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IJCP Group of Publications Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor Dr Deepak Chopra Chief Editorial Advisor

Volume 22, Number 9, February 2012

FROM THE DESK OF GROUP EDITOR-IN-CHIEF 429 Irisin: The Hormone for Obesity and Diabetes Control

Dr KK Aggarwal CMD, Publisher, Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor

IJCP Editorial Board

KK Aggarwal

ORIGINAL STUDY 431 Risk Assessment for Congestive Heart Failure in a South Indian Population: A Clinical Pharmacist’s Perspective

Obstetrics and Gynaecology Dr Alka Kriplani Dr Thankam Verma, Dr Kamala Selvaraj

N Vanitha Rani, G Kannan, Vasantha J, P Thennarasu, C Uma Maheswara Reddy

DRUG REVIEW

ENT Dr VP Sood

437 Role of Phenazopyridine in Urinary Tract Infections

Cardiology Dr Praveen Chandra Dr M Paul Anand, Dr SK Parashar

Paediatrics Dr Swati Y Bhave Dr Balraj Singh Yadav Dr Vishesh Kumar Diabetology Dr Vijay Viswanathan Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty Dentistry Dr KMK Masthan Dr Rajesh Chandna

OP Gupta, KK Aggarwal

REVIEW ARTICLE 443 Clinical Safety and Efficacy of Pilex Tablets and Ointment in the Management of Hemorrhoids

Dibyendu Gautam, Manasi Basu Banerjee, Shib Shankar Roy Chowdhury, Jaydev Pramanik

CLINICAL STUDY 450 Clinical Outcome in Malaria - Reiterating the Role of Parasitic Index

Gastroenterology Dr Ajay Kumar

Dermatology Dr Hasmukh J Shroff

454 A Study of Clinical Profile of 50 Patients with Portal Hypertension and to Evaluate Role of Noninvasive Predictor of Esophageal Varices

Nephrology Dr Georgi Abraham Neurology Dr V Nagarajan Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

Aarthi Rajkumar, Shalinee Rao, Sandhya Sundaram

BC Kaji, Yagnesh R Bhavsar, Nitin Patel, Anupam Garg, Hiren Kevadiya, Zishan Mansuri

CASE REPORT 458 Allergic Contact Stomatitis: A Case Report and Review of Literature

P Lokesh, T Rooban, Joshua Elizabeth, K Umadevi, K Ranganathan

CASE REPORT

Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at E - 219, Greater Kailash, Part - 1 New Delhi - 110 048 E-mail: editorial@ijcp.com

463 Wireless Capsule Endoscopy Requiring Surgical Intervention

Printed at IG Printers Pvt. Ltd., New Delhi E-mail: igprinter@rediffmail.com printer_ig@yahoo.com

Neha Kantawala, JS Rajkumar, S Yuvaraja, T Perungo

466 Pseudo-infarct in ECG in A Case of Asymmetric Septal Hypertrophy

Š Copyright 2012 IJCP Publications Ltd. All rights reserved.

The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

S Parthasarathy, M Ravishankar

468 Unusual Presentation of Blindness

SA Kareem, Siva Nambi

Editorial Policies The purpose of IJCP Academy of CME is to serve the medical profession and provide print continuing medical education as a part of their social commitment. The information and opinions presented in IJCP group publications reflect the views of the authors, not those of the journal, unless so stated. Advertising is accepted only if judged to be in harmony with the purpose of the journal; however, IJCP group reserves the right to reject any advertising at its sole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP group of a particular policy, product or procedure. We believe that readers need to be aware of any affiliation or financial relationship (employment, consultancies, stock ownership, honoraria, etc.) between an author and any organization or entity that has a direct financial interest in the subject matter or materials the author is writing about. We inform the reader of any pertinent relationships disclosed. A disclosure statement, where appropriate, is published at the end of the relevant article.

LEGAL QUESTION 470 What should Doctors and Nursing Homes do to Prevent and Manage Violence by Patients/Relatives?

MC Gupta

PHOTO QUIZ 474 Adolescent with a Diffuse, Progressive Rash

PRACTICE GUIDELINES

Note: Indian Journal of Clinical Practice does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.

476 ACCP Releases Statement on Dyspnea Treatment in Patients with Advanced Lung or Heart Disease

LIGHTER READING 478 Lighter Side of Medicine

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from the desk of group editor-in-chief Dr KK Aggarwal

Padma Shri and Dr BC Roy National Awardee Sr. Physician and Cardiologist, Moolchand Medcity, New Delhi President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS Chairman Ethical Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) emedinews@gmail.com http://twitter.com/DrKKAggarwal Krishan Kumar Aggarwal (Facebook)

Irisin: The Hormone for Obesity and Diabetes Control Researchers from the Dana-Farber Cancer Institute, Massachusetts, Harvard Medical School, University of California and Denmark’s Odense University Hospital, among others, have found that some of the most widely recognized effects of exercise on muscle are mediated by irisin, a hormone secreted by muscle cells. The study has been published in the latest issue of scientific journal Nature.

Irisin is induced with exercise in mice and humans, and mildly increased irisin levels in the blood cause an increase in energy expenditure in mice with no changes in movement or food intake. This results in improvements in obesity and glucose homeostasis. The hormone has been found to act in two ways. It promotes the conversion of inert (white) yellow fat to the metabolically more active brown fat, and facilitates insulin action, thus decreasing blood glucose levels. While white fat is used to store energy (calories), brown fat seems to be more involved in burning it. The researchers found irisin to be present in the blood of human volunteers who had undergone 10 weeks of exercise.

When irisin was introduced in sedentary mice, the physiological effects of exercise like higher metabolism, stabilization of blood glucose levels through better uptake of glucose from blood - one of the mechanisms by which insulin works - were mimicked in the laboratory. In the last few years, brown fat has begun to increasingly intrigue scientists. In many ways, it physically resembles muscle more than it does typical fat. While little is known about it, it seems to play a major role in maintaining normal weight. One study found that the more brown fat a person has, the lower their BMI will be. Another study found that mice with a genetic abnormality that eliminated their brown fat became obese even without overeating.

Brown fat is common in infants but was once thought to disappear in adults. Recent studies have shown that it merely decreases. It is found mainly in the neck and upper chest of adults. In infants, brown fat is an important regulator of body temperature, helping to keep the infant warm. Unlike white fat, when brown fat is metabolized (burned), most of its energy content is converted into heat. Adults don’t seem to need this system of keeping warm.

It’s not yet known precisely what function brown fat serves in adults. So far, most studies of brown fat have been done in mice, because adult mice have more brown fat than adults humans do.

In the current study, the Dana-Farber researchers injected small amounts of irisin into the muscles of sedentary adult mice that were both obese and prediabetic. Within 10 days of treatment, the mice showed better control of blood sugar and insulin levels - possibly preventing the onset of full-blown diabetes - and also lost a small amount of weight. The researchers suspect that longer therapy would have led to greater weight loss.

Irisin was named after a Greek messenger Goddess (Iris) because it’s a chemical messenger. It’s normally present as part of a larger protein in a muscle cell’s outer membrane, where it lies dormant and inactive. Exercise (and, most likely, other unknown factors) cause this protein to be split, releasing irisin, which exits the muscle cell and carries its message to other cells of the body. Ultimately, some white fat cells are told to convert to brown fat cells and islet cells of the pancreas are told to produce more insulin.

Source: Indian Express

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

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Original Study

Risk Assessment for Congestive Heart Failure in a South Indian Population: A Clinical Pharmacist’s Perspective N Vanitha Rani*, G Kannan, Vasantha J, P Thennarasu, C Uma Maheswara Reddy

Abstract Congestive heart failure (CHF) is becoming an increasingly prevalent healthcare problem. Hypertension (HT) is a major risk factor for CHF and it commonly coexists with other cardiovascular risk factors. The quality of risk that HT represents has to be thoroughly compared with other risk factors. This could have significant implications for primary prevention strategies including drug treatment. A study was conducted in 137 heart failure patients, to assess the contribution of cardiovascular risk factors like age, sex, obesity, HT, diabetes, dyslipidemia, alcohol, smoking and family history, individually and in combination, in the progression of CHF using multivariate logistic regression analysis and odds ratio (OR) (95% confidence interval). Of the various individual factors, HT showed 3.8 times greater risk (p = 0.003; OR-3.773) for heart failure; dyslipidemia exhibited 2.5 times risk (p = 0.07; OR-2.49), followed by others. Patients with HT, but no diabetes or dyslipidemia had 1.2 times risk (OR-1.17) for CHF; patients with hypertension and diabetes had 1.7 times risk (OR-1.69) and patients with HT, diabetes and dyslipidemia had two times greater risk (OR-1.87). Though, the present study emphasizes that HT is the most common risk factor in the progression of heart failure, the risk is high when it coexists with other risk factors like diabetes and dyslipidemia. A clinical pharmacist can work in collaboration with healthcare team in achieving the goal of long-term control of hypertension and other cardiovascular risk factors in millions of patients, by providing services ranging from monitoring drug therapy and improving patients compliance to drug therapy, to, health maintenance care such as ordering screening procedures and counseling regarding lifestyle modification.

Keywords: Hypertension, heart failure, diabetes, dyslipidemia, cardiovascular risk factors

C

ongestive heart failure (CHF), also referred to as congestive cardiac failure (CCF) or just heart failure, is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood through the body.1 It is becoming an increasingly prevalent healthcare problem with notable socioeconomic consequences.2 Because not all patients have volume overload at the time of initial or subsequent evaluation, the term ‘heart failure’ is preferred over the older term ‘CHF’.3 Hypertension (HT) and chronic ischemic heart disease (one or the other or, more frequently, in association) are responsible for the highest percentage of cases of CHF in the industrialized world. Obesity, diabetes, sedentary lifestyle and

*Lecturer, Dept. of Pharmacy Practice, Sri Ramachandra College of Pharmacy, Sri Ramachandra University, Chennai Address for correspondence Dr N Vanitha Rani Lecturer, Dept. of Pharmacy Practice Sri Ramachandra College of Pharmacy, Sri Ramachandra University Porur, Chennai - 600 116 E-mail: vanithak9@rediffmail.com

smoking also play unmistakable roles, favoring the development of CHF. HT as such is an independent risk factor for heart failure and plays a key role in the evolution of the disease.4 In the Framingham heart study cohort, HT antedated the development of heart failure in 91% cases and was associated with 2- to 3-fold risk, after adjusting for age and other cardiovascular risk factors.5 The primary cardiac mechanism that underlies the clinical syndrome of heart failure is systolic and diastolic dysfunction, usually in combination.6 The earliest functional cardiac changes in HT are in left ventricular systolic and diastolic function, which evolve and progress to left ventricular hypertrophy (LVH) and then to left ventricular failure, which can be diagnosed by echocardiogram.7 The spectrum of HT, LVH and left ventricular failure represent an under-diagnosed and undertreated problem. Too few patients have their blood pressure (BP) under good control and too many progresses to heart failure. BP control continues to be important in reducing cardiovascular risk.

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

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Original Study Major problems in control of BP are patient’s noncompliance to drug therapy, lack of patient education about importance of BP control and high costs of medical and pharmaceutical care which can be effectively addressed by a clinical pharmacist. As a member of healthcare team, the clinical pharmacist can act as a bridge between the patients and the prescribers to achieve the goal of long-term control of the cardiovascular risk factors.

A clinical pharmacist can work in collaboration with healthcare team in achieving the goal of longterm control of HT in millions of patients, by providing services ranging from monitoring drug therapy and improving patients compliance to drug therapy to, health maintenance care such as ordering screening procedures and counseling regarding lifestyle modification.8 METHODOLOGY The study was carried out for a period of eight months (January 2008 to August 2008) in the intensive coronary unit of a South Indian tertiary care teaching hospital after obtaining approval from the Institutional Ethics Committee and consent from the patients. The study population comprised of 137 patients (100 men and 37 women, age range 30-90 years; mean age 62.31 ± 12.09) and diagnosed with left ventricular failure.

Detailed medical history elicitation including demographic data (age, sex, body mass index [BMI]), presence of contributing cardiovascular risk factors namely HT, diabetes mellitus, obesity, dyslipidemia, smoking, alcohol and family history of cardiovascular diseases were collected for each patient and recorded in the data collection forms designed exclusively for the study. Cardiovascular risk factors were defined as follows: Smoking was defined as current smoking of ≥1 pack/day, obesity as the BMI >30 kg/m2, family history as history of cardiovascular disease or sudden cardiac death before the age of 55 years in the father or any other first-degree male relative or before the age of 65 years in the mother or any other first degree female relative, HT as having a BP of >140/90 mmHg on two separate examinations or usage of antihypertensive agents, diabetes mellitus as fasting glucose ≥126 mg/dl, postprandial glucose ≥200 mg/dl and random blood sugar ≥200 mg/dl, respectively or usage of insulin or antidiabetic drugs, metabolic dyslipidemia as the fasting cholesterol ≥200 mg/dl, triglyceride ≥150 mg/dl, low-density lipoprotein (LDL) ≥100 mg/dl, high-density lipoprotein (HDL) level <40 mg/dl in men and <50 mg/dl in women.

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

STATISTICAL ANALYSIS All data were entered prospectively in a computerized data base. Analysis was done with the SPSS Statistical software (10.0 version). All categorical values were presented as mean ± standard deviation. A multivariate logistic regression analysis and odds ratio (OR) (95% confidence interval [CI]) was performed to identify the contribution of major cardiovascular risk factors in the progression of CHF in the study population. The risk of CHF when HT coexists with diabetes and dyslipidemia was also analyzed. A p value of <0.05 was considered significant.

RESULTS A total of 137 patients with left ventricular dysfunction were included in the study of which, 100 (73.0%) were males and 37 (27.0%) were females. The mean age and standard deviation of males were 62.09 ± 12.39 and females were 61.41 ± 11.59. Prevalence of left ventricular dysfunction was higher in males (73%) than in females (27%) in this study.

Risk Factor Profile The overall cardiovascular risk factor profile observed in the study population was HT in 105 (76.6%) patients, diabetes in 75 (54.7%), dyslipidemia in 32 (23.4%), alcoholics 20 (14.6%), smoking in 38 (27.7%) and family history of cardiovascular disease in 31 (22.6%). The contribution of individual and combined risk factors in the progression of heart failure in the study population were analyzed using multivariate logistic regression analysis and OR (95% CI). The statistical analysis was carried out using all the cardiovascular risk factors (age, sex, BMI ≥ 30 kg/m2, HT, diabetes, dyslipidemia, alcohol, smoking and family history) as independent variables and left ventricular dysfunction as dependent variable.

HT was found to be significant risk factor in the progression of left ventricular failure (p = 0.003) followed by dyslipidemia which was moderately significant (p = 0.07). Based on OR, HT showed 3.8 times greater risk (OR-3.773) for cardiac failure than other cardiovascular risk factors studied. Dyslipidemia exhibited 2.5 times greater risk (OR-2.49) for cardiac failure which establishes it to be a second major risk factor for the progression of heart failure (Table 1 and Fig. 1).

Based on the regression analysis and OR of combined risk factors, patients with HT without diabetes or

Original Study

Dependent variable - Cardiac failure

Table 1. Results of Multiple Logistic Regression Analysis of Risk Factors Independent variables

Reg. coeff ‘b’

Standard error of ‘b’

p value

Odds ratio

95% CI

Age

0.026

0.016

0.120

1.026

0.993-1.060

Sex

0.136

0.466

0.780

0.878

0.352-2.188

0.82

0.062

0.185

1.086

0.962-1.226

Hypertension

1.329

0.446

0.003

3.773

1.575-9.052

Diabetes

0.274

0.384

0.476

1.315

0.619-2.792

Dyslipidemia

0.914

0.518

0.078

2.494

0.903-6.887

Smoking

0.308

0.471

0.513

1.360

0.541-3.421

Family history

0.258

0.468

0.581

0.772

0.309-1.934

BMI ≥30

kg/m2

p value of <0.05 is considered significant.

Dependent variable-Cardiac failure

Table 2. Results of Multiple Logistic Regression Analysis of Combined Risk Factors Independent variables

Reg. coeff ‘b’

Standard error of ‘b’

p value

Odds ratio

95% CI

Hypertension

0.159

0.4

0.692

1.172

0.535-2.568

Hypertension + Diabetes

0.525

0.374

0.16

1.69

0.813-3.516

Hypertension + Diabetes + Dyslipidemia

0.623

0.628

0.321

1.865

0.545-6.378

p value of <0.05 is considered significant.

complex clinical syndrome characterized by inadequate systemic perfusion to meet the body’s metabolic demands as a result Smoking 1.36 of impaired cardiac function.9 HT and Dyslipidemia 2.494 ischemic heart disease are the two cardinal causes of heart failure and they commonly Diabetes 1.315 coexist. The relative contributions of Hypertension 3.773 hypertension and ischemic heart disease to heart failure have been difficult to Obesity 1.086 disentangle.10 The mechanisms involved Sex 0.878 in progression from HT to heart failure have been the focus of many recent Age 1.026 studies. HT should not be considered in 0 0.5 1 1.5 2 2.5 3 3.5 4 isolation because other risk factors such as plasma lipid levels, cigarette smoking Odds ratio and presence of diabetes mellitus, obesity Figure 1. Odds ratio of risk factors. and family history of cardiovascular disease have also been a considerable impact on the progression of heart dyslipidemia had 1.2 times risk (OR-1.17) for heart failure.11 failure, whereas patients with HT and diabetes had The quality of risk that HT represent has to be 1.7 times risk (OR-1.69) and patients with HT, diabetes thoroughly compared with other factors. This could and dyslipidemia had two times greater risk (OR-1.87) have significant implications for primary prevention (Table 2 and Fig. 2). strategies including drug treatment in the progression of heart failure. The framingham heart study DISCUSSION demonstrated HT to be the most common and one Heart failure is increasing in prevalence in many of the strongest risk factors for heart failure, especially areas of the world. It can be defined as a progressive in patients aged between 60-70 years.12 Family history

0.772

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

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Original Study

1.865

HT + DM + DYS 1.69

HT + DM

REFERENCES

1.172

HT 0

0.5

1

1.5

control of the risk factors by educating the patients about early screening and regular monitoring of BP, blood sugar and serum cholesterol levels; the importance of compliance with the therapy and lifestyle modification.

1.

Neubauer S. The failing heart: an engine out of fuel.

N Engl J Med 2007;356(11):1140-51.

2.

Coats AJ. Is preventive medicine responsible for the increasing prevalence of heart failure? Lancet 1998;352 Suppl 1:SI39-41.

3.

Krumholz HM, Chen YT, Wang Y, Vaccarino V, Radford MJ, Horwitz RI. Predictors of readmission among elderly survivors of admission with heart failure. Am Heart J 2000;139(1 Pt 1):72-7.

4.

Gaasch WH. Diagnosis and treatment of heart failure based on left ventricular systolic or diastolic dysfunction.

JAMA 1994;271(16):1276-80.

5.

Vasan RS, Levy D. The role of hypertension in the pathogenesis of heart failure. A clinical mechanistic overview. Arch Intern Med 1996;156(16):1789-96.

6.

Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA 1996;275(20):1557-62.

7.

Paul E Nolan Jr, Dawn G. Zarembski. Heart Failure.

In: Textbook of Therapeutics â&#x20AC;&#x201C; Drug and Disease Management. 7th edition, Helms, Quan, Harfindal, Gouley (Eds.), Lippincott Williams & Wilkins: USA 2000: p.825-66.

8.

Gandhi SK, Powers JC, Nomeir AM, Fowle K, Kitzman DW, Rankin KM, et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 2001;344(1):17-22.

9.

American Society of Health System Pharmacists. ASHP statement on pharmaceutical care. Am J Hosp Pharm 1993;50:1720-3.

2

Odds ratio Figure 2. Odds ratio of combined risk factors.

HT = Hypertension; DM = Diabetes; DYS = Dyslipidemia

In the present study, HT was found to be a major risk factor for the progression of heart failure in 76.6% of cases. This was followed by dyslipidemia, diabetes, smoking, obesity and family history of cardiovascular diseases. Hypertensive patients without diabetes or dyslipidemia had 1.2 times risk of heart failure, whereas patients with both HT and diabetes had 1.7 times risk and patients with HT, diabetes and dyslipidemia had 1.9 times greater risk.

A study done by Verdecchia 2000, had suggested that the risk of developing heart failure is 0.9% in the presence HT but if diabetes and dyslipidemia coexist then the risk of heart failure rises to 5.1%. Although, the contribution of HT in the progression of heart failure is high when compared to other risk factors, the absolute risk in individuals with HT remains low in the absence of other risk factors. HT clusters with other risk factors including hyperglycemia and hyperlipidemia, all of which have been implicated in intimal thickening and worsening after load.13 CONCLUSION Though, the study shows that HT is a common cause for cardiac failure, practitioners need to realize that HT is typically accompanied by other cardiovascular risk factors, especially dyslipidemia and hyperglycemia, and that control of all these factors with appropriate therapy will have a positive effect on progression of heart failure. As a member of the healthcare team, a clinical pharmacist may play a pivotal role in effective

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

10. Gillum RF. Epidemiology of heart failure in the United States. Am Heart J 1993;126(4):1042-7.

11. Wilson PW. An epidemiologic perspective of systemic hypertension, ischemic heart disease, and heart failure.

Am J Cardiol 1997;80(9B):3J-8J. 12. Mitchell GF, Pfeffer JM, Pfeffer MA. The heart and conduit vessels in hypertension. Med Clin North Am 1997;81(6):1247-71.

13. Verdecchia P. Cardiac failure in hypertensive cardiopathy.

Ital Heart J 2000;1 Suppl 2:72-7.

drug review

Role of Phenazopyridine in Urinary Tract Infections op gupta*, kk aggarwal**

Abstract Irritative voiding symptoms, urinary urgency, frequency, nocturia, painful voiding, bladder discomfort or stranguria, are to the urinary tract much as a cough is to the pulmonary system, i.e., they are a nonspecific manifestation of multiple potential underlying causes. Urinary tract infections (UTIs) are usually associated with irritative voiding symptoms, such as painful urination (dysuria), urinary urgency and frequency. Anticholinergic drugs like flavoxate, oxybutynin provide beneficial symptomatic relief. However, they have associated adverse anticholinergic effects, such as dry mouth, which hinders patient compliance. Phenazopyridine hydrochloride acts as a topical analgesic on the mucosal lining of the urinary tract and thus relieves the irritative symptoms associated with UTI. It is compatible with antibiotics and relieves pain during the interval before the antibiotic begins to control the infection. It is well-tolerated as it lacks the anticholinergic side effects of other anticholinergics.

Keywords: Irritative voiding symptoms, anticholinergics, UTI, patient compliance, phenazopyridine hydrochloride

I

rritative voiding symptoms are to the urinary tract much as a cough is to the pulmonary system, i.e., a nonspecific manifestation of multiple potential underlying causes. Similar to the lungs, the urinary bladder responds to a spectrum of pathologic processes with a limited repertoire of symptoms. Irritative symptoms of the lower urinary tract generally refer to urinary urgency, frequency, nocturia, painful voiding, bladder discomfort or stranguria.1 An Internet-based questionnaire found that 20-30% of adults >40 years reported symptoms of urgency, frequency, nocturia or urge incontinence. The study also noted that 5% of men and 8% of women reported bladder pain; painful urination was found in 3% of adults. In addition, patients with the most severe lower urinary tract symptoms (LUTS) had the greatest degree of bother, highest rates of clinical anxiety or depression, and the lowest quality-of-life.2 LUTS are associated with lower urinary tract dysfunction. They can also indicate pathologies other than lower urinary tract dysfunction, such as urinary tract infection (UTI).3 Many patients with indwelling catheter experience catheter cramp. Irritation of the trigone causes detrusor contractions, known as bladder spasms, in these patients. Bladder spasms are a distressing complication for the patient.4 Placement of *Professor, Dept. of Medicine MGIMS, Sevagram, Wardha **Senior Physician and Cardiologist Moolchand Medcity, New Delhi

a ureteral stent after ureteroscopy is a common practice in urology. It has been reported that 38-80% of patients experience stent-related symptoms such as flank pain, lower abdominal discomfort, urinary urgency, urinary frequency, infection.5 Anticholinergic medications provide useful beneficial symptomatic management in these patients.1 Anticholinergics The anticholinergic/antispasmodic drugs are used to relieve cramps or spasms of the bladder6 and to reduce irritative voiding symptoms.7 Anticholinergic drugs reduce detrusor contractions by blocking antimuscarinic receptors in the detrusor.

Since, muscarinic receptors are found in many different organs, urinary antispasmodics are associated with adverse anticholinergic effects, such as blurred vision, dry mouth, constipation, urinary retention, and central nervous system effects such as dizziness, somnolence and headaches.8 The elderly, so also the children, are usually more sensitive to these effects of anticholinergics.6 Flavoxate: A tertiary-amine antimuscarinic, flavoxate is used for its antispasmodic properties in the symptomatic treatment of many urological conditions including overactive bladder and incontinence.

Randomized studies9,10 and one Cochrane review7 have found flavoxate to be no better than placebo for urge incontinence. Given the lack of demonstrated effect of flavoxate in placebo-controlled studies it is

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

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Drug Review difficult to recommend its use and it is definitely not a first-line treatment. Bilateral acute angle closure glaucoma following flavoxate administration has been reported.11 Briggs and associates reported essentially no effect of flavoxate in elderly patients with detrusor hyperreflexia.12 Oxybutynin: Oxybutynin is a tertiary-amine with anticholinergic, antispasmodic and local anesthetic properties.13 Its usefulness is however limited by classic antimuscarinic side effects. Dry mouth is the most common and bothersome complaint, followed by constipation, blurred vision, dry eyes, urinary retention and drowsiness. These adverse effects, particularly dry mouth, are often severe enough to cause poor patient compliance, suboptimal dosing and even drug discontinuation.14 The mean pharmacokinetic parameters (i.e., Cmax and AUC) of oxybutynin may be altered when co-administered with antibiotics like macrolides (erythromycin, clarithromycin). These drugs should therefore be used together with caution.15 Oxybutynin was no better than placebo in patients with bladder spasm after transurethral surgery16 or for the treatment of incontinence in the presence of detrusor instability in elderly institutionalized people.17 Clinically, oxybutynin appears more potent in causing dry mouth than in inhibiting detrusor instability.14 Role of phenazopyridine Phenazopyridine hydrochloride is an azo dye with local analgesic and anesthetic effects on the urinary tract.18 Chemically, phenazopyridine is 2,6-Pyridinediamine, 3-(phenylazo), monohydrochloride.19 It is used as a urinary tract antiseptic and analgesic as brief adjuvant therapy for treatment of UTI. Additionally, the drug is used for many urologic problems involving dysuria.20

Clinical Pharmacology The exact mechanism of action of phenazopyridine hydrochloride is not known. It is excreted in the urine, where it exerts a topical analgesic effect on the mucosa of the urinary tract. This action helps to relieve pain, burning, urgency and frequency. Phenazopyridine has no antimicrobial actions.

Phenazopyridine exerts its clinical effect in conditions of urinary bladder hypersensitivity by direct inhibition

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

Table 1. Pharmacokinetics: Salient Features  



Half-life: 7.35 hours.22 Metabolism: Mainly metabolized by hydroxylation;23 the extent of azo bond cleavage is low. 5-hydroxyl PAP is the major metabolite (48.3% of the dose).24 Excretion: Rapidly excreted by the kidneys directly into the urine (65% of the drug is excreted unchanged into the urine); about 40% is excreted in the bile.23 Major urinary metabolites: 4-acetylaminophenol (NAPA) followed in order by 5,4’-dihydroxy-PAP, 5-hydroxy-PAP, 4’-hydroxy-PAP and 2’-hydroxy-PAP.24

of the mechanosensitive Aδ fibers as demonstrated by Aizawa et al in their study. They evaluated the effect of phenazopyridine on afferent nerve activity by direct measurement of both Aδ- and C-fibers, and compared the outcome with the effects of a local anesthetic (lidocaine) and of an analgesic (acetaminophen).

Intravenous administration of phenazopyridine was found to significantly decrease dose-dependently only the Aδ-fiber but not the C-fiber activity. Acetaminophen significantly decreased only Aδ-fiber activity, but it was not dose-dependently completely. Lidocaine inhibited both the Aδ- and C-fiber activities.21 Table 1 describes the salient pharmacokinetic properties of phenazopyridine.

Phenazopyridine Efficacy: Clinical Evidence Phenazopyridine hydrochloride acts as a topical analgesic on the mucosal lining of the urinary tract and thus relieves pain, burning, urgency and frequency.19 

Phenazopyridine relieves symptoms of urogenital infections: A study was done on 118 cases of urogenital infections with symptoms of pain on urination, burning, frequency and nocturia.

The patients were administered phenazopyridine 500 mg in dose of two tablets thrice-daily. In 65 (55.1%) cases, all the characteristic symptoms of urogenital infections were relieved: Pain on urination was alleviated or abolished in 95.3%; burning on urination was relieved in 93.6%; frequency decreased in 85%, nocturia was eliminated or reduced in 83.7%, with reduction the organized sediment. In the remaining 53 cases, symptomatic relief was also observed in all but a few, although, there was no concomitant reduction in the organized urinary sediment. No toxic effects from phenazopyridine were observed during the two weeks of its administration.25

Drug Review 

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Phenazopyridine is very useful as adjuvant to antimicrobial therapy in uncomplicated UTIs: Phenazopyridine when administered along with antibiotics is efficacious as short-term analgesic in the treatment of uncomplicated UTIs (uUTIs) as shown in a randomized, open label study.

Phenazopyridine, when given with antibiotics such as ciprofloxacin, doxycycline within 48 hours of diagnosis, resulted in marked reduction in urinary symptoms of burning micturition (91%) and pain during voiding of urine (89%).23 Phenazopyridine co-administration enhances ciprofloxacin bioavailability: A study compared the pharmacokinetic behavior of ciprofloxacin administered alone versus ciprofloxacin plus phenazopyridine. While there were no differences between the two treatments in terms of peak plasma concentration (Cmax) and elimination constant (ke), area under the concentration-time curve to last measurable concentration (AUCt) and area under the concentration-time curve extrapolated to infinity (AUC∞) were 35% and 29% higher, respectively, in the combined treatment arm.

In addition, a significant delay in tmax (from 1 to 1.5 hours) and a statistical increase of 29% in mean residence time (MRT) were also observed in the combination group. The study concluded that phenazopyridine, when given together with antibiotic (ciprofloxacin) enhances its bioavailability with regard to the amount absorbed and MRT in the body, which is beneficial during treatment.26 Phenazopyridine does not alter efficacy of sulfonamides against uropathogenic bacteria: Phenazopyridine is widely used as an adjunct to sulfonamides in the treatment of bacterial UTIs and has been shown not to alter the effectiveness of sulfonamides (sulfacytine, sulfisoxazole and sulfamethoxazole) against uropathogenic bacteria.27 The combined bacteriostatic activity of sulfonamide compounds and phenazopyridine upon Balantidium coli has also been demonstrated earlier by Neter and Loomis.27,28 When used along with an antibiotic for the treatment of a UTI, phenazopyridine should not be given for more than two days as there is insufficient data to support benefits of administration beyond this time period.19 Phenazopyridine relieves pain due to bladder spasms: Indwelling urinary catheters can cause severe pain and discomfort and can impair a

person’s quality-of-life. A catheter is a foreign body and its presence may trigger bladder spasm and pain.29 Phenazopyridine helps to relieve the pain caused by catheters.4 

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Phenazopyridine relieves postoperative ureteral stent discomfort: Stent placement after ureteroscopy results in considerable morbidity in the form of irritative lower urinary tract symptoms.30 Norris et al published their findings of a small but well-conducted double-blind, placebo-controlled study comparing ER oxybutynin, phenazopyridine and placebo in patients who had a stent place after ureteroscopy. Each of 60 patients who received a unilateral stent after ureteroscopy was given a blister pack containing 21 unmarked capsules of either extended-release oxybutynin 10 mg, phenazopyridine 200 mg or placebo in a prospective, randomized and double-blinded fashion. Patients were instructed to take 1 capsule 3 times daily immediately after the procedure.

Patients were given 50 tablets of oral narcotic to be taken as needed. Assessment tools included a questionnaire for stent symptoms, visual analog scale scores and requirement of narcotic medications. Results did not show differences for flank pain, suprapubic pain, urinary frequency, urgency and dysuria.

The phenazopyridine group reported less hematuria on postoperative Day 1 when compared with placebo, which was statistically significant.5 Phenazopyridine relieves autonomic dysreflexia associated with cystitis: Autonomic dysreflexia (AD) in individuals with spinal cord injury and other neurologic disorders is due to a genitourinary cause 81-87% of the time. Urinary bladder distension due to urinary retention, blocked catheters or of defective catheter tubing or drainage bags is the commonest precipitant. UTIs can also induce AD, albeit not as commonly as bladder distension.31 Phenazopyridine is useful in the management of AD associated with cystitis as documented by Paola and coauthors.32

Conclusion 

Irritative voiding symptoms occur with a high prevalence in the general population1 and can greatly affect patients’ quality-of-life. These symptoms can be a source of great discomfort, embarrassment and loss of confidence, causing withdrawal from social life and affecting physical and mental health.33 UTIs are usually associated

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with irritative voiding symptoms, such as painful urination (dysuria), urinary urgency and frequency.

3.

Takeda M, Araki I, Kamiyama M, Takihana Y, Komuro M, Furuya Y. Diagnosis and treatment of voiding symptoms.

Urology 2003;62(5 Suppl 2):11-9.

Anticholinergic drugs are widely used in clinical practice to reduce irritative voiding symptoms.7

4.

Sulzbach LM. Ask the experts. Crit Care Nurse 2002;22(3):84-7.

5.

Norris RD, Sur RL, Springhart WP, Marguet CG, Mathias BJ, Pietrow PK, et al. A prospective, randomized, doubleblinded placebo-controlled comparison of extended release oxybutynin versus phenazopyridine for the management of postoperative ureteral stent discomfort.

Urology 2008;71(5):792-5.

6.

Kulkarni SK. Antispasmodics – A new perspective.

JAMA India 2001;4(8):119-21.

7.

Roxburgh C, Cook J, Dublin N. Anticholinergic drugs versus other medications for overactive bladder syndrome in adults. Cochrane Database Syst Rev 2007;(3): CD003190.

8.

Therapeutic Class Review Urinary Antispasmodics http://ovha.vermont.gov/advisory-boards/urinaryantispasmodics.3.09.pdf.

9.

Chapple CR, Parkhouse H, Gardener C, Milroy EJ. Double-blind, placebo-controlled cross-over study of flavoxate in the treatment of idiopathic detrusor instability. Br J Urol 1990;66(5):491-4.

Anticholinergics/Antispasmodics help relieve dysuria and provide relief from bladder spasms.

Optimal control is obtained if both infection and bladder spasms are treated simultaneously.34 Urinary antispasmodics such as oxybutynin and flavoxate are muscarinic receptor antagonists and exert beneficial direct relaxant effect on smooth muscle of the urinary tract. But they have high incidence of side effects, predominantly dry mouth, which is a major disadvantage leading to poor patient compliance and discontinuation of treatment.

The lack of demonstrated effect of flavoxate in placebo-controlled studies makes it difficult to recommend the use of flavoxate and it is definitely not a first-line treatment.11 Clinically, oxybutynin appears more potent in causing dry mouth than in inhibiting detrusor instability, which precludes its use.14 Also, drug interactions are known to occur when co-administered with antibiotics like macrolides.

Phenazopyridine is a urinary tract analgesic, which is used to treat symptoms of dysuria,34 while the patient is awaiting medical evaluation and treatment.35 When taken orally, majority of the drug enters the urine unchanged, where it acts as a topical analgesic within the bladder.34 Phenazopyridine is also frequently used for adjunctive treatment of pain associated with UTIs in addition to antibiotics aimed at the underlying microbial infection.35 It relieves pain and discomfort during the interval before antibiotic therapy begins to control the infection.19 Most doctors prefer to use phenazopyridine as a first choice drug in dysuria.

References 1.

Guralnick ML, O’Connor RC, See WA. Assessment and management of irritative voiding symptoms. Med Clin North Am 2011;95(1):121-7.

2.

Coyne KS, Sexton CC, Thompson CL, Milsom I, Irwin D, Kopp ZS, et al. The prevalence of lower urinary tract symptoms (LUTS) in the USA, the UK and Sweden: results from the Epidemiology of LUTS (EpiLUTS) study. BJU Int 2009;104(3):352-60.

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10. Dahm TL, Ostri P, Kristensen JK, Walters S, FromodtMøller C, Rasmussen RB, et al. Flavoxate treatment of micturition disorders accompanying benign prostatic hypertrophy: a double-blind, placebo-controlled multicenter investigation. Urol Int 1995;55(4):205-8.

11. Mohammed ZS, Simi ZU, Tariq SM, Ali KR. Bilateral acute angle closure glaucoma in a 50 year old female after oral administration of flavoxate. Br J Clin Pharmacol 2008;66(5):726-7.

12. Briggs RS, Castleden CM, Asher MJ. The effect of flavoxate on uninhibited detrusor contractions and urinary incontinence in the elderly. J Urol 1980;123(5): 665-6.

13. Kirkali Z, Whitaker RH. The use of oxybutynin in urological practice. Int Urol Nephrol 1987;19(4):385-91.

14. Lai HH, Boone TB, Appell RA. Selecting a medical therapy for overactive bladder. Rev Urol 2002;4 Suppl 4:S28-37.

15. Oxybutynin chloride extended release tablets. http:// www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4295b_ 02_05_Ditropan%20XL%202004%20Label.pdf.

16. Wein AJ, Hanno PM, Raezer DM, Benson GS. Effect of oxybutynin chloride on bladder spasm following transurethral surgery. Urology 1978;12(2):184-6.

17. Zorzitto ML, Holliday PJ, Jewett MA, Herschorn S, Fernie GR. Oxybutynin chloride for geriatric urinary dysfunction: a double-blind placebo-controlled study.

Age Ageing 1989;18(3):195-200.

Drug Review 18. Iqbal J, Gupta A, Husain A. Photochemistry of phenazopyridine hydrochloride. Pharmazie 2006;61(9): 747-50.

27. Heifetz CL, Fisher MW. Phenazopyridine-sulfonamide combination antibacterial therapy in mice. Antimicrob Agents Chemother 1973;3(1):134-5.

19. Pyridium drug description. Available at: www.rxlist.com.

28. Neter E, Loomis TA. The combined bacteriostatic activity of sulfonamide compounds and pyridium upon B. coli in vitro. Urol Cutan Rev 1941;45:295-7.

20. Gaines KK. Phenazopyridine hydrochloride: the use and abuse of an old standby for UTI. Urol Nurs 2004;24(3):207-9.

21. Aizawa N, Wyndaele JJ. Effects of phenazopyridine on rat bladder primary afferent activity, and comparison with lidocaine and acetaminophen. Neurourol Urodyn 2010;29(8):1445-50.

22. Thomas BH, Whitehouse LW, Solomonraj G, Paul CJ. Metabolism and disposition of phenazopyridine in rat.

Xenobiotica 1993;23(2):99-105.

23. Deepalatha C, Deshpande N. A comparative study of phenazopyridine (pyridium) and cystone as short-term analgesic in uncomplicated urinary tract infection. Int J Pharm Sci 2011;3 Suppl 2:224-6.

24. Thomas BH, Whitehouse LW, Solomonraj G, Paul CJ. Excretion of phenazopyridine and its metabolites in the urine of humans, rats, mice and guinea pigs. J Pharm Sci 1990;79(4):321-5.

25. Kirwin TJ, Lowsley OS, Menning J. The effects of pyridium in certain urogenital infections. Am J Surg 1943;62(3):330-5.

26. Marcelín-Jiménez G, Angeles AP, Martínez-Rossier L, Fernández SA. Ciprofloxacin bioavailability is enhanced by oral co-administration with phenazopyridine: a pharmacokinetic study in a Mexican population. Clin Drug Investig 2006;26(6):323-8.

29. Nazarko L. Bladder pain from indwelling urinary catheterization: case study. Br J Nurs 2007;16(9): 511-2, 514.

30. Nabi G, Cook J, N’Dow J, McClinton S. Outcomes of stenting after uncomplicated ureteroscopy: systematic review and meta-analysis. BMJ 2007;334(7593):572.

31. Shergill IS, Arya M, Hamid R, Khastgir J, Patel HR, Shah PJ. The importance of autonomic dysreflexia to the urologist. BJU Int 2004;93(7):923-6.

32. Paola FA, Sales D, Garcia-Zozaya I. Phenazopyridine in the management of autonomic dysreflexia associated with urinary tract infection. J Spinal Cord Med 2003;26(4):409-11.

33. Rovner ES, Gomes CM, Trigo-Rocha FE, Arap S, Wein AJ. Evaluation and treatment of the overactive bladder. Rev Hosp Clin Fac Med Sao Paulo 2002;57(1): 39-48.

34. Radiation therapy: Toxicities and management. Chapter 14. In: Cancer Nursing Principles and Practice. Connie Henke Yarbro, Debra Wujcik, Barbara Holmes Gobel (Eds.), 7th edition, Jones and Bartlett Publishers, LLC 2011:p.338.

35. Shi CW, Asch SM, Fielder E, Gelberg L, Nichol MB. Consumer knowledge of over-the-counter phenazopyridine. Ann Fam Med 2004;2(3):240-4.

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review article

Clinical Safety and Efficacy of Pilex Tablets and Ointment in the Management of Hemorrhoids Dibyendu Gautam*, Manasi Basu Banerjee**, Shib Shankar Roy Chowdhury†, jaydev Pramanik‡

Abstract Hemorrhoids are an abnormal swelling of the blood vessels in the anal canal; treatment is indicated only when they become symptomatic. Conservative treatment typically consists of increasing dietary fiber, oral fluids to maintain hydration, nonsteroidal anti-inflammatory drugs (NSAIDs), sitz baths and rest. Surgery is indicated when conservative treatment fails; but, the results are often unsatisfactory and recurrence may occur. However, in the general management of hemorrhoids, colorectal surgeons agree that severe painful thrombosed hemorrhoids should be excised. The main ingredients of Pilex tablet are Terminalia chebula, Cassia fistula, Emblica officinalis, which improve appetite, correct hepatic function and have mild laxative properties thereby facilitating bowel evacuation and reducing local trauma to the hemorrhoidal vessels. The main ingredients of Pilex ointment are Mimosa pudica, Vitex negundo, Eclipta alba and Solanum nigrum. These herbs possess styptic and antiinflammatory properties and help in regeneration of the vascular endothelium. Pilex tablets orally and ointment locally have been very favorably reported for the amelioration and treatment of piles in various clinical trials and also established by a large number of clinicians and surgeons. This review summarizes the effects of the polyherbal formulations Pilex tablets and ointment in patients of hemorrhoids.

Keywords: Pilex tablets, Pilex ointment, hemorrhoids

H

emorrhoids, or piles, as they are commonly known as, have plagued humankind since ancient times. On the day of the decisive battle at Waterloo, Napoleon Bonaparte was in pain because of a severe case of thrombosed hemorrhoids, which impaired his battlefield conduct.1 Hemorrhoids are an abnormal swelling in the blood vessels in the anal canal. The most common symptom is bright red blood in stool. Other symptoms range from itchiness, pain, swelling, protrusion, bleeding, constipation and difficulty evacuating, to large fungating masses or prolapsed piles.2 These symptoms occur due to a vicious circle of events. Vascular, submucosal cushions protrude through a tight anal canal, become further congested by the sphincter and hypertrophy so that they then protrude more easily. Management of hemorrhoids is directed at breaking this circle.

There are two types of hemorrhoids, external and internal, according to their position with respect to the dentate line.3 The internal hemorrhoids develop within *Professor, Dept. of Surgery **Associate Professor, Dept. of Pharmacology †Associate Professor, Dept. of Surgery Medical College and Hospital, Kolkata ‡Ayurvedic Consultant Kawagachhi Gramin Health and Research Centre, Parganas, West Bengal Address for correspondence Prof. Dibyendu Gautam, Dept. of Surgery Medical College and Hospital, Kolkata, West Bangal E-mail: drdivyendu@gmail.com

the anus beneath the lining. An internal hemorrhoid can cause severe pain if it is completely prolapsed.4 The external hemorrhoids develop near the anus and are covered by very sensitive skin. If a blood clot (thrombosis) develops in an external hemorrhoid, it becomes a painful, hard lump and may bleed if it ruptures.5 Internal hemorrhoids are classically divided into four categories (I-IV) based on the degree of prolapse. Recently, it has been suggested that it is more appropriate to classify them on the basis of presence or absence of bleeding or prolapse.6 The prevalence of symptomatic hemorrhoids ranges from 4.4% in the general population to 36.4% in general practice.7 The pathophysiology is not completely understood other than that structural and vascular changes are involved.8 A detailed history is important.

Besides the routine physical examination (visual inspection of the anal region, digital examination, anoscopy), patients <50 years should undergo a flexible sigmoidoscopy. Colonoscopy is recommended for patients >50 years, patients of any age with bleeding and anemia, those with persistent bleeding despite medical therapy, select patients with significant family history of colorectal malignancy and those with other symptoms such as abdominal pain and bloating and diarrhea.9 Treatment is only indicated if they become symptomatic. But, colorectal surgeons agree that all painful thrombosed hemorrhoids should be excised.

Conservative treatment typically consists of increasing

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review article dietary fiber, oral fluids to maintain hydration, analgesics, sitz baths and rest.3 Increased fiber intake improves outcomes.10 There is scant evidence to support use of topical agents and suppositories for treatment.3 Steroid-containing agents should not be used for >14 days as they may cause thinning of the skin.3 Hemorrhoidectomy is indicated for large thirdand fourth-degree hemorrhoids, mixed hemorrhoids with a prominent external component and incarcerated internal hemorrhoids requiring urgent intervention.

Hemorrhoids that fail to respond to medical management may be treated with rubber band ligation, sclerosis and thermotherapy. Rubber band ligation has been demonstrated to be the most effective method to treat symptomatic internal hemorrhoids that have failed conservative management.11-14 Complications of this procedure include vasovagal response, anal pain, bleeding from early dislodgment and pelvic sepsis.15 This review summarizes six clinical studies wherein Pilex tablets and ointment were evaluated in hemorrhoids.

against Staphylococcus aureus.23 It is useful in viral hepatitis, premature atherosclerosis, anemia, acne, fistula, etc.24 

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Pilex Tablet and its Pharmacology Pilex tablets contains various herbs: Their pharmacological actions are as described below.

Pharmacological Actions of Principal Herbs 

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Balsamodendron mukul (Syn. Commiphora mukul): The guggulusterone fraction showed antiinflammatory activity, comparable to approximately one-fifth that of hydrocortisone and equal to phenylbutazone and ibuprofen.16 Shilajeet (Purified): It has been used as antiinflammatory agent. Results of its use in diabetes, fever, anemia, anorexia, spasmodic pain, obesity, abdominal disorders and skin diseases have been documented. It also has cardiotonic activity.17,18

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Emblica officinalis: It has antiviral, antibacterial and antiallergic activities and is rich in phenols.

The aqueous extract has antibacterial activity

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Terminalia belerica: It has hepatoprotective action.26 Being one of the ingredients of Triphala, T. belerica also has gastroprotective and laxative properties.27 Cassia fistula: It is used in conditions of hematemesis, pruritus, leukoderma, diabetes and other common dermatological infestations, inflammatory disorders and constipation.28 C. fistula pod infusion has been safely utilized as a laxative and as a substitute for the official Senna.29 Bauhinia variegata: It has laxative, antibacterial, blood purifying, antioxidant, antitumor and hepatoprotective properties.30,31 Mesua ferrea: It has potent broad-spectrum antimicrobial actions.32 Its astringent and styptic actions are useful in bleeding piles.33

Pilex Ointment and its Pharmacology Pilex ointment is a herbomineral formulation. The synergistic actions of constituent herbs reduce varicosities of venous plexus in hemorrhoids. 

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Melia azadirachta (Syn. Azadirachta indica): The leaves and bark have antimicrobial, antifungal, anthelmintic, insecticidal, antiviral, antipyretic and anti-inflammatory activities. It has been used in inflammatory gum diseases, boils, sores, measles, small pox and other cutaneous infections.19,20 Berberis aristata: The extract has bitter, cholagogue, antidiarrheal, stomachic, laxative, antipyretic and antiseptic activities. It also has anti-inflammatory, hypotensive and antiamebic activities.21 The laxative activity is useful in hemorrhoids.22

Terminalia chebula: It has antibacterial, antifungal activity against many dermatophytes and enhances immunity. It also has antispasmodic and potent wound healing activities. It is widely prescribed in constipation, ulcer, gastroenteritis, cough, hemorrhoids and other skin diseases.25

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Mimosa pudica: It’s astringent and styptic actions are useful in bleeding piles.34 Eclipta alba: It has anti-inflammatory and analgesic activities.35 Vitex negundo: It’s potent broad-spectrum antimicrobial action prevents secondary microbial infection.36 V. negundo also has potent and directly dose-dependent analgesic, strong antihistamine activity (which helps to control associated itching), membrane stabilizing and antioxidant activities.37,38 Anti-inflammatory activity due to triterpenoids and antihistamine activity have been demonstrated.39 Calendula officinalis: It has anti-inflammatory and analgesic activities and accelerates wound healing by epithelial regeneration.40 C. officinalis improves network of basal membrane collagenous substance, which re-normalizes the capillary membranes resistance. It subsequently induces reduction in the hemorrhoidal mass of the dilated veins of hemorrhoidal plexus.40 It also has potent free radical scavenging activities.41

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Cinnamomum camphora: It has analgesic activity and relieves pain by reducing sensitivity of the brain or nervous system to pain.42 It accelerates wound healing by epithelial regeneration and has potent broad-spectrum antimicrobial actions43 including free radical scavenging activities.44 Tankana: Its potent broad-spectrum antimicrobial actions prevent secondary microbial infections.45 Yashada Bhasma: It has potent anti-inflammatory and analgesic actions and accelerates wound healing by epithelial regeneration.46

Clinical Studies of Pilex Tablet and Ointment Pilex has been put to stringent safety and tolerability evaluation. Six clinical studies are summarized below.

Study 1: Indigenous drug therapy for hemorrhoids47 Material and methods: The study included 100 patients with first- and second-degree uncomplicated hemorrhoids. Fifty patients were given a placebo; the remaining 50 patients were given Pilex therapy.

Bleeding was the most common symptom in all the patients, followed by pain during/after defecation (92%) and mucus discharge (72%). A detailed history including digital examination and proctoscopy was done to exclude other causes of bleeding per rectum. Initially, Pilex tablets were given in a dose of two tablets thricedaily for 1 week, followed by two tablets twice-daily for 4 weeks. A maintenance dose of one tablet twicedaily was given till symptomatic relief was obtained.

Pilex ointment was used in all as a supplement.

Conclusion: Treatment with Pilex was highly satisfactory; it was unsatisfactory in the placebo group.

Study 2: Pilex versus Daflon in hemorrhoids48 Material and methods: Thirty patients with Grades I, II and III of internal and external hemorrhoids were included in the trial. Patients with evidence of rectal prolapse, malignancy and systemic debilitating illness were excluded from the trial. All the patients were subjected to history taking and physical examination including digital examination and proctoscopy. Patients were divided into two groups of 15 each. Group A patients received Pilex tablets, two tablets thrice-daily after meals for 1 week, followed by two tablets twicedaily for 5 weeks. All the patients were advised to apply Pilex ointment twice-daily before and after evacuation of the bowel. Group B patients received Daflon tablets one tablet thrice-daily for 6 weeks. All the patients were examined at weekly intervals of six weeks for subjective evaluation, which was graded with scores: 1 - Mild relief, 2 - Moderate relief and 3 - Complete relief. Objective evaluation was done at the beginning and at six weeks at end of study.

Results Group A: Patients treated with Pilex tablet and ointment. 

Results 

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Pilex Group: Fifty percent showed remarkable improvement in the form of complete cessation of bleeding, pain and discharge. Proctoscopy in these patients revealed significant shrinkage of the pile masses and improvement in hemoglobin.

Good response in the form of marked regression of bleeding, pain and discharge was seen in 26% of cases. The shrinkage of pile mass was to a lesser extent in these patients. Poor response, either subjectively or objectively, was seen in 24%.

Placebo Group: In first-degree hemorrhoids, improvement was seen only in 20%. Ten percent showed some improvement in symptoms with some shrinkage of pile masses and reduction in discharge. Remaining 70% had a poor subjective or objective response in the follow-up period of six months. Several of them later switched over to some other form of therapy like injection and surgery as they were unwilling to continue.

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Grade I: Pilex tablet and ointment was found very effective in controlling bleeding. About 90% of patients reported complete recovery; on proctoscopy after four weeks of treatment, the mucosa was normal. Bleeding was checked within 2-3 weeks of treatment. Shrinkage in piles gradually occurred over 3-4 weeks in 80%.

Grade II: Moderate reduction in size and inflammation on hemorrhoidal mass; bleeding was controlled in over 90% of cases.

Grade III: Mild reduction in size and inflammation of hemorrhoid mass. But, bleeding stopped within four weeks of treatment.

Group B: Patients treated with Daflon 

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Grade I: More than 90% of patients responded in terms of bleeding per rectum. There was a mild decrease in size and inflammation of pile mass.

Grade II: Bleeding was controlled in >90% of cases.

Minimal to mild reduction in size and inflammation of mass was reported after 4-6 weeks of treatment.

Grade III: Effective in controlling bleeding; minimal change in size and inflammation was reported.

Conclusion: Daflon tablets and Pilex tablet and ointment are equally effective in controlling bleeding,

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review article irrespective of the grade of hemorrhoids. Bleeding was checked in both the groups over a period of 2-3 weeks.

Pilex tablet and ointment are better than Daflon tablet in reducing inflammation and size of hemorrhoidal mass in Grades I and II. Pilex tablet and ointment induced complete remission in most cases with Grade I hemorrhoids. They also had better efficacy in reducing pain than Daflon, in terms of early recovery.

Study 3: Role of Pilex tablets and ointment in the treatment of piles and fissures49 Material and methods: One hundred eight cases of piles, with/without anal fissures, were treated with a combination of Pilex tablets and Pilex ointment for six weeks; for the first two weeks with 2 tablets of Pilex thrice-daily orally and Pilex ointment applied locally twice-daily (at bedtime and in the morning after defecation). For the next four weeks, the dose of the tablets was reduced to one tablet thrice-daily and the application of ointment was continued as earlier.

Patients with other associated conditions like fistula-inano and anorectal growths were excluded. Every week, the patients were assessed regarding subjective feeling, symptomatic improvement, proctoscopic assessment of the size of the pile mass and complications, if any.

Bleeding at the time of defecation was the predominant symptom, followed by pain and heaviness in the anorectal region (n = 81).

Results: Eighty-two cases of piles of all degrees and 26 cases of fissure-in-ano were treated with Pilex tablets and ointment. Almost all patients reported subjective improvement within a week of starting treatment.

An objective improvement was found in all cases of fissures and in most cases of piles.

Conclusion: In early cases of piles and fissure-in-ano, Pilex tablets and ointment constitute a good alternative to surgery. Even in late cases, when surgery is contraindicated, or is to be postponed, this conservative regimen can provide adequate remission for a relatively longer period.

were completely relieved from bleeding; four cases (13.3%) showed improvement and only two cases (6.7%) reported no improvement. Mucous discharge and perineal pain was completely relieved in 60% and 80% cases, respectively. Three cases (10%) showed complete disappearance of piles and reduction in pile mass was observed in 21 cases (70%). There was no change at all in six cases (20%). Symptomatic relief was noted from 2nd week after the start of therapy and was dramatic at the end of eight weeks.

In second-degree hemorrhoids, response to Pilex therapy was also good. Bleeding completely stopped in 10 cases (66.6%), improved in three cases (20%) and continued in two cases (13.4%). Six (40%) out of total 15 cases showed complete relief of prolapse of the pile mass. Sixty percent showed reduction in the size of piles and one case (6.6%) had complete reduction of pile mass. Discharge and perineal pain were also relieved in 57.1% and 60% of cases, respectively.

Symptomatic relief was observed from 3rd week after the start of therapy and was remarkable at the end of eight weeks.

In five cases of third-degree hemorrhoids, response to Pilex therapy was satisfactory and a notable change was found in the relief of symptoms. One case showed complete relief from prolapse; three cases showed improvement and only one case reported no improvement. Forty percent of patients showed complete relief from bleeding probably due to relief of congestion, reduction in prolapse and size of pile mass.

One patient had recurrence, who presented after six months; but was relieved after a further 30-day therapy with Pilex tablets and Pilex ointment.

Conclusion: Most cases showed complete relief from bleeding probably due to relief of congestion, reduction in prolapse and size of pile mass with Pilex therapy.

Study 5: Clinical trial of Pilex tablets and ointment in the treatment of hemorrhoids51

Material and methods: Fifty patients were studied.

Each patient irrespective of degree of hemorrhoids was treated with Pilex tablets (2 tablets thrice-daily) and Pilex ointment (applied twice-daily) simultaneously for eight weeks.

Material and methods: Fifty patients with bleeding per rectum who had piles, mainly first- and second-degree and a few third-degree were recruited. Patients were grouped into the following three: First-degree (congested blood vessels, but no prolapse), second-degree (prolapsed on straining but, regressed spontaneously) and third-degree (continuously prolapsed). All patients were subjected to Pilex therapy with both tablets and ointment from the day of attendance for six weeks in the following schedule:

Results: Thirty cases of first-degree of piles showed very good response to Pilex therapy; 24 cases (80%)

Dose: Pilex tablet; two tablets thrice-daily for 1 week or till symptomatic relief (usually 2-3 weeks) followed by

Study 4: Pilex therapy in the treatment of hemorrhoids50

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

review article one tablet thrice-daily for the rest of the course. Pilex ointment applied per rectum at least thrice a day.

Follow-up: Every week for six weeks; fortnightly for three months and then monthly for rest of the trial period (upto 1 year) or as deemed necessary.

All 10 females and 20 males had constipation and used some laxatives in the form of drugs or diet. These patients were prescribed easily digestible high residue diet and antianemic supportive therapy. If there was no response after a full course of six weeks, a gap of two weeks was allowed and then Pilex course was repeated. A total of 4-5 such courses were tried before declaring trial cases as failed. Failed trial cases were subjected to other forms of treatment, mainly surgical.

Results 







Out of 42 Group ‘A’ cases classified (Good), 33 were first-degree piles and nine were early seconddegree piles, all of them were symptom-free after Pilex therapy during the follow-up period.

Group ‘B’ cases with (Fair) response consisted of two first-degree and three second-degree piles.

During follow-up, they had mild recurrence of symptoms usually at 4-6 weeks after the first course and required another course of Pilex therapy.

During the rest of the follow-up period they were symptomless.

All Group ‘C’ cases classified as (Poor) were thirddegree piles with long history and were subjected to operative treatment; Pilex therapy gave them temporary relief from symptoms.

Forty-two cases had disappearance of all symptoms and no relapse. Fair results i.e., symptoms persisted slightly and required further course of Pilex, were noticed in five cases. Failed trial cases, 3 in number, required surgical intervention. There were no toxic or side reactions in any case.

Conclusion: Eighty-four percent of first-degree and early second-degree piles remained symptom-free in the 1-year follow-up period. This study had 50 cases.

An extensive study with prolonged follow-up is required for definite assessment of Pilex therapy in piles.

Study 6: Clinical trial of Pilex combination therapy in the treatment of hemorrhoids52 Material and methods: This study included 60 cases of internal piles. All patients had bleeding (100%); 34 cases had constipation (55.6%), 26 had discomfort or pain (43.3%), 16 had itching (26.6%) and only 12 had discharge (20%) as a presenting symptom. Twentyfive cases had already received some form of medical

treatment; of these, five cases had received injections for piles. Pilex tablets were given in the dose of two tablet t.i.d. for 4 weeks followed by one t.i.d. for 2 months along with local application of Pilex ointment b.i.d.

Results: At the end of 6-8 weeks, bleeding completely stopped in 51 cases (85%) and diminished in the remaining nine cases (15%); constipation was completely checked in 22 (64.7%), diminished in 10 (29.4%) and remained the same in 2; pain or discomfort was relieved in 15 (57.6%), diminished in nine (34.6%) and remained the same in 2; itching was relieved in 10 (62.5%), decreased in five and remained the same in 1; discharge was relieved in eight (66.6%), diminished in 3 and remained the same in one. Proctoscopic examination also showed control of congestion and reduction in pile masses.

Conclusion: Combination treatment with Pilex tablets and ointment gives excellent results in all cases of firstdegree piles (100%) and in 15 cases of second-degree piles (75%). Three cases of second-degree piles, three cases of third-degree showed good response and three cases of third-degree showed fair response. Only three cases of third-degree piles showed poor response. No local or general side-effects or toxicity were observed with Pilex combination therapy in our study.

Summary and conclusion of the review Hemorrhoids are a common anorectal disorder worldwide. Avoidance of constipation is key in treating hemorrhoids. Most patients can be effectively treated with fiber supplementation and local ointments. Surgery is indicated in patients with acute complications or those in whom conservative treatment has failed. Pilex tablet and ointment, a polyherbal formulation, has been extensively studied and has been found to be safe and effective in patients suffering from hemorrhoids.

Pilex tablet has beneficial effects due to the synergistic activity of its potent constituent herbs. The antiinflammatory action reduces swelling of hemorrhoidal tissue and expedites healing; its styptic action controls bleeding. It also has antimicrobial, antifungal, anthelmintic, insecticidal, antiviral, antipyretic, laxative, antipruritic, blood purifying and antioxidant activity.

Pilex ointment has useful astringent and styptic actions; the anti-inflammatory, analgesic, membrane stabilizing activities and strong antihistamine activity help to control associated itching, accelerate wound healing. It improves the network of basal membrane collagenous substance, which leads to re-normalization of the capillary membranes resistance and reduction in

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

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review article hemorrhoidal mass of the dilated veins of hemorrhoidal plexus. Results of the clinical studies reviewed show rapid and effective relief in symptoms like shrinkage of hemorrhoidal mass, control of bleeding per rectum, relief from itching, reduction of pain and discomfort during defecation, relief from constipation, control of secondary infection and recurrence and clinical improvement in local condition. Pilex combination therapy is safe and effective in the management of uncomplicated early hemorrhoids as was shown in the substantial sample size of the patients reviewed.

24. Asolkar LV, et al. Second supplement to glossary of Indian Medicinal Plants with active principles. CSIR. Govt. of India: New Delhi 1992:p.291-2.

References

30. Asolkar LV, et al. Second supplement to glossary of Indian Medicinal Plants with active principles. CSIR, Govt. of India: New Delhi 1992:p.113-4.

1.

Welling DR, et al. Dis Colon Rectum 1988;31(4):303-5.

2.

Tse GN. Can Fam Physician 1988;34:655-9.

3.

Lorenzo-Rivero S. Am Surg 2009;75(8):635-42.

4.

Hosking SW, et al. Lancet 1989;1(8634):349-52.

5.

Johansen K, et al. JAMA 1980;244(18):2084-5.

6.

Abcarian H, et al. Am J Gastroenterol 1994;89(Suppl 8): S182-93.

7.

Abramowitz L, et al. Gastroenterol Clin Biol 2001;25 (6-7):674-702.

8.

Beck DE. Hemorrhoidal disease. In: Fundamentals of anorectal Surgery. Beck DE, Wexner SD (Eds.), 2nd edition. WB Saunders: London 1998:p.237-53.

9.

Villalba H, et al. Perm J 2007;11(2):74-6.

10. Alonso-Coello P, et al. Cochrane Database Syst Rev 2005;(4):CD004649.

11. MacRae HM, et al. Dis Colon Rectum 1995;38(7):687-94.

12. Templeton JL, et al. Br Med J (Clin Res Ed) 1983;286(6375): 1387-9.

13. Walker AJ, et al. Int J Colorectal Dis 1990;5(2):113-6.

14. Johanson JF, et al. Am J Gastroenterol 1992;87(11):1600-6.

15. Russell TR, et al. Dis Colon Rectum 1985;28(5):291-3.

16. Khare CP. Encylopedia of Indian Medicine. Springer: Germany 2007:p.159-60.

17. Ayurvedic Formulary of India. Part-II. 1st English Edition. Ministry of H & FW, Dept. of ISM & H. Govt of India. New Delhi 2000:p. 373-4.

18. Mishra S. Ayurvediya Rasashastra. Chaukhamba Orientalia: Varanasi, 7th edition 1997:p.399.

19. Khare CP. Indian Medicine: An illustrated dictionary.

Springer: New Delhi 2007:p.75.

20. Biswas K, et al. Current Science 2002;82(11):1336-45.

21. Khare CP. Indian Medicine: An illustrated dictionary.

Springer: New Delhi 2007:p.88-9.

22. Asolkar LV, et al. Second supplement to glossary of Indian Medicinal Plants with active principles. CSIR, Govt. of India: New Delhi 1992:p.120.

23. Nair R, et al. Turk J Biol 2007;31:231-6.

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25. Chattopadhyay RR, et al. Pharmacogn Rev 2007;1(1):151-6.

26. Khare CP. Indian Medicine: An illustrated dictionary.

Springer: New Delhi 2007:p.652-3.

27. Yoganarasimhan SN. Medicinal Plants of India - Tamil Nadu, Bangalore., 1st edition 2000:p.540.

28. Asolkar LV, et al. Second supplement to glossary of Indian Medicinal Plants with active principles. CSIR, Govt. of India: New Delhi 1992:p.177-8.

29. Akanmu MA, et al. African J Biomed Res 2004;7:23-6.

31. Mali RG, et al. Pharmacogn Rev 2007;1:314-9.

32. Mazumder R, et al. Phytother Res 2004;18(10):824-6.

33. Chopra RN, et al. Mesua ferrea. Glossary of Indian Medicinal Plants. National Institute of Science Communication, New Delhi; 4th Reprint 1996:p.166.

34. Chopra RN, et al. Mimosa pudica. Glossary of Indian Medicinal Plants. National Institute of Science Communication, New Delhi; 4th Reprint 1996:p.167.

35. Leal LK, et al. J Ethnopharmacol 2000;70(2):151-9.

36. Perumal Samy R, et al. J Ethnopharmacol 1998;62(2):173-82.

37. Jagetia GC, et al. J Med Food 2004;7(3):343-8.

38. Dharmasiri MG, et al. J Ethnopharmacol 2003;87(2-3): 199-206.

39. Chawla AS, et al. J Nat Prod 1992;55(2):163-7.

40. Lavagna SM, et al. Farmaco 2001;56(5-7):451-3.

41. Cordova CA, et al. Redox Rep 2002;7(2):95-102.

42. Chopra RN, et al. Cinnamomum camphora. Glossary of Indian Medicinal Plants. National Institute of Science Communication, New Delhi; 4th Reprint 1996:p.65.

43. Asolkar LV, et al. Cinnamomum camphora. Glossary of Indian Medicinal plants with Active principles.

Publications & Information Directorate (CSIR), New Delhi. 1992; Second Supplement, Part-I (A-K), (1965-1981): p.203.

44. Lee HJ, et al. J Ethnopharmacol 2006;103(2):208-16.

45. Mishra S. Tankana. Ayurvediya Rasashastra. Chaukhambha Orientalia, Varanasi; 7th edition 1997:p.699-702.

46. Sri Sadananda Sharma. Rasatarangini. Yashada bhasma.

Motilal Vanarasi Das, Delhi; 11th edition 1994:p.482-3.

47. Vijayasarathy V, et al. Med Surg 1981;XXI:1-2.

48. Tripathi A. Antiseptic 2000;97(9):317-21.

49. Reddy SS, et al. Probe 1984;XXIII(4):213-7.

50. Shafi M, et al. Indian Medical Gazette 1977;XVI (9):353-6.

51. Gupta SK, et al. Indian Medical Journal 1980;8:109.

52. Dâ&#x20AC;&#x2122;Silva V, et al. Indian Practitioner 1976;8:527.

clinical Study

Clinical Outcome in Malaria - Reiterating the Role of Parasitic Index aarthi rajkumar*, shalinee rao**, sandhya sundaramâ&#x20AC;

Abstract Malaria is a common parasitic infection seen in the tropics. The most common clinical presentation of malaria is fever with chills and rigors. However, it can also manifest with systemic complications depending on the immune status of the individual and degree of parasitemia. This study was undertaken to look at the various clinical patterns of presentation of malaria and the impact of parasitemia on disease progression and recovery. Parasitic index (PI) was calculated and graded and was found to correlate with the severity of disease.

Keywords: Complications, malaria, parasitic index

M

alaria is a major health hazard in India and other tropical countries. Approximately 300 million people worldwide are inflicted with malaria and each year, between 1-1.5 million die due to malaria.1,2 Though malaria presents as an uncomplicated fever with prompt recovery, it may mimic many systemic illness confounding the treating physician in individuals with low immunity. The classic triad of fever with chills and rigors is often masked by other symptoms like jaundice, renal failure, acidosis, hypoglycemia and electrolyte imbalance. Many patients with malaria present with systemic complications, especially renal and hepatic failure.3 The present study was undertaken to analyze the various clinical presentation of malaria with their hematological and biochemical parameters and to correlate the severity and outcome of the disease with the parasitic index (PI). material and methods This was a retrospective study done in the post monsoon period between October 2006 and March 2007. Cases, which were diagnosed as malaria, on Leishman stained thin smears and confirmed by quantitative buffy coat

*Assistant Professor **Associate Professor â&#x20AC; Professor Dept. of Pathology Sri Ramachandra Medical College and Research Institute, Porur, Chennai Address for correspondence Dr Aarthi Rajkumar Assistant Professor Dept. of Pathology Sri Ramachandra Medical College and Research Institute, Porur, Chennai - 600 116 E-mail: aarthirajkumar96@gmail.com

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

(QBC) analysis were included in the study. PI was estimated by counting the number of parasitized red blood cells (RBCs) among 1000 RBCs. Only asexual forms (ring, trophozoite and schizont) were included for calculating the PI. The parasitic load was graded on a scale of I-IV corresponding to 0-5%, 6-10%, 11-20% and >20%, respectively. Hematological parameters like hemoglobin, white blood cell count, platelet count, reticulocyte count, prothrombin time (PT), partial thromboplastin time (PTT) and biochemical parameters like blood urea nitrogen (BUN), creatinine, bilirubin, glucose and electrolytes were also noted from the clinical case sheets archived from the medical record department.

RESULTS Forty-six cases were identified as malaria-positive in this period. Plasmodium vivax was found to be the commonest form of infection followed by falciparum.

Mixed infections with falciparum and vivax were also seen (Fig. 1).

Fever was the most common presenting symptom observed in 96% of cases (Table 1). Thrombocytopenia was the commonest lab hematological abnormality seen in 48% of cases. Hyperbilirubinemia, electrolyte imbalance, raised BUN/creatinine was also noted (Fig. 2). Systemic complications were seen in only 27 cases (Table 2).

PI was <10% in 89% of cases and these patients had a good outcome and recovered, while five patients (11%) succumbed to the infection. All the five patients who died, developed disseminated intravascular coagulation (DIC) and had a PI >10% (Table 3).

clinical study

Vivax Falciparum Mixed

3

5 5

16

7

27

22 7

Figure 2. Laboratory abnormalities

Figure 1. Species specific case distribution.

DISCUSSION

Table 1. Signs and Symptoms Symptoms

Number and percentage of cases

Fever

44 (96%)

Chills

20 (43%)

Vomiting

7 (16%)

â&#x2020;&#x201C;Urine output

7 (16%)

Headache

5 (11%)

Dark urine

5 (11%)

Diarrhea

5 (11%)

Altered sensorium

5 (11%)

Stupor/Unconsciousness

Table 2. Complications Complication

2

Thrombocytopenia Hemoglobin <5 gm% Reticulocyte BUN/Creatinine Electrolyte imbalance Bilirubin

Falciparum

Vivax

Total

Acute renal failure

5

2

7

Cerebral malaria

5

0

5

Jaundice

4

1

5

DIC

4

1

5

ARDS/Sepsis

4

1

5

Malarial parasite is a protozoa belonging to genus Plasmodium with four species, namely vivax, ovale, malariae and falciparum that are pathogenic to man. Of these, P. vivax malaria is prevalent in many regions of the world and accounts for more than half of all malaria cases in Asia and Latin America.4 A study done by Koh et al showed that P. vivax accounted for upto 50% of malaria cases in South-East Asian population.5 In our study too, the commonest species causing malaria was P. vivax, (58%), followed by falciparum (35%) and mixed infection with falciparum and vivax infection (7%).

The clinical manifestation of malaria is variable ranging from fever with chills and rigors to vomiting, malaise, headache and myalgia. These symptoms are nonspecific and cannot be distinguished reliably from other febrile illnesses.6 Some patients can also present with symptoms resulting from complications such as renal failure, coma, diarrhea, jaundice and severe anemia. Recently, there has been a change in the trend of clinical manifestations of malaria, with more and more patients presenting to tertiary care hospitals.3,5 High fever is the commonest clinical presentation in any species of malaria, a finding which was also noted in our study. Fever with chills and rigors is seen more often in vivax infection than falciparum and

Table 3. Parasitic Index and Clinical Outcome Parasitic index

Falciparum

Vivax

Mixed

Total

0-5%

5

22

2

6-10%

7

4

1

11-20%

2

1

>20%

2

-

-

Complication

Outcome

29

Nil

Recovered

12

IVH and ARF

Recovered

3

DIC, IVH, ARF Electrolyte imbalance

Expired

2

DIC, ARF, ARDS

Expired

IVH = Intravascular hemolysis; ARF = Acute renal failure; DIC = Disseminated intravascular coagulation; ARDS = Acute respiratory distress syndrome.

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

451

clinical study this is thought to coincide with the period of schizont rupture.6 Surprisingly, we found fever with chills and rigors in only 48% of our cases and these were mostly seen in vivax infection.

Many systemic complications are seen in malaria such as renal failure, jaundice, cerebral malaria, acute respiratory distress syndrome (ARDS) and DIC. Renal involvement in malaria varies widely from asymptomatic proteinuria to acute renal failure (ARF). Dehydration and increased catabolism has been attributed to development of renal derangement in malaria patients.

Mild renal dysfunction in the form of albuminuria is seen in 20-90% of patients in Plasmodium falciparum malaria but only a few of these progresses to renal failure. The development of renal failure and mortality in these patients is influenced by the parasitic load.7 Our study also demonstrated that a high PI leads to the development of ARF and was a poor prognostic factor as five of the seven cases that developed ARF expired and all of them had severe parasitemia (>10%).

Hepatic dysfunction can also be seen in malaria.

Jaundice is believed to occur as a result of intravascular hemolysis of parasitized erythrocytes, hepatic dysfunction and possibly due to microangiopathic hemolysis associated with DIC.2 Hemolysis usually causes an unconjugated hyperbilirubinemia, while hepatic dysfunction produces conjugated bilirubinemia. The incidence of jaundice in malaria ranges from 20 to 31% and it is predominantly hemolytic with a high parasitic load.3 In our study, all five cases of jaundice had a high PI though intravascular hemolysis was noted in only two of these.

Cerebral malaria is observed more frequently in falciparum than vivax. The pathogenic mechanism in cerebral malaria involves sequestration of parasitized RBCs in microvasculature of brain due to cytoadherence, rosette formation and decreased deformability of infected erythrocytes. This causes hypoxia and release of cytokine tumor necrosis factor-β (TNF-β), which in turn upregulates nitric oxide synthetase activity interfering with calcium influx thereby producing coma.3 In our study, five patients were diagnosed with cerebral malaria as per WHO criteria. Although, the parasitic load was high in these patients all of them recovered after treatment with intravenous quinine as there were no associated systemic complications.

Thrombocytopenia is the commonest hematological derangement noted in patients with malaria. In our

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

study too, it was observed in 22 cases. Sequestration of platelets in the spleen or their consumption as in DIC are thought to be important causes of thrombocytopenia in malaria.2 Anemia is also a common feature of acute malarial infection. It may develop rapidly in falciparum infection due to heavy parasitemia and destruction of parasitized RBCs.3 Severe anemia with a hemoglobin concentration <5 gm% was seen in only two cases in our study.

Malaria is an important cause of multiple organ failure in India. Mortality rate is 6.4% when one organ fails but increases to 48.8% with failure of â&#x2030;Ľ2 organs.8 Hyperparasitemia is believed to be an important cause of multiorgan failure and death in malaria.3,5,9 In our study, the mortality rate due to malaria was 10.8%. Thirty-nine cases with low parasitemia had no complications and complete recovery. Two cases with ARF and low PI recovered, while five cases with severe parasitemia developed multiorgan failure with DIC and expired. This highlights the fact that parasitic load remarkably influences clinical outcome.

The incidence of mixed infection with vivax and falciparum is reported to be <2%. Concurrent infections with different Plasmodium species may have important role in the development of cross-species immunity and a milder clinical course. Mixed infections with vivax appear to reduce the severity of disease with falciparum, decreasing the risk of complications and treatment failure.4 This was also evident in our study as all cases of mixed infection had a low parasitemia and showed prompt recovery.

Complications and fatality are more common with falciparum than vivax infection.9,10 In our study, of the five who expired, only one died due to vivax infection. Systemic complications like renal failure, hepatic dysfunction, ARDS and DIC occurred with falciparum infection showing that it was more fulminant than vivax.

Cases without any complication responded well to antimalarials regardless of the causative species.

In this study, PI correlated well with the severity and course of disease. Complications and mortality was seen more often in patients with a higher degree of parasitemia. Hence, knowledge of PI could be a valuable tool for predicting clinical outcome and planning appropriate therapy.

clinical study 6.

Muddaiah M, Prakash PS. A study of clinical profile of malaria in a tertiary referral centre in South Canara.

J Vector Borne Dis 2006;43(1):29-33.

Mandell, Douglas, and Bennnet. Principles and Practice of Infectious Diseases. 6th edition, Churchill Living Stone Publication; 2005.

7.

Banzal S, Ayoola EA, El Sammani EE, Gadour MO, Jain AK. The clinical pattern and complications of severe malaria in the Gizan region of Saudi Arabia.

Ann Saudi Med 1999;19(4):378-80.

Trang TT, Phu NH, Vinh H, Hien TT, Cuong BM, Chau TT, et al. Acute renal failure in patients with severe falciparum malaria. Clin Infect Dis 1992;15(5): 874-80.

8.

Krishnan A, Karnad DR. Severe falciparum malaria: an important cause of multiple organ failure in Indian intensive care unit patients. Crit Care Med 2003; 31(9):2278-84.

Kochar DK, Saxena V, Singh N, Kochar SK, Kumar SV, Das A. Plasmodium vivax malaria. Emerg Infect Dis 2005;11(1):132-4.

REFERENCES 1.

2.

3.

Nand N, Aggarwal H, Sharma M, Singh M. Systemic manifestations of malaria. J Indian Acad Clin Med 2001;2(3):189-94.

4.

Price RN, Tjitra E, Guerra CA, Yeung S, White NJ, Anstey NM. Vivax malaria: neglected and not benign.

Am J Trop Med Hyg 2007;77(6 Suppl):79-87.

9.

5.

Koh KH, Chew PH, Kiyu A. A retrospective study of malaria infections in an intensive care unit of a general hospital in Malaysia. Singapore Med J 2004;45(1):28-36.

10. Sitalakshmi S, Srikrishna A, Devi S, Damodar P, Mathew T, Varghese J. Changing trends in malariaa decadeâ&#x20AC;&#x2122;s experience at a referral hospital. Indian J Pathol Microbiol 2003;46(3):399-401.

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

453

CLINICAL Study

A Study of Clinical Profile of 50 Patients with Portal Hypertension and to Evaluate Role of Noninvasive Predictor of Esophageal Varices BC Kaji*, Yagnesh R Bhavsar**, Nitin Patel†, Anupam Garg‡, Hiren Kevadiya‡, Zishan Mansuri§

Abstract Objective: To study the predictive power of noninvasive investigative parameters (clinical, biochemical, radiological) for detection of esophageal varices in patients with portal hypertension (PHT) as compared to invasive parameters (upper gastrointestinal endoscopy). Materials and methods: Fifty patients with PHT, between May 2008 to September 2010, were studied. Those who had decompensated liver diseases, HIV, hepatocellular carcinoma, metastasis in liver, parentral drug addiction, chronic febrile illness, H/O treatment taken for PHT in the form of surgery or endoscopic bending or sclerotherapy were excluded. Detailed clinical history was taken and physical examination was done. All patients underwent the required hematological, biochemical, radiological, endoscopic and histopathological investigations. Results: Platelet count/splenic size showed a significant correlation between presence or absence and grade of esophageal varices (p < 0.00015). If a cut-off value of 1,000/cu mm is taken, then 87.5% (35/40) patients with esophageal varices have ratio <1,000 while 20% (2/10) of patients with ratio <1,000 did not have any varices. It was also observed that lower the ratio, higher the grade of varices. Conclusion: Asymptomatic esophageal varices, which is quite common, can be easily diagnosed with invasive endoscopy or otherwise can be suspected with noninvasive predictors like platelet/spleen size ratio in our country, where financial constraint is a major problem for investigations like endoscopy.

Keywords: Portal hypertension, noninvasive predictors, asymptomatic esophageal varices, platelet/spleen size ratio

P

ortal hypertension (PHT) commonly accompanies cirrhosis of liver. Development of esophageal varices is one of the major complications of PHT. A major cause of PHT-related morbidity and mortality is the development of variceal hemorrhage, which occurs in 25-40% of patients.1 Esophageal varices are diagnosed by endoscopy.

Further follow-up should then relate to the initial size of varices. In case of large varices, endoscopic follow-up is not necessary and primary prophylaxis with a nonselective β-blocker should be started.

Endoscopic band ligation is useful in preventing variceal bleeding in patients with medium or large varices.

Accurate identification of patients at the highest risk of bleeding allows stratification in an attempt to avoid unnecessary preventive measures in 60-75% of patients who will never have variceal bleeding2,3 in future.

In order to reduce the increasing burden that endoscopy units will have to bear, some studies have attempted to identify characteristics that noninvasively predict the presence of large esophageal varices like platelet count and splenomegaly.4-17 In this study, we have used the platelet count/spleen diameter ratio as a noninvasive predictive parameter. Apparently, the decrease in platelet count in all these patients was most likely due to hypersplenism because of PHT. objectives

*Professor, Dept. of Medicine **4th Year Resident †3rd Year Resident ‡2nd Year Resident §1st Year Resident Civil Hospital, Ahmedabad Address for correspondence Dr BC Kaji A1, Payal Apartment Behind Iffco Tokyo Insurance Company Navrangpura, Ahmedabad - 380 009 E-mail: bckaji@hotmail.com

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012







To study clinical and investigative profile of selective patients of PHT. To study the predictive power of noninvasive investigative parameters (clinical, biochemical, radiological) for detection of esophageal varices in patients with PHT as compared to invasive parameter (upper gastrointestinal endoscopy).

To discuss the etiopathogenesis of PHT.

clinical study Materials and methods This study was conducted at Civil Hospital, Ahmedabad, a tertiary care hospital in Gujarat. The study was conducted from May 2008 to September 2010 and 50 patients were studied.

Adult patients with PHT, which had been diagnosed clinically, biochemically, radiologically and endoscopically were included. Those who had decompensated liver diseases, HIV, hepatocellular carcinoma, metastasis in liver, parentral drug addiction, chronic febrile illness, H/O treatment taken for PHT in form of surgery or endoscopic banding or sclerotherapy were excluded.

All patient were subjected to following tests: Hemogram with thin peripheral smear and ESR, RBC indices, prothrombin time and INR, serum bilirubin, alkaline phosphate (ALKP), alanine transaminase (ALT), aspartate transaminase (AST), total serum proteins, albumin and globulin levels, serum electrolytes and blood urea, serum creatinine, random blood sugar, ascitic fluid analysis, HbsAg, chest X-ray and abdominal ultrasonography and portal vein Doppler and barium swallow, upper gastrointestinal endoscopic examination and percutaneous liver biopsy.

Esophageal varices are graded as follows:18 

Grade 0: No varices



Grade 1: Varices small and straight





Grade 2: Varices obliterating less than one-third of esophageal lumen Grade 3: Varices obliterating more than one-third of esophageal lumen.

Results There was a male preponderance (M:F = 2.1:1), with mean age of 41 ± 10.9 years. Most were from lower socioeconomic class. This is due to high prevalence of alcoholism in this group.18 Constitutional symptoms (100%) and abdominal distension (80%) were most common presenting features, followed by jaundice and pedal edema.

Pallor (88%), ascites (80%) and splenomegaly (70%) were common signs followed by icterus (52%).

Anemia with hemoglobin (Hb) <9 g/dl was found in 52% of patients. Raised prothrombin time (88%), serum albumin <2.9 g/dl (64%) and platelet count <1,00,000/cu mm (60%) in decreasing order of frequency were the common abnormalities.

The etiology was alcoholic in 52%, cryptogenic in

30%, noncirrhotic portal fibrosis in 10%, chronic viral etiology in 6% and portal vein thrombosis in 2% of patients.

As a specialized investigation, ultrasonography showed splenomegaly in 80% of patients and ascites in 88% of patients. Portal vein diameter was >13 mm in 58% of patients; splenic vein diameter was >7 mm in 70%. Asymptomatic esophageal varices were found in 80% of patients, 20% had Grade 1, 26% had Grade 2 and 34% had Grade 3 esophageal varices. It was observed that Hb, packed cell volume (PCV), mean corpuscular volume (MCV) and WBC count did not show any significant correlation with esophageal varices. Serum bilirubin and liver enzymes like ALT, AST, ALKP failed to show any significant correlation with size and presence or absence of esophageal varices. Similarly, portal vein diameter, splenic vein diameter and serum albumin had nothing to do with esophageal varices.

There was significant correlation between platelet count and esophageal varices (Table 1). In the present study, 70% (28/40) patients with esophageal varices had platelet count <1,00,000/cu mm, while 80% (8/10) of patients without esophageal varices had platelet count above 1,00,000 cu mm. Eighty percent (32/40) patients with esophageal varices had longitudinal spleen diameter >120 mm. Forty percent (5/11) with normal longitudinal spleen diameter had no varices. Ninety-two percent (26/28) patients with Grade 2 or 3 varices had spleen diameter >120 mm (Table 2). Eighteen percent (2/11) patients with normal spleen size had Grade 2 or 3 esophageal varices (p < 0.014). Platelet count/ spleen size ratio showed a significant correlation between presence or absence of esophageal varices and grade of esophageal varices (p < 0.00015) (Table 3). If a cut-off value of 1,000/cu mm is taken, then 87.5% (35/40) patients with esophageal varices have ratio <1,000 while 20% (2/10) of patient with ratio <1,000 did not have any varices. It was also observed that lower the ratio, higher the grade of varices.

Table 1. Correlation between Platelet Count and Esophageal Varices Platelet count (cu mm/dl)

Esophageal varices Grade 0 Grade 1 Grade 2 Grade 3

<50,000

0

1

0

5

50,000-10,0000

2

6

8

8

1,00,001-1,50,000

0

3

3

2

1,50,001-2,00,000

4

0

1

2

>2,00,000

4

0

1

0

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clinical study Table 2. Correlation between Splenic Size and Esophageal Varices Spleen (mm)

Esophageal varices Grade 0

Grade 1

Grade 2

Grade 3

â&#x2030;¤120

5

4

1

1

>120

5

6

12

14

Table 3. Correlation between Platelet Count/Splenic Size and Esophageal Varices Platelet splenic size ratio

Esophageal varices Grade 0

Grade 1

Grade 2

Grade 3

<500

0

3

2

10

5,00-1,000

2

6

9

5

1,001-1,500

4

1

1

2

>1,500

4

0

1

0

Discussion Most commonly affected patients were middle-aged males coming from lower socioeconomic class. Most common etiology for PHT was alcoholic cirrhosis of liver, which is a potentially preventable form.

Abdominal distension was the most common specific presenting complaint followed by jaundice and edema over feet. Pallor, ascites were common signs followed by splenomegaly and icterus.

Incidence of esophageal varices in patients with PHT is approximately 90-95%, but only 30-50% develop variceal bleeding, which is usually associated mainly with fatal outcome. Therefore, regular control and evaluation of esophageal varices with timely introduction of nonselective b-blockers and variceal ligation play an important role in prevention of bleeding.

Endoscopy procedure. parameters esophageal studies.

is an invasive and costly diagnostic Therefore, introduction of noninvasive for assessment of presence and size of varices is a major goal of numerous

To date, seven studies have been published concerning the noninvasive diagnosis of the presence of either any esophageal varices or large esophageal varices in patients with PHT.3-11 The reason for this effort is simple: the number of patients undergoing screening for the presence of esophageal varices is going to increase in the near future as a result of the growing pool of patients with chronic liver disease.

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In general, most important noninvasive parameters esophageal varices are decreased platelet count and splenomegaly. A p value of <0.05 was observed for both of these parameters in our study, but the specificity was low. If cut-off value for platelet count <1,00,000/cu mm was taken then, it has specificity of 70% and sensitivity of 60%. If splenic size was >120 mm then it has specificity of 85% and sensitivity of 50%. We also tried to corroborate other parameters like portal vein diameter, splenic vein diameter and serum albumin with presence or absence of esophageal varices or grade of esophageal varices but specificity was low and p < 0.5, which is not significant.

Only 12% of patients with esophageal varices (10% had large varices) were missed considering a cut-off value of platelet count/splenic diameter <1,000/cu mm. Eighty-seven percent of patients with varices had ratio <1,000/cu mm. The sensitivity was 87% and specificity was 80%. P value was <0.00015.

Nevertheless, this platelet count and splenic size ratio may serve for selection of patients who need more frequent endoscopies. This ratio will help to identify patients at higher risks for development of esophageal varices. It will provide insight into the relationship between clinical, biochemical, hematological and imaging abnormalities and development of clinically significant esophageal varices.

Conclusion Portal hypertension is largely a preventable condition because the commonest etiology is alcoholism. Asymptomatic esophageal varices, which is quite common, can be easily diagnosed with invasive endoscopy or otherwise suspected with noninvasive platelet/spleen size ratio in country like ours, where financial constraint is a main problem. It can be very useful and applicable at small centers like community health centers (CHCs) and primary health centers (PHCs) in our country with limited resources.

References 1.

Grace ND. Prevention of initial variceal hemorrhage.

Gastroenterol Clin North Am 1992;21(1):149-61.

2.

Dâ&#x20AC;&#x2122;Amico G, Garcia-Pagan JC, Luca A, Bosch J. Hepatic vein pressure gradient reduction and prevention of variceal bleeding in cirrhosis: a systematic review.

Gastroenterology 2006;131(5):1611-24.

3.

Merli M, Nicolini G, Angeloni S, Rinaldi V, De Santis A, Merkel C, et al. Incidence and natural history of small esophageal varices in cirrhotic patients. J Hepatol 2003;38(3):266-72.

clinical study 4.

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Gorka W, al Mulla A, al Sebayel M, Altraif I, Gorka TS. Qualitative hepatic venous Doppler sonography versus portal flowmetry in predicting the severity of esophageal varices in hepatitis C cirrhosis. AJR Am J Roentgenol 1997;169(2):511-5.

Chalasani N, Imperiale TF, Ismail A, Sood G, Carey M, Wilcox CM, et al. Predictors of large esophageal varices in patients with cirrhosis. Am J Gastroenterol 1999;94(11):3285-91.

Zaman A, Hapke R, Flora K, Rosen HR, Benner K. Factors predicting the presence of esophageal or gastric varices in patients with advanced liver disease. Am J Gastroenterol 1999;94(11):3292-6.

Pilette C, Oberti F, Aubé C, Rousselet MC, Bedossa P, Gallois Y, et al. Non-invasive diagnosis of esophageal varices in chronic liver diseases. J Hepatol 1999;31(5): 867-73.

8.

Ng FH, Wong SY, Loo CK, Lam KM, Lai CW, Cheng CS. Prediction of oesophagogastric varices in patients with liver cirrhosis. J Gastroenterol Hepatol 1999;14(8):785-90.

9.

Schepis F, Cammà C, Niceforo D, Magnano A, Pallio S, Cinquegrani M, et al. Which patients with cirrhosis should undergo endoscopic screening for esophageal varices detection? Hepatology 2001;33(2):333-8.

10. Zaman A, Becker T, Lapidus J, Benner K. Risk factors for the presence of varices in cirrhotic patients without a history of variceal hemorrhage. Arch Intern Med 2001;161(21):2564-70.

11. Madhotra R, Mulcahy HE, Willner I, Reuben A. Prediction of esophageal varices in patients with cirrhosis. J Clin Gastroenterol 2002;34(1):81-5.

12. Amarapurkar DN, Parikh SS, Shankaran K, Chopra K, Dhawan P, Kalro RH, et al. Correlation between splenomegaly and oesophageal varices in patients with liver cirrhosis. Endoscopy 1994;26(6):563.

13. Zeijen RNM, Caenepeel P, Stockbrügger RW, Arends JW, Oei TR. Prediction of esophageal varices in liver disease: preliminary results. Gastroenterology 1994;106(Suppl): A1013.

14. Lavergne J, Molina E, Reddy KR, Jeffers L, Leon R, Nader AK, et al. Ascites predicts the presence of high grade varices by screening gastroscopy. Gastrointest Endosc 1997;45(4):AB187.

15. Garcia-Tsao G, Escorsell A, Zakko M. Predicting the presence of significant portal hypertension and varices in compensated cirrhotic patients. Hepatology 1997;26:927-30.

16. Freeman JG, Darlow S, Cole AT. Platelet count as a predictor for the presence of oesophageal varices in alcoholic cirrhotic patients. Gastroenterology 1999;116: A1211.

17. Riggio O, Angeloni S, Nicolini G, Merli M, Merkel C. Endoscopic screening for esophageal varices in cirrhotic patients. Hepatology 2002;35(2):501-2.

18. Sherlock S. Diseases of liver and biliary system. 11th edition 2002:p.147-80.

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case report

Allergic Contact Stomatitis: A Case Report and Review of Literature P Lokesh, T Rooban, Joshua Elizabeth, K Umadevi, K Ranganathan

Abstract Allergic contact stomatitis is a well-recognized entity, which may be easily overlooked by the clinician since its signs and symptoms are similar to various other oral lesions. Accurate diagnosis warrants adequate treatment that will help in providing prompt relief and will also prevent further recurrences. We present a case report of a 27-year-old South Indian male student, who presented with multiple erythematous erosions involving much of the nonkeratinized oral mucosa. History revealed that there was a previous episode of a similar lesion, associated with intake of food with flavoring agents. Based on the history and clinical features, we arrived at a diagnosis of allergic contact stomatitis and successfully treated the lesions with topical and systemic antihistamines.

Keywords: Allergic contact stomatitis, oral mucosa, antihistamines

A

llergic contact stomatitis is a rare disorder, which most clinicians are not familiar with.

A wide variety of substances are known to elicit adverse oral mucosal reactions. Flavoring agents, preservatives and dental materials are the most common causes of allergic/hypersensitivity reactions related to oral mucosa. Flavoring agents and preservatives have been used widely in commercially available personal hygiene products and foods, thereby increasing the risk hypersensitivity reactions.

Previous exposure with an allergen is essential for diagnosis of allergic contact stomatitis. Sensitization usually occurs through contact of allergen with the oral mucosa. Rarely, sensitization may also occur by contact of allergen with skin. Memory T cells are activated soon after the initial exposure. On re-exposure to the same allergen, a type IV hypersensitivity reaction occurs. This reaction may be delayed by at least 48 hours and the clinical presentation may vary depending on the severity of the reaction.

Case report A 26-year-old dental postgraduate student presented with a complaint of pain and diffuse intraoral erythematous lesions for the past three days. The patient first experienced roughness and discomfort in the left

Dept. of Oral and Maxillofacial Pathology, Ragas Dental College and Hospital, Chennai

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buccal mucosa four days ago. The following day he developed erythematous lesions and pain in the left buccal mucosa, followed by lesions on the anterior part of ventral tongue, soft palate, right buccal mucosa and lower labial mucosa. Difficulty in brushing, speech and burning sensation while eating were experienced, for which 2% benzocaine gel was applied 3-4 times every day before food intake.

Intraoral examination revealed carious 26, glass ionomer cement (GIC) Class I restoration in 46, buccally inclined 18 and 28. Diffuse erythema involving the whole of soft palate, without extension on to the hard palate was seen (Fig. 1). Ventral surface of anterior tongue was bright red in color with few small whitish plaques, suggestive of necrosis (Fig. 2).

Lower labial mucosa exhibited irregular zones of erythema. Large oval to irregular bright red patches surrounded by whitish edematous zones were seen on buccal mucosa, extending some distance into the vestibule on both right (Fig. 3) and left side (Fig. 4). The keratinized mucosa of the hard palate, gingiva and dorsum of the tongue was not involved.

Further questioning did not reveal history of any change or use of oral hygiene products, recent dental treatment or drug intake. Eventually, patient did recall an episode of having food at a restaurant 2-3 days before developing the lesions. Patient also gave a history of episodes of recurrent minor aphthous ulcers.

One such episode occurred about two years ago and was characterized by multiple painful oral lesions,

case report

Figure 1. Diffuse erythema of soft palate.

Figure 3. Erythematous lesions on right buccal mucosa.

Figure 2. Erosive lesions on ventral surface of tongue.

Figure 4. Erythematous lesions on left buccal mucosa.

which developed soon after intake of specific food, which the patient has been avoiding since then. Based on the history and clinical features, a provisional diagnosis of allergic stomatitis was made.

(Figs. 5-8). A mild increase in the pigmentation was seen on the buccal mucosa. Two new lesions, which were not present during the initial examination, were seen on both the left and right sides of buccal mucosa, adjacent to the upper canine and premolars (Figs. 9 and 10). These lesions were erythematous areas, 2 Ă&#x2014; 1 cm in size with whitish necrotic plaques. Patient was advised to continue the same medications for three more days, following which all the oral lesions healed completely.

Management Patient was advised to avoid foods with preservatives and flavoring agents. Cetirizine hydrochloride 10 mg tablet hs, 5 ml of diphenhydramine hydrochloride syrup mixed with equal amount of an antacid liquid in a swish and swallow method 3-4 times daily were prescribed to alleviate the symptoms.

During the follow-up visit, four days later, most of the initial lesions had healed without any scarring

Discussion Contact stomatitis is an inflammation of the oral mucosa caused by external substances. It can be caused by a

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Figure 5. Soft palate - 4 days after therapy.

Figure 7. Right buccal mucosa - 4 days after therapy.

Figure 6. Ventral surface of tongue - 4 days after therapy.

Figure 8. Left buccal mucosa - 4 days after therapy.

variety of substances, which can either act as irritant or allergic agents. These substances include dental materials, preservatives and flavoring agents in foods or oral hygiene products. Oral mucosa is less commonly prone to contact allergic reactions, when compared to skin, though the latter is exposed to a wide variety of antigenic stimuli. This can be attributed to the various biologic and physiologic differences between the two.

Saliva acts as a solvent that solubilizes, dilutes and also starts digesting potential allergens and helps to wash them there by limiting the duration and number of molecules that contact oral mucosa. Limited keratinization makes hapten binding more difficult and the limited number of antigen presenting cells

in the oral mucosa decreases the chance of antigen recognition. Irritants and allergens that do contact the oral mucosa are removed more quickly because of higher vascularity and faster epithelial renewal rates than in keratinized skin.

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Balsam of peru, cinnamon, cinnamic aldehyde, menthol, peppermint and eugenol are some of the common oral flavoring allergens.

These reactions can be either acute or chronic.

Clinical presentations vary based on the nature of reaction, type of allergen site and duration of contact.

Patients with acute lesions may present with burning or redness. Vesicles are rarely seen and if present rupture in a short while after formation. Some patients

case report Table 1. Differential Diagnoses

Pemphigus

Lupus erythematosus

Pemphigoid

Syphilis

Lichen planus

Friction-induced

Drug reactions

Contact stomatitis

Erythema multiforme

Erythematous candidiasis

lesions during clinical examination. Erosions can also be caused by trauma arising from friction between the teeth or irregular dental restorations. Burns from hot foods, radiation and caustic chemicals also cause similar erosions.

Figure 9. Lesions on right buccal mucosa, during review visit.

Figure 10. Lesions on left labial vestibule, during review visit.

may experience edema, itching or stinging sensation.

Contact allergy lesions occur directly at the site of exposure to the causative agent. Acute lesions develop soon after antigenic exposure; diagnosis of these may be straightforward since a cause-and-effect relationship can be easily established.

Chronic lesions typically present as areas of erythema, edema, desquamation and occasionally ulceration. In addition, allergic contact stomatitis can also present as erosions with rough surface and irregular borders, often surrounded by a red halo. These lesions may be indistinguishable from aphthous ulcers and other

Hence, it is essential to elicit a thorough history and exclude other pathosis presenting with similar lesions clinically (Table 1). Patch testing of oral mucosa is difficult and may yield false-negative results. Some common conditions which can present as erosive lesions in the oral mucosa are listed in Table 1.

Identification and elimination of the allergen that initiated the reaction is essential to treat the condition, as well as to prevent recurrences. If an association is not established, cutaneous patch testing may be useful.

Lesions respond well once the antigenic stimulus is eliminated. Antihistamines, topical anesthetics and topical corticosteroids are the commonly used pharmacological agents. Use of antihistamine suspensions in a swish and swallow method provide the advantage of both local and systemic action. Some of these agents may not be tolerable when there is a mucosal breach. Hence, a well-tolerated, flavored antacid was included in the prescription.

Conclusion Allergic contact stomatitis is a well-recognized entity, the incidence of which could be far more than that reported. Clinical presentation and histopathologic features are not always specific. Hence, a high-degree of suspicion and careful history taking to establish a cause-and-effect relationship is essential. Biopsy findings may be confirmatory but not always essential.

Health practitioners should consider contact allergic stomatitis in the differential diagnosis of nonspecific oral lesions so as to provide proper treatment and avoid recurrences.

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case report Consent

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Written informed consent was obtained from the patient for publication of this case report and accompanying images.

Nevelle B, Damm D, Allen C, Bouquot J. Oral and Maxillofacial Pathology. 3rd edition.

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Ostman PO, Anneroth G, Skoglund A. Amalgamassociated oral lichenoid reactions. Clinical and histologic changes after removal of amalgam fillings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;81(4): 459-65.

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Kowitz G, Jacobson J, Meng Z, Lucatorto F. The effects of tartar-control toothpaste on the oral soft tissues. Oral Surg Oral Med Oral Pathol 1990;70(4):529-36.

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Tremblay S, Avon SL. Contact allergy to cinnamon: case report. J Can Dent Assoc 2008;74(5):445-61.

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De Rossi SS, Greenberg MS. Intraoral contact allergy: a literature review and case reports. J Am Dent Assoc 1998;129(10):1435-41.

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Raap U, Stiesch M, Reh H, Kapp A, Werfel T. Investigation of contact allergy to dental metals in 206 patients.

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Competing Interests The authors declare that they have no competing interests.

Acknowledgments We thank our Principal, Dr S Ramachandran, for encouraging the publication of this case report and Dr Yakob Martin, for the images.

suggested reading 1.

LeSueur BW, Yiannias JA. Contact stomatitis. Dermatol Clin 2003;21(1):105-14, vii.

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Tosti A, Piraccini BM, Peluso AM. Contact and irritant stomatitis. Semin Cutan Med Surg 1997;16(4):314-9.

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Ophaswongse S, Maibach HI. Allergic contact cheilitis.

Contact Dermatitis 1995;33(6):365-70.

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10. Torgerson RR, Davis MD, Bruce AJ, Farmer SA, Rogers RS 3rd. Contact allergy in oral disease. J Am Acad Dermatol 2007;57(2):315-21.

case report

Wireless Capsule Endoscopy Requiring Surgical Intervention NEHA KANTAWALA*, JS RAJKUMAR**, S YUVARAJA*, T PERUNGO†

Abstract Wireless capsule endoscopy is a relatively new diagnostic technique for the detection of small bowel disease. Currently represents an increasingly used method for diagnostic evaluation of the small intestine. It is important for surgeons to be familiar with its uses and complication that may arise. We report an interesting case of spontaneous video capsule entrapment in small bowel Crohn’s disease in which diagnosis was made radiologically.

Keywords: Wireless capsule endoscopy, minimally invasive, capsule battery, intestinal strictures

W

ireless capsule endoscopy is a relatively new diagnostic technique for the detection of small bowel disease. This minimally invasive procedure generally poses few risks to the patients and reported complications typically are related to capsule retention. The retrospective analysis of some series indicates that the incidence of capsule retention depends on the indication for the capsule examination 0% in healthy controls, 1.4% in obscure gastrointestinal bleeding, 1.48% in suspected Crohn’s disease, 5-13% in known Crohn’s disease and 21% in suspected small bowel obstruction. We report an interesting case of spontaneous video capsule entrapment in small bowel Crohn’s disease in which diagnosis was made radiologically. case report A 35-year-old woman was evaluated for persistent fever and weight loss in a known case of Crohn’s disease. She had no gastrointestinal symptoms. CT scan of abdomen was normal and colonoscopy revealed terminal ileal Crohn’s disease. Small intestine evaluation was thus pursued and wireless capsule endoscopy was

*Consultant Surgeon **Chief Surgeon †Surgical Registrar Dept. of Surgical Gastroenterology and Minimal Access Surgery Lifeline Group of Hospitals, Chennai Address for correspondence Dr JS Rajkumar Chief Surgeon and Chairman Lifeline Multi Speciality Hospital 5/639, Old Mahabalipuram Road Kandanchavadi, Perungudi, Chennai - 600 096

performed. Unfortunately, as the endoscopic images revealed, the capsule became lodged in small intestine segment containing stagnant contents and eventually lost battery power. As patient had no symptoms of obstruction, he was called for review after 15 days.

An abdominal radiograph showed video capsule in the right lower quadrant. CT of the abdomen revealed that the video capsule was caught in the ileum. As patient had persistent weight loss and persistent fever with capsule retention, it was planned to proceed with diagnostic laparoscopy, which revealed multiple strictures in terminal ileum with capsule retained in proximal stricture. There were five complete strictures in terminal ileum so we decided to proceed with resection with ileotranseverse anastomosis. Postoperatively, the patient recovered well.

Discussion Wireless capsule endoscopy was approved for clinical use in United States in 2001 and currently represents an increasingly used method for diagnostic evaluation of the small intestine. It is important for surgeons to be familiar with its uses and complication that may arise. In our case, CT scan of the abdomen was done to rule out strictures. The endoscopic capsule examination begins when the patient swallows the 1.1 × 2.6 cm, 4 g capsule, which contains a camera, light source, batteries and transmitter. As the capsule transverses the small intestine, it relays images to a recorder wore on a belt around the patient’s waist. The capsule battery has a life span of about eight hours, typically enough time for it

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case report Suggested reading 1.

Delaney CP, Fazio VW. Crohnâ&#x20AC;&#x2122;s disease of the small bowel.

Surg Clin North Am 2001;81(1):137-58, ix.

2.

Iddan G, Meron G, Glukhovsky A, Swain P. Wireless capsule endoscopy. Nature 2000;405(6785):417.

3.

Gong F, Swain P, Mills T. Wireless endoscopy. Gastrointest Endosc 2000;51(6):725-9.

4.

Swain P. Wireless capsule endoscopy. Gut 2003;52 Suppl 4:iv48-50.

5.

Fritscher-Ravens A, Swain CP. The wireless capsule: new light in the darkness. Dig Dis 2002;20(2):127-33.

6.

Bar-Meir S, Bardan E. Wireless capsule endoscopy - pros and cons. Isr Med Assoc J 2002;4(9):726.

7.

Fireman Z, Glukhovsky A, Jacob H, Lavy A, Lewkowicz S, Scapa E. Wireless capsule endoscopy. Isr Med Assoc J 2002;4(9):717-9.

8.

Ge ZZ, Hu YB, Gao YJ, Xiao SD. Clinical application of wireless capsule endoscopy. Zhonghua Xiaohua Zazhi 2003;23:7-10.

9.

Ang TL, Fock KM, Ng TM, Teo EK, Tan YL. Clinical utility, safety and tolerability of capsule endoscopy in urban Southeast Asian population. World J Gastroenterol 2003;9(10):2313-6.

Figure 1.

10. Appleyard M, Fireman Z, Glukhovsky A, Jacob H, Shreiver R, Kadirkamanathan S, et al. A randomized trial comparing wireless capsule endoscopy with push enteroscopy for the detection of small-bowel lesions.

Gastroenterology 2000;119(6):1431-8.

Figure 2.

11. Costamagna G, Shah SK, Riccioni ME, Foschia F, Mutignani M, Perri V, et al. A prospective trial comparing small bowel radiographs and video capsule endoscopy for suspected small bowel disease. Gastroenterology 2002;123(4):999-1005.

to image the entire small bowel as it passes through.

Recorded images are downloaded and analyzed later.

12. Bardan E, Nadler M, Chowers Y, Fidder H, Bar-Meir S. Capsule endoscopy for the evaluation of patients with chronic abdominal pain. Endoscopy 2003;35(8):688-9.

Most capsules are naturally expelled within 72 hours of ingestion. Current imaging techniques can show long or medium stenosis, with great reduction of lumen size; however, short stenosis usually cannot be detected by standard methods. This fact explains that in most of the reported cases of capsule retention, the previous performance of the usual radiological studies was not capable of diagnosing the intestinal strictures which the capsule clearly showed. It is therefore, proven that the lack of findings in radiological techniques does not rule out the existence of bowel stenosis.

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13. Schreyer AG, GĂślder S, Seitz J, Herfarth H. New diagnostic avenues in inflammatory bowel diseases.

Capsule endoscopy, magnetic resonance imaging and virtual enteroscopy. Dig Dis 2003;21(2):129-37.

14. Tibble JA, Bjarnason I. Non-invasive investigation of inflammatory bowel disease. World J Gastroenterol 2001;7(4):460-5.

15. Lewis BS. Radiology versus endoscopy of the small bowel. Gastrointest Endosc Clin N Am 1999;9(1):13-27.

16. Chong AK. Comments regarding article comparing small bowel radiographs and video capsule endoscopy.

Gastroenterology 2003;125(1):276.

case report 17. Liangpunsakul S, Chadalawada V, Rex DK, Maglinte D, Lappas J. Wireless capsule endoscopy detects small bowel ulcers in patients with normal results from state of the art enteroclysis. Am J Gastroenterol 2003;98(6):1295-8.

20. Seensalu R. The sonde exam. Gastrointest Endosc Clin N Am 1999;9(1):37-59.

18. MacKenzie J. Push enteroscopy. Gastrointest Endosc Clin N Am 1999;9(1):29-36.

22. Ge ZZ, Xiao SD. Prospects for wireless capsule endoscopy. Wei Chang Bing Xue 2002;7:326-30.

19. Gay GJ, Delmotte JS. Enteroscopy in small intestinal inflammatory diseases. Gastrointest Endosc Clin N Am 1999;9(1):115-23.

23. Barkin J, Friedman S. Wireless capsule endoscopy (WCE) requiring surgical intervention: The worldâ&#x20AC;&#x2122;s experience.

2nd Conference on Capsule Endoscopy, Berlin 2003:171.

21. Delmotte JS, Gay GJ, Houcke PH, Mesnard Y. Intraoperative endoscopy. Gastrointest Endosc Clin N Am 1999;9(1):61-9.

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case report

Pseudo-infarct in ECG in A Case of Asymmetric Septal Hypertrophy S Parthasarathy*, M Ravishankar**

Abstract A 68-year-old male with a history of type 2 diabetes and hypertension presented for a routine check-up. His routine ECG revealed recent inferior infarct. He was admitted and later echocardiography showed it to as asymmetric septal hypertrophy.

The ECG findings of the disease and various causes of pseudo-infarct are discussed.

Keywords: Asymmetric septal hypertrophy, pseudo-infarct, inferior wall

Case capsule A 68-year-old male with a history of type 2 diabetes for a decade and hypertension for five years presented for a routine check-up. He was on the following drugs; glipizide, metformin, atenolol, enalapril atorvastatin and vitamins. He was asymptomatic.

A routine ECG revealed inferior infarct of recent onset (Fig. 1). There was no evidence of either left atrial overload or left ventricular hypertrophy. He was hospitalized; injection heparin, tablet ecospirin were added.

He was asymptomatic. His random blood sugar was 163 mg/dl and blood pressure was 136/84 mmHg. A repeat ECG the next day was similar. His other investigations like blood urea, creatinine and electrolytes were normal; urine ketones were negative. Echo heart on the following day revealed asymmetric septal hypertrophy (ASH) of septal lateral wall and apex.

There was no evidence of aortic stenosis or regional wall motion abnormality. Injection heparin was withdrawn after a diagnosis of pseudo-infarct was made. We do not have the facilities for an enzyme analyses or angiography. The patient was discharged the next day at his request. As he was asymptomatic, he was not willing for further evaluation.

*Chief Anesthesiologist and Intensivist Govt. Dist. Headquarters Hospital Kumbakonam, Tamil Nadu **Professor and Head Dept. of Anesthesiology Mahatma Gandhi Medical College and Research Institute, Pondicherry Address for correspondence Dr S Parthasarathy 20, Palanisamy Nagar, Chennai Road Kumbakonam - 612 002, Tamil Nadu E-mail: painfreepartha@gmail.com

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Figure 1. ECG showing inferior infarct of recent onset.

Discussion ASH may be asymptomatic or manifest as pain in the chest, syncope, congestive heart failure or sudden death.

Some patients have left ventricular outflow obstruction, and it is this subgroup which was originally described as having idiopathic hypertrophic subaortic stenosis.1 Our patient had no symptoms except for very occasional giddiness, which was elicited on repeated probing. It has been suggested that a basic marker for the disease is ASH, defined echocardiographically as a septal to posterior wall thickness ratio1 >1.3 although diseases other than hypertrophic cardiomyopathy may result in echocardiographic ASH. A variety of ECG findings have been reported in association with hypertrophic cardiomyopathy, including ventricular hypertrophy, â&#x20AC;&#x2DC;pseudo-infarctionâ&#x20AC;&#x2122; Q waves, atrial enlargement and abnormalities of the S-T segment and T waves. In a separate study, on description of ECG changes in ASH probable or definite, left ventricular hypertrophy was present in 33% of the patients; Q-wave patterns consistent with transmural myocardial infarction (MI)

case report were present in 21% of patients. A 35-year-old woman with 40-msec Q waves in both inferior and anterior leads had normal coronary arteries, no disorders of wall motion, and a subaortic gradient only after a premature ventricular contraction occurring during Valsalva’s maneuver. A 70-year-old man with 40-msec Q waves in leadsV1-V4 had a provocable gradient and coronary atherosclerosis but no myocardial scar at autopsy.

Three patients with anterior and four with inferior 40-msec Q-wave patterns did not undergo cardiac catheterization. None of these patients had a clinical history of MI. Our patient had no clinical history of MI.2 The various causes of pseudo-infarct patterns are described below. 

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In left ventricular hypertrophy, there is often a QS deflection or poor R-wave progression in the right precordial leads that suggests anterior MI. The secondary ST-segment elevation in these leads may be mistaken as a current of injury.

In pulmonary emphysema, the R waves in the right precordial and sometimes mid-precordial leads become quite small or are absent, suggesting anterior MI. These QRS changes are explained by the vertical displacement of the heart secondary to a low-lying diaphragm and the intervention of hyperinflated lungs.

The pseudo-infarction pattern may be seen in patients with pneumothorax. The voltage of the QRS complex may be reduced. QS deflection may appear in the right precordial leads.

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Left anterior hemiblock is occasionally associated with small Q waves in the precordial leads that mimic anterior MI. The δ waves in Wolff-Parkinson-White syndrome are frequently interpreted as abnormal Q waves of MI. Pheochromocytoma may be associated with striking ECG changes mimicking ischemic heart disease.

Other conditions that may be associated with ECG changes simulating MI include intracranial hemorrhage, hyperkalemia and acute pericarditis.

Pseudo-infarct patterns in ECG can occur in diabetic ketoacidosis with normokalemia.

Pseudo-infarct patterns in ECG can occur after intravenous flecainide.

In postoperative period after cardiac transplantation.3-10

In our patient, the renal parameters were normal with no evidence of any other systemic illness. Hence, the pattern is probably due to ASH. Conclusion 





Infarct patterns can occur in asymptomatic individuals and ASH is one of the causes.

We were mistaken because of the presence of associated risk factors like diabetes and hypertension.

We can be criticized because of the lack of establishment of normal coronaries with angiography.

In pulmonary embolism, the Q waves in lead III (as part of the S1Q3 pattern), and sometimes in lead aVF, that are accompanied

by ST-segment and T-wave changes are often interpreted as inferior MI. QS complexes with ST-segment elevation may occasionally develop in these leads and mimic acute anterior myocardial infarction.

Acknowledgments

1.

Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA 2002;287(10):1308-20.

In hypertrophic cardiomyopathy (ASH), abnormal Q waves are often seen, especially in the left precordial leads and lead I. These Q waves have been attributed to ventricular septal hypertrophy.

2.

Engler RL, Smith P, LeWinter M, Gosink B, Johnson A. The electrocardiogram in asymmetric septal hypertropy.

Chest 1979;75(2):167-73.

3.

Hung SC, Chiang CE, Chen JD, Ding PY. Images in cardiovascular medicine: pseudo-myocardial infarction. Circulation 2000;101(25):2989-90.

4.

Cheng TO, Bashour TT. Striking electrocardiographic changes associated with pheochromocytoma.

Masquerading as ischemic heart disease. Chest 1976;70(03):397-9.

5.

Burris AC, Chung EK. Pseudomyocardial infarction associated with acute bifascicular block due to hyperkalemia. Cardiology 1980;65(2):115-20.

Cont’d on page 469...

Myocardial fibrosis is responsible for the pseudoinfarction pattern in patients with dilated cardiomyopathy, progressive muscular dystrophy, Friedreich’s ataxia, scleroderma, amyloidosis and tumors of the heart.

QS deflections are often seen in the right precordial leads in patients with complete left bundle branch block in the absence of MI.

Our sincere acknowledgments to Dr T Anbalagan, Superintendent, Govt. Dist. Headquarters Hospital, Kumbakonam for allowing to publish the article.

References

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

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case report

Unusual Presentation of Blindness SA Kareem*, Siva Nambi**

Abstract A 38-year-old male patient suffered significant bilateral visual loss by putting fingers in his eyes on and off in order to keep his eyes clean. He also used to bite his lips till they bled. Detailed report of the case with psychiatric management and ocular treatment is discussed herein.

Keywords: Obsessive-compulsive disorder, leucoma cornea, SSRI, cognitive-behavioral therapy, STOP technique, insight oriented therapy, punishment therapy

T

here are several causes for blindness. Psychosomatic disorder is one of the causes of blindness.

We report an interesting case, which was seen in our institution with a psychosomatic disorder, with self-inflicted injury to both eyes leading to blindness.

Case report The patient was a 38-year-old male, and complained of repetitive thoughts and compulsion to poke his eyes in order to keep them clean since three years and repetitive thoughts and compulsion to bite his lips till they bled since three months. He was above average in school and college and participated in outdoor games.

He worked as salesman and was not working now because of poor vision in both eyes.

Both as a student and salesman, he was very particular in keeping up with time and arranging books and other articles in proper order. Other than this, he had no other illness. There was no family history of similar complaint. He was wearing teeth guard, which is usually worn by boxers to prevent injury to lips and tongue. He had covered both his hands with gauze so that he could avoid putting fingers in the eyes. He had adopted both these precautions to prevent further damage to his eyes and lips. His higher functions were normal and orientation was good. He said that he was doing these acts despite knowing well that they would harm his eyes and lips. Ocular examination showed corneal opacities, otherwise known as leucoma cornea, almost involving the whole cornea in both *Head, Dept. of Ophthalmology **Former Head, Dept. of Psychiatry Sri Balaji Medical College and Hospital, Chennai Address for correspondence Dr SA Kareem Head, Dept. of Ophthalmology Sri Balaji Medical College and Hospital, Chennai

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

eyes. He demonstrated how he was putting his fingers in the eyes for cleaning the cornea, upper and lower fornices of the conjunctiva. Vision in the right eye was counting fingers (2 meters) and left eye counting fingers (6 meters). Other details of the eyes including the fundi were seen through the hazy corneas and appeared normal. Tension in both eyes was normal.

He also had scars in the lips due to repeated biting.

Investigations All investigations relevant to this case were normal.

Diagnosis Severe obsessive-compulsive disorder (OCD) with leucoma cornea both eyes.

Management This patient, a case of severe OCD was managed by the psychiatrist with medications, behavioral therapy (BT) and cognitive behavioral therapy (CBT). The selective serotonin reuptake inhibitors (SSRIs) are effective in this condition. Clomipramine, fluoxetine, fluvoxamine and sertraline are approved for the treatment of OCD. Thought STOP technique was taught to him and the patient would say loudly â&#x20AC;&#x2DC;STOPâ&#x20AC;&#x2122;, the movement he had the compulsion to put his fingers in the eyes.

The other therapies given by the psychiatrist were: Insight oriented therapy and punishment therapylike putting rubber bands in his hands to cause mild pain by pulling, whenever he had the compulsion to put fingers in his eyes. The leucoma cornea was managed by lubricating eye drops. Patients condition was improving gradually and his OCD is much under control and patient is being followed up regularly.

Once his psychiatric condition is well-controlled,

case report keratoplasty can be done for his leucoma cornea to improve his vision.

Discussion OCD is characterized by persistent and uncontrollable thoughts and irrational beliefs that can cause an individual to perform compulsive rituals that interfere with the daily life. It is an anxiety disorder. Obsessions are thoughts that are observed and the patients want to avoid them, but such thoughts will keep on coming with more and more force, which produce a lot of anxiety.

Common obsessions are fear of contamination, precise arranging, aggressive thoughts, doubts like door locked, cooking gas switched off, unwanted thoughts on sex and religion. Compulsions are repetitive acts carried out in stereotyped manner like repeated washing of the hands, taking bath for long time, repeated checking, counting and asking for reassurance.

Obsessions and compulsions may occur separately.

But they occur together so often that they are considered two aspects of a single disorder called OCD. It is gradual in onset and the illness may last for 2-3 years before treatment. There is accompanying anxiety when the person takes countermeasures against certain ideas.

Apart from this, a significant number of patients may have co-morbid depression.

Deficiency of the neurotransmitter, serotonin (5-HT) is considered to be the cause for OCD. About 1-2% population in India suffer from this, but only 10-15% come for medical help. OCD is a chronic disorder.

Those with OCD often do not seek treatment. They often feel shame regarding their symptoms and take great effort into concealing them. While many patients experience moderate symptoms, OCD can be a severe and disabling illness, causing serious illness like loss of vision as in this case.

Conclusion Severe clinical complications like blindness can occur in psychosomatic disorders.

Suggested reading 1.

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th edition, Text Revision (DSM-IV-TR). American Psychiatric Association: Washington, DC, 2000.

2.

Bartz J, Hollander E. Is obsessive-compulsive disorder an anxiety disorder? Prog Neuropsychopharmacol Biol Psychiatry 2006;30(3):338-52.

3.

Greist JH, Jefferson JW, Kobak KA, Katzelnick DJ, Serlin RC. Efficacy and tolerability of serotonin transport inhibitors in obsessive-compulsive disorder: a metaanalysis. Arch Gen Psychiatry 1995;52(1):53-60.

4.

Lin PY. Meta-analysis of the association of serotonin transporter gene polymorphism with obsessivecompulsive disorder. Prog Neuropsychopharmacol Biol Psychiatry 2007;31(3):683-9.

5.

Koran LM, Hanna GL, Hollander E, Nestadt G, Simpson HB; American Psychiatric Association. Practice guideline for the treatment of patients with obsessive-compulsive disorder. Am J Psychiatry 2007;164(7 Suppl):5-53.

6.

Foa EB, Wilson R. Stop Obsessing! How to Overcome Your Obsessions and Compulsions. Bantam Books: New York, 1991.

7.

Grayson J. Freedom from Obsessive-Compulsive Disorder: A Personalized Recovery Program for Living with Uncertainty. Berkley Publishing Group.

New York, 2004.

8.

Torres AR, Domingues Mde S, Shiguematsu AI, Samira SI. Loss of vision secondary to obsessivecompulsive disorder: a case report. Gen Hosp Psychiatry 2009;31(3):292-4.

...Contâ&#x20AC;&#x2122;d from page 467 6.

7.

8.

Makaryus AN, Adedeji O, Ali SK. Acute pancreatitis presenting as acute inferior wall ST-segment elevations on electrocardiography. Am J Emerg Med 2008;26(6):734.e1-4.

Lustik SJ, Wojtczak J, Chhibber AK. Wolff-ParkinsonWhite syndrome simulating inferior myocardial infarction in a cocaine abuser for urgent dilation and evacuation of the uterus. Anesth Analg 1999;89(3):609.

Aksakal E, Duman H, Ulus T, Bayram E. Acute inferior pseudoinfarction pattern in a patient with normokalemia

and diabetic ketoacidosis. Am J Emerg Med 2009;27(2): 251.e3-5.

9.

van Aubel KJ, Ruiter JH, Arnold AE, Burgersdijk C. Pseudo infarction ECG pattern occurring during intravenous treatment with flecainide acetate. Eur Heart J 1992;13(1):137-9.

10. Aziz TA, Pereira NL. Electrocardiographic changes simulating a myocardial infarction after cardiac transplantation. J Heart Lung Transplant 2004;23(11): 1301-3.

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legal question

What should Doctors and Nursing Homes do to Prevent and Manage Violence by Patients/Relatives?

MC Gupta

Q. Doctors in Jharkhand are endangered by violent attendants of the patients. There is no medical protection act in our state. What should we do?

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Ans. You should do as follows: One: preventive Action by Individual Practitioners

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A. The Indian Medical Council (Professional conduct, Etiquette and Ethics) Regulations, 2002, should be strictly complied with.

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B. Keep liaison with the local police.

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C. Keep proper records.

D. Do not commit negligence. Be knowledgeable in your subject. Do not venture out of your area of work/expertise.

Two: preventive Action by Nursing Homes/ hospitals It needs to be appreciated that violence against hospitals occurs mainly because of lack of information and misunderstanding. It also occurs because of negligence or crudeness or arrogance or greed on the part of nursing homes. The nursing homes should do the following: A. They should take steps to minimize the possibility of such attacks. Examples of such steps are: 

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470

The Indian Medical Council (Professional conduct, Etiquette and Ethics) Regulations, 2002, should be strictly complied with by the doctors working in the nursing home.

A notice should be prominently displaced providing information to the public about the actions that an aggrieved patient may take. Such information may include:  Name and mobile telephone number of the person/doctor who is officially assigned the duty of attending patient complaints/ emergencies on 24-hour basis.  Name of the person in charge and the members of the “Patients Grievance Redressal Committee” of the hospital or nursing home concerned and the time limit (say, 48 hours)

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

during which the Committee would take initial necessary action.

The mechanism for supplying a copy of patients’ medical records on request, including the fees and time limit for the same.

Name and address of the local Indian Medical Association (IMA) “Patients Grievance Cell”, if such a cell exists.

Name and address of the State Medical Council.

Name and address of the District Consumer Forum.

The following information should also be prominently displayed:  Schedule of hospital charges  Names, qualifications and medical council registration numbers of all doctors.

B. They should buy a hospital professional indemnity policy through a legal risk cover company. While choosing the legal risk cover company, they should choose that company whose terms and conditions include a written clause that the company will provide legal services in connection with criminal/ police complaints related to violence against the hospital.

C. They should organize a collective nursing home defence mechanism through the local IMA. If this is not possible, a few nursing homes should come together on their own to form such a joint mechanism. Such joint defense mechanism, Joint Defense Academy (JDM), would do the following: 

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

It would collect fees from members and keep proper accounts of the funds collected and spent.

It would provide the following services to the members:  Liaising with the police.  Organizing joint seminars on the issues related to nursing home protection. The local police officers; CMO; DM; media and some persons from the legal field, if possible the magistrate or sessions judge, should be invited on these occasions and they should be requested to express their views.

legal question 

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Engaging the services of an advocate on the criminal side to act as a standing counsel for the member nursing homes for any legal help at times of violence.

Engaging the services of a security agency to provide security cover in normal times as well, additionally, in emergencies, to the member nursing homes.

D. The cost of the JDM incurred by the member nursing homes should be recovered, in part or full, as appropriate, from the patients by adding an item in the bill, such as, “Protection against violence charges”. Such charges should be levied in a transparent manner and should be supported by proper accounting procedures. The consent form signed by the patient at the time of admission should clearly state that the signatory consents to pay the “hospital patients protection charges”.

E. They should take the following miscellaneous actions/precautions: 

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Only MBBS doctors should be employed in the hospital. Paramedical staff should be adequately qualified/trained.

A written undertaking should be taken from the patient and two relatives that they would not indulge in violence and that any loss to hospital property as a result of violence caused by them would be recoverable from them by various means, including but not restricted to adjustment against the advance deposit and any bank guarantee or any other guarantee provided on behalf of the patient at the time of admission.

Hospital records in respect of patients (case sheets) should be properly kept.

Treating doctors should spend sufficient time with the patients and relatives to answer their doubts and queries.

The consent form should not be got signed in a cursory manner. It should be an informed consent in the true sense.

No false assurances, even verbal, should be given to patients.

Patients should be clearly and documentedly told that they are free to shift their patient to any other hospital at any time.

Prompt police complaints should be made against those who commit violence. Video cameras should be installed at a few places to record the

photographs and voice of any bad elements who commit violence. This would greatly help in making a police complaint and pursuing it. 

Patient records should be properly maintained.

They should be kept in proper custody of the hospital and should not be loosely displayed.

However, proper and detailed referral letters and discharge summaries, containing necessary details, should be given to patients under signature when they leave the hospital.

Note: Some nursing homes may be small nursing homes with only a few beds. However, all the above measures need to be taken for every nursing home, big or small. The smaller the hospital, the more the chances of violence against it.

Three: preventive Action by the IMA A. The state IMA and the city/district branches should establish patient grievance redressal cells to look into complaints of medical negligence. These cells, if they function properly, would avoid or minimize the incidents of this type.

B. The state and district IMA branches should organize discussion meetings with the police regarding atrocities and injustice against doctors.

C. The state and district IMA branches should organize regular medicolegal updates for members with focus on medical negligence and grievances of doctors.

Four: action to be taken when Violence Occurs A. Depute someone (preferably beforehand) to take photographs and, even, audio records of the violence.

B. Depute someone to immediately get the medical record of the patient photocopied, preparing at least three copies. These will be useful for giving to the patient’s relatives and the police and to the court. If the mob carries away the original record, the photocopies will be useful.

C. Inform your advocate.

D. Inform the police immediately by phone, etc. and keep a record of such phone call, etc.

E. Identify the troublemakers/leaders in the mob and talk to them and try to pacify them, even though you may have to go out of the way to a certain extent.

F. Get written, signed statements from the persons present (doctors, staff, patients, relatives, others)

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legal question regarding the occurrence of violence. An advocate’s help in this would be specially useful. (Note: Such statements are crucial as regards the legal course of the incident and may not be easily available later).

G. Lodge an FIR with the police. It is better to let the advocate prepare the FIR. H. Issue a press statement about the incident.

I.

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472

The aggrieved doctor should not be left alone. The local IMA should provide him all support in the interest of the profession. The support should be on the following lines: It should immediately constitute a high powered committee including, amongst others, its counsel and also, preferably, a retired judge (and may be also a police officer), to probe into the incident and submit its report along with the plan of action.

It should get published in the newspapers a balanced and correct version of the incident so that the public understands the facts of the situation.

This may be by way of a press release or an advertisement.

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012



It should take direct action within law against the culprits. It should circulate amongst the members the names of those involved in the incident with a request that members may, at their discretion, decline to provide services to them except in emergency unless they submit apology to the concerned doctor and to the state IMA in writing.

Five: getting the Protection Act Passed in your State Press the state IMA to pursue with the state government to pass an act on the lines of the acts in other states such as the “Punjab Protection of Medicare Service Persons and Medicare Services Institutions (Prevention of Violence and Damage to Property) Act, 2008” or the Tamil Nadu Medicare Service Persons and Medicare Service Institutions (Prevention of Violence and Damage or Loss to Property) Act, 2008. Demand from the local MLAs and the health minister that pending the framing of a regular act, an ordinance may be passed immediately as was done in Andhra Pradesh.

At the same time, in consultation with an advocate, file a Public Interest Litigation (PIL) in this connection after necessary ground work.

photo quiz

Adolescent with a Diffuse, Progressive Rash

A

15-year-old boy presented with a diffuse rash that began on his lower extremities and rapidly progressed over the previous two weeks to his upper extremities, chest, and back. A basic metabolic panel and complete blood count were unremarkable.

Topical steroids were ineffective. The rash was associated with mild muscle aches, joint pain, and one day of emesis.

On physical examination, the patient was nontoxic and had no fever. Skin examination revealed multiple, diffuse, nonblanching purpura scattered on the distal lower extremities, lower abdomen, lower back, and distal upper extremities (Figure 1). In addition, there were several areas of coalescence with a few scattered vesicles that varied in level of progression (Figure 2).

Urine dipstick testing was unremarkable.

Figure 1.

Question Based on the patientâ&#x20AC;&#x2122;s history and physical examination, which one of the following is the most likely diagnosis?

A. Contact dermatitis.

B. Henoch-SchĂśnlein purpura.

C. Idiopathic thrombocytopenic purpura.

D. Meningococcemia.

E. Rocky Mountain spotted fever.

Figure 2.

SEE THE NEXT PAGE FOR DISCUSSION...

Source: Adapted from Am Fam Physician. 2010;82(11):1401-1402.

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Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

photo quiz Discussion

Summary Table

The answer is B: Henoch-Schönlein purpura.

Condition

Characteristics

Henoch-Schönlein purpura is the most common systemic vasculitis of childhood.1 The disease is characterized by a tetrad of clinical manifestations, including palpable purpura without thrombocytopenia or coagulopathy, arthritis and arthralgias, abdominal pain, and renal disease. The rash often begins with erythematous, macular, or urticarial wheals that coalesce into ecchymosis, petechiae, and palpable purpura.2 The purpura are typically located on pressuredependent areas, often in a symmetric distribution.

Contact dermatitis

Pruritic papules and vesicles on an erythematous base that typically do not coalesce; distribution related to exposure (e.g., poison ivy, nickel)

Henoch-Schönlein purpura

Henoch-Schönlein purpura is less common in adults, often occurring between three and 15 years of age.

The condition appears primarily in the fall, winter, and spring, but rarely in the summer. Approximately 50 percent of cases are preceded by an upper respiratory infection, particularly streptococcal pharyngitis3; however, the underlying cause is unknown. HenochSchönlein purpura is an immune complex–mediated vasculitis associated with immunoglobulin A (IgA) deposition in small vessels. The diagnosis is clinical but may be confirmed with skin or renal biopsies, which demonstrate leukocytoclastic vasculitis with a predominance of IgA deposition. The clinical manifestations may develop over days to weeks and may vary in order of presentation.

Immune complex–mediated vasculitis associated with immunoglobulin A deposition in small vessels; characterized by palpable purpura without thrombocytopenia or coagulopathy, arthritis and arthralgias, abdominal pain, and renal disease; usually occurs between three and 15 years of age

Idiopathic thrombocytopenic purpura

Nonpalpable petechia; associated with thrombocytopenia and coagulopathy; lesions do not coalesce

Meningococcemia

Fever and malaise in severely ill patients; petechiae, purpura, ecchymosis; associated with neurologic symptoms

Rocky Mountain spotted fever

Rickettsial infection; blanching maculopapular eruption; may be pruritic; lesions start distally and spread centripetally to the trunk and extremities

Henoch-Schönlein purpura is usually self-limited.

Treatment includes supportive care and symptomatic therapy for arthralgias, abdominal pain, and skin irritation. Acetaminophen and nonsteroidal antiinflammatory drugs are the mainstays of treatment.

Hospitalization may be required in patients who cannot maintain hydration and in those with severe abdominal pain, gastrointestinal bleeding, mental status changes, or renal disease. Early, aggressive oral prednisone is recommended for patients with severe renal involvement.1 Contact dermatitis is characterized by pruritic papules and vesicles on an erythematous base that typically do not coalesce.4 A causative exposure typically can be identified, such as poison ivy or nickel, and distribution of the rash is usually related to exposure.

Idiopathic thrombocytopenic purpura is characterized by nonpalpable petechiae, which occur mostly in areas that are subject to pressure, such as the lower extremities, belt line, and buttocks.5 The lesions do not coalesce.

The condition is associated with thrombocytopenia and coagulopathy.

Meningococcemia is a severe systemic infection that usually causes fever and malaise. The condition can occur at any age.4 The rash appears as petechiae, purpura, and ecchymosis. Patients often have neurologic symptoms (e.g., mental status changes) at presentation.

Rocky Mountain spotted fever is a rickettsial infection that appears as a classic blanching, maculopapular eruption on the wrists and ankles, then spreads centripetally to involve the trunk and extremities.6 REFERENCES 1.

Reamy BV, Williams PM, Lindsay TJ. Henoch-Schönlein purpura. Am Fam Physician. 2009;80(7):697-704.

2.

Roane DW, Griger DR. An approach to diagnosis and initial management of systemic vasculitis. Am Fam Physician. 1999;60(5):1421-1430.

3.

Masuda M, Nakanishi K, Yoshizawa N, Iijima K, Yoshikawa N. Group A streptococcal antigen in the glomeruli of children with Henoch-Schönlein nephritis.

Am J Kidney Dis. 2003;41(2):366-370.

4.

Ely JW, Seabury Stone M. The generalized rash: part I. Differential diagnosis. Am Fam Physician. 2010;81(6): 726-734.

5.

Blanchette V, Bolton-Maggs P. Childhood immune thrombocytopenic purpura: diagnosis and management.

Hematol Oncol Clin North Am. 2010;24(1):249-273.

6.

Elston DM. Tick bites and skin rashes. Curr Opin Infect Dis. 2010;23(2):132-138.

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practice guidelines

ACCP Releases Statement on Dyspnea Treatment in Patients with Advanced Lung or Heart Disease

M

ore than 90 percent of patients with advanced chronic obstructive pulmonary disease and more than 60 percent with advanced heart disease experience breathlessness. Approximately 94 percent of patients with chronic lung disease experience dyspnea in the last year of life. One study found that many patients who died of chronic obstructive pulmonary disease had dyspnea, with serious dyspnea more common than serious pain. Although it is not known what causes dyspnea, physicians should provide treatment for this symptom. Patients have not received consistent or effective treatment for dyspnea; therefore, the American College of Chest Physicians (ACCP) wrote a consensus statement to influence clinical practice and provide suggestions regarding the management of dyspnea in patients with advanced lung or heart disease.

Measurement Physicians are ethically obligated to treat dyspnea.

They should routinely ask patients about the intensity of their breathlessness, which should then be documented in the medical record. Physicians should also reassure patients and their families that they will treat dyspnea.

Evaluation of dyspnea should include asking about the distress, meaning, and needs that come with breathlessness. Three instruments are available to measure dyspnea: the Borg scale, visual analog scale, and numerical rating scale. Currently, there is no reason to use one instrument over another. Physicians should start treatment with the understanding that they should reassess whether the treatment is improving dyspnea without causing adverse effects.

Treatment

Nonpharmacologic Oxygen therapy is the standard of care for patients with hypoxemia, but only a limited number of studies have assessed the short-term effects of supplemental oxygen on breathlessness at rest in patients with advanced lung Source: Adapted from Am Fam Physician. 2010;82(8):999-1000.

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disease. Two studies found significant improvements in dyspnea with oxygen therapy, whereas two found no benefit. No randomized controlled trials have evaluated the effect of oxygen therapy in patients with advanced heart disease. The ACCP determined that supplemental oxygen can provide relief for patients with dyspnea who are hypoxemic at rest or during minimal activity.

No studies were found that evaluated the effect of supplemental oxygen in patients without hypoxemia at rest.

Pursed-lip breathing, a breathing strategy often used by patients with airway obstruction, can provide relief of dyspnea. When performed at rest, pursed-lip breathing improves oxygen saturation, reduces carbon dioxide levels, and promotes slower, deeper breathing.

Relaxation therapy can also relieve dyspnea. One study found that, compared with patients who sat quietly, those who listened to a recorded relaxation message reported less dyspnea. Another study found that progressive muscle relaxation reduced dyspnea in patients with chronic obstructive pulmonary disease after each of four weekly sessions, but not at the end of the four-week period.

Noninvasive positive pressure ventilation can provide some relief. Three systematic reviews of noninvasive positive pressure ventilation concluded that it improved the patientâ&#x20AC;&#x2122;s perception of dyspnea. Four other studies found modest to significant improvement of dyspnea, as reported by the patient.

Pharmacologic Oral and parenteral opioids can improve dyspnea.

One review of 13 studies of persons with a variety of advanced chronic diseases found that morphine was effective for treating dyspnea. Two reviews of palliative care determined that short-term opioid therapy is effective for treating dyspnea at the end of life. Dosing and titration considerations should include renal, hepatic, and pulmonary function, and current and past opioid use.

Respiratory depression and overdose are concerns with the use of opioids. One study found that higher doses of opioids used in the withdrawal of life-sustaining treatment were not associated with decreased time

from withdrawal of life support to death. Other studies determined that survival time was not related to the dosage of morphine. Only one of 11 studies on arterial blood gases or oxygen saturation reported significant changes in oxygenation with opioids. Arterial carbon dioxide partial pressure did increase with the use of opioids; however, it did not exceed 40 mm Hg. Opioids may cause other adverse effects, including constipation, confusion, drowsiness, hallucinations, nausea or vomiting, and psychosis.

Ethical Issues Treatment of dyspnea should not be limited by concerns about addiction or dependence. The principle of double effect is a rationale for using opioids or sedatives that may hasten death, assuming the reason for increasing the dose is to provide relief from dyspnea. Physicians

should assess patients for anxiety and depression, which often accompany dyspnea.

Physicians should communicate with patients about end-of-life care. Although it has been shown that most patients with advanced disease want to discuss end-of-life care with their physicians, few physicians discuss such issues with their patients. It is important to understand the barriers to this communication. In some cultures, family members may have different views regarding the role of family and who should be involved in decision making about treatment at the end of life. Differences in family perspectives or spiritual beliefs on the value of maintaining consciousness at the end of life, as well as the value of suffering, should be anticipated. Physicians should be prepared to apply principles of culturally effective end-of-life care in these situations.

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lighter reading

The American investment banker was at the pier of a small coastal Mexican village when a small boat with just one fisherman docked. Inside the small boat were several large yellow fin tuna.

The American complimented the Mexican on the quality of his fish and asked how long it took to catch them. The Mexican replied, “Only a little while.”

The American then asked, “Why didn’t you stay out longer and catch more fish?” The Mexican said, “With this I have more than enough to support my family’s needs.” The American then asked, “But what do you do with the rest of your time?” The Mexican fisherman said, “I sleep late, fish a little, play with my children, take siesta with my wife, Maria, stroll into the village each evening where I sip wine and play guitar with my amigos, I have a full and busy life.”

The American scoffed, “I am a Harvard MBA and could help you. You should spend more time fishing; and with the proceeds, buy a bigger boat: With the proceeds from the bigger boat you could buy several boats. Eventually you would have a fleet of fishing boats. Instead of selling your catch to a middleman you would sell directly to the processor; eventually open your own cannery. You would control the product, processing and distribution. You would need to leave this small coastal fishing village and move to Mexico City, then Los Angeles and eventually New York, where you will run your ever - expanding enterprise.”

lab update

Working Towards What you Already Have

Stool Examination O and P (Ova and Parasite) testing: A microscopic evaluation of stool for parasites and the ova (eggs, cysts) of parasites. A basic test but very important!!

—Dr Arpan Gandhi, Dr Navin Dang

laugh a while

An Inspirational Story

Lighter Side of Medicine

Boss: Have you ever seen an owl?

Man (looking down): No Sir……

Boss: Don’t look down. Look at me.

—Dr GM Singh

Make Sure

During Medical Practice A 28-year-old male presents with increased frequency and occasional blood in urine. Examination of urine shows sterile pyuria.

Oh my God! Why didn’t you check for TB?

Make sure to rule out TB in patients with frequency, dysuria, hematuria. Sterile pyuria is the first clue to diagnosis.

—Ms Ritu Sinha

KK Aggarwal

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©IJCP Academy

The Mexican fisherman asked, “But, how long will this all take?” To which the American replied, “15-20 years.” “But what then?” asked the Mexican.

The American laughed and said that’s the best part.

“When the time is right you would announce an IPO and sell your company stock to the public and become very rich, you would make millions.” “Millions? Then what?” The American said, “Then you would retire.

Move to a small coastal fishing village where you would sleep late, fish a little, play with your kids, take siesta with your wife, stroll to the village in the evenings, where you could sip wine and play your guitar with your amigos.”

Information for Authors Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767).

Indian Journal of Clinical Practice strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so.

The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript.

Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper.

Covering letter –

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The covering letter should explain if there is any deviation from the standard IMRAD format (Introduction, Methods, Results and Discussion) and should outline the importance of the paper.

Principal/Senior author must sign the covering letter indicating full responsibility for the paper submitted, preferably with signatures of all the authors.

Articles must be accompanied by a declaration by all authors stating that the article has not been published in any other Journal/Book. Authors should mentioned complete designation and departments, etc. on the manuscript.

Manuscript – Three complete sets of the manuscript should be submitted and preferably with a CD; typed double spaced throughout (including references, tables and legends to figures).

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The manuscript should be arranged as follow: Covering letter, Checklist, Title page, Abstract, Keywords (for indexing, if required), Introduction, Methods, Results, Discussion, References, Tables, Legends to Figures and Figures.

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All pages should be numbered consecutively beginning with the title page.

departments and institutions where the work was performed, name of the corresponding authors, acknowledgment of financial support and abbreviations used.

– The title should be of no more than 80 characters and should represent the major theme of the manuscript.

A subtitle can be added if necessary.

– A short title of not more than 50 characters (including inter-word spaces) for use as a running head should be included.

– The name, telephone and fax numbers, e-mail and postal addresses of the author to whom communications are to be sent should be typed in the lower right corner of the title page.

– A list of abbreviations used in the paper should be included. In general, the use of abbreviations is discouraged unless they are essential for improving the readability of the text.

Summary – The summary of not more than 200 words. It must convey the essential features of the paper.

– It should not contain abbreviations, footnotes or references.

Introduction – The introduction should state why the study was carried out and what were its specific aims/objectives.

Methods – These should be described in sufficient detail to permit evaluation and duplication of the work by others.

– Ethical guidelines followed by the investigations should be described.

Statistics The following information should be given: – The statistical universe i.e., the population from which the sample for the study is selected.

– Method of selecting the sample (cases, subjects, etc. from the statistical universe).

– Method of allocating the subjects into different groups.

– Statistical methods used for presentation and analysis of data i.e., in terms of mean and standard deviation values or percentages and statistical tests such as Student’s ‘t’ test, Chi-square test and analysis of variance or non-parametric tests and multivariate techniques.

Note: Please keep a copy of your manuscript as we are not responsible for its loss in the mail. Manuscripts will not be returned to authors.

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Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the

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Confidence intervals for the measurements should be provided wherever appropriate.

Results These should be concise and include only the tables and figures necessary to enhance the understanding of the text.

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Discussion –

This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g., practicality and cost.

References These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited (Sinha12 confirmed other reports13,14...). References cited only in tables or in legends to figures should be numbered in the text of the particular table or illustration. Include among the references papers accepted but not yet published; designate the journal and add ‘in press’ (in parentheses). Information from manuscripts submitted but not yet accepted should be cited in the text as ‘unpublished observations’ (in parentheses).

At the end of the article the full list of references should include the names of all authors if there are fewer than seven or if there are more, the first six followed by et al., the full title of the journal article or book chapters; the title of journals abbreviated according to the style of the Index Medicus and the first and final page numbers of the article or chapter. The authors should check that the references are accurate. If they are not this may result in the rejection of an otherwise adequate contribution.

Examples of common forms of references are: Articles

Figures – Two complete sets of glossy prints of high quality should be submitted. The labelling must be clear and neat.

– All photomicrographs should indicate the magnification of the print.

– Special features should be indicated by arrows or letters which contrast with the background.

– The back of each illustration should bear the first author’s last name, figure number and an arrow indicating the top. This should be written lightly in pencil only. Please do not use a hard pencil, ball point or felt pen.

– Color illustrations will be accepted if they make a contribution to the understanding of the article.

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Do not use clips/staples on photographs and artwork.

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Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in the text and abbreviated as “Fig.”.

Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected

Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes.

Q. J. Expt. Physiol. 1955;40:89-111.

2. Total number of pages ________________________

Books

5. Special requests _____________________________

Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985.

6. Suggestions for reviewers (name and postal address)

Articles in Books

2.____________

2._ _______________

Strong MS. Recurrent respiratory papillomatosis. In: Scott Brown’s Otolaryngology. Paediatric Otolaryngology Evans JNG (Ed.), Butterworths, London 1987;6:466-470.

3.____________

3._ _______________

4.____________

4._ _______________

Tables –

These should be typed double spaced on separate sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.

Legends – These should be typed double spaces on a separate sheet and figure numbers (in Arabic numerals) corresponding with the order in which the figures are presented in the text.

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482

The legend must include enough information to permit interpretation of the figure without reference to the text.

Indian Journal of Clinical Practice, Vol. 22, No. 9, February 2012

summary, etc.)_______________________________ 3. Number of tables ____________________________ 4. Number of figures ___________________________

Indian 1.____________Foreign 1._ _______________

7. All authors’ signatures________________________ 8. Corresponding author’s name, current postal and e-mail address and telephone and fax numbers __________________________________________

Online Submission Also e- Issue @ www.ijcpgroup.com For Editorial Correspondence

Dr KK Aggarwal

Group Editor-in-Chief Indian Journal of Clinical Practice E-219, Greater Kailash, Part-1 New Delhi - 110 048. Tel: 40587513 E-mail: editorial@ijcp.com Website: www.ijcpgroup.com