Meenakshi Medical Journal May 2011 by Meenakshi Mission Hospital and Research Centre

Madurai Medical Journal

From the Editor’s Desk

EDITORIAL BOARD PATRONS

Dr. N. Sethuraman, M.S., M.Ch.(Uro), MNAMS.(Uro), FICS. FOUNDER CHAIRMAN

Dr. S. Gurushankar, M.B.B.S., M.B.A. VICE CHAIRMAN

ADVISORS

Prof. Dr. V.N. Rajasekaran, Ph.D., M.D., DTM&H MEDICAL DIRECTOR

Prof. Dr. N. Krishnamurthy

M.S., M.Ch.(Uro), D.H.&HM. BGL, M. Phil(Tamil), M.A(Phi&Rel) PGDIM., PGDHRM.

ACADEMIC DIRECTOR

Dr. T.R. Murali, M.S., M.Ch.(Uro), CHAIRMAN ACADEMIC

EDITOR IN CHIEF

Dr. S. Kumar, M.D. (Anaes), D.Diab., (

PGHSc).,

CONSULTANT CARDIAC ANAESTHESIOLOGIST

MEMBERS

Dr. Ramesh Ardhanari, M.S., M.Ch.(GE), FRCS. (Glasgow) Dr. K. Sampath Kumar, M.D., DNB., DM.(Nephro) Dr. A.R. Raghuram, M.S., M.Ch.(CTS), D.N.B., FIACS. Dr. S. Jayabose, M.B.B.S., D.C.H., A.B(Paed)., A.B(Paed. Hematology - Oncology)., Dr. P. Krishnamoorthi, M.D., FIAMS., FCGP., Dr. T. Mukuntharajan, M.B.B.S., DMRD. Dr. N. Panchavarnam, M.S., M.Ch. (Plastic) Dr. S. Lakshmi, M.D., D.A. Dr. N. Maharajan, M.D., DA. Dr. K.S. Anand, M.D. (Anaes) Dr. V. Sathya Narayana, M.S., D.Ortho., DNB Dr. S. Balasubramanian, M.S.(Ortho), Dr. S. Padma, M.D., DNB. (OG), Dr. R. Sivakumar, M.D., DNB.(Cardio) Dr. S. Selvamani, DNB. (GM), DNB. (Cardio), Dr. M. Sampthkumar, M.D., DM. (Cardio), Dr. N. Karunakaran, M.B.B.S., DMRD., DNB.(Radiology), Dr. K.S. Kirushnakumar, M.D.(RT), Dr. A. Kannan, M.D. (Paed) Dr. K. Selva Muthu Kumaran, M.Ch.(Neuro) Dr. M.S. Senthilnathan, M.D. (Nuc.Med) Dr. Narendra Nath Jena, M.B.B.S., DFM., PG. Diab., FAEM. Dr. R. Vijaya Bhaskar, M.S., M.Ch. (Surg. Onco) Co-ordination & Compilation

Mr. V.M. Pandiarajan, Sr.Manager - Marketing Mr. R. Saravanan, M.Sc., M.B.A., PGDFRM., Mr. P. Madhusudhanan, B.A., PGDHM.,PGDCA., M.B.A., PGDFRM., Mr. S. Balaji, M.Com., M.B.A., Editorial Address

Meenakshi Mission Hospital and Research Centre (Run by S.R. Trust)

Lake Area, Melur Road, Madurai - 625 107

Managing Asthma – A Shift in Focus ! Asthma was first recognized and named by Hippocrates circa 450 BC. According to World Health Organisation (WHO) estimate, there are between 15 and 20 million people with asthma in India. The defining aspects of the bronchial asthma include the presence of chronic inflammatory changes, reversible airflow limitation and bronchial hyper-responsiveness. There is a better understanding of the airflow limitation, the inflammatory cascade, bronchial hyper responsiveness and even of the genetic domain of asthma. A joint US and UK consortium of researchers have identified a gene ADAM33 (a disintegrin and metallo protease 33)-located on chromosome 20p13 to be associated with airway remodeling in asthma, which offers a potential new target for developing drugs that can prevent changes in lung tissue that result in hyper-responsiveness. Care of the asthmatic patient at the physician level should not focus solely on symptom relief, but also on the need to maintain good pulmonary function and the importance of treating the underlying inflammatory changes. The focus has shifted to a result-driven philosophy: total asthma control versus uncontrolled asthma. Management of the asthmatic patient should be based on Severity (intrinsic intensity of the disease process) and Control (degree to which asthma-related symptoms, functional impairment, and risk of untoward events are minimized and the goals of therapy are met). The importance of treating the underlying inflammation is in the forefront of asthma management. Despite this, the use of inhaled corticosteroids has remained significantly less in countries like India. Current guidelines also now note that that these agents do not appear to prevent disease progression. Many practitioners both general and specialist still have some difficulty in adequately manipulating the commonly utilized drugs. Although inhaled corticosteroids remain central to achieving long-term asthma control, current guidelines recognize combination therapy as a preferred choice for achieving control in many patients with persistent asthma. Most adults with asthma will require ongoing and regular daily management with preventer therapy in addition to as-needed short acting β2 agonist (SABA) therapy. Preventive therapy with inhaled corticosteroids (ICS), alone or in combination with long acting β2 agonist (LABA), is recommended for patients with mild, moderate or severe persistent asthma. A leukotriene receptor antagonist (LTRA) may be considered as an alternative to ICS where there is reason to avoid ICS or according to patient preference. Therefore, major responsibility lies upon the shoulders of health authorities and local medical societies to set up continuous health education programs to improve asthma management and to clarify to patients the merits of the drugs used for treatment and to alleviate any fears of using them.

Tamilnadu, INDIA Phone : 0452 - 2588741 - 750, 4263000 Fax : 0452 - 2586353 E-mail : mmjmmhrc@gmail.com Website : http://www.meenakshimission.org Thee Classic Printers, 27 Kakathope Street, Madurai - 625 001 & 0452 - 2323819, 2624466, 4381603

Dr. S. Kumar

Editor in Chief – MMJ, Sr. Consultant Cardiac Anaesthesiologist Mobile : 94422 44084, E-mail : skumardr@yahoo.com

All Medical practitioners, PGâ&#x20AC;&#x2122;s & CRRI can answer this quiz

MMJ

SPOTTER - 5

What is the Diagnosis?

A 42 year old man underwent Routine Health Check up at MMHRC. The Patient is asymptomatic. The ECG is presented here. What is the diagnosis ?

Send your answer within 20th of June.

Corner

Write your full name, qualifications and place of practice. Answers can be sent through SMS - 97874 41050 / E-mail - drskumarima@gmail.com For enquiries you can contact above phone numbers.

Last month Quiz Answer SPOTTER - 4 Question A 53 yrs old female, a known case Rheumatic heart Disease, admitted for evaluation & further management. The ECG is presented here. What is the diagnosis ?

Diagnosis : Atrial Fibrillation (Controlled Ventricular Rate) ECG shows varying R-R interval, absent (or) variable size P wave with Controlled Ventricular Rate. Highest incidence of AF in Rheumatic Heart Disease occurs in Mitral Stenosis, Mitral Regurgitation and Tricuspid Regurgitation in combination. AF occurs in only 29% of isolated MS, 16% of isolated MR and 1% of Aortic Valve Disease.

Madurai Medical Journal May 2011

Contents Editorial

Page No.

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MMJ Quiz Corner

Glanzmannâ&#x20AC;&#x2122;s thrombasthenia presenting with severe epistaxis - A Case Report

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1 2 4

Dr. R. Priya, Dr. Lakshmi Leela & Dr. S. Jayabose Osteoarthritis - Pain Killers - Hypertension - A Review Article

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Dr. S. Murugan Epidermodysplasia Verruciformis - Rare Cause of Skin Cancer - A Case Report

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Dr. G. Sathishkumar, Dr. O.L. Sadasivam & Dr. R. Vijayabhaskar Extra Systoles - A Brief Communication .................................................................................................................................................................................................................

Dr. M. Palanisamy & Prof. Dr. V.N. Rajasekaran Doctorâ&#x20AC;&#x2122;s Diary

Nodal yield - is it a treasure hunt in cancer treatment ? PG Corner

...................................................................................................................................

Dr. Krishnakumar Rathnam Up Coming Events

MMHRC Congratulates the following Doctors who correctly answered the last month quiz (Spotter - 4) Chennai Dr. H. Ahamed Ashar Ali Dr. B. Madhumitha Dr. Prince Vedaraj

Dr. Selvin Dr. S. Senthur

MMHRC

Dr. Amudhanilavan

Coimbatore

Pondichery

Dr. V. Mahendran

Dr. T. Ashwini

Erode

Pudukottai

Dr. P. Shanthi Shanmugam

Kanyakumari

Dr. M. Periyasamy Dr. D. Dharmabalan

Dr. G. Madhusudhanan (Susindram) Dr. R.K. Mony (Nagercoil)

Dr. S.R. Raja

Madurai Dr. Dr. Dr. Dr. Dr. Dr. Dr. Dr.

N. Castro Hemamalini (Thirumangalam) Jude Vinoth Karthiyayini N. Raja A. Rajiv C. Ramesh K.R. Santharam

Ramnad Tanjore Dr. David Baskar Dr. Rajeswari

Tirunelveli Dr. R. Loganathar (Ambai) Dr. S. Mohan Dr. S. Paulthurai (Sankarankovil)

Theni

Dr. S. Sivakumar (Bodi)

Thiruvarur

Dr. M. Chandrasekaran Dr. P. Thiyagarajan Dr. S. Vinoth Kanna

Trichy

Dr. Hussain (Perambalur) Dr. Jayasree (Lalgudi) Dr. Ramesh (Lalgudi)

Tuticorin Dr. Dr. Dr. Dr. Dr. Dr. Dr.

A.P. Aarthi (Vilathikulam) Amol. P. Supe K. Arumugam (Thiruchendur) C.K. Chidambaram (Kovilpatti) M. Dhanushkodi Hariramakrishnan N. Kathiresan

Virudhunagar

Dr. M. Arul Prakash (Aruppukottai) Dr. T. Selvan (Aruppukottai)

Madurai Medical Journal May 2011

Glanzmann’s thrombasthenia presenting with severe epistaxis

Dr. R. Priya M.B.B.S., A.B.(Ped),

Jr. Consultant Dept. of Pediatric Hematology-Oncology, MMHRC

Dr. Lakshmi Leela M.B.B.S., DCH., (DNB),

Registrar Dept. of Pediatric Hematology-Oncology, MMHRC

- A Case Report

Dr. S. Jayabose M.B.B.S., DCH., A.B. (Ped), A.B. (Ped. Haem-Oncol) Director Dept. of Pediatrics & Pediatric Hematology-Oncology, MMHRC

Abstract Glanzmann’s thrombasthenia is a rare congenital bleeding disorder. Patients usually present with mucocutaneous bleeding and excessive bleeding associated with trauma or surgery. The platelet count is normal, bleeding time is prolonged, and platelet aggregation is deficient or absent. Bleeding is effectively managed by platelet transfusions. Key words Glanzmann’s thrombasthenia, GPIIb/GPIIIa, platelet dysfunction. Introduction examination were normal. Hb - 6.8, WBC - 15,000 with P55L38M6 and platelets – 270,000. PT was mildly Glanzmann’s thrombasthenia is an autosomal recessive elevated with INR - 1.26, aPTT was normal. Factor VIII bleeding disorder characterized by mucocutaneous [1] assay was normal. Liver and renal function tests were hemorrhage of varying severity . Globally, it is normal. He received 2 units of packed red cells and 3 extremely rare but it has a relatively high incidence units of FFP with no significant control of the epistaxis. in consanguineous populations where intermarriage is [2] ENT was consulted and nasal packing was done. Bone common . In this report, we describe a patient with marrow aspirate was negative for storage disorder. Glanzmann’s thrombasthenia who presented with severe epistaxis. Case Report A 6 yr old male presented to MMHRC with severe epistaxis of one day duration. He had several similar episodes since 2 years of age for which he had received various treatments at a local hospital, including transfusion of red cells and fresh frozen plasma. [During the most recent admission in addition to epistaxis, he had a subconjunctival hemorrhages as well as subconjunctival hematomas in the palperbral conjunctiva. (Figure 1.)] He never had gum bleeds, hemarthrosis, malena or hematuria although there Figure 1. a Subconjunctival hemorrhage in our patient is a history of prolonged bleeding after trauma, and generalized bruises off and on. There was no family history of bleeding disorder. On exam, he was short statured, and pale with profuse epistaxis from both nostrils. There was diffuse petechiae and purpura, and mild hepatosplenomegaly, but no significant lymphadenopathy. Heart and lung Corresponding Author

Dr. R. Priya

M.B.B.S., A.B. (Ped),

Jr. Consultant, Department of Pediatric Heamtology-Oncology Meenakshi Mission Hospital and Research Centre, Madurai - 625 107 Phone : 0452 2588741, Mobile : 80123 07718 E-mail : drpriya79@gmail.com

Madurai Medical Journal May 2011

Figure 1 b. Subconjunctival palpebral hematoma in our patient

Platelet function studies (done at CMC, Vellore) revealed the following: a) Clot retraction was absent b) platelet aggregation was absent in response to collagen, ADP, arachidonic acid and epinephrine, but normal in response to ristocetin- findings diagnostic of Glanzmann thrombasthenia (GT). Bleeding time in their lab was abnormal: 15 min (normal 2 to 9 min). Since the diagnosis of GT he has had two more episodes of severe epistaxis which were controlled effectively with transfusion of platelet concentrates. Discussion Galanzmann thrombasthenia (GT) is an autosomal recessive disorder characterized by increased bleeding time and a normal platelet count with abnormal platelet function assays. Clinical features Severe epistaxis is the most common bleeding of clinical significance. Gingival bleeding is more often found in those with poor dental hygiene. Menorrhagia occurs in most female patients at the time of menarche causing considerable concern, usually requiring transfusion. Pathology

presence of ristocetin. Platelet aggregation is absent in the presence of epinephrine, collagen, arachidonic acid and ADP due to the dependence of these factors on fibrinogen attachment to the platelet for aggregation. Platelet aggregation occurs normally in response to ristocetin due to its independence from fibrinogen. Treatment There is no known cure for GT. Platelet transfusion is necessary for the treatment of severe bleeding or for the prevention of bleeding during surgery or invasive procedures . Drugs that affect platelet function, such as NSAIDS or aspirin, should be avoided. Immunizations for hepatitis B should be given due to the infectious risks of frequent transfusion. Oral contraceptives may be used to treat menorrhagia. Desmopressin has been attempted as therapy but has not shown any proven clinical usefulness. Bone marrow transplants have been used successfully in rare cases [3]. Conclusion In summary, Glanzmann’s thrombasthenia is a rare inherited bleeding disorder arising from a number of mutations that affect GPIIb, GPIIIa, and/or the GPIIb/ IIIa complex. Supportive treatment is the best means for care, and bleeding is managed by platelet transfusions.With proper supportive care Glanzmann’s thrombasthenia has a very good prognosis. Reference 1. Glanzmann E. Hereditaire Hamorrhagische thrombasthenic. Ein Beitrag Zur Pathologie der Blutplattchen. Jahrbuch Kinderheilkde. 1918;88:1–42 2. Khanduri U, Pulimood BM. A review and report of 42 cases from South India. Thromb Haemost. 1981;46:717–21. 3. Bellucci S, Socié G, Gluckman E. Bone marrow transplantation in severe Glanzmann’s thrombasthenia with antiplatelet alloimmunization. Bone Marrow Transplant. 2000;25:327–330. Source of support - Nil Conflict of Interest - None declared

Figure 2. Platelet adhesion and platelet aggregation Platelet activation confers a conformational change in the complex allowing it to bind to fibrinogen on both subunits. The binding of fibrinogen to this complex allows it to bridge two platelets in the presence of calcium to initiate primary and secondary platelet aggregation. Platelet aggregation is deficient when any component of the complex is mutated or the complex is present in subnormal amounts. GT is caused by deficiency or abnormality of the platelet glycoprotein IIb and/or IIIa. Thus, patients with thrombasthenia have a normal platelet count but these platelets cannot bind fibrinogen after stimulation and thus cannot aggregate properly. Laboratory Diagnosis Glanzmann’s thrombasthenia is characterized by normal platelet morphology and normal platelet count, prolonged bleeding time, absent or decreased clot retraction, and normal platelet aggregation in the

Condolence MMHRC expresses its deepest condolence for the demise of Dr. T.E. Manley Ex. Major / Surgeon Army Medical Corps, Tuticorin

Dr. M. Deivanai Sujatha Clinic, Paramakudi

Dr. K. Bose Former Dean Incharge of Madurai Medical College, Madurai

Dr. C. Pradeep S/o. Dr. Chandrasekaran

Retd. Prof. of Surgery, Theni Medical College,

Theni

Mrs. V. Iyyammal M/o. Dr. V. Neethiarasu Madurai

Madurai Medical Journal May 2011

Osteoarthritis – Pain Killers – Hypertension

- A Review Article

Dr. S. Murugan M.D., D.M. (Cardio)

Visiting Consultant - Interventional Cardiologist Dept. of Cardiology, MMHRC

Abstract Osteoarthritis in elderly population warrants painkillers - NSAID & COX - 2 inhibitors. Both these agents cause rise of BP, especially in known hypertensives, CKD patients & those on ACEIS, β - Blockers and Diuretics. The rise of BP has significant deleterious CVS effects that can’t be ignored. Key words Osteoarthritis, hypertension, NSAID & COX - 2 inhibitors. Introduction Osteoarthritis and Hypertension are the growing problems in the elderly population. Acetaminophen, Selective & Nonselective cyclooxygenase ( COX )-2 inhibitors, Conventional NSAIDs, Nonacetylated salicylate & other analgesics like tramadol are commonly used pain killers for Osteoarthritis. NSAID use and the prevalence of hypertension are both increased in the elderly. About 40% of patients taking NSAIDs have preexisting hypertension. Effects of NSAIDs on BP Nonselective NSAIDs increase systolic BP by about 7 – 10 mm of Hg, Diastolic BP by about 3 – 4 mm of Hg & Mean arterial pressure by about 6 mm of Hg.The increase in BP is greater in patients with hypertension and in those treated with ACE inhibitors, diuretics, or beta-blockers [1, 2 ]. In one study Rofecoxib use for 6 weeks resulted in increase of systolic BP of 3.1 mm of Hg (average) [3]. Even small changes in blood pressure correlate with increased cardiovascular adverse events, including stroke, MI, and death [4] Epidemiologically, each mm Hg increase in systolic Blood pressure translates into a 2%-3% increase in Stroke, heart failure, and coronary disease. Corresponding Author

Dr. S. Murugan

M.D., D.M. (Cardio),

Visiting Consultant - Interventional Cardiologist, Dept. of Cardiology Meenakshi Mission Hospital and Research Centre, Madurai - 625 107 Phone : 0452 2588741, Mobile : 90251 35271 E-mail : drsmurugan@rediffmail.com

Madurai Medical Journal May 2011

Data From NHANES III An increase of 1 mm Hg in systolic blood pressure was associated with 7100 additional CAD and stroke events over 1 year. An increase of 5 mm Hg in systolic blood pressure was associated with 35,700 additional CAD and stroke events over 1 year [5]. CV Mortality Risk Doubles With Each 20/10mm Hg Increase in BP [6]. Pathophysiological Mechanisms

NSAIDs can increase BP by a complex cascade of events. Conventional NSAIDs and to a variable degree COX – 2 drugs inhibit peripheral vascular “vasodilator” prostacyclin production with increase of BP. Conventional NSAIDs and to a variable degree COX – 2 drugs stimulate salt an water retention ( Pg/ RAS / vasopressin / ANP ) with increase of BP. These agents interfere with the transition of arachidonic acid to form Prostaglandins. Prostaglandin E is an important mediator of salt and water balance. Rofecoxib & Naproxen cause greater increase of BP. For most patients with good renal function, there’s no problem, but certain subgroups of patients are at risk. Patients at risk for BP destabilization 1. Those who have underlying renal disease. 2. Patients with a history of heart disease. 3. Patients who are taking medications that make them salt-sensitive – primarily, rennin-angiotensin blocking drugs and, to some extent, diuretics and beta-blockers. When these patients take NSAIDs, their BP increase more in order to maintain homeostasis of renal function and blood flow. CLASS trial and VIGOR trial reveal the fact of increased thromboembolic CV adverse events due to Rofecoxib & Naproxen [7]. CRESCENT trial concludes that Rofecoxib increases systolic BP more than Celecoxib or Naproxen[8]. Target trial demonstrates larger increase in BP with Naproxen and Ibuprofen comparing with Lumiracoxib [9]. Endothelial dysfunction is strongly linked to both hypertension and increased CV risk. Nitric Oxide (NO) is a key mediator of both endothelial and renal function. Maintenance and/or restitution of the physiological bioactivity of NO is critical to preserve the homeostasis of the vascular wall in hypertension and atherosclerosis. Conventional NSAIDs and selective COX-2 inhibitors negatively affect both endothelial and renal function. Linking NO to an NSAID may mitigate the deleterious effects of these drugs on vascular and renal function.

Potential Benefits of combining an NO Donor with an NSAID [10] 1. Maintenance of normal BP 2. Protection of endothelium 3. Reduced Oxidative stress 4. Decreased levels of pro-inflammatory cytokines and reduced vascular inflammation. 5. Inhibition of platelet aggregation 6. Potential enhancement of analgesia. Naproxcinod, a compound in which NO is linked to the naproxen molecule, is effective for relieving pain and improving function in patients with OA. Naproxcinod, is not different from placebo in its BP effects and is less likely to increase BP in normotensive and hypertensive patients than traditional NSAIDs (Naproxcinod is not yet approved by the FDA).Endoscopy studies have shown that naproxcinod has a GI safety profile than may be superior to naproxen.Naproxcinod is an alternative to conventional NSAIDS for treatment of OA in hypertensive patients. In a study by White and colleagues, 916 patients with OA were given naproxen (500 mg bid), naproxcinod (375 or 750 mg bid), or placebo for 13 weeks. Naproxcinod did not differ from placebo in its effect on BP; compared with naproxen, naproxcinod 750 mg reduced systolic BP [11]. Conculsion v Don’t underestimate the potential CV risks of NSAIDs & Cox – 2 inhibitors. v Be vigilant about monitoring patients’ blood pressures. v Don’t assume that all small increases in blood pressure are insignificant. v Remember that NSAIDs differ in their potential to have adverse effects. v NSAIDs do not affect all patients the same way; their effects on blood pressure are highly variable. Reference 1. 2. 3. 4. 5. 6.

Pope JE, et al. Arch Intern Med. 1993;153:477-484. Johnson AG, et al. Ann Intern Med. 1994;121:289-300 Whellon. A. et al Am J Cardio. 2002. Grover SA, et al. Hypertension. 2005;45:92-97. & Julius S, et al. Lancet. 2004;363:2022-2031. Singh G, et al. j Rheumotol.2003;30:714-719. Lewington S,et al. Lancet. 2002;60:1903-1913 & Chobanian AV, et al JNCVII – JAMA. 2003;289:2560-2571. 7. Silverstein FE, et al JAMA.2000; 284:1247-1255 & White WB, et al Am J Cardiol 2002;89: 425-430. 8. Sowers JR, et al. Arch Intern Med. 2005;165:161-168. 9. Farkouh ME, et al. Lancet. 2004;364:675-684 & Farkouh ME, et al. Ann Rheum Dis. 2007;66:764-770. 10. Miller MR. Megson IL. Br J Pharamcol.2007;1521:305-321:Abramson 58. Arthritis Res Ther 2008:10 ( Suppl 2 )52. 11. White WB, et al. Am j Cordiol. 2009;109:840-845 Source of support - Nil Conflict of Interest - None declared

Madurai Medical Journal May 2011

Epidermodysplasia Verruciformis - Rare Cause of Skin Cancer

Dr. G. Sathish Kumar M.B.B.S., DNB (General Surgery) Resident Surgery Dept. of Surgical Oncology, MMHRC

Dr. O.L. Sadasivam MS.,F.I.C.S.,

Consultant Dept. of Surgical Oncology, MMHRC

- A Case Report

Dr. R. Vijayabhaskar MS., M.Ch.(Onco), Consultant Surgical Oncologist, MMHRC

Abstract A 41 yr Old Male presented with recurrent proliferative growth over the left upper chest wall, with tinea versicolor like skin lesions involving all over the body, He was evaluated with skin wedge biopsy and punch biopsy of growth which was reported as Epidermodysplasia Verruciformis and associated Squamous cell carcinoma of skin. Key words EV (epidermodysplasia verruciformis), HPV (human papilloma virus), wide excision, SSG(split skin graft), cryotherapy, Squamous cell carcinoma Case Summary A 41 yr old male patient, farmer by occupation presented to our hospital with the complaints of recurrent growth over the chest wall. The patient had skin lesions from childhood, these lesions were distributed all over the body and more commonly on the trunk (fig- 1). One of these lesions started growing like a wart in left upper anterior chest wall, for which he consulted a dermatologist at a government hospital. He was admitted and evaluated.

He underwent skin biopsy and was diagnosed as a case of Epidermodysplasia Verruciformis. Wide excision with SSG was done for chest wall lesion on feb 2005. HPE was reported as well differentiated squamous cell carcinoma. He defaulted for further followup. Now he presented to us with proliferative growth at previous operated site with warty lesions on the back and right forehead. He has no comorbidities and no family history of similar skin diseases. On examination, a 7x8cm irregular, proliferative fungating growth with everted edges was present over the manubrium sterni, which is foul smelling and bleeds on touch. Another proliferative exophytic lesion of size 6x5cm was noted in the back, and a wart like lesion in right forehead. He is also having small flat warty lesions over the upper back(fig-2) and tinea versicolor like lesions(fig-3) with irregular borders and scaling surfaces of varying sizes noticed all over the body ,abundant on the trunk.

Fig-1 Distribution of EV Lesions Over Back. Corresponding Author

Dr. G. Sathish Kumar

M.B.B.S., DNB (Gen.Surgery)

Resident Surgery, Dept. of Surgical Oncology Meenakshi Mission Hospital and Research Centre, Madurai - 625 107 Phone : 0452 2588741, Mobile : 99948 18743 E-mail : drsathishganesan@gmail.com

Madurai Medical Journal May 2011

Fig-2 Warty Lesions over Upper Back.

had uneventful post op period with graft take >90%, Histopathology report showed features of poorly differentiated squamous cell carcinoma (fig 6 & 7) with adequate tumor free margin.

Fig-3 Tinea Versicolor Like Skin Lesions With Irregular Borders And Scaling Surface. Patient was evaluated with CECT chest, which showed an enhancing mass lesion measuring 8x4cm in anterior chest wall. Underlying manubrium sterni appears normal. There were no mediastinal lymphnodes and the lung fields appear clear. Punch biopsy from the chest wall lesion showed features of squamous cell carcinoma. This patient was discussed in tumor board and was planned for surgery. He underwent wide excision of chest wall and back lesions with SSG (fig-4&5). Patient

Fig-4 Well Taken Graft On Chest Wall - 10 th POD

Fig-5 Back Wound With Graft (minimal graft necrosis on medial side)-10 th POD.

Fig-6 Large polygonal cells with vesicular nuclei and abundant eosinophilic cytoplasm.

Fig-7 Cells shows moderate pleomorphism ,some have bizarre nucleus and areas of necrosis. Discussion EV also called Lewandowsky-Lutz Dysplasia or Lutz Lewandowsky Epidermodysplasia Verruciformis is an extremely rare hereditary skin disorder associated with high risk of carcinoma of skin[1]. It is characterized by abnormal susceptibility to HPV of the skin[2]. The resulting uncontrolled HPV infection result in the growth of scaly macules & papules. It is typically associated with HPV types 5 & 8[3], which is found in about 80% of the normal population as asymptomatic infection. Although other types may also contribute, HPV 5 & 8 have been isolated in >90% of EV associated squamous cell carcinoma [4], which is most commonly inherited as autosomal recessive manner, sporadic sex-linked, autosomal dominant forms have been reported. The cause of this condition is an inactivating mutation in either EVER 1or EVER 2 genes, which are located adjacent to one another on chromosome 17[1]. The precise function of these genes is not fully understood, but they play a role in regulating the distribution of ZINC in the cell nucleus. It has been shown that zinc is a necessary co-factor for many viral proteins, and the activity of EVER gene complex to restrict the access of viral proteins to cellular zinc stores, limiting their growth[5]. The condition usually has an onset of between the age of 1-20[6].

Madurai Medical Journal May 2011

The wart usually starts to develop during childhood, 61% of cases appears in childhood aged 5-11 yrs[8]. It is universal and affects persons of all ages and both sexes. Malignant tumors typically appears during the 4th or 5th decade of life. The reported frequency of malignant change ranges from 30-60%[7]. Clinical Features Two types of EV lesions have been described, 1) Flat wart like lesions that look like plane warts. These can be flat-topped papules ranging from light pink to violet in colour. In some places papules join together to form large plaques, these may be reddish-brown and have scaly surfaces and irregular borders. 2) Verrucous or seborrhoeic keratosis like lesions,these are most commonly seen on sun-exposed skin and are often slightly raised, brown coloured lesions[8]. Treatment EV is an life long disease,eventhough lesions can be treated or removed as they appear, patient with EV will continue to develop these lesions throughout life. Currently there is no treatment to prevent new EV lesions from occuring, the management of EV involve a combination of medical and surgical treatments alongside patient counselling and education. • Stress the importance of following sun protection strategies. (exposure to UVA&UVB rays has been shown to increase the rate of EV lesions turning into malignancy). • Treat and remove warts. This includes chemical treatment, cryotherapy with liquid nitrogen and electrosurgery [8]. • Wide excision of malignant lesion with suitable reconstruction.

Madurai Medical Journal May 2011

• Oral and topical treatment with RETINOIDS (isotretinoin&acitretin), fluorouracil and imiquimod are proving to be useful agents. Experimental therapies for EV lesions skin tumors include intralesional interferons and retinoids, also combination of isotretinoin and interferon alpha or cholecalciferol(vit-D) analoques[8]. Reference 1) ^ a b Ramoz N, Rueda LA, Bouadjar B, Montoya LS, Orth G, Favre M (December 2002). “Mutations in two adjacent novel genes are associated with epidermodysplasia verruciformis”. Nature Genetics 32 (4): 579–81. 2) ^ Lazarczyk M, Pons C, Mendoza JA, Cassonnet P, Jacob Y, Favre M (January 2008). “Regulation of cellular zinc balance as a potential mechanism of EVER-mediated protection against pathogenesis by cutaneous oncogenic human papillomaviruses”. The Journal of Experimental Medicine 205(1): 35–42. 3) ^ a b Orth G (1986). “Epidermodysplasia verruciformis: a model for understanding the oncogenicity of human papillomaviruses”. Ciba Foundation Symposium 120: 157–74. 4) ^ Antonsson A, Forslund O, Ekberg H, Sterner G, Hansson BG (December 2000). “The ubiquity and impressive genomic diversity of human skin papillomaviruses suggest a commensalic nature of these viruses”. Journal of Virology 74 (24): 11636–41. 5) ^ Lazarczyk M, Favre M (December 2008). “Role of Zn2+ ions in host-virus interactions”. Journal of Virology 82 (23) 6) Gül U, Kiliç A, Gönül M, Cakmak SK, Bayis SS (October 2007). “Clinical aspects of epidermodysplasia verruciformis and review of the literature”. Inter national Journal of Dermatology 46 (10)tions”. Journal of Virology 82 (23) 7) Grace F Kao, MD Clinical Professor of Dermatopathology, Department of Dermatology, University of Maryland School of Medicine and George Washington University Medical School; Director, Dermatopathology Section, Department of Pathology and Laboratory Medicine, Veterans Affairs Maryland Healthcare System, Baltimore, Maryland 8) :OMIM – Online Mendelian Inheritance in Man (search term Epidermodysplasia verruciformis) Book: Textbook of Dermatology. Ed Rook A, Wilkinson DS, Ebling FJB, Champion RH, Burton JL. Fourth edition. Blackwell Source of support - Nil Conflict of Interest - None declared

Extra Systoles - A Brief Communication

Dr. M. Palanisamy M.B.B.S., M.D.(Gen) Consultant, Dept. of Medicine MMHRC

Prof. Dr. V.N. Rajasekaran M.D., Ph.D., DTM&H., Medical Director & Head of the Department of Medicine MMHRC

Abstract Extrasystoles are nothing but the extrabeats of the heart. Extrasystoles consist of atrial, AV nodal and ventricular. Extrasystoles are due to the premature discharge of ectopic focus in atria, Av node and ventricles. The arrthymia of extrasystoles are common among people, which may be benign and malignant under the underlying heart diseases, which may endanger the life if not diagnosed earlier and management with appropriate measures. Key words Extrasystoles, Premature Atrial Contraction(PAC), Junctional premature contraction (AV nodal extrasystoles), Premature Ventricular Contraction (PVC), paroxysmal ventricular tachycardia, Amidarone. Non Communicable Diseases (NCDS). Introduction The focus on communicable diseases has prevented sufficient attention being paid to a rapidly growing health features of our societies - Non Communicable diseases or NCDS. NCDS posses a threat to nation by inflicting sufficient injuries on social, economical and work forces. There is a tall claim that most of the communicable diseases have been prevented, but inspite NCDS like diabetes, HTN, Storke, Cardiovascular problems and mental illness have become priority of our country to contain. Major NCDS have already taken root in many of our countries and must be urgently dealt with systematically and rapidly. Early diagnosis of the disease, can with effective treatment, avert potentially life threatening and disabling consequence. For this to happen, routine screening or health check ups and timely treatment will have to be given more priority, than before. Separate Health check-up division under the department of medicine, in MMHRC, is functioning with all modern facilities with adequate wings and all specialty departments. Health check-up division aims to screen individual, detect diseases, initiates early medical or surgical Corresponding Author

Dr. M. Palanisamy M.D. (Gen), Consultant, Department of Medicine

Meenakshi Mission Hospital and Research Centre, Madurai - 625 107 Phone : 0452 2588741, Mobile : 96772 95469

interventions. Interventions of speciality departments have become routine both for diagnostic and curative purposes. Reporting early in the morning and leaving in the afternoon with all related documents of an individual, have become day today routine. Health check-up division takes care of the health care of individual, attending. An annual health check-up in this department will definitely keep a person from diseases or if diseased, addressed subsequently. In routine health check-up, it was noticed that most of the cases had ignored their diseases which they had. Several cases of Diabetes, HTN, Cardiovascular diseases, dyslipidamia, thyroid diseases, Renal diseases, Gastro intestinal diseases, Respiratory diseases and Mental diseases were diagnosed and appropriate treatment have been initiated. About 200 cases of ectopic or extrasystoles have been made out and appropriate measures have been taken. Following few cases are given here as instances. Illustration of cases Case 1 A 43 yrs old male moderately obese agriculturist hailing from sivagangai district has reported for difficulty in breathing on exertion, extraordinary fatigue, malaise. Unable to have normal sleep during night hours. He used to have compensation for sleep by having chronic smoking, average 10-20 cigarattes per day invariably ends his day by drinking alcohol. This way of life is going on for more than 10 years and subsequently becomes his life style. On examination patients pulse, BP and all systems are normal. Other parameters like laboratory test, X-Ray chest, Echo are all within the normal limits.

Madurai Medical Journal May 2011

His abdomen scan has shown fatty liver. His ECG revealed ST depression with T wave inversion in L II, L III, AVF and V5 - V6. Other interesting finding in ECG includes RBBB and ventricular extrasystoles. His TMT suggested strong positiveness which warrants coronary Angiogram (CAG). He was further advised to have β - blockers.

Case 2 A 57 years male, a bank employee from Aruppukottai, has reported for sleeplessness, lower limb numbness and general debility 2yrs. On examination the patient was lethargic, his pulse and BP was normal. Systemic examination maintains normality. Other tests like laboratory revealed increased in Total Cholesterol (TC), Low density lipoprotien (LDL). His X-Ray, Abdomen scan, Echo cardiogram and Treadmill test are normal. His ECG showed sinus tachycardia, RBBB, and ventricular extrasystole.

The PAC and PVC may be palpated either a premature beat (extra beat) or a sudden pause (skipped beat). Extrasystoles often occur in normal individuals and that do not necessarily imply underlying heart disease or a poor pragnosis. * PREMATURE ATRIAL CONTRACTIONS (PAC) An atrial extrasystole is due to the premature of an ectopic atrial focus. Etiology  Rheumatic heart diseases notably mitral valve disease congenital or acquired not rheumatic MR  Ischaemia heart disease  Thyrotoxicosis  Acute or chronic lung diseases  ASD  Thoracic surgery  Tobacco  Excessive intake of coffee or tea  Idiopathic I. Atrial extrasystole Atrial extrasystole may appear occasionally with viral infection. Occasional atrial extrasystole may occur in normal individual. Alternate conducted atrial extrasystole area cause of both atrial and ventricular bigeminal rythm. Frequently occuring atrial extrasystoles often lead on to atrial fibrillation. Three or more consequetive atrial extra systoles constitute a paroxysmal atrial tachycardia. ECG

ECG showing alternate conducted atrial extrasystole.

To make an early diagnosis and treat, it is imperative to go into the details of the importance of the Extrasystoles. Enlightment of Extrasystoles is very useful and negligence on Extrasystole have to be averted. Extrasystoles The most but not the least arrthymias of heart, are extrasystoles. Friends of mine, of more than 20 have developed this arrthymia, which provoked a desire to write this article. Extrasystole are nothing but ectopic beats which are characterised by Cardiac contractions which arise prematurely from a normal or abnormal foci (pace maker) Extrasystoles are of three types * Premature atrial contractions (PAC) * Junctional (nodal) premature contractions * Premature ventricular contractions (PVC)

Madurai Medical Journal May 2011

 Atrial extrasystole characterised by presence of bizarre p wave, which may be pointed, notched, biphasic or inverted  The p wave may be hidden with in the preceding T wave  PR interval more than 0.12 seconds  The QRS complex is normal  Compensatory pause is relative II. Junctional premature contractions (AV nodal extrasystole)

1. This is similar in appearance to atrial extrasystole on the ECG 2. P wave may either precede, merge with or follow the QRS complex depending on whether the ectopics arise from upper, mid, or lower part of the AV node respectively. 3. PR interval is less than 0.12 seconds 4. Full compensatory pause Proxysmal Av Nodal Tachycardia This may be defined as a succession of three or more AV nodal extrasystoles and has similar characteristics of Atrial tachycardia. Blocked Atrial Ectopic No QRST complex following P wave, if impulse reaches AV node when it is refractory. III. Premature Ventricular Contractions (PVC)

PVC is also known as premature ventricular complex, ventricular premature contraction (PVC), ventricular premature beat (VPB) or extrasystole, is a relatively common event where the heart beat is initiated by the Heart ventricles rather than by the sinoatrial node. In a PVC, the ventricles contract first, which means that the circulation is inefficinet. However, single beat PVC arrthymias do not usually pose a danger and can be asymptomatic in a healthy individuals. Etiology A) Ventricular ectopics may be benign, due to excessive ingestion of coffee, tea, alcohol, cold water, smoking or emotional stress. B) organic heart diseases * IHD (Ischaemic heart disease) * Hypertensive Heart disease * Myocarditis * Ventricular hypertrophy of any cause such as cardiomypathy, mitral valve prolapse. C) Drugs - digitalis, procainamide, amphetamine, caffeine, thyroxine, adrenaline, nicotine. D) General - after major illness or surgery or physical instability. E) Idiopathic. Clinical Significance 1) Idiopathic ectopic may occur in health and it may be caused by emotional upset or during pregnancy. 2) Effect of exercise: If extrasystole is abolished by exercise it is considered as benign. Extrasystole

induced by exercise, it may suggest the presence of coronary insufficiency. 3) In acute myocardial infarction PVC’s are warning for more serious arrthymias. In LBBB, PVC’s may be the only ECG evidence of cardiac infarction. 4) Patients with mitral valve prolapse are at higher risk for serious ventricular arrthymias. 5) A complex and frequent ectopic is always associated with increased risk of sudden death, while low grade ectopic is a benign pragnosis. Besides, the above described three types of extrasystoles, are also worth to mention here. Interpolated Extrasystole: Occurance of three beats in rapid succession in the time normally occupied by two and without a long pause. Common with ventricular ectopic beats. Fusion Beats: QRS complex intermediate in shape between a normal and aberrant QRS and preceded by a P wave. ECG of Ventricular Extrasystole Ventricular extrasystole is characterised by appearance of a premature and bizarre (widened, slurred or notched) QRS complex, with associated secondary ST - T changes (when the QRS complex dominantly upright the ST segment is depressed and T wave is inverted. When the QRS complex dominantly downwards, the ST segment is elevated and T wave is upright). The ventricular extrasystole is followed by an absolute compensatory pause. Signs and Symptoms of Extrasystoles Mostly no symptoms in about 50% of patients. In majority of patients there may be disagreeable sensation due to a large beat, or fear of heart stopping due to a long pause. Pain in hypersensitive patients. Dizziness and faintness if premature beats numerous. Fluttering sensation if premature beats in quick succession. Pulse Quick beat followed by pause less than compensatory in atrial and nodal and equivalent to two sinus cycles in ventricular premature beats ending in pulse more forcible than it’s predecessor. Early beat faintly palpable or impalpable at peripheral pulse. Heart Sound First sound always accentuated in all ectopic beats. Second heart sounds normal splitting in atrial and nodal and wide splitting due to ventricular asynchrony. If extrasystole is so premature that there is insufficient ejection of blood, no second sound. JVP Cannon waves are seldom occur in PVC. Cannon A wave in PVC coincidence with or just follows first heart

Madurai Medical Journal May 2011

sound or carotid impulse in contrast with cannon waves in PAC with just precedes first sound or cartoid impulse. Poor manâ&#x20AC;&#x2122;s stress test T wave inversion if present in normal complex immediately following the ventricular ectopic indicates the presence of underlying ischaemia. Right Ventricular Extrasystole Ventricular ectopics with a predominantly negative QRS complex in the right precardial leads (V1 - V2) indicate that ectopics originate from right ventricle and are usually benign. Left Ventricular Extrasystole The presence of ventricular ectopics with predominant negative QRS complex, in the left precardial leads (V4, V5, V6) indicate that the ectopics originate from left ventricle and are invariably pathological. Types Of Ventricular Extrasystole 1) Ventricular bigeminy

Extrasystole ventricular bigeminy: Alternate ventricular extrasystole ( Extrasystoles occur after every other sinus beat, this is common in digitalis toxicity). Unifocal ventricular extrasystole are usually indicative of cardiac diseases. The occur in crops or showers. They occur in association with cardiac disease and in persons over 40 years of age and precipitated by exercise. 2) Multifocal or Multiform Ventricular Extrasystoles

Multifocal or multiform ventricular extrasystole: Extrasystoles that arises from different focus and consequently give rise to different QRS complex. Multifocal ventricular extrasystole and ventricular trigeminy are are always abnormal and usually indicative of serious myocaradial disease. 3) Ventricular Trigeminy

Madurai Medical Journal May 2011

Extrasystoles in pairs (Ventricular trigeminy): When a ventricular ectopic foci discharge prematurely and twice in succession, the rhythm will manifest as a pair of extrasystole, namely a sinus beat followed by two extrasystoles. Frequent ventricular extrasystole especially those occuring in pairs often lead to ventricular tachycardia or ventricular fibrillation. 4) Paroxysmal Ventricular Tachycardia

Extrasystolic paroxysmal ventricular tachycardia: Three or more successive ventricular ectrasystoles constitute it. Ventricular extrasystoles are always significant when associated with myocardial disease. A ventricular extrasystole occuring prematurely so as to be superimposed on the T wave of the preceding complex, may prone to precipitate ventricular fibrillation. Diagnosis and Treatment Diagnosis of extrasystoles are purely on the basis of ECG manifestation. HOLTER - 24 hours monitoring is invariably used to detect the types, chronicity and fixing the appropriate management of the extrasystoles. Treatment of Atrial Extrasystoles Treatment is not always, normally required unless the ectopic beats provoke more significant arrthymias, when beta blockers may be effective. Treatment of Ventricular Extrasystoles Ventricular extrasystoles are most uncomfortable especially when frequent. The patient may complaint of extra beat, missed beat or heavy beat because of its prematurity, the post ectopic part of the next sinus beat (ie) noticed by the patient. The pulse is irregular owing to the premature beat, occurs regularly after every normal beat, pulses bigeminus may occur. If premature beats highly symtomatic, treatment with beta blocker may be helpful. If the ectopic stems from a singe focus, especially when in the right ventricle, catheter ablation can be very effective. Ventricular extrasystoles usually treated only if symptomatic. Simple measures such as reassurance and beta blocker therapy are all required. The symptomatic ventricular extrsystoles are better treated with amidarone. Amidarone has unique pharmacological properties beyond its effects on the cardiac sodium and potassium channels. Amidarone is also a beta adrenergic receptor - blocker and calcium channel blocker with anti ischaemic effect. While considering the supremacy of the amidarone, its adverse reactions like photo sensitivity, rhabdomyolysis have to be kept in mind. The dosage and root of administration of amidarone are purely depending on the frequency, chronicity, the type and severity of the condition.

Early detection and confirmation of the diagnosis by applying routine methods and management with appropriate measures will save life. Reference 1. 2. 3.

4. 5. 6. 7. 8.

Harrison’s Internal Medicine Davidson’s Principles And Practice Of Medicine Golwala’s Clinical Medicines Principles Of Clinical Electrocardiography By Mervin J.Coldman M.D., An Introduction To Electrocardiography By Leo Schamroth

Hurst’s - The Heart Volume I Braun Wald’s Heart Disease Lange - Current Medical Doagnosis And Treatment 2010

Source of support - Nil Conflict of Interest - None declared

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Post Graduates Corner Nodal yield – is it a treasure hunt in cancer treatment ?? Part I

Dr. Krishna Kumar Rathnam M.D., (Med.), DM. (Med. Onco.), Consultant, Dept. of Medical Oncology MMHRC

Introduction Addressing primary tumor by surgery is the main stay of treatment in many cancers. This just does not include clearing the primary tumor, but also includes clearing it’s nodal basin. This is not only prognostic but is very important from medical oncologist’s point of view for deciding necessity of adjuvant treatment. We shall discuss role of lymph node dissection in breast and head and neck cancers in this edition’s PG corner. Nodal Dissection in Breast Cancer Days have advanced from the time old Halstead’s mastectomy to modified radical mastectomy and to breast conserving surgery (BCS), however one fact remains constant - the need to address axilla. This has shown to be important by many randomised studies in patients younger than 70 years of age. Today the standard procedure of“ Modified Radical Mastectomy” includes dissection of level I and Level II axillary lymph node dissection (ALND) along with the mastectomy / BCS. Certain institutes go upto dissecting Level III nodes if level II nodes are grossly involved. So, why is this important ? First of all, studies have shown that axillary dissection has decreased local recurrence rates, had some minimal benefit on survival [1] and is important in deciding who needs adjuvant treatment and what type of adjuvant treatment. In patients whose axillary nodes are involved, it is mandatory to give radiotherapy to chest wall. These candidates also have to receive chemotherapy with anthracyclines and now with latest data, taxanes also. On the contrary, after proper dissection of atleast ten nodes or more [2], if the nodes are found to be

Corresponding Author

Dr. Krishna Kumar Rathnam MD.(Med.), DM.(Med. Onco.), Consultant, Medical Oncologist

Meenakshi Mission Hospital and Research Centre, Madurai - 625 107 Phone : 0452 2588741, Mobile : 93804 17299 E-mail : kkrathnam@gmail.com

Madurai Medical Journal May 2011

pathologically not involved by tumor, depending on the size of primary tumor, hormone receptor status and HER2 status there is a possibility that the patient may be saved from toxic chemotherapy. So here lies the importance of a proper axillary dissection in cases of breast cancer. Can axillary dissection be avoided in breast cancer patients? In patients with clinically node negative breast cancer, if sentinel lymph node biopsy facility is available and is done and found to be negative, studies show that these patients may be deprived of further axillary dissection[3]. Many studies are still trying to identify the low risk group of sentinel lymph node biopsy positive patients, where an ALND can be avoided, but are still unclear. Also patients who under go palliative toilet mastectomy can escape axillary dissection. Nodal dissection in head and neck cancer Cancer of head and neck region is a loco regional cancer, notoriously involving draining neck nodes. Sometimes the squamous cell carcinoma is detected in a metastatic neck node and the primary is never found until in very late stages[4]. In advanced head and neck cancers definitive chemo radiotherapy is the first line of treatment in most cases, however when it comes to early operable head and neck cancers, selective/comprehensive neck dissection becomes very important as it may be curative and also very important in deciding who are candidates for adjuvant chemoradiotherapy. Managing early head and neck cancers includes addressing the primary tumor and the draining nodes in the neck. Usually both are addressed using the same modality of primary treatment, either by radiotherapy or surgery depending on the site of tumor (ref table 1), chances of complete resection and cosmetic outcome. Further the extent of neck dissection also depends on the nature of the primary disease and the propensity to involve neck nodes. In patients who clinically have a N0 neck, the estimated subclinical disease in the neck is presented in TABLE 1 below.

Table 1 Definition of risk groups for the clinically N0 neck Site Group Risk of neck disease T stage Low risk < 20 % T1 Oral tongue, Floor of mouth, RMT, gingival, palate, buccal mucosa 20 – 30 % T1 Soft palate, Pharyngeal Intermediate risk wall, Supraglottic larynx, tonsil T2 Floor of mouth, oral tongue, RMT, gingival, hard palate, buccal mucosa T1-T4 Nasopharynx, Pyriform >30 % High risk sinus, Base of tongue T2-T4 Soft palate, pharyngeal wall, supraglottic pharynx, tonsil T3-T4 Floor of mouth, oral tongue, RMT, gingival, hard palate, buccal mucosa T – Tumor, RMT – retro molar trigone, ( From reference – 5 ) Addressing the neck nodes by surgery can be by either a classic radical neck dissection (RND) or selective neck dissection. In classic RND, the superficial and deep cervical fascia with it’s enclosed lymph nodes from Level I - V is removed in continuity with the sterno cleidomastoid and omohyoid muscles, internal and external jugular veins, spinal accessory nerve and the submandibular gland. The RND may be modified (modified RND) to decrease morbidity and improve cosmetic and functional outcomes without compromising disease control. Selective neck dissections are more limited and include lateral (Level II - IV neck nodes), postero lateral (Levels II - V neck nodes) and supra omohyoid (Levels I - III neck nodes). In a clinically negative neck, when the primary tumor is treated by surgery, the neck should be electively dissected when the chance of occult involvement is > 10 - 15%. A modified / selective neck dissection achieves good local control. However in a clinically positive neck, addressing the neck is the rule either by surgery or radiotherapy, which ever be the primary modality of treatment. In such instances selective neck dissections are usually recommended for clinically negative neck, selected clinically positive necks (mobile, 1-3 cm nodes) and for removing residual nodes after radiation if there is an excellent regression of the N2 or N3 disease [6]. Anything beyond, usually demands a more comprehensive neck dissection.

Why such neck dissection and what after ? Good neck dissection after primary surgery achieves excellent local control and patients found to have multiple positive nodes, extracapsular extension and lymphovascular invasion, have higher risk of local and systemic recurrence and have to receive adjuvant chemotherapy + radiotherapy[7,8]. It is a well known fact that once recurrences occur after primary definitive therapy, salvage therapy is a repeat surgery and this is not just technically demanding in an irradiated / operated field, but also mutilating in most cases as recurrences are extensive. “FIRST HIT”, should be the “BEST HIT”; there, remains the importance of a complete surgery followed by chemoradiotherapy if needed, without compromising cosmetic or functional outcome as much as possible. Conclusion Breast cancer incidence is increasing in India and it is very important to stage the disease correctly. It not only decides the necessity but also the type of adjuvant chemotherapy and whether radiotherapy is needed for the patient. So a proper and adequate nodal dissection is important in breast cancer patients. Head and neck cancer has always been a very common cancer in our sub continent and here again proper neck nodal dissection is important not only because it is therapeutic in early cancer but also predictive of adjuvant chemotherapy and radiotherapy. Acknowledgements 1. Dr. R. Vijaya Bhaskar M.S, M.Ch (Sur. Onco) Consultant Surgical Oncologist, MMHRC, Madurai 2. Dr. K.S. Kirushna Kumar MD ( RT ) - Senior Consultant Radiation Oncologist, MMHRC, Madurai

Reference 1.

Hayward J,Caleffi M.The significance of local control the primary treatment of breast cancer. Lucy Wortham James Clinical award. Arch Surg 1987;122(11):1244.

Axellson CK, Mouridson HD et al. Axillary dissection of level I and level II Lymph node dissection is very important in breast cancer staging.The Danish breast Cancer Cooperative Group. Eur J Cancer 1992;28A:1415-1418

Naik AM,Fey J,Gemignani M et al.The risk of sentinel lymph node biopsy for breast cancer is comparable with that of axillary lymph node dissection: a follow up study of 4008 procedures. Ann Surg 2004;240(3):462;discussion.

Medenhall WM,Mancuso AA,Parsons JT et al. Diagnostic evaluation of squamous cell carcinoma metastatic to cervical lymph nodes from an unknown primary head and neck site. Head Neck 1998;20:73

Mendenhall WM , Million RR.Elective neck irradiation for squamous cell carcinoma of head and neck:analysis of time-dose factors and causes of failure. Int J Radiat Oncol Biol Phys 1986;12:741

Memdenhall WM, Villaret DB , Amdur RJ et al.Planned neck dissection after radiotherapy for squamous cell carcinoma of head and neck. Head Neck 2002;24:1012

Memdenhall WM, Amdur RJ, Hinnerman RW et al. Post operative radiotherapy for squamous cell carcinoma of head and neck. Am J Otolaryngol 2003;24:41

Cooper JS , Pajak TF , Forastiere AA et al. Long term results of phase III intergroup trial ( RTOG 95-01 ) of surgery followed by radiotherapy versus radiochemotherapy for resected high risk squamous cell carcinoma of head and neck. Int J Radiat Oncol Biol Phys 2006;66:S14 ( abst )

Madurai Medical Journal May 2011

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TRAC - 2011 (Tamil Nadu State RSSDI Annual Conference) July 30th & 31st, 2011 Venue : Hotel DSF Grand Plaza, Tuticorin

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Meenakshi Mission Hospital and Research Centre, Madurai & Indian Medical Association CGP in affiliation with George Washington University, USA and IIEMS (USA) announces one year

2nd Batch Post Graduate Diploma in Emergency Medicine PGDEM (USA) From July 2011 Emergency medicine is a recognised speciality in India and the demand for an Emergency Medicine trained doctor will overwhelm the job market. This course is designed to provide essential training in Emergency Medicine. Eligibility criteria : MBBS with MCI registration Seats available :10 Last date for application : 15 June 2011

Madurai Medical Journal May 2011

Course Highlights â&#x20AC;˘ A well designed course curriculum by George Washington University that meets the requirements to work as an efficient GP & Emergency Physician. â&#x20AC;˘ Experienced Core faculty & Visiting faculty from USA For details and application Contact Dr. Narendra Nath Jena

Course Co-ordinator - PGDEM(USA) Consultant & Head, Dept of Accident & Emergency Medicine Meenakshi Mission Hospital and Research Centre, Madurai-625107 Phone: 91-9944384994 Email: emergency.mmhrc@gmail.com