evidence of the oncologic superiority of cylindrical abdominoperineal excision for low rectal cancer. J Clin Oncol 2008;26:3517–22.

54. Nagtegaal ID, van de Velde CJ, Marijnen CA, et al. Low rectal cancer:a call for a change of approach in abdominoperineal resection. J Clin Oncol 2005;23:9257– 64.

55. Wibe A, Syse A, Andersen E, et al. Oncological outcomes after total mesorectal excision for cure for cancer of the lower rectum: anterior vs. abdominoperineal resection. Dis Colon Rectum 2004;47:48 –58.53.

56. Hida JI, Yasutomi M, Fujimoto K, et al: Analysis of regional lymph node metastases from rectal carcinoma by the clearing method. Dis Colon Rectum 39:12821-11285, 1996.

57. Sugihara K, Kobayashi H, Kato T, et al: Indication and benefit of pelvic sidewall dissection for rectal cancer. Dis Colon Rectum 49:1663-1672, 2006.

58. Weiser MR, Quah HM, Shia J, et al. Sphincter preservation in low rectal cancer is facilitated by preoperative chemoradiation and intersphincteric dissection. Ann Surg. 2009;249:236–242.

59. Guillem JG, Chessin DB, Shia J, et al. A prospective pathologic analysis using whole-mount sections of rectal cancer following preoperative combined modality therapy: implications for sphincter preservation. Ann Surg. 2007; 245:88–93.

60. Chamlou R, Parc Y, Simon T, et al. Long-term results of intersphincteric resection for low rectal cancer. Ann Surg. 2007; 246:916–921.

61. Christoforidis D, Cho HM, Dixon MR, et al. Transanal endoscopic microsurgery versus conventional transanal excision for patients with early rectal cancer. Ann Surg. 2009; 249:776–782.

62. Bentrem DJ, Okabe S, Wong WD,et al. T1 adenocarcinoma of the rectum: transanal excision or radical surgery? Ann Surg. 2005;242:472–477.

63. Bach SP, Hill J, Monson JR, Simson JN, Lane L, Merrie A, Warren B, Mortensen NJ. A predictive model for local recurrence after transanal endoscopic microsurgery for rectal cancer.

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64. Bedrosian I, Rodriguez-Bigas MA, Feig B, et al. Predicting the node-negative mesorectum after preoperative chemoradiation for locally advanced rectal carcinoma. J Gastrointest Surg.

2004;8:56–62.

65. Habr-Gama A, Perez RO, Nadalin W, et al. Operative versus nonoperative treatment for stage 0 distal rectal cancer following chemoradiation therapy: long-term results. Ann Surg.

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66. Habr-Gama A, Perez RO. Non-operative management of rectal cancer after neoadjuvant chemoradiation. Br J Surg. 2009; 96:125–127.

67. Smith JJ, Heriot AG, Tekkis PP et al. Comparison of circumferential margin involvement between restorative and non-restorative resections for rectal cancer. Colorectal Dis 2004;6

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68. Daniels I, on behalf of the Mercury Study Group. Magnetic resonance imaging can predict clear margins and avoid the need for pre-operative neo-adjuvant therapy. Br J Surg 2004;6(Suppl. 1): 27.

69. M. Davies, D. Harries, G. Hirst, et al. Local recurrence after abdomino-perineal resection.

Colorectal Disease, 11, 39–43.

70. Holm T, Ljung A, Haggmark T, et al: Extended abdominoperineal resection with gluteus maximus flap reconstruction of the pelvic floor for rectal cancer. Br J Surg 94:232-238, 2007.

71.West NP, Anderin C, Smith KJE, et al. Multicentre experience with extralevator abdominoperineal excision for low rectal cancer. Br J Surg 2010; 97: 588–599.

72. Han JG, Wang ZJ, Wei GH, et al. Randomised clinical trial of conventional versus cylindrical abdominoperineal resection for locally advanced lower rectal cancer.Am J Surg 2012; 204(3):274-282.

73. West NP, Finan PJ, Anderin C, et al. Evidence of the Oncologic Superiority of Cylindrical Abdominoperineal Excision for Low Rectal Cancer. J Clin Oncol 2008; 26: 3517-3522.

74. Fujita S, Yamamoto S, Agasu M et al. Lateral pelvic lymph node dissection for advanced lower rectal cancer. Br J Surg 2003; 90: 1580–5.

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16. THE COLONIC ESOPHAGEAL CONDUIT

INTRODUCTION Diseases of the oesophagus, benign or malignant may necessitate esophagectomy. This of course requires that the functional element of the esophagus be replaced or maintained. The stomach is usually the first choice in an esophageal substitute because of its ease of use and rich submucosal vascular network.

Unfortunately, there are situations in which use of the stomach is not possible.

These include concomitant injury by chemicals or other diseases such as previous gastrectomy for ulcer disease or involvement with cancer. Other potential esophageal substitutes include the colon or jejunum. The jejunal esophageal conduit is technically more challenging and often requires microvascular surgery. Because of this the jejunal conduit is not as common and experience with this is limited.

As an esophageal conduit, a colon graft is more commonly used. This was described just over a century ago. The technical aspects have improved considerably to effect the desired role when used. Despite it being the conduit more commonly used and recommended, it is associated with considerable potential mortality and complications.

A case of a 30 year old gentleman is presented here. He presented with dysphagia following lye ingestion 2 months previously. It was also discovered in addition to his lower third esophageal stricture that he also had developed pyloric 303

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outlet obstruction related to the causative etiology. Subsequent to his gastrojejunostomy and feeding jejunostomy, he underwent esophagectomy and reconstruction with a colonic graft. A discussion follows which focuses on the role of the colonic esophageal conduit and some of the controversial issues with this.

CASE History: A 43 year old gentleman was referred from the A&E with a complaint of dysphagia and vomiting. This gentleman at the age of 33 years drank lye following a family dispute. Three months later he was admitted to hospital for progressive dysphagia. A barium swallow done at that time illustrated a stricture in the mid and distal third of the esophagus.

In order to maintain his nutrition he was taken to the operating theatre for a feeding gastrostomy. At surgery it was discovered that he also developed gastric outlet obstruction from presumed lye induced stricturing. A gastrojejunostomy was fashioned and a feeding jejunostomy constructed instead.

He was subsequently referred to another institution to be seen by the thoracic surgeon. He was advised about esophageal reconstruction and this was performed. The native esophagus was removed; a left colon graft was mobilized and placed orthotopic. The proximal anastomosis was performed at 18cm from the incisors.

The patient explained that he developed a proximal stricture thereafter. This was managed initially by endoscopic dilatation and subsequently by self dilatation using a Savary-Gillard dilator. (Fig1)

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However, in the recent weeks prior to this presentation he noted episodes of vomiting and dysphagia despite dilatation. On the day of presentation he experienced retrosternal pain. This was quite sharp, did not radiate and was constant.

It was not associated with palpitations, cold sweating or syncopy.

Physical Examination: A slim but well looking gentleman presented in no obvious distress. His vital signs were normal (P 64min-1, RR 18 min-1, BP 122/ 72 mmHg, T 366 0C).

His cardio-respiratory systems were clinically normal. The following scars were noted: left anterior sternocleidomastoid incision, left antero-lateral thoracotomy via the 7th intercostal space, and a midline abdominal incision which extended from the xiphisternum to subumbilical. (Fig 2)

His abdomen was not distended, moved with respiration, non-tender and bowel sounds were normal with no succusion splash. The hernial orifices were normal and the digital rectal examination was also normal.

Investigations: His full blood count, renal function tests and amylase levels were normal. An ECG was requested to exclude myocardial ischemia and this was normal.

X-rays of the chest and abdomen were both normal. Endoscopic examination was requested and arranged for two weeks later. At upper gastrointestinal endoscopy there was stricturing at the cervical esophagocolonic anastomosis. This was dilated using pneumatic dilatation (15mm at 60 psi). (Fig 3)

There was a large residual volume of fluid within the distal colon graft. The distal aspect of the colon conduit was poorly visualised. A subsequent CT scan 305

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indicated that the distal aspect of the graft appeared redundant with mild compression of the base of the right lung.

A further gastroscopy was attempted 4 weeks later. The distal anastomosis was slightly strictured and the residual stomach appeared normal. The cause of his symptoms was most probably related to acid or bile induced lower sphincter inflammation or the redundant colon graft.

The patient is willing to cope with the intermittent nature of the symptoms. He is not contemplating surgery. At this point, his further care resides with the gastroenterologist and consists of intermittent endoscopic dilatation.

DISCUSSION Successful reconstruction of the gastrointestinal tract following esophagectomy can be challenging even in the hands of experienced esophageal surgeons. Undeniably the stomach has proved to be the most reliable of all available esophageal substitutes. Many reports have praised its extraordinary plasticity and stretchability as well as its rich blood supply making the stomach suitable for this role. Recent technological advances in mechanical stapling have allowed the simplification of formerly time consuming procedures of gastric lengthening and tubularisation and lends greater acceptance to the use of the stomach (1) Occasionally, however, the stomach is either undesirable or unavailable for use due to prior resection or coexistent gastric pathology. In this instance, the colon and jejunum can be used as a substitute. Procedures involving the jejunum are challenging and more likely to require microvascular surgery. The colon is more commonly used for esophageal reconstruction when required. Either the right colon or the left colon can be utilized. This is a point of controversy as there are proponents for each.

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Fig 1: A Savary-Gillard esophageal dilator

The use of long segments of colon, either for replacement or bypass of all or part of the thoracic esophagus, was introduced independently by Kelling and Vulliet in 1911.(2) Since then, the colon has emerged as a well functioning and durable esophageal substitute. Two critical factors in the success of using colon as an esophageal substitute are the adequacy of the blood supply to the colon graft used and its ability to transport food effectively from pharynx to stomach.

The indications for esophageal reconstruction are generally related to cancer or benign conditions: stricture, advanced motility disorders and failed multiple anti reflux procedures. Patients with esophageal cancer generally belong to an older age group with more attendant comorbidities. The survival of esophageal cancer is poor (overall 5 year survival <15%) (3). These patients are often quite cachectic with poor physical reserve to allow them to withstand the surgical stress of esophageal reconstruction. Many present with advanced stage disease and so generally require palliation. The use of endoscopic stents is helpful for many of these patients. In those patients who undergo surgical treatment of their cancer, limited survival makes it difficult to assess long term graft function.

Despite this, recent reports indicated that colonic interposition is feasible for 307

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Fig 2: Left Anterior sternocleido mastoid incision Midline abdominal incision

Left thorcotomy incision

Fig 3: Handheld device to perform endoscopic pneumatic dilatation of esophageal stricture.

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such patients and that the mortality and morbidity is related to comorbidity and tumor effects.(4,5) Patients with benign disease are generally younger and in the active period of their lives. Consequently, long term function is more relevant and there is greater need for meticulous surgical skills and preparation. Knezevic et al in a report of 40 years experience in the treatment of caustic strictures identified an average age of 38 years.(6)

Both the left and right colon can be used as conduits for esophageal replacements. The decision weighs heavily on the related blood supply. Opponents to right coloplasty argue that the vascular anatomy of the right colon is remarkably variable making its use hazardous.(1) According to autopsy and arteriographic analysis, a continuous right marginal artery is present in 30- 95% of cases.

Conversely the left marginal artery is almost constant.

(1,7)

The direct result of

insufficient blood supply results in increase in anastomotic leak rates, fistula formation and stenosis. Despite this anatomical knowledge, there are literature which describes the use of the use of right colon/ ileo-colic grafts for esophageal replacement. The leak rates range from 6.9 - 46% and are comparable to those of left coloplasties. In particular conduit necrosis range from 1.4- 2.4%.(2,6,8,9,10) However, Bothereau et al observed a 20% graft necrosis rate when the right colon graft was implemented. Within the same group, graft failure due to impaired blood supply was noted in 1 of 10 (10%) left coloplasties (7).

For those who are proponents of the ileocolon/ right coloplasty, they respectfully describe meticulous dissection and attention to dissecting the colon graft off the retroperitoneum and its subsequent mobilization into the thorax. Several authors have described the value of clamping the right marginal arcade and the ileocolic vessels for 10-20 minutes before dissection of the colon. In this way, if the blood supply to the graft is likely to be compromised this could be detected. In fact, with careful intraoperative consideration some authors have 309

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recommended more ileum in the graft than colon (4,8).

Apart from the relevance of the blood supply to the integrity of the graft, other anatomical attributes have contributed to the use of different parts of the colon as an esophageal conduit. The ileo-colon is preferred by some because the similar diameter of the cervical esophagus and the ileum improves the facility of anastomotic procedures relative to the colon. The ileum is less bulky than the colon, which sometimes result in cervical wound bulging. Preservation of the ileocecal valve within the graft may help regurgitation of digestive juices.(4,11) To this end, Popovici et al recommended harvesting as long a terminal ileum segment as possible.(8)

Short segment colon interposition grafts usually, the right or transverse colon, are targeted for reconstruction of the intrathoracic esophagus. Long colon interposition grafts, often of the left colon, are employed for anastomosis to the cervical esophagus or pharynx. Classically isoperistaltic colon interposition grafts are employed in the reconstruction of the esophagus when long term survival of the patient is anticipated. The left colon has been considered by many to be a preferable conduit for several reasons. First, the diameter of the left colon is smaller and less prone to dilatation. The blood supply has been shown in anatomic studies to be more reliable than the right colon. The left colon provides adequate length for reconstruction of not only the intra thoracic esophagus but also the cervical esophagus and pharynx. Finally, the left colon is quite effective at propelling a solid bolus and is acid resistant.(12,13) Significant reported results utilizing the left colon graft for esophageal replacement are illustrated in the table below:

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LEFT COLOPLASTIES Reference

No. of Pt

Left Colo-

Operative

Graft Ne-

Anastomot-

Anastomotic

plasty (% of

Mort-

crosis %

ic Leakage

strictures %

procedures)

abilty %

DeMeester12

92

92

5

7.6

4.3

4.3

Cerfolio 14

32

63

9.4

9.4

3.3

24

Isolauri 15

248

54

16

3

4

No report

Thomas 16

60

88

8.3

5.0

10

13.5

Kolh 17

38

63

2.5

0

0

No report

258

76.7

4.16

1.55

7.76

4.46

Knezevic

6

%

Compared with the preferred gastric pull up, the disadvantages of left coloplasty include the long operative times caused by mobilization of the colon and the additional anastomoses which increases the risk of complications. The overall rates of complications seem to be higher with this approach with average rates of ischemic complications for stomach 3.2% and that for colon 5.1%.(18,19) Briel and colleagues compared stomach versus colon conduit use after esophagectomy and noted an overall incidence of ischaemia of 9.2%. In their series, the incidence of ischemia for stomach and colon was 10.4% and 7.4% respectfully.

Anastomotic leaks and stricture rates, both thought to be sequelae of ischemia, also were lower for colon conduit use than for stomach conduit. Multivariate analysis identified patient comorbidities as the only independent risk factor for conduit ischemia. These findings supported their preferential use of colon conduits.(20) Other reports from high volume centres demonstrate no significant difference in operative morbidity and mortality rates between colon interposition and gastric pull up. (20,21)

With time, technical advances have been made in improving the outcomes of this challenging procedure. De Meester is credited for the improvement in the technical aspects of the left coloplasty that preserves adequate blood supply and 311

A CASEBOOK OF TWENTY SURGICAL CASES

inserting the graft in such a manner so as to maximize its ability to transport food. These are summarized as follows :(12)

There are five techniques that are helpful in preserving optimal blood supply to a left coloplasty based on the left colic artery:

1) Preserve both the ascending branch of the left colic artery and the distal marginal artery and vein when mobilizing the colon. This allows further blood supply to the graft from the sigmoid arteries and venous drainage via the haemorrhoidal and sigmoid veins.

2) The second technique is to ligate the middle colic artery and vein below the division in to their left and right branches. This provides an adequate arcade between the two branches to maintain the blood supply to the right half of a long graft.

3) The distal end of the graft is divided without dividing the mesentery and its vessels.

4) When using the substernal route, the acute angle at the diaphragm should be changed to a smooth rounded curve to prevent kinking of the vessels of the graft.

5) The graft should be delayed if there is any concern regarding its blood supply.

There are five techniques that are important in inserting the colon graft in a manner to maximise its transport function.

1) Perform the proximal anastomosis with a single layer of interrupted sutures to prevent narrowing.

2) Anchor the colon graft in as straight a line as possible to the diaphragm thus avoiding redundancy and upward movement of the colon into the chest.

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3) The gastric anastomosis on the posterior wall of the stomach, one third the distance from the fundus to the pylorus. This reduces regurgitation and development of an ulcer in the graft.

4) Avoid performing a pyloroplasty unless based on the preoperative gastric emptying studies it is deemed necessary. This prevents against bile reflux gastritis in the stomach and colitis in the graft.

5) When using the substernal route, the left half of the manubrium and the sternal head of left clavicle should be resected to avoid compression and obstruction of the graft.

As previously explained properties of the stomach make it a suitable conduit for esophageal replacement and is widely used once available. It does have some drawbacks however. The most pertinent of these are significant loss of capacity of the gastric reservoir and long term gastroesophageal reflux with its attendant pulmonary complications and possible recurrent peptic stricture.(6) The experience of De Meester on colon replacement of the esophagus for benign disease creates a point of debate. In a review of 104 cases of esophageal replacement for benign disease colon was used for reconstruction in 84 patients, stomach in 10 patients, jejunum in 9 and a composite in 1. The primary underlying esophageal pathology was a severe end- stage motility disorder (36%), undilatable stricture(25%), traumatic, spontaneous or iatrogenic perforation (13%), end- stage gastroesophageal reflux (11%), corrosive injury (8%) or others (8%). The results indicate that overall hospital mortality was 2%. Graft necrosis occurred in 3% of patients and anastomotic leak in 2% of anastomoses. The most commonly affected anastomosis was the esophagocolonic anastomosis. Thirty percent of patients undergoing a gastric pull-up required postoperative dilatation, while this was necessary in only 5% of patients with colonic interposition. Long 313

A CASEBOOK OF TWENTY SURGICAL CASES

term outcome which extended over 4 years reflected that 83% of respondents could eat three meals a day without difficulty while 69% reported the pleasure of an unrestricted diet. For these patients a recommendation was made for colon interposition in patients with benign esophageal diseases refractory to more conservative measures. This is particularly so if a vagal sparing esophagectomy can be performed. They argue that with the stomach maintained in its native location, it allows for normal gastric and bowel function after colon interposition.

With benign disease, a vagal sparing esophagectomy may be possible allowing the interposed colon to be anastomosed to a fully innervated stomach and distal gastrointestinal tract.

From a technical standpoint, this report highlighted the importance of excluding any evidence of delayed gastric emptying or a denervated stomach. In this situation, delayed gastric emptying results in the regurgitation of gastric contents back up through the interposed stomach. Consequently many of the problems ascribed to colon interposition are due to poor gastric emptying. They recommend in such cases that a two third proximal gastric resection be done whenever a colon interposition connects to the stomach. This give a better functional result in that the interposed colon functions as a reservoir for the retained antrum which under these conditions, continues its innate three contractions per minute, maintaining its pump function. (21)

The literature reflects that the colon has been widely used as an esophageal conduit following esophagectomy for both malignant and benign conditions.

Though this procedure can be associated with significant complications and mortality, several reported series indicate that these can be kept within acceptable limits. The choice between right or left colon for esophagoplasty is still debatable and generally depends on surgeon preference. As noted earlier the decision weighs heavily on the available blood supply, with that of the right colon being 314

A CASEBOOK OF TWENTY SURGICAL CASES

more variable. In order to analyse colonic vascularisation, pre operative arteriography has been used by several investigators.(6,12). Conversely, others opine that despite precise anatomical analysis, arteriography does not allow functional assessment of blood supply and especially the quality of venous outflow. Also that arteriography should not replace intra- operative clamping tests which is the only reliable means to assess, in a reversible way, the future vascular conditions after pedicle ligation.(16) Bothereau et al observed a 20% graft ischaemia despite successful clamp testing.(7). Others have suggested a selective approach for mesenteric arteriography for patients with pervious vascular insufficiency of the lower limbs, abdominal aortic aneurysm repair or previous laparotomy.(14)

An interesting point to note is that the temporal order of graft selection should be considered. With proponents of right and left coloplasties defending the use of each graft, it may be wise when the colon is available to consider the use of a right sided graft first. This suggestion is based on the possibility of using the left colon as a rescue transplant in case of postoperative right colic transplant necrosis. The opposite on the other hand may not be feasible, as during left coloplasty, proximal colic division is performed at the right part of the transverse colon. The remaining right colon may be of insufficient length for a rescue right coloplasty.(7)

During reconstruction of the esophagus, position of the graft is relevant. The graft could be positioned subcutaneously, substernally or in the esophageal bed within the posterior mediastinum. These locations have implications for both the procedure and outcome. The subcutaneous route requires a longer graft to be harvested and positioned other than orthotopic offers a greater propensity for twisting and kinking which may contribute symptoms of dysphagia. Reconstruction using the retrosternal route is common in many surgical departments because anastomotic leakage or necrosis of the colon graft within the poste315

A CASEBOOK OF TWENTY SURGICAL CASES

rior mediastinum can lead to severe infection and sepsis.(5,23). Others postulate the posterior mediastinal route as the route of first choice, which provides better long term functional outcomes after operative therapy than the retrosternal route(16,24). The subcutaneous route has been largely abandoned because of its required length and poor functional and aesthetic results.

The colon can be placed isoperistaltically or anisoperistaltically. From a functional standpoint, the colon graft has poor motility, therefore the passage of food is slow and occurs mainly due to gravity. It is the opinion of many that the colon graft must be transposed in an isoperistaltic position. Experiential studies showed that the isoperistaltic colon has a reasonable reservoir function and clearance is completed by peristaltic activity that prevents regurgitation and aspiration.(6,12,25).

Despite the plethora of reports in support of colonic grafts for esophageal reconstruction, there are instances where this would be inappropriate. Absolute contraindications to colon interposition are the presence of intrinsic colonic disease such as inflammatory bowel disease or malignancy and inadequate arterial blood supply to the colon. Relative contraindications to the use of the colon include portal hypertension, extensive diverticular disease and multiple colonic polyps.

Mild diverticulosis without extensive inflammatory changes and the presence of a few colonic polyps that can be removed before surgery do not preclude the use of the colon for interposition. Advanced age or the presence of severe cardiac or pulmonary diseases is also relative contraindications. Colonoscopy is advocated by many in the pre- operative planning of these procedures to identify any relevant pathology.(22)

The colonic conduit provides good long term function. However, unique to the colonic conduit is the risk for redundancy. This may be related to technical 316

A CASEBOOK OF TWENTY SURGICAL CASES

failure and has been reported for 15% to 30% of patients. Redundancy of the colonic conduit can also manifest years later.(2,26) Over time, this may cause obstructive symptoms such as dysphagia and regurgitation and correction can be a complex undertaking. Very few cases of revision are reported in the literature, with few indications on how to avoid or reliably repair this complication. A host of other symptoms may be experienced as long term sequelae and these include: regular regurgitation, early satiety, diarrhoea, nausea, bloating, dumping and halitosis.(12,16)

The case described here involved a non dilatable stricture related to lye ingestion. This particular problem presents its own peculiarities which may influence the outcome following esophageal reconstruction. Accidental or intentional ingestion of caustic substances can cause very severe destruction of the tissues and organs of the foregut. Intentional, mainly suicidal ingestion of caustic substances is very common in Eastern Europe, South America and Asia.(6) Prognosis of the esophageal lesions is mainly influenced by the type, concentration and amount of the caustic material ingested. Esophageal strictures related to lye ingestion appear in up to 85% of patients.(6) Though some of these are amenable to repeated dilatation, many require esophageal reconstruction.

In a recent review of esophageal reconstruction after caustic injury, a cervical anastomotic rate of 38% was observed with colonic conduit. This high rate related to the pathophysiology of caustic injury. The proximal extent of the caustic injury is variable and may include the esophageal os, hypopharynx and oropharynx. As a result it may require a colonic transplant sufficient to reach the pharynx or sometimes the tongue base .Inherent in this attempt, is the risk of blood supply insufficiency at the tip of the transplant. The cervical anastomosis has to be constructed with previously injured esophageal or pharyngeal tissues.

While this may appear macroscopically healthy at the time of anastomosis, such 317

A CASEBOOK OF TWENTY SURGICAL CASES

tissues are at increased risk of fistulisation or stenosis (7).

It has been noted that postoperative upper digestive tract stenosis after reconstruction for caustic injury often result from delayed progressive caustic scarring of the tissue where the anastomosis is performed.(27) To avoid such stenosis, it is important to delay the date of reconstruction after caustic ingestion up to 3 months in the absence of pharyngeal injury and up to 6 months in cases of pharyngeal injury. In fact, it has been established that the duration of healing was longer at the pharyngeal level.(28) This is a critical issue and some authorities recommend that even in the absence of pharyngeal lesions, an effort should be made to resect all of the cervical esophagus. Even if macroscopically healthy, it is suggested that the cervical anastomosis be performed with the hypopharynx. (7).

The location of the transplant is a point to debate for these patients. Some regard the retrosternal route as mandatory due to the combination of previous esophagectomy and mediastinal caustic injury resulting in a sclerous posterior mediastinum.(7) Knezevic et al employed the posterior mediastinum for patients who underwent esophagectomy. This route was shorter and reportedly better as noted previously. However, they encountered abundant bleeding in two patients.

While esophagectomy makes the esophageal bed available to the conduit, it is questionable whether to perform routine esophagectomy or not. Some authors who back this position, assume that corrosively changed esophagus has a high risk of developing malignancy. According to the literature, the incidence of carcinoma development on corrosively scarred esophagus after a period of 40-50 years from caustic ingestion is about 4%.

(29,30)

Others are of the opinion that

this standpoint relates only to patients whose esophagus has been constantly exposed to the thermal and chemical effects of food. If the reconstruction is performed 6- 12 months after the caustic ingestion and the esophagus is ex318

A CASEBOOK OF TWENTY SURGICAL CASES

cluded from the passage of food, the risk of developing malignancy is becoming irrelevant.(30) Knezevic holds a selective approach in this group of patients in view of the risk of serious complications. An esophagectomy is suggested only in patients who have a complete caustic stricture of the thoracic portion of esophagus. Exclusion of this portion of the esophagus from the passage may result in an esophageal mucocele. Esophagectomy may also be considered when the reconstruction is performed decades after the caustic ingestion, due to its malignant potential.(6)

The final point of note for these patients is whether there is stomach involvement and to what extent the stomach, if not injured, may be used for the conduit.

If it is injured and requires resection, then a colonic graft can be made available.

In the case described, the stomach had injury limited to the pyloric area. Distal continuity was facilitated by the use of a previously constructed gastrojejunostomy. This allowed the stomach to retain its native place and function while receiving the distal aspect of the colon graft.

CONCLUSION The use of colon graft for esophageal reconstruction may be associated with significant morbidity and mortality. Several authors demonstrate that with careful preparation the colon graft can provide acceptable results particularly in the long term which is desirable, as for the case presented here. The right and left colon could be utilised as an esophageal conduit but surgeons must be aware of the disadvantages of each. The stepwise use of the right colon before the left colon may prove strategic in case of graft failure. This will increase flexibility and offer another chance of graft replacement if necessary in the future.

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REFERENCES 1.Pascal T, Fuentes P, Giudicelli R, et al. Colon interposition for esophageal replacement: current indications and long-term function. Ann Thorac Surg 1997; 64: 757– 64.

2.Davis PA, Law S, Wong J. Colonic interposition after esophagectomy for cancer. Arch Surg 2003; 138: 303-308.

3. Marks JL, Hofstetter WL. Esophageal reconstruction with alternative conduits. Surg Clin North Am 2012; 92(5): 1287-97.

4. Mine S, Udagawa H, Tsutsumi K, et al. Colon interposition after esophagectomy with extended lymphadenectomy for esophageal cancer. Ann Thorac Surg 2009;88:1647–54.

5.Klink CD, Binnebo..sel M, Schneider M, et al. Operative outcome of colon interposition in the treatment of esophageal cancer: A 20-year experience. Surgery 2010; 147: 491-6.

6.Knezevic JD, Radovanovic S, Simic P, et al. Colon interposition in the treatment of esophageal caustic strictures: 40 years experience. Diseases of the Esophagus 2007; 20: 530–534.

7.Bothereau H, Munoz-Bongrand N, Lambert B, et al. Esophageal reconstruction after caustic injury: is there still a place for right coloplasty? Am J Surgery 2007; 193: 660–664.

8. Popovici Z. A new philosophy in esophageal reconstruction with colon. Thirty-years experience. Dis Esophagus 2003;16: 323–7.

9. Shiraka Y, Naomoto Y, Noma K, et al. Colonic interposition and supercharge for esophageal reconstruction. Langenbecks Arch Surg 2006; 391:19 –23.

10. Doki Y, Okada K, Miyata H, et al. Long-term and short-term evaluation of esophageal reconstruction using the colon or the jejunum in esophageal cancer patients after gastrectomy. Dis Esophagus 2008;21:32– 8.

11. Metzger J, Degen L, Beglinger C, et al. Clinical outcome and quality of life after gastric and distal esophagus replacement with an ileocolon interposition. J Gastrointest Surg 1999;3: 383– 8.

12. DeMeester TR, Johansson K-E, Franze I, et al. Indications, surgical technique, and longterm functional results of colon interposition or bypass. Ann Surg 1988; 208: 460–74.

13.Mansour KA, Bryan CF, Carlson GW. Bowel interposition for esophageal replacement: Twenty five year experience. Ann Thorac Surg 1997; 64:752– 6.

14.Cerfolio RJ, Allen MS, Deschamps C, et al. Esophageal replacement by colon interposition.

Ann Thorac Surg 1995; 59: 1382-1384.

15.Isolauri J, Markkula H, Autio V, et al. Colon interposition in the treatment of carcinoma of the esophagus and gastric cardia. Ann Thorac Surg 1987; 43: 420-424.

16.Thomas P, Fuentes P, Giudicelli R, et al. Colon interposition for esophageal replacement : current indications and long term treatment. Ann Thorac Surg 1997; 64: 757-764.

17. Kohl P, Honore P, Degauque C, et al. Early stage results after oesophageal resection for malignancy: colon interposition vs gastric pull-up. Eur J Cardiothorac Surg 2000; 18: 293-300.

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18. Kao CH, Wang SJ, Chen CY, et al. The motility of interposition in patients with esophageal carcinoma after reconstructive esophageal surgery. Clin Nucl Med 1993; 18: 782-5.

19.Wormuth JK, Heitmiller RF. Esophageal conduit necrosis. Thoracic Surg Clinics 2006: 16(1): 11-22.

20.Briel JW, Tamhankar AP, Hagen JA, et al. Prevalence and risk factors for ischemia, leak and stricture of esophageal anastomosis: gastric pull-up versus colon interposition. J Am Coll Surg 2004;198: 536–542.

21. Hagen JA, DeMeester SR, Peters JH, et al. Curative resection of esophageal adenocarcinoma. Ann Surg 2001;234:520 –31.

22.De-Meester TR. In :Operative Techniques in Cardiac & Thoracic Surgery, Vol 2, (1), 1997.

WB Saunders: pp 73-86.

23. Wain JC, Wright CD, Kuo EY,et al. Long-segment colon interposition for acquired esophageal disease. Ann Thorac Surg 1999; 67: 313-7.

24. Motoyama S, Kitamura M, Saito R, et al. Surgical outcome of colon interposition by the posterior mediastinal route for thoracic esophageal cancer. Ann Thorac Surg 2007; 83: 1273-8.

25. Dreuw B, Fass J, Titkova S. Colon interposition for esophageal replacement: isoperistaltic or antiperistaltic: experimental results.Ann Thorac Surg 2001; 1: 303–8.

26.Urschel JD. Does the interponat affect outcome after esophagectomy for cancer? Dis Esophagus 2001; 14: 124-130.

27. Cattan P, Chiche P, Berney T, et al. Surgical approach by cervicosternolaparotomy for the treatment of extended cervical stenoses after reconstruction for caustic injury. J Thorac Cardiovasc Surg 2001; 122: 384–6.

28. Brette MD, Aidan K, Halimi B, et al. Pharyngo-esophagoplasty by right coloplasty for the treatment of post-caustic pharyngo-laryngealesophageal burns: a report of 13 cases. Ann Otolaryngol Chir Cervicofac 2000;117:147–54.

29. Young T K, Sook W S, Yoo H K. Is it necessary to resect the diseased esophagus in performing reconstruction for corrosive esophageal stricture? Eur J Cardiothorac Surg 2001; 20: 1–6.

30. Gerzic Z, Knezevic J, Miliæevic M. Esophagocoloplasty in the management of postcorrosive strictures of the esophagus. Ann Surg 1990; 211: 329–36.

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17. PERFORATED DUODENAL ULCER Role of H pylori in ulcer disease and treatment limitations. Changing paradigms in acid suppression (is there a role for surgical acid suppression?

INTRODUCTION The main consequences of peptic ulcer disease are pain, perforation, haemorrhage and obstruction. Operative management of patients who have chronic problems (pain, obstruction) has all but disappeared. The majority of operations performed in the current era are for emergencies: bleeding and perforation.

Duodenal and pyloric channel perforations are the most common sites of ulcer perforation and are functionally grouped as duodenal perforations. Operative intervention is almost always indicated in the treatment of perforated peptic ulcers. About two decades ago, controversy existed about the most appropriate operative approach for acute perforation of duodenal ulcers. Simple suture or omental patch closure was complicated by recurrent ulcers in more than half of cases followed long term. In appropriately selected patients, acid reducing operations such as proximal gastric vagotomy or truncal vagotomy and drainage were shown to reduce recurrence rate to about 10%.

However, our current understanding of peptic ulcer pathogenesis has decreased the need for acid reducing surgical procedures. Increased understanding of the biology of Helicobacter pylori (H. pylori), indicates that infection of the gastric mucosa with H. pylori is responsible for most of the observed changes in gastric acid secretion seen in peptic ulcers. Following the discovery of H. Pylori, multiple trials demonstrated that effective eradication of H. pylori with a short course of antibiotics and proton pump inhibitors (PPI) resulted in relapse â&#x20AC;&#x201C; free cure 322

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of the vast majority of ulcers. In addition, the use of aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) by inhibiting mucosal defence mechanisms against an acid mediated injury are able to cause peptic ulcers, either independently or synergistically with H. pylori. This new understanding of peptic ulcer disease implies that the great majority of peptic ulcer disease is the result of modifiable causes.

Omental patch closure is an appealing surgical solution as it is expeditious.

These patients are quite ill and recurrence can be limited by H. pylori eradication therapy. This form of therapy may be suited for the elderly and those with multiple co-morbidities. On occasion, complicated ulcers do present. Also, there are limitations to the management of H. pylori. This includes compliance with medications, increasing antibiotic resistance and compliance by clinicians and patients to confirm eradication. Younger patients are also more likely to indulge in ulcerogenic habits such as smoking and alcohol consumption.

While the need for acid reducing procedures has diminished considerably, they may not have vanished completely. An even bigger challenge is the lack of expertise to perform these procedures. Laparoscopic repair of perforated duodenal ulcers has been introduced and is becoming an increasing trend. It brings the usual advantages of laparoscopy- smaller incision, minimal pain and early ambulation. Similarly, a particular challenge is the ability to perform acid reducing procedures laparoscopically.

Despite the success of medical management of peptic ulcer disease, it is prudent that the current day surgeon understand the surgical options available in the management of perforated peptic ulcers. Changing epidemiology of the disease may demand a change in surgical strategies, perhaps even a need for acid reducing procedures.

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A CASEBOOK OF TWENTY SURGICAL CASES

A summary of cases of perforated peptic ulcers that were managed during residency is presented. Following this is a discussion on the role of H. pylori in ulcer pathogenesis and its treatment. The surgical management perforated duodenal ulcers is also described which includes a comment on the role of acid reducing procedures.

CASE SERIES: Age/Sex Loca-

Procedure

tion

Comor-

Complica-

Out-

bidities/

tions

comes

Risk fac1

70yr /M

D1

Graham Patch

tors Rh ar-

Blow out of Died of

thritis,

Patch, Burst MODS

DM, IHD, abdomen CVA, 2

71yr/M

D1

Antrectomy

NSAIDS HTN

and Bilroth II 3 4 5 6 7

63yr/M

Pre-

78yr/M

pyloric Pre-

62yr/M

pyloric Pre-

62yr/F

pyloric Pre-

40yr/F

pyloric D1

Duodenal

Died of

stump blow sepsis

reconstruction out Graham Patch DM, HTN nil

dis-

Graham Patch

charged DM, HTN, Burst abdo- Died (MI)

Graham Patch

Alcohol Alcohol,

men nil

> 30 days dis-

Graham Patch

Smoker Rh ar-

Wound

charged dis-

Graham Patch

thritis, Rh ar-

infection nil

charged dis-

thritis, NSAIDS

324

charged

A CASEBOOK OF TWENTY SURGICAL CASES

8 9

76yr/M 19yr/M

Pyloric Prepy-

Graham Patch Graham Patch

Marijuana nil

dis-

Alcohol

charged dis-

loric

nil

charged

CASE 1 History: This gentleman presented 3 days after the onset of symptoms. He was tachycardic and was admitted to the ICU for resuscitation before undergoing laparotomy. On day 7 there was discharge from the midline epigastric wound.

On closer inspection bile stained fluid and pus was noted to be discharging with separation of the abdominal closure.

This patient had a re-laparotomy and the omental patch was redone. The abdomen was also repaired and he returned to ICU. Unfortunately he never recovered from the sepsis, developed multi-organ dysfunction syndrome (MODS) and died.

CASE 2 History: This gentleman presented with peritonitis. He was resuscitated preoperatively and taken for a laparotomy. At laparotomy the first part of duodenum bore a 3cm perforation with edematous friable edges. This would not have supported sutures and so a resection including the antrum of the stomach was undertaken. He was admitted to ICU post operatively.

Despite a tube duodenostomy, the stump broke down. He died of sepsis.

All the others had a Graham patch repair (Fig 1 & 2) and was given H. pylori eradication therapy for presumed H. pylori infection. Case 8 actually had serology performed privately. This was negative though and subsequent gastroscopy was also normal. No specific cause was found.

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Case 9 , a 19 year old boy attended for post-operative follow up 6 weeks after discharge. He was encouraged to have his H. pylori titres checked and never did. He eventually absconded from follow up.

Fig 1. Vicryl sutures placed but not tied

Fig2. Vicryl sutures tied over tongue of omentum (Graham Patch)

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DISCUSSION Multiple reports from several countries have indicated a decrease in elective surgery for peptic ulcer disease (PUD), as much as 90%, over the last two decades. This is in keeping with the changing and greater understanding of the pathogenesis of peptic ulcer disease. Major improvements in medical treatments for PUD, including the introduction of histamine (H2) receptor antagonists, use of proton pump inhibitors and H. pylori eradication with antibiotics, have significantly reduced the need for surgical treatment of the disease.

Initial ideas regarding ulcerogenesis held the concept of excessive acid secretions as the major culprit and that this was further compounded by smoking, alcohol and stress. As a result, long term solutions to decrease acid secretion lead to surgical procedures (vagotomy and/or surgical elimination of acid secreting gastric mucosa), or chronic use of medications to suppress acid secretion (H2 antagonist, proton pump inhibitors (PPI). The major player in pathogenesis of PUD was identified by Warren and Marshall in 1982. (1) They identified H. pylori as a causative agent in PUD and changed the acid dogma to one of an infectious disease. Decades of dominance of surgical intervention and subsequently long term acid suppression therapy was replaced with a short-term antibiotic regimen targeting eradication of H. pylori infection.

H. pylori is a gram negative, helical shaped, microaerophilic bacterium found in the stomach. More than 50% of the worldâ&#x20AC;&#x2122;s population has a chronic H. pylori infection of the gastric mucosa, yet only 5-10% of those infected develop ulcers. Infection is more prevalent in developing countries, and the incidence is decreasing in western countries. (2) Factors determining whether the infection will produce disease are the pattern of histological gastritis induced, changes in homeostasis of gastric hormones and acid secretion, gastric metaplasia in the duodenum, interaction of H. pylori with the mucosal barrier and immunopatho327

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genesis, ulcerogenic strains and genetic factors.

H. pylori colonises the entire gastric epithelium, from the pre-pyloric antrum to the cardia. Clinical outcomes are dependent on the pattern of chronic mucosal inflammation induced. In patients with the duodenal ulcer, density of infection and severity of inflammation are greatest in the distal antral region with sparing of the acid-secreting body mucosa. After H. pylori eradication, gastric mucosa changes are usually fully reversible. In gastric ulcer, inflammation affects the body and antral mucosa to a similar degree, although it varies dependent on ulcer location. Unlike in duodenal ulcer, acid secretion in gastric ulcer can be decreased because of the more severe involvement of acid-secreting body mucosa. However, a crucial amount of acid production is always conserved.(3)

In antrum-predominant non-atrophic H. pylori gastritis, both basal and stimulated gastric acid output is increased. This effect is most pronounced in patients with duodenal ulcer. Patients with duodenal ulcer and H. pylori infection produce more acid than do infected people without ulcers in response to the same stimulation with gastrin. Patients with duodenal ulcers also have more acidsecreting parietal cells than do people without ulcers and produce more acid in response to maximum gastrin stimulation. A highly constitutive acid secretory capacity might therefore promote development of antral predominant body sparing gastritis and thus duodenal ulceration. (4)

H. pylori infection impairs negative feedback regulation of gastrin release and thus acid secretion. A low antral pH stimulates release of somatostatin from D cells in the antral gland, and this somatostatin exerts paracrine inhibitory control of gastrin release from adjacent G cells. H. pylori has very high urease activity, producing ammonia to protect the organism from its acidic gastrin environment.

Production of alkaline ammonia by bacteria on the surface epithelium and in 328

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the glands of the antrum prevents D cells in the gland from sensing the level of acidity. This leads to inappropriate decrease of somatostatin and an increase in gastrin and consequently excess acid secretion. The trophic effect of hypergastrenemia induced by H. pylori also induces hyperplasia of the enterochromaffin- like and acid- secreting parietal cells. (5, 6) Further increase of the acid output in patients with H. pylori associated duodenal ulcer may result from functional disruption of antral- fundic neural connections. Impairment in this inhibitory neural control, in association with the hypergastrenemia previously described leads to further increase of acid output. (7)

Colonization with H. pylori is specific and exclusive to gastric epithelial cells.

The resulting acid overload in the duodenum results in development of metaplasia of the duodenal bulb. Metaplasia is a prerequisite for H. pylori colonization of duodenal epithelium. Once colonized, this inflamed duodenal mucosa becomes more susceptible to peptic acid attack and ulceration. (8) The ulcerogenesis of H. pylori related gastric ulcers are somewhat different. Infection involving the antrum and body of the stomach results in an inflammatory response in gastric mucosa. Influx of neutrophil and macrophage into the gastric mucosa with release of lysosomal enzymes, leukotrienes and reactive oxygen species, impairs mucosal defenses resulting in gastric ulcers.(3)

H. pylori isolated from patients with ulcer disease carry a high virulence. Features of increase virulence include a strong adhesive property and an increased production of enzymes with toxic potential. Strains of H. pylori from ulcer patients might produce higher amounts of urease than do those from people without ulcers. Urease catalyses the production of ammonia, which in high concentrations is followed by formation of toxic complexes. Specific H. pylori genotypes are associated with severe morbidity. The most prevalent genotypes in patients with peptic ulceration are vac A+ (vacuolating cytotoxin) and cag A 329

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(cytotoxin associating gene A). These cause greater cellular injury and enhance the local inflammatory response. (9) A genetic predisposition to acquire H. pylori has been shown in twins with an increased affinity in monozygotes versus dizygotes. (10) Earlier studies indicate that people with blood group O carry a higher risk for ulcer disease than do those with other blood groups. (11) H. pylori adhesion to gastric mucosa is increased in patients positive for Lewis b antigens, which are expressed on blood and gastric epithelial cells. (12) The pathogenetic importance of this finding is controversial. The presence of these antigens is believed by some to contribute to more severe mucosal damage through increased adhesion. On the other hand, others suggest that binding of H. pylori to these antigens would help to eliminate the organism by shedding of the surface of gastric epithelial cells. (3)

H. pylori- host interactions in the ulcer pathogenesis are complicated and aggravated by environmental risk factors. The greater understanding of the role of H. pylori in ulcerogenesis has been proven by a multitude of studies repeatedly demonstrating greater ulcer healing and reduced ulcer relapse rates once H. pylori eradication is instituted. These findings led to the 1994 National Institute of Health consensus statement, which said that antibiotic treatment in addition to anti-secretory therapy is needed in all patients with H. pylori positive ulcers.

This has been implemented in all subsequent guideline recommendations for therapy of peptic ulcer disease. (13) The use of aspirin and non- steroidal anti- inflammatory (NSAIDs) has long been recognized as an important cause of peptic ulcer disease. These drugs inhibit the production of prostaglandin in the stomach that plays a critical role on the mucosal defences of the stomach against acid induced and pepsin induced injury. In the stomach, the prostaglandin stimulates mucin and bicarbonate production and plays an important role in the regulation of gastric mucosal blood flow. By inhibitory mucosal defense mechanism against acid mediated injury, 330

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NSAIDs are able to cause peptic ulceration independently, but also synergise with H. pylori infection to cause peptic ulcer.

(14)

From a clinical standpoint,

there is data to suggest that H. pylori has no effect on, or decrease ulcer risk in NSAID users. Two systematic reviews have shown that H. pylori infection substantially increases risk of peptic ulcer and ulcer bleeding in chronic NSAID users. (14, 15)

In one study, risk of ulcer bleeding was increased by a factor of 1.79 with H. pylori infection, by 4.85 with NSAID usage and by 6.13 in the presence of both NSAID use and H. pylori infection. (14) In patients who are about to start NSAIDS, eradication of H pylori substantially reduces subsequent risk of endoscopic and complicated ulcers. Additionally, no difference is reported between H. pylori eradication and continued therapy with a PPI in primary prevention of ulcers in a regular NSAID user with average gastrointestinal risk.

(17)

How-

ever, eradication of H. pylori alone is not sufficient to prevent ulcer bleeding in NSAID users with a high gastrointestinal risk, such as a history of ulcer bleeding.

Before the role of H. pylori in ulcerogenesis was clearly defined, medical therapies targeted gastric acid suppression and mucosal defense mechanisms. The most successful classes of drugs were those inhibiting gastric acid secretion. H2 receptor antagonists were associated with high rates of ulcer healing and remission when given as maintenance therapy. More potent acid suppression was provided by the introduction of the proton pump inhibitors (PPIs) in the late 1980s.

However, after the healing phase, ulcers were usually seen to recur and for years standard practice was to keep patients on maintenance acid suppression, until the introduction of H. pylori eradication therapy. Reinforcement of the mucosal barrier is another means by which ulcer healing may be achieved. Its major application is protection against NSAID induced ulcers and includes drugs such 331

A CASEBOOK OF TWENTY SURGICAL CASES

as Misoprotol, Sulcrafate and Bismuth salts. Bismuth salts with some intrinsic anti H. pylori activity are used in ulcer therapy only in combination with antibiotics. (3)

Our current understanding of peptic ulcer disease suggested that H. pylori and NSAID use, either alone or in combination, are the causative agents for the vast majority of peptic ulcers. As such the great majority of peptic ulcer disease is the result of treatable or modifiable causes. Previous surgical strategies to reduce acid production has largely been replaced by H. pylori eradication in H. pylori positive peptic ulcer and PPI for healing and preventing peptic ulcers induced by gastrotoxic drugs.

H. pylori eradication is usually achieved with a combination of acid- inhibiting therapy and antibiotics. Antibacterial therapy alone does result in healing, but the process is accelerated by addition of acid supplements (i.e. PPI therapy).

The Maastricht Consensus Report provides recommendations on treatment of H. pylori infection19:

First-line options (7–14 days) • In populations with less than 15–20% clarithromycin resistance and greater than 40% metronidazole resistance: proton-pump inhibitor (PPI) standard dose, clarithromycin 2×500 mg, and amoxicillin 2×1000 mg, all given twice a day • Less than 15–20% clarithromycin resistance and less than 40% metronidazole resistance: PPI standard dose, clarithromycin 500 mg, and metronidazole 400 mg or tinidazole 500 mg, all given twice a day • In areas with high clarithromycin and metronidazole resistance: bismuth-containing quadruple therapy

Second-line option (10–14 days) 332

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• Bismuth-containing quadruple therapy • PPI plus metronidazole and amoxicillin, if clarithromycin was used in firstline treatment (in Latin America and China, furazolidone 2–4×100 mg is often preferred over metronidazole)

Rescue therapies (10–14 days) • PPI twice a day plus amoxicillin 2×1000 mg with either levofloxacin 2×250 (500) mg, or with rifabutin 2×150 mg

Eradication rates depend on several factors: a) drug regimen b) resistance rate to the antimicrobial agent used c) compliance with the drug d) duration of therapy e) genetic variations in drug- metabolizing enzymes. Two antimicrobials often used in eradication regimens are clarithromycin and metronidazole. H. pylori can be resistant to either of these drugs, causing reduced eradication rates.

Checking for antimicrobial sensitivity before treatment of H. pylori is not routine. However, if a patient has previous exposure to these antimicrobials or lives in a region where these drugs are frequently prescribed, they are more likely to have a resistant strain and alternative antimicrobials should be prescribed. The H. pylori eradication failure rate of 16% among patients completing the antibiotic regimen is typical and emphasizes that resistance to metronidazole has become common in developed countries (greater than 40% in the United States).

Even resistance to clarithromycin, the most effective single agent currently used in FDA-approved regimens, is now estimated to be 8% in the United States. (20) This is particularly relevant to our patient population where patients can avail themselves of medication over the counter at various pharmacies and general practitioners, particularly when not indicated.

Testing for H. pylori infection is largely unavailable at our public hospitals.

Several simple tests have been devised to indicate infection (serology, stool 333

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antibody, C14 Urease breath test) with H. pylori. These however are not readily available. This presents two particular problems: we are unable to identify the presence or rate of infection with H. pylori. Many patients are treated empirically; however no follow up testing is done/ available to confirm eradication.

Monitoring of eradication rates is important to detect emergence of resistant strains and alert clinicians of the need to modify the treatment regimen. A recent report from the UK revealed that for 697 patients with complicated duodenal ulcer (perforation or bleeding) more than 80% of surgeons prescribed H. pylori eradication therapy while less than 60% performed any confirmatory test of eradication.(21)

The duration of eradication therapy remains controversial. In Europe 1-week triple regimens are used, whereas US guidelines recommend 10 or even 14 days of therapy. A meta-analysis showed that increasing the duration of triple therapy from 7 days to 10 days increased the eradication rate by 4% and from 7 days to 14 days by 5%. However they were unable to quantify the clinical significance as the difference were not statistically noteworthy. (22) Quadruple therapies- PPI, tetracycline, metronidazole, and a bismuth salt- are alternative first line therapies in areas of high prevalence of antibiotic resistance and achieves excellent eradication rates (>80%) as first line treatment. (23)

The most effective treatment regimens fail in about 10- 20% of patients. Bismuth- based quadruple therapy is the main option for second- line therapy if these compounds were not used previously, with eradication rates of 57- 95%.

(24)

However, since bismuth is not available in some countries because of puta-

tive toxic effects, triple therapies of various combinations have been tested as second line options. PPI combined with amoxicillin and metronidazole is recommended as second line therapy if PPI, clarithromycin and amoxicillin were 334

A CASEBOOK OF TWENTY SURGICAL CASES

used as first line. Another combination with few data but a high eradication rate (91%) is PPI, clarithromycin and metronidazole. Clarithromycin should be avoided in second line unless resistance tests confirm that the H. pylori strain is susceptible. (3)

Patients, who are not cured with two consecutive treatments, including clarithromycin and metronidazole, will have at least single and usually double resistance. No standard third line therapy exists and European guidelines recommend culture and susceptibility testing in these patients to select an eradication regimen according to microbial sensitivity to antibiotics. Classes of antibiotics that include either levofloxacin or rifabutin as a third component besides PPI and amoxicillin can be used for treatment of H. pylori infection after failure.

The eradication rate of levofloxacin containing triple salvage therapies ranges from 63% to 94%. (25) Rifabutin combined with a PPI and amoxicillin given for more than 7 days is well tolerated and highly effective against double- resistant (metronidazole and clarithromycin) H. pylori after failure of standard triple therapy. However, rifabutin can select resistance in mycobacteria, and should therefore be used cautiously and never on a large scale. When a high prevalence of metronidazole resistance is suspected, this drug can be replaced by furazolidone; there is no potential for cross resistance. In clinical trials, high eradication rates have been achieved when patients tolerated these drugs. Moxifloxacin combined with metronidazole and omeprazole is reported to be as effective, as are omeprazole, bismuth, metronidazole and tetracycline in patients failing standard triple therapy, but experience is limited and needs further validation.(26, 27)

The greater acceptance of the role of H. pylori in PUD is reflected in the decreasing incidence of unresolved dyspepsia. With the relevant constellation of symptoms, clinicians readily institute H. pylori eradication therapy. This has resulted in a steady decline in the rate of elective surgery for PUD over the last 20- 30 years. Data from the American surgical training programmes and 335

A CASEBOOK OF TWENTY SURGICAL CASES

Scandinavian national audits have shown a decrease in the rate of elective ulcer surgery of between 80- 97% during the 1980â&#x20AC;&#x2122;s and 1990â&#x20AC;&#x2122;s.(28, 29) During the residency no acid reducing procedure for peptic ulcer disease has been performed.

While operation for PUD related to pain or progressive obstruction has all but disappeared, reports from some populations indicate the incidence of operation for emergency ulcer related problem is actually increasing.(30, 31) The remainder of this discussion relates to management of perforated duodenal ulcers.

Several factors contribute to the noted increase in perforated peptic ulcers. These include the aging of the population and the increase in the numbers of persons who smoke cigarettes or take NSAIDs. The two major factors associated with perforation of peptic ulcer are thought to be cigarette smoking and NSAID use; these are thought to contribute to perforation in greater than 75% and 20- 30% of patients who perforate, respectively. In patients on NSAID therapy, there is a greater risk of ulcer perforation with a history of prior ulcer, age older than 60 years, concomitant use of medications; alendronate, selective serotonin reuptake inhibitors, steroids or anticoagulants. (32, 33)

Despite the revolutionization in understanding and medical management of PUD related to H. pylori infection, the role of H. pylori in perforation is less clear. A study from Hong Kong showed that 70% of patients who had perforated duodenal ulcer had positive biopsies for H. pylori. This infection rate was not remarkably different from the 55% prevalence of H. pylori in the general population. (34) A study from the United Arab Emirates reported that 29 patients who underwent simple closure of perforated duodenal ulcers, were tested for Helicobacter by urease breath test on postoperative day 8. Twenty four of the 29 patients were positive for urease activity.

(35)

In a report from the United

Kingdom 47% of patients who had perforated duodenal ulcers was found to be positive for Helicobacter by enzyme linked immunosorbent assay. This com336

A CASEBOOK OF TWENTY SURGICAL CASES

pared to 50% of the control population, and suggested no relationship between Helicobacter and perforation. (36) Although the relationship of perforated PUD and H. pylori seems variable, by these reports, the evidence for H. pylori in ulcerogenesis demand eradication therapy be offered to these patients. None of these tests have 100% sensitivity.

Duodenal and pyloric channel perforations are the most common sites of ulcer perforation and are functionally grouped as duodenal perforation. In an analysis of 40 trials of perforated peptic ulcer disease, perforation was most common at the duodenal bulb (62%), followed by the pyloric region (20%) and the gastric body (18%). (37) In the series presented all the patients were found to have duodenal and prepyloric ulcers.

It is important to quickly diagnose a perforated peptic ulcer. The prognosis is improved if treatment is provided within 6 hours of perforation whereas a delay in treatment beyond twelve hours following perforation is associated with an increase in both morbidity and mortality.

(38)

It is important to strati-

fy patients into different categories based on the likelihood of morbidity and mortality, so that high risk patients can receive more appropriate treatment and greater intensive care. Several risk scores exist for the prediction of outcomes in PUD however the Boey scoring system is among the commonest risk stratifications used because of its simplicity and high predictive value for mortality in perforated peptic ulcers39. Boey risk factors include: preoperative shock (<100mmHg), perforation present for more than twelve hours, and associated medical co- morbidities. Each of these risk factors scores 1 point to a maximum of 3 points with corresponding mortality rates as follows:

337

A CASEBOOK OF TWENTY SURGICAL CASES

Boey Scoring System RISK FACTORS 0 1 2 3

MORTALITY RATES % 0 10 45.5 100

The incidence of mortality of perforated PUD is 5 to 10%. Mortality increases up to 50% if the perforation has been >24 hours. (39)

Surgery is the mainstay of treatment for perforated duodenal ulcers, the objective of which is to repair the hole and treat peritoneal contamination. Boey et al. endorsed omental patch repair as it was simple and fast. The long term results of omental patch repair for perforated duodenal ulcer were unsatisfactory with ulcer recurrence rates of 50% or more. (20) Therefore, some surgeons advocated immediate acid- reduction procedures in addition to repair of the ulcer as a preventative measure against subsequent ulcer relapse. It was demonstrated that immediate definitive surgery in selected patients is safe, without increasing the rate of postoperative complications or death.

(40)

This therefore presented con-

troversy about the most appropriate operative approach for acute perforation of duodenal ulcers.

Recent advances in the anti- ulcer medical therapy (PPI and H. pylori eradication) have somewhat solved this problem. One of the sentinel papers in shifting the emphasis on perforated duodenal ulcer away from definitive intervention was presented by Ng et al. This was a randomized trial following simple closure and treatment of H. pylori. In that study, eradication of H. pylori was almost universal among patients given a multiple drug regimen. The omeprazole group, however, rarely healed. The recurrence rates at 1 year of the ulcer were only 5% in the H. pylori treatment group but 38% in the control group, thus the argument 338

A CASEBOOK OF TWENTY SURGICAL CASES

that treatment of H. pylori obviates the need for definitive treatment. (41) More recently, further support for the omental patch repair of perforated duodenal ulcer and H. pylori eradication therapy was revealed by a systematic review and meta-analysis. In this review of controlled trials of duodenal ulcer perforation, the pooled incidence of 1- year ulcer recurrence in H. pylori eradication group was 5.2%, which is significantly lower than that of the control group (35.2%).

They concluded H. pylori eradication after simple closure of duodenal ulcer perforation gives improved results. These results are better than the operation plus anti- secretory non- eradication therapy for prevention of ulcer recurrence.

They recommend that all duodenal ulcer perforated patients should be tested for H. pylori infection and eradication therapy is required in all infected patients. (42)

The omental patch closure of the ulcer can be created by fashioning a tongue of omentum and securing the tissue over the perforation with absorbable sutures.

This technique, sometimes referred to as a Graham patch, was actually first described by Cellen-Jones in 1929. Grahamâ&#x20AC;&#x2122;s description, reported in 1937, involved suturing of an omentum either free or attached without attempt at closing the perforation.

(43)

Most patients respond well to post-operative treatment

of H. pylori and chemical vagotomy with proton pump inhibitors; mortality, morbidity and ulcer recurrence with omental patch repair have all been shown to be extremely low (10%). (41,44)

One variation of the classical technique used by some surgeons is the modified omental patch. After sutures are placed between the edges of the perforation in a standard fashion, they are tied in an attempt to close the wall defect. Without cutting the sutures, a segment of omentum is then brought on top of the closed perforation and tied knots and the same sutures are used to secure the omental patch over the already approximated perforation. Opponents of this modified technique express concern regarding the seal obtained from the omentum when 339

A CASEBOOK OF TWENTY SURGICAL CASES

suture knots are interposed between the duodenal serosa and the omental patch.

At the same time, the apposition of omentum is not as broad as with the original patch. However, no definitive conclusions can be drawn from the literature regarding the difference in morbidity or mortality associated with each of these techniques. (33)

Another variation of the standard technique is the use of the sero- muscular suture placement (Lembert) instead of full thickness bites. This is accomplished without entering the duodenal lumen, and these sutures theoretically have a lower risk of passing the needle through the posterior wall, minimising the risk of obstruction.(45) In patients in whom the omentum is not available because of previous surgery, necrosis or anatomy, a variant technique is that of the Thal patch, in which a loop of jejunum is used to patch the perforation. In this case, seromuscular sutures are used to attach the serosal side of a loop of jejunum across the ulcer defect.

(45)

While the majority of perforated duodenal ulcers are simple anterior wall perforations, sometimes associated complications are involved. As such, the surgeon should be adept at dealing with these:

路 If an element of gastric outlet obstruction is suspected with a duodenal perforation it is safest to perform a pyloroplasty, or consider simple omentopexy with a diverting gastrojejunostomy, before a partial gastrectomy is considered. If post-operatively the patient develops gastric outlet obstruction, treatment options include pyloroplasty or antral resection, balloon dilatation or insertion of a removable stent.(33) 路 Large perforations are between 1 and 3cm in size, with giant perforations exceeding 3cm in size occurring in only 2.5% of peptic ulcers.

It should be stressed that simple patch closure may not be suitable for 340

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large perforations .The leak rates with its attendant morbidity and mortality are high in these patients. Various surgical options are described as these large perforations are particularly hazardous because of the extensive duodenal tissue loss and surrounding tissue inflammation.

These options include resection of the perforation bearing duode-

(46)

num and the antrum in the form of a partial gastrectomy with either a Billroth I or Billroth II anastomosis or the creation of a tube duodenostomy with antrectomy and feeding jejunostomy with GI continuity restored in 4 weeks. Others have recommended conversion of the perforation into a pyloroplasty or closure of the perforation using a serosal jejunal patch or a pedicled jejunal graft. It is probably advisable where possible to attempt the simplest closure technique. Omentopexy is still safe to perform in perforations of up to 3cm; it is simple and avoids a major resection in an already compromised patient.

(47,48)

Omental plugging can be safely performed with giant perforated duodenal ulcers with indurated, fibrotic, friable margins and seems to have a better long term outcome with regards to gastric outlet obstruction when compared to omentopexy. The technique of omental plugging is as follows: The tip from the nasogastric tube is guided through the perforation. The free edge of the omentum is then sutured to the tip of the tube which is then carefully withdrawn, pulling the plug of omentum in the stomach. The omentum is then fixed with interrupted sutures taken between the omentum and the healthy duodenum, approximately 3- 4cm from the margin of the perforation. (47) 路 Perforation with duodenal destruction Any repair will be challenging due to much inflammation and friable, fibrotic tissue edges. A higher than normal duodenal leak rate must be 341

A CASEBOOK OF TWENTY SURGICAL CASES

anticipated. Management would include similar strategies as noted previously including partial gastrectomy or gastric disconnection. (33)

These difficult situations represent a subset of patients with perforated duodenal ulcers. The surgical options described to deal with them mean that definitive anti- acid surgical procedures are required less and less. Current surgical trainees are therefore deprived of any experience with vagotomies compared with the previous surgical generation. In fact, such is the rarity of these procedures that the current focus of surgical management has shifted to open omental patch versus laparoscopic omental patch repair for perforated duodenal ulcers.

The feasibility of laparoscopic repair of perforated peptic ulcer was reported in 1990. (49) Despite this, the technique has not been widely adopted. Several of the earlier studies have documented that perforated duodenal ulcer treated by laparoscopic closure had a 20% to 25% incidence of conversion to open laparotomy, for a number of technical reasons. Three randomized clinical trials for laparoscopic versus open repair of perforated peptic ulcers have demonstrated comparable or better outcome in the laparoscopic group, revealing benefits in terms of reduced wound pain and analgesic requirement, decreased hospital stay and earlier resumption of daily activities. (50, 51, 52)

A recent meta- analysis of a number of reports of laparoscopic repair has demonstrated that this approach is superior in the short term because of lesser postoperative pain than with the open approach. This meta- analysis also demonstrated that laparoscopic repair confirmed a significant reduction in wound infection, as compared to open repair. This might in turn, reduce the future occurrence of incisional hernia. Successful laparoscopic repair will bear shorter scars and attain better cosmesis. Furthermore, the open approach in contrast to laparoscopic repair was associated with a higher incidence of chest infection 342

A CASEBOOK OF TWENTY SURGICAL CASES

and prolonged ileus. The main drawbacks of the laparoscopic approach were an increased operating time and a significantly increased re- operative rate. These are important considerations in a patient group where the technique of repair has a considerable effect on the eventual outcome. Several factors contributed to conversion include: difficulty identifying the site of perforation, large perforation, technical problems, perforated non- pyloric gastric ulcer, cardiovascular instability, iatrogenic injury, bleeding and adhesion. (53)

While the laparoscopic approach to repair of perforated duodenal ulcer can be advantageous, the evidence is not strongly in favour or against this intervention. This was demonstrated in a recent Cochrane review.

(54)

It is

probable that in the future greater benefit from the laparoscopic approach may be identified with perfection and standardization of the technique.

At this time, the most appropriate approach to the treatment of perforated duodenal ulcers is omental patch closure of the ulcer, the most desirable operation by a laparoscopic approach, once the expertise is available. This is followed by intensive medication both to block acid output and to treat H. pylori.

Although this simplistic view is welcomed for a patient group who can present in extremely ill states, it still bears a few controversial points. The obvious prerequisite for this approach in management of these patients is knowing the H. pylori status of patient. Of course it is rare that H. pylori status is known at the time of the operation for perforated ulcer. Moreover many of these patients are managed at night time hours when investigative tools are at a minimum.

A multitude of studies reconfirmed the association of H. pylori with duodenal ulcers. Non- invasive testing is the best option for these patients as endoscopic biopsy and microscopy is impractical in the situation of peritonitis related to a 343

A CASEBOOK OF TWENTY SURGICAL CASES

perforated duodenal ulcer. Options for non- invasive testing include: urea breath testing, stool antigen testing and serology.

The urea breath test requires ingestion of radioactive C14 labelled or non- radioactive C13 labelled urea. Base line levels in exhaled gases are noted prior to testing and half hour after ingestion using scintillation or mass spectrometry respectively. The diagnostic accuracy of this test is >95%. The test is accurate, practical and readily available. (55)

Serology is a widely available and inexpensive non- invasive test, but the diagnostic accuracy is low (80- 84%). Tests that detect active infection, although more expensive are preferable to serology as these reduce the number of patients inappropriately treated for presumed H. pylori infection. Kits are available to diagnose H. pylori antibodies in urine and saliva. Their main advantages are their non- invasiveness and convenience. Unfortunately, their sensitivity is low. (1)

Stool antigen testing is a modern and rapid method of gaining information on a patientâ&#x20AC;&#x2122;s H. pylori status in the pre- operative period. A monoclonal stool antigen test has 94% sensitivity, 97% specificity and can be processed in an hour.

(56)

A rapid stool antigen test may be processed within 5 minutes; however, the

sensitivity is 76% and the specificity is 98%. (57)

Despite the relative simplicity of these tests, none of the patients tested in the series presented had H. pylori testing pre-operatively. Testing for H. pylori is unavailable at our institution and they were all treated with H. pylori eradication therapy and acid suppression. While the data presented by Ng et al (41) strongly recommends simple patch closure, H. pylori eradication therapy and acid suppression, closer inspection of the results reveals more conflicting findings. Data 344

A CASEBOOK OF TWENTY SURGICAL CASES

from only 52% of the patients with perforated duodenal ulcers contributed to the conclusion that acid- reducing surgery is unnecessary in the absence of other concurrent ulcer complications. Using information provided in the article, a minimum of 37 (22%) and as many as 59 (34%) of the total 172 patients would not have benefited from post- operative antibiotic treatment due to absence of the organism as an etiologic factor.

Although the literature reflects that acid reducing procedures for the management of perforated duodenal ulcers have vanished practicalities are, this may not be the case. Knowing that the antibiotic regimen will fail in some 5% to 10% of infected patients at 1 year follow up and that another 25%- 30% of patients may not be infected at all, offers limited assurance that simple closure alone is an optimal safety margin. Other practical issues associated with reliance on post- operative multiple- drug regimens are those of patient compliance and emerging antibiotic resistance. Significant side effects are not uncommon with multiple- drug antimicrobial therapy and are a major source of patient non- compliance. The H. pylori eradication failure rate of 16% among patients completing the antibiotic regimen is typical and emphasizes that resistance to metronidazole has become common (as noted earlier).

(20)

For all that has been discovered about H. pylori some countries are noting a decreasing frequency of H. pylori infection. The lower rate of infection in Western countries is largely attributed to higher hygiene standards and widespread use of antibiotics. (58) Other investigators have noted that perforated duodenal ulcers is becoming common in older patients with associated co- morbidities and is associated with a high incidence of recent consumption of NSAIDs. (59) This point is relevant to the series of patients presented here as 3 patients were noted to be on long term NSAIDs for arthritic symptoms. A history of ulcer complications is the most important predictor of future ulcer complication associated with NSAID 345

A CASEBOOK OF TWENTY SURGICAL CASES

use. (60) The youngest patient in the series had no obvious cause for his ulcer. With a long life expectancy ahead of him chances are he may use NSAIDs again for future ailments or simply because of non- compliance with the advice to avoid them.

Taken together, these facts underscore the practical limitations of the currently available non- surgical cures for real and presumed H. pylori mediated duodenal ulcer disease. It therefore requires judicious thinking on the part of the surgeon to consider these practicalities in the surgical treatment of perforated duodenal ulcers.

The mainstay of treatment of NSAID induced dyspepsia or previous PUD is acid suppression therapy with PPI. While these drugs are excellent at ulcer healing and gives good support to the omental patch repair of perforated duodenal ulcers, their long term use has been called into question.

The PPI’s are generally safe with rates of minor side effects being low, while several adverse events are rare. There have been cases of interstitial nephritis, hepatitis and visual disturbances associated with PPI therapy.

(61)

PPI’s reduce gastric acid, and thereby reduce the bioavailability of drugs requiring intragastric acidity to maximise their absorption and bioavailability.

Several PPI’s are metabolized by the hepatic cytochrome enzymes and thus may alter the intestinal first pass metabolism or hepatic clearance of some drugs. The most notable drug interaction is the reduced effectiveness of clopidogrel and a resulting 40% increased risk of coronary stent occlusions.(62)

Long term use of PPI is associated with an increased risk of bone fractures and their increased risk depends on the duration and dose of chronic use of PPI. The use of PPI for greater than 5 years can increase the risk of pre- operative fractures by 1.62 fold, while other studies confirm that 346

A CASEBOOK OF TWENTY SURGICAL CASES

use of PPI more than 7 years increase the risk of osteoporotic hip fractures by 4.55 fold. PPI use for 6- 12 months has been reported to be associated with an increased risk of osteoporotic hip and spine fractures.

(63)

Other metabolic derangements have been noted with proton pump inhibitor therapy. A growing number of case reports have indicated that hypomagnesemia can result from prolonged PPI therapy. The cases of PPI induced hypomagnesemia show severe symptoms of magnesium depletion. Magnesium homeostasis is essential for many intracellular processes and depends on the balance of intestinal absorption and renal excretion. Clinical awareness of this occurrence is required by clinicians to detect and avoid related complication of hypomagnesemia. The cause of hypomagnesemia remains poorly understood, but it responds rapidly to withdrawal of the PPI. (64)

The success of omental patch repair followed by H. pylori eradication therapy and long term proton pump inhibitor therapy has seen a further and further shift away from surgical procedures to reduce acid production. Whether or not, these recent developments noted with prolonged PPI therapy skews this balance in the opposite deviation, is a possible future development.

Within the current strategies for managing the patient with perforated duodenal ulcers there are relative indications for adding surgical acid control to an omental patch which can be categorized as follows:

路 Hemodynamic stability (localised peritonitis and minimal spillage of gastro- duodenal contents) 路 Short duration of pre- operative acute symptoms (<12- 24 hours) 路 Failure of medical therapy 347

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· Non- compliance with medical therapy · Need for post- operative NSAIDs · H. pylori negative testing · Chronic history of peptic ulcers It is worth reviewing therefore the surgical options for addressing perforated duodenal ulcer and acid suppression. In the setting of a patient who is hemodynamically stable with minimal intra- abdominal contamination, the relevant procedures are: a truncal vagotomy and pyloroplasty, omental patch and parietal cell vagotomy or an antrectomy with truncal vagotomy. Vagotomy and pyloroplasty is the easiest operation to perform, but has a 10%- 15% ulcer recurrence rate and exposes the patient to all of the complications of dumping and postvagotomy syndrome. (65) Truncal vagotomy and antrectomy can be applied to a variety of situations and the ulcer recurrence rate is low (0- 2%). This procedure represents the gold standard, as far as recurrence rates go, but post- gastrectomy and post- vagotomy syndromes are of the order of 20%. The disadvantages are that the operative mortality is higher than either of the other two procedures and the surgeon is forced to deal with an often chronically scarred duodenal stump and the complications of duodenal stump leak or anastomotic failure. (65)

Highly selective vagotomy or parietal cell vagotomy divides the vagus nerve supplying the acid producing cells of the fundus and preserves the pyloric- antral pump function. This procedure is the least traumatic and least complication prone because there is no anastomosis, technically demanding in the sense that surgeons must be more meticulous in maintaining innervation of the distal antrum, at the crow’s foot, but also must be sure that the proximal vagal interruption includes, if present, the criminal nerve of Grassi. Recurrence rates are expected in the 10-15% range and are regarded as acceptable as these respond to PPI therapy. (65) 348

A CASEBOOK OF TWENTY SURGICAL CASES

In a landmark study more than twenty years ago, Boey et al reported a remarkable series of 213 patients operated on for perforated duodenal ulcer with a very low 4.2% mortality rate. The factors that suggested higher morbidity and mortality rates included serious concurrent medical illness, pre- operative hemodynamic instability (including shock) and perforations more than 48 hours in duration at the time the patient presented.

(66)

They concluded that closure

of perforated ulcer alone is a better choice when any of these risk factors were identified and suggested further study of definite ulcer surgery in good- risk patients. A number of studies were subsequently reported and by the mid 1990â&#x20AC;&#x2122;s, omental patch closure coupled with parietal cell vagotomy had become the procedure of choice. (45)

If Helicobacter resistance and drug related adverse effects become clinically significant in the future, surgical acid suppression may be needed again.

Unfortunately, the surgical craft of acid reducing procedures will have to be re- learnt due to the absence of these procedures since the 1980â&#x20AC;&#x2122;s. Parietal cell vagotomy can be demanding even without the edema and inflammation of the tissue adjacent to the stomach and duodenum that accompany perforation. Of relevance also is whether the laparoscopic surgeonâ&#x20AC;&#x2122;s skill allows performance of a definitive ulcer operation such as parietal cell vagotomy along with patch repair of the perforation as expeditiously as can be done via the open approach.

CONCLUSION Helicobacter pylori is a major etiological factor in peptic ulcer disease. Unavailability of tests to confirm its presence and subsequent eradication are limitations in proper treatment. Given the developing uncertainties of H. pylori, the dropout rate from treatment and the emergence of resistant strains, acid reducing procedures may resurface in the management of perforated duodenal ulcer. More so 349

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with the increasing prevalence of NSAID induced ulcers in the elderly population and notable complications related to prolonged anti- ulcer therapy with PPI.

The trade- off in doing a definite ulcer operation with better chance of permanent cure may be to increase morbidity and mortality when it may not be necessary. As the pendulum continues to swing the management of perforated duodenal ulcers requires awareness of the pathogenesis and limitations of medical treatment of acid suppression. Surgeons need to be aware of their limitations and offer the simplest, safest operation, in a disorder where patients are quite ill even without hemodynamic instability or a short history of perforation.

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References 1. Malfertheiner P, Megraud F, O’Morain C, et al. Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report. Gut 2007; 56: 772–81.

2. Brown LM . Helicobacter pylori: epidemiology and routes of transmission. Epidemiol Rev 2000; 22 (2): 283–97.

3. Malfertheiner P, Chan FKL, McColl KEL. Peptic ulcer disease. Lancet 2009; 374: 1449-61.

4. Kuipers EJ, Uyterlinde AM, Pena AS, et al. Increase of Helicobacter pylori-associated corpus gastritis during acid suppressive therapy: implications for longterm safety. Am J Gastroenterology 1995; 90: 1401–06.

5. Moss SF, Calam J, Legon S, et al. Effect of Helicobacter pylori on gastric somatostatin in duodenal ulcer disease. Lancet 1992; 340: 930–32.

6. El-Omar EM, Penman ID, Ardill JE, et al. Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease. Gastroenterology1995; 109: 681–91.

7. McColl KE, Fullarton GM, Chittajalu R, et al. Plasma gastrin, daytime intragastric pH, and nocturnal acid output before and at1 and 7 months after eradication of Helicobacter pylori in duodenal ulcer subjects. Scand J Gastroenterol 1991; 26: 339–46.

8. Harris AW, Gummett PA, Walker MM, et al. Relation between gastric acid output, Helicobacter pylori, and gastric metaplasia in the duodenal bulb. Gut 1996; 39: 513–20.

9. Atherton JC. The clinical relevance of strain types of Helicobacter pylori. Gut 1997; 40: 701–03.

10. Malaty HM, Engstrand L, Pedersen NL, et al. Helicobacter pylori infection: genetic and environmental influences. A study of twins. Ann Intern Med 1994; 120: 982–86.

11. Cowan WK. Genetics of duodenal and gastric ulcer. Clin Gastroenterol1973; 2: 539–46.

12. Boren T, Falk P, Roth KA, et al. Attachment of Helicobacter pylori to human gastric epithelium mediated by blood group antigens. Science 1993; 262: 1892–95.

13. NIH Consensus Conference. Helicobacter pylori in peptic ulcer disease. NIH Consensus Development Panel on Helicobacter pylori in peptic ulcer disease. JAMA 1994; 272: 65–69.

14. Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and nonsteroidal antiinflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet2002;359(9300):14–22.

15. Papatheodoridis GV, Sougioultzis S, Archimandritis AJ. Effects of Helicobacter pylori and nonsteroidal anti-infl ammatory drugs on peptic ulcer disease: a systematic review. Clin Gastroenterol Hepatol 2006; 4: 130–42.

16. Chan FKL, To KF, Wu JCY, et al. Eradication of Helicobacter pylori and risk of peptic ulcers in patients starting long-term treatment with non-steroidal anti-inflammatory drugs: a randomised trial. Lancet 2002; 359: 9–13.

17. Labenz J, Blum AL, Bolten WW, et al. Primary prevention of diclofenac associated ulcers and dyspepsia by omeprazole or triple therapy in Helicobacter pylori positive patients: a randomised, double blind, placebo controlled, clinical trial. Gut 2002; 51: 329–35.

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A CASEBOOK OF TWENTY SURGICAL CASES 18. Chan FK, Chung SC, Suen BY, et al. Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen. N Engl J Med 2001; 344: 967–73.

19. Malfertheiner P, Megraud F, O’Morain C, et al. Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report. Gut 2007; 56: 772–81.

20. Stabile BE. Ann Surg 2000; 231 (2): 159-160.

21. Gilliam AD, Speake WJ, Lobo DN, et al. Current practice of emergency vagotomy and Helicobacter pylori eradication for complicated peptic ulcer in the United Kingdom. Br J Surg 2003; 90: 88-90.

22. Fuccio L, Minardi ME, Zagari RM, et al. Meta-analysis: duration of first-line proton-pump inhibitor based triple therapy for Helicobacter pylori eradication. Ann Intern Med 2007; 147: 553–62.

23. Fischbach L, Evans EL. Meta-analysis: the effect of antibiotic resistance status on the efficacy of triple and quadruple first-line therapies for Helicobacter pylori. Aliment Pharmacol Ther 2007; 26: 343–57.

24. Gisbert JP, Pajares JM. Review article: Helicobacter pylori “rescue” regimen when proton pump inhibitor-based triple therapies fail. Aliment Pharmacol Ther 2002; 16: 1047–57.

25. Saad RJ, Schoenfeld P, Kim HM, et al. Levofloxacin-based triple therapy versus bismuthbased quadruple therapy for persistent Helicobacter pylori infection: a meta-analysis. Am J Gastroenterol 2006; 101: 488–96.

26. Qasim A, Sebastian S, Thornton O, et al. Rifabutin- and furazolidone-based Helicobacter pylori eradication therapies after failure of standard first- and second-line eradication attempts in dyspepsia patients. Aliment Pharmacol Ther 2005; 21: 91–96.

27. Bago J, Pevec B, Tomic M, et al. Second-line treatment for Helicobacter pylori infection based on moxifloxacin triple therapy: a randomized controlled trial. Wien Klin Wochenschr 2009;121: 1–2.

28. Paimela H, Paimela L, Myllykangas-Luosujarvi R, et al. Current features of peptic ulcer disease in Finland: incidence of surgery, hospital admissions and mortality for the disease during the past twenty-five years. Scand J Gastroenterol 2002; 37(4):399–403.

29. Schwesinger WH, Page CP, Sirinek KR, et al. Operations for peptic ulcer disease: paradigm lost. J Gastrointest Surg 2001;5(4):438–43.

30. Liu TJ, Wu CC. Peptic ulcer surgery: experience in Taiwan from 1982–1993. Asian J Surg 1997;20:305.

31. Groenen MJ, Kuipers EJ, Hansen BE, et al. Incidence of duodenal ulcers and gastric ulcers in a Western population: back to where it started. Can J Gastroenterol 2009;23(9):604–8.

32. Svanes C. Trends in perforated peptic ulcer: incidence, etiology, treatment and prognosis.

World J Surg 2000; 24:277.

33. Lee CW, Sarosi Jr GA. Emergency ulcer surgery. Surg Clin N Am 2011; 91: 1001-1013.

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Ng EKW, Chung SCS, Sung JJY, et al. High prevalence of Helicobacter pylori infection in duodenal ulcer perforations not caused by non-steroidal anti-inflammatory drugs. Br J Surg 1996; 83:1779.

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A CASEBOOK OF TWENTY SURGICAL CASES 35. Sebastian M, Prem Chandran VP, El Ashaal YIM, et al. Helicobacter pylori infection in perforated peptic ulcer disease. Br J Surg 1995; 82:360.

36. Reinbach DH, Cruickshank G, McColl KEL. Acute perforated duodenal ulcer is not associated with Helicobacter pylori infections. Gut 1993; 34:1344.

37. Bertleff MJ, Lange JF. Laparoscopic correction of perforated peptic ulcer: first choice? A review of literature. Surg Endosc 2010; 24(6):1231–9.

38. Svanes C, Lie RT, Svanes K, et al. Adverse effects of delayed treatment for perforated peptic ulcer. Ann Surg 1994; 220(2):168–75.

39. Lohsiriwat et al. Perforated Peptic Ulcer: Clinical Presentation, Surgical Outcomes, and the Accuracy of the Boey Scoring System in Predicting Postoperative Morbidity and Mortality.

World J Surg (2009) 33:80-85.

40. Hay JM, Lacaine F, Kohlmann G, et al. Immediate definitive surgery for perforated duodenal ulcer does not increase operative mortality: a prospective controlled trial. World J Surg 1988; 12:705–709.

41. Ng EKW, Lam YH, Sung JJY, et al. Eradication of Helicobacter pylori prevents recurrence of ulcer after simple closure of duodenal ulcer perforation: randomized controlled trial. Ann Surg 2000; 231:153–158.

42. Tomtitchong P, Siribumrungwong B, Vilaichone RK, et al. Systematic review and metaanalysis: Helicobacter pylori eradication therapy after simple closure or perforated duodenal ulcer. Helicobacter 2012;17(2): 148-52.

43. Ronald F, Martin MD. Surgical management of Ulcer Disease. Surg Clin N Am 2005; 85: 907-929.

44. Kate V, Ananthakrishnan N, Badrinath S. Effect of Helicobacter pylori eradication on the ulcer recurrence rate after simple closure of perforated duodenal ulcer: retrospective and prospective randomized controlled studies. Br J Surg. Aug 2001;88(8):1054-8.

45. Baker RJ. Perforated Duodenal Ulcer. In Book: Fischer JE, Bland KI .Mastery of Surgery 5th. edition. Philadelphia:Lippincott Williams & Wilkins;2007 . p 891- 901.

46. Gupta et al. The management of large perforations of duodenal ulcers. BMC Surg 2005; 5:15- 28.

47. Jani et al. omental plugging for large sized duodenal peptic perforations. A prospective randomized study of 100 patients. South Med J. 2006 ; 99(5):467-71.

48. Shyu et al. gastric body partition for Giant Perforated Peptic Ulcer in Critically ill Elderly patients. World J Surg 2006 ;30: 12, 2204-2207.

49. Nathanson LK, Easter DW, Cuschieri A. Laparoscopic repair/peritoneal toilet of perforated duodenal ulcer. Surg Endosc 1990; 4: 232–233.

50. LauWY, Leung KL, Kwong KH, et al. A randomized study comparing laparoscopic versus open repair of perforated peptic ulcer using suture or sutureless technique. Ann Surg 1996; 224: 131–138.

51. Druart ML, Van Hee R, Etienne J, et al. Laparoscopic repair of perforated duodenal ulcer. A prospective multicenter clinical trial. Surg Endosc 1997; 11: 1017–1020.

52. Siu WT, Leong HT, Law BKB, et al. Laparoscopic repair for perforated peptic ulcer: a ran-

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53. Lau H. Laparoscopic repair of perforated peptic ulcer: a meta-analysis. Surg Endosc 2004; 18(7): 1013-21.

54. Sanabria AE, Morales CH, Villegas MI. Laparoscopic repair of perforated peptic ulcer disease. Cochrane Database Syst Rev 2005;19(4): CD004778.

55. Gisbert JP, Pajares JM. Review article: C-urea breath test in the diagnosis of Helicobacter pylori infection—a critical review. Aliment Pharmacol Ther 2004;20:1001–17.

56. Gisbert JP, de la Morena F, Abraira V. Accuracy of monoclonal stool antigen test for the diagnosis of H. pylori infection: a systematic review and meta-analysis. Am J Gastroenterol 2006;101(8):1921–30.

57. Leodolter A, Wolle K, Peitz U, et al. Evaluation of a near-patient fecal antigen test for the assessment of Helicobacter pylori status. Diagn Microbiol Infect Dis 2004; 48(2):145–7.

58. Malaty HM. Epidemiology of Helicobacter pylori infection. Best Pract Res Clin Gastroenterol 2007; 21 (2): 205-214.

59. Lanas A, Serrano P, Bajador E, Esteva F, Benito R, Sainz R.Evidence of aspirin use in both upper and lower gastrointestinal perforation. Gastroenterology 1997; 112:683–689.

60. Garcia Rodriguez LA, Jick H. Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs. Lancet 1994; 343: 769–72.

61. Thomson ABR, Sauve MD, Kassam N, et al. Safety of the prolonged use of protn pump inhibitors. World J Gastroenterol 2010; 16(19): 2323-30.

62. Juurlink DN, Gomes T, Ko DT, et al. A population based study of the drug interaction between proton pump inhibitors and clopidogrel. CMAJ 2009; 180: 713-718.

63. Targownik LE, Lix LM, Metge CJ, et al. Use of proton pump inhibitors and risk of osteoporosis-related fractures. CMAJ 2008; 179: 319-326.

64. Cundy T, Mackay J. Proton pump inhibitors and severe hypomagnesemia. Curr Opin Gastroenterol 2011; 27 (2): 180-5.

65. Mercer DW, Robinson EK. Stomach. In Book: Townsend CM, Beauchamp RD, Evers BM, Mattox KL. Sabiston’s Textbook of Surgery: the biological basis of modern surgical practice, 18th edition. Philadelphia: Saunders Elsevier; 2008. p. 1223-1277.

66. Boey J, Wong J, Ong GB. A prospective study of operative risk factors in perforated duodenal ulcers. Ann Surg 1982; 195(3): 265-9.

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18.

PANCREATicODUODENECTOMY: PJ VS PG INTRODUCTION Ampullary carcinoma accounts for 20% of all tumor-related obstructions of the common bile duct, representing 2% of all gastrointestinal (GI) malignancies and 20% of all tumors of the extrahepatic biliary tree. The mainstay of treatment for ampullary cancer is pancreaticoduodenectomy (Whipple procedure), which involves removal of the distal half of the stomach with or without preserving the pylorus, gallbladder, distal common bile duct, head of the pancreas, duodenum, proximal jejunum, and regional lymph nodes.

Pancreaticoduodenectomy (PD) increases overall survival in patients with ampullary cancer without nodal involvement or distant metastases.

Pancreaticoduodenectomy (PD) is performed to treat benign and malignant pancreatic and periampullary diseases. It is a complex and challenging surgical procedure with a high mortality rate of up to 30%. Recent technical advances, however, have decreased the mortality rate to < 3â&#x20AC;&#x201C;5%, although the morbidity rate remains high (30â&#x20AC;&#x201C;50%), even at high-volume centers. Among the complications, postoperative pancreatic fistula (POPF) is the most common major complication of PD with a frequency ranging from 2 to 20%.

POPF induces abscess formation, vascular injuries, pseudoaneurysm rupture, and fatal hemorrhage or sepsis, all of which eventually result in a prolonged hospital stay or in a potentially serious and life-threatening event. Consequently, a reduced rate of POPF after PD is an important challenge for surgeons.

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Numerous risk factors predisposing patients to POPF after PD have been proposed, including advanced age, male sex, preoperative jaundice, impaired renal function, diabetes mellitus , ampullary disease , intraoperative blood loss , prolonged operation, and anastomotic techniques. Among these factors, the anatomic features of the pancreatic remnant, a small diameter pancreatic duct, and a soft pancreatic texture seem to be the most frequently reported and generally accepted risk factors.

Surgical technique might be one improvable aspect of pancreaticoduodenectomy that can reduce the pancreatic leakage rate; it is critical in the management of the pancreatic remnant because of the various methods used by surgeons.

Reconstruction by anastomosing the pancreas and jejunum is the most widely used and can be oriented in end-to-side, with or without duct-to-mucosa anastomosis or end-to-end invagination styles. Arguably, anastomosis of the remnant pancreas with the stomach is also another method.

A 49 year old gentleman presented with intermittent obstructive jaundice. He was diagnosed with an ampullary neoplasm for which he underwent a Whipple procedure. The case, including the post-operative course is described followed by a discussion regarding the evidence relating to pancreatojejunostomy (PJ) and pancreatogastrostomy(PG) in reducing the rate of POPF.

CASE History: A 49 year old gentleman was referred to hospital by his general practitioner. He complained of jaundice (noticed by his wife) and darkening of the urine. The jaundice was initially intermittent but by the end of two weeks became persistent. Although he described his stool as yellow, he experienced pruritus which was progressively worse. He experienced no pain, his appetite was maintained and reported that his weight was stable. Systematic enquiry 356

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was otherwise non-contributory.

This patient, a warehouse manager, had no chronic illnesses and had no previous surgery. He did not smoke and had stopped drinking alcohol 9 years previously. He lived with his wife and kids.

Physical Examination The patient appeared to be comfortable. His vital signs revealed: P 70min-1, BP 122/70 mmHg, RR 18min-1, T 36.80C. Examination of his eyes revealed he was icteric. There was no clinical lymphadenopathy.

There were no signs of chronic liver disease.

Cardio-respiratory examination was normal.

The abdomen appeared symmetrical and moved with respiration. There was no tenderness and neither were there any masses. There was no clinical ascites and the bowel sounds were normal. The digital rectal examination revealed normal anal tone and mucosa. The stool was pasty and clay coloured.

Investigations: Hb 13.38 g/dl, WCC 9.9 x 103 /Âľl, Plt 346 x 103 /Âľl, Urea 22 mgdl-1, Cr 0.8 mgdl, Na 134 mmol, K 3.7 mmol, Amylase 122 u,

1

Total Bilirubin 3.9 (D 2.6), ALP 404, GGT 1235, HbA1c 4.9%.

CXR, AXR: both normal USS: The common bile duct was dilated at 10.1mm (8.3mm in the intrapancreatic segment). The solid organs were sonographically normal and there was no evidence of gallstones.

CT (Abdomen and Pelvis): There was no free fluid, pancreatic head tumour or metastatic disease. A double duct sign was noted and the superior mesenteric vessels were normal and demonstrated clear planes in relation to the surround357

A CASEBOOK OF TWENTY SURGICAL CASES

ing tissues.

MRCP: This confirmed a dilated CBD but no gallstones within.

ERCP: An adenomatous polyp was noted at the ampulla. An 18-20mm sphincterotomy was done and biopsies of the polyp were taken.

Histology: elements of a Tubulo-villous adenoma in which arises a well differentiated adenocarcinoma.

Surgical Treatment: Whipple Procedure (see Fig 1 & 2) Intraoperative finding: No ascites, no liver metastases or peritoneal nodules.

The superior mesenteric artery and vein were both uninvolved with any disease.

The common bile duct was 10mm. The pancreas felt soft and on the dividing at the neck the pancreatic duct was 3mm in diameter.

The Proximal jejunal limb was oriented in a Bilroth II fashion to allow reconstruction of gastrointestinal continuity: - End to side Pancreaticojejunostomy (PJ) (3/0 prolene interupted) (Invagination followed by omental wrapping) - End to side Hepaticojejunostomy (3/0 vicryl interrupted) - Side to side Gastrojejunostomy (GIA 55mm stapler) Two suction drains were placed at the end, one in the subhepatic space next to the choledocho jejunostomy and the other in the vicinity of the PJ. The estimated blood loss was 800mls.

Postoperatively the patient was admitted to the high dependency unit. The epidural catheter was removed after 48 hours. He was sufficiently stable to be transferred to the surgical ward on day 3.

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Drain contents: Postopera- Right Drain Right Drain Left Drain Left Drain Serum tive Day Day 3 Day 6 Day 10 Day 11

volume 80 15 20 5

Amylase

volume

44 29 15 --

54 50 64 20

Amylase

amy-

11570 1306 414 182

lase 38 25 26 40

The effluent from the left drain was of a light beige colour. This observation along with the high drain amylase indicated that he had a POPF (ISGPF Grade B). Although the drain volume was decreasing, the patient developed a tachycardia. This prompted a CT (Day 5): no abscess, hematoma or indication of a collection was noted. Both drains were withdrawn on day 13. By this time the patient was tolerating orally, more self caring and his appetite was improving.

He was discharged home.

The patient was re-admitted to hospital 2 weeks later with an abscess pointing through the epigastric aspect of the rooftop incision. A CT scan of the abdomen revealed that this was confined to the anterior abdominal wall with no evidence of an intra-abdominal communication or abscess. This was incised and drained.

The pus was sent to the pathology laboratory for culture and antibiotic sensitivity. There was no bacterial growth and the wound was healing with topical dressings. He was discharged 3 days later to continue dressings at the local health center.

The histology of the Whipple specimen (pT2N0M0) described a 1.5cm ampullary adenocarcinoma with some infiltration to the duodenal wall. There was no 359

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involvement of the pancreas or lymph node metastasis.

After 1 year of follow up he continues to do well with no evidence of recurrent disease.

Fig 1: Whipple specimen

Fig 2:The opened duodenum demonstrating the ampullary carcinoma 360

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DISCUSSION Ampullary carcinoma is a malignant tumor arising from the ampulla of Vater.

It may originate from the epithelium of the distal bile duct, or the distal pancreatic duct, or the duodenal mucosa overlying or within the deeper tissues of the papilla. Regardless of the epithelium of origin, carcinomas involving the major papilla appear as an enlarged or redundant mass encroaching upon the duodenal lumen. Ampullary carcinoma accounts for 20% of all tumor-related obstructions of the common bile duct, representing 2% of all gastrointestinal malignancies and 20% of all tumors of the extrahepatic biliary tree.(1,2)

The overall incidence is 6 cases per 1 million individuals. The average age at time of diagnosis of ampullary carcinoma is 60â&#x20AC;&#x201C;70 years. Earlier presentation may occur with inherited colorectal cancer syndromes such as familial adenomatous polyposis (FAP). Patients with FAP must undergo endoscopic surveillance of their small bowel to assess for the development of ampullary and duodenal adenomas.(3,4)

The mainstay of treatment for ampullary cancer is pancreaticoduodenectomy (Whipple procedure), which involves removal of the distal half of the stomach with or without preserving the pylorus, gallbladder, distal common bile duct, head of the pancreas, duodenum, proximal jejunum and regional lymph nodes.

Pancreaticoduodenectomy increases overall survival in patients with ampullary cancer without nodal involvement or distant metastases.(5)

An alternative to pancreaticoduodenectomy is surgical transduodenal ampullectomy with sphincteroplasty, where the ampulla is removed and the common bile duct and pancreatic duct are reimplanted into the duodenal wall. Outcomes are less impressive with this procedure, as compared to pancreaticoduodenectomy, given the increased risk of leaving behind adenomatous tissue and/or involved 361

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lymph nodes, and this should be reserved for patients who are felt to be poor candidates for pancreaticoduodenectomy.(6)

Endoscopic ampullectomy involves local resection of ampullary masses during per-oral endoscopy. It is typically reserved for benign ampullary adenomas and is not advocated for use in patients with ampullary cancer who are acceptable surgical candidates. Palliation of malignant obstructive jaundice due to ampullary cancer is most commonly performed via endoscopically placed biliary stents.(7)

Codvilla is credited with the first en bloc resection of the head of the pancreas and the duodenum for periampullary carcinoma at the turn of the twentieth century, but the patient died of postoperative complications.(8) Following this development, this surgery continued to evolve but despite technical advances, the outcome remained dismal. Crile in 1970 reported that pancreatic cancer was incurable by pancreaticoduodenectomy, and that the disease could be palliated just as effectively by performing a biliary bypass, with survival being prolonged in the bypass group.(9) Shapiro reported similar survival in patients undergoing pancreaticoduodenectomy and palliative biliary bypass. He reviewed the literature and found that of the 496 patients with adenocarcinoma of the head of the pancreas who had undergone pancreaticoduodenectomy between 1962 and 1974, the hospital mortality rate was 21% and 5-year survival was 4%.(10)

Improvement in support services mainly anesthesia and intensive care with better support for organ failure, among other improvements in critical care surgery resulted in improved mortality. During the 1980s, many centers reported reduced hospital mortality rates, and some large series from centers with extensive experience in pancreatic resections reported no mortality.(11)Increasing experience and familiarity with anatomy, shortening of operative time and decreasing 362

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operative blood loss, and better anticipation and management of postoperative complications have all played a role in decreasing hospital mortality which now generally ranges 3-5%.(12) With improvement in mortality over the past decade, indications have greatly expanded to include benign neoplasms and other nonneoplastic conditions such as chronic pancreatitis.(13,14)

During the last decade, although the rate of operative mortality significantly decreased after PD, the incidence of postoperative morbidity still remains high.

Among the complications, postoperative pancreatic fistula (POPF) is the most common major complication of PD with a frequency ranging from 2 to 20% .(15) POPF induces abscess formation, vascular injuries, pseudoaneurysm rupture, and fatal hemorrhage or sepsis, all of which eventually result in a prolonged hospital stay or in a potentially serious and life-threatening event . Consequently, reduced rates of POPF after PD is an important challenge for surgeons and in recent times have become the main focus of outcomes following PD.

Most of the large pancreaticoduodenectomy series have reported rates of pancreatic fistula of over 10% .(17,18,19.20) Risk factors for pancreatic fistula depend upon (12): 1) general patient factors, including age , sex, diabetes mellitus and nutrition 2) disease-related factors, including pancreatic duct size, pancreatic texture and pathology 3) procedure-related factors, including blood loss operative time and anastomotic method

Among these risk factors, the most important might be the texture of the remnant pancreas.(21) Indeed, despite an occurrence rate of pancreatic fistula of 5% in cases of hard pancreatic tissue, the rate rises to nearly 20% in cases of soft pancreatic texture. (18,19,20) The risk of developing a pancreatic fistula is significantly 363

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associated with the final histopathological diagnosis of the resected specimen. A lower risk is observed in adenocarcinoma and higher risk in cystic neoplasms or disease originating from the bile duct. (22) This is because pancreatic malignancy usually causes main pancreatic duct dilatation and associated chronic pancreatitis. The resulting fibrotic hard remnant pancreas and enlarged duct are easily anastomosed. In contrast a soft pancreas remains at risk of pancreatic fistula due to its fragility and its secretion of a large amount of pancreatic juice.(23)

Surgical technique might be one improvable aspect of pancreaticoduodenectomy that can reduce the pancreatic leakage rate; it is critical in the management of the pancreatic remnant because of the various methods used by surgeons.

Methods of reconstruction used between the remnant pancreas and the intestine include end-to-side, with or without duct-to-mucosa anastomosis, end-to-end invagination styles, and arguably, anastomosis of the remnant pancreas with the stomach is also another method.

The greatest challenge in comparing different techniques of pancreatico-enteric reconstruction is the diagnosis of a POPF. The diagnosis of pancreatic fistula is suspected on the basis of many clinical or biochemical findings. There is no universally accepted definition of PF. While some researchers have emphasized on the volume (and colour) of the drain output, and its duration, others have stressed more on the amylase content of the drainage fluid. In a study published in 2004, Bassi et al summarized 4 definitions of POPF and applied each definition to 242 patients who had undergone pancreatic resection. The results revealed wide variations in the incidence of PF, from 10% to 29% depending upon the definition used.(24) Therefore, it is essential to standardize the reporting of post-PD complications, especially POPF. This led to the unified definition, now known as the International Study Group on Pancreatic Fistula (ISGPF) definition.(15) The definition was intended to standardize the reporting of POPF. 364

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The essential component of an anastomotic leak was the high amylase content (> 3 times the upper normal serum value), of the drain fluid (of any measurable volume), at any time on or after the 3rd postoperative day. In addition, pancreatic fistula was classified according to three clinical grades: grade A, pancreatic fistula with no clinical impact; grade B, pancreatic fistula that requires specific treatment and a change in management or adjustment in the clinical pathway; and grade C, pancreatic fistula that requires a major change in clinical management or deviation from the normal clinical pathway. Since the initiation of clinical grading of pancreatic fistula as defined by the ISGPF, several authors have evaluated pancreatic fistula according to this classification.

POPF is the cause of most complications after PD. Not surprisingly much effort has gone into preventing its occurrence. These measures primarily include technical modifications of constructing a pancreatic anastomosis. The correct management of a pancreatic remnant after a PD is a matter of much debate and this is reflected in the variety of techniques that have evolved over the years for the construction of a safe pancreatic anastomosis.

The original Allen Whipple description involved occlusion of the pancreatic duct, which he later modified to the procedure of pancreaticojejunostomy. Simple ductal ligation was advocated in the past, but has largely been abandoned because of the high fistula rate of 50%.(25,26) A recent prospective randomized trial by Tran et al. comparing PJ versus duct occlusion without PJ, showed no significant difference in postoperative complications, mortality, and exocrine insufficiency, but the incidence of diabetes mellitus was significantly higher in patients with duct occlusion.(27) Dicarlo et al, proposed pancreatic ductal occlusion with neoprene; in their 51 patients they observed a 33.3% overall morbidity and a 5.8% operative mortality.(28)

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Total pancreatectomy obviates the need for a pancreatic anastomosis. Sarr et al, reported mortality, morbidity, and survival equivalent to PD after total pancreatectomy.(29) However, total pancreatectomy is inevitably associated with severe endocrine and exocrine abnormalities, and its use is therefore greatly discouraged. Clearly, the high incidence of pancreatic fistula following pancreatic duct ligation and the associated pancreatic insufficiency and diabetes, have restricted the use of duct occlusion as a reliable method for the management of pancreatic remnant after PD.

PJ has been the most commonly employed method of restoring pancreatico-enteral continuity since the initial use of the Whipple operation in the 1970s. There is, however, a lack of agreement among surgeons about the technique used in creating this anastomosis. PJ anastomosis is carried out either as an end-to-end anastomosis with invagination of the pancreatic stump in to the jejunum or as an end-to-side anastomosis with or without duct-to-mucosa suturing. In an early single-institution experience using the duct-to-mucosa PJ technique and an internal stent, Strasberg and colleagues reported a PF rate of only 1.6% in 123 patients.(30) In another experience reported by Tani and colleagues, the fistula rate was 11% for a stented duct-tomucosa PJ technique and 6.5% for a two-layer invaginated end-to-side externally stented technique.(31) Other modifications include the orientation of the jejunal loop with the pancreas. A separate Roux loop of jejunum is suggested by some researchers for the PJ so that not more than two anastomoses are carried on one loop of jejunum.(31,32) This theoretically reduces the risk of activation of pancreatic enzymes near the PJ by avoiding contact with the biliary secretions. A review of series PJ where >100 cases were performed indicate a POPF rate of 0-17% and mortality rate of 0-2%. (Table 1)

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TABLE 1 Major series (>100 cases) of pancreaticojejunostomy (PJ)

Author

Year

PJ (N)

Leakage (%) Mortality (%)

Marcus et al.(34)

1995

114

17

0.8

Ohwada et al.(35)

2001

100

4

2

Z’graggen et al.(36)

2002

331

2

0.0

Strasberg et al.(30)

2002 123

1.6

0.8

Peng et al.(37)

2002 150

0.0

0.0

These results are difficult to interpret in view of the multiple variations of the PJ anastomosis. Regardless of the orientation of the jejunal loop, the two widely used method of anastomosis are invagination PJ (or ‘‘dunking’’ the pancreatic remnant into the jejunum) or duct-to-mucosa PJ.

There have been two prospective randomized trials evaluating a duct-to-mucosa PJ versus an end-to-side PJ reported in the literature. In the first trial, Bassi and his coauthors randomized 144 patients undergoing PD to either a two-layer duct-to-mucosa PJ anastomosis or a single-layer end-to-side anastomosis. POPF were seen in 14% of patients—13% in the duct-to-mucosa group and 15% in the end-to-side group, and there was no difference in complications between the groups (overall rate of 54% in both groups). There were no statistically significant differences between the groups with regard to abdominal complications, abdominal fluid collections, or length of stay. The authors concluded that the anastomotic technique did not change the operative risk.(38)

A subsequent dual institution trial by Berger et al. randomized 197 patients to either a two-layer duct-to mucosa PJ anastomosis or a two-layer end-to-side PJ anastomosis. The majority of cases were performed by five surgeons across two 367

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institutions. Patient demographics, including age and gender, were comparable between the two groups. This study revealed an advantage to the two layer endto-side invagination technique. The POPF rate in the duct-to-mucosa group was 24%, while the rate in the invagination group was only 12% (P< 0.05). There were significant differences in the rates of major complications between the groups (25% duct-to mucosa versus 12% invagination; P = 0.03) and the need for interventional radiologic procedures (11 vs. 3%; P = 0.03). The length of stay was comparable between the groups. In the multivariate analysis for PF, there were factors that were found to be independent predictors of a fistula. The most powerful predictor was the texture of the pancreatic remnant, with soft or normal glands being associated with a higher PF risk. Patients with a soft pancreas had a much higher likelihood of a PF developing than those with a hard pancreas ( P = 0.003). The authors also observed a much higher likelihood of PF developing in those patients who underwent a duct-to mucosa anastomosis.(23)

Attempts to decrease the rates of POPF and its sequelae encouraged experimentation with other methods of anastomosis. Waugh and Clagett in 1946 were the first to introduce PG in the clinical setting. (8) Certain advantages have been put forth as regards the use of PG. First, the anastomosis is considered to be easier to perform, because the posterior wall of the stomach lies immediately anterior to the mobilized pancreatic remnant. The proximity of the pancreas to the posterior wall of the stomach allows for potentially less tension on the anastomosis. Second, the excellent blood supply to the stomach wall is considered to be favorable for anastomotic healing. Nasogastric decompression provides for continuous emptying of the stomach, and therefore, less tension on the anastomosis. Furthermore, with PG, the pancreatic exocrine secretions enter the acidic gastric environment, where the low pH and lack of enterokinase prevents their activation. This lack of enzymatic activation may help prevent auto-digestion of the anastomosis. Furthermore, the performance of PG reduces the number of 368

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anastomoses in a single loop of retained jejunum, thereby potentially decreasing the likelihood of loop kinking. Pancreaticogastrostomy also avoids creation of a long jejunal limb between the pancreatic and biliary anastomoses, where biliary and pancreatic secretions could collect and cause increased pressure, possibly resulting in tension at both the pancreatic and biliary anastomosis.

Mason did a meta-analysis of PG between 1946 and 1997. Between 1946 and 1990, 199 cases were described in the literature with a mortality of 4.5% (9/199) and a leakage rate of 1% (2/199). The 9 deaths were not attributed to PG. The numbers of PG between 1991 and 1997 described in the literature rose to 614.

The mortality rate in this group was 3.3% (20/614) and the leakage rate was 4.87% (29/614).(39) As experience grew PG was demonstrated to be feasible and results indicated the potential to decrease POPF rates. (Table 2)

TABLE 2 Major series of pancreaticogastrostomy (PG) (> 100 cases)

Author

Year

PG (N)

Leakage (%) Mortality

1998

125

0

(%)

Kapur et al.(40)

4.8

Oâ&#x20AC;&#x2122;Neil et al.(41) 2001 102 8.8 3.9 Schlitt et al.(42) 2002 260 2.8 4.4

The potential benefits of PG led to various non-randomized studies comparing outcomes of PG and PJ. Several of these studies indicated improved POPF rates in favor of PG. Aranha et al, in a series of 214 patients, did not find a difference in the leak rate between PG and PJ, but they found that leakage at PJ anastomosis was more likely to be fatal and require re-exploration and infection control.

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PJ leaks were also associated with a high incidence of bile leaks at the hepaticojejunal anastomosis and took a longer time to close.(43) A very recent study by Oussoultzoglou et al, of 250 patients showed a lower fistula rate (2.3%) in the PG group than in the PJ group (20.4%). Nine (52.9%) of 17 patients with pancreatic fistula in the PJ group underwent re-laparotomy, and all 9 subsequently underwent completion pancreatectomy (n = 7) or removal of peripancreatic necrotized tissue (n = 2) with a postoperative mortality rate of 22.2%. However, of the four patients who developed a pancreatic fistula following PG, none required re-laparotomy because medical therapy succeeded in all 4 patients.

Moreover, the overall relaparotomy rate was significantly lower in the PG group (4.7%) than in the PJ group (18.0%). Length of hospital stay was significantly lower in the PG group (17.2 – 7.7days) than in the PJ group (23.3 – 11.7 days).

No mortality related to pancreatic fistula occurred in the PG group.(44)

McKay and colleagues reported on a meta-analysis of PG vs PJ following PD. (45)

Eleven articles were identified for inclusion: one prospective randomized

trial, two nonrandomized prospective trials and eight observational cohort studies. The meta-analysis revealed a higher rate of POPF associated with PJ reconstruction (relative risk (RR) 2·62 (95 per cent confidence interval (C.I.) 1·91 to 3·60)). A higher overall morbidity rate was also demonstrated in this group, as was a higher mortality rate. Despite the findings of the study the author identified several limitations. Several differences between the studies served as sources of heterogeneity, including differences in the nuances of surgical technique, adjunctive measures to decrease fistula formation (stents, somatostatin analogues), and advances in perioperative care during the fairly long time periods over which some of the studies were conducted. Other areas of heterogeneity included the quality of the pancreatic parenchyma (hard versus soft), which was not commented on in most of these studies, as well as surgeon volume of procedures, which is strongly linked to outcomes after pancreaticoduodenectomy.

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The other main risk to the validity of the conclusions involves the differences in the quality of the studies included in the meta-analysis. Only one study was a randomised controlled trial, in two studies the data were collected prospectively, and the others were observational with several inherent biases.

Wente et al. reported on a systematic review and meta-analysis of PG vs PJ.(46) Sixteen articles were included; meta-analysis of 3 randomized controlled trials (RCT) revealed no significant difference between PJ and PG regarding overall postoperative complications, pancreatic fistula, intra-abdominal fluid collection, or mortality. On the contrary, analysis of 13 nonrandomized observational clinical studies showed significant results in favor of PG for the outcome parameters with a reduction of pancreatic fistula and mortality in favor of PG. All the observational studies reported superiority of PG over PJ. The authors commented that this may be influenced by institutional/publication bias. In contrast, all RCTs failed to show advantage of a particular technique, suggesting that both PJ and PG provide equally good results.

There are four randomised controlled trials which compared the results of PJ versus PG following PD. Three of these studies did not show any significant difference in the incidence of pancreatic fistula. Only one showed a benefit of PG in terms of reducing the incidence of pancreatic fistula and overall complications.

Yeo et al. analyzed the findings of 145 patients between May 1993 and January 1995, in a prospective trial at The Johns Hopkins Hospital. Patients were randomly assigned to PG or PJ after completion of the pancreaticoduodenal resection. The PG (n = 73) and PJ (n = 72) groups were comparable with regard to multiple parameters, including demographics, medical history, preoperative laboratory values, and intraoperative factors, such as operative time, blood 371

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transfusions, pancreatic texture, length of pancreatic remnant mobilized, and pancreatic duct diameter. The overall incidence of pancreatic fistula after PD was 11.7% (17/145). The incidence of POPF was similar for the PG (12.3%) and PJ (1 1.1 %) groups. (47)

Bassi et al. randomised 151 patients undergoing PD with soft residual tissue to be reconstructed with either PG or end-to-side PJ. The two treatment groups showed no differences in vital statistics or underlying disease, mean duration of surgery, and need for intraoperative blood transfusion. Overall, the incidence of surgical complications was 34% (29% in PG, 39% in PJ, p not significant).

Patients receiving PG showed a significantly lower rate of multiple surgical complications (p= 0.002). POPF was the most frequent complication, occurring in 14.5% of patients (13% in PG and 16% in PJ, p not significant). Five patients in each treatment arm required a second surgical intervention; the postoperative mortality rate was 0.6%. PG was favored over PJ due to significant differences in postoperative collections (p = 0.01), delayed gastric emptying (p= 0.03), and biliary fistula (P= 0.01). The authors concluded that when compared with PJ, PG did not show any significant differences in the overall postoperative complication rate or incidence of pancreatic fistula. However, biliary fistula, postoperative collections and delayed gastric emptying were significantly reduced in patients treated by PG. In addition, PG was associated with a significantly lower frequency of multiple surgical complications. (48)

In a multicenter (single blind) study from France, Duffas randomized 149 patients (81underwent PG and 68 PJ). The main endpoint was intra-abdominal complications. No significant difference was found between the two groups concerning pre or intraoperative patient characteristics. The rate of patients with one or more intra abdominal collection was 34% in each group. Twenty372

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seven patients sustained a pancreatoenteric fistula (18%), 13 in PG (16%) and 14 in PJ (20%). No statistically significant difference was found between the 2 groups concerning the mortality rate (11% overall), the rate of reoperations and/or postoperative interventional radiology drainages (23%), or the length of hospital stay (median 20.5 days). They concluded that the type of pancreatoenteric anastomosis (PJ or PG) after PD does not significantly influence the rate of patients with one or more intra abdominal collections and/or pancreatic fistula or the severity of complications.(49)

The most recent prospective trial compared the post-operative morbidity of PJ vs PG after a pylorus-preserving pancreaticoduodenectomy (PPPD). In patients having a PG, a gastric partition (GP) was made, creating a separate pouch for the PG. One hundred eight patients undergoing PPPD for benign and malignant diseases of the pancreatic head and the periampullary region were randomized to receive PG (PPPD-GP) or end-to-side PJ (PPPD-PJ).

The two treatment groups showed no differences in preoperative parameters and intraoperative factors. The overall postoperative complications were 23% after PPPD-GP and 44% after PPPD-PJ (P < 0.01). The incidence of pancreatic fistula was 4% after PPPD-GP and 18% after PPPD-PJ (P < 0.01). This study shows that PPPD-GP can be performed safely and is associated with less complication than PPPD-PJ. The authors stated that the advantage of this technique over other PG techniques is that the anastomosis is outside the area of the stomach where the contents empty into the jejunum, but pancreatic juice drains directly into the stomach.(50)

Critical appraisal of the management of the pancreatic remnant performed in the four randomised controlled trials revealed important differences not only in the selection of patients in the study but in the technique used, in the defini373

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tion of pancreatic fistula, and in the use adjuncts (stents, octreotide) to prevent complications.

Patients with periampullary tumors were randomly assigned to PG or PJ after completion of the PD. Only one study was multicenter; 14 centers participated (8 universities and 6 community hospitals) and the median number of patients included per center was 8 (range 2–27).(49) The study by Bassi et al. only enrolled patients with a pancreas that was intraoperatively considered to be soft and with a diameter of the main duct less than 5 mm.(48) No attempt was made to include pancreas according to the pancreas texture and diameter of the duct in the other RCTs.

The lack of uniform definition of POPF was found in three studies. These were reported before the international consensus of POPF definition was published.

Only the study by Fernández- Cruz et al. used the definition by the International Study Group on Pancreatic Fistula.(50)

The analysis of the PJ technique used in the four RCTs is striking: (1) three RCTs show a lack of uniform technique, (2) a duct-to-mucosa technique was used as the standard in one trial and at the surgeon’s discretion in another trial, (3) end-to-end PJ anastomosis was used in two trials at the surgeon’s discretion, and (4) a duct to- mucosa PJ with an internal stent was used in only one trial.

Therefore, the major criticism of three RCTs is that the technique of PJ anastomosis was not standardized. As noted earlier the variations of the PJ technique are associated with important differences in the pancreatic fistula rate.(30,31,32)

The benefit of an internal or external stent across pancreatico-enteric anastomosis remains controversial. Theoretically, a stent may help divert the pancreatic secretion from anastomosis, and it also allows more precise placement of 374

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sutures for duct-to-mucosa anastomosis. Two recent prospective randomized trials have reached different conclusions on the benefit of stenting in reduction of the rate of PF. Winter et al. found that the use of a short internal stent did not reduce the frequency or the severity of PF after PJ. The major criticism of this study is that the technique of PJ anastomosis was not standardized because the use of the duct-to-mucosa invagination technique was at the discretion of the surgeons. There could be a possible bias in that invagination technique was chosen for a pancreatic stump with a small pancreatic duct that is more difficult for duct-to mucosa anastomosis, hence the benefit of a stent could have been missed in such patients.(51) On the other hand, Poon et al. used end-to-side, ductto-mucosa anastomosis, and the patients were randomized to have either an external stent inserted across the anastomosis to drain the pancreatic duct or no stent. This randomized trial showed a reduction of the incidence of pancreatic fistula from 20% in the nonstented group to 6.7% in the stented group.(52) Only one of the four RCTs used an internal stent for PJ reconstruction.

The study by Yeo et al. performed PJ in either end-to end or end-to-side fashion at the surgeon’s discretion. End-to-end PJ was favored and was most commonly performed. End-to-side PJ was used when there was a size discrepancy between the jejunum with a relatively small diameter and a pancreas segment with a relatively large transected end.(47) The study by Bassi et al performed PJ using a single-layer PJ or duct-to-mucosa technique.(48) In the study by Duffas et al, PJ could be performed end-to-end or end-to-side at the surgeon’s discretion.(49) However, the technical aspects of the anastomosis were not recorded. End-toside duct-to-mucosa PJ with an internal stent was performed in all patients in the study by Fernández-Cruz et al.(50)

The techniques of PG anastomosis were different in the four randomised controlled trials. The lack of a uniform technique for PG anastomosis raises the 375

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same controversy as that with PJ anastomosis (dunking vs duct-to-mucosa).

Delcore et al. reported a method of PG in which 3 cm of pancreatic remnant was telescoped into the gastric lumen (small gastrotomy made in the posterior gastric wall) without any stenting of the main pancreatic duct. PG is done in the gastric lumen through either the gastric stump or through an anterior-wall gastrotomy (in the case of pylorus-preserving procedure).(53) Aranha et al described one-layer invaginating PG after a Whipple procedure; the pancreatic remnant is mobilized for a distance of 4 cm, and sutures are placed from the posterior superior wall of the stomach to the anterior wall of the pancreas. A gastrotomy, measuring 3 cm in length, is made and then sutures are placed from the posterior inferior wall of the stomach to the posterior pancreas; 1 cm of the pancreas is invaginated into the stomach when the sutures are tied.(43) Among other alternatives, Telford and Mason reported that direct anastomosis of the pancreatic duct to gastric mucosa provides better patency of the pancreatic duct than does a simple implantation procedure.(54) Takao et al described a modified PG without gastrotomy. The proximal 2 cm of the pancreatic remnant is freed from the retroperitoneum and anastomosed end-to-side to the posterior wall of the stomach.

A 2-cm area of the seromuscular layer of the stomach in this region is excised. A stent in the pancreatic duct is then passed into the stomach through the exposed mucosa/ submucosa of the posterior gastric wall and exited through the anterior gastric wall. A suture anchoring the pancreatic duct is passed through the gastric mucosa/ submucosa and circumferentially around the pancreatic tube. The anastomosis is completed by applying sutures between the anterior pancreatic edge and the stomach.(55)

In the four randomised controlled trials the following PG techniques were employed. PG anastomosis was accomplished by anastomosing the pancreatic remnant to the posterior gastric wall in the study by Yeo et al.(47) The size of the posterior gastrotomy averaged 2.5â&#x20AC;&#x201C;3 cm. The study by Bassi et al telescoped the 376

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pancreatic remnant into the gastric cavity.(48) No mention of the details of PG anastomosis was found in the study by Duffas et al.(49) A new technique, pylorus-preserving pancreaticoduodenectomy with gastric partition, was described in the study by Fernández-Cruz et al.(50) Gastric partition was performed using two Endo-GIA staplers along the greater curvature of the stomach, 3 cm from the border. This gastric segment, 12–15 cm in length, is placed in close proximity to the cut edge of the pancreatic stump. An end-to-side, duct-to-mucosa anastomosis (with a pancreatic duct stent) is constructed.

The differences in these studies, as outlined previously, prohibit meaningful comparisons or conclusions to be made. Whether PG is superior to PJ or vice versa remains to be determined. While several modifications of either technique are reported the most appropriate method to fashion the pancreatico-enteric continues to be disputed.

CONCLUSION Advances in perioperative patient management and intensive care as well as progress in surgical technique have reduced the mortality rate after PD, whereas the morbidity rate remains. Pancreatic fistula and other pancreatic stump-related complications are the most common and serious problem after PD and may result in death. Patients with a fibrotic gland with a big duct have a very low probability of PF, no matter what technique is used. The probability of POPF increases dramatically in patients with a soft gland with a normal size duct.

In addition, the surgeon’s experience makes a difference to the surgical outcome. In the series of PJ (Table 1) and PG (Table 2) low rates of POPF and mortality were demonstrated. These results indicate that patient volume per surgeon may be an independent factor in determining the risk of anastomosis. Despite a lack of global consensus regarding whether PJ or PG is better, it appears that a standardized approach to the pancreatic anastomosis and a consistent practice of 377

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a single technique can help to reduce the incidence of complications after PD. However, given the multitude of factors that may influence the development of a POPF, the surgeon should gain experience in several techniques.

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51. Winter JM, Cameron JL, Campbell KA, et al. Does pancreatic duct stenting decrease the rate of pancreatic fi stula following pancreaticoduodenectomy? Results of a prospective randomized

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52. Poon RT, Fan ST, Loch M, et al. External drainage of pancreatic duct with a stent to reduce leakage rate of pancreaticojejunostomy after pancreaticoduodenectomy. A prospective randomized trial. Ann Surg 2007; 246:425–35.

53. Delcore R, Thomas JH, Pierce GE, et al. Pancreatogastrostomy: a safe drainage procedure after pancreatoduodenectomy. Surgery 1990; 108:641–5.

54. Telford GL, Mason GR. Pancreaticogastrostomy: clinical experience with a direct pancreatic-duct-to-gastric-mucosa anastomoses. Am J Surg 1984;1 47:832–7.

55. Takao S, Shimazu H, Maenohara S, et al. Modified pancreaticogastrostomy following pancreaticoduodenectomy. Am J Surg 1993; 165:317–21.

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19.

CROHN’S DISEASE OF THE COLON INTRODUCTION

Crohn’s Disease (CD) is a chronic inflammatory condition of the intestinal tract of unknown cause. In general, the following three main clinical anatomic patterns of CD are recognized: small bowel pattern 30%, ileocolic pattern 40%, and colonic (including rectum) 10%. For those patients with Crohn’s colitis (CC) the majority will be affected with pancolitis with the remaining 25 – 30% affected segmentally and up to 40% of those will have apparent rectal sparing.

The majority of patients with CD will require surgical intervention during the course of the illness. In the main, the philosophy of surgical management of CD consists of bowel and sphincter preservation. While bowel sparing techniques have been published for treatment of CD of the small bowel, because of its recurrent nature, the extent of resection in CC is still somewhat debatable.

A case of CC in a young woman is presented followed by a discussion related to the surgical options for CC and their related advantages and disadvantages.

CASE History: A 24 year old woman was admitted as an emergency with an abscess on the left lower abdomen. Her medical history began 14 months earlier when she was investigated for iron deficiency anemia and weight loss. A gastroenterologist had investigated her by way of: -Stool cultures: negative 383

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-Barium meal and follow through: normal stomach and small bowel -Colonoscopy: features consistent with inflammatory bowel disease; biopsy reported an indeterminate colitis.

-Mantoux test: negative -HIV :negative

Despite the histology report the diagnosis of Crohn’s disease was entertained.

Treatment was started and consisted of : prednisolone, azathioprine and asacol.

Unfortunately, the patient had poor support from her family (dad and stepmother) and eventually became non-compliant with her medications.

Physical Examination An emaciated young woman; she appeared pale, P 110 min-1, RR 24 min-1, T 372 0C. There was no lymphadenopathy and her Cardiorespiratory examination was normal.

The abdomen was scaphoid. A 4x4 cm fluctuant tender mass was identified just medial to the left anterior superior iliac spine.

Inspection of the perianal area revealed a frond-like skin tag. There was no evidence of fistula or abscess. Digital rectal examination identified normal tone and mucosa. There was no blood or mucus on the gloved finger.

There were no rashes or ulcers indicating pyoderma gangrenosum.

Investigations: Hb 6.1 g/dl, WCC 15 x 103 /µl, Plt 125 x 103/µl Renal function normal; Albumin 2.1 g/dl , Coagulation profile normal, CRP 25mg/dl.

CXR: normal

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The abscess was incised and drained. However 2 days later stool began oozing from the abscess cavity. She had developed a colocutaneous fistula.

Therapeutic measures included: rehydration, blood transfusion x 2units, antibiotics (augmentin 1.2g Intravenously three times daily), clexane 40 mg sc nocte.

After discussing with the gastroenterologist prednisolone (30mg po bd) and azathioprine (60mg po od) were recommenced. Although she was able to eat, her nutrition was augmented by parenteral nutrition via a PICC (peripherally inserted central line catheter). Her caloric intake was started at 1000kcal/ day for 2 days and increased incrementally by 500kcal every 2 days upto 4000 kcal.

A barium meal and follow through was repeated and the stomach and small bowel was normal. Colonoscopy showed that the mucosa of the sigmoid was friable and displayed small fissures/ ulcers. Mucosal nodularity was noted from the distal sigmoid colon to the splenic flexure, beyond which the scope could not progress. The colocutaneous fistula was noted and the rectal mucosa was spared.

The repeat colonic biopsy was reported as a non-specific colitis. The diagnosis was uncertain: ulcerative colitis vs Crohnâ&#x20AC;&#x2122;s disease. A colonic resection was required because of the fistula and the active disease causing malnutrition. The possibilities included: Pancolectomy with permanent stoma, Total colectomy and ileostomy with consideration for second stage ileorectal anastomosis or proctectomy.

The patient was informed of these plans and consented. Her parents had been contacted and educated about her condition and their role in her care. When the serum albumin was 3g/dl the patient was taken to the operating theatre and a Total colectomy and end ileostomy was performed.

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At laparotomy the terminal ileum appeared normal with no creeping fat. The proximal jejunum was adherent to the left colon (thickened) suggesting a entero-colic fistula (Fig1). The rectum was palpably normal.

Her recovery was slow but uneventful. She was taught how to care for the stoma. The patient was discharged 3 weeks after surgery.

Histology: Crohnâ&#x20AC;&#x2122;s Disease Skin overlying the fistula: Fragments of skin and subcutis with active chronic inflammation. Occasional small granulomas are seen in the dermis consistent with Crohnâ&#x20AC;&#x2122;s Disease.

Large Bowel: Colectomy with a strictured segment approximately 18 cm long with cobblestone appearance. Numerous pseudopolyps were noted. The mucosa either side of this appears normal. (Fig 2) The patient has had reviews in the outpatient clinic and is doing well. She has gained weight and is in good health up to one year ago.

Fig 1: Proximal jejunum adherent to the left colon (possible entero-colic fistula)

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Fig 2.: Left-sided colonic Crohn’s Disease with multiple pseudopolyps

DISCUSSION CD was first described by Crohn, Ginsberg, and Oppenheimer in 1932, when it was called regional ileitis (Crohn himself initially denied that regional enteritis occurred in the colon).(1). The most common anatomic presentations are ileocolonic 40%, small bowel disease 30%, while exclusive involvement of the colon and rectum is about 10%. The classic pathologic and gross features of Crohn’s disease of full thickness involvement with “bear claw” ulcerations, fistulization and aphthous ulceration remain the hallmarks of its clinical presentations. For those patients with CC the majority will be affected with pancolitis, with the remaining 25-30% affected segmentally. Interestingly up to 40% will have apparent rectal sparing.(2)

Most patients with CD ultimately require one or more operations in the course of their illness. At the Cleveland Clinic rates of surgery with disease duration of five years were 75%, 50% and 50% for ileocolitis, ileal disease and colonic disease respectively.(3) It has always been the role of the surgeon to rectify the complications of Crohn’s disease through operative intervention: obstruction, fistulization, anemia, bleeding and medically refractory disease. As would be expected, the leading indication for surgery in Crohn’s colitis remains failure of 387

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medical management. With improved radiologic and endoscopic imaging, innovative medical therapies and surgical judgment the surgical tenant of Crohn’s disease management remains bowel and sphincter preservation. Crohn’s disease is recurrent by nature and in order to avoid short bowel syndrome, techniques that limits resection for small bowel disease have been described.(4) Crohn’s disease of the colon and rectum presents many operative challenges and the extent of resection is a matter of debate.

Segmental or skipped areas occur in 25-30% of Crohn’s disease. Although debatable, the best surgical option may be limited or segmental colon resection.

Prabhakar et al on review of 49 patients with segmental resection for colonic Crohn’s disease noted that during follow up 45% required no further intervention.(5) Only 16 patients required another operation (10 required another segmental resection and 6 colostomy). Overall 86% of patients remained stoma free and those who ultimately required a stoma had it delayed by 23 months.

In another report, 55 patients underwent segmental colectomy and a recurrence rate of 38% was noted.(6) The recurrences occurred earlier and was higher for patients undergoing more extensive resections (total abdominal colectomy, proctocolectomy). Martel and colleagues studied 84 patients who underwent segmental colonic resection. After a mean follow up of 111 months 13 patients had a stoma while 36 patients required re-operation. Twenty-six patients suffered with colonic recurrence of which 17 had another segmental resection. The only factor that correlated with the risk of recurrence was youth.(7) Seventy-five percent of the patients without stoma had less than 3 bowel movements per day and 80% were satisfied. They concluded a bowel sparing policy was appropriate for segmental colonic Crohn’s disease as there is no evidence of a higher risk of post operative complications, surgical recurrence or requirement of a permanent stoma, compared with more extensive resections.

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Fortunately, 40% of patients with colonic Crohn’s disease have rectal sparing.

The long term outcome of an ileorectal anastomosis (IRA) is predictably poor in cases where the rectum itself is diseased.(8) The “bug bear” of Crohn’s disease is that of relapse or recurrence and this has been noted in up to 60% of patients in both the ileum and rectum.(9) As a result there is concern by some clinicians over the consequences of recurrence following total colectomy and IRA. It was Goligher’s seminal article that first defined the debate as one which stated that it is in the patients best interest to avoid recurrence and thus undergo completion proctectomy and ileostomy: in a series of 207 patients undergoing resection for colonic CD those undergoing sub total colectomy and IRA had significantly higher recurrence rates than those undergoing proctectomy and ileostomy.(10) This finding has been confirmed by others (11,12,13).

Despite these findings some surgeons have continued to attempt to retain intestinal continuity, particularly in younger patients. To this end, several authors have published on follow up series on IRA. They indicate that long term intestinal continuity and reasonable function can be maintained with a conservative surgical approach.

(14,15)

This success might be due to good patient selection

and improvements in medical management. In addition, Alves et al showed that while proctectomy was often the eventual result in patients who developed recrudescent Crohn’s disease in the rectal remnant, the more common site of recurrence, at and immediately proximal to the IRA, could be dealt with by ileorectal resection and construction of a new IRA.(16)

A more recent report by O’Riordan et al demonstrated functioning IRA at 5 and 10 years were 87% and 72.2% respectively. (17) In this series, 11 of 81 patients underwent small bowel resection plus redo IRA. They identified a re-operative and/or proctectomy rate of 30%. It is prudent that patients are counseled appropriately; in the case described this young lady decided against the risk of IRA 389

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(anastomotic leak, rectal recurrence ± redo surgery) and was willing to revisit the idea of IRA once she had improved and settled a bit in her life. It would appear that assuming good pre operative sphincter control and rectal compliance an IRA will provide most patients with reasonable long term function.

The more radical procedure of total proctocolectomy and end ileostomy, in the setting of severe anorectal CD, is the procedure of choice. The recurrence rate varies from as low as 10 – 25%. This low rate of recurrence is far below that found in other areas of the gastrointestinal tract, which generate a recurrence rate of 50%. The trade off for this low recurrence rate unfortunately has been historically poor healing in the perineal wound.(18)

In patients with CD avoidance of a permanent stoma and maintaining bowel continuity would indeed lessen the physical and psychological ailments seen in patients with CD and hence improve their quality of life. Another surgical option for patients with colonic Crohn’s disease is restorative proctocolectomy.

Since its introduction by Parks and Nicholls, proctocolectomy with ileal pouch anal anastomosis (IPAA) has become the standard treatment for patients with ulcerated colitis (UC) and most of those with familial adenomatous polyposis syndrome.(19) In many of these cases the procedure cures the disease, maintain gastrointestinal continuity and improved the patients functional outcome and quality of life. Although the complication rate ranges from 30-40%, the incidence of pouch failure declines with experience.(20)

The role of restorative surgery in colonic CD, however is controversial. It is often performed in patients who were initially diagnosed with UC but were subsequently found to actually have CD after IPAA. It is often difficult to make discrete preoperative clinical and pathological distinctions between UC and CC, particularly after medical therapy has been instituted. The standard pre-opera390

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tive diagnosis of CD is usually based on the presence of epithelial granuloma or focal chronic ileitis, the presence of deep ulceration, patchy inflammation with rectal sparing, focal chronic ileitis and transmural lymphoid aggregations in non ulcerated areas. Distinguishing CD from UC or indeterminate colitis can be quite a challenge. Fewer than 30% of patients present with classic features and in approximately 8-10% of patients the pathologic diagnosis is changed from UC to CD after IPAA.(21)

Apart from incontinence and excessive bowel frequency, the principal causes of pouch failure in patients with CD are severe perineal disease, recurrent sepsis, outlet strictures, and fistulae. These clinical presentations of severe perineal disease, recurrent sepsis, outlet strictures, and small bowel involvement lead to pouch excisions and re-diversions in a large number of patients whose diagnosis were missed before IPAA. Re-operative surgery, especially redo-pouch with abdominal perineal disconnection might be best avoided in patients with CD and multiple intestinal involvements due to the risk of short bowel syndrome.

Data suggest that IPAA patients with a pre-operative diagnosis of CC generally have a 40-45% chance of pouch failure and often develop life time comorbidities.(22) Crohnâ&#x20AC;&#x2122;s inflammation often recurs within the perineum and pelvic cavity after IPAA which may result in multiple complex fistulae leading to pouch failure hence IPAA is generally contra indicated in patients with colonic CD.(23) Furthermore, other serious implications of IPAA include fecal incontinence due to anal sphincter damage and bladder and sexual dysfunction due to autonomic nerve damage. Fecundity in female patients with either familial adenomatous polyposis syndrome or UC after IPAA is reduced.(24). These were notable concerns of the young lady whose case was described here.

Nevertheless, some authors have reported reasonably good outcomes and have recommended IPAA to be an alternative for selected patients with colonic CD. 391

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Panis and co-workers reported a low complication rate (19%) from selected patients with CC (n=31) who did not have perineal and small intestinal disease. In this prospective study, inflammation within the pouch occurred in 6 patients, 2 (6.4%) required subsequent pouch excision. Short and long term complications occurred in 16% and 19% respectively. Perfect continence was achieved in 74% of cases and 32% of patients required anti diarrheal medication. Overall, sexual function was good.(25) In another study reporting long term (10 years) results Regimbeau and colleagues reported 35% morbidity, with only 10% of patients experiencing pouch failure.(26) Good functional outcome was also reported in a small study by de Oca and colleagues: 12 patients with a post operative diagnosis of Crohnâ&#x20AC;&#x2122;s disease. When compared with 100 patients with UC, the patient satisfaction rate was high and with good physical and social improvements achieved. The long term complications, functional outcomes, and quality of life were comparable with those of UC patients.(27)

IPAA for CD may come about in two ways. Firstly, in patients with known CC, and secondly in patients who underwent IPAA for suspected UC or indeterminate colitis. Other researchers have found that patients with an established diagnosis of CC have a better chance of pouch survival than those with secondary diagnoses. (28,29). While IPAA is a consideration for patients with CC, a thorough discussion regarding the possible complications and expectations of the patients is required.

Due to the overlapping clinical histological and endoscopic findings of pouchitis and CD, managing relapsing inflammatory manifestations and reservoir dysfunction can be challenging in the post operative period. In this respect Infliximab, an antitumor necrosis factor (TNF-Îą) antibody, is associated with good short term and long term clinical responses and satisfactory functional outcomes in refractory post-IPAA CD. As such, further surgical interventions 392

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may be avoided with effective medical therapy which can increase a patient’s quality of life.(30).

CONCLUSION The patient in the case described had a preoperative diagnosis (histological) of indeterminate colitis. She presented with a colocutaneous fistula, which given her age and sparing of the lower rectum, may have suggested a diagnosis of Crohn’s disease. While an ileorectal anastomosis was an option, her current state of health could not risk an anastomotic leak. Also consideration was given to the possibility of her histology ultimately indicating UC, in which case she could be appropriately consented for an IPAA or completion proctectomy. Similarly, an IPAA was not undertaken in view of the possibility of Crohn’s disease.

Also, her wishes to have a family were considered and given due respect, and so unnecessary pelvic dissection was avoided. Having had a total colectomy and end ileostomy, this young lady still has the option of restoring bowel continuity via an IRA. In her follow up over eighteen months her quality of life is much better, she has gained weight and her decision is awaited.

The majority of patients with CC eventually require surgical excision of the disease. The decision regarding which operation to perform depends on the extent and site of disease, distensibility of the rectum, the presence of perianal disease, the age and attitude of the patient and their acceptance or otherwise of a stoma.

Total proctocolectomy and ileostomy gives the best long term results for CC in terms of recurrence rate. Abdominal colectomy and ileorectal anastomosis often restores young patients to good health without the risk of impaired sexual function from pelvic dissection and a permanent stoma is delayed and sometimes avoided. Segmental colonic resection should be considered for isolated short segments of CC. While a small subset of patients with CC may do well with IPAA, this procedure is generally not recommended.

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REFERENCES 1. Wolf BG. Crohn’s colitis. Current Therapy in Colon and Rectal surgery. Decker, Ontario, 1990,pp 195-198.

2. Prabhakar LP, Wolff BG: Crohn’s colitis, in Cameron JL (ed): Current Surgical Therapy.

Mosby, St. Louis, 1998, pp 184-186.

3. Whelan G, Farmer RG, Fazio VW, et al: Recurrent after surgery in Crohn’s disease: Relationship to location of disease (clinical pattern) and surgical indication. Gastroenterology, 1985; 88:1826-1833.

4. Talamini MA, McLemore EC: Use of strictureplasty in Crohn’s disease, in Cameron JL, Cameron AM (ed): Current Surgical Therapy. Elsevier,Saunders, 2011, pp 101- 105.

5. Prabhakar LP, Laramee C, Nelson H, et al: Avoiding a stoma: role for segmental or abdominal colectomy in Crohn’s colitis. Dis Colon Rectum 40(1):71-78, 1997.

6. Fichera A, McCormack R, Rubin MA, et al. Long term outcome of surgically treated Crohn’s colitis: a prospective study. Dis Colon Rectum, 2005; 48(5): 963-9.

7. Martel P, Betton PO, Gallot D, et al. Crohn’s colitis: experience with segmental resections; results in a series of 84 patients. J Am Coll Surg, 2002; 194 (4): 448-53.

8. Ekelund G, Lindhagen T: Controversies in the surgical management of Crohn’s disease. Perspect Colon Rectal Surg 1989, 1-17.

9. Lindhagen T, Ekelund G, Leandoer L, et al: Crohn’s disease in a defined population course and results of surgical treatment. Part II. Large bowel disease Acta Chir Scand, 1983; 149(4):415421.

10. Goligher JC: The long-term results of excisional surgery for primaryand recurrent Crohn’s disease of the large intestine. Dis Colon Rectum, 1985; 28(1):51-55.

11. Andrews HA, Lewis P, Allan RN: Prognosis after surgery for colonic Crohn’s disease. Br J Surg, 1989; 76(11):1184-1190.

12. Andrews HA, Keighley MR, Alexander-Williams J, et al: Strategy for management of distal ileal Crohn’s disease. Br J Surg, 1991; 78(6):679-682.

13. McLeod RS, Wolff BG, Steinhart AH, et al: Prophylactic mesalamine treatment decreases postoperative recurrence of Crohn’s disease. Gastroenterology, 1985; 109(2):404-413.

14. Pastore RL, Wolff BG, Hodge D: Total abdominal colectomy and ileorectal anastomosis for inflammatory bowel disease. Dis Colon Rectum 1997; 40(12):1455-1464.

15. Cattan P, Bonhomme N, Panis Y, et al: Fate of the rectum in patients undergoing total colectomy for Crohn’s disease. Br J Surg, 2002; 89:454-459.

16. Alves A, Panis Y, Joly F, et al: Could immunosuppressive drugs reduce recurrence rate after second resection for Crohn’s disease? Inflamm Bowel Dis, 2004; 10:491-495.

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A CASEBOOK OF TWENTY SURGICAL CASES 17. O’Riordan JM, O’Connor BI, Huang H, et al. Long term outcome of colectomy and ileorectal anastomosis for Crohn’s colitis. Dis Colon Rectum, 2011; 54(11): 1347-54.

18. Larson DW, Wolff BG. Colectomy for Crohn’s disease, What Operation? Semin Colon Rectal Surg, 2006; 17: 76-90.

19. Parks AG, Nicholls RJ: Proctocolectomy without ileostomy for ulcerative colitis. BMJ, 1978; 2:85-88.

20. Tulchinsky H, Hawley PR, Nicholls J: Long-term failure after restorative proctocolectomy for ulcerative colitis. Ann Surg, 2003; 238:229-234.

21. Sagap I, Remzi FH. Ileal pouch anal anastomosis and Crohn’s disease. Semin Colon Rectal Surg, 2006; 17: 91-95.

22. Braveman JM, Shoetz DJ, Marcello PW, et al: The fate of the ileal pouch in patients developing Crohn’s disease. Dis Colon Rectum, 2004; 47:1613-1619.

23. Hyman NH, Fazio VW, Tuckson WB, et al: Consequences of ileal pouch-anal anastomosis for Crohn’s colitis. Dis Colon Rectum, 1991; 34(8): 653-657.

24. Averboukh F, Kariv Y. Ileal pouch rectal anastomosis: technique, indications and outcomes.

Semin Colon Rectal Surg 2009;20: 93-102.

25. Panis Y, Poupart B, Nemeth J, et al. Ileal pouch-anal anastomosis for Crohn’s disease. Lancet 1996; 347: 854-857.

26. Regimbeau JM, Panis Y, Pocard M, et al: Long-term results of ileal pouch-anal anastomosis for colorectal Crohn’s disease. Dis Colon Rectum 2001; 44:769-778.

27. de Oca J, Sanchez-Santos R, Rague JM, et al: Long-term results of ileal pouch-anal anastomosis in Crohn’s disease. Inflamm Bowel Dis 2003; 9(3): 171-175.

28. Mylonakis E, Robert NA, Keighley MRB: How does pouch construction for a final diagnosis of Crohn’s disease compare with ileoproctostomy for established Crohn’s proctocolitis? Dis Colon Rectum 2001; 44:113-143.

29. Hartley JE, Fazio VW, Remzi FH, et al: Analysis of the outcome of ileal pouch-anal anastomosis in patients with Crohn’s disease. Dis Colon Rectum 2004; 47:1808-1815.

30. Orlando A, Colombo E, Kohn A, et al: Infliximab in the treatment of Crohn’s disease: predictors of response in an Italian multicentric open study. Dig Liver Dis 2005; 37(8):577-583.

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RUPTURED ABDOMINAL 20. AORTIC ANEURYSM Is there an EVAR-lasting improvement in the high mortality?

INTRODUCTION The incidence of abdominal aortic aneurysm (AAA) is increasing with our aging population. The most feared complication is rupture of AAA (RAAA). This situation presents several challenges starting with its diagnosis and management. Unfortunately, rupture has a high mortality (80%). These patients require intense treatment strategies which exhaust significant resources.

As a result of this high mortality many surgeons are selective regarding to whom surgery is offered. Several scoring systems have been developed to prognosticate the outcome of critically ill patients. The Hardman Index (HI) and Glasgow Aneurysm Score (GAS) are two such scoring systems. Their validity and use to select patients with ruptured AAA for surgery has met with controversial results.

Despite improvement in peri-operative care and operative strategies, attempts to improve the mortality associated with RAAA have been unsuccessful. In the last decade, repair of ruptured AAA has seen a shift from open surgical repair to more frequent use of Endovascular Aneurysm Repair (EVAR), in an attempt to decrease mortality and provide another option to those deemed unsuitable for open surgery.

Two cases of ruptured AAA are described followed by a discussion regarding the challenges in diagnosis of ruptured AAA, the difficulty in predicting mortal396

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ity and strategies to improve the survival, particularly the role of EVAR in the management of ruptured AAA.

CASE 1 History: A 74year old woman (RS) suffered vague epigastric pain for 1 week.

There was occasional radiation to the back but no history of fatty food intolerance. Apart from being hypertensive this woman was otherwise well. Her medications included enalapril and simvastatin. Having seen her private GP for the pain, an ultrasound of the abdomen was ordered. She attended for the US the following day when she had a further episode of pain. The severity was much worse and it was felt in the back. The US had noted a 5cm infra-renal abdominal aortic aneurysm.

Physical Examination: On arrival to the emergency room: Her BP 110/60 mmHg, P60/ min and appeared drowsy but GCS was 15/15. Physical examination revealed a pulsatile mass in the left abdomen. Her peripheral pulses were present but of low volume.

Laboratory investigations included: Hb 11.8, Plts 168, WCC 6.5, Cr 1.0, BUN 16, Na 140, K 3.7, Cl 107.

An urgent contrast enhanced CT confirmed a leaking infra-renal AAA.

Surgical Treatment: Emergency laparotomy and Aneurysmorraphy: Midline laparotomy with induction of anaesthesia. A juxta-renal aneurysm was identified with the distal limit 3cm from the bifurcation of the aorta. After aortic cross clamping at the level of the crus (supraceliac ) an infra-renal aortic clamp was placed and repair was effected with a 16 mm Gelatin impregnated woven vascular graft. The aortic clamp time was 96 minutes and estimated blood loss was 2700 mls. Intra-operatively Mrs. RS was transfused 4 units of blood and 6 397

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units of FFP. (See Fig 1 and 2)

Post-operative course: Admitted to the ICU: -Ionotrope dependent for 2 days (weaned off) -Extubated day 2 -Chest and Limb physiotherapy commenced -Naso-gastric feeds commenced on day 4

On day 5, the patient developed respiratory distress and required re-intubation.

Her CVP was persistently elevated (14-16cmH20) with a BP 100mmHg systolic. A cardiology review was requested, the ECG and echocardiogram was normal, as were serial cardiac enzymes. Her deterioration was most probably related to a transfusion related lung injury (TRALI).

The patient had a tracheostomy done on day 7 and made very slow progress over the next two weeks. By this time she remained very lethargic and physically weak. During the 4th week she experienced episodes of bradycardia and eventually had a cardiac arrest and died (day 25).

Fig 1: Retroperitoneal hematoma related to infra-renal aortic aneurysm

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Fig 2: Pre-clotting of the woven graft

CASE 2 History (As per A&E): A 64 year old man was admitted to A&E with epigastric pain for 3 days. This pain had an insidious onset, was unrelated to meals with no specific aggravating or relieving factors. This was not associated with any back pains or syncope. Although he was hypertensive he reported no cardiac symptoms and had good exercise tolerance.

Physical examination (As per A&E): His admitting vital signs were normal (BP 132/84mmHg, P92min-1 , RR 20 min, T 36.8oC. Abdominal examination revealed mild distention with vague dis-

1

comfort, not associated with guarding or rebound. There was epigastric fullness but no expansile, pulsatile features. Bowel sounds were present and normal as were examination of the groin and digital rectal examination.

Peripheral pulses were present and equal.

Relatives reported he did not smoke and lived on his own.

X rays were not possible (equipment malfunction) so a CT scan (suspected acute pancreatitis) was ordered. Initial blood results were : Hb 9.4 g/dl, WCC 399

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9 x 103, Plts 222 x 103, Cr 3.2 mgdl-1, BUN 28 mgdl-1, Na 132, K 5.1, Cl 105.

On return from CT, his pain became acutely worse and he was now unconscious. His BP measured a systolic in the 70s which was subsequently maintained at 120/ 80 mmHg with intravenous crystalloids. Resuscitation continued and blood investigations repeated. A surgical consult was requested.

CT scan revealed a ruptured abdominal aortic aneurysm (infra-renal). He was taken to the operating theatre within 15 mins. On transfer to the operating table his blood pressure became unrecordable, suffered a cardiac arrest and died. His blood investigations revealed a fall in Hb to 7.6mmHg.

Fig 3: Ruptured abdominal aortic aneurysm with retro-peritoneal hematoma

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Fig 4: Ruptured aortic aneurysm (broken calcified ring)

DISCUSSION The difficulties in diagnosis and management of AAA was noted more than a century ago by Sir William Osler.(1) Misdiagnosis of ruptured AAA remains a serious challenge to all practitioners and the real rate is probably difficult to identify due to under reporting. One report indicates that in 61% of cases, ruptured AAA was missed on initial diagnosis. In nine (9) of fourteen (14) patients who were hemo-dynamically stable at presentation, diagnosis was not made until shock developed.(2) On reviewing the literature, it appears that clinical presentation may mimic other illnesses, such as, urinary tract obstruction or infection; spinal disease and diverticulitis..(1)

A high index of suspicion is required as these patients sometimes are reviewed less urgently or are extensively investigated before the diagnosis is arrived at.

Misdiagnosis is quite a serious issue as ruptured AAA is associated with an overall mortality of 80%.(3)

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Some historical clues have a well-established relationship with AAA. These include, advanced age, cardiovascular disease, peripheral vascular disease, and cerebrovascular disease and of course their associated risk factors (smoking, hyperlipidemia and hypertension). Recent advances in identifying those at risk for AAA have come in the fields of genetics and molecular biology. Engstrom and colleagues(4) studied five (5) inflammation – sensitive plasma proteins (fibrinogen, alpha 1 antitrypsin, haptoglobin, ceruloplasmin, orosomucoid) and noted an association with elevated levels and fatal AAA or increased fatality after surgically repaired AAA. The presence of susceptibility loci for AAA has been identified by Shimbura and colleagues(5) on chromosome 19q13 and 4q31.

These discoveries show promise for earlier identification of patients at high risk.

On presentation to the emergency room, the clinician must turn to the bedside examination as the next step in the diagnostic pathway for a time-sensitive condition. The classic examination finding is a pulsatile, expansile abdominal mass. However, the accuracy of the physical examination in diagnosis of a ruptured and non-ruptured AAA remains highly controversial. For bedside identification of AAA by physical examination, the sensitivity rates range from 33% to 100% and specificity rates range from 75% to 100%. The sensitivity of abdominal palpation increases with aneurysm size (29% for 3–3.9cm; 50% for 4-4.9cm; 70% for ≥5.0cm) but is quite variable.(6)

With physical findings and examination skills being so variable, other diagnostic tools are very important. Plain abdominal x-rays and ultrasound (US) are common place in accident and emergency. The plain abdominal x-ray can be helpful as it may display the following signs: calcification of aneurysm, complete loss of one or both psoas shadows, complete loss of one or both renal outlines, and renal displacement. A recent review of the plain abdominal film for ruptured AAA indicated these findings to be quite variable leaving room for 402

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error or misdiagnosis.(7)

USS is now commonly performed by emergency room doctors for abdominal catastrophes. Despite being observer dependent with sufficient training and experience, emergency room USS can provide a timely diagnosis of ruptured AAA. Numerous studies have actually demonstrated 100% accuracy of diagnosis of ruptured AAA by USS. Tayal et al (8) on review of 125 scans performed by emergency room doctors, had 100% sensitivity and 98% specificity for AAA on confirmatory testing with radiology, ultrasound, abdominal CT, abdominal MRI or laparotomy.

Most clinicians will accept that in unstable patients, hemodynamic instability plus identification of AAA by USS is an indication for laparotomy. In view of the varied presentations, however, in stable patients, further imaging may be necessary to determine if the finding of AAA is causal or incidental. CT findings in patients with ruptured AAA include retroperitoneal hematoma, focal discontinuity in circumferential calcification, high attenuating peripheral crescent, indistinct aortic wall, and frank contrast medium extravasation. In addition to better identification of a leaking aortic aneurysm, a CT scan provides more information regarding other causes of intra-abdominal pathology.(6) A further role of CT of course is to help plan endovascular repair (EVAR) which is becoming more popular. The use of CT in the diagnosis and evaluation of the patient who presents with suspected ruptured AAA remains controversial. On one hand, it is a risk to allow the potentially unstable patient to leave the emergency department for a test which would delay the transport to the operating room. On the other hand, CT is more sensitive for aneurysm leakage and can provide a better road map for endovascular repair when compared with ultrasound alone. In an interesting study by Lloyd and colleagues(9), time to death in patients who present with ruptured AAA was reported to be over two (2) hours in 87.5% of pa403

A CASEBOOK OF TWENTY SURGICAL CASES

tients. They concluded that most patients with a ruptured AAA who survive to the hospital are therefore stable enough to undergo CT scanning before surgery.

The high mortality associated with ruptured AAA has stimulated ideas regarding patient selection for operative treatment. The definitive management, surgical repair, is not debated, however the high mortality rate has stimulated ideas about being more selective about who should be operated on. Patientâ&#x20AC;&#x2122;s age is an often quoted prohibitive factor. It is generally thought that the outcome will be poor with such a vascular catastrophe in elderly patients. Many of them have other co-morbidities with perceived limited life expectancies, particularly in octogenarians and nonagenarian.

Nevertheless, vascular and general surgeons are called upon to evaluate and treat the very elderly with a ruptured AAA and are thus faced with an ethical and clinical dilemma of whether to operate or not. At present, decisions made in these situations are based on clinical judgment as there is no clear support by literature data. This effect was demonstrated in a questionnaire study performed in Great Britain and Ireland in 1998 which indicated that age > 80 years, significantly influenced surgeons decision not to treat patients with ruptured AAA(10).

Biancari et al

(11)

reported on a systematic review and meta-analysis of obser-

vational studies reporting on the outcome following open repair of ruptured AAA in patients > 80 years. They identified that those patients > 80 years had a significant risk of immediate post operative mortality compared with younger counterparts (risk difference of 19.4%). However looking at intermediate survival in 6 of 29 studies where the information was available survival rates at 1, 2, 3, years were 82.4%, 75.6% and 68.7% respectively. Therefore some patients >80 years old may benefit from emergency surgery for ruptured AAA. Other researchers, have also reported acceptable survival rates for open repair for ruptured AAA in octo and nonagenarians and as such these patients should not be 404

A CASEBOOK OF TWENTY SURGICAL CASES

denied surgery based on advanced age alone.(12)

Harris et al, identified that mortality related to ruptured abdominal aortic aneurysm were related to pre-operative, intra-operative and post â&#x20AC;&#x201C;operative factors.

They observed a mortality of 64% on review of 113 cases. Pre-operative factors including cardiac arrest, loss of consciousness and acidosis influenced early post-operative deaths (<48 hrs) but not late deaths. Late deaths were related to development of multi-organ failure, specifically renal and respiratory, and the need for re-operation.(13) Others have identified similarly high mortality rates and have identified, advanced age along with multiple co-morbidities, particularly renal failure as factors which influence mortality.(14,15)

As noted previously the high mortality and resource implications for patients with ruptured AAA gives great appeal to the ability to select patients that are likely to survive surgery for ruptured AAA. About fifteen years ago, two scoring systems were developed which were thought to predict mortality for patients with ruptured AAA. These statistical models the Glasgow Aneurysm Score (GAS)(16) and Hardman Index (HI)(17) predicted high mortality (> 80% GAS >95, 100% HI â&#x2030;Ľ 3) and it was hoped that they may provide a tool by which to risk stratify patients. The scoring systems for both of these are shown in the tables below:

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TABLE 1 THE GLASGOW ANEURYSM SCORE PARAMETER

POINTS AWARD-

CASE 1

CASE 2

(years)

74

64

Shock

17

0

0

Myocardial Disease

7

0

0

Cerebrovascular disease

10

0

0

Renal Disease

14

0

14

ED Age

TABLE 2 THE HARDMAN INDEX PARAMETER

POINTS

CASE 1

CASE 2

AWARDED

Age >76 years

1

0

0

Loss of consciousness

1

0

1

Hemoglobin <9mg/dl

1

0

0

Serum Cr >190mmol/L

1

0

1

1

0

0

(>2.1 mg/dl) Ischemic

changes

on

ECG

406

A CASEBOOK OF TWENTY SURGICAL CASES

According to these scores survival was expected to be more favorable but unfortunately both patients died. The past decade has seen numerous articles published in relation to these statistical models. While a trend of increased mortality with increased scores are noted they are poor predictors of mortality.(18, 19, 20) Most recently, Gatt and colleagues identified that neither of these two systems helped to predict mortality nor did they correlate with each other.(21) There is now an abundance of evidence to dispense with statistical models to predict patient outcomes for ruptured AAA. The only way to predict a patientâ&#x20AC;&#x2122;s outcome with some certainty is not to offer surgery.

Conventional open repair is performed with the patient under general anaesthesia. The patient is prepped and draped from the neck to mid thighs. The midline laparotomy is done simultaneously with induction of anaesthesia. The aorta is cross clamped sequentially at the supraceliac and infra-renal level to minimize decompensation following the loss of sympathetic tone with anaesthesia on board. The small bowel mesentery is safe guarded, the related clot/ hematoma is dissected off. A further clamp was applied below the aneurysm and the aneurysm sac is opened longitudinally. Back bleeding from the lumbar vessels are sutured and an aortic graft is placed. In the case described (Case 1) woven Dacron (16mm) graft was sutured in place with 2/0 prolene. The graft was pre-clotted with blood to prevent leakage of blood into the sac. The sac was then sutured over the graft.

The ruptured abdominal aortic aneurysm is itself an extreme physiological challenge to the patient however other factors contribute to the high mortality associated with emergency repair of ruptured AAA. In addition a significant proportion of patients are elderly with comorbidities. Consequently cardiac complications are the most frequent peri-operative complication and include myocardial infarction, arrhythmia and congestive cardiac failure. Renal failure 407

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after repair of a ruptured AAA occurs in 15-21% of cases and carries a high mortality. It is more frequent in patient with pre-existing renal impairment but may occur as a result of hypoperfusion, suprarenal aortic clamping, atheroembolism and contrast administration.(22)

Post-operative bleeding may continue from the anastomotic suture lines, from unrecognized venous injuries, and as a result of coagulapathy due to intra-operative hypothermia and blood loss. Post-operative acute pancreatitis may ensue from injury inflicted by retractors. The most serious gastrointestinal complication is ischemia of the left colon and rectum. In ruptured AAA this can be observed in 30% of cases. Intestinal ischemia develops when critical hypogastric arteries are not revascularised or when a patent inferior mesenteric artery is ligated in the setting of superior mesenteric artery or bilateral hypogastric artery occlusion. Improper ligation of the inferior mesenteric artery too far from the aneurysm wall can interfere with the collateral blood supply to the rectosigmoid and lead to ischemia. Post-operative hypotension and hemodynamic instability may contribute.(22)

Lower extremity ischemia may result from embolisation of mural thrombus or atherosclerotic plaque from the aneurysm, or thrombus distal to the vascular clamp. Occasionally microembolisation can occur resulting in small patchy areas of ischemia, usually on the plantar aspect of the foot, referred to as thrash foot. A more extreme situation is massive embolisation with extensive buttock and lower extremity ischemia associated with high mortality.(22)

Ischemic injury to the spinal cord or lumbosacral plexus is much more frequent after ruptured AAA (1.4%) than after elective open AAA repair (0.1%). Preservation of the pelvic blood supply, avoiding prolonged suprarenal clamping and carefully removing aortic thrombus from the aneurysm to prevent lumbar or in408

A CASEBOOK OF TWENTY SURGICAL CASES

ternal iliac artery embolisation are important to further decrease this devastating complication. The mortality rate associated with this complication is 50 %. (23) Most patients end up in the intensive care unit. Respiratory complications can occur after any painful abdominal operation which discourages deep breathing and coughing, particularly when patients are elderly and likely to have smoked in the past. Early extubation and mobilisation with aggressive pulmonary toilet can help prevent the onset of nosocomial pneumonia and pulmonary dysfunction. The post-operative pneumonia rate is about 5%.(22)

Transfusion â&#x20AC;&#x201C;related lung injury (TRALI) is estimated to occur in 1 case per 5000 units of blood transfused. The term was first coined by Popovsky in 1983 and is now known to be the most common cause of fatal transfusion reactions.

(24)

TRALI is a clinical syndrome associated with the transfusion of all blood

components, especially platelets and plasma. TRALI is characterized by the onset of dyspnea, hypotension, hypoxemia, fever, and bilateral non-cardiogenic pulmonary edema within 6 hours of transfusion. The diagnosis is one of exclusion after volume overload, cardiogenic pulmonary edema or acute respiratory distress syndrome has been ruled out. The pathophysiology is thought to be due to transfusion of donor leukocyte antibodies or biologically active lipids from donor blood cell membranes into recipients. The donor antibodies attack recipient leukocytes that localize to the pulmonary microvasculature and release cytokines that lead to an increase in vascular permeability and fluid exudation.

Overall mortality is 5-10%.(25)

The perioperative mortality is still largely determined by the patientâ&#x20AC;&#x2122;s hemodynamic status at presentation. Somewhat paradoxically, it has been established that in circumstances with major arterial bleeding, restricted blood transfusions and fluid resuscitation can actually decrease blood loss and improve patient outcomes.(26) As early as 1991, fluid restriction was advocated for the preoperative 409

A CASEBOOK OF TWENTY SURGICAL CASES

management of RAAAs.(27) When patients are over-resuscitated, the pressure elevates and a formed clot at the site of rupture or arterial injury can get dislodged, causing more bleeding. In addition, if excessive fluids are used, coagulation factors get diluted, which can contribute to a coagulopathy. As such several reports have indicated the use of this strategy in order to minimize hemodynamic decompensation in the perioperative management of ruptured AAA(28, 29,30) The use of vasopressors is avoided and blood pressures as low as 50 mmHg are accepted so long as the patient is moving and responsive. Fluid restriction is continued until the patient is in the operating room. If the patient becomes unresponsive with an unobtainable blood pressure, fluid and blood resuscitation may become necessary while achieving vascular control.

Although Dubost performed the first aortic aneurysm repair in 1951 by an extraperitoneal thoraco-abdominal approach (33), most surgeons now use an anterior midline transperitoneal exposure for aneurysmorraphy. The advantages of the extraperitoneal approach to aortic aneurysmorraphy are: it eliminates bowel exposure and manipulation and the associated fluid and electrolyte loss of the transperitoneal approach. These were highlighted more recently in a series by Naraynsingh et al.(31) Growing experience with the left retro-peritoneal exposure for elective aortic surgery has allowed surgeons to extend the use of this approach to the repair of ruptured AAA. In one study the extended left retroperitoneal approach using a posterolateral exposure through the 10th intercostal space allowed the surgeon expeditiously and reliably to obtain supraceliac aortic control by dividing the left crus of the diaphragm in all patients. In total, 104 aortic replacements were performed for ruptured abdominal aortic aneurysm over a 7 year period. Of these patients, 87 were men and 17 women; mean (range) age was 72 (52-95) years. Hemodynamic instability (as defined by a systolic blood pressure of < 90 mmHg) was present before surgery in 41% (43/104) of patients.

The operative mortality rate was 27.9% (29/104). Preoperative hemodynamic 410

A CASEBOOK OF TWENTY SURGICAL CASES

instability, time of operative delay and aortic cross-clamp time did not correlate with operative mortality. The median duration of intensive care unit stay was 4 (range 1-60) days and hospital stay 11 (range 6-175) days. The results of this series identified that a change in the operative technique for the repair of ruptured abdominal aortic aneurysm beneficially affected patient survival. The authors suggest that expeditious supraceliac control without thoracotomy is an excellent alternative and offers an advantage in the surgical management of ruptured abdominal aortic aneurysm.(32)

While refinement of the open approach to aneurysmorraphy for ruptured AAA is welcomed to quell the historically high mortality of this condition, the advent of endovascular techniques have presented the opportunity to substantially alter and improve the outcomes of ruptured AAA. The treatment of aortic aneurysmal disease was changed forever when Parodi and colleagues (33) implanted the first endograft to treat an infra-renal abdominal aortic aneurysm. Among the advantages of endovascular repair of ruptured aneurysms are the ability to obtain proximal control without general anesthesia and the ability to deploy the graft from a remote access site. In a series by Peppelenbosch et al, 58% of patients had local or regional anesthesia(34). In addition, blood loss is reduced and hypothermia minimized by eliminating laparotomy, thus limiting a spiraling, uncontrolled coagulopathy.

Patients with ruptured AAAs may be severely hypotensive. However, many patients may have their blood pressure stabilized at a nonlethal level due to sympathetically mediated vasoconstriction in response to hypotension. It is not uncommon for this vasoconstriction to be released during the induction of general anesthesia, which results in a sudden drop in blood pressure. Therefore, a relatively stable patient may become severely hypotensive, mandating urgent application of a proximal aortic clamp. However, a guidewire can be inserted 411

A CASEBOOK OF TWENTY SURGICAL CASES

in the upper abdominal or lower thoracic aorta through a percutaneous puncture under local anesthesia, while maintaining the vasoconstriction. Once the guidewire is inserted in the aorta, the patient can then safely undergo induction of general anesthesia because proximal control can be rapidly and relatively safely obtained by placement of a large sheath and an occlusion balloon using the previously inserted guidewire.(34)

Endovascular grafts are inserted and deployed through a remote access site, thereby obviating the need for laparotomy and, more importantly, eliminating the technical difficulties that are encountered when performing a standard repair in the rupture setting. With the associated bleeding, the anatomy of the retroperitoneal structures is often distorted and obscured by a large hematoma, which may lead to technical difficulties as well as inadvertent injury of the inferior vena cava, the left renal vein or its genital branches, the duodenum, or other surrounding structures. These iatrogenic injuries have been the cause of significant operative morbidity and mortality following standard surgery for RAAAs. In contrast, endograft repair is performed within the arterial tree, which is unaffected by extravasated blood or previous operative scarring. (33)

Endovascular repair for RAAAs has been accomplished with a relatively small amount of additional blood loss compared with that which occurs during open RAAA repair. This advantage is more important in patients with RAAAs because these patients have already lost a significant amount of blood following rupture, and coagulopathy or disseminated intravascular coagulation secondary to further blood loss can be serious and often lethal complications. There are several reasons why blood loss is limited, including the maintenance of the tamponade effect within the retro-peritoneum. In addition, back-bleeding from the iliac and lumbar arteries, bleeding from the anastomotic suture lines and from iatrogenic venous injuries are eliminated. Furthermore, hypothermia secondary 412

A CASEBOOK OF TWENTY SURGICAL CASES

to poor perfusion and laparotomy can exacerbate coagulopathy, which is one of the causes of mortality following open surgical repair. Endovascular graft repair can minimize the extent of hypothermia by avoiding laparotomy. (33)

This technology has reduced the mortality risk compared with open repair and it has eliminated the associated morbidity of an abdominal operation in high risk patients.(35, 36) Not surprisingly, in an attempt to curtail the high mortality associated with open surgical treatment of ruptured AAA numerous reports have been published on the use of EVAR for ruptured AAA. The increased use of EVAR is reflected in an American study which indicated the use of EVAR rose from 35% in 2001 to 63% in 2005 and comprised 78% of repairs by 2008 for intact AAA. During this time, the use of EVAR for ruptured AAA rose to 31% (37) A systematic review by Rayt et al (38) identified a pooled mortality of 24% across 31 studies from ruptured AAA after EVAR. Other benefits included intra operative blood loss of 525mls and hospital stay of 10.1 days.

Accurate preoperative imaging is important for ascertaining the feasibility for endovascular stenting and for measuring anatomic dimensions, and contrastenhanced CT scan remains the gold standard.(39) One of the major concerns is the time delay for the scan, especially in unstable patients. A preoperative CT scan in patients with ruptured AAA increases the time before the operation and does impose some risk. One option is the percutaneous insertion of an aortic occlusion balloon, which can be inflated if patients become unstable.(40, 41) Urgent angiography in the operating room can also be used to assess suitability for EVAR.(41) These two techniques may be used together in unstable patients with ruptured AAA, the group with the highest mortality rate.

One of the most challenging obstacles in evaluating this patient population is the disparate nature of their presentation and the variations of their clinical co413

A CASEBOOK OF TWENTY SURGICAL CASES

morbidities. There are factors beyond the operative approach themselves which may influence the outcomes following open or endovascular repair. Hospital volume-outcome improvements have been observed in elective vascular procedures(42) as well as coronary artery bypass

(43)

, pancreatic cancer(44) and hip

replacement surgeries.(45) The mobilization of the vascular team and surgical staff must be rapid and proficient, and immediate availability of CT resources is critical; increased experience with RAAA including pre- and postoperative care will undoubtedly improve survival. Egorova et al demonstrated an improvement in survival with increasing in both surgeon- volume and institution- volume for open and endovascular repair for RAAA.

(29)

This finding underlines

the importance of the experience of the team rather than just the surgeon.

Although the physiological stress may be less in patients undergoing EVAR, they have the same spectrum of complications after open repair of RAAA. However, abdominal compartment syndrome is a major cause of morbidity and mortality after EVAR for RAAA. It is advantageous to keep a high index of suspicion for this entity. Laparotomy and hematoma evacuation have alleviated the hypotension, high ventilatory compliance, and oliguria that occurs with the full-blown syndrome. Monitoring bladder pressure has been helpful in the early detection of the syndrome and early laparotomy with open abdomen treatment and suction/sponge dressings may decrease mortality and allow survival in otherwise hopeless circumstances when small bowel and mesenteric edema cause loss of domain for the abdominal viscera.(46)

The sole prospective randomized controlled trial comparing open and endovascular treatments found a 53% mortality amongst patients treated by either modality. This study was under powered and contrary to numerous cohort series that showed reduced mortality with EVAR.(47) The overall analyses of EVAR compared to open surgery showed a 38% reduction in 30 day or hospital mortal414

A CASEBOOK OF TWENTY SURGICAL CASES

ity rate.(48) At present, the mainly observational studies do show that EVAR for ruptured AAA is feasible with a trend towards lower peri-operative mortality.

However, they suffer from considerable heterogeneity. Furthermore, potential selection bias select patients for endovascular repair constituting a hemodynamically lower risk category with a more favorable EVAR suitable anatomic configuration, makes a proper comparison unlikely. While the answer to this burning issue is as yet unknown, randomized control trials are needed to identify the benefits of EVAR in ruptured AAA over open surgery.

Although some groups have achieved excellent results with EVAR for RAAA and have reported a low 30 day mortality ranging from 10-25% other centers have not reproduced these results(34,47). However there are paradigms that can be used from the EVAR technique that may also improve the mortality after open repair of RAAA. The most significant is probably the use of a protocol and organization for the treatment of RAAA, the presence of trained staff committed to an endovascular protocol and a ready stock of endovascular grafts.

Identification that outcomes are better with increasing surgeon-volume and institution-volume endorses the need for centralization of services. This will result in a concentration of skill and experience in the resuscitation, repair (open or EVAR) and post operative care for this challenging group of patients.

Moreover, the use of fluoroscopic techniques to facilitate placement of proximal occlusion balloons for RAAA, which is an old idea(49), will make this endovascular adjunct a practical and valuable one, even if an endovascular graft procedure is not possible and an open repair is required.

Despite the current trend by enthusiasts for the technique of EVAR for RAAA use of open repair cannot be abandoned due to limitation in endovascular skill as well as many patients suffer from adverse anatomy, hemodynamic instability and unavailability of suitable grafts. This point is crucial for poorer countries 415

A CASEBOOK OF TWENTY SURGICAL CASES

and calls for continued search for innovative efforts to limit mortality associated with RAAA.

CONCLUSION Ruptured AAA, though an uncommon clinical problem, is a catastrophe with a high mortality. Its diagnosis is very challenging and requires a high index of suspicion in the at-risk patient. Reliable clinical examination and judicious use of investigations can help to realize a diagnosis in an acceptable period of time. The risk stratification of patients and the appropriate mode of treatment are currently areas of controversy and interest. While the results of randomized control trials regarding EVAR are awaited, clinicians will need to use some judgment in identifying patients who may be suitable for EVAR and in whom surgical intervention should be with held in favor of palliative measures.

416

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3. Biancari F, Mazziotti MA, Paone R et al (2011) Outcome afteropen repair of ruptured abdominal aortic aneurysm inpatients[80 years old: a systematic review and meta-analysis.World J Surg 35(7):1662–1670 4. Engstrom G, Borner G, Bengt L, et al. Incidence of fatal or repaired abdominal aortic aneurysm in relation to inflammation-sensitive plasma proteins. Arterioscler Thromb Vasc Biol 2004;24:337–41.

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A CASEBOOK OF TWENTY SURGICAL CASES 17. Hardman DT, Fisher CM, Patel MI, et al. Ruptured abdominal aortic aneurysm: who should be offered surgery? J Vasc Surg 1996; 23: 123-9.

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39. Hinchcliffe RJ, Yusuf SW, Macierewicz JA, et al. Endovascular repair of ruptured abdominal aortic aneurysm- a challenge to open repair? Results of a single centre experience in 20 patients. Eur J Vasc Endovasc Surg 2001;22:528-34.

40. Okhi T, Veit VF, Sanchez LA, et al. Endovascular graft repair of ruptured aortoiliac aneurysms. J Am Coll Surg 1999; 189: 102-12.

41. Veit VF, Okhi T. Endovascular approaches to ruptured infra-renal aortoiliac aneurysms. J Cardiovasc Surg 2002; 43: 369-78.

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44. Hannan EL, Kilburn H Jr, Bernard H, et al. Coronary artery bypass surgery: the relationship between in-hospital mortality rate and surgical volume after controlling for clinical risk factors.

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46. Mayer D, Pfammatter T, Rancic Z, et al. 10 years of emergency endovascular aneurysm repair for ruptured aortoiliac aneurysms: lessons learned. Ann Surg 2009; 249: 510-515.

47. Hinchcliffe RJ, Bruijstens L, MacSweeney STR, et al. A randomised trial of endovascular and open surgery for ruptured abdominal aortic aneurysm: results of a pilot study and lessons learned for future studies. Eur J Vasc Endovasc Surg 2006; 32:506-513.

48. Ten Bosch JA, Cuypers PW, van Sambeek M, et al. Current insights in endovascular repair of ruptured abdominal aortic aneurysms. Eurointervention 2011; 7(7): 852-8.

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DR. SUNILDATH JUGOOL (MBBS,UWI) The University of the West Indies