Indian journal of clinical practice july 2014

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Indexed with IndMED

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Volume 25, Number 2

July 2014, Pages 101-200

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

Volume 25, Number 2, July 2014 from the desk of THE group editor-in-chief

105 Union Budget 2014 KK Aggarwal

Dr Deepak Chopra Chief Editorial Advisor Padma Shri, Dr BC Roy National & DST National Science Communication Awardee

Dr KK Aggarwal Group Editor-in-Chief

Dr Veena Aggarwal MD, Group Executive Editor

IJCP Editorial Board Obstetrics and Gynaecology Dr Alka Kriplani Dr Thankam Verma, Dr Kamala Selvaraj Cardiology Dr Praveen Chandra, Dr SK Parashar Paediatrics Dr Swati Y Bhave Diabetology Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty ENT Dr Jasveer Singh Dr Chanchal Pal Dentistry Dr KMK Masthan Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar Dr Rajiv Khosla Dermatology Dr Hasmukh J Shroff Dr Pasricha Dr Koushik Lahiri Nephrology Dr Georgi Abraham Neurology Dr V Nagarajan Dr Vineet Suri Journal of Applied Medicine & Surgery Dr SM Rajendran, Dr Jayakar Thomas Orthopedics Dr J Maheshwari

Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

This journal is indexed in IndMED (http://indmed.nic.in) and full-text of articles are included in medIND databases (http://mednic.in) hosted by National Informatics Centre, New Delhi.

American Family Physician

107 Sick Sinus Syndrome: A Review

Michael Semelka, Jerome Gera, Saif Usman

113 Practice Guidelines 115 Photo Quiz Anesthesiology

119 TURP Syndrome – A Quick Review and Update

Parinita C Hazarika

CARDIOLOGY

124 Pseudo Right Ventricular Myocardial Infarction in ECG of

Patients with Isolated Left Ventricular Anterior Myocardial Infarction

Monika Maheshwari

Community Medicine

126 Efficacy of Vitamin Supplementation on Plasma Homocysteine Levels Among Hyperlipidemic Patients: A Spectral and Clinical Analysis

A Bright, TS Renuga Devi, S Gunasekaran

diabetology

132 Gender-related Difference in Socioeconomic and Behavioral Factor in Relation to BP and BMI of Type 2 Diabetic Workers from Match Factories and Fireworks in Sivakasi, Tamil Nadu

V Priya, Mazher Sultana, Babuji, Kamaraj

Drug

141 Everlasting Gold Standard Amoxicillin in the Era of Antimicrobial Resistance

Pawan Mangla

Endocrinology

144 A Comparative Study to Analyze the Association of Metabolic

Syndrome in Females with Diagnosed Polycystic Ovarian Syndrome

Richa Singh, Saroj Singh, Poonam Yadav, Harpreet Kaur

ENT

150 Self-Inflicted Styloid Process Fracture Cures Styalgia

Anupama Kaur, Amanpreet Singh

Gastroenterology

155 A Case Report on Perforated Duodenal Ulcer in Early Puerperium

Pradeep MR, Nandish VL, Lalithashivanna

Notifications

158 Drugs and Cosmetics


Obstetrics and Gynecology 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

161 Mature Teratoma of the Ovary Associated with Contralateral Huge Mucinous Cystadenoma: A Case Report

Nalini Sharma, WK Shullai, AS Singh, WBC Sangma

164 Paraparesis Following Spinal Anesthesia in a Patient after Cesarean Section: A Rare Entity

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166 Unilateral Atresia of Cervix Uteri and Uterus Didelphys in

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a Girl with Operated Congenital Pouch Colon

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Sangeeta Gupta, Taru Gupta, Akshay Sharma, Pushpa Bhatia, Nupur Gupta

170 Acquired Vaginal Atresia: A Case Report

Reena Yadav, Rani Reddi

173 Septic Abortion: An Unusual Case of Intrauterine Foreign Body

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.

Priyanka Mandve

Pediatrics

176 Effect of Protein and Energy Supplementation on Growth of Infants ≤1,500 g at Birth: A Randomized Trial

Janardhan Shenoy, Nivethitha, Suchetha Rao

Psychiatry

180 Body Dysmorphic Disorder – Borderline Category Between Neurosis and Psychosis

K Raman, R Ponnudurai, OS Ravindran

184 Pediatric Bipolar Disorder

Prerna Malik, Raghu Gandhi, Aparna Goyal, Savita Kundu, Anil Kumar Gulia

AROUND THE GLOBE

187 News and Views mediLAW

189 Contributory Negligence by Patient can Come to Your Rescue

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.

What’s New

194 Disease Prevention LIGHTER READING

196 Lighter Side of Medicine

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

Padma Shri, Dr BC Roy National & DST National Science Communication Awardee Sr. Physician and Cardiologist, Moolchand Medcity President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group and eMedinewS National Senior Vice President, IMA Member, Ethics Committee, MCI Chairman, Ethics 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)

Union Budget 2014

T

he Honorable Minister of Finance, Arun Jaitley, tabled Union Budget 2014, a comprehensive agenda to bolster India's long-term economic strengths and promote growth in other sectors too. This Union Budget 2014 takes an important step to address the challenges and help to take advantage of the opportunities of the global economy, while ensuring sustainable social programs and sound public finances for future generations. As far as the healthcare sector is concerned, Union Budget 2014 has a lot to cheer. The sector is the growth engine for any developing country. Huge amount of money has been pumped into the medical sector. To move towards ’Health for All‘, the two key initiatives i.e., the Free Drug Service and Free Diagnosis Service are proposed to be taken up on priority.

The Finance Minister proposes to set aside a sum of ` 500 crore to set up four more All India Institutes of Medical Sciences (AIIMS) like institutions at Andhra Pradesh, West Bengal, Vidarbha in Maharashtra and Poorvanchal in Uttar Pradesh with the ultimate aim of an AIIMS to be built and function in every state. This augers well from the affordability perspective as it would bring down the cost of healthcare services. In order to achieve universal access to early quality diagnosis and treatment to TB patients, two National Institutes of Aging have been proposed to be set up at AIIMS, New Delhi and Madras Medical College, Chennai. A national level research and referral institute for higher dental studies would be set up in one of the existing dental institutions. Presently, we have 58 government aided and approved medical colleges. The Finance Minister proposes to add 12 more government medical colleges, a step that will go some distance in bridging the supply demand gap for qualified medical personnel. In addition, dental facilities are proposed to be provided in all the hospitals Impetus has been given to preventive aspect of treatment. A sum of ` 3,600 crore has been earmarked under National Rural Drinking Water Program for providing safe drinking water through community water purification plants in next 3 years. The Central Government plans to provide central assistance to strengthen the States’ Drug Regulatory and Food Regulatory Systems by creating new drug testing laboratories and strengthening the 31 existing State laboratories. This is a welcome step as it would ensure quality healthcare delivery in the country. With the Government’s focus on improving affordable healthcare and to augment the transfer of technology for better healthcare facilities in rural India, the Finance Minister proposes to set up 15 Model Rural Health Research Centers in the states, which shall take up research on local health issues concerning rural population.

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from the desk of THE group editor-in-chief A national program in Mission Mode is urgently required to halt the deteriorating malnutrition situation in India, as present interventions are not adequate. The Finance Minister proposes to put in place a comprehensive strategy including detailed methodology, costing, time lines and monitorable targets within 6 months. To improve the plight of people with disabilities including better aids, the Finance Minister promised universal inclusive design, to include people of all abilities. He also promised to print currency notes in Braille to help the visually impaired. Other key features from the budget are summarized below: ÂÂ ` 28658 crore for sanitation and safe drinking water for girls in rural schools and ` 200 crore on women safety

will help the health status of the women. Additionally, better sanitation in the society with Swastha Bharat Abhiyan campaign will help to check communicable disease.

ÂÂ ` 50,000 crore for Rural roads and 50 crores for road safety will reduce the burden of road traffic accidents. ÂÂ Costly pan masala, tobacco and soft drinks will help lowering of disease burden. ÂÂ Introduction of e-visas will promote medical tourism. ÂÂ Increase in FDI in insurance sector by 49% will help in health insurance coverage. ÂÂ Separate schemes for differently abled people and tax exemption for senior citizen will help the society. ÂÂ Releasing of more budgets for bio-research and indigenous manufacturing units will help cheaper medical

treatments. Apart from this, free drugs and investigations will provide primary healthcare to the needy. ■■■■

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American Family Physician

Sick Sinus Syndrome: A Review MICHAEL SEMELKA, JEROME GERA, SAIF USMAN

Abstract Sick sinus syndrome refers to a collection of disorders marked by the heart’s inability to perform its pacemaking func­tion. Predominantly affecting older adults, sick sinus syndrome comprises various arrhythmias, including bradyar­rhythmias with or without accompanying tachyarrhythmias. At least 50 percent of patients with sick sinus syndrome develop alternating bradycardia and tachycardia, also known as tachy-brady syndrome. Sick sinus syndrome results from intrinsic causes, or may be exacerbated or mimicked by extrinsic factors. Intrinsic causes include degenerative fibrosis, ion channel dysfunction, and remodeling of the sinoatrial node. Extrinsic factors can be pharmacologic, metabolic, or autonomic. Signs and symptoms are often subtle early on and become more obvious as the disease pro­gresses. They are commonly related to end-organ hypoperfusion. Cerebral hypoperfusion is most common, with syn­cope or near-fainting occurring in about one-half of patients. Diagnosis may be challenging, and is ultimately made by electrocardiographic identification of the arrhythmia in conjunction with the presence of symptoms. If electrocardi­ography does not yield a diagnosis, inpatient telemetry monitoring, outpatient Holter monitoring, event monitoring, or loop monitoring may be used. Electrophysiologic studies also may be used but are not routinely needed. Treat­ment of sick sinus syndrome includes removing extrinsic factors, when possible, and pacemaker placement. Pace­makers do not reduce mortality, but they can decrease symptoms and improve quality of life.

Keywords: Sick sinus syndrome, tachy-brady syndrome, cerebral hypoperfusion, holter monitoring, pacemaker placement

S

ick sinus syndrome is a collection of disorders defined by abnormal cardiac impulse formation and by abnormal propagation from the sino­ atrial node, which prevents it from perform­ ing its pacemaking function. This condition, also known as sinus node dysfunction, is associated with an atrial rate that does not meet the body’s physiologic requirements. It manifests clinically as arrhythmias that can include sinus bradycardia, sinus pauses or arrest, sinoatrial exit block, or alternating bradyarrhythmias and tachyarrhythmias. These manifestations can lead to chrono­tropic incompetence, which is an inadequate heart rate response to exercise or stress.1-6

Prevalence Sick sinus syndrome usually occurs in older adults, but it can affect persons of all ages. One in 600 cardiac patients older than 65 years has this syndrome.1 In one

MICHAEL SEMELKA, DO, FAAFP, is the residency director and chairman of the Department of Family Medicine at Excela Health Latrobe (Pa.) Hospital. JEROME GERA, MD, is a faculty physician at Excela Health Latrobe Hospital. SAIF USMAN, MD, is a sports medicine fellow at the University of Missouri–Kansas City School of Medicine. At the time this article was writ­ten, Dr. Usman was a resident physician at Excela Health Latrobe Hospital. Source: Adapted from Am Fam Physician. 2013;87(10):691-696.

study of patients older than 21 years with sick sinus syndrome, the median age was 74 years.7 Men and women are affected equally.7 Causes The etiology of sick sinus syndrome can be divided into intrinsic causes and extrinsic factors that disrupt the function of the sino­atrial node (Table 1).1,3,6,8-10

Intrinsic Causes Intrinsic causes of sick sinus syndrome include degenerative fibrosis of the sinoatrial node, ion channel dysfunction, and remod­eling of the sinoatrial node. Historically, the most common intrinsic cause is thought to be age-related, idiopathic degenerative fibro­sis of the sinoatrial node.8 Recent research and understanding of familial and con­ genital sick sinus syndromes, however, have shown that an inherited dysfunction of ion channels within the sinoatrial node also plays a significant part in age-related sick sinus syndrome.1,9,11-13 Remodeling of the sinoatrial node occurs in heart failure and atrial fibrillation, and this appears to play a role in the development of sick sinus syndrome for some patients.1,14,15 Certain infiltrative disease processes, including connective tissue diseases,

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American Family Physician hemo­ chromatosis, sarcoidosis, and amyloidosis, may also cause intrinsic dysfunction of the sinoatrial node.10 Atherosclerotic changes of the sinus node artery, which originates from the proximal right coronary artery in 65 per­cent of patients,10 may contribute to chronic ischemia and subsequent fibrosis of the sinoatrial node, but are not considered to be a major cause of sick sinus syndrome.3,16

Extrinsic Factors Extrinsic factors that can mimic or exacerbate sick sinus syndrome include the use of certain pharmaco­ logic agents, metabolic disturbances, and autonomic dysfunction. The pharmacologic agents that commonly cause dysfunction of the sinoatrial node are beta block­ ers, calcium channel blockers, digoxin, sympatholytic medications, antiarrhythmic medications, and lith­ium.10,17 The most common electrolyte abnormalities leading to dysfunction of the sinoatrial node are hyper­kalemia, hypokalemia, and hypocalcemia. Other extrinsic factors include hypothyroidism, hypoxia, hypothermia, and toxins. Autonomic dysfunc­ tion can mimic or exacerbate sick sinus syndrome via neurally mediated bradycardia in vasova­ gal syncope, neurocardiogenic syncope, and carotid sinus Table 1. Causes of Sick Sinus Syndrome Intrinsic causes Degenerative fibrosis Infiltrative disease processes Amyloidosis Connective tissue diseases Hemochromatosis Sarcoidosis Ion channel dysfunction Remodeling of the sinoatrial node

Extrinsic factors that mimic or exacerbate sick sinus syndrome (continued) Hypocalcemia Hypokalemia Hypothermia Hypothyroidism Hypoxia Obstructive sleep apnea Pharmacologic agents

Extrinsic factors that mimic or exacerbate sick sinus syndrome

Antiarrhythmic medications (class I and III)

Autonomic dysfunction Carotid sinus hypersensitivity

Calcium channel blockers (nondihydropyridine)

Neurocardiogenic syncope

Digoxin

Vasovagal syncope

Lithium

hypersensitivity.10,18-20 Although rare, findings of sick sinus syn­drome can be associated with other cardiac abnormalities such as Brugada syndrome, which is an ion channel disorder that can lead to sudden cardiac death.5,21 Signs and Symptoms Sick sinus syndrome tends to be progres­sive. Patients often are asymptomatic early in the disease course, whereas those with more advanced disease can present with symptoms and signs of end-organ hypoper­fusion. Cerebral hypoperfusion is the most common, and approximately 50 percent of patients with sick sinus syndrome have near-fainting spells or syncope.3,4,22 End-organ hypoperfusion can also manifest as transient lightheadedness, confusion, fatigue, palpitations, angina, congestive heart failure, stroke, transient ischemic attacks, vague gastrointestinal symptoms, or oliguria.3,4,22,23 Electrocardiographic Findings The diagnosis of sick sinus syndrome requires electro­ cardiographic findings of bradyarrhythmias, such as sinus bradycardia, sinoatrial pause of three seconds or more, sinoatrial exit block, or sinus arrest1-6 (Table 23,24). However, findings often are normal in patients with sick sinus syndrome, particularly early in the disease course, making the diagnosis a challenge. Although bradyarrhythmias are required for the diagnosis, supraventricular tachyarrhythmias are pres­ent in at least 50 percent of patients with sick sinus syndrome.6,25 Episodes of alternating tachyarrhyth­ mias and bradyarrhythmias are known as tachycardia-bradycardia, or tachy-brady, syndrome1,3,6,25 (Figure 13). The most common tachyarrhythmias are atrial fibril­ lation or flutter with rapid ventricular response.5,6 These tachyarrhythmias are more common in older patients with advanced sinoatrial nodal disease in whom sino­ atrial node fibrosis may favor reentrant beats or tachy­

Beta blockers

Increased vagal tone (occurs in Sympatholytic medications athletes and during sleep) Toxins Metabolic disturbances Hyperkalemia Information from references 1, 3, 6, and 8 through 10.

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Figure 1. Electrocardiogram from a patient with tachybrady syndrome.


American Family Physician cardia.8,26 Additionally, there is evidence that atrial fibrillation and flutter can lead to atrial remodeling and subsequent dysfunction of the sinoatrial node.1,14,15 Clinical Diagnosis Sick sinus syndrome is diagnosed by correlating symp­ toms of end-organ hypoperfusion with the occurrence of bradycardia, with or without accompanying tachy­ cardia.3 Electrocardiographic abnormalities and clini­ cal symptoms must be present. Marked bradycardia, including sinoatrial pauses of three seconds or more, is not diagnostic of sick sinus syndrome in the absence of symptoms. Electrocardiographic abnormalities in the absence of symptoms may be explained by physiologic and pathophysiologic processes such as increased vagal tone during sleep or obstructive sleep apnea.6,27,28 When 12-lead electrocardiography does not yield a diagnosis, prolonged cardiac monitoring should be con­sidered.5,29 Depend­ing on the severity of symptoms and the overall clinical picture, this can be done in the

hospital via telemetry moni­toring or on an out­patient basis with a 24- to 48-hour Holter monitor.30 If no definitive diagnosis is made, Holter monitoring can be repeated. If clinical suspicion of arrhythmia remains high and Holter monitoring results are negative, the next step should be longer-duration cardiac monitoring.31-33 Monitoring can occur for weeks at a time with external continuous or event monitors, or for months at a time with an implantable loop recorder; Table 3 lists available ambulatory monitoring devices.30,34,35 Although rhythm monitoring is the diagnostic stan­ dard, electrophysiologic studies are sometimes useful in the evaluation of sick sinus syndrome. These stud­ ies evaluate patients in whom sick sinus syndrome is strongly suspected but no arrhythmia has been demon­ strated that correlates with symptoms after prolonged cardiac monitoring.7 The rhythm abnormalities of sick sinus syndrome occasionally are detected or suspected as an incidental finding during evaluation and treatment of other car­

Table 3. Ambulatory Cardiac Monitoring Devices Type of monitor

Typical duration of use

Description

Activation and transmission of data

Holter

24 to 48 hours

Continuous Data stored on monitoring device monitoring; all that is uploaded at the conclusion recorded data stored of monitoring period

Indication

Cost

First-line choice in ambulatory monitoring

$104

Mobile One to four cardiovascular weeks telemetry

Continuous prolonged monitoring; all recorded data stored

Data transmitted daily by cell phone device and in real time when triggered by arrhythmia or manually by patient

Nondiagnostic Holter monitoring and/or intermittent symptoms of syncope, dizziness, or palpitations

$780

Presymptom event monitor

Two to four weeks

Continuous loop monitoring; data deleted every few minutes if device not activated

Triggered by arrhythmia or manually by patient; five to 30 minutes of pre- and postevent monitoring is recorded and transmitted by patient via telephone or e-mail

Nondiagnostic Holter monitoring and/or intermittent symptoms of syncope, dizziness, or palpitations

$305

Postsymptom event monitor

Two to four weeks

Intermittent patientinitiated monitoring

Triggered by patient activating device on wrist or placing device on chest to initiate recording; data transmitted by patient via telephone or e-mail

Nondiagnostic Holter monitoring and/or intermittent symptoms of syncope, dizziness, or palpitations

$261

Implantable loop recorder

Months to three years

Continuous loop monitoring; data deleted every few minutes if device not activated

Triggered by arrhythmia or manually by patient; five to 40 minutes of pre- and postevent monitoring is recorded; data uploaded in physician office or transmitted by patient via telephone or e-mail

Nondiagnostic, noninvasive monitoring for recurrent, intermittent symptoms of syncope, dizziness, or palpitations

$4,374

Information from references 30, 34, and 35.

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American Family Physician diac conditions.36 For example, two small studies of patients undergoing exercise treadmill testing found that 38 to 57 percent of patients with known sick sinus syndrome were unable to achieve a maximal heart rate of 120 beats per minute.37,38 This inadequate response to exercise suggests chronotropic incompetence that occurs in persons with sick sinus syndrome, but there are no well-validated standards for diagnosing sick sinus syndrome in this setting.6 Carotid sinus massage or pressure that results in a sinoatrial pause for more than three seconds is also suggestive, but not diagnostic, of sick sinus syndrome.3,5,18 Complications of Sick Sinus Syndrome More than 50 percent of patients with sick sinus syn­ drome develop tachy-brady syndrome with atrial fibril­ lation or flutter as the tachyarrhythmia, leading to an increased risk of embolic stroke. Anticoagulation ther­ apy has been shown to decrease the number of embolic events and strokes, and the decision to start anticoagu­ lant medication can be based on American College of Cardiology Foundation/American Heart Association guidelines.39 Patients with sick sinus syndrome are also at risk of developing atrioventricular block. This occurs in 0.5 to 1.5 percent of patients per year,6,40 and eventually Table 4. Reasons for Permanent Pacemaker Implantation in Patients with Sick Sinus Syndrome

Table 5. Pacemaker Options for Patients with Sick Sinus Syndrome Indication

Type of pacemaker

Sick sinus syndrome with normal atrioventricular conduction*

Dual chamber pacing or atrial inhibited pacing

Sick sinus syndrome with known atrioventricular conduction abnormality (including bundle branch block and bifascicular block)

Dual chamber pacing

*Dual chamber pacing is the preferred pacemaker setting for this indication because of the propensity of patients to develop atrioventricular block; however, atrial inhibited pacing can also be used. Information from references 6, and 44 through 50.

develops in as many as one-half of patients with sick sinus syndrome.41 Treatment Permanent pacemaker placement is recommended only in patients with symptomatic sick sinus syndrome and documented bradycardia;6 it is the only effective treat­ ment for chronic symptomatic sick sinus syndrome that is not caused by correctable extrinsic factors.1,3,25 In 2009, there were 235,567 new pacemakers implanted in the United States.42 Historically, sick sinus syndrome accounts for one-half of pacemaker implantations.1,3,25

Symptomatic sinus bradycardia caused by medication required for medical condition

Pacemaker therapy has not been shown to affect sur­vival rates in this population. Rather, the primary goal of pacemaker placement is to relieve symptoms and improve quality of life.43 Tables 46 and 56,44-50 list indica­ tions for pacemaker implantation in patients with sick sinus syndrome. Given the propensity for these patients to develop atrioventricular block, dualchamber pace­makers are generally preferred.6,44-50

Implantation is reasonable

For complete article see; www.aafp.org/afp.

Significant symptoms of bradycardia and documented heart rate less than 40 beats per minute without documentation of bradycardia during symptoms

REFERENCES

Implantation is indicated Documented symptomatic bradycardia with frequent sinus pauses that produce symptoms Symptomatic chronotropic incompetence

Syncope of unexplained origin with dysfunction of sinoatrial node discovered or provoked in electrophysiologic studies Implantation may be considered Minimally symptomatic patients with chronic heart rate less than 40 beats per minute while awake Note: The American College of Cardiology/American Heart Association/ Heart Rhythm Society guidelines rated the supporting evidence for these recommendations as Level C (consensus, disease-oriented evidence, usual practice, expert opinion, or case series). Information from reference 6.

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1. Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. Circulation. 2007;115(14):1921-1932. 2. Melzer C, Witte J, Reibis R, et al. Predictors of chronotropic incompe­ tence in the pacemaker patient population. Europace. 2006;8(1):70-75. 3. Adán V, Crown LA. Diagnosis and treatment of sick sinus syndrome. Am Fam Physician. 2003;67(8):1725-1732. 4. Guidelines for Clinical Intracardiac Electrophysiological and Catheter Ablation Procedures. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. (Com­mittee


American Family Physician on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures). Developed in collaboration with the North American Soci­ety of Pacing and Electrophysiology. Circulation. 1995;92(3):673-691. 5. Keller KB, Lemberg L. The sick sinus syndrome. Am J Crit Care. 2006;15(2):226-229. 6. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/ HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormali­ties: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collabo­ration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons [published corrections appear in J Am Coll Cardiol. 2009;53(16):1473, and J Am Coll Cardiol. 2009;53(1):147]. J Am Coll Cardiol. 2008;51(21):e1-e62. 7. Lamas GA, Lee K, Sweeney M, et al. The mode selection trial (MOST) in sinus node dysfunction: design, rationale, and baseline characteristics of the first 1000 patients. Am Heart J. 2000;140(4):541-551. 8. Demoulin JC, Kulbertus HE. Histopathological correlates of sinoatrial disease. Br Heart J. 1978;40(12):1384-1389. 9. Holm H, Gudbjartsson DF, Sulem P, et al. A rare variant in MYH6 is associ­ated with high risk of sick sinus syndrome. Nat Genet. 2011;43(4):316-320. 10. Mangrum JM, DiMarco JP. The evaluation and management of brady­cardia. N Engl J Med. 2000;342(10):703-709. 11. Benson DW, Wang DW, Dyment M, et al. Congenital sick sinus syn­drome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). J Clin Invest. 2003;112(7):1019-1028. 12. Jones SA, Boyett MR, Lancaster MK. Declining into failure: the age-dependent loss of the L-type calcium channel within the sinoatrial node. Circulation. 2007;115(10):1183-1190. 13. Yeh YH, Burstein B, Qi XY, et al. Funny current downregulation and sinus node dysfunction associated with atrial tachyarrhythmia: a molec­ular basis for tachycardia-bradycardia syndrome. Circulation. 2009;119(12):1576-1585. 14. Elvan A, Wylie K, Zipes DP. Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Electrophysiological remodeling. Circulation. 1996;94(11):2953-2960. 15. Sparks PB, Jayaprakash S, Vohra JK, Kalman JM. Electrical remodeling of the atria associated with paroxysmal and chronic atrial flutter. Circula­tion. 2000;102(15):1807-1813. 16. Alboni P, Baggioni GF, Scarfò S, et al. Role of sinus node artery disease in sick sinus syndrome in inferior wall acute myocardial infarction. Am J Cardiol. 1991;67(15):11801184. 17. Oudit GY, Korley V, Backx PH, Dorian P. Lithium-induced sinus node disease at therapeutic concentrations: linking lithium-induced block­ade of sodium channels to impaired

pacemaker activity. Can J Cardiol. 2007;23(3):229-232. 18. Moya A, Sutton R, Ammirati F, et al.; Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); Euro­ pean Heart Rhythm Association (EHRA); Heart Failure Association (HFA); Heart Rhythm Society (HRS). Guidelines for the diagnosis and manage­ment of syncope (version 2009). Eur Heart J. 2009;30(21):2631-2671. 19. Gauer RL. Evaluation of syncope. Am Fam Physician. 2011;84(6):640-650. 20. Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. BMJ. 2004;329(7461):336-341. 21. Hayashi H, Sumiyoshi M, Yasuda M, et al. Prevalence of the Brugada-type electrocardiogram and incidence of Brugada syndrome in patients with sick sinus syndrome. Circ J. 2010;74(2):271-277. 22. Rodriguez RD, Schocken DD. Update on sick sinus syndrome, a cardiac disorder of aging. Geriatrics. 1990;45(1):26-30, 33-36. 23. Wozakowska-Kapłon B, Opolski G, Kosior D, et al. Cognitive disor­ders in elderly patients with permanent atrial fibrillation. Kardiol Pol. 2009;67(5):487-493. 24. Wahls SA. Sick sinus syndrome. Am Fam Physician. 1985;31(3):117-124. 25. Lamas GA, Lee KL, Sweeney MO, et al.; Mode Selection Trial in Sinus-Node Dysfunction. Ventricular pacing or dual-chamber pacing for sinus-node dysfunction. N Engl J Med. 2002;346(24):1854-1862. 26. Davies MJ, Pomerance A. Quantitative study of ageing changes in the human sinoatrial node and internodal tracts. Br Heart J. 1972;34(2):150-152. 27. Hilgard J, Ezri MD, Denes P. Significance of ventricular pauses of three seconds or more detected on twenty-fourhour Holter recordings. Am J Cardiol. 1985;55(8):10051008. 28. Ferrer MI. The sick sinus syndrome in atrial disease. JAMA. 1968;206(3):645-646. 29. Linzer M, Yang EH, Estes NA III, Wang P, Vorperian VR, Kapoor WN. Diagnosing syncope. Part I: Value of history, physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the Ameri­can College of Physicians. Ann Intern Med. 1997;126(12):989-996. 30. Zimetbaum P, Goldman A. Ambulatory arrhythmia monitoring: choos­ing the right device. Circulation. 2010;122(16):1629-1636. 31. Assar MD, Krahn AD, Klein GJ, Yee R, Skanes AC. Optimal duration of monitoring in patients with unexplained syncope. Am J Cardiol. 2003;92(10):1231-1233. 32. Sivakumaran S, Krahn AD, Klein GJ, et al. A prospective randomized comparison of loop recorders versus Holter monitors in patients with syncope or presyncope. Am J Med. 2003;115(1):1-5. 33. Edvardsson N, Frykman V, van Mechelen R, et al.; PICTURE Study Inves­tigators. Use of an implantable loop

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American Family Physician recorder to increase the diagnostic yield in unexplained syncope: results from the PICTURE registry. Euro­pace. 2011;13(2):262-269. 34. Olson JA, Fouts AM, Padanilam BJ, Prystowsky EN. Utility of mobile cardiac outpatient telemetry for the diagnosis of palpitations, presyn­ cope, syncope, and the assessment of therapy efficacy. J Cardiovasc Electrophysiol. 2007;18(5):473-477. 35. Krahn AD, Klein GJ, Skanes AC, Yee R. Insertable loop recorder use for detection of intermittent arrhythmias. Pacing Clin Electrophysiol. 2004;27(5):657-664. 36. Rosenqvist M. Atrial pacing for sick sinus syndrome. Clin Cardiol. 1990;13(1):43-47. 37. Abbott JA, Hirschfeld DS, Kunkel FW, Scheinman MM, Modin G. Graded exercise testing in patients with sinus node dysfunction. Am J Med. 1977;62(3):330-338. 38. Holden W, McAnulty JH, Rahimtoola SH. Characterisation of heart rate response to exercise in the sick sinus syndrome. Br Heart J. 1978;40(8):923-930. 39. Fuster V, Rydén LE, Cannom DS, et al. 2011 ACCF/ AHA/HRS focused updates incorporated into the ACC/ AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the Ameri­ can College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2011;123(10):e269-e367. 40. Kühne M, Schaer B, Kaufmann C, et al. A randomized trial compar­ing two different approaches of pacemaker selection. Europace. 2007;9(12):1185-1190. 41. Stockburger M, Trautmann F, Nitardy A, et al. Pacemakerbased analysis of atrioventricular conduction and atrial tachyarrhythmias in patients with primary sinus node

dysfunction. Pacing Clin Electrophysiol. 2009;32(5):604-613. 42. Mond HG, Proclemer A. The 11th world survey of cardiac pacing and implantable cardioverter-defibrillators: calendar year 2009—a World Society of Arrhythmia’s project. Pacing Clin Electrophysiol. 2011;34(8):1013-1027. 43. Gregoratos G. Indications and recommendations for pacemaker ther­apy. Am Fam Physician. 2005;71(8):15631570. 44. Masumoto H, Ueda Y, Kato R, et al. Long-term clinical performance of AAI pacing in patients with sick sinus syndrome: a comparison with dual-chamber pacing. Europace. 2004;6(5):444-450. 45. Jarcho JA. Resynchronizing ventricular contraction in heart failure. N Engl J Med. 2005;352(15):1594-1597. 46. Nielsen JC, Thomsen PE, Højberg S, et al.; DANPACE Investigators. A comparison of single-lead atrial pacing with dual-chamber pacing in sick sinus syndrome. Eur Heart J. 2011;32(6):686-696. 47. Healey JS, Toff WD, Lamas GA, et al. Cardiovascular outcomes with atrial-based pacing compared with ventricular pacing: meta-analysis of randomized trials, using individual patient data. Circulation. 2006;114(1): 11-17. 48. Lamas GA, Ellenbogen KA. Evidence base for pacemaker mode selec­tion: from physiology to randomized trials. Circulation. 2004;109(4):443-451. 49. Leclercq C, Hare JM. Ventricular resynchronization: current state of the art. Circulation. 2004;109(3):296-299. 50. Burkhardt JD, Wilkoff BL. Interventional electrophysiology and cardiac resynchronization therapy: delivering electrical therapies for heart fail­ure. Circulation. 2007;115(16):22082220.

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American Family Physician

Practice Guidelines AASM Updates Treatment Guidelines for Restless Legs Syndrome and Periodic Limb Movement Disorder The American Academy of Sleep Medicine (AASM) last published recommendations on the treatment of restless legs syndrome (RLS) and periodic limb movement disor­ der in 2004. It recently updated these recommendations based on a literature review and meta-analysis. Recom­ mendations were graded based on the balance of benefits and harms, and on the quality of evidence. Standard recommendations include those with high- to moderate-quality evidence that the benefits outweigh the harms; guideline recommendations are based on low-quality evidence that the benefits outweigh the harms, or high- to moderate-quality evidence that the benefits and harms are closely balanced or uncertain. Other options include those based on low-quality evidence that the benefits and harms are closely balanced or uncertain.

Restless Legs Syndrome Standard Recommendations Pramipexole and ropinirole should be used to treat patients with moderate to severe RLS. They are typically well tolerated, and adverse effects (e.g., nausea, somnolence, and nasopharyngitis with prami­ pexole; nausea and vomiting, headache, dizziness, and somnolence with ropinirole) are self-limited with cessa­tion of therapy. Guideline Recommendations Levodopa is effective in the treatment of RLS, but carries the risk of augmentation (i.e., worsening of symptoms with ongoing treatment). This agent may be most benefi­cial in patients with intermittent symptoms who do not require daily therapy. Cabergoline is more effective than levodopa but is not as well tolerated. Because of the potential for serious adverse effects, including heart valve damage, cabergoline should be used only if other recommended agents have been ineffective, and if close follow-up can be assured. Source: Adapted from Am Fam Physician. 2013;87(4):290-292.

Opioids are effective in the treatment of RLS, espe­cially for patients whose symptoms are not relieved by other medications. They are generally well tolerated and have a lower risk of augmentation than dopaminergic agents. However, patients should be monitored closely for adverse effects, including medication abuse and new or worsening sleep apnea.

Other Options Low-quality evidence supports the use of gabapentin in patients with mild to moderate RLS, par­ticularly in those with both RLS and pain. However, its potential adverse effects (e.g., sedation, dizziness, vision changes, suicidal ideation) make the balance of benefits and harms uncertain. Low-quality evidence supports the use of pregabalin in the treatment of moderate to severe RLS. However, long-term follow-up is lacking; thus, other betterstudied therapies should be considered before prescribing pregabalin. Carbamazepine has been downgraded from a guideline recommendation in a previous guideline to an option in the current update. Although its effec­tiveness was shown in earlier studies, no new studies have been performed, and other therapies have better evidence for their use. Potential adverse effects include sedation, liver abnormalities, suicidal ideation, and StevensJohnson syndrome. Clonidine has minimal supporting evidence in the treatment of RLS and carries a considerable risk of adverse effects (e.g., hypotension in normotensive patients). It may be considered in patients with con­ comitant RLS and hypertension. Iron supplementation has not been proven effective in the treatment of RLS, except in patients with low ferritin levels or refractory symptoms. Parenteral high molecular–weight iron dextran therapy carries the risk of anaphylaxis. Oral iron supplementation is associated with fewer adverse effects (primarily constipation and in rare cases, iron overload) and is recommended over parenteral therapy whenever possible.

No Recommendation There is insufficient evidence to support the use of benzo­ diazepines, valproic acid, valerian, and

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American Family Physician nonpharmacologic therapies (e.g., sleep hygiene, behavioral and nutritional strategies, compression devices, exercise) in the treatment of RLS. Transdermal rotigotine was withdrawn from the U.S. market in 2008 because of concerns about incon­ sistent absorption from the patch. It was reapproved in 2012, but because of its market status at the time the AASM guideline was published, it was given a “no recommendation” rating, despite high-level evidence of effectiveness in the treatment of moderate to severe RLS. Amantadine has been downgraded from a treatment option in the previous guideline because several superior options are available, and because there has been no new evidence for its use in patients with RLS. There is conflicting evidence on whether antidepres­sants

can cause or exacerbate RLS symptoms, and no recommendation can be made on whether patients with RLS may benefit from avoiding their use.

Periodic Limb Movement Disorder There is insufficient evidence to recommend the use of pharmacologic therapy in patients diagnosed with isolated periodic limb movement disorder. However, existing data for RLS therapy support medical interventions in some patients with RLS who have periodic limb movements. Some studies have shown statistically significant decreases in periodic limb movement indices in patients with RLS who were taking pramipexole, ropinirole, and carbidopa/ levodopa/entacapone. Gabapentin and pregaba­lin also showed improved indices in patients with RLS.

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American Family Physician

Photo Quiz Nodule Arising in a Surgical Scar A 79-year-old woman presented with a rap­idly growing nodule on her leg six months following surgical excision of a basal cell car­cinoma. The nodule was about 1 × 1 cm in size and located at the surgical site. Physical examination revealed an ery­ thematous and centrally hyperkeratotic nodule at the inferior margin of the surgical scar (see accompanying figure). The lesion began to regress after two months without treatment.

Question Based on the patient’s history and physical examination findings, which one of the fol­lowing is the most likely diagnosis? A. Basal cell carcinoma recurrence. B. Dermatofibrosarcoma protuberans.

D. Keratoacanthoma.

C. Keloid.

E. Subcutaneous fungal infection.

SEE THE FOLLOWING PAGE FOR DISCUSSION.

Source: Adapted from Am Fam Physician. 2013;87(4):285-286.

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American Family Physician Discussion The answer is D: keratoacanthoma. Kera­toacanthomas are rapidly growing tumors that are generally considered a variant of squamous cell carcinoma. Rarely, kerato­acanthomas can develop in postoperative wounds or scars.1 Keratoacanthomas are characterized by rapid growth over several weeks or months, usually followed by spontaneous resolu­ tion over four to six months. Most occur in sun-exposed areas of the skin. These lesions begin as a papule, which becomes a welldefined, uniform, firm, flesh-colored to brown nodule. Keratoacanthomas are ele­ vated away from the surrounding skin and have a central hyperkeratotic plug. They are usually 1 to 2 cm in size, but may be larger. Summary Table Condition

Characteristics

Basal cell carcinoma recurrence

Solid, flesh-colored, often translucent nodule with mother-of-pearl reflectance; telangiectasias; eventual central ulceration; no initial keratosis

Dermatofibrosarcoma protuberans

Firm, indurated, flesh-colored to redbrown plaque; slow growing; multiple exophytic nodules possible

Keloid

Firm to hard, flesh-colored to red nodule with smooth surface; may take months or years to develop; no spontaneous regression, and usually recurs after excision

Keratoacanthoma

Subcutaneous fungal infection

Initial papule becomes a welldefined, uniform, firm, flesh-colored to brown nodule with a central hyperkeratotic plug; rapid growing; usually regresses spontaneously Single or multiple, painless, erythematous or bluish nodules or plaques; slow growing, no spontaneous regression

The recurrence of basal cell carcinoma after nonradical surgical excision is typically characterized by telangiectasias and even­tual central ulceration. Nodules are solid, flesh-colored, and often translucent with mother-of-pearl reflectance. There is no initial keratosis. Dermatofibrosarcoma protuberans is a rare, nodular, sarcomatous neoplasm that can clinically resemble a keloid.2 It is a low-grade, slow-growing malignancy that appears as a firm, indurated, flesh-colored to redbrown plaque. Multiple exophytic nodules are often present. Keloids are elevated hypertrophic scars that extend beyond the borders of the origi­ nal wound, do not regress spontaneously, and usually recur after excision. They are more common in persons with darker skin pigmentation and appear as firm to hard, flesh-colored to red nodules with a smooth surface. Keloids may take months or years to develop.3 Subcutaneous fungal infections may lead to a single or multiple slow-growing, painless, erythematous or bluish nodules or plaques. These fungal infections have been reported in patients who have had a transplant, who are immunocompromised, who are from countries with poor sanitary conditions, or who have a history of a con­taminated injury.4 They require surgical or antifungal therapy. REFERENCES 1. Kimyai-Asadi A, Shaffer C, Levine VJ, Jih MH. Keratoac­ anthoma arising from an excisional surgery scar. J Drugs Dermatol. 2004;3(2):193-194. 2. Seo JK, Cho KJ, Kang JH, Lee D, Sung HS, Hwang SW. Dermatofibrosarcoma protuberans arising from a burn scar. Ann Dermatol. 2009;21(4):416-418. 3. Murray JC. Keloids and hypertrophic scars. Clin Derma­ tol. 1994;12(1):27-37. 4. Tambasco D, D’Ettorre M, Bracaglia R, et al. A sus­ pected squamous cell carcinoma in a renal transplant recipient revealing a rare cutaneous phaeohypho­mycosis by Alternaria infectoria. J Cutan Med Surg. 2012;16(2): 131-134.

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Anesthesiology

TURP Syndrome – A Quick Review and Update PARINITA C HAZARIKA

Abstract Transurethral resection of prostate syndrome (TURP-S) is one of the commonest and dreaded complications of urological endoscopic surgery. It is characterized by cardiocirculatory and neurological changes consequent to acute changes in intravascular volume and plasma solute concentrations occurring as a result of excess absorption of irrigating fluid. Even in best of hands, incidence of TURP-S is up to 20% and carries a significant mortality rate- 0.5-5% die perioperatively. It may occur at any time perioperatively and has been observed as early as few minutes after surgery has started and as late as several hours after surgery has been completed. Symptoms and signs are varied and unpredictable, and result from fluid overload and disturbed electrolyte balance and hyponatraemia. Treatment is largely supportive and relies on removal of the underlying cause, and organ and physiological support. Preoperative prevention strategies are extremely important.

Keywords: TURP syndrome, constant vigilance, prevention, early diagnosis, treatment

T

ransurethral resection of the prostate syndrome (TURP-S), first described by Creevy in 1947 is defined as a clinical condition characterized by cardiocirculatory and neurological changes consequent to acute changes in intravascular volume and plasma solute concentrations occurring as a result of excess absorption of irrigating fluid. It is one of the commonest and dreaded complications of urological endoscopic surgery. Even in best of hands, incidence of TURP-S is up to 20% and carries a significant mortality rate- 0.5 to 5% die perioperatively. It may occur at any time perioperatively and has been observed as early as few minutes after surgery has started and as late as several hours after surgery has been completed. TURP-S like syndrome may occur during endoscopic procedures such as ureterorenoscopy (URS), hysteroscopic submucosal fibroid resection, transcervical resection of endometrium (TCRE), percutaneous nephrolithotomy (PCNL), etc. Pathophysiology TURP-S affects many systems and the pathophysiology can be summarized under the following heads: ÂÂ

ÂÂ

Hypervolemia

Increased fluid absorption

Antidiuretic response to stress

Alteration in concentration of plasma solutes

Hyponatremia (dilutional)

Dept. of Anesthesiology Rajan Babu Institute of Pulmonary Medicine and Tuberculosis Kingsway Camp, Delhi

Hypo-osmolality

Hyperglycinemia

Hyperammonemia

Hypocalcemia

Hypoproteinemia (Hypoalbuminemia)

Decreased hematocrit

ÂÂ

Role of anesthesia and drugs

ÂÂ

Hemolysis

ÂÂ

Role of bacterial endotoxins

Important considerations

Hemolysis When hypotonic irrigant such as distilled water is used, there is acute hypo-osmolality with massive hemolysis. Bleeding and red cell destruction are additional sources of volume and oxygen carrying capacity losses. The hemoglobinemia and hemoglobinuria coupled with hypotension can cause acute renal failure and death. Again, hyperkalemia occurring due to cell breakdown may cause cardiac arrest.

Hyponatremia Dilutional hyponatremia (serum Na+ <130 mmol/L) is the hallmark of TURP-S syndrome. Hyponatremia causes lowering of cell membrane potential. Thus, there is disturbance of nerve conduction and muscle contraction. Also, hyponatremia leads to a reduction in plasma osmolality. Hence, water enters the intracellular space causing cell edema, hemolysis, pulmonary edema, kidney failure and in severe cases cerebral edema.

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Anesthesiology Hypo-osmolality The real cause of neuronal disturbance is the rapidly established hypo-osmolality and not hyponatremia. The effective pore size of blood brain barrier is such that it makes the barriers essentially impermeable to sodium but freely permeable to water. Physiologically, the neurons react to serum hypo-osmolality with a mechanism called ‘idiogenic osmoles’. When there is acute change of serum osmolality (within minutes to hours), this compensatory mechanism may not be triggered fast enough to prevent neuronal expansion, cerebral edema and increased intracranial pressure, which in term cause bradycardia and hypertension by cushing’s reflex. A volume of more than 2 liters, gained in 1 hour can lead to TURP-S; > 3.5 liters precipitates shock and multiple system dysfunction.

Hyperglycinemia Although glycine is accepted as the most likely cause of ‘visual disturbance’ following TURP, it may also result in’ glycine-induced encephalopathy and seizure’ and’ toxic renal effects’. The glycine absorbed with the irrigating fluid is metabolized at the hepatic and kidney level with the synthesis of ammonia, glyoxylic acid, glylcolic acid, serine and elastase, which are accumulated both in blood and cerebrospinal fluid (CSF). Glycine is the major inhibitory neurotransmitter at the levels of retina, whereas glyoxylic acid and glycolic acid are neurotoxic. Its link with the receptor of γ-aminobutyric acid (GABA) opens channels for the chloride located at the neurone surface with consequent hyperpolarization of ganglion cells (retina) thus inhibiting the neuronal impulses. Normal plasma glycine levels are 13-17 mg/ L whereas levels as high as 1,029 mg/L (up to 65 times normal) can be reached leading to transient blindness. Glycine may also lead to encephalopathy and seizure via “NDMA (N-methyl-D-aspartate), an excitatory neuro transmitter. Renal toxic effects of glycine may occasionally occur from hyperoxaluria (glycine metabolites-oxalate and glycolate).

Hyperammonemia Ammonia is a major by-product of glycine metabolism. High ammonia concentration suppresses norepinephrine and dopamine release in the brain. This causes the encephalopathy of TURP-S. Fortunately ammonia toxicity is rare in man. Characteristically the toxicity oc­curs within 1 hour after surgery. The patient develops nausea and vomiting and then lapses into coma. Blood

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ammonia rises above 500 µmol/L (normal value is 11-35 µmol/L). Hyperammonemia lasts for over 10 hours postoperatively, probably because glycine contin­ues to be absorbed from the periprostatic space. It is not clear why hyperammonemia does not develop in all TURP patients. Hyperammonemia implies that the body cannot fully metabolize glycine through the glycine cleavage system, citric acid cycle and conversion to glycolic acid and glyoxylic acid. Another possible ex­ planation is arginine deficiency. Ammonia is normally con­verted to urea in the liver via the ornithine cycle. Arginine is one of the intermediary products necessary for this cy­cle. When a patient has arginine deficiency, ornithine cycle is not fuelled and thus ammonia accumulates. SIGNS OF SYMPTOMS OF TURP-S The first sign of significant fluid absorption is a gradual or sudden rise of blood pressure (BP) (generally between 20 and 60 mmHg) accompanied by a bradycardia (10-25 beats/ min). Retrosternal chest pain is another early symptom.

Cardiopulmonary Hypertension Hypotension Tachycardia Bradycardia Dysrhythmia Cyanosis Respiratory distress Shock-death

Hemolytic and Renal ÂÂ

Hyponatremia

ÂÂ

Hemolysis/Anemia

ÂÂ

Hyperglycinemia

ÂÂ

Acute renal failure-death

Central Nervous System ÂÂ

Nausea and vomiting

ÂÂ

Visual disturbance- Temporary total blindness

ÂÂ

Confusion, restlessness

ÂÂ

Twitches - seizures Lethargy - Paralysis Dilated, nonreactive pupils Coma - death

Prevention of TURP-S This has two aspects: Surgical and anesthetic, but no method ensures that TURP-S will be avoided. Surgical preventive aspects are all designed to limit the absorption of excess irrigant during TURP.


Anesthesiology Surgical Aspects of Prevention ÂÂ

Avoidance of early capsular perforation and opening of various sinuses during TURP.

ÂÂ

Limiting the intravesical pressure by:

Adjusting the height of the irrigation bag.

Use of continuous suprapubic trocar.

flow

systems

or

ÂÂ

Limiting the resection time to 1 hour and proper selection of gland size.

ÂÂ

Selection of proper irrigation fluid.

ÂÂ

Use of bipolar saline TURP (using sodium chloride irrigation).

ÂÂ

ÂÂ

zz

Plasma sodium

zz

Plasma glycine concentration.

(The above blood samples should be monitored just before surgery, every 15 minutes during surgery and 30 minutes after termination of operation)

Other relevant measurements are: Breath ethanol content

zz

Plasma magnesium level susceptibility to seizures)

zz

Serum acid phosphates

Selecting alternative intervention in high-risk cases.

zz

Arterial blood gases metabolic acidosis)

Novel and experimental approaches:

zz

Plasma concentration of fluorescein

(indicates

(may

herald

Intraoperative intra-prostatic vasopressin.

zz

Plasma concentration of potassium

Use of 5a-reductase inhibitors.

zz

Use of load cell transducers.

Anesthetic Aspects of Prevention

ÂÂ

Osmolality

zz

Although TURP is still considered the gold standard, there are other attractive techniques such as HO; YAG and potassium-titanyl-phosphate lasers, microwave ablation and cryosurgery. Their main advantages over conventional TURP include minimal blood loss, low morbidity and minimal fluid absorption.

ÂÂ

zz

Preoperative screening

Recognizing high-risk patients for TURP-S.

Assigning proper ASA grade.

Optimization of cardiopulmonary system.

Ethanol Monitoring Highly specific and inexpensive method. This simple and safe method clearly requires a 1% ethanol marker in the irrigating fluids. It is measured by instrument called Alcomed. Cut-off level is 0.2 mg/L. TREATMENT ÂÂ

Intraoperatively as soon as the signs and symptoms of TURP-S appear, the following measure should be taken.

Intra-and postoperative aspects

Proper choice of anesthetic technique

Intense monitoring of vitals:

zz

SpO2

zz

ECG

zz

Noninvasive BP

zz

Heart rate/Pulse rate

zz

End tidal CO2 (EtCO2)

zz

Respiration

Prevention of hypothermia: zz

Adjusting OT temperature

zz

Use of warm blankets, mattresses

zz

Intravenous (IV) fluids and irrigating fluids pre-warming to 37˚C.

Blood sample measurements:

In the early phase:

ÂÂ

Alert the operating surgeon.

Try to minimize fluid absorption (adjusting reservoir height or putting a suprapubic trocar) and sometimes it is advisable to terminate surgery as soon as possible after proper hemostasis.

IV furosemide (40-100 mg) to induce diuresis.

Draw arterial blood sample for ABG and serum electrolytes.

In the late intraoperative or early postoperative phase:

Mannitol is useful in promoting diureris and eliminating intravascular volume overload.

Ascertain normal gaseous between lungs and blood.

Packed RBC

exchange

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Anesthesiology

O2 by mask

Calcium and magnesium ions to give positive inotropic effects, when needed.

If required, support respiration by endotracheal intubation and intermittent positive pressure ventilation.

Correct hyponatremia by using hypertonic saline (3%).

When there is hypotension, peripheral vasoconstrictors are useful.

In case of convulsion, short-acting anticonvulsants (diazepam or midazolam IV and in resistant cases, phenytoin or barbiturates can be given.

Packed RBC rather than whole blood is indicated in case of significant blood loss.

Restricted and cautious administration of IV fluid is necessary as these patients are very prone to pulmonary edema.

For temporary total blindness, reassurance that unimpaired vision is expected to return within 24 hours is the best treatment as half-life of glycine is only 85 minutes.

Clinical Relevance Circulatory overload occurs when weight of prostate is >45 g. Ideal height of irrigating fluid is 60 cm, so that approximately 300 mL. of fluid is obtained per minute for good vision. Symptoms of water intoxication appear when serum sodium level falls 15-20mEq/L below normal levels. Clonus and positive babinski responses are seen. Papilloedema with dilated, sluggishly reacting pupils and low voltage EEG can occur. When serum sodium level is below 120 mEq/L there is, hypotension due to reduced myocardial contractility. Below 115 mEq/L, bradycardia, widening of QRS complexes, ventricular ectopics and T-wave inversion are seen. At levels below 100 mEq/L generalized seizures coma, respiratory arrest, ventricular tachycardia, ventricular fibrillation and finally cardiac arrest occurs. Sodium deficit = Normal serum sodium-estimated serum sodium × volume of body water (body water is usually 60% of body weight). The most feared complication of correcting hyponatremia is central pontine myelinolysis (CPM), also referred to as ‘osmotic demyelination syndrome’ as demyelination can occur in extrapontine areas. Also CPM is most commonly seen in women, probably

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due to sex differences in cellular ion pump capacity. It has been reported after rapid as well as slow correction of serum sodium concentration in TURP patients. About 1.5 to 2 mmol./L/hr correction in the serum sodium levels has been suggested to be safe. Visual disturbances: Transient blindness, foggy vision and patients see halos around objects. Pupils may be dilated and unresponsive. Optic disc appears normal. Perception to light and blink responses are preserved but pupillary responses to light and accommodation are lost in TURP blindness. Summary TURP is a procedure carried out on predominantly elderly population with a higher incidence of co-existing disease. Consequently anesthetizing for the procedure may present a challenge. Early detection and prompt treatment of the syndrome are vital for a favorable outcome. Newer techniques of TURP promise a reduced risk of TURP-S. REFERENCES 1. Creevy CD. Hemolytic reactions during transurethral prostatic resection. J Urol 1947;58(2):125-31. 2. Ghanem AN, Ward JP. Osmotic and metabolic sequelae of volumetric overload in relation to the TUR syndrome. Br J Urol 1990;66(1):71-8. 3. Gravenstein D. Transurethral resection of the prostate (TURP) syndrome: a review of the pathophysiology and management. Anesth Analg 1997;84(2):438-46. 4. Malhotra V. Transurethral resection of the prostate. Anesthesiol Clin North America 2000;18(4):883-97, x. 5. Bakan N, Gedik E, Ersoy O. Early detection of the TURP syndrome. Anesth Analg 2000;91(1):250-1. 6. Moorthy HK. Philip S. Serum electrolytes in TURP syndrome - is the role of potassium underestimated? Indian J Anaesth 2002;46(6):441-4. 7. Norris HT, Aasheim GM, Sherrard DJ, Tremann JA. Symptomatology, pathophysiology and treatment of the transurethral resection of the prostate syndrome. Br J Urol 1973;45(4):420-7. 8. Hoekstra PT, Kahnoski R, McCamish MA, Bergen W, Heetderks DR. Transurethral prostatic resection syndrome - a new perspective: encephalopathy with associated hyperammonemia. J Urol 1983;130(4):704-7. 9. Olsson J, Hahn RG. Ethanol monitoring of irrigating fluid absorption in transcervical resection of the endometrium. Acta Anaesthesiol Scand 1995;39(2):252-8. 10. Hahn RG. Ethanol monitoring of irrigating fluid absorption. Eur J Anaesthesiol 1996;13(2):102-15. 11. Olsson J, Nilsson A, Hahn RG. Symptoms of the transurethral resection syndrome using glycine as the irrigant. J Urol 1995;154(1):123-8.


Anesthesiology 12. Hahn RG, Ekengren JC. Patterns of irrigating fluid absorption during transurethral resection of the prostate as indicated by ethanol. J Urol 1993;149(3):502-6. 13. Mebust WK. Transurethral surgery. In: Campbell’s Urology. Walsh PC, Retik AB, Stamey TA, Vaughan ED (Eds.), Saunders: Philadel­phia 1992:p.2900-19. 14. Henderson DJ, Middleton RG. Coma from hyponatremia following transurethral resection of prostate. Urology 1980;15(3):267-71. 15. Bernstein GT, Loughlin KR, Gittes RF. The physiologic basis of the TUR syndrome. J Surg Res 1989;46(2):135-41. 16. Zhang W, Andersson BS, Hahn RG. Effect of irrigating fluids and prostate tissue extracts on isolated cardiomyocytes. Urology 1995;46(6):821-4. 17. Hahn RG, Essén P. ECG and cardiac enzymes after glycine absorption in transurethral prostatic resection. Acta Anaesthesiol Scand 1994;38(6):550-6. 18. Evans JW, Singer M, Coppinger SW, Macartney N, Walker JM, Milroy EJ. Cardiovascular performance and core temperature during transurethral prostatectomy. J Urol 1994;152(6 Pt 1):2025-9. 19. Ashton CM, Lahart CJ, Wray NP. The incidence of perioperative myocardial infarction with transurethral resection of the prostate. J Am Geriatr Soc 1989;37(7):614-8. 20. Krohn JS. Dilutional hypocalcemia in association with dilutional hyponatremia. Anesthesiology 1993;79(5):1136-8. 21. Roesch RP, Stoelting RK, Lingeman JE, Kahnoski RJ, Backes DJ, Gephardt SA. Ammonia toxicity resulting from glycine absorption during a transurethral resection of the prostate. Anesthesiology 1983;58(6):577-9. 22. Hahn RG, Stalberg HP, Ekengren J, Rundgren M. Effects of 1.5% glycine solution with and without 1% ethanol on the fluid balance in elderly men. Acta Anaesthesiol Scand 1991;35(8):725-30. 23. Périer C, Mahul P, Molliex S, Auboyer C, Frey J. Progressive changes in glycine and glycine derivatives in plasma and cerebrospinal fluid after transurethral prostatic resection. Clin Chem 1990;36(12):2152-3. 24. Harrison RH 3rd, Boren JS, Robison JR. Dilutional hyponatremic shock: another concept of the transurethral prostatic resection reaction. J Urol 1956;75(1):95-110. 25. Hahn RG. Fluid and electrolyte dynamics during development of the TURP syndrome. Br J Urol 1990;66(1):79-84. 26. Hahn RG. Acid phosphatase levels in serum during transurethral prostatectomy. Br J Urol 1989;64(5):500-3. 27. Sohn MH, Vogt C, Heinen G, Erkens M, Nordmeyer N, Jakse G. Fluid absorption and circulating endotoxins during transurethral resection of the prostate. Br J Urol 1993;72(5 Pt 1):605-10. 28. Ovassapian A, Joshi CW, Brunner EA. Visual disturbances:

an unusual symptom of transurethral prostatic resection reaction. Anesthesiology 1982;57(4):332-4. 29. Hahn RG. Irrigating fluids in endoscopic surgery. Br J Urol 1997;79(5):669-80. 30. Hahn RG. Transurethral resection syndrome from extravascular absorption of irrigating fluid. Scand J Urol Nephrol 1993;27(3):387-94. 31. Weber S, Acuff JH, Mazloomdoost M, Kirimli BI. Transurethral prostatectomy complicated by intraperitoneal extravasation of irrigating fluid. Can J Anaesth 1987;34(2):193-5. 32. Hahn RG. Transurethral resection syndrome after transurethral resection of bladder tumours. Can J Anaesth 1995;42(1):69-72. 33. Stjernström H, Henneberg S, Eklund A, Tabow F, Arturson G, Wiklund L. Thermal balance during transurethral resection of the prostate. A comparison of general anaesthesia and epidural analgesia. Acta Anaesthesiol Scand 1985;29(7):743-9. 34. Ekengren J, Zhang W, Hahn RG. Effects of bladder capacity and height of fluid bag on intravesical pressure during transurethral resection of the prostate. Eur Urol 1995;27(1):26-30. 35. Madsen PO, Frimodt-Møller PC. Transurethral prostatic resection with suprapubic trocar technique. J Urol 1984;132(2):277-9. 36. Ekengren J, Hahn RG. Continuous versus intermittent flow irrigation in transurethral resection of the prostate. Urology 1994;43(3):328-32. 37. Singer M, Patel M, Webb AR, Bullen C. Management of the transurethral prostate resection syndrome: time for reappraisal? Crit Care Med 1990;18(12):1479-80. 38. Hahn RG, Nilsson A, Hjelmqvist H, Zhang W, Rundgren M. Renal function during intravenous infusion of urological irrigating fluids in the sheep. Acta Anaesthesiol Scand 1996;40(6):671-8. 39. Hoffman RM, MacDonald R, Wilt TJ. Laser prostatectomy for benign prostatic obstruction. Cochrane Database Syst Rev 2004;(1):CD001987. 40. O’Donnell AM, Foo IT. Anaesthesia for transurethral resection of the prostate. Contin Educ Anaesth Crit Care Pain 2009;9(3):92-6. 41. Jennifer Heisler,RN, About.Com. Guide May 27, 2010. Available at: http://surgery.about.com/bio/JenniferHeisler-RN-41438.htm 42. Rocco B, Albo G, Ferreira RC, Spinelli M, Cozzi G, Dell’orto P, et al. Recent advances in the surgical treatment of benign prostatic hyperplasia. Ther Adv Urol 2011;3(6):263-72.

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Cardiology

Pseudo Right Ventricular Myocardial Infarction in ECG of Patients with Isolated Left Ventricular Anterior Myocardial Infarction MONIKA MAHESHWARI

Abstract We describe herein one interesting case of ST-segment elevation in right precordial leads in the setting of an acute isolated left ventricular anterior myocardial infarction.

Keywords: Right ventricular myocardial infarction, left ventricular anterior myocardial infarction, pseudo ST-segment elevation

E

arliest recognition of right ventricular myocardial infarction (RVMI) is important as it defines a significant clinical entity, which is associated with considerable immediate morbidity and mortality and has a well-delineated set of priorities for it’s management. The sensitivity and specificity of ST-segment elevation in the right-sided precordial leads, especially lead RV4, for the diagnosis of RVMI is well over 90%. However, at times electrocardiogram (ECG) changes are inconsistent and bedside diagnosis may be misleading. We describe herein a case of isolated left ventricular anterior myocardial infarction (LVMI) presenting with pseudo ST-segment elevation in right precordial leads. Case Report

Figure 1a. Electrocardiogram showing ST- segment elevation in leads RV4, RV3 and V1-V4.

A 45-year-old male presented in the casualty outdoor with complaints of severe, retrosternal chest pain since 45 minutes. The pain was radiating to back and to both the arms, associated with profuse cold sweating. On physical examination, his pulse rate was 88/min, blood pressure 130/80 mmHg and respiratory rate was 26/min. Jugular venous pressure (JVP) was normal. There was no pedal edema, pallor, icterus or lymphadenopathy. Cardiovascular examination was unremarkable. Lungs were clear. Chest skiagram Associate Professor Dept. of Medicine Jawaharlal Nehru Medical College, Ajmer, Rajasthan Address for correspondence Dr Monika Maheshwari Naveen Niwas, 434/10, Bapu Nagar, Ajmer, Rajasthan E-mail: opm11@rediffmail.com

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Figure 1b. Sequential electrocardiogram showing settled ST-segment in both right-sided and left precordial leads.


Cardiology Discussion

Figure 2. Left coronary angiogram showing 90% stenosis in proximal LAD.

Figure 3. Right coronary angiogram showing normal RCA.

showed mild cardiomegaly. ECG revealed ST-segment elevation in leads RV4, RV3 and V1-V4 (Fig. 1a). Transthoracic echocardiogram showed hypokinetic LV apex and upper two-thirds of interventricular septum. However, RV walls showed no regional wall motion abnormality. The next ECG done 6 hours showed sequential changes with settled ST-segment in both right-sided and left precordial leads (Fig. 1b). Finally, coronary angiogram was planned to specify the coronary artery involved and area of myocardium jeopardized. Left coronary angiogram revealed 90% stenosis in proximal left anterior descending (LAD) artery (Fig. 2). However, to our surprise right coronary angiogram was absolutely normal (Fig. 3). Patient underwent immediate percutaneous coronary angioplasty with stenting to LAD followed by heparin, nitrates, aspirin and b-blockers. Patient had no recurrence of chest pain. He had an uncomplicated and uneventful hospital stay and was discharged on 10th day as per our hospital protocol for acute MI.

RVMI is usually associated with inferior MI and rarely with acute anterior MI. The classic triad of hypotension, elevated JVP with clear lung fields is highly specific but insensitive clinical parameters for identification of associated RVMI.1 The sensitivity and specificity of ST-segment elevation in the right-sided precordial leads, especially lead RV4, for the diagnosis of RVMI is well over 90%.2 However, at times ECG changes are atypical and bedside diagnosis of RVMI may be misleading. Shah et al, reported ST-segment elevation in left-sided anterior precordial leads in patients presenting with RVMI.3 The following electrocardiographic features helped to differentiate between RVMI and anterior LVMI: ÂÂ

When the magnitude of ST-segment elevation in V1-V5 decreases from right to left without the development of sequential Q waves, the ECG is suggestive of RVMI.4

ÂÂ

When the magnitude of ST-segment elevation in RV4 is more than the ST-segment elevation of lead V3 it is RVMI, in contrast to the ST-segment elevation in anterior MI, which is always more in V3 than the ST-segment elevation in RV4.5

In our patient, the ST-segment elevation increased progressively from lead V1-V3 and the lead RV4 showed lesser ST-segment elevation than the lead V3. Further no regional wall motion abnormality in right ventricle on echocardiography and normal right coronary artery ruled out RVMI and confirmed pseudo ST-segment elevation in right precordial leads in our patient. REFERENCES 1. Dell’Italia LJ, Starling MR, O’Rourke RA. Physical examination for exclusion of hemodynamically important right ventricular infarction. Ann Intern Med 1983;95(5):608-11. 2. Maheshwari M, Gokhroo RK. Inferior myocardial infarction with associated anterior ST-segment elevation: a rare presentation or right ventricular infarction. Indian J Electrocardiol 2011;2:17-9. 3. Shah PK. New insights into the ECG of acute myocardial infarction. In: Current Topics in Cardiology. Elsevier Science Publishing Co. Inc: NewYork 1991:128-43. 4. Chou TC, Van der Bel-Kahn J, Allen J, Brockmeier L, Fowler No. Electrocardiographic diagnosis of right ventricular infarction. Ann J Med 1981;70(6):1175-80. 5. Lopez-Sendon J, Coma-Canella I, Alcasena S, Seoane J, Gamallo C. Electrocardiographic findings in acute right ventricular infarction: sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V2 and V3. J Am Coll Cardiol 1985;6(6):1273-9.

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Community Medicine

Efficacy of Vitamin Supplementation on Plasma Homocysteine Levels Among Hyperlipidemic Patients: A Spectral and Clinical Analysis A Bright, TS Renuga Devi, S Gunasekaran*

Abstract Homocysteine, 2-amino-4-mercaptobutyric acid is a sulfur-containing nonessential amino acid biosynthesized from methionine in blood plasma. It is metabolized through two pathways, remethylation and transulfuration, which use as cofactors folate, vitamin B6 and vitamin B12. Hyperhomocysteinemia has been identified as a risk factor for cerebrovascular disease, dementia, impaired cognitive function and depression. Several drugs may interfere with metabolic pathways of homocysteine, leading to an alteration of plasma homocysteine levels. Lipid-lowering drugs used by patients with high levels of plasmatic lipids can increase plasma homocysteine levels. For the present study, five hyperlipidemic patients were enrolled. Before the initiation of vitamin supplements along with their regular medication the Fourier transform infrared (FTIR) spectra of the blood plasma was recorded and their homocysteine levels were clinically tested. They were orally administered a daily dosage of folic acid (5 mg), vitamin B12 (250 Âľg) and vitamin B6 (25 mg) supplements for a period of 2 months. Efficacy of these vitamin supplements were analyzed both clinically and spectroscopically. The FTIR spectra were recorded at the end of the first and the second month and also the homocysteine levels were clinically tested. The absorption values of the specific modes of vibration pertaining to homocysteine of both pre- and post-treatment spectra were noted and the percentage of efficacy of the multivitamins was calculated. The spectral and clinical investigation showed that the addition of these vitamins can markedly reduce the homocysteine levels in blood plasma.

Keywords: FTIR spectroscopy, plasma homocysteine, vitamin supplementation, hyperlipidemia.

H

omocysteine is a thiol-(sulfhydryl-) containing nonessential amino acid, which converts itself to several beneficial compounds required for energy including adenosine triphosphate (ATP), cysteine and S-adenosylmethionine (SAM-e). If homocysteine is not completely broken down it begins to cause oxidative damage to the walls of the arteries, oxidation of blood fats and abnormal blood clotting by making the platelets stick together.1 Homocysteine also enhances the binding of lipoprotein(a) to fibrinogen initiating a series of biochemical reactions eventually leading to blockages.2 Blocking may be followed by heart attacks, strokes and other circulation calamities. The enzyme co-factors especially vitamin B6, vitamin B12 and folic acid play a vital tool in the metabolism of homocysteine.3 Homocysteine is metabolized via remethylation, resulting in the formation of methionine, or via transulfuration, resulting in the formation of Post Graduate, Dept. of Physics Women’s Christian College, Chennai *Registrar, Periyar University, Salem, Tamil Nadu

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cysteine and finally taurine.4 The remethylation pathway of homocysteine is strongly dependent on the availability of folic acid in the active form of 5-methyltetrahydrofolate and vitamin B12. The latter is essential for optimal activity of the enzyme methionine synthase, which is responsible for methylation of homocysteine to methionine.5 In the transulfuration pathway an essential co-factor is the active form of vitamin B6, pyridoxal-5’phosphate (P5P). Deficiency of any of these vitamins is associated with hyperhomocysteinemia.6 Many drugs increase the level of homocysteine either by interfering with the metabolism of folate or vitamin B6 or vitamin B12.7 Certain lipid-lowering drugs administered in patients with high levels of plasmatic lipids can increase homocysteine levels.8 Elevated levels of plasma homocysteine have been documented in epileptic patients after chronic treatment with anti-epileptic drugs.9 There have been a number of clinical reports about the role of vitamin supplementation in normalizing homocysteine levels among hyperlipidemic and epileptic patients.10 Only a very few researchers have


Community Medicine analyzed the efficacy of drugs spectroscopically.11,12 The goal of this study is to determine the percentage of efficacy spectroscopically and substantiate it with the clinically obtained results. The former has lot of advantages and hence can be implemented as a prospective tool for the diagnosis and monitoring of plasma homocysteine levels. Material and Methods A group of five hyperlipidemic patients of the same age and blood group were enrolled for the study. They were undergoing treatment in the Deepam Hospital, Chennai. Before the administration of vitamin supplements along with their regular medication, the Fourier transform infrared (FTIR) spectra of the blood plasma were recorded and their homocysteine levels were clinically tested. They were orally administered a daily dosage of folic acid (5 mg), vitamin B12 (250 µg) and vitamin B6 (25 mg) supplements for a period of 2 months. The FTIR spectra were recorded at the end of the first and the second month and also the homocysteine levels were clinically tested.

Clinical Analysis Two milliliter of blood of each individual were collected in ethylenediaminetetraacetic acid (EDTA) vacutainers. The blood was centrifuged immediately and the plasma was separated. It was subjected to a clinical test (immunoassay-chemiluminescence) and the homocysteine levels were measured clinically in the reference range of 10-12 µmol/L.13 Almost all the patients enrolled for the study had homocysteine levels much greater than 12 µmol/L before they were administered with vitamin supplements (pretreatment). There was a marked reduction in the plasma homocysteine levels at the end of the first month (Day 30) and second month (Day 60). The clinical values of the measured homocysteine levels are shown in Table 1.

FTIR Spectra Acquisition The capillary blood samples (approximately 2 mL) of the patients, before they were administered with vitamin supplements, were collected. The blood was immediately centrifuged to separate plasma from erythrocytes. The samples were then stored at –20°C before analyses. After the samples returned to room temperature (around 25-30°C), a volume of 1 mL of serum was spread evenly over the surface of a thallium chromide pellet. The specimen was air-

dried for 30 minutes prior to measuring the spectra.14 The strong absorption band of water in the midinfrared- region poses hindrance and hence to eliminate this, the serum samples were air-dried. The dried serum forms a thin uniform film on the pellet.15 Infrared transparent thallium chromide without the sample was scanned as background for each spectrum and 16 scans were co-added at a spectra resolution of ±1 cm–1. The spectra were baseline corrected and they were normalized to acquire identical area under the curves. The spectra were recorded in the wave number range of 400-4,000 cm–1 on a Perkin-Elmer FTIR spectrometer at Sophisticated Analytical Instrumentation Facility, Indian Institute of Technology, Chennai, India. The spectra of the patients were recorded again at the end of the first month (Day 30) and second month (Day 60) after administrating the vitamin supplements. Results and Discussion

Assignment of Absorption Bands of Plasma Homocysteine By careful inspection of the obtained spectra, several spectral parameters can be identified as possible biomarkers for the detection of elevated levels of plasma homocysteine. The wide multiple bands between 3,300 and 2,300 cm–1 corresponds to the antisymmetric and symmetric stretching frequencies of NH.15 –1 An absorbance peak was noticed at 3,295 cm due to NH stretching vibrations. The spectra were dominated by absorbance bands at 1,542 and 1,656 cm–1 i.e., the amino acid and amide I bands, respectively.16 The peak at 1,542 cm–1 was due to the bending vibration of NH2. The amide I band showing a peak at 1,656 cm–1 was due to stretching vibrations of C = O. The absorbance at 2,930 and 1,456 cm–1 were due to the asymmetric bending and asymmetric stretching vibrations of the CH2 molecule. The bands at 2,996-2,819 cm–1 were assigned to symmetric and asymmetric stretching vibrations of CH2. The absorbance peak at 1,480-1360 cm–1 was attributed to stretching vibrations characteristic of amino acids (COO–).17 The C-S vibrations resulted in a band at 570-710 cm–1 with a maximum absorption at 698 cm–1. No significant peaks could be detected for the weak vibrations corresponding to the disulfides (S-S) at 500-540 cm–1.18,19 The absorption bands corresponding to the weak stretching vibrations of thiols (S-H) were also insignificant due to its dimeric nature.15

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Community Medicine Table 1. Efficacy of Vitamin Supplements on Homocysteine among Hyperlipidemic Patients Sample

1

2

3

4

5

128

Status

Clinical values µmol/L

3,295

2,930

2,848

1,656

1,542

1,456

1,402

698

Day 1

26.82

0.7799

0.3843

0.1825

1.4711

0.9234

0.2963

0.3463

0.1196

Day 30

20.33

0.7565

0.3654

0.1443

1.4547

0.8785

0.2603

0.3158

0.0944

% of efficacy

-24.20

-3.00

-4.9

-20.9

-1.10

-4.8

-12.15

-8.8

-10.36

Day 60

16.75

0.7122

0.3166

0.1342

1.4451

0.8746

0.2520

0.3084

0.0972

% of efficacy

-37.55

-8.70

-17.6

-26.4

-1.76

-5.2

-14.95

-10.9

-12.35

Day 1

16.03

0.8016

0.4807

0.2373

1.4319

0.9653

0.3643

0.3946

0.1103

Day 30

15.15

0.7925

0.4496

0.2157

1.4244

0.9214

0.3188

0.3705

0.1098

% of efficacy

-5.49

-1.14

-6.46

-9.14

-0.52

-4.55

-12.49

-6.11

-0.45

Day 60

14.64

0.7687

0.4579

0.2070

1.4020

0.9190

0.3170

0.3694

0.1095

% of efficacy

-8.64

-4.10

-4.74

-12.80

-2.09

-4.80

-12.98

-6.39

-0.45

Day 1

15.84

0.9835

0.4046

0.2314

1.4712

0.9169

0.3072

0.3386

0.1536

Day 30

12.44

0.8144

0.3447

0.1512

1.4657

0.8851

0.2774

0.3177

0.1437

% of efficacy

-21.46

-17.19

-14.78

-34.66

-0.37

-3.47

-9.70

-6.17

-6.45

Day 60

11.26

0.7592

0.3367

0.1497

1.4598

0.8753

0.2782

0.3058

0.1300

% of efficacy

-28.91

-22.81

-16.76

-35.31

-0.77

-4.54

-9.44

-9.69

-15.43

Day 1

17.12

0.8081

0.4439

0.2335

1.4615

0.9108

0.3422

0.3781

0.1181

Day 30

12.90

0.7952

0.4275

0.2,039

1.4414

0.9063

0.2951

0.3385

0.0977

% of efficacy

-24.65

-1.60

-3.69

-12.68

-1.38

-0.49

-13.76

-10.47

-17.02

Day 60

11.64

0.7763

0.4007

0.1961

1.4242

0.8858

0.2899

0.3301

0.0900

% of efficacy

-32.01

-3.94

-9.73

-16.02

-2.55

-2.74

-15.28

-12.70

-31.41

Day 1

20.81

0.8569

0.4006

0.2277

1.4737

0.9091

0.2981

0.3487

0.1286

Day 30

17.81

0.8324

0.3366

0.1501

1.4467

0.8619

0.2767

0.3229

0.0972

% of efficacy

-14.45

-2.86

-15.98

-34.08

-1.83

-5.19

-7.15

-7.40

-24.41

Day 60

16.43

0.6826

0.3268

0.1497

1.4051

0.8542

0.2654

0.358

0.0954

% of efficacy

-21.05

-20.34

-18.42

-34.26

-4.65

-6.04

-10.97

-9.44

-25.82

Absorbance of specific modes of vibration (cm–1)

Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014


Community Medicine

1.6 1.4

Day 1 Day 30 Day 60

1.2

Healthy

Absorbance

1 0.8 0.6 0.4 0.2 0 4000

3600

3200

2800

2400

2000

1600

1200

800

Wave number (cm–1) Figure 1. An overlaid spectrum to show the efficacy of vitamin supplements on homocysteine in an hyperlipidemic patient.

Calculation of Percentage of Efficacy In order to find the efficacy of folic acid, vitamin B6 and vitamin B12 in bringing down the homocysteine levels, the absorption values of the vibrational bands at 3,295 cm–1, 2,930 cm–1, 2,848 cm–1, 1,656 cm–1, 1,542 cm–1, 1,456 cm–1, 1,402 cm–1 and 698 cm–1 corresponding to plasma homocysteine of both pre- and post-treatment spectra were noted. The percentage of efficacy was calculated using the formula: Percentage of efficacy of vitamin supplements = ([Pre Post]/Pre) *100 The results are shown in Table 1. Conclusion The present study was undertaken to utilize the potential of FTIR spectroscopy in analyzing the efficacy of vitamin supplementation on plasma homocysteine levels among epileptic patients. The specific modes of vibrations pertaining to plasma homocysteine were identified. The percentage of efficacy after 30 days and 60 days of initialization of vitamin supplementation were calculated using the absorption values at the specific modes of vibration.

The plasma homocysteine levels had decreased with the progress of the treatment. The spectroscopical outcome was substantiated with the clinical results. This study forms a promising basis for employing spectroscopy in the follow-up of patients undergoing treatment for various ailments. This technique requires a small amount of plasma and the results can be obtained in a short duration. It is much costeffective when compared to clinical tests. It is therefore worthwhile to continue developing spectroscopy as an effective and reliable tool for the diagnosis and follow-up of disease pattern. References 1. Ueland PM, Refsum H, Brattstorm L, Francis RBJ (Eds.). Atherosclerotic Cardiovascular Disease 1992:p.183-236. 2. Wilcken DE, Wilcken B. The pathogenesis of coronary artery disease. A possible role for methionine metabolism. J Clin Invest 1976;57(4):1079-82. 3. McCully KS. Homocysteine theory of arteriosclerosis development and current status. Atherosclerosis Rev 1983;11:157-246. 4. Duerre JA, Briske-Anderson M. Effect of adenosine metabolites on methyltransferase reactions in isolated rat livers. Biochim Biophys Acta 1981;678(2):275-82.

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Community Medicine 5. Watkins D, Ru M, Hwang HY, Kim CD, Murray A, Philip NS, et al. Hyperhomocysteinemia due to methionine synthase deficiency, cblG: structure of the MTR gene, genotype diversity, and recognition of a common mutation, P1173L. Am J Hum Genet 2002;71(1):143-53.

11. Gunasekaran S, Renuga Devi TS, Sakthivel PS. Asian J Clin Cardiol 2007;10(5):19-29. 12. Gunasekaran S, Renuga Devi TS, Sakthivel PS. Asia J Chem 2008;20(1):167-76.

6. Selhub J, Jacques PF, Bostom AG, Wilson PW, Rosenberg IH. Relationship between plasma homocysteine and vitamin status in the Framingham study population. Impact of folic acid fortification. Public Health Rev 2000;28(1-4):117-45.

13. Frantzen F, Faaren AL, Alfheim I, Nordhei AK. Enzyme conversion immunoassay for determining total homocysteine in plasma or serum. Clin Chem 1998;44(2):311-6.

7. Dierkes J, Westphal S. Effect of drugs on homocysteine concentrations. Semin Vasc Med 2005;5(2):124-39.

15. Budinova G, Salva J, Volka K. Applied Spectroscopy.

8. Dierkes J, Luley C, Westphal S. Effect of lipid-lowering and anti-hypertensive drugs on plasma homocysteine levels. Vasc Health Risk Manag 2007;3(1):99-108. 9. Bottiglieri T, Hyland K. S-adenosylmethionine levels in psychiatric and neurological disorders: a review. Acta Neurol Scand Suppl 1994;154:19-26. 10. Siniscalchi A, Mancuso F, Gallelli L, et al. Pharmacological Research 2005; 5(5):367-75.

14. Heise HM, Bilter AJ. Molecular structure 1995;348:21. 16. Ivanova BB, Arnaudov MG, Bontchev PR. Linear-dichroic infrared spectral analysis of Cu(I)-homocysteine complex. Spectrochim Acta A Mol Biomol Spectrosc 2004;60(4): 855-62. 17. Gerard Deleris, Cyril Petribois. Vibrational Spectroscopy 2003;32:129-36. 18. Shaw RA, 2000;54:885.

Mantseh

HH.

Applied

Spectroscopy

■■■■

Work-related Stress can kill Job stress raises the risk of heart disease by disrupting the body’s internal systems. The findings from a long-running study involving more than 10,000 British civil servants also suggest stressinduced biological changes may play a more direct role than previously thought. The researchers measured stress among the civil servants by asking questions about their job demands such as how much control they had at work, how often they took breaks, and how pressed for time they were during the day. The team conducted seven surveys over a 12-year period and found chronically stressed workers - people determined to be under severe pressure in the first two of the surveys - had a 68 percent higher risk of developing heart disease. The link was strongest among people under 50. Stressed workers also eat unhealthy food, smoke, drink and skip exercise - all behaviors linked to heart disease. In the study, stressed workers also had lowered heart rate variability - a sign of a poorly-functioning weak heart and higher than normal levels of cortisol, a “stress” hormone that provides a burst of energy for a fight-or-flight response. Too much cortisol circulating in the blood stream can damage blood vessels and the heart.

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diabetology

Gender-related Difference in Socioeconomic and Behavioral Factor in Relation to BP and BMI of Type 2 Diabetic Workers from Match Factories and Fireworks in Sivakasi, Tamil Nadu V Priya*, Mazher Sultana*, Babuji†, Kamarajâ€

Abstract Objective: The prevalence of diabetes has been steadily increasing in workers of Match factories and Fireworks in Sivakasi area. We investigated the difference between male and female diabetic patients on impact of socioeconomic, behavioral and other risk factors like blood pressure (BP) and body mass index (BMI). Methods: Total 112 persons (64 male and 48 female) with type 2 diabetes were selected for this study, from various hospitals situated in Sivakasi area. Socioeconomic status (SES) and other behavioral factors ascertained by physical examination and interview. Result: There was significant difference between male and female diabetics only in certain factors. SES was found significant and inversely related to physical activity, marital status, food habit, duration and systolic blood pressure (SBP) in female diabetics. In male, these association were weaker or absent, when education level was considered. But in income level significant differences found in SBP and detected age. Statistical significance was found between behavioral and other risk factors in both male and female diabetics. Conclusion: Physical inactivity leads to high BMI and increased SBP. Due to lack of knowledge, these diabetic patients did not avail any type of medical attention for treating diabetic till they got other complications due to untreated diabetes.

Keywords: Prevalence of diabetes, blood pressure, body mass index, socioeconomic status, physical inactivity, smoking, alcohol intake

D

iabetes prevalence is increasing in all population groups in India, but this increase seems to be greater in lower level people. The prevalence of type 2 diabetes has been reported more in fire works and match factory workers in Sivakasi area. Socioeconomic status which plays an important role in healthcare and disease prevention, is a complex indicator of health services accessibility, knowledge of health promotion, willingness to seek treatment and lifestyle behavior (Mei Tang 2003). Educational attainments and income adequacy are important indicators of socioeconomic status (SES). Low SES tends to be associated with a high prevalence of diabetes in developed countries (Evans et al 2000, Robbins et al 2001, Connolly et al 2000). Obesity, physical inactivity, smoking and alcohol intake are implicated in the development of type 2 diabetes and are also associated with low socioeconomic position (Emilie et al 2004).

*Presidency College, Chennai, Tamil Nadu †Kani Lakshmi Clinic, Sivakasi, Tamil Nadu

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Research suggests an association between low SES and high blood pressure (BP), although this association is not consistent. A study on smoking, alcohol consumption and body mass index (BMI) reveals that the lifestyle increases the risk of high BP. And it is more common among people with low SES. (Mathews et al 1997, Lynch et al 1997, Porton et al 1999, Dyer et al 1999). Diagnostic and treatment services for high BP may be more accessible to people with high SES (Bunker et al 1995, Hoddard et al 1997). The health impact of SES and behavioral factors may not be the same in male and female. Only a few studies have assessed sex difference in the relationship between SES and diabetes. The pathway by which SES may differently affect the development of type 2 diabetes in male and female are unclear. The impact of behavioral factors like BMI, physically inactive, smoking, alcohol consumption and family history of diabetes are closely linked with insulin resistance. But the variation of BP in SES and behavioral factors has rarely been studied. So, the aim of the study was to assess the sex specific


diabetology association of SES, behavioral factor and the difference in BP and BMI with diagnosed type 2 diabetic workers from match factories and fireworks in Sivakasi area.

Table 1. Socioeconomic, Behavioral and Other Risk Factors Among Males and Females Factor

Male

Female

P value

Method

Age (years) Mean SD

51.13 10.17

48.77 10.10

0.23

Diabetes detected age (years) Mean SD

47.48 9.62

44.88 9.91

0.17

Duration (years) Mean SD

3.67 2.37

3.92 2.67

0.62

SBP (mmHg) Mean SD

132.53 12.70

131.29 10.82

0.58

DBP (mmHg) Mean SD

80.03 8.09

79.23 6.84

0.57

Plasma glucose (mg/dL) Mean SD

170.02 39.78

172.83 42.61

0.72

BMI ( kg/m²) Mean SD

26.59 1.99

25.38 2.60

0.0086

Marital status Married (%) Single/widow (%)

89.06 10.94

81.25 18.75

0.24

Food habit NV (%) Veg (%)

81.25 18.75

70.83 29.17

0.196

Physically Inactive (%) Active (%)

31.25 68.75

43.75 56.25

0.174

Smoking habit Smoker (%) Nonsmoker (%)

43.75 56.25

0 100

0.000

Alcohol intake Alcoholic (%) Nonalcoholic (%)

45.31 54.69

0 100

0.000

Family history of diabetes FH+ (%) FH - (%)

76.56 23.44

70.83 29.17

0.49

Education Primary (%) Secondary (%) Higher (%)

25.00 56.25 18.75

60.42 29.17 10.42

0.0008

Income Low (%) Medium (%) High (%)

28.13 37.50 34.37

54.17 25.00 20.83

0.02

Area This study was carried out on workers working in match factories and fire works in Sivakasi area. Sivakasi is situated in Virudhunagar district, Tamil Nadu state, India. This place is very dry and is ideally suited for the manufacturing of fireworks, printed materials, paper and the match factories. About 3,500 match factories are situated in and around Sivakasi area. Around 30,000 persons are directly employed in these factories.

Participants For this present study 112 samples (64 male and 48 female) were collected from various hospitals situated in Sivakasi area. The participants were interviewed and completed questionnaires on SES and behavioral characters were collected.

Socioeconomic Variables Information on educational attainment was divided into primary (Class 1-5), secondary (Class 6-10) and higher (>10th class) education and income was divided in low (< ` 3,000), medium (` 3,000 to ` 5,000) and higher level (> ` 5,000).

Behavioral Variables Body weight was measured in light clothing in kg and height was measured in centimeters. BMI was calculated by weight in kg divided by square of height in meters. BP was measured in a sitting position for 2 times at the right arm after 15 minutes rest using sphygmomanometer by a well trained nurse. All subjects were interviewed and asked about their physical activity. It was divided into ‘active’ and ‘inactive’. Alcohol drinking habit was categorized as ‘alcoholic’ and ‘nonalcoholic’. Cigarette smoking was divided into ‘smokers’ and ‘nonsmokers’. Their family history about diabetes was analyzed and grouped into FH+ and FH-. Their age, diabetes detected age and duration also asked during interview.

Laboratory Measurement Plasma glucose was measured using an enzymatic method by using ready made kits manufactured by Prison Diagnostic Pvt. Ltd. Mumbai.

FH+: Family history of diabetes present; FH- : Family history of diabetes absent; NV: Nonvegetarian; SBP: Systolic blood pressure; DBP: Diastolic blood pressure.

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diabetology or proportions for categorical variables were calculated among the SES groups.

Statistical Analysis Analysis was carried out separately for males and females using Systat 12 (2007) statistical software. Descriptive analyses were obtained for all variables and differences between males and females were assessed using ‘t’ test, X2 tests and ANOVA. Sex differences in SES indicators were evaluated using linear or logistic regression models including original SES variables. Means [standard deviation (SD)] for normal distribution and means for log normal distributed continuous variables

Result Socioeconomical, behavioral and other risk factors among male and female participants are shown in Table 1. Systolic BP (SBP), diastolic BP (DBP) and BMI were higher and blood sugar was lower among males than females. Physical inactivity was more in female compared to males. Smoking and alcohol intake was

Table 2a. The Distribution of Risk Factor of Type 2 Diabetes by SES in Men Factor

Education

Income

P value

Primary

Secondary

Higher

P value

Low

Medium

High

Marital status Married (%) Single (%)

75.00 25.00

94.44 5.55

91.67 8.33

0.11

83.33 16.67

83.33 16.67

100 --

0.127

Food habit NV (%) Veg (%)

93.75 6.25

75.00 25.00

83.33 16.67

0.27

72.22 27.78

83.33 16.67

86.36 13.64

0.49

Physically Active (%) Inactive (%)

62.50 37.50

66.67 33.33

83.33 16.67

0.46

16.67 83.33

79.17 20.83

100 --

0.000

Smoking habit Smoker (%) Nonsmoker (%)

43.75 56.25

44.44 55.56

41.67 58.33

0.98

38.89 61.11

45.83 54.17

45.45 54.55

0.88

Alcohol intake Alcoholic (%) Nonalcoholic (%)

37.50 62.50

47.22 52.78

50.00 50.00

0.76

38.89 61.11

45.83 54.17

50.00 50.00

0.77

Family history of diabetes FH+ (%) FH - (%)

6.25 93.75

30.56 69.44

25.00 75.00

0.16

27.78 72.22

16.67 83.33

27.27 72.73

0.61

SBP (mmHg) Mean SD

137.00 13.06

130.39 13.19

133.00 9.67

NS

139.67 11.19

133.58 11.72

125.55 11.66

**

DBP (mmHg) Mean SD

81.75 9.18

78.94 7.61

81.00 8.16

NS

83.11 7.36

81.00 8.89

76.45 6.59

**

Plasma glucose (mg/dL) Mean SD

166.94 48.99

174.97 35.79

159.25 38.66

NS

167.61 33.39

173.33 42.59

168.36 42.88

NS

BMI (kg/m²) Mean SD

26.94 1.59

26.43 2.06

26.61 2.34

NS

27.70 2.24

26.73 1.73

25.23 1.52

NS

Detected age (years) Mean SD

48.94 9.46

46.44 9.67

48.67 10.11

NS

54.11 9.37

46.00 8.80

43.68 8.15

**

Duration (years) Mean SD

3.56 2.34

3.67 2.53

3.83 2.08

NS

4.39 2.64

3.63 2.64

3.14 1.69

NS

NS: No significance; **Significance p < 0.01

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diabetology found only in males. Nonvegetarians were more in males (81.25%) compared to females (70.81%). Family history of diabetes was seen more in males than females. Significant difference was found in income (p = 0.02) and educational status (p = 0.0008) between male and female subjects. The age at which the diabetes detected was high in males (47 years) and low in females (44 years). The distributions of various risk factors by SES are shown in Table 2a and 2b. In patients with secondary education level, more male (94.44%) members were

found married than female (92.86%). In male diabetics with primary education level number of singles or widows was high. But for female diabetics number of single or widows was high in higher education level. There was significant difference in education level and marital status among female diabetics (p = 0.03). Most of the male nonvegetarians were found in primary education group. But female nonvegetarians were more in secondary education group. While comparing income level, there was no significant difference noticed in male food habits. But in females there was a

Table 2b. The Distribution of Risk Factor of Type 2 Diabetes by SES in Women Primary

Secondary

Higher

P value

Low

Medium

High

P value

Marital status Married (%) Single (%)

Factor

82.76 17.24

92.86 7.14

40.00 60.00

0.03

76.92 23.08

83.33 16.67

90.00 10.00

0.65

Food habit NV (%) Veg (%)

68.97 31.03

78.57 21.43

60.00 40.00

0.69

84.62 15.38

58.33 41.67

50.00 50.00

0.067

Physically Active (%) Inactive (%)

37.93 62.07

78.57 21.43

100.00 --

0.004

30.46 61.54

75.00 25.00

80.00 20.00

0.025

Smoking habit Smoker (%) Nonsmoker (%)

0 100

0 100

0 100

0.0001

0 100

0 100

0 100

0.008

Alcohol intake Alcoholic (%) Nonalcoholic (%)

0 100

0 100

0 100

0.0001

0 100

0 100

0 100

0.008

Family history FH+ (%) FH - (%)

20.69 79.31

42.86 57.14

40.00 60.00

0.28

26.92 73.08

33.33 66.67

30.00 70.00

0.92

SBP (mmHg) Mean SD

134.41 9.01

128.29 12.19

121.60 10.14

**

133.92 11.01

129.33 8.06

126.80 12.15

NS

DBP (mmHg) Mean SD

80.45 7.16

78.29 6.27

74.80 5.02

**

80.27 7.41

76.33 6.14

80.00 5.58

NS

Plasma glucose (mg/dL) Mean SD

170.79 40.89

177.36 51.08

172.00 32.33

NS

178.00 38.22

161.08 49.62

173.50 46.38

NS

BMI (kg/m²) Mean SD

26.00 2.78

24.71 2.05

23.64 1.92

NS

25.68 2.99

25.39 2.26

24.58 1.84

NS

Detected age (years) Mean SD

45.97 10.38

43.86 8.58

41.40 11.46

NS

46.31 11.61

42.92 9.13

43.5 7.15

NS

Duration (years) Mean SD

4.28 3.17

3.79 1.58

2.20 0.84

***

3.96 3.21

3.83 1.69

3.90 2.28

NS

NS: No significance; ** Significance p < 0.01; *** p < 0.001

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diabetology Table 3a. The Relationship Between Behavioral and Other Risk Factors in Male Factor

Food habit

Smoker Yes

No

Alcohol

P value Yes

No

Physically

P value Inactive

P value

Nonveg

Veg

P value

Active

Family history FH + (%) FH - (%)

21.15 78.85

33.33 66.67

0.37

25.00 22.22 75.00 77.78

0.79

31.03 17.14 68.97 82.86

0.19

70.00 30.00

79.55 20.45

0.40

Marital status Married (%) Single (%)

90.38 9.62

83.33 16.67

0.48

96.43 83.33 3.57 16.67

0.09

100.0 80.00 20.00

0.01

85.00 15.00

90.91 9.09

0.48

SBP (mmHg) Mean SD

131.8 13.22

135.5 10.06

0.29

135.0 130.6 8.83 14.88

0.15

134.0 131.2 110.1 13.98

0.37

138.9 10.53

129.6 12.64

0.004

DBP (mmHg) Mean SD

80.08 7.74

79.83 9.85

0.94

81.07 79.22 8.70 7.61

0.38

81.59 78.74 8.20 7.88

0.16

81.30 8.81

79.45 7.78

0.43

Plasma glucose mg/dL Mean SD

168.7 40.36

175.5 38.36

0.59

171.8 168.5 35.02 43.57

0.74

176.7 164.4 30.08 40.83

0.21

164.3 38.19

172.6 40.65

0.43

BMI (kg/m²) Mean SD

26.43 1.93

27.29 2.18

0.22

27.23 26.09 1.36 2.26

0.01

26.72 26.48 1.80 2.15

0.63

27.79 1.87

26.05 1.81

0.001

Detected age (years) Mean SD

46.50 9.69

51.75 8.38

0.07

47.36 47.58 8.17 10.73

0.92

47.24 47.69 8.83 10.35

0.85

55.05 5.19

44.05 9.22

0.000

Table 3b. The Relationship Between Behavioral and Other Risk Factors in Female Factor

Smoker

Alcoholic

Nonveg

Veg

P value

No

No

Inactive

Active

Family history FH+ (%) FH - (%)

29.41 70.59

28.57 71.43

0.95

29.17 70.83

29.17 70.83

19.05 80.95

37.04 62.96

0.17

Marital status Married (%) Single (%)

76.47 23.53

92.86 7.14

0.19

81.25 18.75

81.25 18.75

76.19 23.81

85.19 14.82

0.43

SBP (mmHg) Mean SD

132.8 10.72

127.5 10.50

0.13

131.2 10.82

131.2 10.82

136.5 8.42

127.1 10.82

0.001

DBP (mmHg) Mean SD

79.38 6.77

78.86 7.26

0.82

79.23 6.84

79.23 6.84

79.86 7.21

78.74 6.64

0.58

Plasma glucose (mg/dL) Mean SD

170.2 41.56

179.2 46.01

0.53

172.8 42.61

172.8 42.61

168.48 38.72

176.2 45.83

0.53

BMI (kg/m²) Mean SD

25.49 2.80

25.12 1.93

0.61

25.38 2.60

25.38 2.60

26.46 2.86

24.54 2.07

0.01

Detected age (years) Mean SD

44.44 11.33

45.93 5.21

0.54

44.88 9.91

44.88 9.91

51.33 5.33

39.85 9.78

0.000

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Food habit

Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014

Physically

P value


diabetology significant difference (p = 0.06). Physical inactivity was high in primary education level and low income group in both males and females. But, there was significant difference in education level (p = 0.004) and income level (p = 0.02) in females. In males, smoking habit was high in secondary education level with medium income. And there was no smoking habit among female of any education and income level. Alcohol intake was high in higher education level and high income level male. Family history of diabetes reported high among both male (30.56%) and female (42.86%) with secondary education and no significant association found in income groups. SBP was more in primary educated (137 mmHg) and lower income level (139 mmHg) males. Also similar trend found in female diabetics. There was statistical significance found in diastolic pressure in males at income level and female at education levels. Plasma glucose level was high in both male (174.9 mg/dL) and female (177.3 mg/dL) subjects with secondary education level. Male (173.3 mg/dL) diabetics with medium income and female (178 mg/dL) diabetics in lower income level had high glucose level. Male diabetics in lower income level had high BMI 27.7 kg/m². But female diabetics with primary education level had high BMI 26.9 kg/m². Diabetes detected age was high among male diabetics (54 years) and low among female diabetics (46 years) who were in low income level. And diabetes was detected very early in both the males and females in high income level. Table 3a and 3b shows the relation between behavioral factors and other risk factors. Among male diabetics, significant association found between marital status and smoking habit (p = 0.09). Systolic pressure in male diabetics was more in vegetarians (135.5 mmHg), smokers (135 mmHg), alcoholic (134 mmHg) and physically inactive (138.9 mmHg). But, there was statistical significance found only in physical activity and SBP (p = 0.003). In male diabetics, plasma glucose was more in vegetarians (175.58 mg/dL), smokers (171.86 mg/dL) and alcoholic (176 mg/dL). BMI was also more in vegetarians (27.2 kg/m²), smokers (27.23 kg/m²) and physically inactive (27.79 kg/m²) males. But, BMI showed statistical significance between smokers and nonsmokers (p = 0.015) and physically active and inactive (p = 0.01) males. In female diabetics, SBP was high in nonvegetarians (132.8 mmHg) and physically inactive (136.57 mmHg). Statistical significance (p = 0.01) was found between

physical activity and SBP in females. Plasma glucose was found more in vegetarians (179.21 mg/dL) and physically active (176.22 mg/dL) females. In female diabetics, BMI showed significance (p = 0.01) with physical activity, it was more (26.46 kg/m²) in case of physically inactive females. Duration of diabetes shows significant difference between physical active and inactive females (p = 0.02). discussion This study shows that there is significant difference between male and female diabetics only in certain factors. In the third National Health and Nutrition Examination Survey (2001), SES was significantly associated with type 2 diabetes in both African American and white women. But, no relationship was found for men. Rathmann et al (2005) found that patients with long- standing diabetes along with severe disabling diabetic complication and poor health may result in low SES. According Tang et al (2003) in the National Population Health Survey in Canada, low income and education remained significantly associated with self-reported diabetes after controlling for BMI and physical activity in women. In men, the association was weaker and did not persist after controlling for risk factors. In the present study, there was significant difference in male only in few factors and SES. But, female showed significant inverse association with SES. This study reveals BMI was more among low income level male diabetics. Poor diet, lack of physical activity and smoking habit had lead to increase in BMI of these diabetic cases. Female diabetics in primary education level have more BMI. Lack of knowledge, consumption of junk food and sedentary lifestyle has increased the BMI of female diabetics. The association between SES and obesity was found in several studies, obesity being stronger in women than in men. Rathman et al (2005) analyzed that an inverse association of BMI and SES was found only in women. Ramachandran et al (2002) found that obesity is common in Indians and the adverse effect of central obesity is manifested in increasing tertiles of BMI both in men and women. BMI was found more in Indian women. Physical inactivity is another major behavioral risk factor of type 2 diabetes. Lantz et al (1998) found in US adult that physical activity was less in low SES groups. Ford et al found women with higher SES were more physically active than women with low SES; whereas this social gradient may be less pronounced in men. Rathman et al (2005) in KORA survey proved that physical inactivity was reported more in men

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diabetology and women in low SES. In the present study, physical inactivity is high among both male and female diabetics who were in low income level. Physically inactive female were more in low education level. Normally welleducated and those who earn more are more likely to engage in high physical activity. Mathews et al (1997) identified people with high occupational status and in particular high education attainments were less likely to smoke and drink excess alcohol. Study conducted in Canada showed that lower income was inversely associated with smoking and diet intake. But in this present study there was no difference in smoking habit between education level and income level in males. Alcohol intake was more in higher income group. Because of more work, stress, body pain and work tension they may resort to take alcohol. Kivimaki et al (2004) identified that there was a weak inverse relationship between SES and BP. Higher education attainment was associated with lower SBP. But association involving occupational status and DBP did not reach statistical significance. Stronger links with lifestyle and risk factor may partially explain the greater BP differences between educational levels and occupational status. Marmot et al (2001) in the Whitehall study found difference in SBP was no more than 3-5 mmHg between the highest and lowest employment grade. INTER-SALT study, Stamler (1992) proved an inverse association between years of education and BP. He found that, for men 28 out of 47 populations and for women 38 of 47 populations, this inverse association was seen. The US Hanes III study showed no association between SES and BP. In this present study SBP was more in primary education and low income level in both males and females. Tension, worry about the uncertainty in life, work pressure and poor diet regulation may increase the BMI. Previous researches consistently showed a positive relationship between body weight and BP. Increased BMI was the predictor of higher BP. Hoskins et al found that a family history of diabetes was a risk factor for diabetes in Melanesians and Indians living in Fiji. Ramachandran et al (1988) reported a high prevalence of diabetes among Indian children who had one or two diabetic parents. But in the present study, there was no significant difference in family history of diabetes and SES between males and females. This study shows low income male diabetic had longer duration of diabetes and diabetes detected age was also higher. Even in female diabetics primary

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education group had diabetes over long duration and the detected age was high. Due to poverty and lack of knowledge these diabetic patients were not aware of the free healthcare facilities and never tried to avail any type of medical attention for treating diabetes, till they got complication due to prolonged untreated diabetes. In conclusion, in female diabetics SES was found to be significantly and inversely related to physical activity, marital status, food habit, duration and SBP. In males these association were weaker or absent when education level was considered. But in income level significant differences, found were in SBP and detected age. Significant differences found in both male and female behavioral characters and other risk factors like SBP and BMI. Physical inactivity leads to high BMI and it increases SBP. But, the differences between male and female diabetic patients needs to be further investigated.

Acknowledgment We thank Mr. Ramadas, Mr Navaneethan and Mrs. Asha for the help they extended while collecting the samples. Also we thank Mr Ponmurugan for the statistical and secretarial help.

Suggested Reading 1. Adler NE, Boyce WT, Chesney MA, Folkman S, Syme SL. Socioeconomic inequalities in health. No easy solution. JAMA 1993;269(24):3140-5. 2. Ramachandran A, Jali MV, Mohan V, Snehalatha C, Viswanathan M. High prevalence of diabetes in an urban population in south India. BMJ 1988;297(6648):587-90. 3. Brown AF, Ettner SL, Piette J, Weinberger M, Gregg E, Shapiro MF, et al. Socioeconomic position and health among persons with diabetes mellitus: a conceptual framework and review of the literature. Epidemiol Rev 2004;26:63-77. 4. Connolly V, Unwin N, Sherriff P, Bilous R, Kelly W. Diabetes prevalence and socioeconomic status: a population based study showing increased prevalence of type 2 diabetes mellitus in deprived areas. J Epidemiol Community Health 2000;54(3):173-7. 5. Choi BC, Shi F. Risk factors for diabetes mellitus by age and sex: results of the National Population Health Survey. Diabetologia 2001;44(10):1221-31. 6. Dyer AR, Liu K, Walsh M, Kiefe C, Jacobs DR Jr, Bild DE. Ten-year incidence of elevated blood pressure and its predictors: the CARDIA study. Coronary Artery Risk Development in (Young) Adults. J Hum Hypertens 1999;13(1):13-21. 7. Agardh EE, Ahlbom A, Andersson T, Efendic S, Grill V, Hallqvist J, et al. Explanations of socioeconomic differences in excess risk of type 2 diabetes in Swedish men and women. Diabetes Care 2004;27(3):716-21.


diabetology 8. Evans JM, Newton RW, Ruta DA, MacDonald TM, Morris AD. Socio-economic status, obesity and prevalence of Type 1 and Type 2 diabetes mellitus. Diabet Med 2000;17(6):478-80. 9. Brancati FL, Kao WH, Folsom AR, Watson RL, Szklo M. Incident type 2 diabetes mellitus in African American and white adults: the Atherosclerosis Risk in Communities Study. JAMA 2000;283(17):2253-9. 10. House JS, Lepkowski JM, Kinney AM, Mero RP, Kessler RC, Herzog AR. The social stratification of aging and health. J Health Soc Behav 1994;35(3):213-34. 11. House JS, Kessler RC, Herzog AR. Age, socioeconomic status, and health. Milbank Q 1990;68(3):383-411. 12. Ismail AA, Beeching NJ, Gill GV, Bellis MA. Capturerecapture-adjusted prevalence rates of type 2 diabetes are related to social deprivation. QJM 1999;92(12):707-10. 13. Lynch JW, Kaplan GA, Salonen JT. Why do poor people behave poorly? Variation in adult health behaviours and psychosocial characteristics by stages of the socioeconomic life course. Soc Sci Med 1997;44(6):809-19. 14. Lantz PM, House JS, Lepkowski JM, Williams DR, Mero RP, Chen J. Socioeconomic factors, health behaviors, and mortality: results from a nationally representative prospective study of US adults. JAMA 1998 ;279(21):1703-8. 15. Tang M, Chen Y, Krewski D. Gender-related differences in the association between socioeconomic status and selfreported diabetes. Int J Epidemiol 2003;32(3):381-5.

18. Poston WS 2nd, Foreyt JP. Obesity is an environmental issue. Atherosclerosis 1999;146(2):201-9. 19. Robbins JM, Vaccarino V, Zhang H, Kasl SV. Socioeconomic status and type 2 diabetes in African American and nonHispanic white women and men: evidence from the Third National Health and Nutrition Examination Survey. Am J Public Health 2001;91(1):76-83. 20. Stamler R, Shipley M, Elliott P, Dyer A, Sans S, Stamler J. Higher blood pressure in adults with less education. Some explanations from INTERSALT. Hypertension 1992;19(3):237-41. 21. Shah SK, Saikia M, Burman NN, Snehalatha C, Ramachandran A. High prevalence of type 2 diabetes in urban population in north eastern India. Int J Diabetes Dev Countries 1999;19:144-7. 22. Maty SC, Everson-Rose SA, Haan MN, Raghunathan TE, Kaplan GA. Education, income, occupation, and the 34year incidence (1965-99) of Type 2 diabetes in the Alameda County Study. Int J Epidemiol 2005;34(6):1274-81. 23. Gary TL, Brancati FL. Commentary: socioeconomic position and the risk of type 2 diabetes. Int J Epidemiol 2005;34(6):1282-3.

16. Kivimäki M, Kinnunen ML, Pitkänen T, Vahtera J, Elovainio M, Pulkkinen L. Contribution of early and adult factors to socioeconomic variation in blood pressure: thirty-four-year follow-up study of school children. Psychosom Med 2004;66(2):184-9.

24. Rathmann W, Haastert B, Icks A, Giani G, Holle R, Meisinger C et al; KORA Study Group. Sex differences in the associations of socioeconomic status with undiagnosed diabetes mellitus and impaired glucose tolerance in the elderly population: the KORA Survey 2000. Eur J Public Health 2005;15(6):627-33.

17. Power C, Matthews S. Origins of health inequalities in a national population sample. Lancet 1997;350(9091):1584-9.

25. Williams DR. Socioeconomic differentials in health: a review and redirection. Soc Psychol Q 1990;53(2):81-99.

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ÂÂ

A study published online in Diabetes Care has stated that people with impaired glucose tolerance (IGT) have evidence of neuropathy that can be detected through the eye using corneal confocal microscopy.

ÂÂ

Spanish researchers have recently reported that gestational diabetes mellitus (GDM) screening using the recent International Association of Diabetes in Pregnancy Study Group (IADPSG) guidelines improves outcome and ultimately cuts costs. With the new approach, the GDM rate increased from 10.6% to 35.5%, reported the researchers online in Diabetes Care.

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Drug

Everlasting Gold Standard Amoxicillin in the Era of Antimicrobial Resistance Pawan Mangla

Abstract Antimicrobial resistance (AMR) is an increasingly serious threat to public health. AMR is emerging across the globe and cannot be eradicated completely. However, a multidisciplinary approach involving a wide range of stake holders may be able to limit the risk of AMR. The rational use of antibiotics should be advocated among the clinicians, prescribers and the general public. Using broad-spectrum antibiotics such as second-generation macrolides, cephalosporins, quinolones as first-line therapy not only increases the development of resistant strains, but also adds to costs substantially. Hence, there is a growing need to optimize the use of first-generation antibiotics like amoxicillin to treat the infections.

Keywords: Antimicrobial resistance, rational use of antibiotics, broad-spectrum antibiotics, amoxicillin

A

ntimicrobial resistance (AMR) is an increasingly serious threat to public health. AMR has sinister implications:

ÂÂ

Standard treatments no longer work

ÂÂ

Infections are difficult, rather impossible to control

ÂÂ

The risk of the spread of infection in community settings is increased

ÂÂ

Illness and hospital stays are prolonged, with added economic and social costs

ÂÂ

Increased risk of morbidity and mortality—in some cases, twice that of patients who have infections caused by non-resistant bacteria.

The recent report ‘Antimicrobial Resistance: Global Report on Surveillance’ published by World Health Organization (WHO), presents the most comprehensive data on antibiotic resistance.1 Data from 114 countries reveals that resistance to common intestinal bacteria such as Klebsiella pneumoniae has spread to all regions of the world. According to this report, resistance to antibiotics poses a ‘major global threat’ to public health.1 The report comes as a warning for India and for developing countries. The infectious disease burden in India and in developing countries is among the highest in the world and the inappropriate, irrational use of antimicrobial agents has led to an increasing trend in the development of AMR. The WHO report primarily points to the poor regulations in the

Chest Physician Moolchand Medcity, New Delhi

medical sector especially with respect to the rational prescription of antibiotics. Rational and effective use of antibiotics has enabled us to live longer, live healthier and to get maximum benefit when the infections are encountered. Unless significant efforts are made and effective actions taken to prevent infections, and rational use of antibiotics practiced and advocated, the world will stand to lose the efficacy of the antibiotics and the implications will be devastating for the future generations. Rationale use of antibiotics AMR is emerging across the globe and cannot be eradicated completely. However, a multidisciplinary approach involving a wide range of stake holders may be able to limit the risk of AMR.2 The rational use of antibiotics should be advocated among the clinicians, prescribers and the general public. This will prevent the misuse, abuse and overuse of these life-saving drugs. Using broad-spectrum antibiotics such as secondgeneration macrolides, cephalosporins, quinolones as first-line therapy not only increases the development of resistant strains, but also adds to costs substantially. There has been a reduction in the usage of firstgeneration antibiotics such as amoxicillin, due to the increased and indiscriminate usage of higher generation antibiotics. This has created a favorable impact and pathogens are becoming more susceptible to first-generation antibiotics, when compared to the second- or third-generation. Hence, in times to come, the first-generation antibiotics should be the major lines of defense, when it comes to the battle against multidrug-resistant pathogens.

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Drug The following steps should be taken whenever a patient comes with an infection: ÂÂ

Empirical treatment should be initiated with firstgeneration antibiotics with proven efficacy like amoxicillin, ampicillin and their combinations. Antibiotics should be given in proper doses and treatment durations should be kept at minimum prescribed limits.

ÂÂ

The second- and third-generation antibiotics like ceftriaxone and azithromycin should be used only when necessary and in cases where patient does not respond to older antibiotics.

ÂÂ

An attempt should be made to isolate the microbiological pathogen. Pathogen isolated should be subjected to a sensitivity test to select the most effective antibiotic. The antibiotic should be prescribed based on sensitivity test results.

ÂÂ

Attempt should be made to select the antibiotics having a limited and minimum impact on the environment.

Efficacy of Amoxicillin in clinical practice There is an evident gap between the current worldwide spread of multi-resistant bacteria and the pipeline of newer antibiotics with limited efforts to develop new molecules. Hence, there is a growing need to optimize the use of first-generation antibiotics like amoxicillin to treat the infections. Amoxicillin is the gold standard antibiotic and the drug of choice in various respiratory tract infections such as acute otitis media (AOM) in children and most episodes of acute bacterial sinusitis. Sincere efforts should be made to continue using this wonderful molecule and also to follow the prescribing guidelines while using it. A study was undertaken to find out the standard of practices about antibiotic use in the infections in a pediatric emergency department.3 A departmental database was reviewed from July 2005 to October 2007 under the category ‘respiratory infection’, including variables such as age, antibiotic prescription and compliance with current clinical recommendations. Out of the 23,114 reviewed reports, 32.7% (7,567) were upper respiratory tract infections (URTIs) (cold, AOM, sinusitis and tonsillopharyngitis) or lower respiratory tract infections (LRTIs) (laryngitis, bronchitis, bronchiolitis and pneumonia). Antibiotic therapy- mainly amoxicillin was prescribed in 30.8% of URTI (5.7% rhinopharyngitis, 96.5% AOM and 36.7% tonsillopharyngitis) and in 12.4% of LRTI. A retrospective cohort study compared the outcomes

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and resource utilization among children hospitalized with community-acquired pneumonia (CAP) between 2005 and 2011 receiving either first-generation penicillin or ceftriaxone/cefotaxime.4 It was seen that clinical outcomes and costs for children hospitalized with CAP were not different, when treatment was with firstgeneration antibiotics as compared to the treatment with broad-spectrum therapy. In another multicenter retrospective cohort study, medical records of children aged 2 months to 18 years at four pediatrics hospitals with a discharge diagnosis of CAP were analyzed in 2010.5 The effectiveness of empiric treatment with first-generation antibiotics was compared with broadspectrum therapy for children hospitalized with uncomplicated CAP and it was observed that both were associated with similar outcomes. The most common bacteria that can be isolated in patients with acute rhinosinusitis are Streptococcus pneumoniae and Haemophilus influenzae. For many years, the first drug of choice has been penicillin V, and treatment with penicillin V has followed Scandinavian recommendations. However, the resistance patterns in respect of H. influenzae have changed over the years and if the dominant flora is H. influenzae, then oral penicillin is not sufficient anymore, and should be replaced by amoxicillin with or without clavulanate.6 Group A streptococcal pharyngitis is a significant cause of community-associated infections. Inappropriate antimicrobial use for URTIs, including acute pharyngitis, has been a major contributor to the development of AMR among common pathogens. Based on its efficacy, infrequency of adverse reactions and modest cost, amoxicillin is the recommended drug of choice for those nonallergic to these agents.7 People with nonsevere CAP can be given empirical antibiotic treatment at home without the need for microbiological and radiological investigations. It is seen that only a limited range of pathogens cause CAP, the commonest being S. pneumoniae. Amoxicillin at higher doses 500 mg to 1.0 g three times daily remains the preferred agent for community managed CAP. Chronic obstructive pulmonary disease is the collective name for a number of lung diseases including chronic bronchitis, emphysema and chronic obstructive airways disease. Amoxicillin 500 mg to 1.0 g three times daily for 7-10 days is appropriate as first-line therapy. Amoxicillin is safe in Pregnancy and Lactation Another major advantage with the use of amoxicillin is its safety during pregnancy. Amoxicillin has been


Drug assigned to pregnancy category B by the Food and Drug Administration (FDA). In the Collaborative Perinatal Project involving 50,282 mother-child pairs, there were 3,546 mother-child pairs exposed to penicillin derivatives in the first trimester. As a group, there was no significant increase in the risk of malformations.8 A Danish study of 401 women exposed to amoxicillin during pregnancy from 1991 to 2000 did not find an increased risk of birth defects or adverse outcomes compared to women who had taken no medication.9 As regards the use of amoxicillin during lactation, studies suggest that less than .095% of the maternal dose enters the breast milk making amoxicillin a safe drug. Amoxicillin is one of the safest antibiotics to be used during breastfeeding and is categorized as an L1 drug.

minimum impact on the environment and the planet. Thus, the truly enzymatic amoxicillin produced by enzymatic process is not only effective and safe, but also ecofriendly. In a nutshell, the benefits of the truly enzymatic amoxicillin to the patients can be summarized as follows: ÂÂ

Better efficacy as the assay is more than 99.5%

ÂÂ

Enhanced safety and tolerability, as there is less chemical load

ÂÂ

Increased patient compliance due to better taste.

Over and above, the enzymatic amoxicillin also offers better stability of the formulation throughout the shelflife of the formulation. References

Enzymatic Production of Amoxicillin: Safe and Ecofriendly With newer technologies and increased focus on sustainability, the production of antibiotics has also evolved over a period of time. From a purely chemical process involving variety of solvents, the production of the first-generation antibiotics has evolved over the time. Now amoxicillin is being manufactured by an enzymatic process, which has minimum use of solvents.10 The absence of solvents in the enzymatic process offers a better quality of amoxicillin, making it more effective. The reduced toxicity owing to the absence of most residual solvents is an aspect, which is highly valued by doctors and patients. When it comes to palatability, the enzymatic amoxicillin offers a better taste due to the absence of most residual solvents. In the manufacture of amoxicillin suspensions and syrups, the taste of the chemically-produced amoxicillin and active pharmaceutical ingredient (API) can be dominant and children may discard the prescribed formulation, if the taste is not palatable. In such cases, use of enzymatic amoxicillin comes handy and the formulations based on enzymatic amoxicillin are preferred over the alternatives based on chemically-produced amoxicillin. Hence, the absence of the chemicals makes the antibiotics safer and more palatable, thereby reducing the need of sweeteners and masking agents in the final formulations. The enzymatic process also ensures lesser energy consumption, lesser production of waste and lesser emissions to the environment as compared to conventional chemical process. This results in

1. World Health Organization. Antimicrobial resistance: global report on surveillance 2014. www.who.int/ drugresistance/documents/surveillancereport/en. 2. https://www.gov.uk/.../20130902_UK_5_year_AMR_ strategy.pdf. 3. Guzmán Molina C, Velasco Rodríguez-Belvís M, Coroleu Bonet A, Vall Combelles O, García-Algar O. Antibiotics in Respiratory Tract Infections in Hospital Pediatric Emergency Departments. Arch Bronconeumol 2014 Mar 11. pii: S03002896(14)00068-4. 4. Williams DJ, Hall M, Shah SS, Parikh K, Tyler A, Neuman MI, et al. Narrow vs broad-spectrum antimicrobial therapy for children hospitalized with pneumonia. Pediatrics 2013;132(5):e1141-8. 5. Queen MA, Myers AL, Hall M, Shah SS, Williams DJ, Auger KA, et al. Comparative effectiveness of empiric antibiotics for community-acquired pneumonia. Pediatrics Peds 20131773; published ahead of print December 9, 2013. 6. Hansen JG. Acute rhinosinusitis (ARS). Diagnosis and treatment of adults in general practice. Dan Med J 2014;61(2):B4801. 7. Shulman ST, Bisno AL, Clegg HW, Gerber MA, Kaplan EL, Lee G, et al. Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America. Clin Infect Dis 2012;55(10):1279-82. 8. Klebanoff MA. The Collaborative Perinatal Project: a 50-year retrospective. Paediatr Perinat Epidemiol 2009;23(1):2-8. 9. Jepsen P, Skriver MV, Floyd A, Lipworth L, Schønheyder HC, Sørensen HT. A population-based study of maternal use of amoxicillin and pregnancy outcome in Denmark. Br J Clin Pharmacol 2003;55(2):216-21. 10. Schroen CG, Van Roon JL, Beefink HH, Tramper J, Boom RM. Membrane applications for antibiotics production. Desalination 2009;236:78-84.

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143


Endocrinology

A Comparative Study to Analyze the Association of Metabolic Syndrome in Females with Diagnosed Polycystic Ovarian Syndrome Richa Singh*, Saroj Singh*, Poonam Yadav†, Harpreet Kaur‡

Abstract Objectives: Polycystic ovarian syndrome (PCOS) is a common female endocrinopathy affecting 5-6% of women within the age group 12-45 years. This study was contemplated with the aim to study the prevalence of metabolic syndrome in patients of PCOS and to study the spectrum of clinical features of metabolic syndrome in patients of PCOS. Material and methods: This case-controlled study was conducted on 50 cases of diagnosed PCOS females and compared with 50 healthy age and body mass index (BMI) matched controls. Results: The prevalence of metabolic syndrome in PCOS patients was found to be 24% and in control group it was 6%. Among patients with metabolic syndrome 14% of patients had high blood pressure, 12% had impaired fasting glucose, 38% have high waist-hip ratio, 14% have raised serum triglycerides and 44% had decreased highdensity lipoprotein (HDL). Conclusion: It is observed that metabolic syndrome manifests at an early age in women with PCOS. In order to prevent metabolic syndrome one should maintain BMI <25 and waist circumference <35 inches.

Keywords: Metabolic syndrome, polycystic ovarian syndrome, hyperinsulinemia

P

olycystic ovarian syndrome (PCOS) is one of the most common female endocrinopathy affecting 5-6% of women within the age group 12-45 years. These patients are at high-risk of developing infertility, dysfunctional uterine bleeding, endometrial carcinoma and a number of metabolic disorders including insulin resistance, hyperinsulinemia, type 2 diabetes mellitus, hypertension, dyslipidemia and cardiovascular disease. Due to these facts, early diagnosis of the syndrome should be emphasized. This background knowledge demands the necessity to work out the prevalence of metabolic syndrome in women with PCOS in our society and to measure the strength of their association in the Indian scenario. Aims and Objectives ÂÂ

To study the prevalence of metabolic syndrome in patients of PCOS.

*Professor †Lecturer ‡Jr - III Dept. of Obstetrics and Gynecology SN Medical College, Agra, Uttar Pradesh Address for correspondence Dr Richa Singh Professor Chauhan Nursing Home, 1/120-G, Delhi Gate Agra - 282 002, Uttar Pradesh E-mail: chauhan.richavishal@gmail.com

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Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014

ÂÂ

To study the spectrum of clinical features of metabolic syndrome in patients of PCOS.

Material and Methods This study was conducted on 50 cases of diagnosed PCOS coming to our hospital and was compared with 50 healthy age and body mass index (BMI) matched women (control group) over a period of 1 year.

Inclusion Criteria Around 50 cases diagnosed to have PCOS by the Rotterdam European Society of Human Reproduction Embryology/The American Society of Reproductive Medicine (ESHRE/ASRM) PCOS group’s revised 2003 criteria, with presence of any two of the three criteria, were recruited for the study. These criteria are: ÂÂ

Oligo and/or anovulation

ÂÂ

Clinical and/or biochemical signs of hyperandrogenism

ÂÂ

Polycystic ovaries (as confirmed by USG)

The criteria for metabolic syndrome in women with PCOS. According to National Cholesterol Education Program (NCEP), Adult Treatment Panel III (ATP III) 2001.


Endocrinology Three out of these five will qualify for the syndrome: ÂÂ

Abdominal obesity (waist circumference ≥88 cm or 35 inches) and ≥80 cm for Asian females

ÂÂ

Triglycerides ≥150 mg/dL

ÂÂ

High-density ≤50 mg/dL

ÂÂ

Blood pressure ≥130/85 mmHg

ÂÂ

Fasting plasma glucose ≥100 mg/dL or previously diagnosed type 2 diabetes.

lipoprotein

(HDL)

cholesterol

After taking careful history from the patient and conducting examination, following investigations were carried out - hemogram, fasting blood sugar, oral glucose tolerance test (OGTT), fasting insulin, fasting lipid profile, hormonal estimations for leuteinizing hormone, follicle-stimulating hormone, testosterone, estrogen, progesterone and ultrasound abdomen. In these women, fasting blood was drawn for glucose, insulin and lipid profile, which included triglycerides, total cholesterol, HDL and low-density lipoprotein (LDL) cholesterol. A 2-hour 75 g glucose tolerance test was done in all PCOS patients. Two markers for obesity, such as BMI and waist-hip ratio, which depicts central obesity were used to study relationship of obesity to lipid parameters. Height (m) and weight (kg) measurements can be used to calculate the BMI (BMI = Weight in kg/height in m2). Waist-hip ratio can be calculated after measuring waist circumference between pelvic brim and costal margin, while hip circumference is taken at the level of the greater trochanter. Waist-hip ratio >0.85 is considered abnormal, while <0.85 normal. The results were subjected to statistical analysis wherever applicable. Results The profile of patients included in the study is shown in Table 1. The distribution of cases and controls according to BMI (kg/m2) is shown in Table 2. It is seen that 67% of patients included in the study were overweight or obese. Table 3 shows distribution of cases according to fasting insulin levels. Fasting insulin levels were raised in 24% of cases and 10% of controls. Distribution of cases according to components of metabolic syndrome in patients of PCOS is shown in Table 4. It was seen that ↓HDL-C levels were seen in 44% of cases and 12% of controls. Waist-hip

Table 1. Patient Profile Age group

Socioeconomic status

15-25

26-35

Total

Low

High

No.

21

29

50

20

30

%

42

58

100

40

60

No.

16

34

50

22

28

%

32

68

100

44

56

Cases

Controls

P value <0.04.

Table 2. Distribution of Cases and Controls according to BMI (kg/m2) Category according to BMI (kg/m2)

Cases

Controls

No.

%

No.

%

Underweight (≤19.9)

3

6

2

4

Normal (20-24.9)

13

26

15

30

Overweight (25-29.9)

30

60

28

56

Obese (≥30)

4

8

5

10

Total

50

100

50

100

Table 3. Distribution of Cases according to Fasting Insulin Levels Category

Cases

Controls

No.

%

No.

%

Normal

38

76

45

90

Increased

12

24

5

10

Table 4. Distribution of Cases according to Components of Metabolic Syndrome in Patients of PCOS Clinical components

Cases

Controls

Positive

%

Positive

%

BP >130/85 mmHg

7

14

2

4

Impaired fasting blood glucose (>100 mg/dL)

6

12

2

4

Waist-hip ratio >0.85 cm

19

38

7

14

↑STG (>150 mg/dL)

8

16

5

10

↓HDL-C (<50 mg/dL)

22

44

6

12

PCOS = Polycystic ovarian syndrome; BP = Blood pressure; HDL-C = High-density lipoprotein cholesterol; S. = Serum; TG = Triglyceride.

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Endocrinology Table 5. Comparative Evaluation of Clinical Spectrum of Metabolic Syndrome in Cases and Controls Clinical parameters Controls (50) Cases (50) P value Age (years) 26 25 0.52 BMI 23.75 24.25 0.78 SBP (mmHg) 110 120 0.06 DBP (mmHg) 70 74 0.06 S. cholesterol (mg/dL) 175.2 201.2 0.02 S. TG (mg/dL) 110.7 133.3 0.03 HDL (mg/dL) 35.2 25.4 0.04 LDL (mg/dL) 105.2 130.8 0.04 VLDL (mg/dL) 12.2 18.12 0.02 Insulin (ÂľIU/mL) 5.1 6.5 0.04 Fasting glucose (mg/dL) 77 86 0.04 ANOVA test is used for calculating p value. BMI = Body mass index; SBP = Systolic blood pressure; DBP = Diastolic blood pressure; S = Serum; TG = Triglyceride; HDL = High-density lipoprotein; LDL = Low-density lipoprotein; VLDL = Very low-density lipoprotein.

Table 6. Prevalence of Metabolic Syndrome in Various Studies Study

Year

Our study

Prevalence of metabolic syndrome (%)

2012-13

24

Glueck et al (USA)1

2003

43-46

Dey (India)2

2011

42

2006

33.4

2005

47.3

Ehrmann et Dokras et

al3

al4

ratio >0.85 cm was seen in 38% of cases and 14% of controls. Comparative evaluation of clinical spectrum of metabolic syndrome in cases and controls is depicted in Table 5. The prevalence of metabolic syndrome in various studies is shown in Table 6. Discussion This was a cross-sectional case-control study of 100 females attending our OPD over a period of 1 year. If we compare BMI matched cases and controls, then also lipid profile derangement is associated more with PCOS obese than non-PCOS obese (p < 0.04). This is in accordance with the study of Macut et al5 who found that overweight and normal weight women with PCOS have higher incidence of lipid profile derangement than their controls. Wild et al6 found that dyslipidemia is more common in PCOS. In our study, among patients with lipid profile derangement, 44% had decreased

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HDL as compared to 12% of controls (p < 0.05). Low HDL is having more detrimental effect on lipid profile derangement predictions among cases, which is in accordance with a study in Teharian women by Moini et al,7 where low HDL was found in 96.9% of cases of metabolic syndrome in PCOS. Study by Dey et al2 showed decreased HDL in 50% cases. In our study, waist circumference, which depicts central obesity ≼80 cm was found in 38% of cases and 14% of controls (p < 0.05). It is different from the study done by Ehrmann et al,3 which supports high value of waist circumference by citing 80% of subjects above 88 cm. In our study, fasting insulin level showed increase in 24% of cases and 10% of controls (p < 0.05) it shows a significant difference among women with metabolic syndrome in comparison to those without metabolic syndrome as supported by Dokras et al4 study in 2005. We observed that, while USA women and Indian women have similar androgen levels, similar blood pressure, similar total cholesterol and LDL, USA women have higher body weight, higher fasting insulin, higher fasting glucose level, lower HDL and raised triglycerides. Most of these difference occurred as a result of higher prevalence of obesity in USA group, but other factors including characteristics of diet may also be responsible. Thus, in our study prevalence of metabolic syndrome is 24% among cases and 6% among age and BMI matched controls, which shows a statistically significant difference (p < 0.05) and thus PCOS per se is responsible for prevalence of metabolic syndrome. Conclusion It is observed that metabolic syndrome manifests at an early age in women PCOS. Hyperinsulinemia, a central factor in the pathogenesis of PCOS, also appears to be a critical link between PCOS and metabolic syndrome. Thus, there is an urgent necessity to assess the rising trend of metabolic syndrome among the women with PCOS and to take early measures for primary prevention of its long-term sequel. In order to prevent metabolic syndrome maintain BMI <25 and waist circumference <35 inches to prevent the development of metabolic syndrome or cardiovascular disease. An independent panel convened by the National Institutes of Health has recommended that well-designed, multicentric studies be conducted to determine


Endocrinology factors such as obesity, that exacerbate a genetic predisposition. The panel also determined the need for additional research to identify risks and treatments for complications and how to manage the common symptoms. References 1. Glueck CJ, Papanna R, Wang P, Goldenberg N, SieveSmith L. Incidence and treatment of metabolic syndrome in newly referred women with confirmed polycystic ovarian syndrome. Metabolism 2003;52(7):908-15. 2. Dey R, Mukherjee S, Roybiswas R, Mukhopadhyay A, Biswas SC. Association of metabolic syndrome in polycystic ovarian syndrome: an observational study. J Obstet Gynaecol India 2011;61(2):176-81. 3. Ehrmann DA, Liljenquist DR, Kasza K, Azziz R, Legro RS, Ghazzi MN; PCOS/Troglitazone Study Group. Prevalence and predictors of the metabolic syndrome in women with

polycystic ovary syndrome. J Clin Endocrinol Metab 2006;91(1):48-53. 4. Dokras A, Bochner M, Hollinrake E, Markham S, Vanvoorhis B, Jagasia DH. Screening women with polycystic ovary syndrome for metabolic syndrome. Obstet Gynecol 2005;106(1):131-7. 5. Macut D, Damjanovic S, Panidis D, Spanos N, Glisic B, Petakov M, et al. Oxidised low-density lipoprotein concentration - early marker of an altered lipid metabolism in young women with PCOS. Eur J Endocrinol 2006;155(1):131-6. 6. Wild RA, Rizzo M, Clifton S, Carmina E. Lipid levels in polycystic ovary syndrome: systematic review and metaanalysis. Fertil Steril 2011;95(3):1073-9.e1-11. 7. Moini A, Javanmard F, Eslami B, Aletaha N. Prevalence of metabolic syndrome in polycystic ovarian syndrome women in a hospital of Tehran. Human Reprod Med 2012;10(2):127-30.

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Can Diabetes Be Warded Off? Adhering to Mediterranean diet, rich in fruits and vegetables and low in animal products may protect from type 2 diabetes. The Mediterranean diet gives emphasis to olive oil, vegetables, fruits, nuts, cereals, legumes and fish and de-emphasizes meat and dairy products. It is a healthy eating plan that prevents heart disease. In the study published in the British Medical Journal, researchers tracked the diets of 13,380 Spanish university graduates with no history of diabetes. The study participants filled out a 136-item food questionnaire, which measured their entire diet (including their intake of fats), their cooking methods and their use of dietary supplements. During an average of 4.4 years of follow-up, the researchers found that people who adhered to a Mediterranean diet had a lower risk of developing type 2 diabetes. In fact, those who very closely adhered to the diet reduced their risk by 83 percent. Moreover, the people who tended to stick closest to the diet were those with factors that put them at the highest risk for developing diabetes, such as being older, having a family history of diabetes and being an ex–smoker. These people were expected to have a higher rate of diabetes, but when they adhered to the Mediterranean diet this was not the case. Type 2 diabetes is typically brought on by poor eating habits, too much body weight and too little exercise. One key factor that might be responsible for the protective effect of the Mediterranean diet is its emphasis on olive oil for cooking, frying, putting on bread and mixing in salad dressings. Tips to prevent diabetes ÂÂ

Eat less

ÂÂ

Omit refined carbohydrates (white sugar, white rice and white maida)

ÂÂ

Use olive oil, vegetables, fruits, nuts, cereals, legumes and fish, and reduce meat and dairy products.

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Every citizen of India should have the right to accessible, affordable, quality and safe heart care irrespective of his/her economical background

Sameer Malik Heart Care Foundation Fund An Initiative of Heart Care Foundation of India

E-219, Greater Kailash, Part I, New Delhi - 110048 E-mail: heartcarefoundationfund@gmail.com Helpline Number: +91 - 9958771177

“No one should die of heart disease just because he/she cannot afford it” About Sameer Malik Heart Care Foundation Fund

Who is Eligible?

“Sameer Malik Heart Care Foundation Fund” it is an initiative of the Heart Care Foundation of India created with an objective to cater to the heart care needs of people.

Objectives Assist heart patients belonging to economically weaker sections of the society in getting affordable and quality treatment. Raise awareness about the fundamental right of individuals to medical treatment irrespective of their religion or economical background. Sensitize the central and state government about the need for a National Cardiovascular Disease Control Program. Encourage and involve key stakeholders such as other NGOs, private institutions and individual to help reduce the number of deaths due to heart disease in the country. To promote heart care research in India.

All heart patients who need pacemakers, valve replacement, bypass surgery, surgery for congenital heart diseases, etc. are eligible to apply for assistance from the Fund. The Application form can be downloaded from the website of the Fund. http://heartcarefoundationfund.heartcarefoundation. org and submitted in the HCFI Fund office.

Important Notes The patient must be a citizen of India with valid Voter ID Card/ Aadhaar Card/Driving License. The patient must be needy and underprivileged, to be assessed by Fund Committee. The HCFI Fund reserves the right to accept/reject any application for financial assistance without assigning any reasons thereof. The review of applications may take 4-6 weeks. All applications are judged on merit by a Medical Advisory Board who meet every Tuesday and decide on the acceptance/rejection of applications. The HCFI Fund is not responsible for failure of treatment/death of patient during or after the treatment has been rendered to the patient at designated hospitals.

To promote and train hands-only CPR.

Activities of the Fund Financial Assistance

The HCFI Fund reserves the right to advise/direct the beneficiary to the designated hospital for the treatment.

Financial assistance is given to eligible non emergent heart patients. Apart from its own resources, the fund raises money through donations, aid from individuals, organizations, professional bodies, associations and other philanthropic organizations, etc.

The financial assistance granted will be given directly to the treating hospital/medical center.

After the sanction of grant, the fund members facilitate the patient in getting his/her heart intervention done at state of art heart hospitals in Delhi NCR like Medanta – The Medicity, National Heart Institute, All India Institute of Medical Sciences (AIIMS), RML Hospital, GB Pant Hospital, Jaipur Golden Hospital, etc. The money is transferred directly to the concerned hospital where surgery is to be done.

Drug Subsidy

The HCFI Fund has the right to print/publish/webcast/web post details of the patient including photos, and other details. (Under taking needs to be given to the HCFI Fund to publish the medical details so that more people can be benefitted). The HCFI Fund does not provide assistance for any emergent heart interventions.

Check List of Documents to be Submitted with Application Form Passport size photo of the patient and the family A copy of medical records Identity proof with proof of residence Income proof (preferably given by SDM)

The HCFI Fund has tied up with Helpline Pharmacy in Delhi to facilitate

BPL Card (If Card holder)

patients with medicines at highly discounted rates (up to 50%) post surgery.

Details of financial assistance taken/applied from other sources (Prime Minister’s Relief Fund, National Illness Assistance Fund Ministry of Health Govt of India, Rotary Relief Fund, Delhi Arogya Kosh, Delhi Arogya Nidhi), etc., if anyone.

The HCFI Fund has also tied up for providing up to 50% discount on imaging (CT, MR, CT angiography, etc.)

Free Diagnostic Facility

Free Education and Employment Facility

The Fund has installed the latest State-of-the-Art 3 D Color Doppler EPIQ 7C Philips at E – 219, Greater Kailash, Part 1, New Delhi.

HCFI has tied up with a leading educational institution and an export house in Delhi NCR to adopt and to provide free education and employment opportunities to needy heart patients post surgery. Girls and women will be preferred.

This machine is used to screen children and adult patients for any heart disease.

Laboratory Subsidy HCFI has also tied up with leading laboratories in Delhi to give up to 50% discounts on all pathological lab tests.


About Heart Care Foundation of India

Help Us to Save Lives The Foundation seeks support, donations and contributions from individuals, organizations and establishments both private and governmental in its endeavor to reduce the number of deaths due to heart disease in the country. All donations made towards the Heart Care Foundation Fund are exempted from tax under Section 80 G of the IT Act (1961) within India. The Fund is also eligible for overseas donations under FCRA Registration (Reg. No 231650979). The objectives and activities of the trust are charitable within the meaning of 2 (15) of the IT Act 1961.

Heart Care Foundation of India was founded in 1986 as a National Charitable Trust with the basic objective of creating awareness about all aspects of health for people from all walks of life incorporating all pathies using low-cost infotainment modules under one roof. HCFI is the only NGO in the country on whose community-based health awareness events, the Government of India has released two commemorative national stamps (Rs 1 in 1991 on Run For The Heart and Rs 6.50 in 1993 on Heart Care Festival- First Perfect Health Mela). In February 2012, Government of Rajasthan also released one Cancellation stamp for organizing the first mega health camp at Ajmer.

Objectives Preventive Health Care Education Perfect Health Mela Providing Financial Support for Heart Care Interventions Reversal of Sudden Cardiac Death Through CPR-10 Training Workshops Research in Heart Care

Donate Now... Heart Care Foundation Blood Donation Camps The Heart Care Foundation organizes regular blood donation camps. The blood collected is used for patients undergoing heart surgeries in various institutions across Delhi.

Committee Members

Chief Patron

President

Raghu Kataria

Dr KK Aggarwal

Entrepreneur

Padma Shri, Dr BC Roy National & DST National Science Communication Awardee

Governing Council Members Sumi Malik Vivek Kumar Karna Chopra Dr Veena Aggarwal Veena Jaju Naina Aggarwal Nilesh Aggarwal H M Bangur

Advisors Mukul Rohtagi Ashok Chakradhar

Executive Council Members Deep Malik Geeta Anand Dr Uday Kakroo Harish Malik Aarti Upadhyay Raj Kumar Daga Shalin Kataria Anisha Kataria Vishnu Sureka

This Fund is dedicated to the memory of Sameer Malik who was an unfortunate victim of sudden cardiac death at a young age.

Rishab Soni

HCFI has associated with Shree Cement Ltd. for newspaper and outdoor publicity campaign HCFI also provides Free ambulance services for adopted heart patients HCFI has also tied up with Manav Ashray to provide free/highly subsidized accommodation to heart patients & their families visiting Delhi for treatment.

http://heartcarefoundationfund.heartcarefoundation.org


ENT

Self-Inflicted Styloid Process Fracture Cures Styalgia ANUPAMA KAUR,* AMANPREET SINGH†

Abstract The treatment of styalgia varies from region to region. Initially, the patients are treated medically and if not relieved styloidectomy is advised. Styloid process fracture has also given favorable results in many patients. The authors report a 45-year-old man who accidentally fractured his own styloid process and got relieved of styalgia. In this case report, authors discuss clinical presentation, differential diagnosis of styalgia and various lines of management for styalgia.

Keywords: Styloid process, styalgia, styloidectomy

T

he styloid process is a cylindrical, long cartilaginous bone located on the posterior lower surface of the petrosal bone. Direction of this process is downwards to the front and slightly to the inside. The normal styloid process length is between 20-30 mm. It develops from the second brachial arch.1 Watt W Eagle coined the term stylalgia to describe the pain associated with elongation of styloid process. Patients can be categorized into two groups: Patients who have classical symptoms of a foreign body sensation in the throat with a palpable mass in the tonsillar region and those with pain in the neck following the carotid artery distribution.2 The elongated styloid process can be palpated orally by inserting a finger orally along the occlusal line in posterior tonsillar fossa.3 If palpation of the styloid process produces pain that is either referred to ear, head or face, it is very likely that styloid process is elongated.4 Initially, the clinician should try to decrease any muscle spasm and scar tissue around the styloid process. Some clinicians have also tried fracturing of styloid process with mixed results. Steroid injections have also been injected into affected tissues with varying results.5,6 If not relieved, traditional method of surgical excision of styloid process is followed. Eagle in 1949, described a syndrome as Eagle’s syndrome characterized by elongated styloid process or ossified *Assistant Professor Dept. of Physiology †Assistant Professor Dept. of ENT MM Institute of Medical Sciences, Mullana, Ambala, Haryana Address for correspondence Dr Amanpreet Singh Assistant Professor Dept. of ENT MM Institute of Medical Sciences, Mullana, Ambala, Haryana E-mail: dr.apsarora@gmail.com

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stylohyoid ligament.7 Here we report a case of a patient who accidentally fractured his styloid process that cured his styalgia. CASE REPORT A 45-year-old man farmer by occupation came with the following sequence of events. Around 4-5 years back the patient started having pain in the throat. It was more during swallowing food and predominantly on the left side. With time his symptoms started to aggravate and he also started to experience pain radiating to ear and sometimes to ipsilateral face and rarely to clavicle. He presented to us with the abovementioned symptoms. Intraoral palpation revealed bilateral enlargement of styloid process. Thinking in terms of styalgia carbamazepine was started with a dosage of 200 mg twice a day. Patient was advised to come after 10 days for follow-up. He did turn up but after

Figure 1. Showing healed fracture of left styloid process.


ENT around 3 months. As his symptoms were not relieved, he went to a quack, who rubbed salt-like powder (locally called as manjun) in the region of palatine tonsils. As the patient describes, it gave him a moment of relief. Patient started rubbing the powder by himself in the tonsillar region for relief. Once while applying the powder he vigorously rubbed and pressed and felt something snapping. He experienced severe excruciating pain, which subsided with pain killers in a week. In 2 weeks time, he realized that he had no further pain and its radiation to ear and other regions had also stopped. He presented to us to know whether he had caused himself an unknown trauma. Intraoral palpation still revealed bilateral enlargement of the styloid process. X-ray of skull, Townes view was done. In addition to bilateral enlargement of styloid process, it also showed a healed fracture of styloid process left side. DISCUSSION Normally, styloid process is not palpable on bimanual palpation of tonsillar fossa. If palpable, it confirms the diagnosis. X-ray of skull, Townes view can also be done to confirm the diagnosis. An ossified stylohyoid ligament or an elongated styloid process may not be symptomatic in every patient. Symptoms may vary from foreign body sensation, throat pain, dysphagia, headache, ipsilateral otalgia and sometimes facial and carotid pain.8-10 In medical literature, there are not many cases of fractures of ossified ligaments reported. Either these fractures are spontaneous or traumatic.10,11 Elongated styloid process can be caused by congenital elongation of styloid process due to persistence of cartilaginous analog of styloid and can also be due to calcification of stylohyoid ligament by unknown mechanism and growth of osseous tissue at the insertion of stylohyoid ligament. Glossopharyngeal nerve, vagus and 3rd branch of trigeminal nerve and chorda tympani can be stimulated by styloid process and induce pain. There are various claims that fracture of styloid process can lead to granular tissue formation thus releasing pressure on nearby structures. For symptomatic cases, therapy may vary from medical to surgical line of management, depending upon the intensity of pain and dysphagia. Medical line includes anti-inflammatory and corticosteroid drugs. Surgery is planned in patients who do not respond to medical line of management. Elongated styloid

process can be excised, but some authors do not agree for excision of styloid process.5,6 Excision of styloid process can be done by transoral approach or external approach. Nowadays, styloid process is also resected endoscopically through transoral route.12 The advantage of following external approach is proper exposure of styloid process and other vital structures.13 In spite of medical research going all over the world and new drugs and treatment modalities coming every other day, few diseases still are not satisfactorily treated, neuralgia being one of them. Our patient was not relieved with the treatment we had advised him to follow. Under the influence of a quack, patient started rubbing salt-like powder in his tonsillar region which on one day led to fracture of styloid process. Patient is now relieved of the pain. These sequences of events highlights three major issues. Firstly, to confirm the diagnosis of styloid process enlargement clinically by proper history and examination which should be further consolidated by X-ray, Townes view. Secondly, the unsatisfactory treatment of styalgia and associated neuaralgias due to the lack of a set of guidelines for the treatment of the same. Treatment ranges from medicines to styloidectomy to fracture of styloid process, and last but not the least the invasion of health industry in India by unqualified and underqualified practitioners. Our patient was relieved of symptoms and he is full of praise for the quack, but we as a medical fraternity should recognize this as a failure on our part. CONCLUSION Styloid process enlargement is not uncommon. History should be taken thoroughly and in detail and physical examination of head and neck are mandatory. Traditionally, surgical excision of styloid process is the treatment of choice. But there have been cases all over the world in which the patients felt totally relieved of the neuralgic symptoms by infracture of styloid process after tonsillectomy. A patient infracturing a styloid process accidentally and getting relieved of styalgia is a rare and probably the first case in the world. References 1. Standing S. Skull and Mandible. In: Gray’s Anatomy. The Anatomical Basis of Clinical Practice. 39th edition, Elsevier: Edinburg 2005:p.470. 2. Camarda AJ, Deschamps C, Forest D. I. Stylohyoid chain ossification: a discussion of etiology. Oral Surg Oral Med Oral Pathol 1989;67(5):508-14.

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ENT 3. Keur JJ, Campbell JP, McCarthy JF, Ralph WJ. The clinical significance of the elongated styloid process. Oral Surg Oral Med Oral Pathol 1986;61(4):399-404.

9. Unlu Z, Orguc S, Eskiizmir G, Aslan A, Bayindir P. Elongated styloid process and cervical spondylosis. Clin Med Case Rep 2008;1:57-64.

4. Mendelsohn AH, Berke GS, Chhetri DK. Heterogeneity in the clinical presentation of Eagle’s syndrome. Otolaryngol Head Neck Surg 2006;134(3):389-93.

10. Blomgren K, Qvarnberg Y, Valtonen H. Spontaneous fracture of an ossified stylohyoid ligament. J Laryngol Otol 1999;113(9):854-5.

5. Evans JT, Clairmont AA. The nonsurgical treatment of Eagle’s syndrome. Eye Ear Nose Throat Mon 1976;55(3):94-5.

11. Correll RW, Jensen JL, Taylor JB, Rhyne RR. Mineralization of the stylohyoid-stylomandibular ligament complex. A radiographic incidence study. Oral Surg Oral Med Oral Pathol 1979;48(4):286-91.

6. Steinmann EP. Styloid syndrome in absence of an elongated process. Acta Otolaryngol 1968;66(4):347-56. 7. Eagle WW. Elongated styloid process; further observations and a new syndrome. Arch Otolaryngol 1948;47(5):630-40.

12. Matsumoto F, Kase K, Kasai M, Komatsu H, Okizaki T, Ikeda K. Endoscopy-assisted transoral resection of the styloid process in Eagle’s syndrome. Case report. Head Face Med 2012;8:21.

8. Moffat DA, Ramsden RT, Shaw HJ. The styloid process syndrome: aetiological factors and surgical management. J Laryngol Otol 1977;91(4):279-94.

13. Beder E, Ozgursoy OB, Karatayli Ozgursoy S. Current diagnosis and transoral surgical treatment of Eagle’s syndrome. J Oral Maxillofac Surg 2005;63(12):1742-5.

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A new study conducted at the Seoul National University, Korea has stated that polyps that develop on the vocal cords may resolve on their own in up to one third of patients. Researchers noted that among 94 patients presenting to a tertiary referral center treated conservatively and observed for at least three months, 46% of polyps diminished significantly in size and 38% resolved completely without requiring surgery. Of the polyps that resolved on their own, 44% were resolved by three months and 81% by eight months. The study was published online in JAMA Otolaryngology-Head & Neck Surgery.

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A study published recently in Otolaryngology-Head and Neck Surgery has pointed that adults have a high rate of complications after tonsillectomy, with one in five adults also having serious complications within two weeks of surgery. The study authors evaluated the records of 36,000 adult outpatient tonsillectomies in a nationwide insurance database and noted that after one week of surgery, 15% of patients had at least one possible complication, which further increased to 20% by the two- and four- week points.

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Caloric vestibular stimulation (CVS), a test commonly used by ENT specialists and audiologists to test patients' balance, could transiently enhance illness awareness in patients with schizophrenia, reports a pilot proof-of-concept study presented at the American Society of Clinical Psychopharmacology (ASCP) 2014 Annual Meeting.

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Gastroenterology

A Case Report on Perforated Duodenal Ulcer in Early Puerperium Pradeep MR*, Nandish VL†, lalithashivanna‡

Abstract Perforated duodenal ulcer is a uncommon disease in pregnancy and puerperium. An 18-year-old primigravida was admitted to our hospital at term in labor. She underwent emergency cesarean section for deep transverse arrest. On 8th postoperative day, patient had sudden pain in the upper abdomen and found to have hypovolemic shock with distention of abdomen. Emergency laparotomy was done after resuscitation. Per operatively, 2 liters of bilious fluid in the abdominal cavity with huge anterior wall perforated duodenal ulcer was present. Bile drained, Graham patch closure carried out. Patient was discharged on 10th day. Symptoms of peptic ulcer disease (PUD) and pregnancy often overlap and difficult for diagnosis. Early diagnosis and timely management of complicated PUD with pregnancy or puerperium is challenging for a treating doctor.

Keywords: Pregnancy, puerperium, perforated duodenal ulcer, peptic ulcer disease, laparotomy, Graham patch closure

P

erforated duodenal ulcer is a rare disease in pregnancy and puerperium. There is not enough data for exact incidence of disease in pregnancy and puerperium; however, older literature suggest an incidence of 0.005%,1 whereas incidence of peptic ulcer disease (PUD) is 0.1-0.19% in general population.2 It is interesting to note that symptoms of PUD decrease in pregnancy and recur after 3-6 months of parturition.3 The improvement in symptoms may be due to decrease in gastric acid production and increased gastric mucus synthesis in pregnancy.3,4 The symptoms of PUD like nausea, vomiting and epigastric discomfort also overlap with symptoms of pregnancy. So, diagnosis and timely management of PUD is challenging for a treating doctor. We report one such case of perforated duodenal ulcer in early puerperium. Case Report An 18-year-old primigravida was admitted at 38 weeks in labor. Patient was admitted twice for threatened

*Assistant Professor Dept. of Obstetrics and Gynecology †Professor and Head Dept. of Surgery ‡Professor and Head Dept. of Obstetrics and Gynecology Mandya Institute of Medical Sciences, Mandya, Karnataka Address for correspondence Dr Pradeep MR H. No: 201B, Doctors Quarters, Mandya Institute of Medical Sciences Mandya - 571 401, Karnataka E-mail: majormrp@gmail.com

preterm labor at 28 and 34 weeks of gestation, subsided with short course of tocolytics and antibiotics. Steroid prophylaxis (injection betamethasone 12 mg two doses 24 hours apart) was given for lung maturity. There was no history of vomiting or epigastric pain at that time. Patient underwent emergency cesarean section under spinal anesthesia for deep transverse arrest. Operative findings were within normal limits. Injection diclofenac sodium 50 mg IM b.i.d. as analgesic and H2 receptor antagonist (injection ranitidine 50 mg b.i.d.) was given for 3 days. Same in tablet form was given for two more days along with 5 days of antibiotics. Patient was started on oral diet after 24 hours of operation. On 8th postoperative day, patient developed sudden pain in the upper abdomen; on examination, pulse rate - 110/min blood pressure (BP) - 90/60 mmHg. Tenderness and distention of abdomen was present. Emergency ultrasound revealed moderate to gross ascites. Abdominocentesis was done, ascitic fluid aspirated. On cytology cell count 2,760 cells/mm3, protein - 2.8 g/dL, polymorphs - 99% and occasional lymphocytes seen. Smear was negative for malignant cells, 6 hours later patient’s condition deteriorated further. Other investigation: Renal function tests (RFTs), liver function tests (LFTs) and serum electrolytes were within normal limits. Provisional diagnosis of septic peritonitis was made. Intravenous (IV) antibiotic piperacillin with tazobactam was started. After stabilizing patient by IV fluids, emergency laparotomy was carried out.

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Gastroenterology PREGNANCY

Duodenal Perforation

Increased anterior pituitary like hormones

Increased progesterone

Hypochlorohydria

Increased placental histamine synthesis

Increased gastric mucus synthesis

Decreased maternal histamine Decreased gastric acid production

Figure 1. Anterior wall duodenal perforation seen at emergency laparotomy.

Per operatively, 2 liters of bilious fluid in the abdominal cavity, huge anterior wall duodenal perforation was present (Fig. 1). Bilious fluid drained, duodenal perforation closed in layers with omental patch, peritoneal wash was given and abdomen closed in layers. The patient was on IV antibiotics for 7 days and proton pump inhibitors for 10 days. On Day 4, patient developed acute respiratory distress syndrome (ARDS) but responded well to treatment. Patient also had wound gaping. Secondary suturing was done and patient was discharged on 10th day. Discussion Even though, there is paucity of data, multiple epidemiological studies shows decreased incidence of PUD in pregnancy and early puerperium.1 Hormones and other factors secreted during pregnancy cause hypochlorohydria, increased gastric mucus synthesis, decreased maternal histamine and decreased gastric acid production. Risk factors for PUD like cigarette smoking, alcohol, nonsterodial anti-inflammtory drugs (NSAIDs) are generally avoided during pregnancy. So, PUD becomes a rare disease in pregnancy and early puerperium (Fig. 2).3,4 Symptoms of PUD are same in pregnant and non-pregnant women. Clinical symptoms often overlap with symptoms of pregnancy (Table 1). Management of severe cases of PUD with pregnancy and puerperium require obstetrician, surgeon and a gastroenterologist. On suspicion of complication of PUD in pregnancy and puerperium baseline investigations - complete blood count, LFT, RFT, serum amylase and serum electrolytes

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Protective factors for PUD during pregnancy

Avoiding NSAIDs, cigarette smoking, alcohol in pregnancy

Figure 2. Factors contributing towards decreased incidence of PUD in pregnancy.

Table 1. Symptoms of PUD in Pregnancy Symptoms

Pregnancy

Pregnancy with PUD

Nausea and vomiting

More in the morning hours

More in the night and after food increases with gestational age, severe in 3rd trimester5

Present in 1st and early 2nd trimester Pain abdomen6

Often lower part

Epigastric pain: May have hematemesis Fecal occult blood, tender ness and rebound tenderness in the abdomen

Treatment of PUD depends upon severity of symptoms Mild symptoms of PUD

Lifestyle modifications avoid fatty food caffeine, NSAIDs alcohol, cigarette smoking.

(Cimetidine, ranitidine famotidine, nizatidine) Histamine receptor Antagonists FDA Cat B Drugs

Lansoprazole and sucralfate FDA Cat B Drugs.7

must be carried out. Abdominal ultrasound is a useful tool to exclude cholelithiasis and gallstone pancreatitis. If duodenal ulcer perforation is suspected following steps should be taken:


Gastroenterology ÂÂ

Fluid resuscitation and correction of electrolyte imbalance

ÂÂ

Laparotomy - Graham patch closure

ÂÂ

If preterm pregnancy steroids should be given for lung maturation

ÂÂ

Proton pump inhibitor and oral IV antibiotics should be given for a week.

References 1. Baird RM. Peptic ulceration in pregnancy: report of a case with perforation. Can Med Assoc J 1966;94(16):861-2.

PUD is challenging during pregnancy and puerperium. Diagnosis is often made late leading to very high morbidity and mortality in a woman. In 1962, Paul et al described 14 cases of perforated duodenal ulcer in pregnancy in which all patients lost their life.8 Conclusion Pregnancy and puerperium is protective against PUD. But complications from PUD do occur during pregnancy and puerperium. Since symptoms of PUD often overlap with symptoms of pregnancy, obstetrician must be cautious in treating pain abdomen for detection of PUD. Early detection and management of complications from PUD in pregnancy/in puerperium certainly reduce high morbidity and mortality.

2. Sung JJ, Kuipers EJ, El-Serag HB. Systematic review: the global incidence and prevalence of peptic ulcer disease. Aliment Pharmacol Ther 2009;29(9):938-46. 3. Cappell MS. Gastric and duodenal ulcers during pregnancy. Gastroenterol Clin North Am 2003;32(1): 263-308. 4. Horwich M. Perforated duodenal ulcer during pregnancy. Br Med J 1958;2(5089):145. 5. Barnes LW. Serum histaminase during pregnancy. Obstet Gynecol 1957;9(6):730-2. 6. Essilfie P, Hussain M, Bolaji I. Perforated duodenal ulcer in pregnancy--a rare cause of acute abdominal pain in pregnancy: a case report and literature review. Case Rep Obstet Gynecol 2011;2011:263016. 7. Singer AJ, Brandt LJ. Pathophysiology gastrointestinal tract during pregnancy. Gastroenterol 1991;86(12):1695-712.

of the Am J

8. Paul M, Tew WL, Holliday RL. Perforated peptic ulcer in pregnancy with survival of mother and child: case report and review of the literature. Can J Surg 1976;19(5):427-9.

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ÂÂ

A study presented at the Digestive Disease Week (DDW) annual meeting has reported that MUSETM System (less invasive surgical anterior fundoplication with standard surgical staples) is safe and effective for patients with PPI-responsive, moderate-to-severe GERD. Researchers noted that the majority of patients (74%) treated with the MUSETM System remained off daily PPI at 3 years post-procedure.

ÂÂ

A phase II study from Finland has reported that celiac patients treated with a gluten-specific enzyme may be less exposed to gluten and its potentially harmful effects. Researchers noted that the gluten-specific protease ALV003 could attenuate gluten-induced injury to the small intestinal mucosa in celiac disease patients. The study was published online in Gastroenterology.

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Notifications

Drugs and Cosmetics Ministry of Health and Family Welfare (Department of Health and Family Welfare) Dated 30th August, 2013 Whereas certain draft rules further to amend the Drugs and Cosmetics Rules, 1945, were published, as required by sections 12 and 33 of the Drugs and Cosmetics Act, 1940 (23 of 1940), without consulting the Drugs Technical Advisory Board vide notification of the Government of India, Ministry of Health and Family Welfare (Department of Health/and Family Welfare), number G.S.R.228(E), dated the 20th March, 2012, published in the Gazette of India, Extraordinary, Part II, Section 3, Sub-section (i), dated the 20th March, 2012, inviting objections and suggestions from all persons likely to be affected thereby before the expiry of a period of forty-five days from the date on which the copies of the Official Gazette containing the said notification were made available to the public; And whereas the copies of the Gazette in which the said notification was published were made available to the public on the 20th March, 2012; And whereas, the Drugs Technical Advisory Board has been consulted in the matter, And whereas, objections and suggestions received in respect of the said draft rules have been considered by the Central Government; Now, therefore, in exercise of the powers conferred by sections 12 and 33 of the Drugs and Cosmetics Act, 1940 (23 of 1940), the Central Government, after consultation with the Drugs Technical Advisory Board, hereby makes the following rules further to amend the Drugs and Cosmetics Rules, 1945, namely:1. (1) These rules may be called the Drugs and Cosmetics (Fourth Amendment) Rules, 2013. (2) They shall come into force after 6 months of their publication in the Official Gazette. 2. In the Drugs and Cosmetics Rules, 1945 (here in after referred to as said rules),(i) in rule 65,(a) in condition (3), in clause (1),(A) in sub-clause (f) and in item (ii) of the third proviso to sub-clause (g), for the words and letter ‘Schedule H’, the words and letters “Schedule H and Schedule H1” shall respectively be substituted;

(B) after clause (g) and the provisos thereof, the following shall be inserted, namely:

“(h) the supply of a drug specified in Schedule H1 shall be recorded in a separate register at the time of the supply giving the name and address of the prescriber, the name of the patient, the name of the drug and the quantity supplied and such records shall be maintained for 3 years and be open for inspection.

(b) in condition (9), in clauses (a) and (b), for the words and letter ‘Schedule H’, the words and letters “Schedule H and Schedule H1” shall respectively be substituted;

(c) in condition (11), for the words and letter ‘Schedule H’, the words and letters “Schedule H and Schedule H1” shall be substituted;

(d) in condition (11A), for the words and letter ‘Schedule H’, the words and letters “Schedule H and Schedule H1” shall be substituted;

(ii) in rule 97, in sub rule (1), after clause (d), the following shall be inserted, namely,‘(e) if it contains a drug substance specified in Schedule H1, the drug formulation shall be labelled with the symbol Rx which shall be in red and conspicuously displayed on the left top corner of the label, and shall also be labelled with the following words in a box with a red border:

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Notifications “SCHEDULE H1 DRUG - WARNING: -It is dangerous to take this preparation except in accordance with the medical advice. -Not to be sold by retail without the prescription of a Registered Medical Practitioner.”

3. In the said rules, in Schedule H, the following entries shall be omitted, namely:1. Alprazolam 2. Cefdinir 3. Cefepime hydrochloride 4. Cefetamet pivoxil 5. Cefpirome 6. Cefpodoxime poxetil 7. Ceftazidime pentahydrate 8. Ceftizoxime sodium 9. Chlordiazepoxide 10. Clofazimine 11. Codeine 12. Diazepam 13. Diphenoxylate and its salts

14. Ethambutol hydrochloride 15. Ethionamide 16. Levofloxacin 17. Meropenem 18. Midazolam 19. Moxifloxacin 20. Nitrazepam 21. Pentazocine 22. Pyrazinamide 23. Sparfloxacin 24. Thiacetazone 25. Tramadol hydrochloride 26. Zolpidem”

4. In the said rules, after Schedule H, the following Schedule shall be inserted, namely:“Schedule H1 (See rules 65 and 97) 1. Alprazolam 2. Balofloxacin 3. Buprenorphine 4. Capreomycin 5. Cefdinir 6. Cefditoren 7. Cefepime 8. Cefetamet 9. Cefixime 10. Cefoperazone 11. Cefotaxime 12. Cefpirome 13. Cefpodoxime 14. Ceftazidime 15. Ceftibuten 16. Ceftizoxime 17. Ceftriaxone 18. Chlordiazepoxide 19. Clofazimine 20. Codeine 21. Cycloserine 22. Diazepam 23. Diphenoxylate

24. Doripenem 25. Ertapenem 26. Ethambutol hydrochloride 27. Ethionamide 28. Feropenem 29. Gemifloxacin 30. Imipenem 31. Isoniazid 32. Levofloxacin 33. Meropenem 34. Midazolam 35. Moxifloxacin 36. Nitrazepam 37. Pentazocine 38. Prulifloxacin 39. Pyrazinamide 40. Rifabutin 41. Rifampicin 42. Sodium para-aminosalicylate 43. Sparfloxacin 44. Thiacetazone 45. Tramadol 46. Zolpidem

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Notifications Note.- Preparations containing the above drug substances and their salts excluding those intended for topical or external use (except ophthalmic and ear or nose preparations) containing above substances are also covered by this Schedule.”

Sd/(Arun K. Panda) Jt. Secy. G.S.R.588(E) F.No.X-11014/6/2010-DFQC Issued by: Ministry of Health and Family Welfare (Department of Health and Family Welfare) New Delhi Foot note: The principal rules were published in the Official Gazette vide notification No.F.28-10/45-H (1), dated 21st December, 1945 and last amended vide notification number G.S.R.72(E), dated the 8th February, 2013. ■■■■

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Obstetrics and gynecology

Mature Teratoma of the Ovary Associated with Contralateral Huge Mucinous Cystadenoma: A Case Report Nalini Sharma*, WK Shullai†, AS Singh‡, WBC Sangma#

Abstract Mucinous tumors are multiloculated cysts lined by epithelium resembling that of the endocervix. Mature cystic teratomas of the ovary are among the common benign neoplasms of the ovary derived from germ cells, which are commonly seen occurring in young patients mostly in the reproductive years. We report a mature teratoma of one ovary associated with mucinous cystadenoma of the other ovary. The case is being presented due to its rarity.

Keywords: Mucinous cyst adenoma, mature cystic teratoma, contralateral ovary

M

ucinous tumor is the second most common epithelial tumor of ovary.1 Mucinous tumors are multiloculated cysts lined by epithelium resembling that of the endocervix. These tumors can grow up to a large size and are usually unilateral and only 8-10% are bilateral.1 Mature cystic teratomas of the ovary are among the common benign neoplasms of the ovary derived from germ cells, which are commonly seen occurring in young patients mostly in the reproductive years. The histology of these tumors reveals tissues originating from the ectoderm, mesoderm and endoderm. We report a mature teratoma of one ovary associated with mucinous cystadenoma of the other ovary. The case is being presented due to its rarity.

On physical examination, her abdomen was markedly distended and a huge mass was filling the whole abdomen. The mass was cystic, nontender with a smooth surface and restricted mobility. The abdominopelvic computed tomography (CT) showed a large cystic multiseptated mass measuring 16 × 26 × 34 cm. Another well-defined mass lesion measuring 4.2 × 6.6 cm of mixed attenuation. Imaging study suggested a large ovarian mass and dermoid cyst (Fig. 1). Cancer antigen (CA) 125, carcinoembryonic antigen (CEA) were normal. At laparotomy, a huge multiloculated cystic mass originating from left ovary was seen. Right ovarian cyst was about 4.5 × 6.5 cm, uterus and right tube was normal. Left ovariotomy

CASE REPORT A 22-year-old unmarried G0P0 girl presented in the outpatient clinic of the gynecology department with gradual distension of abdomen since 8 years. Her menstrual cycles were regular. *Assistant Professor †Senior Resident ‡Professor and Head Dept. of Obstetrics and Gynecology North Eastern Indira Gandhi Regional Institute of Health and Medical Sciences (NEIGRIHMS) Shillong, Meghalaya # Consultant Radiologist, Roberts Hospital, Shillong, Meghalaya Address for correspondence Dr Nalini Sharma Assistant Professor Dept. of Obstetrics and Gynecology NEIGRIHMS, Mawdiangdiang, Shillong, Meghalaya E-mail: nalinisharma100@rediffmail.com

Figure 1. CT scan showing huge ovarian mass.

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Figure 2. Magnification is 100x mucinous cystadenoma.

Figure 5. Picture showing hair and pultaceous material removed from dermoid cyst of right ovary.

Figure 4 shows mucin-filled huge multilobed cyst of left ovary. Figure 5 shows hair and pultaceous material removed from dermoid cyst of right ovary. DISCUSSION Ovarian mucinous cystadenomas have a controversial histogenesis. Different theories have been proposed suggesting origin from metaplasia of surface epithelium or a teratomatous origin. The surface metaplasia theory has been supported by ultrastructure studies3 and by mucin histochemical studies.4 Figure 3. Magnification is 100x mature cystic teratoma (mesodermal and endodermal).

Figure 4. Picture showing mucin filled huge multilobed cyst of left ovary.

and right cystectomy was done. Patient did wellpostoperatively. Microscopically, sections studied from the left ovarian cyst shows features consistent with mucinous cystadenoma with papillary excrescences (Fig. 2). Sections studied from the right ovary shows features consistent with mature teratoma (Fig. 3).

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The teratoma theory is based on the frequent observation of co-existence of mature cystic teratoma and mucinous cystadenoma, borderline, benign as well as mucinous cystadenocarcinoma.5,6,8 and on the evidence that mucinous cystadenoma can be lined by intestinal epithelium, sometimes with intestinal specific structures like goblet cells, paneth cells and endocrine cells and sometimes with complete colonic wall,5 which may be due to endodermal growth of teratomas. In the present case, huge mucinous cystadenoma of one ovary was associated with a mature cystic teratoma of the other ovary. Though, the occurrence of the above mentioned tumors in the same ovary is not unusal.6-8 Two to 11% mature teratomas contain a mucinous tumor and 3-8% of mucinous tumors contain a teratoma. Their presence in two different ovaries as a solitary entity has not been reported so commonly. References 1. Berek and Novak’s Gynaecology. 15th edition, 2012.1355. 2. Wu RT, Torng PL, Chang DY, Chen CK, Chen RJ, Lin MC, et al. Mature cystic teratoma of the ovary: a clinicopathologic study of 283 cases. Zhonghua Yi Xue Za Zhi (Taipei) 1996;58(4):269-74.


Obstetrics and gynecology 3. Fenoglio CM, Ferenczy A, Richart RM. Mucinous tumors of the ovary. Ultrastructural studies of mucinous cystadenomas with histogenetic considerations. Cancer 1975;36(5):1709-22. 4. Nomura K. Mucin histochemistry of ovarian mucinous cystadenomas expressing gastrointestinal characteristics. Pathol Int 1995;45(6):430-5. 5. Tang P, Soukkary S, Kahn E. Mature cystic teratoma of the ovary associated with complete colonic wall and mucinous cystadenoma. Ann Clin Lab Sci 2003;33(4):465-70. 6. Hwang JH, So KA, Modi G, Lee JK, Lee NW, Lee KW, et al. Borderline-like mucinous tumor arising in mature cystic

teratoma of the ovary associated with pseudomyxoma peritonei. Int J Gynecol Pathol 2009;28(4):376-80. 7. McKenna M, Kenny B, Dorman G, McCluggage WG. Combined adult granulosa cell tumor and mucinous cystadenoma of the ovary: granulosa cell tumor with heterologous mucinous elements. Int J Gynecol Pathol 2005;24(3):224-7. 8. Mandal S, Kawatra V, Khurana N. Mucinous cystadenocarcinoma arising in mature cystic teratoma ovary and associated pseudomyxoma peritonei: report of a case. Arch Gynecol Obstet 2008;278(3):265-7.

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Women who eat a lot of meat are apt to weigh more than those who do not. Previous studies have consistently shown that vegetarians are lighter and have a lower body mass index than their omnivorous counterparts.

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A study from Brigham Young evaluated 284 premenopausal women, an average of 40-year-old and did not smoke. The researchers separated the women into groups classified by low, moderate and high meat intake per 1,000 calories consumed per day.

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Over the 7-day study, the investigators found that the low-intake group ate <1.9 three-ounce servings of meat per day, as opposed to more than 3.18 servings for the high-intake group.

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More than half (52.8%) of the women classified as having a high meat intake were obese, defined in this study as having greater than 35% body fat. Conversely, 37.3% of women in the moderate meat intake group were obese and only 15.6% of those in the low meat intake group were obese.

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This was a cross-sectional study, so the findings do not show that meat causes obesity, while that could be the case, it could also be that obesity caused women to eat more meat-like more obese women following the Atkins diet, which is rich in meat.

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There are a number of physiological mechanisms by which meat could fuel weight gain. Meat proteins may elevate insulin levels, and thereby growth factors, that could influence weight and percent body fat. It has also been shown that consumption of saturated fat - most of which comes from animal products – is associated with obesity.

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It may be worth recognizing that eating less meat may be beneficial in a weight management program. It is possible to eat a healthy diet that is limited in meat. Alternative protein sources such as, lentils, nuts and legumes can provide sufficient protein and actually be beneficial in dieting.

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Obstetrics and gynecology

Paraparesis Following Spinal Anesthesia in a Patient after Cesarean Section: A Rare Entity Pallab Kumar Mistri*, Bandana Biswas†, Tapan Kumar Naskar†, Suhrita De‡, Sujata Dalai#, Sibsankar Barman$

Abstract Paraparesis, as a complication after spinal anesthesia, is very rare. It may occur due to presence of undiagnosed spinal tumor or spinal shock after lumbar puncture. We describe a 22-year-old mother who had cesarean section under spinal anesthesia and developed paraparesis in postoperative period. She had history of facial palsy and hearing impairment for last 9 years. Magnetic resonance imaging (MRI) revealed spinal space-occupying lesion (extramedullary meningioma) at D-5/D-6 level. Careful observation and examination in postoperative period after regional anesthesia is necessary for early diagnosis and management.

Keywords: Spinal anesthesia, meningioma, paraparesis, cesarean section

P

ost-spinal paraparesis is an uncommon complication after applying spinal anesthesia. It may occur due to neuronal injury at lumbar vertebrae level or spinal shock. This type of incidence may happen with history of previous neurological morbidity or presence of previously undiagnosed spinal tumor.1

Case Report Mrs. CD, a 22-year-old female P1+0 with previous history of lower-segment cesarean section (indications: Severe pre-eclampsia with scar tenderness in post-cesarean pregnancy with 39 weeks 5 days gestational age) on 10.12.2012 at Eden Hospital, Kolkata. Her blood pressure (BP) was 174/112 mmHg during admission. Labetalol and prophylactic magnesium sulfate was administered. Spinal anesthesia was given for cesarean section. A healthy girl baby weighing 2.5 kg was delivered with Apgar score 8 and 10 at 1 minute and 5 minutes, respectively after birth. The vital signs were normal throughout cesarean section. Total operative *Associate Professor †Professor ‡Assistant Professor Dept. of Obstetrics and Gynecology #RMO-cum-Clinical Tutor Dept. of Anesthesiology $Post Graduate Trainee Dept. of Obstetrics and Gynecology Medical College, Kolkata, West Bengal Address for correspondence Dr Pallab Kumar Mistri Flat No. 1B, Durga Apartment, SD More, Sonarpur Station Road Sonarpur, RK Pally, Kolkata - 150, West Bengal E-mail: bandana.biswas2010@gmail.com

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time was 50 minutes. She was kept in observation ward for observation and transferred to postoperative ward after 6 hours. During postoperative follow-up, the patient developed paraparesis in both lower limbs with loss of sensory response to pain and temperature. The degree of motor block was scale 2 (according to Bromage scale). The patient had right-sided Bell’s palsy and hearing impairment for the last 9 years and history of 3-4 episodes of generalized convulsions during the last antenatal period. She subsequently developed urinary retention after removal of Foley’s catheter. Her BP was gradually normalized with medications and investigations were done to rule out renal, liver, cardiac dysfunctions, whose levels were found within normal limits. Hb% - 12.8 g/dL, TC - 14,900/mm3, D/C - N78L10M7E5B0, platelet count - 3.2 lac/mm3, total bilirubin - 0.5 mg/dL, PPBS - 139 mg/dL, blood

Figure 1. Marginated isotense extramedullary lesion involving posterior and left side of spinal canal at D-5/D-6 level.


Obstetrics and gynecology lead to neurological deficit as a result of compression effect.2-4 But paraparesis as a complication of spinal anesthesia is very rare. It may be due to presence of space-occupying lesion (intradural extramedullary tumor) or spinal shock. In our case, though some neurological morbidity was present previously, no clinical signs or symptoms were found suggestive of compressive spinal cord tumor before the incident. The diagnosis of meningioma was revealed after developing post-operative paraparesis.

Figure 2. Lateral view of dorso-lumbar spine showing the space-occupying lesion.

urea - 33 mg/dL, creatinine - 0.7 mg/dL). She was referred to Anesthesiologists and Dept. of Neuromedicine for opinion and they advised MRI of dorsal and lumbosacral spine for diagnosis. MRI features were suggestive of marginated isotense extramedullary lesion involving posterior and left side of spinal canal at D-5/D-6 level favoring for meningioma that almost blocked the spinal cord canal with dorsal cord thinned out and shifted towards right side with cord edema. A small marginated lesion was also seen intraspinally at L-3 level likely to be small meningioma or neurogenic tumor. Then, the patient was transferred to a neurosurgeon for specific management. Laminectomy with resection of the tumor was done in the Dept. of Neurosurgery. She attended Gynecology OPD after 3 months without any paraparesis. Discussion Spinal or epidural anesthesia is commonly given during cesarean section or related procedures. It may be associated with variety of complications. Immediate complications may be in the form of high neuronal block causing hypotension, bradycardia, respiratory insufficiency, apnea, unconsciousness or even cardiac arrest. The delayed complications may be post-dural puncture headache or neuronal injury. Neurological injury may occur due to direct accidental injury to the spinal cord or damage to the conus medullaris leading to paraplegia, isolated sacral dysfunctions, etc. Transient neurological symptoms may occur in the form of back pain without sensory or motor deficit. In some patients, intraspinal or epidural hematoma or abscess may

Probably, the space-occupying lesion created a pressure gradient above and below the level of nearly obliterated spinal cord canal. When the lumbar puncture was done in the lower compartment, the cerebrospinal fluid continued to leakout through the puncture site causing spinal-coning. MRI, a better diagnostic procedure in the present case, revealed the space-occupying lesion and the patient was referred to a neurosurgeon for definitive management (laminectomy for the resection of the tumor mass). For spinal anesthesia, 0.5% hyperbaric bupivacaine is commonly used. It’s duration of action is 90-120 minutes. During postoperative follow-up of our patient, there was motor and sensory deficit even after 6 hours. The case report suggested that close post- operative monitoring with special emphasis on motor or sensory dysfunctions (neurological assessment) is needed and immediate investigations are needed to rule out spinal pathology. During preoperative anesthetic check-up, any pre-existing neurological disorders should be enquired.5 References 1. Dureja J, Singh I, Kad N, Bhai V, Lal J. Paraparesis following spinal anesthesia in a patient with an undiagnosed metastatic spinal tumor. The Indian Anaesthesists Forum, 2013. 2. Gerancher JC, Waterer R, Middleton J. Transient paraparesis after postdural puncture spinal hematoma in a patient receiving ketorolac. Anesthesiology 1997;86(2):490-4. 3. Kane RE. Neurologic deficits following epidural or spinal anesthesia. Anesth Analg 1981;60(3):150-61. 4. Morgan GE, Mikhail MS, Murray MJ. Clinical Anaesthesiology. 4th edition, Tata McGraw-Hill Education Private Limited 2009:p.316-21. 5. Cherng YG, Chen IY, Liu FL, Wang MH. Paraplegia following spinal anesthesia in a patient with an undiagnosed metastatic spinal tumor. Acta Anaesthesiol Taiwan 2008;46(2):86-90.

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Obstetrics and gynecology

Unilateral Atresia of Cervix Uteri and Uterus Didelphys in a Girl with Operated Congenital Pouch Colon Sangeeta Gupta*, Taru Gupta†, Akshay Sharma‡, Pushpa Bhatia¶, Nupur Gupta§

Abstract This case report describes a girl with uterus didelphys with unilateral hematometra and hematosalpinx with congenital pouch colon (CPC) condition, where all or part of the colon is replaced by a pouch-like dilatation (5-15 cm in diameter), which communicates distally with the urogenital tract through a large fistula and associated with anorectal agenesis (supralevator anorectal malformation). CPC is seen in Asia and more specifically in northern India, Pakistan and Nepal. The management summary of this condition is creation of diverting colostomy at birth with or without the excision of pouch followed by pull through (abdominoposterior saggital anorectoplasty) later on. The girl underwent similar procedure at birth and subsequent definitive surgery (pull through), to create a neoanus at 15 months of age. Subsequently since menarche, the child had severe cyclical abdominal pain, which on investigation was found due to hematometra and hematosalpinx in right-sided uterus. Laparotomy with removal of right-sided uterus and right fallopian tube was performed. Right-sided uterus had atresia of cervix uteri. This report emphasizes the need for comprehensive evaluation and a long-term management strategy for associated gynecologic anomalies in girls with CPC, especially with regard to patency of the outflow tract.

Keywords: Anorectal malformation, congenital pouch colon, cervical atresia, hematometra, uterus didelphys

U

terus didelphys with unilateral cervical atresia is an unusual mullerian duct anomaly with defect of vertical-lateral fusion. A well-known clinical association of congenital pouch colon (CPC) with genital anomalies exists.1 At puberty, they present with incapacitating dysmenorrhea shortly after menarche. Similar findings in a girl with CPC have not been reported earlier in the literature. Case Report A 10.5-year-old girl attended gynecology OPD with complaint of severe colicky abdominal pain since attainment of menarche. Pain was cyclical in nature occurring at monthly intervals. Periods were regular. There was history of multiple surgeries for associated *Senior Consultant †Associate Professor ‡Specialist ¶Professor §Assistant Professor Dept. of Gynecology and Pediatric Surgery ESI-PGIMSR, New Delhi Address for correspondence Dr Taru Gupta Associate Professor Dept. of Gynecology and Pediatric Surgery ESI-PGIMSR, Basaidarapur, New Delhi E-mail: tarugupta1971@yahoo.com

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CPC. On examination, there were three scars on abdomen. Available old records of child revealed that she was a diagnosed case of CPC, for which an emergency laparotomy with ileostomy was done at age of 15 days, followed by pull through to create a neoanus operation at age of 18 months and intraoperative findings suggested a type III CPC. Closure of colostomy was done at 2 years of age. Menarche was attained at the age of 10 years and she started having cyclical pain lower abdomen, unrelieved with medications. She was subsequently imaged in the private sector. Ultrasound (whole abdominal and pelvis) showed both kidneys, uterus as normal and cystic mass in midline and towards right, 7.7 × 4.3 cm with internal echoes with a volume of 75 cc. Left ovary was normal. Contrast-enhanced computed tomography (CECT) abdomen showed a normal uterus with tubo-ovarian mass in right adnexa probably of infective etiology. CT urography and micturating cystourethrogram showed normal urethra and urinary bladder. Local examination showed normal perineum with patulous vagina and normally placed neoanus with visible rim of anal mucosa. Magnetic institute

resonance showed

imaging (MRI) at our uterus didelphys with


Obstetrics and gynecology obstructing hemivaginal septum with right hematometra and hematosalpinx (Fig. 1). Left uterine cervix was identified while cervix could not be identified in right uterus. Right ovary was not visualized separately. Clinical diagnosis of mullerian duct anomaly, Class IV American Fertility Society (AFS) classification of uterovaginal anomalies, unusual configuration of vertical-lateral fusion was made. Lateral fusion defect of mullerian ducts may be the cause of uterus didelphys and vertical fusion disorder might have resulted in right cervical agenesis. Examination under anesthesia showed a normal urethral orifice, patulous vagina and normally placed patulous neoanus. Per speculum examination showed normal vagina except a partial vaginal septum in the upper third of vagina. Normal well-developed cervix was present on left side. Menstrual blood was coming through the os. Per vaginum examination showed small-sized uterus in continuation with cervix on left side. On right side, no cervix could be felt, a firm mass of 5 × 4 cm was felt. Uterine sound was put through left cervical os into uterine cavity. Left uterocervical length was 6 cm. Laparotomy was done, which revealed uterus didelphys with right uterus distended with blood and a large right hematosalpinx. Right-sided ovary could not be visualized. Left-sided uterus, fallopian tube and ovary were normal. Removal of right-sided uterus and right hematosalpinx was done. There was complete cervical atresia on right side. The postoperative period was uneventful. The histopathological examination confirmed rightsided hematosalpinx and right-sided uterus with no cervix. Discussion Mullerian ducts represent the primordial components of the female reproductive system. They differentiate into fallopian tubes, uterus, cervix and superior aspect of vagina. Overall published data suggest prevalence of uterovaginal anomalies of 1-6%.2 Complete failure of medial fusion of two mullerian ducts can result in complete duplication, partial failure of fusion can result in a single vagina with a single or duplicate cervix and complete or partial duplication of the uterine corpus. If uterine anomaly is associated with obstruction of menstrual flow, then it causes symptoms that will come to the attention of the gynecologist shortly after menarche.3 Early diagnosis offers significant advantages in patient care.

Right uterus with hematometra

Left uterus

Pull through colon

Figure 1. Showing MRI pelvis showing uterus didelphys with obstructing hemivaginal septum with right hematometra and hematosalpinx.

Right uterine cavity with collected blood

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Right hematosalpinx

Figure 2. Showing cut section of removed right uterus with hematometra and hematosalpinx.

Incapacitating dysmenorrhea shortly after menarche with regular menstrual periods in young girls can be due to unicornuate uterus with a noncommunicating rudimentary anlagen containing functional endometrium, unilateral obstruction of a cavity of a double uterus (complete septum), a clinical syndrome consisting of a double uterus, obstruction of vagina and ipsilateral renal agenesis or unusual configuration of vertical-lateral fusion defects Class IV AFS, as in our case where there was uterus didelphys with unilateral cervical atresia. It is important to make diagnosis as soon as possible, because if lumen of tube communicates with functional endometrial cavity and is patent at fimbrial end, then retrograde menstruation and pelvic endometriosis can develop, destroying reproductive potential. Removal of

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Obstetrics and gynecology associated fallopian tube is strongly recommended to minimize risk of an ectopic pregnancy.3 There are very few reports of uterus didelphys, a finding that appears to be invariable in girls with types I-III CPC.4 Chadha et al described a girl with CPC, uterus didelphys with bilateral cervical atresia. At puberty, child had primary amenorrhea with severe cyclic abdominal pain due to hematometra, hematosalpinx and endometriosis. Laparotomy with removal of both uteri was done. Both uteri had atresia of cervix uteri.5 In a recent review on the subject of gynecologic concerns in girls with anorectal malformation (ARM), Breech6 emphasized the role of vaginoscopy before puberty, preferably at the time of definitive repair of the ARM. Vaginoscopy allows evaluation of the vaginal anatomy and can also document the appearance, development and position of the cervices in vagina and the presence or absence of mucus at the ectocervix (to infer patency). Any underdevelopment of the Müllerian structures can be detected by serial US starting soon after the onset of breast development.6 If neglected, onset of menarche in the presence of obstruction to the outflow tract may result in hematometra and/or hematocolpos, hematosalpinx, adnexal cysts, endometriosis and chronic abdominal pain. Conclusion In conclusion, our report emphasizes the need for a comprehensive evaluation and long-term management strategy for associated gynecologic anomalies in girls with CPC, especially with regard to the patency of the outflow tract. Uterus didelphys with a septate vagina appears to be invariable in girls with types I-III CPC4 and needs to be assessed and managed appropriately with

awareness of the possibility of obstetric complications in later life.7,8 Therefore, it is strongly recommended that the parents of such patients are duly counseled and the entire case record with operative findings are to be preserved. It is also advocated that treating pediatric surgeon should team up with gynecologist for ideal long-term management. References 1. Gupta DK, Sharma S. Congenital pouch colon. In: Anorectal Malformations in Children. Holschneider AM, Hutson J (Eds.), Springer: Heidelberg 2006:p.211-21. 2. Rock JA, Zacur HA, Dlugi AM, Jones HW Jr, TeLinde RW. Pregnancy success following surgical correction of imperforate hymen and complete transverse vaginal septum. Obstet Gynecol 1982;59(4):448-51. 3. Rock JA, Breech LL. Surgery for anomalies of the Mullerian ducts. In: Telinde’s Operative Gynecology. Rock JA, Jones HW. Lippincott Williams & Wilkins 2008:p.539-84. 4. Chadha R, Choudhury SR, Pant N, Jain V, Puri A, Acharya H, et al. The anomalous clinical anatomy of congenital pouch colon in girls. J Pediatr Surg 2011;46(8):1593-602. 5. Chadha R, Puri M, Saxena R, Agarwala S, Puri A, Choudhury SR. Congenital pouch colon in a girl associated with bilateral atresia of cervix uteri and uterus didelphys. J Indian Assoc Pediatr Surg 2013;18(2):81-3. 6. Breech L. Gynecologic concerns in patients with anorectal malformations. Semin Pediatr Surg 2010;19(2):139-45. 7. Levitt MA, Bischoff A, Breech L, Peña A. Rectovestibular fistula-rarely recognized associated gynecologic anomalies. J Pediatr Surg 2009;44(6):1261-7; discussion 1267. 8. Grimbizis GF, Camus M, Tarlatzis BC, Bontis JN, Devroey P. Clinical implications of uterine malformations and hysteroscopic treatment results. Hum Reprod Update 2001;7(2):161-74.

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Corrigendum In the May 2014 issue of IJCP, name of the principal author of the article “A Randomized, Double-blind, PlaceboControlled Study of a Synbiotic (Bifilac) in Children with Acute Diarrhea in South India” was wrongly published as B Vishu Bhat. It should read as B Vishnu Bhat. The error is regretted.

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Obstetrics and gynecology

Acquired Vaginal Atresia: A Case Report REENA YADAV*, RANI REDDI*

Abstract Acquired vaginal atresia is rare and a preventable condition that can be devastating, particularly in the reproductive age group. With improvement of health education, avoiding difficult vaginal deliveries and proper repair of any vaginal lacerations, acquired vaginal atresia can be avoided altogether. We present here an interesting case of acquired vaginal atresia following a difficult delivery.

Keywords: Acquired vaginal atresia, laparotomy, vaginoplasty

V

aginal atresia can be congenital or acquired. Acquired vaginal atresia is rare and a preventable condition that can be devastating, particularly in the reproductive age group. It is relatively more common in the developing countries. Adhesions develop after the delvery of the baby, if tears in the vagina are left unnoticed or improper stiching is carried out. We present here an interesting case of acquired vaginal atresia following a difficult delivery.

case report Mrs. XY, now 36 years old, has been married for 13 years. She had her first full-term delivery at home conducted by dai in 1991. She gave history that it was a difficult delivery; she delivered a fresh stillborn male child. There was no previous history of any coital difficulty or menstrual irregularity prior to first delivery. Three months after first delivery, she consulted a local doctor for amenorrhea and difficulty in having coitus. She was diagnosed with vaginal atresia. In 1992, vaginoplasty was performed in a private hospital. She was free of symptoms for 7 months. Again she complained of difficulty in coitus. She was told that restenosis had occurred and she was 4 months pregnant at that time. At 5 months of gestation, she had pain and bleeding, diagnosed as inevitable abortion on ultrasonography. Since the vagina was stenosed, hysterotomy was done at a private *Professor Dept. of Obstetrics and Gynecology Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER) Pondicherry Address for correspondence Dr Reena Yadav Professor Dept. of Obstetrics and Gynecology, JIPMER, Pondicherry - 605 006 E-mail: reenay27@hotmail.com

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hospital in January 1993. She conceived again in 2002. This time, she presented at 5 months of gestation with pain abdomen and bleeding to our hospital, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER) and she was admitted here. As per clinical examination, rupture uterus was suspected. She was subjected to laparotomy. Intraoperatively, there was posterior colporrhexis; fetus and placenta were lying in the pouch of Douglas. Hemoperitoneum was present. Vagina was dilated from above and a Foley’s catheter put from below. Rent was repaired. Foley’s catheter was kept for 10 days. She was advised vaginoplasty after 6 months. She was admitted with us in April 2003 for vaginoplasty. McIndoe vaginoplasty was done on 28th April 2003. Intraoperative findings were - lower half of vagina stenosed, upper part normal. Atresia released. Bladder base injured at the time of surgery. Laparotomy was done; there was 2 cm rent close to left ureteric orifice. During repair of bladder injury, left ureteric orifice was injured. Left ureter implantation was done. Omentum was placed between bladder and uterus. She stayed in the hospital for 6 weeks after surgery. At the time of discharge, she was voiding normally, and was advised to use mould for 6 weeks. She became symptom-free after the surgery; she had regular periods and no difficulty during coitus. In March 2005, she presented to us as G4P1A2L0, with 32 weeks pregnancy. Ultrasound showed a single live fetus in cephalic position, with adequate liquor, with no anomalies. She was admitted. Her routine investigations were within normal limits. At 37 weeks, on 6th May 2005, elective lower-segment cesarean section (LSCS) was done, an alive term male, 2.85 kg delivered. Her postoperative period was uneventful. Stitches were removed on 8th postoperative day. She was discharged on 14th May 2005.


Obstetrics and gynecology Discussion Congenital vaginal atresia cases are seen more frequently as compared to acquired vaginal atresia. Acquired vaginal atresia is rare and a preventable condition. Acquired vaginal atresia or loss can be devastating, particularly in the reproductive age. Most of the studies in literature are reported from Nigeria. Unuigbe et al1 reported an incidence of 85/1,000 of acquired vaginal atresia. In their study, caustic vaginitis secondary to local herbal pessary insertion and following circumcision were the most common causes of atresia. The resulting atresias were effectively treated successfully by simple adhesiolysis. Ozumba2 studied 78 cases of acquired vaginal atresia. In their study, ritual circumcision was the leading cause followed by birth injuries and postoperative injuries. Symptoms in their study were dysuria or retention of urine, coital difficulties, dyspareunia and apareunia. They used modified Fenton’s operation in majority of cases with good result. Occasionally, McIndoe operation was used when lesion was more extensive. Recurrence rate was low, 11 women in their study got pregnant during

period of follow-up. Arowojolu et al3 reported an incidence of 7/1,000; peak incidence in the age group of 20-30 years. Chemical vaginitis from insertion of caustic vaginal pessary for various reasons was the most common cause. Dyspareunia or apareunia were most common symptoms. Various surgical procedures in their study included McIndoe vaginoplasty or simple dilation of vagina. Acquired vaginal atresia is a preventable condition. With improvement of health education, avoiding difficult vaginal deliveries and proper repair of any vaginal lacerations, acquired vaginal atresia can be avoided altogether. References 1. Unuigbe JA, Ojobo S. Oronsaye AU. The challenges of vaginal atresia and stenosis: Nigerian experience. Int J Gynaecol Obstet 1984;22(1):1-4. 2. Ozumba BC. Acquired gynetresia in eastern Nigeria. Int J Gynecol Obstet 1992;37(2):105-9. 3. Arowojolu O, Okunlola MA, Adenkunle AO, Ilesanssi AO. Three decades of acquired gynaetresia in Ibadan: clinical presentation and management. J Obstet Gynaecol 2001;21(4):375-8.

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A study published in the journal Psychoneuroendocrinology has revealed that intuitive thought commonly ascribed to women under the title of “female intuition” could have a biological influence, rooted in lower prenatal exposure to testosterone in the womb.

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According to a new study, women diagnosed with gestational diabetes before 24 weeks gestation are 10.4 times more likely to deliver a preterm baby compared with women diagnosed after 24 weeks. The findings were presented recently at the annual meeting of the American College of Obstetricians and Gynecologists (ACOG).

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171



Obstetrics and gynecology

Septic Abortion: An Unusual Case of Intrauterine Foreign Body Priyanka Mandve

Abstract Septic abortion is a grave problem contributing to maternal morbidity and mortality in developing countries. This is the case of a 17-year-old unmarried girl who presented with complaints of pain in abdomen and fever on and off, since 4 months. She had history of illegal abortion by a quack 4 months back. Ultrasound showed intrauterine foreign body perforating fundus of uterus. Laparotomy was performed which showed pyoperitoneum and omental cake formation. Wooden stick was removed vaginally. Strict enforcement of Medical Termination Pregnancy (MTP) Act and public participation for awareness and implementation of safe abortion could be important steps for avoiding septic abortions.

Keywords: Septic abortion, intrauterine foreign body, MTP Act

S

eptic abortion is defined as any abortion associated with clinical evidences of infection of uterus and its contents. Each year, 19-20 million women risk their lives to undergo unsafe abortions. In India, inspite of legalization of abortion, the problem of unsafe abortions is very acute. There were 6,20,472 reported abortions in 2012; according to experts true number could be as high as 7 million, with two-thirds of them taking place outside authorized health facilities. According to data on maternal mortality ratio (MMR) and Sample Registration System (SRS) data by Ipas, unsafe abortions are killing a woman every 2 hours in India. As per Lancet paper (2007), there were 6.4 million abortions, of which 3.6 million or 56% were unsafe. Ipas has calculated this based on the latest population and crude birth rates (CBR), which peg the number of induced abortion at 5,007,932.1 According to Census 2011, abortion taking place in institution varies from 32.0% in Chhattisgarh to 73.9% in Assam. Unsafe abortions continue to outnumber safe and legal abortions. The central government constituted an expert committee in the year 2010 to make recommendations. The committee recommends for mid-level providers and medical practitioners with a Bachelor’s Degree in Unani, Ayurveda or Homeopathy.

Assistant Professor Dept. of Obstetrics and Gynecology SVNGMC,Yavatmal, Maharashtra Address for correspondence Dr Priyanka Mandve C/o : Mr. Shivkumar Mandve Bilanpura, Achalpur, Amaravati, Maharashtra - 444 806 E-mail: priyankamandve@yahoo.com

Case report A 17-year-old illiterate, unmarried girl, resident of Adilabad (Andhra pradesh), came on 11/3/2014 with complaints of pain in abdomen since 4 months, amenorrhea since 7 months, on and off fever since 4 months. There were no bladder and bowel complaints. On examination, pulse was 132/min, blood pressure 100/70 mmHg, she was afebrile, pale, abdomen was tense, 18-20 weeks uterine size mass felt, tenderness was present in right iliac fossa. Urine pregnancy test was negative. After thorough examination, on further inquiry her parents revealed history of illegal abortion of 3 months pregnancy 4 months back by a quack. It was also revealed that she was shown to a physician at Adilabad (Andhra pradesh) from where she was referred to us. On per speculum examination, there was pus coming out through cervical os. Tip of foreign body was seen in the cervical canal. Urgent ultrasound was done, which showed a 11 cm foreign body in the uterine canal perforating the fundus (Fig. 1). Initially 4 cm part of foreign body was inside the abdominal cavity (Fig. 2). Also localized collection of around 100 cc was found in the right iliac fossa with enlarged adjacent lymph nodes and there was no obvious injury to bowel and bladder. X-ray abdomen erect was normal, there was no gas fluid level. Blood investigations showed hemoglobin 6.2 g/dL, total leukocyte count 14,400/µL, platelets 3,44,000/µL, erythrocyte sedimentation rate (ESR) at the end of first hour was 60 mm, serum creatinine 0.9 mg/dL.

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Obstetrics and gynecology

Figure 1. Ultrasound picture showing intrauterine foreign body perforating fundus of uterus.

Figure 3. Intraoperative picture showing plastered abdomen.

Figure 2. Intraoperative picture showing pus coming out after opening abdomen.

Two units of blood transfusion was given and exploratory laparotomy was done. Pyoperitoneum of about 100-150 cc was drained. There was plastered abdomen with omental cake formation (Fig. 3). Omentum was adherent to all pelvic organs. Uterus was covered with omentum and could not be reached easily. Hence, uterine rent could not be traced. Around 14 cm long wooden stick was removed through cervical os with difficulty (Fig. 4). Thorough peritoneal wash with antibiotic solution was given. Abdomen was closed in layers. Pus culture showed growth of Escherichia coli. Patient received broad-spectrum antibiotics and recovered well. Postoperative ultrasound showed normal uterine cavity. Anemia was corrected till hemoglobin of 8.2 g/dL and hematinics were continued.

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Figure 4. Wooden stick - foreign body, removed vaginally.

There was decreasing trend of leukocyte count till 8,000/ÂľL. She was discharged on day 10 of surgery. Discussion A septic abortion is a form of abortion that is associated with a serious uterine infection. It may cause septicemia, septic shock in turn leading to renal failure,2,3 bleeding diatheses and disseminated intravascular coagulation (DIC). Intestinal organs may also become infected, potentially causing scar tissue with chronic pain, intestinal blockage and infertility. If not treated quickly and effectively the woman may die. So, early


Obstetrics and gynecology referral of septic cases is important. Once the patient progresses to septicemia, complication rate becomes very high. Complications like fever, wound infection and wound dehiscence, pelvic thrombophlebitis are seen in postoperative period.4-6 eighty-two percent of unintended pregnancies in developing countries occur among women who have an unmet need for modern contraception,7 which further concludes in abortion. Despite legalization of MTP, 4 decades ago only 10% of all abortions are registered or legal in India.8 Gendericide is another different social stigma to Indian population. Septic abortion is associated with high rate of maternal mortality and morbidity especially in developing countries. Lack of knowledge and lack of health seeking practices; especially in poor, illiterate, adolescent and rural population, is the most important factor for illegal abortions not only in unmarried but also in married women. Social taboos and fear of social humiliation prevent; especially unmarried pregnant women from seeking expert advice. Conclusion Social campaign to heighten the awareness of legal abortions, easy availability of expert facilities of newer contraception as well as modes of safe abortion, active

involvement of people from different socioeconomic strata, availability of transport and referral services could help to reduce the burden of maternal morbidity and mortality caused by septic abortion. References 1. Unsafe abortions killing a woman every two hours. The Hindu, May 6, 2013. Available at: http://www.thehindu. com/news/national/unsafe-abortions-killing-a-womanevery-two-hours/article4686897.ece 2. Hawkins DF, Sevitt LH, Fairbrother PF, Tothill AU. Management of septic chemical abortion with renal failure. Use of a conservative regimen. N Engl J Med 1975;292(14):722-5. 3. Reid DE. Assessment and management of the seriously ill patient following abortion. JAMA 1967;199(11):805-12. 4. Konar H. Changing trends in septic abortion. J Obstet Gynaecol India 1992;42:288-92. 5. Rana A, Pradhan N, Gurung G, Singh M. Induced septic abortion: a major factor in maternal mortality and morbidity. J Obstet Gynaecol Res 2004;30(1):3-8. 6. Sharma JB, Manaktala U, Kumar A, et al. Complications and management of septic abortion - A five year study. J Obstet Gynaecol India 2001;51(6):77-9. 7. www.guttmacher.org. 8. Das V, Agarwal A, Mishra A, Deshpande P. Septic abortion. J Obstet Gynecol India 2006;56(3):236-9.

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A re-examination of data from the National Institute of Child Health and Human Development microarray trial published in 2012 has revealed that anomalies detected with ultrasound in fetuses with normal karyotypes could be associated with unusual copy number variants (CNVs). The findings have been published online in Obstetrics and Gynecology.

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A new study conducted in Finland has found that women with a history of eating disorders are at a heightened risk of an array of pregnancy-related complications. The study was published April 7 online in the American Journal of Obstetrics and Gynecology.

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Researchers noted that women with anorexia nervosa had increased odds of developing anemia, and were more likely to have low birth weight babies and very premature births. Additionally, women with bulimia nervosa were more likely to have babies who required resuscitation or had a low Apgar score.

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Pediatrics

Effect of Protein and Energy Supplementation on Growth of Infants ≤1,500 g at Birth: A Randomized Trial Janardhan Shenoy*, Nivethitha†, Suchetha Rao*

Abstract Objective: To study the effect of energy supplements with protein-energy supplementations on the growth patterns of low birth weight (LBW) infants weighing ≤1,500 g. Material and methods: Babies with birth weight of ≤1,500 g and on full enteral feeds on Day 14 of life with expressed breast milk (n = 60) were randomly allocated to energy alone group (n = 30) and protein energy group (n = 30). Babies in energy intervention received medium-chain triglyceride and protein-energy intervention received human milk fortifier supplement added to expressed breast milk. Daily weight, weekly length and head circumference were checked to monitor the growth. Study was continued till the infants reached a weight of 1,600 g or 4 weeks from the start of the study, whichever was earlier. Results: In the energy group mean weight gain was 14.98 ±. 09968 g/kg/day, whereas in the protein-energy group weight gain was 19.79 ±. 08745 g/kg/day (p < 0.001). Increase in length or head circumference did not show any statistical significance. Conclusion: This study was consistent with the importance of providing additional protein intake to achieve increased postnatal growth in LBW babies.

Keywords: Low birth weight, feeding, protein-energy supplements

N

utritional management of the very low birth weight (VLBW) infants is quite a challenge for present neonatal intensive care unit (NICU) teams.1 Most VLBW infants have discharge weight below the 10th percentile of reference intrauterine weights leading to postnatal growth restriction.2,3 Poor neonatal weight gain and head growth have been linked to significant neurodevelopmental outcomes. Interventions to improve antenatal and postnatal growth may contribute to better school-age outcomes.4 To achieve the necessary catch-up growth, nutritional supplements have been added to standard pre term formula or fortified human milk.1 Preterm infants inevitably accumulate a significant nutrient deficit in the first few weeks of life, if fed only with recommended daily allowance of nutrients. This deficit can be directly related to subsequent postnatal growth *Associate Professor Dept. of Pediatrics Kasturba Medical College, Mangalore, Manipal University Karnataka †Consultant Pediatrician Kiruthika Hospital, Tirupur, Tamil Nadu Address for correspondence Dr Suchetha Rao Dept. of Pediatrics Kasturba Medical College, Attavar, Mangalore - 575 001 Manipal University, Karnataka E-mail: suchethasr@gmail.com

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retardation.3 We conducted a randomized control trial to study the effect of energy supplements with proteinenergy supplementations on the growth patterns of low birth weight (LBW) infants weighing ≤1,500 g. Material and methods It was a prospective, randomized controlled trial done in a tertiary care hospital in Dakshina Kannada district of Karnataka. The study was conducted from March 2011 to July 2012. After getting parental consent, babies with birth weight of ≤1,500 g and on full enteral feeds on Day 14 of life were included in the study. Babies with major congenital malformation, suspected or confirmed necrotizing enterocolitis, requiring major surgery, genetic defects, congenital infection, suspected inborn errors of metabolism and on formula feeding were excluded from the study. Study was conducted after Institutional Ethical Committee clearance. A total of 70 infants were included in the study. Infants were randomly assigned into two groups using randomization table, either protein and energy group or energy alone group. Each group comprised of 35 infants. They were categorized into appropriate-for-gestational age (AGA) or small-for-gestational age (SGA) in each group. Study was continued till the infants reached a weight of 1,600 g or 4 weeks from the start of the study, whichever was earlier. Babies developing any feed intolerance or any


Pediatrics

Enrollment

Assessed for eligibility and enrolled (n = 70)

Randomization Allocation

Protein and energy group (n = 35) All received allocated intervention

Follow-up

Energy group (n = 35) All received allocated intervention

Discontinued (n = 5)

Analyzed

Discontinued (n = 5)

n = 30

other complication were excluded from the study. Five babies from each group were excluded during the course of the study due to feed intolerance and insufficient lactation in the mother. Thirty babies in each group were finally analyzed. Babies were feed through nasogastric tube every 2 hours. Trained nurse fed the babies. Those babies randomized to the energy-alone intervention received medium-chain triglyceride (MCT). Each milliliter of MCT oil was added to 50 mL of expressed breast milk (EBM). Those babies randomized to protein-energy intervention received human milk fortifier (HMF). One sachet of 2 g of HMF was added to 50 mL of expressed milk. All babies receiving proteinenergy and energy alone supplement had received only mother’s milk. Protein and calorie content per 100 mL of breast milk given to each group is shown in Table 1. Babies were managed in the same postnatal ward with same ambient temperature. Babies of both groups were provided with cap, gloves, socks and they were rapped with cotton sheet and covered with blankets to prevent the heat loss.

n = 30

Growth rate was measured during the study period by: ÂÂ

Daily weights by electronic weighing machine (Jee-lit with an error of 10 g). The weight was recorded at the same time of the day in all babies.

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Weekly length by infantometer

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Weekly head circumference by nonstretchable inch/centimeter tape.

Mean weight gain in grams per kg per day was calculated by subtracting first day weight from last day weight and dividing it by total number of days and birth weight. Results Thirty-five babies were included to energy alone group and 35 babies to energy and protein group in the beginning of the study. Five babies from each group were excluded during the course of the study due to feed intolerance and insufficient lactation in the mother. Thirty babies in each group were finally analyzed. Birth Table 2. Baseline Characteristics of Each Group Variables

Table 1. Comparison of Caloric and Protein Content of Breast Milk with and without Nutritional Supplements Calories (kcal) per 100 mL

Protein (g) per 100 mL

68

1.1

Human milk + MCT

83.4

1.1

Human milk + HMF

82.94

1.5

Human milk

Energy alone group (MCT) (n = 30)

Protein and energy group (HMF) (n = 30)

P value

Mean birth weight (grams)

1.26

1.19

0.678

Mean gestational age (weeks)

32.94

32.5

0.996

SGA

18 (60%)

17 (57%)

0.943

Gender (males)

16 (53%)

18 (60%)

0.865

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Pediatrics Table 3. Outcome of Nutritional Intervention Parameters

Energy alone group (MCT) (n = 30) mean ± SD

Protein and energy group (HMF) (n = 30) mean ± SD

P value

Weight gain (g/kg/day)

14.98 ± .09968

19.79 ± 0.08745

< 0.001

Length gain (cm/week)

0.375 ± 0.09167 0.402 ± 0.08461

0.632

Head circumference (cm/week)

0.395 ± 0.09534 0.414 ± 0.08567

0.783

Number of days to regain birth weight Duration of study

8 ± 2.598

4.2 ± 2.856

0.15

25.6 ± 3.67157

21 ± 2.74159

0.19

weight, gestational age, gender and other baseline characteristics did not differ significantly between two groups (Table 2). There was no significant difference in weight gain between male and female babies in this study. The weight gain in the infants receiving protein energy supplementation was significantly better than those receiving energy alone group (Table 3). In the energy group mean weight gain was 14.98 ± .09968 g/kg/day, whereas in the protein-energy group weight gain was 19.79 ± 0.08745 g/kg/day (p < 0.001). The infants randomized to protein energy group regained the birth weight and target weight faster than energy alone group but this was not statistically significant. Energy alone group attained birth weight and target weight in 8 ± 2.598 days and in 25.6 ± 3.6715 days, respectively. Protein-energy group attained birth weight and target weight in 4.4 ± 2.856 days and 21 ± 2.74159 days, respectively. SGA babies gained target weight faster than AGA but without statistical significance. There is no significant difference in weight loss in two groups before including into the study. Head circumference increased by 0.395 cm/week in energy alone group and 0.414 cm/week in proteinenergy alone group. Length increased by 0.375 cm/week in energy alone group and 0.402 cm in protein-energy alone group. Increase in length or head circumference did not show any statistical significance. Discussion In LBW infant’s adaptation to extrauterine life is an energy consumptive process.5

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Postnatal growth retardation is a major issue in preterm infants.6 Optimizing growth in the preterm infant continues to be a difficult task and is complicated by a lack of knowledge of the optimal growth pattern. Adequate postnatal growth is necessary for optimal neurological outcome. Prevention of postnatal growth failure requires a comprehensive nutritional regimen that provides adequate nutritional support as soon after birth as possible and is maintained throughout an infant’s hospital course.7 The general trend in many of the NICU in the developing countries to increase the postnatal growth of LBW babies is by addition of MCT oil. HMF is not widely used. Addition of HMF will provide energy as well as protein to the growing babies, but MCTs will provide energy alone. Hence, this study was done to compare the effectiveness of protein-energy supplement over energy supplement. Brumberg et al1 compared the growth in the babies, those received energy alone with those who received protein and energy supplements. The babies in the energy alone gained 11.5 ± 4.8 g/kg/day and proteinenergy group, babies gained 17 ± 2.4 g/kg/day.1 In the present study babies those received energy alone gained 14.98 ± 0.09968 g/kg/day and protein-energy gained 19.79 ± 0.08745 g/kg/day. Gathwala et al8 studied the effect of HMF supplements in SGA babies. The babies who received fortified milk gained a mean weight of 38.77 ± 7.43 g/day, which was significantly better than expressed milk alone group, those babies gained 28.71 ± 3.18 g/day. The present study included both SGA and AGA babies. Mukhopadhyay et al9 study showed that when preterm babies were fed-fortified human milk they had better growth and they compared them with mineral supplements. They followed the babies till they reach 2 kg, whereas in our study we followed them till 1.6 kg. On subgroup analysis, they found that SGA preterm babies fed with fortified milk had significantly better growth than fed-unfortified milk as compared to AGA babies. Our study also shows that SGA babies gained faster than the AGA babies but statistically it was not significant. The mean birth weight of the LBW babies in their study was 1.2 kg, which was similar to our study. Study by Miller et al10 showed that increasing the protein content of HMF improved the growth of LBW babies of <31 weeks gestation. Lucas et al11 showed that developmental scores at 18 months was slightly but not significantly better in the preterm who received protein supplements. Present study has limitation that follow-up was not done.


Pediatrics weight children: neonatal correlates and school-age consequences. Early Hum Dev 2006;82(5):325-34.

Conclusion Present study highlights the continued need of enteral protein in growth of VLBW infants. To improve growth in these infants, supplementation of EBM with protein must be considered. This study has shown the growth benefits of increasing caloric intake with a multinutrient supplement that provides both protein and energy compared with a supplement that provides only energy. References 1. Brumberg HL, Kowalski L, Troxell-Dorgan A, Gettner P, Konstantino M, Poulsen JF, et al. Randomized trial of enteral protein and energy supplementation in infants less than or equal to 1250 g at birth. J Perinatol 2010;30(8): 517-21. 2. Cooke RJ, Ainsworth SB, Fenton AC. Postnatal growth retardation: a universal problem in preterm infants. Arch Dis Child Fetal Neonatal Ed 2004;89(5):F428-30. 3. Embleton NE, Pang N, Cooke RJ. Postnatal malnutrition and growth retardation: an inevitable consequence of current recommendations in preterm infants? Pediatrics 2001;107(2):270-3. 4. Peterson J, Taylor HG, Minich N, Klein N, Hack M. Subnormal head circumference in very low birth

5. Ernst KD, Radmacher PG, Rafail ST, Adamkin DH. Postnatal malnutrition of extremely low birth-weight infants with catch-up growth postdischarge. J Perinatol 2003;23(6):477-82. 6. Cooke R. Postnatal growth in preterm infants: have we got it right? J Perinatol 2005;25 Suppl 2:S12-4. 7. Uhing MR, Das UG. Optimizing growth in the preterm infant. Clin Perinatol 2009;36(1):165-76. 8. Gathwala G, Chawla M, Gehlaut VS. Fortified human milk in the small for gestational age neonate. Indian J Pediatr 2007;74(9):815-8. 9. Mukhopadhyay K, Narnag A, Mahajan R. Effect of human milk fortification in appropriate for gestation and small for gestation preterm babies: a randomized controlled trial. Indian Pediatr 2007;44(4):286-90. 10. Miller J, Makrides M, Gibson RA, McPhee AJ, Stanford TE, Morris S, et al. Effect of increasing protein content of human milk fortifier on growth in preterm infants born at <31 wk gestation: a randomized controlled trial. Am J Clin Nutr 2012;95(3):648-55. 11. Lucas A, Fewtrell MS, Morley R, Lucas PJ, Baker BA, Lister G, et al. Randomized outcome trial of human milk fortification and developmental outcome in preterm infants. Am J Clin Nutr 1996;64(2):142-51.

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As consolidation therapy for Ewing’s sarcoma, a rare bone tumor that predominantly affects children and adolescents, there is little difference in the cure rate between cyclophosphamide and ifosfamide, suggested a new study published online in the Journal of Clinical Oncology.

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Nearly 50% of children with attention deficit hyperactivity disorder experience transient sleeping problems, while about 10% have persistent sleeping problems, reports a new study published online in Sleep Medicine.

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Psychiatry

Body Dysmorphic Disorder – Borderline Category Between Neurosis and Psychosis K RAMAN*, R PONNUDURAI†, OS RAVINDRAN‡

Abstract Body dysmorphic disorder is an under-recognized chronic problem, which is established as an independent diagnostic entity. Its clinical features, comorbidity, course and prognosis have been studied in detail. But, the issue of its psychotic and nonpsychotic variants and the question of dimensional or categorical method of classifying this disorder still poses a diagnostic dilemma. This case report tries to highlight this issue.

Keywords: Body dysmorphic disorder, delusional and nondelusional variant

B

ody dysmorphic disorder (BDD) is an underrecognized chronic problem that is defined as an excessive preoccupation with an imagined or a minor defect of a localized facial feature or body part, resulting in decreased social, academic and occupational functioning. Studies have reported rates of BDD of 7% and 15% in patients seeking cosmetic surgery and a rate of 12% in patients seeking dermatologic treatment.1 BDD has both psychotic and nonpsychotic variants, which are classified as separate disorders in Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) (delusional disorder and a somatoform disorder). Despite their separate classification, available evidence indicates that BDDs delusional and nondelusional forms have many similarities (although the delusional variant appears more severe), suggesting that they may actually be the same disorder, characterized by a spectrum of insight. In fact, it is one of the diagnostic entities that falls on the borderline between neurotic and psychotic spectrum of disorders. CASE Report Mr. S is a 27-year-old male from middle socioeconomic status. Patient was referred to psychiatry OPD *Assistant Professor †Professor and Head ‡Clinical Psychologist Dept. of Psychiatry, Sri Ramachandra University, Porur, Chennai, Tamil Nadu Address for correspondence Dr K Raman Assistant Professor Dept. of Psychiatry Sri Ramachandra University, Porur, Chennai -116, Tamil Nadu E-mail: ramkrish_dr@yahoo.com

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from the plastic surgery department for clearance for rhinoplasty surgery. Patient was interviewed in detail and his history dated back to 17 years of age, when he was in his final year of schooling. He started noticing pimples and acne on his face, which embarrassed him to face his colleagues. He observed that few of them cleared, but few on the face left black marks and those on the nose turned into comedones. Most of them cleared with treatment from a dermatologist. But, the patient’s concern with the healed scars on the face and nose started increasing and he started becoming preoccupied with them. He felt embarrassed in facing his classmates and would feel shy to face the public or relatives who would come to his house. Patient adopted measures like covering his nose with his hands while speaking to others or while listening to the lectures in the class so that others do not watch it. Over time, he started developing rituals such as repeatedly watching his nose in the mirror, frequently washing his face after he returns back home from outside, would apply powder over the nose to cover up the imagined area of scars on the nose and had tried to reshape his nose on his own by using a stone, which resulted in bleeding and worsening of the condition. Patient developed anxiety in social situations because of his referential thinking involving his imagined ugly appearance. He also developed misinterpretations of other people’s behavior and comments linking them to his facial disfigurement. Patient spent enormous amount of time and money in reshaping his nose even at times stealing money from home. He developed


Psychiatry depressed mood, death wishes and suicidal thoughts as a result of lack of improvement with treatment from various doctors. Patient had frequent change of jobs giving the reason as his inability to cope up with works involving social contact as a result of his ugly nose. He also started attributing his failures in academics and professional life to the imagined deformity in the nose. Patient did have recurrent suicidal ideation secondary to preoccupation with imagined deformity and occupational dysfunction but there was no active attempt. Patient did have history of stammering since childhood, which exacerbated after his social anxiety increased. He has history of alcohol and harmful tobacco use. Patient is the first among the five siblings. His mother used to be very critical of his appearance from his childhood. There is family history of stammering but there was no other significant mental illness in the family. He had a difficult temperament from his childhood although adequate information was not available. At the time of presentation to us, patient had nonpervasive sad mood, decreased concentration in his work, significant social anxiety and avoidance of social situations due to referential thinking, stammering, strong beliefs that his nose is ugly and deformed (amounting to delusional level) with absent insight and attributed all his failures to the physical problem. There was significant impairment in social, occupational and academic functioning. There were obsessions related to contamination and compulsive washing, checking and obsessive images, blasphemous thoughts and sexual obsessions. Patient was diagnosed to have BDD delusional variant with obsessive compulsive disorder mixed type, social anxiety disorder, dysthymia with mild depressive episode without somatic complaints and stammering according to DSM-IV criteria. PSYCHOMETRIC ASSESSMENTS On Eysenck Personality Questionnaire, he was found to be a person of introvert personality getting high scores, on neuroticism and low scores on psychoticism. On MiddleSex Hospital Questionnaire, he got significant scores on the scales of free-floating anxiety, phobia, obsession, somatization, depression and hysteria. On Multiphasic Questionnaire, he got significant scores on the clinical scales of paranoid, psychopathic deviation, depression and anxiety. On Social Phobia

Inventory, he got a score of 52, which is interpreted as extreme. On Beck’s Depression Inventory, he got a score of 18 which is interpreted as mild. On BDD-Y-BOCS (Yale Brown Obsessive Compulsive Scale modified for Body Dysmorphic Disorder), he got a score of 24, which is interpreted as moderate. Rorschach record with few popular responses, poor form level, rejection of responses at the time of inquiry, low number of FC responses, C + CF is greater than FC responses, unusual and bizarre responses, emphasis on major detail (D) responses and the presence of m responses is suggestive of a psychotic record with mixed features of anxiety and depression. Themes about sexual preoccupation, extramarital relations, pessimism, lack of assertiveness and delinquent behavior (lying) were brought out on TAT stories. TREATMENT PLAN Contract was established with the patient about avoiding visits to other doctors of different specialties for the treatment of his deformity. His preoccupation with his stammering as one of the reasons for his failure in occupational functioning was taken as the target in the treatment. Patient was educated about his anxiety contributing to his stammering and he was started on progressive muscular relaxation. He was explained about the excess of compulsive rituals that he was performing and home-based exposure response prevention was initiated. He was started on sertraline and clonazepam and their doses were hiked up on subsequent visits. In view of the delusional component, low-dose of risperidone was started, in addition, during the course of treatment to observe for additional improvement. Since, there was no obvious improvement above that obtained with selective serotonin reuptake inhibitor (SSRI), it was stopped. Patient is on continuous follow-up with us for the past 6 months. He reported of decrease in his social anxiety and intensity of stammering. His compulsive rituals also decreased except for mirror watching. His visits with other specialty doctors for change of nasal deformity were reduced to almost one visit in the above period. But, his belief about imagined nasal deformity was still at delusional level. Patient discontinued medications 15 days back and came with relapse of symptoms. He was restarted on medications and he was advised follow-up with his family member.

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Psychiatry DISCUSSION The patient discussed here presents as a prototype case of BDD described in various studies. As described in various studies, the age of onset for the reported case was in adolescence and the duration between the onset of illness and contact with the mental health professional was almost 10 years during which period there were frequent visits to dermatologists and plastic surgeons. His premorbid personality assessment also showed a mixture of avoidant, paranoid and emotionally unstable personality (impulsive type) as observed in literature.2 Factors that may predispose persons to BDD include low self-esteem, critical parents and significant others, early childhood trauma and unconscious displacement of emotional conflict. They also have an earlier onset of major depression and higher lifetime rates of major depression (26%), social phobia (16%), obsessive compulsive disorder (6%) and psychotic disorder diagnoses, as well as higher rates of substance use disorders in first-degree relatives.3,4 The reported case had comorbid obsessive compulsive disorder, social phobia with mild depression and stammering. The co-presence of BDD and obsessive compulsive disorder features appears to possibly individuate a particularly severe form of the syndrome, with a greater load of psychopathology and functional impairment and a more frequent occurrence of other comorbid mental disorders.5 Adults with BDD have markedly impaired functioning and notably poor quality-of-life.2 BDD may have a closely related psychotic subtype that significantly overlaps with, or may even be the same disorder as, the BDD variant of delusional disorder, somatic type. Although, the clinical features and phenomenology are almost similar to nondelusional BDD, delusional BDD patients have significantly lower educational attainment, are more likely to have attempted suicide, have poorer social functioning on several measures, are more likely to have drug abuse or dependence, are less likely to currently be receiving mental health treatment and have more severe BDD symptoms.6 The question arises as to include this category under neurotic or psychotic disorders or whether an intermediate category needs to be created for such disorders whose extreme severity results in a psychotic variant similar to obsessive-compulsive psychosis. This disorder has features predominantly of

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neurotic subtype such as its phenomenology similar to hypochondriasis and obsessive-compulsive disorder, comorbidity with anxiety spectrum disorders and good response to SSRIs. On the other hand, many earlier authors considered BDD a prodrome or variant of schizophrenia.7 Contrary to what might be expected, BDD’s delusional form, although classified as a psychotic disorder, appears to respond to serotonin-reuptake inhibitors alone,8 which questions its existence as a distinctive category under psychotic subtype. In addition, the delusional variant does not differ from the nondelusional variant on many of the measures except its severity, which might point to the existence of a single disorder. The case of BDD discussed above had comorbid anxiety spectrum disorders with impaired insight and significant impairment in occupational functioning and quality-of-life in view of delusional component. This necessitates the inclusion of poor insight or good insight specifiers and dimensional system of classifying such disorders. Although, the initial response to SSRI and anxiolytic showed significant improvement in his symptoms, during the course of illness, a low-dose of neuroleptic was added to augment the response but no added improvement was observed as quoted in the literature. RECOMMENDATIONS It is likely that a number of disorders span a spectrum from delusional to nondelusional thinking, with unlimited shades of gray in between. Future research may indicate that obsessional disorders such as BDD, anorexia, obsessive-compulsive disorder and hypochondriasis, as well as other disorders such as major depression, should have qualifiers or subtypes for example, ‘with good insight,’ ‘with poor insight,’ and ‘with delusional (or psychotic) thinking’ - with an implied continuum of insight embraced by a single disorder. Such approach will not only improve our classification system but also may have important treatment implications. For example, the preliminary finding that delusional BDD responds preferentially to SSRIs but not to neuroleptic agents contradicts conventional wisdom about the treatment of psychosis. Inclusion of a psychotic subtype for BDD should be considered for future editions of DSM.9 These and other data suggest that a dimensional view of psychosis (in particular,


Psychiatry delusions) in these disorders may be more accurate than DSMs current categorical view.

5. Frare F, Perugi G, Ruffolo G, Toni C. Obsessive-compulsive disorder and body dysmorphic disorder: a comparison of clinical features. Eur Psychiatry 2004;19(5):292-8.

REFERENCES

6. Phillips KA, Menard W, Pagano ME, Fay C, Stout RL. Delusional versus nondelusional body dysmorphic disorder: clinical features and course of illness. J Psychiatr Res 2006;40(2):95-104.

1. Phillips KA, Dufresne RG Jr, Wilkel CS, Vittorio CC. Rate of body dysmorphic disorder in dermatology patients. J Am Acad Dermatol 2000;42(3):436-41. 2. Veale D, Boocock A, Gournay K, Dryden W, Shah F, Willson R, et al. Body dysmorphic disorder. A survey of fifty cases. Br J Psychiatry 1996;169(2):196-201. 3. Phillips KA, Gunderson CG, Mallya G, McElroy SL, Carter W. A comparison study of body dysmorphic disorder and obsessive-compulsive disorder. J Clin Psychiatry 1998;59(11):568-75. 4. Gunstad J, Phillips KA. Axis I comorbidity in body dysmorphic disorder. Compr Psychiatry 2003;44(4):270-6.

7. Phillips KA, Menard W, Fay C, Weisberg R. Demographic characteristics, phenomenology, comorbidity, and family history in 200 individuals with body dysmorphic disorder. Psychosomatics 2005;46(4):317-25. 8. McElroy SL, Phillips KA, Keck PE Jr, Hudson JI, Pope HG Jr. Body dysmorphic disorder: does it have a psychotic subtype? J Clin Psychiatry 1993;54(10):389-95. 9. Phillips KA, Grant J, Siniscalchi J, Albertini RS. Surgical and nonpsychiatric medical treatment of patients with body dysmorphic disorder. Psychosomatics 2001;42(6):504-10.

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A new study published online in Sleep Medicine revealed that young adults who exercised vigorously before bedtime ended up getting better sleep than their counterparts who reported less strenuous evening activity.

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Among patients with traumatic brain injury (TBI), neither treatment with erythropoietin nor maintaining a higher hemoglobin concentration using blood transfusion appears to improve neurological outcome at 6 months, suggested the results of a controlled trial. The study was published in the July 2 issue of JAMA.

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Aprepitant, already approved for use in adults for the prevention of chemotherapy–induced nausea and vomiting (CINV), has now been shown to be effective in children and adolescents (ages 6 months to 17 years) too. The data come from a phase 3 study that will be used for regulatory approval submissions. The data was presented at the recent Multinational Association of Supportive Care in Cancer/International Society of Oral Oncology (MASCC/ISOO) Annual International Symposium on Supportive Care in Cancer.

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A new study published in the journal Nature details a test that may predict whether teenagers are likely to engage in binge drinking at the age of 16. Researchers noted that those who engaged in binge drinking at the age of 16 had reduced gray matter volume at age 14, as well as greater activity in the superior frontal gyrus of the brain in response to receiving a reward. Additionally, life events, such as romantic or sexual relationships, and negative life experiences at the age of 14 represented current binge drinking.

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Pediatric emergency medicine researchers at the Children’s Hospital of Eastern Ontario (CHEO) together with the Ontario Neurotrauma Foundation (ONF) have launched the first comprehensive pediatric concussion guidelines. The new guidelines provide evidence-based recommendations to standardize the diagnosis and management of concussion in children aged 5 to 18 years old, from the initial assessment to the period of recovery.

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A Mayo Clinic study published in Pediatric Obesity has reported that physicians using body mass index (BMI) to diagnose children as obese may be missing nearly 25% of kids who have excess body fat despite a normal BMI. Researchers noted that while BMI has high specificity in identifying pediatric obesity, meaning BMI accurately identifies children who are obese, it has a moderate sensitivity, meaning the BMI tool tends to miss children who actually should be considered obese.

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Psychiatry

Pediatric Bipolar Disorder Prerna Malik*, Raghu Gandhi†, Aparna goyal†, Savita Kundu†, Anil Kumar Gulia‡

Abstract Affective disorders in children are considered to be uncommon though they have been reported in several case reports and studies because of their different presentation than adults and also association with other comorbid disorders. We present a case of bipolar affective disorder first episode mania in a 13-year-old boy.

Keywords: Bipolar disorder, children, mania

B

ipolar disorder in children is among the most active and controversial areas of child and adolescent psychiatry research. The diagnostic dilemmas are:

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Whether elevated mood versus irritable mood is essential for diagnosis

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Minimum duration of manic episode

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Comorbid diagnosis.1,2

A manic episode consists of a distinct period of persistently elevated, expansive or irritable mood lasting for more than 1 week or more than 4 days for hypomanic episode and the presence of neurovegetative symptoms such as grandiose thinking or inflated self-esteem, decreased need for sleep, pressured speech or increased verbalizations, racing thoughts or flight of ideas, distractibility, increase in goal-directed activities or ideation and helplessness, which seems to be equally likely at any age. No modifications of manic episodes apply to children or adolescents according to Diagnostic and Statistical Manual Mental Disorders, 4th edition (DSM-IV).3 Here, we report a case of manic episode in a 13-year-old male child. Case report A 13-year-old boy of 6th class from rural Haryana, India was brought to psychiatry outpatient clinic of Postgraduate Institute of Medical Sciences, *Assistant Professor †Junior Resident Dept. of Psychiatry, Pt. BDS University of Health Sciences, Rohtak, Haryana ‡Assistant Professor BPS Govt. Medical College, Khanpur Kalan, Haryana Address for correspondence Dr Prerna Malik Assistant Professor Dept. of Psychiatry, Pt. BDS University of Health Sciences Rohtak - 124 001, Haryana E-mail: pm.malik@yahoo.co.in

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Rohtak, Haryana, India with symptoms of scholastic backwardness, sleep disturbances, running away from school and with increased communication for the past 1 month. He refused to do school assignments, homework and was relatively slow in completing them. He would run away from school or would not listen to teachers and even make fun of other students. The boy’s behavior had become unmanageable at and outside the home. He would talk more and roam around the house. Sometimes he would even run out of the house without informing anyone at home. He started saying that he is very powerful and he could give them money and lots of gold. Whenever, family members contradicted him, he would get violent and aggressive and even hit them. He would try to talk to people in village not known to him and even make fun of them by passing comments and laughing at them. He would visit neighbors and discuss his family issues with them. He would spend long time at other people houses and when asked to go home he would become angry and abuse them. He would order his father to bring new clothes and eatables for him. He also started demanding money. Upon refusal, he would throw household things and on getting money, he would go to the market and eat sweets, fast food. When family members decided not to talk to him thinking that this will improve his behavior, he would sing songs. Throughout the illness, patient’s mood used to remain irritable. He did not manifest hallucinations or had thought alienation, thought broadcasting, passivity or depersonalization. He had no inappropriate or precocious sexual behavior. There was no history of delinquent behavior, bedwetting, sleep talking, seizure, substance abuse and head trauma. Birth and developmental history was normal with no significant past and family history.


Psychiatry Prior to the onset of illness, he was a boy of timid nature, shy and reserved, having very few friends. He had good faith and belief in God and used to offer daily prayers and visit temples often. General physical examination was within normal limits. Mental state examination revealed an average built boy, cooperative, increased psychomotor activity with decrease reaction time, spontaneous speech, inflated self-esteem and delusion of grandiosity. He was found to be irritable throughout the interview. Neurological examination, routine laboratory tests, thyroid, visual examination and CT scan head were normal. He was submitted for psychometric investigation with Binet-Kamat test of mental ability, Wechsler intelligence scale for children, Rorschach Inkblot test. There were no schizophrenic indicators in Inkblot test. His IQ was around 90, with above-average intelligence. Based on the clinical and psychometric assessment, a diagnosis of pediatric bipolar disorder was made. Patient was admitted and started on risperidone 2 mg and later increased to 4 mg with significant improvement. Discussion Bipolar disorder has been recognized in children since 1990s; even then, there was intense debate whether it could occur prior to the age of 12 years. Phenomenology of childhood mania, especially in younger children can vary from the classic description of bipolar disorder in adults. Adolescent presentation may be bizarre, mood incongruent and/or paranoid. Schneiderian first-rank symptoms occur in 20% of cases. Early-onset bipolar disorder may be missed in 50%.4,5 Also, bipolar disorder in children has been found to have symptom overlap with other psychiatric disorders like conduct disorder, attention deficit hyperactivity disorder, substance use and anxiety disorders, etc. Mania in children is seldom characterized by euphoric mood.6,7 Rather, the most common mood disturbance in manic children is severe irritability, with ‘affective storms,’ or prolonged and aggressive temper outbursts.8 The type of irritability observed in manic children is very severe, persistent and often violent.9 The outbursts often include threatening or attacking behavior towards family members, other children, adults and teachers. In between outbursts, these children are described as persistently irritable or angry in mood.6,7,10 Thus, it is not surprising that these children frequently receive the diagnosis of conduct disorder. Conduct disorder according to International of Classification of Diseases 10th Revision (ICD-10) should start before the age of 6 and according to DSM-

IV, before the age of 7 and symptoms of truancy, lying, stealing, cruelty to animals, etc. should be present at least for 6 months or longer and also not as an isolated act.11 The psychopharmacological interventions for childhood mania include lithium, valproate and/or atypical antipsychotics. All mood stabilizers and antipsychotic agents are commonly used for earlyonset bipolar disorder in clinical settings. Lithium has been found to be therapeutically effective in the management of pediatric bipolar disorder.12,13 In a retrospective study of 28 youths with bipolar disorder, 82% of subjects showed improvement in both manic and aggressive symptoms with risperidone treatment.14 In contrast to the duration of treatment required for improvement with mood stabilizers, the average time to optimal response was 1.9 ± 1.0 months of therapy. Conclusion Children with bipolar disorder may be relatively uncommon in outpatient settings, but clinical experience suggests that they may account for a substantial number of child psychiatric hospitalizations and that they are plagued with chronic psychiatric and psychosocial disability.15,16 References 1. Geller B, Zimerman B, Williams M, Delbello MP, Frazier J, Beringer L. Phenomenology of prepubertal and early adolescent bipolar disorder: examples of elated mood, grandiose behaviors, decreased need for sleep, racing thoughts and hypersexuality. J Child Adolesc Psychopharmacol 2002;12(1):3-9. 2. Wozniak J, Biederman J. Childhood mania: insights into diagnostic and treatment issues. J Assoc Acad Minor Phys 1997;8(4):78-84. 3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. Revision: 4th edition, APA: Washington, DC, 2000. 4. James AC, Javaloyes AM. The treatment of bipolar disorder in children and adolescents. J Child Psychol Psychiatry 2000;42(4):439-49. 5. Giedd JN. Bipolar disorder and attention-deficit/ hyperactivity disorder in children and adolescents. J Clin Psychiatry 2000;61 Suppl 9:31-4. 6. Carlson GA. Bipolar affective disorders in childhood and adolescence. In: Affective Disorders in Childhood and Adolescence. Cantwell DP, Carlson GA (Eds.), Spectrum: New York 1983:p.61-83. 7. Carlson GA. Classification issues of bipolar disorders in childhood. Psychiatr Dev 1984;2(4):273-85. 8. Davis RE. Manic-depressive variant syndrome of childhood: a preliminary report. Am J Psychiatry 1979;136(5):702-6.

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Psychiatry 9. Wozniak J, Biederman J, Kiely K, Ablon JS, Faraone SV, Mundy E, et al. Mania-like symptoms suggestive of childhood-onset bipolar disorder in clinically referred children. J Am Acad Child Adolesc Psychiatry 1995a;34(7):867-76. 10. Geller B, Luby J. Child and adolescent bipolar disorder: a review of the past 10 years. J Am Acad Child Adolesc Psychiatry 1997;36(9):1168-76. 11. World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Description and Diagnostic Guidelines. WHO, Geneva; 1992. 12. Brumback RA, Weinberg WA. Mania in childhood. II. Therapeutic trial of lithium carbonate and further description of manic-depressive illness in children. Am J Dis Child 1977;131(10):1122-6.

13. Carlson GA, Rapport MD, Pataki CS, Kelly KL. Lithium in hospitalized children at 4 and 8 weeks: mood, behavior and cognitive effects. J Child Psychol Psychiatry 1992;33(2):411-25. 14. Frazier JA, Meyer MC, Biederman J, Wozniak J, Wilens TE, Spencer TJ, et al. Risperidone treatment for juvenile bipolar disorder: a retrospective chart review. J Am Acad Child Adolesc Psychiatry 1999b;38(8):960-5. 15. Kovacs M, Pollock M. Bipolar disorder and comorbid conduct disorder in childhood and adolescence. J Am Acad Child Adolesc Psychiatry 1995;34(6):715-23. 16. West SA, McElroy SL, Strakowski SM, Keck PE Jr, McConville BJ. Attention deficit hyperactivity disorder in adolescent mania. Am J Psychiatry 1995;152(2):271-3.

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Even Children can have Acidity Children who have continuing recurrence of cough and croup could be suffering from stomach acid reflux problems. Croup or ‘Kali Khansi’, as it is called in local parlance, is recognized by a loud cough that often sounds like the barking of a seal. It can cause rapid or difficult breathing, and sometimes wheezing. Croup is thought to be caused by a virus, but reflux acidity has been suggested as a possible trigger. In gastroesophageal reflux disease, stomach acid causes swelling and inflammation of the larynx, which narrows the airway. It can trigger more swelling with any kind of viral or respiratory infection. Identifying children with gastroesophageal reflux disease could help treat and improve recurring croup. It is unusual for a child to have three or more bouts of croup over a short period of time. These children need to be evaluated. The same is true for adults also. Patients with non responding asthma should be investigated for underlying acidity as the cause of acute asthma.

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Around the Globe

News and Views ÂÂ

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A study published online in BJOG has suggested that about half of hypertensive pregnant women who snore and about a quarter of those who do not snore have unrecognized obstructive sleep apnea (OSA). Researchers noted that of the 51 women with hypertensive disorders, 61% had OSA compared with 19% of 16 normotensive women. Once-daily tedizolid has been found to be noninferior, and to have a similar adverse effect profile, to twice-daily linezolid in the treatment of acute bacterial skin infections and skin-structure infections, report the results from a new phase 3 study. The study is published online June 6 in Lancet Infectious Disease. The US Food and Drug Administration (FDA) and the US Environmental Protection Agency (EPA) have recently suggested that pregnant women should eat more fish, about 8 ounces a week, in order to have smarter children. The US Food and Drug Administration (FDA) has approved efinaconazole 10% topical solution for the treatment of onychomycosis of the toenail. The FDA, however, had earlier declined to approve efinaconazole for onychomycosis in May 2013. A new study published online June 9 in BMJ open has pointed towards a significant increase in the number of people in England who have prediabetes, with 1 in 3 adults now known to be affected and those from poorer backgrounds to be particularly at risk. Prediabetes rates have been noted to increase from around 12% in 2003 to around 35% in 2011. The American Cancer Society has issued new guidelines to help primary care physicians (PCPs) better manage prostate cancer survivors. The new guidelines are both evidence– and expert-based and advice oncologists to provide PCPs with treatment summaries and post-treatment followup recommendations for patients. The guidance has been published online in CA: A Cancer Journal for Physicians. A re-examination of data from the National Institute of Child Health and Human Development microarray trial published in 2012 has revealed that anomalies detected with ultrasound in fetuses with normal karyotypes could be associated with unusual

copy number variants (CNVs). The findings have been published online in Obstetrics and Gynecology. ÂÂ

A review article by investigators from the National Institute on Drug Abuse (NIDA) has suggested that marijuana use is associated with substantial adverse events, including addiction and long-term cognitive dysfunction. The review article was published in the June 5 issue of the New England Journal of Medicine.

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The combination of late life depression and increased cerebral beta–amyloid deposits in patients with mild cognitive impairment appears to be a risk factor for quick progression to Alzheimer’s disease, reports a longitudinal analysis from the Alzheimer’s disease neuroimaging initiative database. The findings were presented at the Society of Nuclear Medicine and Molecular Imaging (SNMMI) 2014 Annual Meeting.

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A new research has suggested that the routine use of alcohol-impregnated disinfection devices on all central-line access ports has the potential to reduce central-line-associated bloodstream infections (CLABSIs). The study was presented at the Association for Professionals in Infection Control and Epidemiology (APIC) 2014 Annual Meeting.

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A new study, published online June 12 in the Journal of Clinical Endocrinology and Metabolism, has shown that African Americans with type 2 diabetes respond better to the glucose-lowering effect of metformin as compared to whites.

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A US national survey that confirms and extends a previous study from a single Veterans Affairs (VA) center has stated that the prevalence of insomnia is extremely high in female veterans in the US. The findings were presented recently at SLEEP 2014, the 28th annual meeting of the Associated Professional Sleep Societies.

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A study published June 12 in the New England Journal of Medicine has stated that continuous positive airway pressure (CPAP) is effective for lowering blood pressure in patients with moderate to severe sleep apnea, even those with blood pressures in the normal range.

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Intake of protein, especially fish, may be associated with a decreased risk for stroke, reported a new meta-analysis published online June 11 in Neurology. Researchers noted that animal protein

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Around the Globe 3 or more years after the drug is discontinued and that early recognition can significantly reduce the amount of visual loss.

intake decreased the risk for stroke by 29% while vegetable protein could decrease it by 12%. ÂÂ

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The number of moles a woman has may be linked with her risk of developing breast cancer, suggest two new studies published online June 10 in PLOS Medicine. One study revealed that women with no moles had an 8.5% chance of developing breast cancer, compared to an 11.4% chance among women with 15 or more moles on their left arm. The second study reported that women having too many moles were 13% more likely to develop breast cancer than women who had no moles. A new study published in Occupational and Environmental Medicine has pointed that hairdressers using permanent hair dye and hair waving products appear to be exposed to carcinogenic aromatic amines. Their blood levels of certain carcinogens appear to be associated with the frequency with which they apply treatments, including hair dyes and permanent waves. A new study presented at the European League Against Rheumatism (EULAR) Congress 2014 has shown that sarilumab plus methotrexate bring about better clinical, radiographic, and functional responses in patients with moderate to severe rheumatoid arthritis (RA), as compared to methotrexate alone. Patients with knee osteoarthritis (OA) can attain significant benefits and avoid physical function limitations just by walking more, reports a study published in Arthritis Care and Research. Researchers noted that walking an additional 1,000 steps each day was associated with a 16-18% reduction in incident functional limitation 2 years later. Use of selective serotonin reuptake inhibitors (SSRIs) for depression is not associated with cerebral microbleeds, reported Dutch researchers in an online report published in Stroke. Italian researchers have identified 4 microRNA (miRNA) biomarkers that are significantly decreased in patients with Alzheimer’s disease (AD) compared with controls. Three of these were also decreased in cerebrospinal fluid (CSF), thereby pointing that circulating miRNAs, along with other biomarkers, can serve as noninvasive indicators of AD. The findings were presented at the 24th Meeting of the European Neurological Society. A study published online June 12 in JAMA Ophthalmology has suggested that hydroxychloroquine retinopathy can continue for

Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014

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Replenishing cholecalciferol reserves in hemodialysis patients can potentially normalize their calcidiol, calcitriol, and calcium levels, reports a new study published online in the American Journal of Kidney Diseases. Oral weekly doses of 25,000 IU cholecalciferol for 13 weeks appear to be effective, safe and inexpensive to increase calcidiol and calcitriol levels in these patients.

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Professional athletes have a more diverse gut microflora as compared to people who are more sedentary, suggesting a beneficial effect of exercise on gastrointestinal health, reported an article published online June 9 in Gut.

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Recording from the dorsal sural nerve may be a favorable method for early detection of oxaliplatin-induced peripheral neuropathy, reports a new study presented at the 24th Meeting of the European Neurological Society (ENS). Oxaliplatin is extensively used in cancer treatment.

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New research shows that low cholesterol is not a good sign for people with kidney cancer, and may be linked with an increased risk of dying. The study is published in BJU International. Researchers noted that patients with high levels of cholesterol had a 43% lower risk of dying from kidney cancer than their counterparts with low levels.

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The oral diabetes drug classes – thiazolidinediones (TZDs) and sulfonylureas – both appear to increase the risk for fractures compared with metformin, reports a large database analysis. The findings were presented at the American Diabetes Association (ADA) 2014 Scientific Sessions.

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A novel study presented at the American Diabetes Association (ADA) 2014 Scientific Sessions has shown that vaccinating people against hepatitis B may prevent the development of diabetes, at least in some individuals. Of the patients without a prior history of diabetes, those previously vaccinated with hepatitis B had a 52% reduction in the risk for subsequent diabetes compared with individuals not vaccinated.

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A study presented at the European League Against Rheumatism (EULAR) Congress 2014 has suggested that erectile dysfunction (ED) is common and quite severe in men suffering from gout, and that all men with gout should be screened for the presence of ED.


mediLAW

Contributory Negligence by Patient can Come to Your Rescue You cannot hold a person liable unless he is made a party to the litigation. Dr KK Aggarwal

Order NATIONAL CONSUMER DISPUTES REDRESSAL COMMISSION NEW DELHI: CONSUMER COMPLAINT NO. 45 OF 2002 1. Manju Anil Chawla 2. Master Ravish Anil Chawla 3. Master Dhruv Anil Chawla ...Complainants Versus 1. Jivandhara Hospital 2. Dr Amit Chadha 3. Dr Vijay Bhomia Before:

HON’BLE MR JUSTICE JM MALIK, PRESIDING MEMBER HON’BLE DR SM KANTIKAR, MEMBER Pronounced on 20th December, 2013 Order Per Dr SM Kantikar

1. Brief facts of the Complaint The complainant Smt. Manju’s husband, late Mr Anil Chawla, (hereinafter, “a patient” consulted the Opposite party (OP-2), Dr at his clinic (OP-1) for his long standing and recurrent cold problem since 10 years and he was taking anti-cold medicines for many years but often he had inability to breathe from the right nostril, snoring at night and bitter taste in throat during nasal infection with running nose. The OP-2 examined him and diagnosed as the cartilaginous nasal septum was grossly deviated to right side and blocking the nose on the right nostril. After X-ray and endoscopy investigations the OP-2 advised the patient to undergo a surgery and date was fixed on 1st October, 1998. As the patient’s son, Dhruva, Complainant No.-3 was suffering from adenoid, OP-2 performed successfully, the adenoid surgery of Dhruva on 30th September, 1998 and was discharged on the same evening. On 1st October, 1998, since it was Dussehra as requested by patient OP-2 rescheduled the surgery for next day at 7.30 pm. Therefore, the patient reached the nursing home of the OP-2 at 7.30 pm on 2/10/1998 straight from his office.

The Defence 2. The OP-2 conducted operation of septoplasty with functional endoscopic sinus surgery with left maxillary clearance using Caldwell Luc approach under general anesthesia on the patient. Dr Rajesh Kolte was the anesthetist.

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mediLAW It was clear that, after proper radiological (X-ray) and blood investigations it was confirmed that the patient had gross deviation of the cartilaginous nasal septum. Surgery performed by OP-2 on the patient was a non-invasive surgery, which has no surgical complications. Also, OP-2 as routine done endoscopy to determine the surgical steps. The operation started at 8:50 pm and was completed in an hour. 3. The OP-2 Dr Amit Chadha submitted that, the attendant of the patient called him at 11.25 PM there was sudden cessation of respiration. The OP-2 examined the patient whose pulse and BP were not recordable. Therefore, all emergency measures were carried out by OP-2 and the Anesthetist Dr Kolte. Immediately cardiac massage was one, patient’s throat was checked for secretions, blood, gauze, which were absent, then the patient was intubated immediately with endotracheal tube by the anesthetist. Intermittent positive pressure ventilation was given with 100% oxygen started by the anesthetist through the tube with the help of portable Boyle’s machine apparatus. Cardiac massage continued, IV adrenaline, atropine, soda bicarb and I/C adrenaline were given but the patient did not respond. The OP-2 called the physician, Dr Vinay Bhomia, (OP-3) who came at about 11.30 p.m. and in a couple of minutes he revived the patient with the help of DC shock and intracardiac adrenaline. There was no secretions/blood, in the oropharyngeal tract. The patient was thereafter shifted to ICCU of Navneet Memorial Hospital and was put on to ventilator with IPPR mode. The patient was attended by Dr Guha, the doctor in-charge of the ICCU, at that time. The OP No. 2, 3 and Dr Kolte were also present there. Also opinion of Dr Parindra Desai, Neuro-Physician was also taken. The patient was diagnosed to have suffered a cardiorespiratory-arrest.

Observations 4. We have perused the affidavit evidences, the interrogatories and replies filed by the concern parties and relevant medical documents on file. The OP-2 is an ENT and Endoscopic Sinus Surgeon holding the Degrees of MS (ENT) and DLO and has been practicing since 1994. He is running a Nursing Home known as Jeevandhara Hospital (OP-1) having all facilities for ENT surgery. 5. The OP-2 further, contended that, the Complainants have concealed the material facts about the true condition/ diseases suffered in pasts, but later on OP-2 came to know about the concealed facts; even the Complainants have also not disclosed the reality in their complaint. In past the patient was admitted and took treatment for his Cardiac and Urinary/Renal problems at various hospitals in year 1997. There upon we found that, the patient late Anil Chawla suffered from cardiac as well as kidney problems in the year 1997, which are discussed further. 6. On 28th June, 1997, at 7.30 pm Anil Chawla was admitted at in Laxmi Heart and Medicare, Ahmedabad because he was suddenly collapsed in the office and experienced uneasiness, heaviness, retrosternal chest pain with perspiration. He was diagnosed as a known case of high blood pressure (HBP) since 1 year and not on regular treatment. The patient was properly treated with antihypertensive drugs like, nitrates, sorbitrate, nifedipine and antiplatelet drugs. The Laxmi Hospital discharged on him 29/6/1997 as against medical advice. 7. Thereafter, the patient was admitted in Muljibhai Patel Urological Hospital, under treatment of Dr Virendra Desai for about 25 days from 29/7/1997, as the Indoor No. 26259. He was diagnosed as right ectopic ureter with hydronephrosis He underwent surgery for the same. The hospital medical record revealed us some important findings as follows: a. The patient had given history of having hypertension for 3 years, he had taken treatment for 3 months but then had stopped taking the medications, and he did not take regular treatment. b. A fresh ECG was taken in Nadiad on 29/7/97 and it was found to have the same changes as at Laxmi Hospital, though minimal, signifying cardiac pathology. The changes may have reduced as he was on antihypertensive and antianginal drugs. We have perused the ICU records of Muljibhai Patel Urological Hospital, which clearly revealed the record of high blood pressure and he was put on antihypertensive drugs. 8. On 1st August, 1997, the patient was further referred to Dharmsingh Desai Memorial Methodist Institute of Cardiology & Cardiovascular Surgery, Nadiad. The Cardiologist Dr Mahpaekar Mashhadi, DM had examined him and advised ECG and 2D echocardiogram, but the Complainant produced only ECG report and concealed the Echo report.

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mediLAW 9. The evidence of OP-3, Dr Vijay Bhomia, revealed that OP-3 was called by the OP-1 & 2 when the patient was in critical situation in postoperative period. The OP-3 tried to revive patient (as stated in para 2 herein), but as there was lack of proper equipment and facility, OP-3 advised to shift patient. Thereafter, the patient was shifted to OP-4, the Navneet Hospital. OP-3 accompanied patient while shifting. The facts submitted by the OP-3 on oath and it are not rebutted by any of the parties of the present case as the bare fact. 10. We do not find any expert evidence is led by the Complainant to establish any negligence or deficiency on service, or any question of the providing short services by any Opposite parties. 11. In the evidence of the OP-4 that since he is in no way concern with the treatment, which was provided by the treating doctor, OP No.-2 & 3. The patient was brought in the late night he was in so much serious condition, who was admitted in ICCU for further management, but subsequently he died. 12. Even, prior to shifting patient to OP-4, during the postoperative period, the patient was under observation of anesthetist who was breathing normally through the mouth. He was given left lateral position. His pulse was regular 96/min and BP was 130/84 mmHg. An emergency was aroused at 11.25 pm, which was managed by OP-2, the anesthetist and OP-3. Thereafter, the patient was shifted to Navneet Hospital ICCU. Therefore, we do not find any deviation of standard of practice adopted by OP-2 and OP-3 during the course of entire treatment. 13. We have referred medical textbooks and literature on ENT surgeries and searched for the complications of “Septoplasty with Functional Endoscopic Sinus Surgery”. There are no reports of fatal complications due to such surgery. It is well known that, there are risks and complications for all surgeries; those for deviated septum and Septoplasty surgeries are very infrequent, but it includes nasal obstruction, bleeding, chronic nasal drainage, eye damage, numbness of facial structures, septal perforation, alteration of sense of smell or taste, and failure to resolve any associated nasal or sinus problem. 14. We are quite surprised to note that, Why the complainants have not made the anesthetist Dr Kolte as a necessary party in this case? The operation was performed under General Anesthesia, and it is known that there are more instances of such fatal complications due to anesthesia. The complications of anesthesia do arise, medical negligence is often a contributing factor. But, at this stage, it is beyond our consideration, because considerable time, of more than a decade has been elapsed now. Also, in the context of “Audi alteram partem” one of the most cherished and sacrosanct principles of the Natural Justice or equity, we are unable to hold anesthetist liable in this case, who was not made a party in this complaint. 15. In our opinion, Anesthetist should fully inform patients of the possible complications from anesthesia. A particular type of serious harm that can occur because of anesthesia error. An anesthetist has the responsibility to correctly regulate a patient’s consciousness during and after a surgical procedure. When used properly, anesthesia is a safe and effective method of sedation. Improperly administered anesthesia can result in significant injury to a patient, including, heart attack, death, nerve damage, stroke, paralysis, etc. 16. In this case, it is apparent to be a “Contributory Negligence”, that there was a mistake on the part of patient as well as the complainant No 1 who did not disclose about the previous medical treatment and disease to the OP2. Sometimes the unexpected results may not be only due to negligence of the doctor but also due to negligence of patients or relatives. If anybody undergoes any medical treatment, or is about to undergo a medical surgical procedure, one should take care to disclose relevant truth and facts to the doctor. The court recognizes, in addition, that patients are responsible for exercising ordinary care in revealing information to their physicians and those physicians have the primary responsibility for eliciting an accurate history from their patients due to their greater wealth of medical knowledge. This responsibility cannot be fully achieved without the truthful admissions of the patient. Thus, if the patient willfully chooses to withhold information from the physician, the physician cannot be liable for a medical negligence. 17. We have relied upon several judgements of Hon’ble apex court on medical negligence and also referred the Bolam’s test in this context. In the Bolam’s case (Bolam Vs. Frien Hospital Management Committee (1957)1 WLR 582) it was also held that a doctor is not negligent if he is acting in accordance with standard practice merely because there is a body of opinion who would take a contrary view. Applying the above principles in the instant case, we are convinced that there is no medical negligence on the part of OP-2 and OP-3 who are qualified doctors, and they have used their best professional judgment and due care during surgery and during complications.

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mediLAW 18. Even on, considering the evidence on record, we could find that the deceased patient Mr Anil Chawla suffered from a heart condition and failed to disclose such condition, which proximately caused his cardiac arrest. If the patient had revealed this information to the OP-2, then OP-2 could have postponed his procedure until it was ideal for surgery. Since, the OP-2 operated without the knowledge of heart disease, he cannot be found negligent. Hence, in our view there is no medical negligence by any opposite party. 19. Accordingly, the complaint is dismissed. Parties have to bear their own costs. (JM MALIK, J) PRESIDING MEMBER (Dr. SM KANTIKAR) MEMBER

Editors Commentary 1. Always keep a copy of all patients records with you. They can help you later if there is a medical dispute and the patient wants to conceal some information. 2. Concealment of any information by the patient amounts to contributory negligence. 3. It goes in your favor if the complainant has not brought any experts evidence in his favor. 4. You cannot hold a person liable unless he is made a party to the litigation. ■■■■

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What’s New

Disease Prevention Fat Intake and Risk of Coronary Heart Disease Guidelines have always recommended reducing intake of saturated fats to reduce the risk of coronary heart disease; whereas, intake of polyunsaturated fatty acids (PUFAs) is said to have a protective effect on the heart. But, findings from a recent meta-analysis of prospective observational studies published in Ann Intern Med 2014;160(6):398-406, do not support cardiovascular guidelines that recommend restricting total saturated fats and increasing the intake of PUFAs. The meta-analysis included 32 observational studies (n = 5,30,525) of fatty acids from dietary intake; 17 observational studies (n = 25,721) of fatty acid biomarkers and 27 randomized, controlled trials (n = 1,03,052) of fatty acid supplementation.1 In the observational studies, relative risks for coronary disease were 1.02 for saturated, 0.99 for monounsaturated, 0.93 for long-chain omega-3 PUFAs, 1.01 for omega-6 PUFAs and 1.16 for trans fatty acids when the top and bottom thirds of baseline dietary fatty acid intake were compared. Corresponding estimates for circulating fatty acids were 1.06, 1.06, 0.84, 0.94 and 1.05, respectively. A heterogeneous association between individual circulating fatty acids and coronary disease was observed but the meta-analysis suggested a decrease in coronary heart disease when omega-3 PUFAs were consumed in higher amounts. However, a beneficial effect of the omega-6 PUFAs is still doubtful. While the authors do not propose avoiding saturated fats, they do affirm that foods that are rich in saturated fats are less healthy as compared to foods that contain saturated foods in lower amounts. They further state that there is insufficient evidence to support choosing low fat dairy fat products. But, they support the recommendation that consumption of trans fats should be reduced. Optimal HPV Vaccine Dosing for Genital Warts In the United States, three doses of human papilloma virus (HPV) vaccine are recommended for protection

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against genital warts. However, it is seen that missed doses and suboptimal adherence to the schedule are frequent. In a Swedish cohort study, over 1 million females, aged 10-24 years were followed for 4 years and receipt of two quadrivalent HPV vaccine doses was shown to be associated with substantial protection against genital warts, although with three doses protection was slightly superior.2 Important outcomes such as cervical intraepithelial neoplasia or cervical cancer were not assessed in this study. Impact of Consumption of Tomato-based Products on Prostate Cancer Risk A large number of studies have been conducted to assess the impact of consumption of lycopenecontaining foods, especially tomato-based products on the risk of prostate cancer, but early reports have given conflicting results. A prospective study in a cohort of over 50,000 men from the Health Professionals Followup Study observed that dietary intake of lycopene was associated with a lower incidence of prostate cancer and a decreased risk of lethal prostate cancer. Analysis of biomarkers suggested that these beneficial effects may be mediated through inhibition of tumor angiogenesis.3 A note of caution, however, that nutritional associations found in observational studies frequently are not confirmed when randomized trials are later performed. Multivitamins and Mineral Supplements: Are they Really Beneficial Vitamin and mineral supplements are frequently given for preventing cancer or cardiovascular disease (CVD). However, limited evidence to support any benefit of vitamin and mineral supplements for preventing cancer or CVD was found in a 2013 systematic review, performed for the US Preventive Services Task Force (USPSTF).4 Randomized trials evaluating efficacy, and both trials and observational studies evaluating supplement safety were included in the review. A borderline significant reduction in the risk of cancer (relative risk [RR] 0.94, 95% confidence interval [CI] 0.89-1.00) and no effect on CVD (RR 1.02, CI 0.941.10) was observed in the meta-analysis of two large


What’s New trials of multivitamin supplements. Multivitamin supplementation also did not appear to reduce the risk of mortality (RR 0.95, CI 0.89-1.01). Also, no benefit on cognitive function was observed in a separate randomized trial that examined long-term multivitamin supplementation in men.5 Inspite of this, many patients choose to take vitamins and it is suggested that clinicians should not be bothered against that practice as long as it is harmless. References 1. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis. Ann Intern Med 2014;160(6):398-406.

2. Herweijer E, Leval A, Ploner A, Eloranta S, Simard JF, Dillner J, et al. Association of varying number of doses of quadrivalent human papillomavirus vaccine with incidence of condyloma. JAMA 2014;311(6):597-603. 3. Zu K, Mucci L, Rosner BA, Clinton SK, Loda M, Stampfer MJ, et al. Dietary lycopene, angiogenesis, and prostate cancer: a prospective study in the prostate-specific antigen era. J Natl Cancer Inst 2014;106(2):djt430. 4. Fortmann SP, Burda BU, Senger CA, Lin JS, Whitlock EP. Vitamin and mineral supplements in the primary prevention of cardiovascular disease and cancer: An updated systematic evidence review for the U.S. Preventive Services Task Force. Ann Intern Med 2013;159(12):824-34. 5. Grodstein F, O’Brien J, Kang JH, Dushkes R, Cook NR, Okereke O, et al. Long-term multivitamin supplementation and cognitive function in men: a randomized trial. Ann Intern Med 2013;159(12):806-14.

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lighter reading

Heaven and Hell A holy man was having a conversation with the Lord one day and said, “Lord, I would like to know what Heaven and Hell are like.” The Lord led the holy man to two doors. He opened one of the doors and the holy man looked in. In the middle of the room was a large round table. In the middle of the table was a large pot of stew which smelled delicious and made the holy man’s mouth water. But the people sitting around the table were thin and sickly. They appeared to be famished. They were holding spoons with very long handles that were strapped to their arms and each found it possible to reach into the pot of stew and take a spoonful, but because the handle was longer than their arms, they could not get the spoons back into their mouths. The holy man shuddered at the sight of their misery and suffering. The Lord said, ‘You have seen Hell.’ They then went to the next room and opened the door. It was exactly the same as the first one. There was the large round table with the large pot of stew which made the holy man’s mouth water. The people were equipped with the same long– handled spoons, but here the people were well nourished and plump, laughing and talking.

HUMOR

Inspiration Story

Lighter Side of Medicine That Darned Cat A man absolutely hated his wife’s cat and decided to get rid of him one day by driving him 20 blocks from his home and leaving him at the park. As he was getting home, the cat was walking up the driveway. The next day he decided to drive the cat 40 blocks away. He put the beast out and headed home. Driving back up his driveway, there was the cat! He kept taking the cat further and further and the cat would always beat him home. At last he decided to drive a few miles away, turn right, then left, past the bridge, then right again and another right until he reached what he thought was a safe distance from his home and left the cat there. Hours later the man calls home to his wife: “Jen, is the cat there?” “Yes”, the wife answers, “why do you ask?” Frustrated, the man answered, “Put that darned cat on the phone. I’m lost and need directions!”

Dr. Good & Dr. Bad Situation: A diabetic patient came with a blood

pressure of 130/80 mmHg.

Lower it further

It is fine

Quote 196

When you are at a loss of what to do, do nothing. Doing nothing can be very wise. When you pause doing things, you become more aware of God’s presence, and often an unexpected solution to your question will arise.

Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014

©IJCP Academy

The holy man said, “I don’t understand.” “It is simple” said the Lord, “In this place the people have learned to feed one another.”

Lesson: The JNC 8 Guidelines recommend a higher

blood pressure model for people who are 60 years or older or patients who are diabetic or patients with chronic kidney disease. Dr KK Aggarwal


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). –

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.

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

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. Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the departments and institutions where the work was performed,

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Confidence intervals for the measurements should be provided wherever appropriate.

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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 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.

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Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected summary, etc.)_______________________________ 2. Total number of pages ________________________ 3. Number of tables ____________________________ 4. Number of figures ___________________________

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.________________

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

Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014

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


lighter reading

Heaven and Hell A holy man was having a conversation with the Lord one day and said, “Lord, I would like to know what Heaven and Hell are like.” The Lord led the holy man to two doors. He opened one of the doors and the holy man looked in. In the middle of the room was a large round table. In the middle of the table was a large pot of stew which smelled delicious and made the holy man’s mouth water. But the people sitting around the table were thin and sickly. They appeared to be famished. They were holding spoons with very long handles that were strapped to their arms and each found it possible to reach into the pot of stew and take a spoonful, but because the handle was longer than their arms, they could not get the spoons back into their mouths. The holy man shuddered at the sight of their misery and suffering. The Lord said, ‘You have seen Hell.’ They then went to the next room and opened the door. It was exactly the same as the first one. There was the large round table with the large pot of stew which made the holy man’s mouth water. The people were equipped with the same long– handled spoons, but here the people were well nourished and plump, laughing and talking.

HUMOR

Inspiration Story

Lighter Side of Medicine That Darned Cat A man absolutely hated his wife’s cat and decided to get rid of him one day by driving him 20 blocks from his home and leaving him at the park. As he was getting home, the cat was walking up the driveway. The next day he decided to drive the cat 40 blocks away. He put the beast out and headed home. Driving back up his driveway, there was the cat! He kept taking the cat further and further and the cat would always beat him home. At last he decided to drive a few miles away, turn right, then left, past the bridge, then right again and another right until he reached what he thought was a safe distance from his home and left the cat there. Hours later the man calls home to his wife: “Jen, is the cat there?” “Yes”, the wife answers, “why do you ask?” Frustrated, the man answered, “Put that darned cat on the phone. I’m lost and need directions!”

Dr. Good & Dr. Bad Situation: A diabetic patient came with a blood

pressure of 130/80 mmHg.

Lower it further

It is fine

Quote 196

When you are at a loss of what to do, do nothing. Doing nothing can be very wise. When you pause doing things, you become more aware of God’s presence, and often an unexpected solution to your question will arise.

Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014

©IJCP Academy

The holy man said, “I don’t understand.” “It is simple” said the Lord, “In this place the people have learned to feed one another.”

Lesson: The JNC 8 Guidelines recommend a higher

blood pressure model for people who are 60 years or older or patients who are diabetic or patients with chronic kidney disease. Dr KK Aggarwal


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 –

– –

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). –

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.

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

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

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 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.

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. –

Do not use clips/staples on photographs and artwork.

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 summary, etc.)_______________________________ 2. Total number of pages ________________________ 3. Number of tables ____________________________ 4. Number of figures ___________________________

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

Indian Journal of Clinical Practice, Vol. 25, No. 2, July 2014

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


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R.N.I. No. 50798/90 Date of Publication 13th of Same Month Date of Posting 13-14 Same Month

POSTAL REGISTRATION NO. DL (S)-01/3200/2012-2014 Posted in N.D. PSO New Delhi


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