Ajcc march 2013

In This Issue —

Smoking Cigarettes: A Health Hazard

—

Anxiety Level Amongst Medical Students

—

Parachute Mitral Valve and a Large Ventricular Septal Defect

—

Corneo-scleral Melting in a Diabetic Patient

—

A Rare Case of Idiopathic Intracranial Hypertension

—

Nerve Damage from Soft Tissue Injury to the Forearm

—

ACC and AHA Update on Chronic Heart Failure Guidelines

—

A Decoy Operation for Catching the Violators of the PC-PNDT Act. Is it Lawful?

Volume 15, Number 11, March 2013 Pages 393-432

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Asian

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CLINICAL CARDIOLOGY

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

Volume 15, Number 11, March 2013

Dr Deepak Chopra Chief Editorial Advisor

Padma Shri and Dr BC Roy National Awardee Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD, Group Executive Editor

from the desk of group editor-in-chief 397 ACC 2013 Update

Dr Praveen Chandra Guest Editor, AJCC praveen.chandra@medanta.org Assistant Editor: Dr Nagendra Chouhan, Dr Dharmendar Jain

AJCC Speciality Panel International Dr Fayoz Shanl Dr Alain Cribier Dr Kohtian Hai Dr Tanhuay Cheem Dr Ayman Megde Dr Alan Young Dr Gaddy Grimes Dr Jung bo Geg Dr Rosli Mohd. Ali Dr S Saito National Dr Mansoor Hassan Dr RK Saran Dr SS Singhal Dr Mohd. Ahmed

Advisory Board Dr PK Jain Dr PK Gupta Dr Naresh Trehan Dr Sameer Shrivastava Dr Deepak Khurana Dr Ganesh K Mani Dr K S Rathor Dr Rajesh Kaushish Dr Sandeep Singh Dr Yugal Mishra Faculty Dr GK Aneja Dr Ramesh Thakur Dr Balram Bhargava Dr HK Bali Dr HM Mardikar

Dr Sanjay Mehrotra Dr Vivek Menon Dr Keyur Parikh Dr Ajit Mullasari Dr Kirti Punamiya Dr MS Hiramath Dr VS Narain Dr SK Dwivedi Dr Raja Baru Panwar Dr Vijay Trehan Dr Rakesh Verma Dr Suman Bhandari Dr Ravi Kasliwal Dr Atul Abhyankar Dr Tejas Patel Dr Samir Dani

Review Article 398 Smoking Cigarettes: A Health Hazard

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 Dentistry Dr KMK Masthan Dr Rajesh Chandna Gastroenterology Dr Ajay Kumar Dermatology Dr Hasmukh J Shroff Neurology Dr V Nagarajan Journal of Applied Medicine and Surgery Dr SM Rajendran, Dr Jayakar Thomas Anand Gopal Bhatnagar Editorial Anchor Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

Shivprasad S, Smita Sonoli, Anuradha Patil, MS Somannavar

CLinical study 402 Anxiety Level Amongst Medical Students

IJCP Editorial Board

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

KK Aggarwal

Rishi Gautam, Kunal Bhatia, SK Rasania, Dhruv Gupta, Rini Sahewalla

Case report 406 Parachute Mitral Valve and a Large Ventricular Septal Defect

Monika Maheshwari, Anand Agarwal

408 Corneo-scleral Melting in a Diabetic Patient

Joginder Pal Chugh, Prachi Jain, Rajender Singh Chauhan, Ashok Rathi

410 A Rare Case of Idiopathic Intracranial Hypertension

Nilay Thakore, Vismay Naik

Photo Quiz 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

417 Nerve Damage from Soft Tissue Injury to the Forearm

Printed at New Edge Communications Pvt. Ltd, New Delhi E-mail: edgecommunication@gmail.com

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

419 ACC and AHA Update on Chronic Heart Failure Guidelines

Around the globe

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.

Note: Asian Journal of Clinical Cardiology 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.

424 News and Views

Medi law 425 A Decoy Operation for Catching the Violators of the PC-PNDT Act. Is it Lawful?

MC Gupta

Lighter reading 426 Lighter Side of Medicine

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

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

ACC 2013 Update ÂÂ

STREAM trial: Fibrinolysis with tenecteplase and contemporary antithrombotic therapy given before transport to a polymerase chain reaction (PCI)-capable hospital coupled with timely coronary angiography is as effective as primary PCI in ST-segment elevation myocardial infarction (STEMI) patients presenting within three hours of symptom onset who cannot undergo primary PCI within one hour of first medical contact. To prevent intracranial hemorrhage the dose of tenecteplase needs to be halved in people aged 75 years and older (New England Journal of Medicine).

ÂÂ

The first prospective international randomized controlled study focusing specifically on angina in patients with diabetes has shown that ranolazine is an effective treatment in this patient population. Results of the Type 2 Diabetes Evaluation of Ranolazine in Subjects with Chronic Stable Angina (TERISA) study were published in the Journal of the American College of Cardiology.

ÂÂ

A lower-profile, next-generation version of the Sapien transcatheter aortic-valve system known as the Sapien XT was associated with similar rates of death and stroke as the first-generation device, results from the PARTNER 2 trial show. The device, tested here in inoperable patients (‘cohort B’), also appeared to improve on several procedural aspects of valve deployment, including lower anesthesia time and fewer vascular complications.

ÂÂ

Community volunteers, namely parents, can be trained to perform an accurate electrocardiogram (ECG) screening, according to the results of a new study presented at the ACC Scientific Sessions. Overall, the rate of technical error in nearly 4,500 ECGs performed by community volunteers on five consecutive screening days was just 0.34%, a rate that was comparable to that of trained ECG technicians.

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Cangrelor cuts complications at PCI versus clopidogrel in CHAMPION-PHOENIX: A >11,000-patient randomized trial found that intravenous cangrelor cut the risk of periprocedural complications at all kinds of PCI compared with taking a pill of clopidogrel, long a mainstay of such procedures.

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Watchman PREVAILs on safety for stroke prevention in Afib: Left atrial appendage closure with the Watchman device has gotten safer for stroke prevention in atrial fibrillation, according to results from the PREVAIL trial designed to allay FDA concerns.

ÂÂ

HPS2-THRIVE may signal the end for niacin: Results from a landmark study of specially formulated niacin in more than 25,000 high-risk patients appears to have extinguished any clinical role for niacin to reduce the risk of cardiovascular events in these patients. mmmmm

Asian Journal of Clinical Cardiology, Vol. 15, No. 11, March 2013

397

review article

Smoking Cigarettes: A Health Hazard Shivprasad S, Smita Sonoli*, Anuradha Patil**, MS Somannavar**

Abstract Tobacco smoke contains various substances, some of which are irritants, oxidants, free radicals and carcinogens. These substances have a direct and profound effect on the human body and are the direct cause of the diseases associated with smoke.

This article depicts the physicochemical properties of smoke and highlights the health hazards of smoking.

Keywords: Tobacco smoke, health hazards, nicotine, carbon monoxide, carcinogen

M

orbidity and mortality is closely associated with smoking habits in individuals. Scientific studies have been conducted for over half a century to determine whether smoking is hazardous to health. The trend of the evidence has been consistent and unambiguous about the health hazards of tobacco.

There is an increasing incidence of mortality due to cigarette/beedi smoking as compared to other causes of death like alcohol, addictive drugs and suicides.

complications. In the United States itself, over 4,00,000 individuals die prematurely each year from cigarette smoking representing approximately one out of every five deaths. Incidence of myocardial infarction in heavy smokers is three times more common compared to nonsmokers. In India, the effects of smoking could be even more harmful than western countries because of widespread practice of smoking beedies, which is more harmful than cigarettes.2-4

This was recognized during industrialized cigarette production and mass use. In the 1950s, there were already reports linking cigarette smoking with the fast rise in the rate of lung cancer. Today knowledge of the deleterious health consequences of smoking is widely recognized, and publicized, but smoking remains as one of the important preventable causes of death in developed as well as developing countries.

Recently, there has been significant concern about the possible health effects of involuntary exposure of nonsmoker to other people’s tobacco smoke i.e. passive smoking. In addition to the irritation and annoying effects of involuntary exposure to cigarette smoke among nonsmokers, specific groups of people have been found to be more susceptible to effects of passive smoking. It is reported to cause exacerbation of asthma and angina and chronic effects like increased risk of lung cancer, respiratory tract infection and atherosclerosis. Approximately 30% increase in risk of death from ischemic heart disease or myocardial infarction is noted in passive smokers.5,6

The first major study associated with smoking predicted risk of cardiovascular disease was published in the year 1985. This was subsequently confirmed by numerous epidemiologic studies. The association has been so strongly consistent that smoking is now considered as one of major risk factors for atherosclerosis.1 In the industrialized world, 50% of deaths are attributed to atherosclerosis and its

*Assistant Professor **Dept. of Biochemistry Jawaharlal Nehru Medical College, Belgaum, Karnataka Address for correspondence Dr Shivprasad S Assistant Professor, Dept. of Biochemistry Jawaharlal Nehru Medical College, Belgaum, Karnataka E-mail: shivprasad273@yahoo.com

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Physicochemical Properties of Cigarette Smoke Cigarette smoke is a complex mixture of over 4,700 chemical compounds including high concentration of oxidants and free radicals present in both gas phase and the tar phase of cigarette smoke. Approximately 92-95% of the total weight of mainstream smoke is present in the gas phase. Nitrogen and carbon dioxide account for 85% of the smoke’s weight and carbon monoxide and nicotine seems to account for most of the acute effects.7-9

review article Pharmacology of Cigarette Smoke Nicotine and carbon monoxide are major substances of cigarette smoke that produce acute effects (Table 1).

Nicotine A highly toxic alkaloid, nicotine is a ganglionic stimulant and depressant. It markedly stimulates the central nervous system (CNS); appropriate dose produce tremors and in larger doses, the tremor is followed by convulsions. Stimulation of the CNS is followed by depression and death results from failure of respiration due to both central paralysis and peripheral blockade of muscles of respiration. At a cellular level, nicotine acts on nicotinic acetylcholine receptors and causes opening of cation channels and neuronal excitation. Along with activation of receptors, Table 1. Cigarette Smoke Constituents10 Substance

Effect(s)

Particulate phase: (Tar phase) Polynuclear aromatic hydrocarbons

Carcinogen

Nicotine

Neuroendocrine stimulant and depressant, addicting drug

Phenol

Cocarcinogen and irritant

Cresol

Cocarcinogen and irritant

β-naphthylamine

Cocarcinogen

N-nitrosonornicotine

Cocarcinogen

Benzo(a) pyrene

Cocarcinogen

Trace metals (e.g. nickel, arsenic, polonium 210)

Cocarcinogen

Indole

Tumor accelerator

Carbazole

Tumor accelerator

Catechol

Cocarcinogen

Gas phase Carbon monoxide

Impair oxygen transport and utilization

Hydrocyanic acid

Ciliotoxin and irritant

Acetaldehyde

Ciliotoxin and irritant

Acrolein

Ciliotoxin and irritant

Ammonia

Ciliotoxin and irritant

Formaldehyde

Ciliotoxin and irritant

Oxides of nitrogen

Ciliotoxin and irritant

Nitrosamines

Carcinogen

Hydrazine

Carcinogen

Vinyl chloride

Carcinogen

nicotine also causes desensitization. Chronic nicotine administration leads to a substantial increase in the number of nicotinic acetylcholine receptors leading to an adaptive response to prolonged receptor desensitization.

It is likely that the overall effect of nicotine reflects a balance between activation of nicotinic acetylcholine receptors, which causes neuronal excitation and desensitization that causes synaptic block. So smokers report that smoking wakes them up when they are drowsy and calms them down when they are tense.

Small doses of nicotine tend to cause arousal and large doses have a reverse effect.

The major action of nicotine on peripheral nervous system consists initially of transient stimulation followed by persistent depression of all autonomic ganglia. Nicotine causes the release of catecholamines in a number of isolated organs. In heart, it causes tachycardia, increased cardiac output and increased arterial pressure. In GIT, it causes nausea, vomiting and occasionally diarrhea. All of these effects decline with repeated dosage, though the central effects remain unaltered. Release of antidiuretic hormone from posterior pituitary causes a decrease in urine flow. The plasma concentration of free fatty acids increase, probably owing to sympathetic stimulation and adrenaline secretion.

Carbon Monoxide Cigarette smoke contains 2-6% of carbon monoxide.

It interferes with oxygen transport and utilization.

Smokers inhale about 400 parts per million (ppm) of carbon monoxide and develop elevated carboxyhemoglobin levels. The range of carboxyhemoglobin found in smokers is 2-15%, while in nonsmokers it is nearly 1%. Chronic mild elevations of carboxyhemoglobin due to smoking are a common cause of mild polycythemia and may produce subtle impairment of CNS function. Cigarette smoke and its condensate are carcinogenic in several species of animals. The major identified carcinogens in cigarette smoke are polynuclear aromatic hydrocarbons, aromatic amines and nitrosamines. Cocarcinogens present in cigarette smoke such as catechol, greatly enhance its carcinogenicity. The sister chromatid exchange rate, a sensitive indicator of mutagenic effects, is higher in the lymphocytes of smokers than in nonsmokers. Cigarette smoke condensate is also mutagenic in microbial system. Potent pulmonary irritants and ciliotoxins are also found in cigarette smoke. These substances increase bronchial mucous secretion and mediate acute

Asian Journal of Clinical Cardiology, Vol. 15, No. 11, March 2013

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review article and chronic decrease in pulmonary and mucociliary function. Cigarette smoke also increases lung epithelial permeability.10-12 Some Diseases Related to Smoking Chronic obstructive pulmonary disease (COPD) refers to a group of conditions that cause difficulty in breathing and are associated with obstruction of air flow within the lung. These conditions are chronic bronchitis, bronchiectasis, asthma and emphysema.

COPD prevalence has increased dramatically in the past few decades and is one of the major causes of bed-confining disability. Diagnosed COPD appears to be more prevalent in men than women, whether expressed in terms of mortality or hospital separation data. This is usually attributed to the historically higher rates of cigarette smoking among men and their greater likelihood of exposure to significant occupational respiratory irritants.11 Studies have found that smoking is associated with an increased rate of respiratory infection and illness. Cigarette smoking is well-recognized to increase the susceptibility to bacterial and viral infections.12 Exposure to cigarette smoking damages the lining of the respiratory tract, reduces mucociliary clearance and impairs both humoral and cellular immune responses.13 In 2003, an estimated 22,400 new cases of stomach cancer were diagnosed, and an estimated 12,100 deaths were expected to occur. Former smokers have lower rates of stomach cancer than those who continue to smoke. For women, the risk of cervical cancer increases with the duration of smoking. In 2003, an estimated 31,900 new cases of kidney cancer were diagnosed, and an estimated 11,900 people died from the disease. In 2003, an estimated 30,700 new cases of pancreatic cancer were diagnosed, attributing to 30,000 deaths.

The median time from diagnosis to death from pancreatic cancer is about three months. In 2003, approximately 10,500 cases of acute myeloid leukemia (AML) were diagnosed in adults. Benzene is a known cause of AML, and cigarette smoke is a major source of benzene exposure. Among US smokers, 90% of benzene exposures come from cigarette.14 There is a growing body of evidence linking smoking and cancer of the hematopoietic system. Twenty to 30% of leukemia cases are related to smoking. In one study, smoking was associated with a two-fold increase in risk for AML among participants aged 60 and older.15

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Most people are amazed at how easy it is to quit smoking while fasting. Fasting makes it easier to overcome a tobacco addiction by reducing the craving for nicotine. An Italian study of men who smoked found that heavy smokers had lower levels of selenium than lighter smokers and nonsmokers.16 One study in 1999 showed that supplemental b-carotene has different effects in smokers and nonsmokers. b-carotene supplementation has been linked to an increase in lung cancer in smokers, but does not appear to increase risk in nonsmokers.17 Smokers have been found to have a lower a-tocopherol level than nonsmokers.

Furthermore, persons with low physical activity levels were found to have a lower level than those with high activity.18 Conclusion Several steps have been taken all over the world through an extensive mass media propaganda whereby public have been warned of the possible health hazard of smoking. In USA, it has already started yielding results.

Situation in India is not encouraging. The famous slogan ‘Cigarette Smoking is Injurious to Health’, found on every the cigarette pack is only confined to the cigarette pack, no one is concerned about it. This may be partially due to the lower literacy rate and lack of health awareness.

More than this, it is because of dependence produced by nicotine. Nicotine is the principal constituent of tobacco responsible for its addictive character.

Addicted smokers regulate their nicotine intake and blood levels by adjusting the frequency and intensity of their tobacco use both to obtain the desired psychoactive effects and to avoid withdrawal effects.

The withdrawal syndrome is characterized by craving for tobacco products, depressed mood, insomnia, irritability, anxiety, difficulty in concentration, restlessness and increased appetite. Most of these symptoms peak in 1-2 days and return to base line within 3-4 weeks of quitting; however, craving for tobacco products may persist for an extended period.

Apart from smoking cessation, further reduction of risk may be achieved by weight loss (when appropriate), a healthier diet (fruits and vegetables) and supplements such as selenium and vitamins C and E. Vitamins C and E work synergistically and a moderate dose of both taken in combination may provide more of a protective effect against lung cancer than either taken separately.19 Encouraging smoking cessation early in life is crucial to help individuals avoid many of the harms related to smoking.20,21

review article References 1. Yasue H, Hirai N, Mizuno Y, Harada E, Itoh T, Yoshimura M, et al. Low-grade inflammation, thrombogenicity and atherogenic lipid profile in cigarette smokers. Circ J 2006;70(1):8-13.

2. McGill HC Jr. The cardiovascular pathology of smoking.

Am Heart J 1988;155(1 Pt 2):250-7.

3. Stringer MD, Görög PG, Freeman A, Kakkal VV. Lipid peroxides and atherosclerosis. BMJ 1989;298:281-4.

12. Arcavi L, Benowitz NL. Cigarette smoking and infection. Arch Int Med 2004;164(20):2206-16.

13. Dye JA, Adler KB. Effects of cigarette smoking on epithelial cells of the respiratory tract. Thorax 1994;49: 825-34.

14. Cancer Statistics. Smoking and Cancer - Statistics for the U.S. Available from: http://quitsmoking.about.com/od/ tobaccostatistics/a/cancerstats.htm.

4. Anand MP, Bakhle DS, Ajay S. Smoking and hypertension Indian scenario. J Assoc Physicians India 1990;38(4):283-4.

15. Sandler DP, Shore DL, Anderson JR, Davey FR, Arthur D, Mayer RJ, et al. Cigarette smoking and risk of acute leukemia: associations with morphology and cytogenetic abnormalities in bone marrow. J Natl Can Inst 1993;85(24):1994-2003.

5. Sorsa M, Einistö P, Husgafvel-Pursiainen K, Järventaus H, Kivistö H, Peltonen Y, et al. Passive and active exposure to cigarette smoke in a smoking experiment. J Toxicol Environ Health 1985;16(3-4):523-34.

16. Jossa F, Trevisan M, Krogh V, Farinaro E, Giumetti D, Fusco G, et al. Serum selenium and coronary heart disease risk factors in southern Italian men. Atherosclerosis 1991;87 (2-3):29-34.

6. Zhu BQ, Sun YP, Sievers RE, Glantz SA, Parmley WW, Wolfe CL. Exposure to environmental tobacco smoke increases myocardial infarct size in rats. Circulation 1994;89(3):1282-90.

7. Tobacco facts and FAQs. WHO. Available from: http:// www.emro.who.int/tfi/facts.htm.

8. Robertson D, Tseng CJ, Appalsamy M. Smoking and mechanism of cardiovascular control. Am Heart J 1988;115(1 Pt 2):258-63.

9. Rahman I, MacNee W. Oxidant/antioxidant imbalance in smokers and chronic obstructive pulmonary disease.

Thorax 1996;51(4):348-50.

17. Welch RW, Turley E, Sweetman SF, Kennedy G, Collins AR, Dunne A, et al. Strain dietary antioxidant supplementation and DNA damage in smokers and nonsmokers. Nutr Cancer 1999;34(2):167-72.

18. Öhrvall M, Tengblad S, Vessby B. Lower tocopherol serum levels in subjects with abdominal adiposity. J Int Med 1993;234(1):53-60.

19. Yong LC, Brown CC, Schatzkin A, Dresser CM, Slesinski MJ, Cox CS, et al. Intake of vitamins E, C, and A and risk of lung cancer. The NHANES I epidemiologic follow up study. First National Health and Nutrition Examination Survey. Am J Epidemiol 1997;146(3):231-43.

10. Harrison’s Principles of Internal Medicine. Vol. -2, 14th edition.

20. Doll R, Peto R, Boreham J, Sutherland I. Mortality in relation to smoking: 50 years’ observations on male British doctors. BMJ 2004;328:1519.

11. Chapman KR, Tashkin DP, Pye DJ. Gender bias in the diagnosis of COPD. Chest 2001;119(6):1691-5.

21. Orleans TC. Helping young adult smokers quit: the time is now. Am J Public Health 2007;97:1353.

My daughter has an MBBS degree and is registered with the Medical Council in India. She wants to get a postgraduate MD degree. Texila American University (TAU) in Guyana offers an MD degree. Should I send her to this University? ÂÂ

The website of the university is www.tauedu.org. The program may be called an MD program but, as per the nomenclature in USA, it is a basic medical degree and not a postgraduate degree.

ÂÂ

I doubt whether degrees awarded by this university are recognized by the MCI.

ÂÂ

The Union Government, exercising powers conferred upon it by the provisions of the Indian Medical Council Act, 1956, has recognized postgraduate medical qualifications being awarded in Australia, Canada, New Zealand, United Kingdom and United States of America, with the condition that these degrees should be recognized in the respective country for enrolment of medical practitioners in the concerned specialties.

This recognition has been notified in the Official Gazette on 10th March 2008.

ÂÂ

The MD degree awarded by TAU will not be covered by the above gazette notification because it is not a postgraduate degree and because Guyana is not included in the list of 6 countries mentioned.

ÂÂ

In the circumstances, it may not be advisable to send your daughter for the above course.

—Dr MC Gupta

Asian Journal of Clinical Cardiology, Vol. 15, No. 11, March 2013

401

Clinical Study

Anxiety Level Amongst Medical Students Rishi Gautam*, Kunal Bhatia*, SK Rasania**, Dhruv Gupta†, Rini Sahewalla †

Abstract Background: The study aims to assess the levels of stress anxiety in medical students and find any correlation with various causative factors. Objectives: 1. To study the levels of anxiety amongst medical students. 2. To compare these levels with different variables and causative factors. Study design: Cross-sectional study at a premier central government medical college called Vardhman Mahavir Medical College, Safdarjung Hospital, New Delhi using a standard anxiety questionnaire.

Participants: Three hundred ten medical students of all batches currently studying in the college. Results: Out of the 310 medical students who participated in the study, 150 (48.4%) were found to have high anxiety levels. The prevalence of abnormally high anxiety levels was maximum in students belonging to the third (66.1%), fifth (47%), ninth (49.3%) semesters. Anxiety levels were significantly higher amongst female students (61.3%) as compared to male students (43.2%) (p < 0.05). Students living in hostel had higher anxiety levels (56.1%) than students living at home (38.9%). Examinations were cited by 66.7% students as the most important cause of high anxiety amongst them. No significant relationship was found between anxiety levels and their medium of schooling, or age. Conclusion: The findings point towards very high prevalence of anxiety amongst medical students, with female students being more prone. Also, examinations instil enormous amounts of stress and anxiety, which is clearly evident from very high anxiety levels amongst the students who had their examinations coming up (students belonging to the third, fifth and ninth semesters). Alcohol and drug abuse are grave consequences that these students are liable to develop and even suicidal ideation. We suggest installation of a psychological support teams in such institutions, which would help the students tide over these stressors in a healthy manner and assure them of full confidentiality regarding their problems.

Keywords: Anxiety, medical students, hostelers, examination, female

A

nxiety is a normal reaction to stress. It helps one deal with a tense situation in the office, study harder for an exam and keep focused on an important speech. In general, it helps one cope.

But when anxiety becomes an excessive, irrational dread of everyday situations, it becomes a disabling disorder.1 Medical students represent a highly educated population under significant pressures.

Their academic responsibilities are a major cause of stress and anxiety amongst them. While a moderate amount of anxiety amongst students helps them achieve an optimum performance, high levels on the other hand can have a deleterious effect on their

*Medical Student Vardhman Mahavir Medical College **Professor Dept. of Community Medicine Vardhman Mahavir Medical College, Safdarjung Hospital, New Delhi †Medical Student Manipal College of Medical Sciences, Manipal Address for correspondence Dr SK Rasania Professor, Dept. of Community Medicine, Vardhman Mahavir Medical College Safdarjung Hospital, New Delhi

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physical as well as their mental health. Their sleep is disturbed and they are distressed to the extent that they are lost. Medical students loaded with heavy texts often suffer from anxiety.2 The prevalence rates of anxiety disorders amongst general population in India and South East Asia range between 0.16-0.20/100 population aged between 18-35 years. And there has been an alarming rise in these cases for the past some years.3 Objectives ÂÂ

To study the levels of anxiety amongst medical students.

ÂÂ

To compare these levels with different variables and causative factors such as examinations, sex, place of residence and medium of schooling.

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To prove or disprove the hypothesis that women are more prone to high anxiety levels.

Material and Methods The study was done amongst the medical students studying at Vardhman Mahavir Medical College, Safdarjung Hospital, New Delhi. It was conducted during August - December 2007.

Clinical Study The design was a cross-sectional study. All the batches of medical students were informed about the purpose of interview and confidentiality assured. Out of the total 443 students in the college, 310 consented to participate. Each student was asked to fill a standard anxiety questionnaire: Sinhaâ&#x20AC;&#x2122;s comprehensive anxiety test. The sociodemographic data was collected along with the test questionnaire keeping the identity confidential.

The test consisted of 90 questions, to which the subjects had to reply as a yes or a no. Each yes response was awarded 1 point, and in the end, the total score for each subject was evaluated (0 as the minimum score and 90 as the maximum score). Based on these scores the subjects were graded into extremely low (1), low (2), normal (3), high (4), extremely high (5) according to the scoring scale provided along with the test questionnaire. The data collected through the questionnaire was then statistically evaluated using the SPSS software to assess the levels of anxiety and its correlation with various causative factors such as examinations, sex, place of residence medium of schooling.

Results Out of the total students, 48.4% of them had abnormally high anxiety levels (Levels 4 and 5).

And the rest 51.6% were in the normal to low anxiety levels after evaluation (Fig. 1). Distribution

40

of anxiety levels varied with sex of the students.

Association was present between sex and anxiety levels, with females having higher anxiety levels than males (p < 0.05); 61.3% of female students had abnormally high anxiety levels (Levels 4 and 5) (Fig. 2).

An association was found between high anxiety levels and students in the third, fifth, ninth semesters, as they had their annual examinations approaching soon (p < 0.05) (Fig. 3). Various causative factors for high anxiety levels are depicted in Figure 4. An association was found between high anxiety levels and examinations, professional future as the major stressors (p < 0.05).

Figure 5 shows the distribution of anxiety levels across students living with their family or at home with those living away from the social support or home.

An association was found between high levels of anxiety and students living in the Hostels, away from their families (p < 0.05).

Variations of anxiety levels in students with prior schooling from an English Medium School as compared to those from a Hindi Medium are shown in Figure 6. The factor was studied to assess if any correlation existed with this aspect, because the standard mode of educational training in medical colleges in India is in English. No significant association was found between anxiety levels and medium of schooling (p > 0.05).

35

60

20

50 21.6

15 5 0

19.7 12.3

10.3

10 1

Students (%)

Students (%)

30 25

Anxiety level Females Males

36.1

2

3

4

5

1 2 3 4 5 Anxiety levels

40 30

27.9

20 10 0

6.6 1 1

8.5

23.6 17.6

11.3 3

2 2

3 Anxiety levels

10.4 12.3 4 4

5

Figure 1. Bar chart showing distribution of the students according their anxiety levels.

Figure 2. Bar chart showing sex-wise distribution of anxiety levels.

Key: X axis-Anxiety levels: 1 = Extremely low anxiety, 2 = Low, 3 = Normal, 4 = High, 5 = Extremely high.

Key: X axis-Anxiety levels: 1 = Extremely low anxiety, 2 = Low, 3 = Normal, 4 = High, 5 = Extremely high.

Y axis: Percentage of total students tested across all batches.

Y axis-Percentage of students

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80

7.60%

Key: X axis: Semester-wise distribution (First, Third, Seventh, etc.)

Y axis: Percentage of students. Bar color coding depicts varying anxiety levels with (1 = Extremely low) to (5 = Extremely high) as graded earlier on a scale of 1-5.

45

30

0

1 2 3 4 5 Anxiety levels

33.3

25

10 5 0

2

1

1

2

4

3

3 Anxiety levels

11.7 16.7

15

36.5

20 20.1

5

Anxiety level English Hindi

16.7

28.8 14 4

10.1

14.6 3

Percentage (%)

42.1 1

10.8 9.9

24.5 24.5 19.3

25.9

20

0

5

40 30

2

4

Y axis-Percentage of students. Bar codes: = Exam-related stress, = Family-related stress, = Friends-related stress/peer pressure, = Professional future-related anxiety, = Other causes.

25

5

3 Anxiety levels

Key: X axis-Anxiety levels: 1 = Extremely low anxiety, 2 = Low, 3 = Normal, 4 = High, 5 = Extremely high.

35

10

2

Figure 4. Bar chart showing relationship between anxiety levels and biggest anxiety causing fears in life.

30

15

1

9.9 13.9

35

40

10

Anxiety level Home Hostel

40

50

20

Ninth

Figure 3. Bar chart showing association between anxiety levels and semester.

Percentage (%)

Percentage (%)

44.90%

8.90%

14.30%

39.40%

17.90%

Third Fifth Seventh Semester-wise distribution

60

21.9 19.4

First

Anxiety level Friends Exams Future Family None

70 37.50%

2 4

25.30%

1 3 5

48.20%

50 45 40 35 30 25 20 15 10 5 0

10.80%

Students (%)

Clinical Study

5

4

5

Figure 5. Bar chart showing association between anxiety levels and place of residence.

Figure 6. Bar chart showing relation between anxiety levels and medium of schooling.

Key: X axis-Anxiety levels: 1 = Extremely low anxiety, 2 = Low, 3 = Normal, 4 = High, 5 = Extremely high.

Key: X axis-Anxiety levels: 1 = Extremely low anxiety, 2 = Low, 3 = Normal, 4 = High, 5 = Extremely high.

Y axis: Percentage of students. Bar codes: = Percentage of students residing at home, = Percentage of students residing in the hostel.

Y axis-Percentage of students. Bar code: schooling, Hindi medium of schooling.

Discussion and Review of Literature

under tremendous stress prior to professional exams.

This stress may manifest with varying magnitude of anxiety4 and decrease in psychological health.5 Further, test anxiety is associated with lower academic performance.6

Medical students are repeatedly subjected to rigorous examinations to check their potential to be a doctor as they have to deal with human life every single day. They have chosen a career which demands not only responsibilities but also ethical and legal liability for other’s lives. The onus of this responsibility and sheer volume of syllabus places a medical student

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English medium of

Our results point towards significant anxiety amongst medical students with 48.4% having abnormally high levels. Females were found to be suffering from more

Clinical Study anxiety than their male counterparts as 61.3% of them had high anxiety levels, in comparison to males, of whom 43.2% fell in this category. This is in agreement with other studies that substantiate presence of sex differences in exam-related anxiety, with female students having higher test anxiety than male students.7,8 Students living in the hostels away from their parents and family were suffering from greater anxiety (56.1% had abnormally high levels), than students living at their homes, with their family and social support, as only 38.9% of them had higher traits 66.2% of the students who had high anxiety stated examinations and future related problems, as their major cause for anxiety.

This is also evident from the findings from the semester-wise variation in the levels of anxiety, with students of the third, fifth, ninth semester having higher anxiety levels as compared to students from the first and the seventh semesters, as they had their examinations around the corner. No significant association was found between anxiety levels and medium of schooling.

Alcohol and drug abuse are grave consequences that these students are liable to develop and even suicidal ideation. We suggest installation of a psychological support teams in such institutions which would help the students tide over these stressors in a healthy manner and assure them of full confidentiality regarding their problems.

Conclusion A total of 310 medical students were interviewed to assess their anxiety levels. These students were studying in the various semesters of MBBS, Vardhman Mahavir Medical College, New Delhi. The salient findings of our study were:

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Significantly higher incidence of anxiety was seen in hostellers (56%) compared to day scholars (38.9%) (p < 0.05).

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Cause of anxiety as cited by the students was stress due to examinations.

Thus, we concluded that in a medical college setting, better hostel facilities and more participation by the faculty in terms of mentors for students, counselors on campus, etc. may help reduce anxiety levels in medical students.

References 1. Vaidya PM, Mulgaonkar KP. Prevalence of depression anxiety and stress in undergraduate medical students and its co-relation with their academic performance. Indian J Occupational Ther 2007;XXXIX(1):7-10.

2. Inam SN, Saqib A, Alam E. Prevalence of anxiety and depression among medical students of private university.

J Pak Med Assoc 2003;53(2):44-7.

3. Mehanza Z, Richa S. Prevalence of anxiety and depressive disorders in medical students. Transversal study in medical students in the Saint-Joseph University of Beirut.

Encephale 2006;32(6 Pt 1):976-82.

4. Kidson M, Hornblow A. Examination anxiety in medical students: experiences with the visual analogue scale for anxiety. Med Educ 1982;16(5):247-50.

5. Aktekin M, Karaman T, Senol YY, Erdem S, Erengin H, Akaydin M. Anxiety, depression and stressful life events among medical students: a prospective study in Antalya, Turkey. Med Educ 2001;35(1):12-7.

6. Zeidner M. Does test anxiety bias scholastic aptitude test performance by gender and sociocultural group? J Pers Assess 1990;55(1-2):145-60.

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Prevalence of high anxiety was 48.4% (n = 150)

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Maximum anxiety levels were seen in the third semester (66%) followed by the ninth semester (49.3%).

7. Chapell MS, Blanding ZB, Silverstein ME, Takahashi M, Newman B, Gubi A, et al. Test anxiety and academic performance in undergraduate and graduate students. J Educ Psychol 2005;97(2):268-74.

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Significantly higher incidence of anxiety was seen in females (61.3%) compared to males (43.2%) (p < 0.05).

8. Eller T, Aluoja A, Vasar V, Veldi M. Symptoms of anxiety and depression in Estonian medical students with sleep problems. Depress Anxiety 2006;23(4):250-6.

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Case report

Parachute Mitral Valve and a Large Ventricular Septal Defect Monika Maheshwari*, Anand Agarwal**

Abstract We report here a rare case of parachute mitral valve associated with a muscular ventricular septal defect and a stenosing supravalvular mitral ring.

Keywords: Ventricular septal defect, parachute mitral valve, supramitral ring

P

arachute mitral valve (PMV) is a severe form of congenital mitral valve (MV) stenosis characterized by the presence of a single papillary muscle, from which the chordae of both valve leaflets divide; thus the resemblance to a parachute.1 This developmental anomaly is most often associated with other obstructive lesions on left side of heart (supravalvular mitral ring, subaortic stenosis and coarctation of aorta) and is known as Shoneâ&#x20AC;&#x2122;s complex.2 When only, two or three of these components are present, the incomplete form of Shoneâ&#x20AC;&#x2122;s complex is diagnosed.3 We describe here a rare case of PMV with a stenosing supravalvular mitral ring and a large muscular ventricular septal defect (VSD).

was a holosystolic murmur at left lower sternum associated with a prominent thrill. Chest skiagram showed cardiomegaly with straightening of left border of heart and cephalization of pulmonary vessels.

Electrocardiogram revealed sinus rhythm admixed with ectopic beats and right ventricular hypertrophy (Fig. 1).

Transthoracic echocardiogram (TTE) parasternal long axis view demonstrated PMV with a single papillary muscle accepting all chordae tendinae and a large

CASE REPORT An 11-year-old girl presented in emergency department with complaints of shortness of breath while playing with her fellows in school. She was underdeveloped for her age and looked pale. Her pulse was 90/minute, regular and of low volume. Cardiac auscultation revealed loud S1 with a mid-diastolic rumbling murmur at the apex increasing with expiration and best heard in left lateral decubitus position. Additionally, there

*3rd Year Resident **Assistant Professor Dept. of Cardiology Jawaharlal Nehru Medical College, Ajmer, Rajasthan Address for Correspondence Dr Monika Maheshwari Navin Niwas, 434/10, Bapu Nagar Ajmer, Rajasthan - 305 001 E-mail: opm11@rediffmail.com

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Figure 1. Electrocardiogram showing sinus rhythm with right ventricular hypertrophy.

case report (10 mm) muscular VSD (Fig. 2). Single papillary muscle was confirmed at the mid-level of left ventricle (Fig. 3) with the typical ‘parachute leaflets’. Transmitral Doppler flow was consistent with severe mitral stenosis with mean gradient across MV of 15 mmHg (Fig. 4).

Aortic valve was normal in morphology and flow.

There was no evidence of coarctation of aorta in suprasternal view. Patient was referred to higher center for surgical correction of the deformity.

DISCUSSION

Figure 2. Transthoracic echocardiogram parasternal long axis view showing PMV with a single papillary muscle accepting all chordae tendinae and a large muscular VSD.

Figure 3. Transthoracic echocardiogram parasternal short axis view at the mid-level of left ventricle showing single papillary muscle with the typical ‘parachute leaflets’.

Parachute deformity of the MV is due to disturbed delamination of the anterior and posterior parts of the trabecular ridge (which normally forms anterolateral and posteromedial papillary muscles, respectively) between 5th and 9th week of gestation, thereby forcing these embryonic predecessors of the papillary muscles to condense into a single papillary muscle.3 Oosthoek et al4 suggested that the valve can be distinguished on the basis of morphological features into parachute-like asymmetrical mitral valves and true PMV. Parachutelike asymmetrical mitral valves have two papillary muscles, with one being elongated located higher in the left ventricle with it’s tip reaching to the annulus, and attached at both it’s base and lateral side to the left ventricular wall, whereas true PMV have a single papillary muscle that receives all chordae. Currently, 2D TTE establishes the diagnosis in majority of the patients with PMV and transesophageal echocardiography is reserved for challenging cases suspected on TTE imaging.5 PMV is very rare as an isolated anomaly6 and usually presents as Shone’s complex. Busacca et al7 reported uncommon association of PMV with Down’s syndrome. Popescu et al8 described for the first time persistent left superior vena cava in patient with Shone’s syndrome. Till date to the best of our knowledge, only two cases of PMV with VSD has been reported.9,10 Hence, it was worth describing this rare association.

REFERENCES 1. Marino BS, Kruge LE, Cho CJ, Tomlinson RS, Shera D, Weinberg PM, et al. Parachute mitral valve: morphologic descriptors, associated lesions, and outcomes after biventricular repair. J Thorac Cardiovasc Surg 2009;137(2):385-93.

Figure 4. Transmitral Doppler flow consistent with severe mitral stenosis.

2. Shone JD, Sellers RD, Anderson RC, Adams P Jr, Lillehei CW, Edwards JE. The developmental complex of “parachute mitral valve,” supravalvular ring of left atrium, subaortic stenosis, and coarctation of aorta.

Am J Cardiol 1963;11:714-25.

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case report

Corneo-scleral Melting in a Diabetic Patient Joginder Pal Chugh, Prachi Jain, Rajender Singh Chauhan, Ashok Rathi

Abstract Scleritis is a rare, usually painful inflammation of sclera causing scleral melt and exposure of underlying uveal tissue.

Although, idiopathic in 50% cases, systemic vasculitides, collagen vascular disorders and autoimmune diseases are wellestablished causes in remaining cases. Diabetes mellitus as an underlying cause of scleritis has not been reported in literature to the best of our knowledge. Microvasculopathy is a well-known complication of diabetes mellitus. We are presenting a case report of a painless scleral melting along with involvement of adjacent cornea in a known diabetic patient without any other systemic cause of scleritis.

Keywords: Scleritis, diabetes mellitus, microvasculopathy

CASE HISTORY A 48-year-old male presented to us with an approximately 5 x 7 mm well-defined localized area of scleral thinning with prolapsed underlying uveal tissue involving inferotemporal region of left eye, which was painless and gradually progressing for last two months. About 2 mm of cornea near the limbus was also involved (Fig. 1). Recorded Snellenâ&#x20AC;&#x2122;s acuity was 6/6 OD and 6/9 OS. Ocular examination revealed mild pupillary distortion in the affected eye and moderate nonproliferative diabetic retinopathy in both eyes. Gonioscopy was not attempted due to corneal involvement. Ultrasound biomicroscopic examination of the affected eye did not reveal any mass lesion underlying the diseased area. There was no evidence of infection in the vicinity of the lesion. There was no history of ocular trauma, topical medication or any ocular surgery. Patient was a known case of diabetes for past 12 years. No history of any other systemic ailment was there. Hematological investigations revealed erythrocyte sedimentation rate (ESR) - 20 mm at the end of first hour, total leukocyte count (TLC) and differential leukocyte count (DLC) were within normal

Figure 1. Showing well-defined area of sclero-corneal melting in a quiescent eye.

limits, Rh factor negative, antinuclear antibodies (ANA) and c-ANCA were negative. Fasting and postprandial blood sugar was 120 and 210 mg % with patient on oral hypoglycemic agents. Glycosylated hemoglobin (HbA1C) was 7.3. Renal function tests were within normal limits and no evidence of diabetic nephropathy was there. Patient was advised corneo-scleral patch grafting, which he deferred.

DISCUSSION

Regional Institute of Ophthalmology PGIMS, Rohtak, Haryana Address for correspondence Dr J oginder Pal Chugh 172-R, Model Town Rohtak, Haryana - 124 001 E-mail: chughjoginder@yahoo.co.in

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Systemic cause of scleritis can be identified in only 50% cases.1 Scleritis is usually noninfectious and associated with systemic vasculitides, connective tissue disorders and autoimmune diseases. Rheumatoid arthritis is the most common disease associated with

case report scleritis.2 Other conditions associated with scleritis are Wegner’s granulomatosis, polyarteritis nodosa, systemic lupus erythematosus, relapsing polychondritis, ankylosing spondylitis and inflammatory bowel diseases. Scleritis is also reported after ocular surgery.3 It is often complicated by involvement of adjacent structures.

All patients with active scleritis require treatment.

Treatment options include oral corticosteroids, nonsteroidal anti-inflammatory agents, intravenous pulsed steroid therapy, cytotoxic agents and surgical reinforcement. Oral corticosteroids are often the firstline agents. Refractory and progressive cases require cytotoxic therapy. Cyclophosphamide in a dose of 2 mg/kg is a drug of choice.4 Surgical reinforcement can be done in patients with severe thinning involving larger area in a quiescent eye. Surgical options include amniotic membrane transplantation, conjunctival flap, scleral and lamellar corneal patch graft. Kim et al reported a series of 16 cases of scleral necrosis in which 13 patients underwent lamellar scleral patch graft along with conjunctival flap and three patients underwent only conjunctival flap reinforcement.5 All cases showed excellent surface restoration except one case of graft melting.

In our case, scleritis was painless and no systemic association was found on investigations except for long-standing diabetes mellitus with poor control.

A case of fungal scleritis in diabetic patients has been reported in the past.6 Diabetes mellitus per se as a cause of scleritis has not been reported to the best of our knowledge. Considering the fact that diabetes can lead to microvasculopathy, it could be the underlying factor responsible for scleral necrosis in our case.

REFERENCES 1. Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol 1976;60(3):163-91.

2. Afshari NA, Afshari MA, Foster CS. Inflammatory conditions of the eye associated with rheumatic diseases.

Curr Rheumatol Rep 2001;3(5):453-8.

3. Joseph A, Biswas J, Sitalakshmi G, Gopal L, Badrinath SS. Surgically induced necrotizing scleritis (SINS) - Report of two cases. Indian J Ophthalmol 1997;45(1):43-5.

4. Hemady R, Tander J, Foster CS. Immunosuppressive drugs in immune and inflammatory ocular disease. Surv Ophthalmol 1991;35(5):369-85.

5. Kim SY, Chung WS, Hahn DK. Surgical management of scleral necrosis. J Korean Ophthalmol Soc 1995;36(1):7-12.

6. Locher D, Adesina A, Wolf TC, Imes CB, Chodosh J. Postoperative Rhizopus scleritis in a diabetic man. J Cataract Refract Surg 1998;24(4):562-5.

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...Cont’d from page 407

3. Hakim FA, Kendall CB, Alharthi M, Mancina JC, Tajik JA, Mookadam F. Parachute mitral valve in adults: a systematic overview. Echocardiography 2010;27(5):581-6.

7. Busacca P, Pozzolini A, Minutiello L. Association between parachute mitral valve and Down’s syndrome. Report of a case. G Ital Cardiol 1998;28(10):1144-8.

4. Oosthoek PW, Wenink AC, Macedo AJ, Gittenberger-de Groot AC. The parachute-like asymmetric mitral valve and its two papillary muscles. J Thorac Cardiovasc Surg 1997;114(1):9-15.

8. Popescu BA, Jurcut R, Serban M, Parascan L, Ginghina C. Shone’s syndrome diagnosed with echocardiography and confirmed at pathology. Eur J Echocardiogr 2008;9(6):865-7.

5. Prunier F, Furber AP, Laporte J, Geslin P. Discovery of a parachute mitral valve complex (Shone’s anomaly) in an adult. Echocardiography 2001;18(2):179-82.

9. Abelson M. Parachute mitral valve and a large ventricular septal defect in an asymptomatic adult.

Cardiovasc J S Afr 2001;12(4):212-4.

6. Almeida S, Cotrim C, Miranda R, Lopes L, Almeida AR, Loureiro MJ, et al. The role of echocardiography in assessing parachute mitral valve. Rev Port Cardiol 2009;28(3):335-9.

10. Suri RK, Jha NK, Sarwal V. Repair of parachute mitral valve with multiple ventricular septal defects: a case report and literature review. J Heart Valve Dis 1997;6(1):63-6.

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Case report

A Rare Case of Idiopathic Intracranial Hypertension Nilay Thakore*, Vismay Naik**

Abstract Idiopathic intracranial hypertension (IIH), sometimes called by the older names benign intracranial hypertension (BIH) or pseudotumor cerebri (PTC), is a neurological disorder that is characterized by increased intracranial pressure (pressure around the brain) in the absence of a tumor or other diseases. The main symptoms are headache, nausea and vomiting, as well as pulsatile tinnitus (buzzing in the ears synchronous with the pulse), double vision, and other visual symptoms. If untreated, it may lead to swelling of the optic disc in the eye, which can progress to vision loss.1 IIH is diagnosed with a brain scan (to rule out other causes) and by measuring cerebrospinal fluid (CSF) opening pressure. Some respond to medications, but others require surgery to relieve the pressure. The condition may occur in all age groups, but is most common in young women, especially those with obesity.1 Here we are presenting a case of a 19-year-old female patient with 67 kg weight who presented with complaints of headache, nausea, vomiting and visual disturbances and was later diagnosed to have PTC on investigations.

Keywords: Pseudotumor cerebri, idiopathic intracranial hypertension, papilledema, CSF opening pressure

CASE REPORT A 19-year-old female patient presented with frontooccipital headache since 15 days, throbbing in nature, continuous, progressively increasing in intensity, worsening on bending forward, coughing, straining and not relieved by taking rest or medication. Patient had nausea and vomiting since 15 days with a frequency 2-3 times/day, projectile in nature, containing water and food particles. Patient had blurring of vision for four days, which was associated with blackouts.

Patient also complained of blurring of vision and headache on seeing illuminated objects for longer time and occasional blurring of vision of surrounding objects while looking straight.

Despite taking medications from family physician patient did not get relief from the symptoms, which increased in intensity. Patient visited our hospital in

*Professor and Head of Unit **Senior Resident Dept. of Medicine Smt. NHL Municipal Medical College Sheth KM School of Postgraduate Medicine and Research Sheth Vadilal Sarabhai General Hospital, Ahmedabad Address for correspondence Dr Vismay Naik 8/A, Rajmugut Society, Near Naranpura Cross Roads Naranpura, Ahmedabad -380 013 E-mail: vismay101@gmail.com

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OPD and was admitted for further investigations and diagnosis.

No complaints of fever, trauma, seizures, photophobia, rhinorrhea, joint pain; no past history of similar complaint, hypertension, ischemic heart disease (IHD), diabetes mellitus (DM), chronic obstructive pulmonary disease (COPD), seizures, major operative procedure, any known drug or food allergy.

Patient gave history of weight gain since last two years.

She gained about 17 kg during last two years. Patient has decreased sleep and appetite since she has started having headache.

On Examination Patient was afebrile, pulse rate - 84/min. Blood pressure 140/84 mmHg. There was no pallor, icterus, cyanosis, lymphadenopathy, jugular venous pressure (JVP) not raised, abdomen was soft, no lump or organomegaly, bowel sounds were present. Height - 150 cm, weight 67 kgs, body mass index (BMI) - 29.7. CVS and RS were within normal limits. On CNS - no NR, pupil-bilateral R/L, plantar - B/L flexion.

Bowel and bladder were normal. Menstrual cycle was regular, five days with moderate amount of blood during cycle.

On blood investigation: Hb - 13.5, TC - 9,270, DC N70,L23,M4,E3,B0; PLT count - 2.6 lakh/mm3. Urea - 10, serum creatinine - 0.71, Na - 139 mEq/l, K - 3.5 mEq/l.

Serum cholesterol - 134 mg/dl, serum triglyceride -

case report

Figure 1. Normal MRI of brain.

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case report

Figure 2. Normal MR venography of brain.

20 18

Right eye

Left eye

Figure 3. Fundus examination of both eyes reveals bilateral papilledema.

100 mg/dl, HDL cholesterol - 38 mg/dl, serum VLDL - 20 mg/dl, serum LDL - 76 mg/dl. Cholesterol/HDL ratio - 3.53 mg/dl, serum total lipid - 568 mg/dl. TSH - 1.523 mIU/ml. CSF routine was normal. Urine routine was normal. Urinary cortisol estimation - 57 mg/24 hours (N-60 to 160) in 1200 ml volume.

Fundoscopy revealed: Bilateral papilledema. Right eye: bilateral disc edema with dilated tortuous vessels with macular edema. Left eye: Flame shaped hemorrhages.

On doing radiological investigations: USG (abd, KUB) was normal (no cystic ovaries). Chest X-ray and ECG were normal. CT scan brain was normal. Magnetic resonance imaging (MRI) study of brain and MR venography revealed no abnormality.

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Cases per 1,00,000

16 14 12

Women

10

Men

8 6 4 2 0

Normal weight

>10% above >20% above ideal body ideal body weight weight

Figure 4. Incidence of IIH.

Inquires were made in different reputed laboratories of the city and the patient was sent to a laboratory, which had the machine to measure maximum cerebrospinal fluid (CSF) opening pressure. Lumbar puncture with manometry and opening pressure in lateral decubitus position was measured as >>350 mm of water, which was much higher than maximum pressure the machine could measure.

case report Follow-up After confirming the diagnosis patient was started tablet acetazolamide 250 mg four times a day and was advised to loose weight. Patient is regularly coming for follow-up and is symptomatically better.

DISCUSSION The first report of idiopathic intracranial hypertension (IIH) was by the German physician Heinrich Quincke, who described it in 1893, under the name serous meningitis.2 The term ‘pseudotumor cerebri (PTC)’ was introduced in 1904 by his compatriot Max Nonne.3 PTC, also known as IIH is a disorder of unknown etiology. It affects predominantly obese women of childbearing age. The primary problem is chronically elevated intracranial pressure (ICP), and the most important neurologic manifestation is papilledema, which may lead to progressive optic atrophy and blindness.4 The cause of IIH is not known. The Monro-Kellie rule states that the ICP (Literally: Pressure inside the skull) is determined by the amount of brain tissue, CSF and blood inside the bony cranial vault. Three theories therefore exist as to why the pressure might be raised in IIH: An excess of CSF production, increased volume of blood or brain tissue, or obstruction of the veins that drain blood from the brain.1 The first theory, that of increased production of CSF, was proposed in early descriptions of the disease.

However, there is no experimental data that supports a role for this process in IIH.1

transverse dural venous sinus was demonstrable on MR venography, while none of the 59 control subjects had this finding.6 These authors suggest that the narrowing is a consequence of elevated ICP and, when the narrowing develops, it exacerbates the pressure elevation by increasing venous pressure in the superior sagittal sinus.

Bateman has shown that some patients with IIH with normal dural venous drainage have increased arterial inflow suggesting that collateral venous drainage occurs in addition to that provided by the superior sagittal sinus and transverse sinuses.7 The same investigator measured MR venography and MR flow quantification in cerebral arteries and veins in a series of 40 patients with IIH, of which 21 patients had venous stenosis. The arterial inflow was 21% higher than normal and superior sagittal sinus outflow was normal, resulting in reduced percentage of venous outflow compared to inflow. The remainder of arterial inflow volume is presumed to have drained via collateral venous channels. With clinical remission of symptoms, the arterial inflow volumes returned to normal.8 Diagnostic criteria for IIH were developed in 1937 by the Baltimore neurosurgeon Walter Dandy; Dandy also introduced subtemporal decompressive surgery in the treatment of the condition.9 The criteria was modified by Smith in 1985 to become the ‘modified Dandy criteria’. Smith included the use of more advanced imaging: Dandy had required ventriculography, but Smith replaced this with CT. In a 2001 paper, Digre and Corbett amended Dandy’s criteria further.10

The second theory posits that either increased blood flow to the brain or increase in the brain tissue itself may result in the raised pressure. Little evidence has accumulated to support the suggestion that increased blood flow plays a role, but both biopsy samples and various types of brain scans have shown an increased water content of the brain tissue. It remains unclear why this might be the case.1

Modified Dandy Criteria10

The third theory suggests that blood flow from the brain may be impaired or congested. Only in a small proportion of patients has underlying narrowing of the cerebral sinuses or veins been demonstrated.

Congestion of venous blood may result from a generally increased venous pressure, which has been linked to obesity.1,5 Farb and colleagues have demonstrated that, in a series of 29 patients with IIH, narrowing of the

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Symptoms of raised ICP (headache, nausea, vomiting, transient visual obscurations or papilledema)

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No localizing signs with the exception of abducens (sixth) nerve palsy

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The patient is awake and alert

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Normal CT/MRI findings without evidence of thrombosis

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LP opening pressure of >25 cmH2O and normal biochemical and cytological composition of CSF

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No other explanation for the raised ICP

In a 2002 review, Friedman and Jacobson proposed an alternative set of criteria, derived from Smith’s. These required the absence of symptoms that could not be explained by a diagnosis of IIH, but did not required

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case report the actual presence of any symptoms (such as headache) attributable to IIH. These criteria also required that the lumbar puncture was performed with patient lying sideways, as a lumbar puncture performed in the upright sitting position could lead to artificially high pressure measurements. Friedman and Jacobson also did not insist on MR venography for every patient; rather, it was required only in atypical cases.11 On average, IIH occurs in about one per 1,00,000 people, and can occur in children and adults. The median age at diagnosis is 30. IIH occurs predominantly in women, especially in the ages 20-45, who are 4-8 times more likely than men to be affected. Overweight and obesity strongly predispose a person to IIH: Women who are more than 10% over their ideal body weight are 13 times more likely to develop IIH, and this figure goes upto 19 times in women who are more than 20% over their ideal body weight. In men, this relationship also exists, but the increase is only 5-fold in those over 20% above their ideal body weight.1 In 1994, Radhakrishnan et al reviewed the literature on IIH associated with other diseases and with drugs. The following data were obtained from this 1994 study and subsequent case reports.12 Increased venous red blood cell aggregation and relatively elevated fibrinogen concentration were demonstrated in patients with IIH compared with matched controls.13 The retinol/retinol-binding protein ratio is elevated in the CSF of patients with IIH compared with non-IIH neurologic controls and with normal controls.14 Because IIH is concentrated in women between puberty and menopause, Fraser and colleagues emphasized the potential role of sex hormones in the pathogenesis of IIH. They also point out that obstructive sleep apnea has been proposed as a risk factor. Since women taking exogenous estrogen and pregnant women are not at particular risk for IIH, they suggest that low levels of testosterone may be the important hormonal link in women with IIH.15 Headache, often unusually severe, is the most common presenting symptom. The headaches are often lateralized and throbbing or pulsatile in character.

They may be intermittent or persistent, daily in some, associated with nausea and vomiting in some.

In addition, a subset of patients describe headache exacerbation with changes in posture and some may report that relief occurs with nonsteroidal antiinflammatory medications and/or rest.

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Retrobulbar pain and pain with eye movement or globe compression are somewhat more specific features for IIH. In some patients, the pain follows a trigeminal or cervical nerve root distribution.

Neck stiffness is also commonly reported. Among younger children, headache is a less universal finding.

In one series, 29% of children with IIH did not have headache, and men are less likely than women to note HA. Transient visual obscurations: Occur in about twothirds of patients with papilledema. These last seconds at a time and can be bilateral or unilateral.

Position changes: Some patients note that these can be precipitated by changes in position (usually standing, but sometimes lying down or bending over), Valsalva, bright light or eye movement. The occurrence of transient visual obscurations does not appear to correlate with the degree of ICP elevation or the extent of disc swelling, and doesn’t predict future visual loss.

Photopsias, brief sparkles or flashes of light, can also occur in patients with IIH and, similar to visual obscurations, can be provoked by positional changes and Valsalva.

Pulsatile tinnitus is common in IIH and in the setting of headache is somewhat specific for the diagnosis.

Patients often describe hearing rushing water or wind.

This symptom can be persistent or intermittent and is believed to represent vascular pulsations transmitted

by CSF under high pressure to the venous sinuses.

Diplopia (Double Vision): Patients with IIH may report intermittent or continuous horizontal diplopia.

On Examination The most common signs of PTC/IIH are: ÂÂ

Papilledema

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Visual field loss

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Sixth nerve palsy

Papilledema is optic disc swelling that is caused by increased ICP. Papilledema is the hallmark sign of PTC/IIH. Severity of the papilledema relates to risk of permanent visual loss. Patients with more severe papilledema are at higher risk of permanent visual loss. ÂÂ

Visual loss: Loss of vision is the major morbidity in IIH and may be present on initial evaluation.

Vision loss is usually gradual but can be abrupt.

Such patients have a more fulminant course and more significant permanent vision loss.

case report ÂÂ

ÂÂ

Visual field loss occurs before loss of acuity: Confrontation visual fields are abnormal (nasal loss, temporal loss, visual blurring) in upto 32% at presentation.

Medications ÂÂ

Glaucoma drugs: One of the first drugs usually tried is tablet acetazolamide 500 mg twice-daily is the usual dose, a glaucoma drug that reduces the production of CSF by at least 50%. Possible side effects include stomach upset, fatigue, tingling of fingers, toes and mouth, and kidney stones

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Diuretics: If acetazolamide alone isn’t effective, it’s sometimes combined with furosemide, a potent diuretic that reduces fluid retention by increasing urine output.

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Migraine medications: Medications typically prescribed to relieve migraines can sometimes ease the severe headaches that often accompany PTC.

Cranial nerve deficits: Cranial nerve deficits are not uncommon with IIH and can resolve with IIH treatment.

MRI: Brain MRI with gadolinium enhancement is probably the study of choice for all patients with IIH since it provides sensitive screening for hydrocephalus, intracerebral masses, meningeal infiltrative or inflammatory disease, and dural venous sinus thrombosis. In a retrospective study of imaging features that have been suggested as typical for patients with IIH, only flattening of the posterior globe was found statistically to be a reliable indicator of IIH, with a specificity of 100% and a sensitivity of 43.5%.16 MR venography: MR venography can be useful for patients who are at greater risk for dural venous sinus thrombosis, such as those with suspected thrombosis on MRI, nonobese or male individuals, or those with a documented procoagulant state. Sagittal T1-weighted images often provide excellent views of the superior sagittal sinus, and these typically are included in routine MRI. Extraluminal narrowing of the transverse sinuses may be a typical feature of IIH as reported by Farb and coworkers.6 CT scan: Brain CT scan is less expensive than MRI and is adequate to rule out larger tumors or lesions, but it is not as sensitive as MRI for meningeal infiltration and/ or dural venous sinus thrombosis.

Ultrasonography: In the emergency department, bedside ultrasonography has been used to identify intracranial hypertension by measuring the diameter of the optic nerve sheath.17 Lumbar puncture ideally is carried out with the patient in the lateral decubitus position with due care to prevent cerebellar herniation. Because finding landmarks is difficult in obese patients, the tap frequently is performed with the patient seated.

Therefore, note that an opening pressure of 500 mm water is extremely high in the lateral decubitus position, but is normal for the sitting position. If possible, the patient should be moved to lateral decubitus position before measuring the pressure.

Treatment typically begins with medications to control the symptoms. Weight loss is recommended for obese individuals. If your vision worsens, surgery to reduce the pressure around your optic nerve or to decrease the ICP may be necessary. Once you’ve had PTC, you should have your vision checked regularly.

Surgery ÂÂ

Optic nerve sheath fenestration: This procedure cuts a window into the membrane that surrounds the optic nerve. This allows excess CSF to escape.

Vision stabilizes or improves in more than 85% of cases. Most people who have this procedure done on one eye notice a benefit for both eyes. However, this surgery isn’t always successful and may even increase vision problems.

ÂÂ

Spinal fluid shunt: Another type of surgery inserts a long, thin tube - called a shunt - into your brain or lower spine to help drain away excess CSF. The tubing is burrowed under your skin to your abdomen, where the shunt discharges the excess fluid. Symptoms improve for more than 80% of the people who undergo this procedure.

Weight Loss is Critical Obesity dramatically increases a young woman’s risk of PTC. In fact, a weight gain of as little as 5% of your body weight can increase the risk - even in women who aren’t obese.

Losing extra pounds and maintaining a healthy weight may help reduce your chances of developing this potentially sight-stealing disorder. The importance of weight loss as the only effective means of reducing the papilledema and with it, the threat of progressive blindness, cannot be overemphasized.18,19

Acknowledgment We are grateful to Dr Pankaj R Patel, Hon. Dean, Smt. NHL Municipal Medical College; Dr ST Malhan, Dy. Superintendent, Sheth VS General Hospital.

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case report We are thankful for the help and support of Dr Mitesh N Suthar, Assistant Professor, Dr Mansurali Ambliyasana and Dr Sanket Dalwadi, Junior Residents of our unit.

REFERENCEs 1. Binder DK, Horton JC, Lawton MT, McDermott MW. Idiopathic intracranial hypertension. Neurosurgery 2004;54(3):538-51; discussion 551-2.

2. Quincke HI. “Meningitis serosa”. Samml Klin Vortr 1893:67: 655.

3. Nonne M. “Ueber Falle vom Symptomkomplex “Tumor Cerebri” mit Ausgang in Heilung (Pseudotumor Cerebri)” (in German). Dtsch Z Nervenheilk 1904;27 (3-4):169-216.

4. Jindal M, Hiam L, Raman A, Rejali D. Idiopathic intracranial hypertension in otolaryngology. Eur Arch Otorhinolaryngol 2009;266(6):803-6.

5. Acheson JF. Idiopathic intracranial hypertension and visual function. Br Med Bull 2006;79-80(1):233-44.

6. Farb RI, Vanek I, Scott JN, Mikulis DJ, Willinsky RA, Tomlinson G, terBrugge KG. Idiopathic intracranial hypertension: the prevalence and morphology of sinovenous stenosis. Neurology 2003;60(9):1418-24.

7. Bateman GA. Association between arterial inflow and venous outflow in idiopathic and secondary intracranial hypertension. J Clin Neurosci 2006;13(5):5506; discussion 557.

8. Bateman GA. Arterial inflow and venous outflow in idiopathic intracranial hypertension associated with venous outflow stenoses. J Clin Neurosci 2008; 15(4):402-8.

9. Dandy WE. Intracranial pressure without brain tumor: diagnosis and treatment. Ann Surg 1937;106(4):492-513.

10. Digre KR, Corbett JJ. Idiopathic intracranial hypertension (pseudotumor cerebri): a reappraisal. Neurologist 2001 Jan 7: 2-67.

11. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension.

Neurology 2002;59(10):1492-5.

12. Radhakrishnan K, Ahlskog JE, Cross SA, Kurland LT, O’Fallon WM. Idiopathic intracranial hypertension (pseudotumor cerebri). Descriptive epidemiology in Rochester, Minn, 1976 to 1990. Arch Neurol 1993;50(1): 78-80.

13. Kesler A, Yatziv Y, Shapira I, Berliner S, EB. Increased red blood cell aggregation in with idiopathic intracranial hypertension. A unexplored pathophysiological pathway.

Haemost 2006;96(4):483-7.

Assayag patients hitherto Thromb

14. Warner JE, Larson AJ, Bhosale P, Digre KB, Henley C, Alder SC, et al. Retinol-binding protein and retinol analysis in cerebrospinal fluid and serum of patients with and without idiopathic intracranial hypertension.

J Neuroophthalmol 2007;27(4):258-62.

15. Fraser JA, Bruce BB, Rucker J, Fraser LA, Atkins EJ, Newman NJ, et al. Risk factors for idiopathic intracranial hypertension in men: a case-control study. J Neurol Sci 2010;290(1-2):86-9.

16. Agid R, Farb RI, Willinsky RA, Mikulis DJ, Tomlinson G. Idiopathic intracranial hypertension: the validity of cross-sectional neuroimaging signs. Neuroradiology 2006;48(8):521-7.

17. Stone MB. Ultrasound diagnosis of papilledema and increased intracranial pressure in pseudotumor cerebri.

Am J Emerg Med 2009;27(3):376.e1-376.e2.

18. Rowe FJ, Sarkies NJ. Assessment of visual function in idiopathic intracranial hypertension: a prospective study.

Eye (Lond) 1998;12(Pt 1):111-8.

19. Kupersmith MJ, Gamell L, Turbin R, Peck V, Spiegel P, Wall M. Effects of weight loss on the course of idiopathic intracranial hypertension in women. Neurology 1998;50(4):1094-8.

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Insomnia Triples Risk of Heart Failure The risk of developing heart failure triples for people who suffer from insomnia.

The finding came from a new study, the largest yet to examine the association, and was published in the European Heart Journal.

Health Secretary Plans to Tackle UK’s High Cardiovascular Disease Death Rate Health Secretary Jeremy Hunt has just announced that the UK is developing a new plan to tackle cardiovascular disease (CVD) which could save upto 30,000 lives over the next several years.

The UK is behind a lot of other western countries in managing CVDs. Jeremy Hunt said that he hopes to change that, as he is striving to make life expectancy in England one of the top in Europe.

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Photo Quiz

Nerve Damage from Soft Tissue Injury to the Forearm

A

24-year-old man sustained penetrating soft tissue injuries just distal to the center of the medial right forearm. Surgery was performed immediately to stabilize his wounds and later to reattach the tendons of his forearm.

The patient had sensory loss to his hand but denied any pain. Motor examination revealed that he had the ability to pronate and supinate the forearm; flex and extend the wrist; and form a normal “OK” sign, with his thumb and index finger pinched together. Figure 1 demonstrates the patient’s attempt to actively open his hand and extend the metacarpophalangeal (MCP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints of his dominant right hand. Figure 2 shows the patient’s hands at rest.

Figure 1.

Question Based on the patient’s history and physical examination, which one of the following nerves was most likely injured?

A. Anterior interosseous nerve.

B. Median nerve.

C. Posterior interosseous nerve.

D. Radial nerve.

E. Ulnar nerve.

Figure 2.

See the following page for discussion.

Source: Adapted from Am Fam Physician. 2009;79(9):793-794.

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photo quiz Summary Table

Figure 3. Muscle wasting and atrophy (arrow) in a patient with ulnar nerve injury to the forearm.

Injured nerve

Characteristics

Anterior interosseous

Inability to form the “OK” sign normally, with the thumb and index finger pinched together; weakened pronation

Median

Thenar eminence wasting; sensory loss to the thumb, index finger, and middle finger; benediction hand

Posterior interosseous

Inability to extend the wrist (wristdrop) without sensory loss to the dorsum of the hand

Radial

Wristdrop with sensory loss to the dorsum of the hand

Ulnar

Clawhand; motor deficits of the intrinsic muscles of the hand; first dorsal interosseous wasting; hypothenar eminence wasting

Discussion The answer is E: ulnar nerve. The patient has the typical presentation of a clawhand, with injury to the ulnar nerve in the forearm. The ulnar nerve originates from the brachial plexus and contains motor and sensory fibers from the C8 and T1 roots.1,2 It innervates many intrinsic muscles of the hand, as well as extrinsic muscles for flexion of the ring and little fingers to allow for the power grip.3 When the patient extends his fingers, the MCP, PIP, and DIP joints remain flexed. The MCP joints flex with passive pull of the denervated medial half of the flexor digitorum profundus muscle, whereas the DIP and PIP joints remain in flexion because of paralysis of the medial lumbrical muscles. Sensory loss is noted in palmar and distal dorsal surfaces of the little finger and in the medial half of the ring finger. Muscle wasting and atrophy of the first dorsal interosseous muscle are present (Figure 3).

Traumatic injury is the most common cause of ulnar nerve damage,4 although leprosy is associated with ulnar nerve lesions. First-degree injury (neurapraxia) is usually reversible within two to three months. Seconddegree injury (axonotmesis) involves axon degeneration distal to the injury site. Recovery is possible, with recovery time dependent on the distance from the injury to the end organ. Third-degree injury (neurotmesis) involves complete disruption of the nerve with little potential for recovery.1 The anterior interosseous nerve is a branch of the median nerve. It innervates the flexor pollicis longus, the lateral half of the flexor digitorum profundus, and the pronator quadratus muscles.

Persons with injury to the anterior interosseous nerve are unable to form a normal “OK” sign.

The median nerve innervates the thenar compartment, allowing for fine control of the pincer grip.2,3 Damage to the median nerve causes motor and sensory loss to

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the thumb, index finger, and middle finger. The clinical picture is similar to that of ulnar nerve injury, except in presentation when the patient attempts to close the hand, rather than open it. The unopposed action of the extensors of the index and middle fingers prevents full flexion as the ring and little fingers flex normally.

Disruption of the flexor digitorum profundus muscle (innervated by the median nerve laterally) causes benediction hand. The posterior interosseous nerve, the deep branch of the radial nerve, is a purely motor nerve. It innervates the extensor muscles of the wrist, hand, thumb, and index finger. Damage to the posterior interosseous nerve leads to the inability to extend the wrist, or wristdrop, without sensory loss to the dorsum of the hand. The radial nerve divides into the superficial and the deep branch (posterior interosseous nerve) at the lateral epicondyle. The superficial branch is a purely sensory nerve. Injury to the superficial branch causes sensory loss in the dorsum of the hand without motor deficits.2 Injury proximal to the branching leads to wristdrop and sensory loss.

REFERENCES 1. Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder and elbow in the athlete. Clin Sports Med. 2006;25(3):465-487.

2. Braddom RL. Physical Medicine and Rehabilitation. 2nd ed. Philadelphia, Pa: Saunders 2000.

3. Daniels JM II, Zook EG, Lynch JM. Hand and wrist injuries: part I. Non-emergent evaluation. Am Fam Physician.

2004;69(8):1941-1948.

4. Wheeless CR. Duke Orthopaedics. Wheeless’ Textbook of Orthopaedics. Intrinsic weakness and claw hand. http:// www.wheelessonline.com/ortho/intrinsic_weakness_ and_claw_hand. Accessed January 27, 2009.

Practice guidElines

ACC and AHA Update on Chronic Heart Failure Guidelines

I

n 2009, the American College of Cardiology (ACC) and the American Heart Association (AHA) published a focused update of the ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult. The guidelines writing committee reviewed recent trial data and other clinical information in the revision process for the 2009 update.

(NT-proBNP) testing for patient evaluation. According to the update, patients with left ventricular dysfunction or heart failure generally present in one of three ways: with a syndrome of decreased exercise tolerance; with a syndrome of fluid retention; or with no symptoms, or symptoms of another cardiac or noncardiac disorder.

The 2005 guidelines described four stages (i.e., stages A, B, C, and D) in the development of heart failure (Figure 1). Patients in stages A and B do not have heart failure, but have risk factors that predispose them toward the development of heart failure. Patients in stage C comprise the majority of patients with heart failure—those who have current or past symptoms of heart failure associated with underlying structural heart disease. Patients in stage D have refractory heart failure and may be eligible for specialized, advanced treatments (e.g., mechanical circulatory support, fluid removal procedures, continuous inotropic infusions, cardiac transplantation) or end-of-life care, such as hospice.

2009 updated recommendation: Measurement of natriuretic peptides (i.e., BNP and NT-proBNP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of heart failure is uncertain.

Measurement of natriuretic peptides can be useful in risk stratification. (Level of Evidence: A) The 2005 guidelines also recommended measurement of BNP for evaluating patients who present in the urgent care setting with possible heart failure; the 2009 update expanded this recommendation to include the measurement of NTproBNP. The level of evidence remained the same for this recommendation. The 2009 update warns that, although elevated natriuretic peptide levels may help confirm a suspected diagnosis of heart failure, the results of this testing alone should not be used to confirm or exclude a heart failure diagnosis.

Updated Recommendations

Reduced LVEF

Updates to the 2005 guidelines are included in sections about the evaluation of patients presenting with heart failure; patients with reduced left ventricular ejection fraction (LVEF); patients with refractory end-stage heart failure; and the treatment of special population groups (e.g., blacks). The updated guidelines also contain a new section with recommendations about heart failure in the hospitalized patient.

The section of the guidelines on patients with reduced LVEF included minor updates on recommendations about the use of angiotensin-II receptor blockers (ARBs) and exercise testing.

Evaluation of Heart Failure Updates to the section on the evaluation of patients presenting with heart failure were made to clarify the role of functional assessment beyond the New York Heart Association (NYHA) classification, and to expand on the use of brain natriuretic peptide (BNP) and N-terminal prohormone brain natriuretic peptide

Source: Adapted from Am Fam Physician. 2010 1;81(5):654-665.

2009 updated recommendation: Use of ARBs is recommended in patients with current or previous symptoms of heart failure and reduced LVEF who have an intolerance to angiotensinconverting enzyme (ACE) inhibitors. (Level of Evidence: A) For this recommendation, the 2009 update modified the text in the 2005 guidelines by eliminating mention of specific agents tested.

2009 updated recommendation: Maximal exercise testing with or without measurement of respiratory gas exchange is reasonable to facilitate prescription of an appropriate exercise program for patients presenting with heart failure. (Level of Evidence: C) The 2009 update changed the class of recommendation from class I (i.e., treatment should be performed) to class IIa (i.e., treatment is reasonable to perform).

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practice guidelines

At risk of heart failure

Management of Patients who have or are at risk of Heart Failure Stage A: At high risk of heart failure, but without structural heart disease or symptoms of heart failure Includes patients with: Atherosclerotic disease Diabetes mellitus Hypertension Metabolic syndrome Obesity Or patients: Using cardiotoxins With a family history of cardiomyopathy

Therapy Goals: Control metabolic syndrome Discourage alcohol intake and illicit drug use Encourage regular exercise Encourage smoking cessation Treat hypertension Treat lipid disorders Drugs: ACE inhibitors or ARBs in appropriate patients for vascular disease or diabetes

Structural heart disease

Stage B: Structural heart disease but without signs or symptoms of heart failure Includes patients with: Asymptomatic valvular disease Left ventricular remodeling, including left ventricular hypertrophy and low ejection fraction Previous myocardial infarction

Therapy Goals: All measures under stage A Drugs: ACE inhibitors or ARBs in appropriate patients Beta blockers in appropriate patients Devices in selected patients: Implantable cardioverter-defibrillators

Development of symptoms of heart failure

Heart failure

Stage C: Structural heart disease, with previous or current symptoms of heart failure Includes patients with: Known structural heart disease and Shortness of breath and fatigue, reduced exercise tolerance

Therapy Goals: Drugs in selected patients: All measures under stages A and B Aldosterone antagonists Restrict dietary sodium ARBs Digitalis Drugs for routine use: Hydralazine/nitrates ACE inhibitors Beta blockers Devices in selected patients: Diuretics for fluid retention Biventricular pacing Implantable cardioverterdefibrillators

Refractory symptoms of heart failure at rest

Stage D: Refractory heart failure requiring specialized interventions Includes patients who have marked symptoms at rest despite maximal medical therapy (e.g., those who are recurrently hospitalized or cannot be safely discharged from the hospital without specialized interventions)

Therapy Goals: All measures under stages A, B, and C Decide appropriate level of care Options: Compassionate end-of-life care, hospice Extraordinary measures (e.g., chronic inotropes, experimental drugs or surgery, heart transplant, permanent mechanical support)

Figure 1. Algorithm of the stages in the development of heart failure, with recommended therapy for patients by stage.

ACE = Angiotensin-converting enzyme; ARB = Angiotensin-II receptor blocker.

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practice guidelines The section on patients with reduced LVEF also included several changes to recommendations concerning implantable cardioverter-defibrillator therapy and cardiac resynchronization therapy.

2009 updated recommendation: Implantable cardioverterdefibrillator therapy is recommended for the primary prevention of sudden cardiac death to reduce total mortality in patients with non-ischemic dilated cardiomyopathy or ischemic heart disease at least 40 days after myocardial infarction (MI); an LVEF of 35 percent or less; and NYHA functional class II or III symptoms while receiving chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for longer than one year. (Level of Evidence: A) This recommendation was modified in the 2009 update to be consistent with the 2008 Device-Based Therapy guidelines from the ACC, AHA, and Heart Rhythm Society (HRS). It replaces recommendations from the 2005 guidelines on implantable cardioverter-defibrillator therapy for patients with ischemic heart disease at least 40 days after MI (2005 Level of Evidence: A) or nonischemic cardiomyopathy (2005 Level of Evidence: B) with an LVEF of 30 percent or less, and for patients with an LVEF of 30 to 35 percent of any origin (2005 Level of Evidence: B).

In two of the major trials reviewed by the guidelines committee, no survival benefit was observed from implantable cardioverter-defibrillator therapy until after the first year of recovery from an acute coronary event. Patients with heart failure and low ejection fraction are typically older than 70 years, although this patient population was not well represented in the trials.

Physicians should consider common comorbidities in older adults (e.g., previous stroke, chronic pulmonary disease, arthritic conditions) when discussing this type of therapy with patients.

Medication may substantially improve LVEF; therefore, consideration of implantable cardioverterdefibrillator therapy should follow documentation of sustained reduction of LVEF despite a course of beta blockers and ACE inhibitors or ARBs. Implantable cardioverter-defibrillator therapy is not warranted in patients with refractory heart failure (stage D) or in those with concomitant diseases that would shorten their life expectancy independent of heart failure.

Before implantation, physicians should inform patients of the effectiveness, safety, and mortality risks of implantable cardioverter-defibrillator therapy; of the morbidity associated with an implantable cardioverterdefibrillator shock; and that the therapy does not improve clinical function or delay progression of heart failure.

2009 updated recommendation: Patients with LVEF of 35 percent or less, sinus rhythm, and NYHA functional class III or ambulatory class IV symptoms despite recommended, optimal medical therapy and who have cardiac dyssynchrony (i.e., a QRS duration of 0.12 seconds or more) should receive cardiac resynchronization therapy, with or without an implantable cardioverter-defibrillator, unless contraindicated.

(Level of Evidence: A) The 2009 recommendation was updated to clarify that cardiac resynchronization therapy may be indicated for patients with or without an implantable cardioverter-defibrillator. Evidence shows that cardiac resynchronization therapy can improve symptoms, exercise capacity, quality of life, LVEF, and survival; it can also decrease hospitalizations in patients with persistently symptomatic heart failure receiving optimal medical therapy who have cardiac dyssynchrony. The use of an implantable cardioverterdefibrillator in addition to cardiac resynchronization therapy should be based on the indications for implantable cardioverter-defibrillator therapy.

End-stage Heart Failure The section of the guidelines on patients with refractory end-stage heart failure (stage D) included a modified recommendation on intermittent infusions.

2009 updated recommendation: Routine intermittent infusions of vasoactive and positive inotropic agents are not recommended for patients with refractory end-stage heart failure. (Level of Evidence: A) The 2009 update changed the level of evidence from B to A for this recommendation, based on evidence from an additional multicenter trial. Intermittent outpatient infusions of vasoactive medications (e.g., nesiritide) or positive inotropic medications have not been shown to improve symptoms or survival in patients with advanced heart failure.

New Recommendations

Hydralazine/Nitrates New recommendation to 2009 update: The combination of hydralazine and nitrates is recommended to improve outcomes for patients with reduced LVEF whose ethnicity is self-described as African American and who have moderate to severe symptoms on optimal therapy with ACE inhibitors, beta blockers, and diuretics. (Level of Evidence: B) Analysis of vasodilator trials showed effectiveness of treatment with isosorbide dinitrate and hydralazine in black participants. Adding these medications to standard therapy with an ACE inhibitor, a beta blocker, or both proved to be beneficial in a subsequent trial.

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practice guidelines Accordingly, this combination is recommended for black patients who remain symptomatic despite optimal medical therapy. However, patient compliance with this combination may be low because of the large number of tablets required and the high incidence of adverse reactions. The combination treatment should not be prescribed in patients who have not previously used an ACE inhibitor, nor should it be substituted for ACE inhibitors in those who are tolerating them without difficulty. It is unclear if this combination is beneficial in non-black patients.

Atrial Fibrillation and Sinus Rhythm New recommendation to 2009 update: It is reasonable to treat patients who have atrial fibrillation and heart failure with strategies to maintain sinus rhythm or to control ventricular rate alone. (Level of Evidence: A)â&#x20AC;ŻFour trials evaluated the effectiveness and safety of restoring and maintaining sinus rhythm in patients with atrial fibrillation.

There were equivalent outcomes for restoring and maintaining sinus rhythm by electrical or pharmacologic conversion compared with controlling ventricular rate in patients with atrial fibrillation. Most patients quickly relapse to atrial fibrillation unless they are treated with a class I or III antiarrhythmic medication, but patients with heart failure are not likely to respond favorably to class I medications. Class III antiarrhythmic medications (e.g., sotalol, dofetilide, amiodarone) can maintain sinus rhythm in some patients, although treatment is associated with an increased risk of organ toxicity (amiodarone) and proarrhythmia (dofetilide).

Cardiac Resynchronization Therapy New recommendations to 2009 update: For patients who have LVEF of 35 percent or less, a QRS duration of 0.12 seconds or more, and atrial fibrillation, cardiac resynchronization therapy, with or without an implantable cardioverter-defibrillator, is reasonable for the treatment of NYHA functional class III or ambulatory class IV heart failure symptoms on optimal recommended medical therapy.

(Level of Evidence: B) Cardiac resynchronization therapy is reasonable for patients with LVEF of 35 percent or less with NYHA functional class III or ambulatory class IV symptoms who are receiving optimal recommended medical therapy and who have frequent dependence on ventricular pacing.

(Level of Evidence: C)â&#x20AC;ŻCardiac resynchronization therapy recommendations were added to be consistent with the ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities.

New Section: The Hospitalized Patient The 2009 update includes a new section on the evaluation and treatment of heart failure in patients

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who are hospitalized. Patients may require hospitalization if they develop acute or progressive symptoms of heart failure. Generally there are three clinical profiles for these patients: those who have volume overload (manifested by pulmonary and/or systemic congestion and often precipitated by an acute increase in chronic hypertension); those with profound depression of cardiac output (manifested by hypotension, renal insufficiency, and/or a shock syndrome); and those with signs and symptoms of fluid overload and shock. Patients with heart failure and preserved LVEF are just as likely to be admitted to the hospital as those with heart failure and low LVEF. Patients are usually admitted to the hospital following a concomitant cardiovascular or cerebrovascular event, and admission often is related to medical or dietary noncompliance. Other common factors that precipitate hospitalization for heart failure include acute myocardial ischemia; uncorrected high blood pressure; atrial fibrillation and other arrhythmias; recent addition of negative inotropic medications; pulmonary embolus; use of nonsteroidal anti-inflammatory drugs; excessive alcohol or illicit drug use; endocrine abnormalities (e.g., diabetes mellitus, hyperthyroidism, hypothyroidism); and concurrent infections (e.g., pneumonia, viral illnesses).

Inpatient Evaluation and Diagnosis The diagnosis of heart failure in hospitalized patients should be based primarily on signs and symptoms, including volume status, the adequacy of circulatory support or perfusion, and consideration of precipitating factors or comorbidities. Many of the evaluation steps are identical to those used in the initial evaluation of heart failure. For an uncertain diagnosis of heart failure, plasma BNP or NT-proBNP concentrations should be considered in patients being evaluated for dyspnea who have signs and symptoms compatible with heart failure. In patients who have already been diagnosed with heart failure, it is important to understand what has caused the clinical symptoms to worsen.

Acute MI is an important cause of worsening or new-onset heart failure, and criteria for an acute coronary event that might indicate the need for further intervention may be present in up to 20 percent of patients hospitalized for heart failure. However, several other patients may have low levels of detectable troponins that do not meet criteria for an acute ischemic event, but that are typical of chronic heart failure with an acute exacerbation. For patients with newly discovered heart failure, physicians should keep in mind the causative role of coronary artery disease in heart failure and be certain that coronary structure

practice guidelines and function are well delineated. Therefore, coronary visualization may be an important step in the evaluation of patients hospitalized with heart failure.

Inpatient Treatment A careful review of each patientâ&#x20AC;&#x2122;s maintenance medications for heart failure is important, and medication adjustments may be necessary as a result of the hospitalization. The majority of patients should continue taking their medications during hospitalization, and most are able to tolerate the continuation of beta blockers, which results in better outcomes.

Patients with substantial fluid overload on hospital admission should be treated with loop diuretics, initiated upon arrival to the emergency department.

After admission, careful and frequent evaluation and monitoring are important and include assessing volume status and circulatory support; monitoring daily weight and vital signs; managing daily fluid input and output; and assessing daily electrolyte levels and renal function, which should be performed while intravenous diuretics or active heart failure medication titration is being done. Optimal dosing of diuretics should produce a rate of diuresis that will benefit volume status and relieve signs and symptoms of congestion without inducing an excessively rapid reduction in intravascular volume, possibly resulting in hypotension, renal dysfunction, or both. Limiting sodium intake and dosing the diuretic multiple times daily can enhance diuresis effectiveness. Patients who present with congestion and moderate to severe renal dysfunction may have a blunted response to diuretics, requiring higher initial doses. If all diuretic strategies are unsuccessful, ultrafiltration or another renal replacement strategy may be considered, as well as consultation with a kidney subspecialist.

Intravenous vasodilators may be added to the treatment regimen in patients who have adequate blood pressure and ongoing congestion that does not adequately respond to diuretics and standard oral therapy. The goals of vasodilator therapy include a more rapid resolution of congestive symptoms; relief of anginal symptoms while awaiting coronary intervention; control of hypertension; and improvement of hemodynamic abnormalities before beginning oral medications for heart failure.

Patients presenting with predominantly low output syndrome or combined congestion and low output

may be considered for intravenous inotropes (e.g., dopamine, dobutamine, milrinone), which may help relieve symptoms caused by poor perfusion and preserve end-organ function in those with severe systolic dysfunction and dilated cardiomyopathy. These medications are most beneficial in patients with relative hypotension and who have intolerance or no response to vasodilators and diuretics. However, the use of inotropes indicates a poor prognosis, and a thorough hemodynamic assessment is necessary. There is no evidence of benefit for routine use of these agents in patients with acute heart failure caused by congestion only; therefore, inotropes should be limited to carefully selected patients with low blood pressure and reduced cardiac output, who will require close monitoring of blood pressure and heart rhythm.

Routine invasive hemodynamic monitoring is not indicated for most patients hospitalized with symptoms of worsening heart failure, but should be considered in those whose volume and filling pressures are uncertain or who are refractory to initial therapy, particularly when filling pressures and cardiac output are unclear.

Routine invasive hemodynamic monitoring also may be beneficial in patients with clinically significant hypotension (i.e., systolic blood pressure typically less than 90 mm Hg or symptomatic low systolic blood pressure) or worsening renal function during initial therapy. Invasive hemodynamic monitoring should be performed in patients with presumed cardiogenic shock that requires escalating pressor therapy and consideration of mechanical support; those with severe clinical decompensation in whom therapy is limited by uncertainty regarding relative contributions of elevated filling pressures, hypoperfusion, and vascular tone; those with apparent dependence on intravenous inotropic infusions after initial clinical improvement; or those with persistent, severe symptoms despite adjustment of recommended treatments.

As patients stabilize and volume status normalizes, oral therapy for heart failure should be initiated or resumed. Caution should be used when starting beta blockers in patients who were treated with inotropes while hospitalized, or when initiating ACE inhibitors in patients who had marked azotemia. Before discharge, patients should be fully transitioned off all intravenous therapy, and oral therapy should be adjusted and maximized. Patients should be given written discharge instructions or educational materials that address activity level, diet, discharge medications, follow-up appointments, weight monitoring, and what to do if symptoms worsen.

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Around the globe

News and Views Spironolactone disappoints in preservedEF HF: Aldo-DHF in print A year of aldosterone blockade failed to improve exercise capacity, symptoms or quality-of-life measures in a placebo-controlled trial of >400 patients with heart failure and LV ejection fractions >50%. However, spironolactone treatment in the study led to significant gains in echocardiographic measures of diastolic function. (Source: Medscape) Nicotine vaccine promising for smoking cessation An experimental nicotine vaccine reduces the amount of nicotine that reaches the brain and binds to nicotinic acetylcholine receptors (nAChRs), helping to reduce cigarette use and cravings, new research shows.

However, at least one expert has some misgivings about its potential as an effective treatment. (Source: Medscape) Increased dietary sugar drives global rise in diabetes The increasing availability of sugary food and drinkindependent of excess calories, excess weight or a sedentary lifestyle - explains part of the rise in cases of type 2 diabetes worldwide, suggests a new study published online February 27 in PLoS ONE. (Source: Medscape) Availability Of Sugar May Impact A Country’s Diabetes Rate A study, published in PLoS One, found, “in the 175 countries studied,” that “a 150-calorie daily increase in the availability of sugar - about the equivalent of a can of Coke or Pepsi - raises the prevalence of type 2 diabetes by 1.1%.”

Cholesterol trial shut down An increase in adverse events, in particular myopathy led to the shut down of a pivotal trial of Tredaptive, the agent that many hoped would improve niacin tolerance.

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At 3.9 years of follow-up, one-quarter of the patients randomized to Tredaptive, a combination of extended-release niacin and the anti-flushing agent laropiprant, had discontinued treatment because of side effects compared with 16.6% of patients in the control arm, according to Jane Armitage, FFPH, FRCP, from the University of Oxford, and colleagues. The finding comes from a substudy of HPS2-THRIVE published online in the European Heart Journal.

Fatal MI more likely after sibling dies The death of an adult brother or sister may boost one’s own risk of dying from a heart attack in the following years, a population-based study showed.

(Source: Medpage Today) Six factors best predict Afib risk in women Researchers have devised a simple method for determining 10-year atrial fibrillation (Afib) risk in women, and the method gained very little when combined with genetic risk markers. (Source: Medpage Today) AIDA STEMI substudy: No benefit for intracoronary abciximab for STEMI PCI A substudy of the AIDA STEMI trial has found no benefit of intracoronary versus intravenous abciximab administration on myocardial damage and/or reperfusion injury in patients with STEMI undergoing PCI. In the analysis, researchers enrolled a subset of 795 patients from the AIDA STEMI trial and used cardiac magnetic resonance (CMR) to visualize myocardial damage and reperfusion injury within one week.

Sitting less trims diabetes risk Just getting out of the chair and moving a little may help ward off type 2 diabetes among individuals at risk even more than engaging in strenuous physical activity, British researchers found. (Source: Medpage Today)

Medi Law

A Decoy Operation for Catching the Violators of the PC-PNDT Act. Is it Lawful? mC Gupta

Q. Is it legal to carry out a decoy operation for catching the violators of the PC-PNDT Act? If yes, what are the guidelines for the same?

Upon learning that the decoy operation has been successful, Appropriate Authorities should take the accused in their custody.

See to it that the accused is not able to make phone calls to anybody. All his phones should be switched off and other contacts not reachable.

Search for the currency notes, verify and record after a Panchnama.

Take a statement from the accused after inquiry.

Statements from the co-accused (other paramedical staff, agent, PRO) should also be taken.

The center should be thoroughly inspected and all important documents in the case should be seized and sealed.

All authorized, unauthorised machines should be taken into custody after sealing them. After a Panchnama, the accused should be given an acknowledgment of all seized machines and documents.

Inspection report should be fully prepared. The entire premises, house, garage, hospital should be thoroughly searched for an unregistered machine.

At the place of the crime, statements of the pregnant woman and the witnesses should be recorded and all the evidence in the form of audio, video cassettes should be taken into custody. The pregnant woman and the witnesses should be given copies of their statements and cassettes.

After making sure that investigation has been carried out thoroughly, a case should be registered in the court after discussing the matter with lawyers.

As the Appropriate Authority is the complainant, she/he or a representative should be present.

Ans. ÂÂ

A genuine and properly planned decoy or sting operation is legally permissible.

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The guidelines for a decoy operation are as follows:

Seek participation of a woman who is 14-22 weeks pregnant and is willing to be involved in the decoy operation. Counsel the selected woman on the purpose of the decoy.

An affidavit from the woman should be obtained stating that she is ready to take part in the decoy operation. Note the numbers on the currency notes to be used. These are to be mentioned in the affidavit. Give these currency notes to the decoy woman or the witness.

Prepare two witnesses to accompany the woman.

Keep an audio-video system handy if possible.

Check beforehand if the pregnant woman and the witness can operate it correctly. They should be comfortable in using these. It is important to avoid any confusion in this regard.

Keep ready three main witnesses and two inspectors. They should be friendly enough with each other to work as a team, with excellent nonverbal communication. They should be trained so as to gather and collect evidence, have a good knowledge of the Act and learn things to keep in mind for a decoy operation.

Appropriate Authorities should be available close by where the decoy operation is to take place.

Advocate and Medicolegal Consultant, New Delhi

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lighter reading

The family ate together nightly at the dinner table. But, the elderly grandfather’s shaky hands and failing sight made eating rather difficult.

Peas rolled off his spoon onto the floor. When he grasped the glass often milk spilled on the tablecloth.

The son and daughter-in-law became irritated with the mess. “We must do something about grandfather,” said the son. I’ve had enough of his spilled milk, noisy eating and food on the floor. So, the husband and wife set a small table in the corner.

There, grandfather ate alone while the rest of the family enjoyed dinner at the dinner table. Since, grandfather had broken a dish or two, his food was served in a wooden bowl. Sometimes when the family glanced in grandfather’s direction, he had a tear in his eye as he ate alone. Still, the only words the couple had for him were sharp admonitions when he dropped a fork or spilled food. The 4-yearold watched it all in silence.

One evening before supper, the father noticed his son playing with wood scraps on the floor. He asked the child sweetly, “What are you making?” Just as sweetly, the boy responded, “Oh, I am making the bowl for you and mama to eat.” The 4-year-old smiled and went back to work. The words so struck the parents that they were speechless. Then tears started to stream down their cheeks. Though no word was spoken, both knew what must be done.

That evening the husband took grandfather’s hand and gently led him back to the family table. For the remainder of his days he ate every meal with the family. And for some reason, neither husband nor wife seemed to care any longer when a fork was dropped, milk spilled or the tablecloth soiled.

Children are remarkably perceptive. Their eyes ever observe, their ears ever listen, and their minds ever process the messages they absorb. If they see us patiently provide a happy home atmosphere for family members, they will imitate that attitude for the rest of their lives. The wise parent realizes that every day those building blocks are being laid for the child’s future. Let us all be wise builders and role models. Take care of yourself, and those you love, today and every day!

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After a Bad Accident Patient: I’m in a hospital! Why am I in here?

Doctor: You’ve had an accident involving a train.

Patient: What happened?

Doctor: Well, I’ve got some good news and some bad news. Which would you like to hear first?

Patient: Well... The bad news first...

Doctor: Your legs were injured so badly that we had to amputate both of them.

Patient: That’s terrible! What’s the good news?

Doctor: There’s a guy in the next ward who made a very good offer on your slippers.

—Dr GM Singh

“What you get by achieving your goals is not as important as what you become by achieving your goals.”

—Henry David Thareau

Dr. Good and Dr. Bad Situation: A patient with normal LDL and high CRP

wanted to know his risk of CAD.

You are not at risk

Get cardiac 64 CT test done

©IJCP Academy

A frail old man went to live with his son, daughter-in-law, and a four-year old grandson.

The old man’s hands trembled, his eyesight was blurred and his step faltered.

laugh a while

The wooden bowl

QUOTE

An Inspirational Story

Lighter Side of Medicine

Lesson: Among asymptomatic individuals with normal

LDL cholesterol levels and elevated highsensitivity CRP measuring the burden of calcium in the coronary arteries with cardiac CT appears to stratify the risk of cardiovascular disease.

Lancet 2011;378:684-92.

KK Aggarwal

Asian

Journal of

CLINICAL CARDIOLOGY

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).

Asian Journal of Clinical Cardiology 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.

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

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

A subtitle can be added if necessary.

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

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

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

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

- It should not contain abbreviations, footnotes or references.

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

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

- Ethical guidelines followed by the investigations should be described.

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

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

- Method of allocating the subjects into different groups.

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

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

-

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

-

Confidence intervals for the measurements should be provided wherever appropriate.

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

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Discussion -

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

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

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

Examples of common forms of references are: Articles

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

- All photomicrographs should indicate the magnification of the print.

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

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

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

-

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.)_______________________________

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

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

2. Total number of pages ________________________

Books

6. Suggestions for reviewers (name and postal address)

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

Indian 1.____________Foreign 1.________________

2.____________ 2.________________

Articles in Books

3.____________ 3.________________

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

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.

-

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

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3. Number of tables ____________________________ 4. Number of figures ___________________________ 5. Special requests _____________________________

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 Asian Journal of Clinical Cardiology E - 219, Greater Kailash, Part - 1, New Delhi - 110 048. Phone: 011-40587513 E-mail: editorial@ijcp.com, emedinew@gmail.com Website: www.ijcpgroup.com

R.N.I. No. 71217/98 Date of Publishing 25 of Same Month Date of Posting 25-26 Same Month

REGISTRATION NO. DL (S)-01/3288/2013-2015 POSTED IN NDPSO NEW DELHI

Dr KK Aggarwal Group Editor-in-Chief Dr Veena Aggarwal MD and Group Executive Editor Dr Alka Kriplani Dr Praveen Chandra Dr Swati Y Bhave Dr CR Anand Moses Dr Sidhartha Das Dr Wiqar Sheikh Dr Ajay Kumar Dr A Ramachandran Dr Samith A Shetty Dr SK Parashar Dr Kamala Selvaraj Dr Georgi Abraham Dr V Nagarajan Dr Thankam Verma Dr KMK Masthan Dr Hasmukh J Shroff Dr Rajesh Chandna Dr SM Rajendran

l

e 22,

er11

Peer Reviewed Journal

Drug Review

Review Article

Original Article

Case Report

Photo Quiz

Lighter Reading

April 2012, Pages 545-596