Retrospective Study
Journal of Veterinary Emergency and Critical Care 19(2) 2009, pp 165–173 doi:10.1111/j.1476-4431.2009.00401.x
Characteristics and outcomes in surgical management of severe acute pancreatitis: 37 dogs (2001^2007) Lisa J. Thompson, DVM; Ravi Seshadri, DVM, DACVECC, DAVBP and Marc R. Raffe, DVM, MS, DACVA, DACVECC
Abstract Objective –Describe clinical characteristics and outcomes associated with canine patients undergoing surgical intervention for treatment of acute pancreatitis. Design –Retrospective outcome study from 2001 to 2007. Animals –Thirty-seven dogs. Interventions –None. Measurements and Main Results –The following data were collected for dogs who underwent surgical intervention in the course of treatment for severe acute pancreatitis: preoperative clinicopathologic and physical data, ultrasonographic findings, surgical procedure detail, histopathologic findings, and transfusion requirements. The survival rate was 80.8% in dogs with extrahepatic biliary obstruction, 64.3% in dogs undergoing necrosectomy, and 40.6% with pancreatic abscess. Overall survival was 63.6%. Surgical complications included intraoperative and postoperative hemorrhage in 12 dogs, postoperative development of diabetes mellitus in 3 dogs, exocrine pancreatic insufficiency in 1 dog, and bacterial peritonitis in 2 dogs. Conclusion –Surgical intervention and aggressive postoperative care may be pursued in select dogs with severe acute pancreatitis. In dogs with extrahepatic biliary obstruction secondary to acute pancreatitis, surgical intervention may be associated with a good prognosis whereas dogs with pancreatic abscess formation may have a more guarded prognosis. (J Vet Emerg Crit Care 2009; 19(2): 165–173) doi: 10.1111/j.1476-4431.2009.00401.x
Keywords: abdominal, gastroenterology, pancreas, pancreatic abscess, pancreatitis, surgery
Introduction Acute pancreatitis is defined as an inflammation of pancreatic tissue that is sudden in onset.1,2 Dogs with acute pancreatitis typically present with clinical signs of abdominal pain, lethargy, vomiting, and anorexia.2–3 There are numerous reported etiologies of acute pancreatitis that vary by species.2–5 Regardless of the species and underlying cause, following initiation of pancreatitis autodigestion of the gland begins to occur.1,2,5 The most common form of acute pancreatitis in humans is acute edema of the pancreas secondary to From the Advanced Critical Care and Internal Medicine, Tustin, CA 92780 (Thompson, Seshadri); and Pfizer Animal Health Inc Veterinary Specialty Team, Mounds View, MN 55112 (Raffe). Address correspondence and reprint requests to Dr. Lisa J. Thompson, Advanced Critical Care and Internal Medicine, 3021 Edinger Ave, Tustin, CA 92780, USA. Email: ljtdvm@hotmail.com & Veterinary Emergency and Critical Care Society 2009
pancreatic inflammation.1,6–8 Edematous pancreatitis causes mild pancreatic damage that responds to appropriate medical therapy and results in full clinical recovery with minimal residual organ dysfunction. Standard treatment in these cases is typically limited to supportive care (nothing per os, pain management, and fluid therapy).1,6–8 A subset of these cases (10–20%) may progress to severe acute necrotizing pancreatitis.5,9,10 In dogs there are no reports as to the prevalence of mild acute pancreatitis in comparison to severe acute necrotizing pancreatitis. Acute pancreatic necrosis is a severe form of pancreatitis that results in pancreatic cell death. There is loss of blood supply (through thrombus formation and disruption of the vasculature during autodigestion) to regional portions of the pancreas and a systemic inflammatory response leading to distant organ dysfunction.5,11 Intrapancreatic sequelae may include formation of a pancreatic abscess 165
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(accumulation of suppurative material localized within the pancreas)2,4,9 or permanently reduced pancreatic function, including development of de novo diabetes mellitus, or exocrine pancreatic insufficiency. Aggressive management is required due to the high morbidity and mortality associated with acute necrotizing pancreatitis.4,6,7 The most appropriate therapy for acute necrotizing pancreatitis remains controversial.4,7,8,10,12–19 Historically, in humans, surgical intervention following medical stabilization was commonly performed to confirm the diagnosis and to treat acute pancreatitic necrosis.20 In recent years, there has been a decreased emphasis on early surgical intervention because improved noninvasive imaging, therapeutic techniques, and intensive care have become more readily available. Access to minimally invasive therapeutic procedures, including laparoscopic debridement, percutaneous aspiration and lavage, and endoscopic retrograde cholangiopancreatography (ERCP) for relief of biliary obstruction, has reduced the need for early surgical intervention in humans.6,8 In humans, delayed surgical intervention has been reported to decrease morbidity and mortality in these cases.8,21 While no specific guidelines have been established, currently accepted criteria for surgical intervention in dogs include evidence of infection, local complications (abscessation or biliary obstruction), diagnostic confirmation (of neoplastic versus nonneoplastic disease), persistent distant organ complications, and failure to respond to aggressive medical management.22–24 The etiopathogenesis of acute pancreatitis differs between humans and companion animals. In humans, a majority of acute pancreatitis cases (80%) are secondary to alcoholism or biliary obstruction.1,9,12 In companion animals, most cases are idiopathic in origin.22,25,26 The difference in etiology and anatomical location calls into question the value of these minimally invasive procedures (such as ERCP) in companion animals. While medical management is successful in many cases of acute canine pancreatitis, there are patients who are unresponsive and clinically deteriorate despite aggressive medical care. Management of these cases continues to be a challenge in veterinary medicine. The previous perception that surgical management is unwarranted in acute pancreatitis has been questioned.27 In fact, there may be a subset of these patients who may benefit from surgical intervention. Identifying these patients and defining the timing of the surgical intervention remains challenging. The purpose of this study was to retrospectively evaluate surgical intervention in the management of severe acute pancreatitis in canine patients. The following factors were evaluated with respect to outcome: 166
biochemical, hematologic, and histopathologic data, and timing of surgical intervention. This study may serve as a future comparison for evaluation of medical versus surgical management in severe acute pancreatitis.
Materials and Methods Medical records from canine patients with a perioperative diagnosis of acute pancreatitis evaluated at our emergency and referral practice between 2001 and 2007 were reviewed. Dogs were included if they demonstrated all of the following: evidence of clinical signs compatible with severe acute pancreatitis (abdominal pain, lethargy, vomiting, and anorexia), ultrasonographic evidence of severe acute pancreatitis or pancreatic abscessation, surgical management, and a confirmed histopathologic diagnosis of pancreatitis or intraoperative gross evidence of acute pancreatitis (pancreatic and peripancreatic tissue destruction or pancreatic abscessation) supported by biochemical parameters consistent with pancreatitis. Medical management, including volume resuscitation with cystalloids and colloids, fasting, analgesia, and supportive care (eg, histamine-2 blockers, antimicrobials, nasogastric suctioning as indicated), was initiated following admission. In addition to supportive care, all dogs underwent nonblinded ultrasonographic imaging by a specialist (internal medicine, radiology, or emergency and critical care) as a component of the initial evaluation. Clients were offered a surgical option in addition to medical therapy. The decision to recommend surgical management was based on subjective assessment of the severity of clinical signs, the response to medical management, clinicopathologic results, ultrasonographic findings consistent with abscessation, peritonitis, biliary obstruction, hyperechoic appearance of omentum in the pancreatitic region, or mass effect suggesting pancreatic neoplasia. Quantitative data collected from each medical record included breed, weight, sex, age, heart rate, rectal temperature, systolic blood pressure, WBC count, band neutrophil count, PCV, presence of free abdominal fluid, respiratory rate, prothrombin time (PT), activated partial thromboplastin time (aPTT), anion gap, and concentrations of ionized calcium (iCa), amylase, lipase, sodium, potassium, total bilirubin, albumin, BUN, creatinine, aspartate transferase, alanine aminotransferase, alkaline phosphatase, blood glucose, and bicarbonate. These parameters were evaluated for potential prognostic value. The values were selected based on a literature review of canine and human pancreatitis severity scores.28–30 Based on a previous report by Ruaux and Atwell that used an organ score system (Table 1), a pancreatitis severity score was retrospec-
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Table 1: Pancreatic severity score based on number of organ systems compromised.29
System
Organ system inclusion factor
Immune Renal
410% band neutrophils or WBC424.0 109/L BUN413.9 mmol/L (39 mg/dL) or creatinine4301 mmol/L (3.4 mg/dL) ALKP, AST, or ALT43 upper reference interval Bicarbonate o13 or 426 mmol/L or anion gap o15 or 438 mmol/L Blood glucose 412.9 mmol/L (232 mg/dL)
Hepatic Acid/Base Endocrine
Each organ system was given a value of either 0 (normal) or 1 (abnormal); the sum of these values equals the pancreatitis severity score. ALKP, alkaline phosphatase; AST, aspartate transferase; ALT, alanine aminotransferase. Units converted from SI to imperial.
tively assigned to each dog.29 In addition to these quantitative parameters, qualitative parameters reviewed for each dog included ultrasonographic interpretation, perioperative management (feeding tube placement and closed suction abdominal drain placement), blood product transfusion (whole blood and packed RBC [pRBCs] or fresh frozen plasma [FFP]), and postoperative complications. Postoperative data reviewed included microbiologic culture and histopathology results. The duration of preoperative medical management is re-
ported in Table 2. Cases for which complete medical records were unavailable were not included. Surgical management was based on gross findings during abdominal exploratory. The pancreas and peripancreatic tissue were carefully examined for evidence of gross abnormality. Necrotic tissue in the peripancreatitic region was bluntly debrided. Biopsies of the pancreas and peripancreatitic tissue were collected. Sampling for aerobic and anaerobic bacterial culture was performed. Following debridement and sample collection, the abdominal cavity was extensively lavaged with sterile saline. In cases where indicated, a feeding tube was inserted (n 5 33). Feeding tube types (gastrotomy, jejunostomy, or jejunal through a gastrotomy tube)a,b,c were inserted using standard techniques as described previously.31 The decision regarding the type and location of the feeding tube was based on presence of vomiting, need for gastric suctioning, or both, with preference toward jejunostomy tubes to minimize pancreatic stimulation. In cases where a pancreatic abscess was present, a closed suction JacksonPratt (J-P) draind was placed in the abscessed region to allow for continued drainage. J-P drains were also placed in dogs when the attending clinician deemed the peritonitis to be severe enough to require continued abdominal drainage. Timing of J-P drain removal was
Table 2: Univariate comparisons of 30-day survival rates with 95% confidence intervals
Factor
Levels
J-tube placed
Yes No 1 2 3 4 Necrosectomy (debridement of pancreatic necrosis)/peritoneal lavage/ feeding tube placement Pancreatic abscess drainage/removal Cholecystoenterostomy Exploratory Yes No Yes No 2 years 3–7 years 47 years 1 2–5 45
Pancreatic severity score29
Surgery type
Free abdominal fluid Major complications Age
Days preoperative
n
30-day survival (%)
Number of patients
Patients surviving
30 7 8 22 5 2 14
19 5 6 11 4 1 9
63.2 68.6 75.0 57.0 80.0 50.0 64.3
48.0–83.1 40.3–100 50.3–100 39.2–82.9 51.6–100 12.5–100 43.5–95.0
11 11 1 26 11 11 26 3 19 15 11 22 4
4 8 1 14 9 5 17 2 12 7 6 12 3
40.9 80.8 100 53.6 90.9 45.5 72.2 66.7 72.9 50.6 62.3 62.4 75.0
19.4–86.3 60.0–100 100 37.4–76.8 75.4–100.0 23.8–86.8 56.5–92.1 30.0–100 55.1–96.4 30.1–84.8 38.9–100 44.8–87.0 42.6–100
95% CI (%)
P-value 0.96 0.63
0.23
0.06
0.17 0.51
0.73
Major complications included transfusion reaction (n 5 1), cardiac failure (n 5 1), postoperative diabetes mellitus (n 5 3), persistent pancreatic effusion (n 5 1), pulmonary infiltrates (n 5 1), jejunostomy tube linear foreign body (n 5 1), duodenal necrosis (n 5 1), exocrine pancreatitic insufficiency (n 5 1), and postoperative bacterial peritonitis (n 5 2).
n
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Statistical methods Median survival time for the study group was determined using a Kaplan-Meier survival curve.32,33 The Mann-Whitney test was used for calculation of nonparametric difference in the median values between survivors and nonsurvivors. Individual variable confidence interval (CI) was determined by FlemingtonHarrington analysis.34 The Mantel-Haenszel test was used to determine P-values,35 except for WBC and iCa values, which were calculated using a t-test.e The risk ratio and Wald CI were calculated.36 Clinicopathologic variables were tested for their influence on major outcome complications (death, additional surgery, longterm medical therapy) with univariate and multivariate logistic regression as appropriate.
Results The study population included 37 dogs with a median age of 7 years (range, 1–12 y). Cases included 18 neutered males, 16 spayed females, 2 intact males, and 1 intact female. Dog breeds represented included mixed breed (n 5 5), Jack Russell Terrier (n 5 3), Rat Terrier (n 5 2), Miniature Poodle (n 5 2), Yorkshire Terrier (n 5 2), Golden Retriever (n 5 2), Shetland Sheepdog (n 5 2), Miniature Schnauzer (n 5 2), Cocker Spaniel (n 5 2), and 1 of each of the following: Keeshond, Chihuahua, Pomeranian, Dachshund, Miniature Pinscher, Welsh Terrier, Basenji, Border Collie, Cavalier King Charles Spaniel, Doberman Pinscher, American Staffordshire Terrier, Lhasa Apso, Labrador Retriever, Beagle, and Dalmatian. The total number of canine accessions seen at the facility during the period from 2001 to 2007 was 39,775, with 583 diagnosed with acute pancreatitis. The prevalence of acute pancreatitis was 1.46% of the total population. Approximately 6.4% of the acute pancreatitis patient population had surgical intervention during the course of their treatment. Of the 37 cases included in this study, 14 (36.4%) died or were euthanized. One was euthanized due to splenic hemangiosarcoma discovered during surgery. Of the dogs that were euthanized the decision was based on financial constraints in 3 of the cases and due to worsening prognosis or status in 4 dogs. Of the animals who survived to discharge (63.6%), the last noted follow-up occurred at a median of 70 days (range, 11–1461 d) postoperatively. The 30-day survival rate for the study population was 63.6% (95% CI, 49.6–81.6%). A KaplanMeier survival curve of the overall survival is shown in Figure 1. 168
1.0 Proportion Surviving
based on volume of fluid produced and results of serial cytological evaluation of the fluid.
0.8 0.6 0.4 0.2 0.0 0
5
10 15 20 Day Post Surgery
25
30
Figure 1: Proportion of animals surviving over time in days with 95% confidence intervals. Vertical lines indicate censored observations and the day of surgery is day 0. The dashed lines indicate confidence intervals, and the solid line indicates the survival curve.
The 30-day survival rates are shown in Table 2. The dogs undergoing surgery for extrahepatic biliary obstruction had an increased survival rate that was not significant (80.8%; 95% CI, 60–100%), compared with those with a pancreatic abscess, who had a survival rate of 40.9% (95% CI, 19.4–86.3%) (P 5 0.23). In comparison, dogs undergoing necrosectomy for surgical debridement, peritoneal lavage, and feeding tube placement in severe acute pancreatitis had a survival of 64.3% (95% CI, 43.5–95.0%). The mean pancreatitis severity score was not significantly different between survivors and nonsurvivors (P 5 0.80). The mean pancreatitis severity score for survivors was 2.0 and 2.1 for nonsurvivors. In this case series, 26 dogs were noted to have free abdominal fluid. Fluid analysis was available for 7, and the results were consistent with a sterile peritonitis in 6 of the 7. In the remaining cases in which free abdominal fluid was present, peritonitis was presumed based on the presence of the fluid as well as abdominal pain and ultrasound evidence of inflammation in these regions, but fluid analysis was not available. Dogs were managed medically for 1–15 days with a median of 2 days before surgical intervention. Postoperative duration of hospitalization ranged from 0 to 8 days with a median of 4 days. Hospitalization times evaluated using univariate and multivariate analyses were not significant between survivors and nonsurvivors. In addition to the survival analysis described in Table 2, univariate and multivariate logistic regression analyses did not identify any significant prognostic indicators. Age was nearly significant (P 5 0.07) in a model that included pancreatitis severity score, bilirubin, and presence of preoperative free abdominal fluid. A t-test comparison of WBC and iCa for survivors versus nonsurvivors did not demonstrate significant differences.
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A blood transfusion was administered in 12 dogs, prompted by a decreased hematocrit or clinical signs consistent with anemia, as well as observation of hemorrhage intraoperatively. These dogs received a whole or pRBC transfusion during the intraoperative or postoperative period. One transfusion resulted in an acute incompatibility reaction leading to death. Six of 12 dogs (50%; 95% CI, 21.1–78.9%) receiving transfusions of whole blood or pRBCs survived. Twenty-seven dogs received a FFP transfusion. Six of these dogs were coagulopathic based on the results of either a prothrombin time, activated partial thromboplastin time, or activated clotting time. Twenty-one dogs received FFP for supplementation of a2-macroglobulin levels or had active bleeding without clotting time prolongation. The risk of death or euthanasia was greater for dogs receiving FFP than for those not receiving FFP, but the difference was not statistically significant (risk ratio 5 1.36; 95% CI, 0.48–3.88; P 5 0.83). Bacterial cultures were obtained from all pancreatic abscesses (n 5 11). Three of these were noted to have a positive culture of abscessed pancreatic tissue. Bacterial cultures were submitted for 12 of 26 dogs with preoperative peritoneal effusion. One of the 12 peritoneal effusion samples had positive culture results. Culture results included growth of Staphylococcus intermedius, Propionbacterium sp., Escherichia coli, and Enterobacter cloacae. Two dogs developed septic peritonitis postoperatively, 1 from the jejunostomy tube site and the other from an unknown source. Both dogs had positive E. coli growth from their abdominal effusion. Cellulitis associated with the jejunostomy site was noted in 6 dogs. Bacterial culture was not performed on these. Histopathology results were not found to be significant factors in predicting survival. Twenty-six dogs had changes consistent with acute pancreatitis. Seventeen dogs had severe necrosuppurative pancreatitis and had a 56.5% (95% CI, 42.6–100%) survival rate. The remaining 9 had diverse histopathology results including severe fibrinonecrotic pancreatitis (n 5 2), severe necrotizing pancreatitis with suppurative steatitis and fibrosis (n 5 2), severe suppurative pancreatitis (n 5 3), and suppurative hemorrhagic pancreatitis with fibrinous deposition (n 5 1). Five dogs with no history to support chronic pancreatitis had histopathology results that were characterized by chronic lymphocytic and fibrosing pancreatitis with gross omental necrosis (n 5 1), fibrotic steatitis, fat necrosis, and severe fibrosis of the associated pancreatic tissue (n 5 1), peripancreatic fibrosis and inflammation (n 5 1), chronic fibrosing pancreatitis with fat necrosis (n 5 1), and nodular hyperplasia (n 5 1). A group of 6 dogs had no biopsy performed but were diagnosed with acute pancreatitis intraoperatively due to gross evidence of
pancreatic necrosis and peripancreatic saponification and inflammation. No deaths were observed in this group.
Discussion Scoring systems have been devised to stratify patients, determine their level of disease, and identify patients that require more aggressive intervention. A pancreatic severity score in dogs has been proposed but is not yet validated.29 The pancreatic severity score did not appear to be helpful in cases with surgical intervention of acute pancreatitis in this study. This was also found with pancreatic abscesses in a previous study.37 In humans, the most common scoring systems for predicting progression and severity in acute pancreatitis include the Ranson criteria and the Glasgow and Acute Physiology and Chronic Health Evaluation II scores.10,14,15,30 Another recently described scoring system for humans is the Pancreatitis Outcome Prediction score.28 There remains some debate as to which of these systems is superior in predicting the outcome or the need for further intervention.10,14 None of these scoring systems are validated for canine patients, and a prospective study is necessary to determine their usefulness in veterinary patients. A Survival Prediction Index has been validated for small animal patients when values are obtained within the first 24 hours of admittance to the intensive care unit.38 This may be a useful index for stratification in future studies of severe acute pancreatitis. Because of the retrospective nature of this study, not all values were available to allow for evaluation of this scoring system. The Balthazar score, for humans, is based solely on computed tomography images.39 In veterinary medicine, computed tomography has not been shown to be more useful in evaluating acute pancreatitis than ultrasonographic imaging.40–42 The cases in this series were imaged solely with ultrasound. With further research it may be possible to devise a pancreatic severity score based on ultrasonographic appearance of the pancreas, peripancreatic fluid accumulation, and evaluation of blood flow to the region.40 None of the variables examined in this study proved useful as a discriminator of disease severity or predictor of outcome. One factor may have been sample size. As other diagnostic tests become more readily available, new parameters may be used as prognostic criteria and allow identification of dogs that would benefit from more aggressive intervention. For example, C-reactive protein has been evaluated in canine patients. While patients with acute pancreatitis were noted to have significantly higher levels of the protein than normal animals, its use in differentiating mild from severe cases has not been defined.43 The Urine Trysinogen
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Activating Peptide: Creatinine ratio (UTCR/Utap:Creat) does, however, appear to allow for discrimination of severe versus mild cases and appears to be a sensitive and specific modality in identification of severe acute pancreatitis in dogs.44 With the improved availability of these tests, larger clinical trials will be needed to determine their optimal use in veterinary medicine. The use of these biomarkers in human studies has not shown any advantage for predicting disease progression or prognosis over the Acute Physiology and Chronic Health Evaluation II and Ranson scoring systems.10,15 As in previous studies WBC and iCa values were not different and do not appear to be useful in predicting outcome in dogs with severe acute pancreatitis.37,45 To the authors’ knowledge, there are no published reports evaluating the value of caninespecific pancreatic lipase tests in predicting severity of acute canine pancreatitis. Recommendations for the management of acute pancreatitis based on human clinical experience (eg, timing of surgical intervention, minimally invasive techniques) may not be valid across species. One reason for this may be the notable difference between humans and companion animals in the anatomical location of the pancreas. In humans, the majority of the pancreas lies in the retroperitoneal space46 versus the peritoneal location in canine patients.47 Because of interspecies differences in anatomy, minimally invasive procedures such as laparoscopic assisted debridment or pecutaneous lavage and drainage may not be appropriate in dogs. In veterinary patients, the peritoneal location makes minimally invasive techniques more difficult due to limited visibility and an increased risk of complications.41 Previously reported surgical techniques for acute pancreatitis vary slightly, but higher morbidity has been noted in cases where open peritoneal drainage has been used.13,37 In cases where continued drainage is required, closed abdominal drainage and lavage systems have also been utilized.6 A previous veterinary study advocated omentalization of pancreatic abscesses based on a trend toward increased survival and decreased hospital stay.37 Dogs with pancreatic abscesses in our study were treated with resection of the diseased tissue and placement of closed suction drains; 5 of 11 of these cases survived. The mortality rate in this subpopulation may be skewed due to 2 dogs being euthanized or dying from nonpancreatic causes (death from transfusion reaction and euthanized due to splenic hemangiosarcoma). This is comparable to previous studies in which there was 0–56% survival.f,27,37,48 Extrahepatic biliary obstruction is a known indication for surgical intervention in acute pancreatitis.49 The current case series of acute pancreatitis-induced biliary 170
obstruction had an improved survival rate (80.8%) over previous reports (50%) including those treated with choledochal tube stenting.50–53 This may be due to client willingness to pursue aggressive postoperative care. There is limited information available regarding medical management of biliary obstruction secondary to pancreatitis. A recent report described ultrasoundguided percutaneous cholecystocentesis resulting in the resolution of the obstruction in 2 of 3 dogs; the third case required surgical intervention despite continued percutaneous aspiration.54 Another recent report described laparoscopic placement of a drainage tube in 3 cases to allow for potential resolution of the obstruction and time for stabilization. All of these animals were later taken to surgery, either for definitive care or due to complications related to the tube.55 Given only these small case studies, it remains unknown whether these procedures are a viable option in place of surgical intervention with either cholecystoenterostomy or choledochal tube stenting. There has also been a recent report regarding the safety of ERCP in canine patients, but the clinical application of this technique remains untried.56 The reported frequency of peritonitis associated with sterile acute necrotizing pancreatitis in human patients is 11.7%.16 The number of patients with free abdominal fluid in our study may indicate that a much larger number of canine acute pancreatitis cases develop chemical peritonitis than is reported in humans. The nonsignificant decrease in survival in those cases with a closed suction J-P drain noted in this series may indicate increased severity of peritonitis in these cases as an explanation for increased mortality. The length of hospitalization before surgical intervention was not found to be significantly related to outcome. This may be due to sample size or may represent a true difference in our cases in contrast to human reports in which early surgical intervention (in both infected and noninfected cases) is associated with higher postoperative mortality.8,13,15,57 In dogs, the lack of significance of surgical timing may be due to decreased postoperative infection rates in comparison to humans, where considerable mortality is associated with postoperative infection of previously sterile necrotic tissues.18 Mortality rates in human cases treated with surgery for sterile necrosis vary from 10% to 25% based on differing reports. Infection of pancreatic necrosis is associated with significantly increased mortality in humans.4,6–8,14,16,18,19 Most reports found in veterinary literature indicate that pancreatic infection is minimal. This case series remains consistent with this observation; although many of the dogs were on antimicrobial therapy before obtaining the tissue or fluid for culture,
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only 2 dogs in this case series were noted to have infection pre- or intraoperatively. Only 2 developed postoperative septic peritonitis, and 1 of these could be attributed to the jejunostomy feeding tube site as a source of sepsis. Previous reports in the veterinary literature also note a lower rate of infection when compared with human reports of acute pancreatitis.22,27,37,48,58–60 In humans, a major determinant of not pursuing surgical intervention of a sterile pancreatic necrosis is the risk of postoperative infection, which can be a significant contributor to postoperative morbidity and mortality.18,57 To the authors’ knowledge, an increased risk of pancreatic infection postpancreatic surgery has not been reported previously in the veterinary literature. Commonly reported complications after surgical intervention in human cases of acute pancreatitis include fistula formation, wound/pancreatic infection, and bleeding.4,8,13,16 Complications in this study population included cellulitis at the jejunostomy tube site (n 5 6) and postoperative septic peritonitis (n 5 2) (1 survived, the other was euthanized at the time of diagnosis). Bleeding did appear to be a significant complication, with 12 dogs requiring transfusion. FFP was administered to 29 dogs, with 6 of those having a documented coagulopathy. The utility of administration of FFP for the treatment of acute pancreatitis (for replacement of a2-macroglobulin) remains anecdotal.49 Administration of FFP did not improve survival in this study, which was consistent previous studies published in the human literature.61 Long-term complications of acute necrotizing pancreatitis in humans include diabetes mellitus (40– 92%)7,12,62 and exocrine pancreatic insufficiency (25%).7,62 There is no previous information on the incidence of diabetes mellitus as a postoperative complication of pancreatic surgery in dogs. In this retrospective case series, 3 of 37 cases developed diabetes mellitus, and 1 was noted to develop exocrine pancreatic insufficiency. One veterinary report describes decreased cTLI concentrations consistent with exocrine pancreatic insufficiency in 2 of 7 cases after medical management of their severe acute pancreatitis.g The true incidence of dogs developing pancreatic insufficiency or diabetes mellitus after severe pancreatitis remains unknown. Veterinary terminology of the histopathologic description of acute pancreatitis is not standardized. In a recent experimental study with rats, histologic changes were seen as early as 3 days after induction of acute pancreatitis; fibrin deposition and neutrophilic, lymphocytic, and histiocytic inflammation predominated.63 Human reports describe fibrin deposition and leukocyte infiltration in cases of acute necrotizing pancreati-
tis.64 Hill and Van Winkle described acute pancreatitis in cats as either a large degree of necrosis or suppurative infiltrate (with no necrosis) with mild to moderate amounts of fibrosis noted.65 Chronic changes are described as replacement of the acini by chronic inflammatory cells and acinar atrophy. Human reports consistently describe the gross appearance of chronic pancreatitis as atrophied, cirrhotic, or both.66 Other veterinary authors describe lesions as chronic if fibrosis exists.27,67–69 Some dogs in this study demonstrated changes that may be considered chronic due to fibrosis with lymphocytic infiltration. These dogs had clinical signs and gross surgical findings (large pancreas with caseous-like debris) that were compatible with acute pancreatitis, but the histopathologic diagnosis was more consistent with chronic pancreatitis as described above. One explanation for this may be that several of these dogs had pancreatitis for more than 7 days before surgical intervention. These dogs would, perhaps, be expected to have chronic (fibrosis and lymphocyte infiltration) histologic changes. Other explanations may involve nonstandardized terminology, the possibility that pancreatic pathology may have been nonhomogenous between biopsied and other visualized sites, and the possibility that the changes are a nondiscrete continuum of inflammation.67,70 Better standardization of histologic criteria and further investigation in this area are needed.
Conclusion The previous notion that surgical intervention has no place in the treatment of severe acute pancreatitis is perhaps unwarranted.27 Surgical intervention in severe acute pancreatitis may be warranted depending on the extent of pancreatic pathology and sequelae found (infection of the tissue, biliary obstruction, pancreatic abscess) or the need for histologic confirmation of the diagnosis. Aggressive postoperative care should be provided as required. Based on this retrospective study, dogs in which surgical intervention is undertaken for biliary obstruction secondary to acute pancreatitis may have a good prognosis. Further prospective studies are needed to compare aggressive medical management to surgical intervention as well as compare differing surgical and minimally invasive techniques and surgical timing. Further evaluation of prognostic indicators and their usefulness in determining the value of surgical intervention is recommended.
Acknowledgment Rebecca Garabed, VMD, MPVM, PhD, Assistant Professor, Department of Preventive Medicine in the
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College of Veterinary Medicine, The Ohio State University, provided stastistical analysis.
Footnotes a
b
c d e
f
g
Kimberly-Clark MIC Percutaneous Endoscopic Gastrotomy (PEG) Kit, Ballard Medical Products, Draper, UT. Kendall Sovereign Feeding Tube and Urethral Catheter, Tyco Healthcare Group LP, Mansfield, MA. Kendall Argyle Feeding Tube, Tyco Healthcare Group LP. Jackson-Pratt Silicone Flat Drain, Cardinal Health McGraw Park, IL. Microsoft Excel Professional Edition 2003, Excel Microsoft Corporation, Redmond, WA. Stimson EL, Espada Y, Moon M, Troy C. Pancreatic abcesses in nine dogs (abstr). J Vet Intern Med 1998;9:202. Sinclair JG, Fleeman LM, Rand JS, et al. Continuing pancreatic inflammation or reduced exocrine function are common in dogs after acute pancreatitis (abstr). J Vet Intern Med 2006;20(3):750.
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