EDITOR SPEAKS

Vol. 8 Issue 2 Jan - March 2009 Dr. Vinay Aggarwal Dr. S. K. Mittal Editorial Board Dr. Vijay Agarwal Atul Gandotra Dr. Sharda Jain Dr. Rajiv Gupta Dr. Deepak Pande Dr. Vineet Jain Dr. B.K. Gupta Dr. Atul Jain Design and Layout Photographer Dr. Ashok Grover Dr. Madhumita Puri Dr. Parkash Gera Dr. S. Arul Rhaj Dr. Yogesh Jhamb Dr. Neeraj Jain Dr. Hariharan Mr. S.K. Singhal Tabassum Mukesh Kapoor
CONTENTS 1. Obesity - A Moribund Epidemic in Children 2. Pneumococcal Vaccination in India: Science and Commerce 3. Diagnostic Approach to Acute Pyrexia in Young Children 4. Celiac Disease Revisited 5. Improving Cure Rates and reducing side-effects by modern Radiotherapy Techniques 6. Office Management of Asthma 7. Common Drugs Acting on Cardiovascular System and Optimal Dosing Time 6. The Role of Spirituality in Medicine 7. Clinical Challenge: Acute Appendicitis with Pregnancy (Three case reports, one in each trimester) 8. Nocturnal Enuresis 9. Is Sunlight an Effective Treatment for Jaundice in Term Infants? 10. Rotavirus Vaccine 11. Recent Advances in Management of Childhood Tuberculosis 12. Pushpanjali Healthcare Events 47 and Initiatiaves 13. Guidelines for submission of Manuscripts 3 5 9 13 19 21 24 29 31 Department of Pediatrics Chairman Dr S K Mittal 9818372811 Consultants Mon-Thurs Dr Ravi Malik 9811078350 Dr Dinesh Aggarwal 9811078283 Dr Rajiv Singh 9810346080 Tues-Friday Dr Deepak Pandey 9810366571 Dr Alok Gupta 9312248808 Dr Anuradha 9899646715 Wed Sat Dr P D Garg 9811109048 Dr. Vineet Jain 9810121098 Dr K K Pandey 9810184791 Dr Manpreet 9811121285 Neonatology Dr Vivek Jain 9999444303 Dr. Sudershan Kumari (Ex. LHMC) Tues-10.00am to 1.00pm

Dear Colleague It gives me great pleasure in presenting to you the latest issue of Medi-Focus, a scientific periodical being published by the Pushpanjali group to update the knowledge and skills of physicians in various fields of Medicine. This issue is entirely devoted to the problems related to child health. I am sure you will find the issue very informative and helpful in your day-to-day practice. You will be glad to know that the Department of Pediatrics and Adolescent Medicine at Pushpanjali Crosslay Hospital is now geared to provide comprehensive services in various areas of child health under the supervision of an expert team of specialists and super specialists. The following facilities are available: i. Round-the-clock emergency facilities with qualified consultants. ii. Outpatient consultations by Senior specialist from 9:00 am to 8:00 pm on all working days. iii. Specialized clinics in the afternoon (2:00 pm to 4:00 pm) Monday: Pediatric Gastroenterology Tuesday: Pediatric Respiratory Thursday: Pediatric Endocrinology Saturday: Pediatric Cardiology and ECHO iv. Special diagnostic facilities like Pediatric GI endoscopy, ECHO cardiography, PFT, Bronchoscopy, Hormonal assays for endocrinal problems. v. Special diagnostic facilities in allied fields like BERA, OAE (For hearing assessment) Detailed retinoscopy (For retinopathy of prematurity) etc. vi. Neonatal Intensive Care with facilities for all levels of neonatal care including monitoring, Ventilation, CPAP, Parenteral alimentation under the supervision of a qualified neonatologist. vii. Pediatric Intensive Care with all Level III facilities under the supervision of pediatric intensivists. viii. Pediatric Surgery by a fully qualified and dedicated Pediatric surgeon. All efforts are being made to continuously upgrade the facilities available in the department .and very soon we will be in a position to provide additional services like: i. Child Guidance and Development services with dedicated Clinical Psychologist, Speech therapist and Occupational therapist. ii. Diagnostic and rehabilitative services for children with Autism, Learning disabilities, Attention Deficit and Hyperactivity Disorders. iii. Special Clinic and Diagnostic facilities in Pediatric Neurology, hemato-oncology, nephrology. The department also conducts weekly clinical meetings with all consultants on Friday afternoons. Further, the department also provides Continuing Medical Education through monthly clinical meetings for neighborhood pediatricians. We invite you to participate in all the academic activities of the Department and also to spare some of your valuable time to visit the hospital and witness first hand the world class facilities being developed in the department. We will be happy to look after all your problem cases with an assurance of developing a long term - partnership for the continued care of your pediatric patients. Dr S K MIttal Chairman Department of Pediatrics, Neonatology and Adolescent Medicine

Editor-in-Chief Sectional Editor

Intensive care Dr Praveen Khilnani 9810159466 Dr Deepika Singhal 39 9811702443 43 Endocrinology Dr I P S Kocher 9910240919 Gastroenterology 51 Dr S K Mittal Dr Manpreet Respiratory Owned, Edited, Printed and Published by Dr Deepak Pandey Dr. Vinay Aggarwal for and on behalf of Pushpanjali Medical Publications Pvt. Ltd., Dr Tilak Raj Dangwal A-14, Pushpanjali, Vikas Marg Extn., Pediatric Surgery Delhi-110092 Dr Rajeev Aggarwal Printed at Kumar Offset Printer, 381, Patparganj 9810032906 Industrial Area, Delhi - 110 092 Development Pediatrics All disputes to be settled in Delhi Courts only. Mr. Sudershan Kumari All rights reserved. Clinical Psychologist No responsibility is taken for returning Dr Sanjeeta Kundu unsolicited manuscripts unless a self-addressed 9811271220 stamped envelope is enclosed. Speech Therapist Views expressed in articles in Medi-Focus do not Dr Mani Bansal necessarily reflect those of the editorial board. 9873880510 33 37

1 Vol. 8, Issue 2 Jan - March 2009

Obesity - A Moribund Epidemic in Children

IPS Kochar
Obesity is defined as a condition of abnormal or excessive fat accumulation in adipose tissue to the extent that health may be impaired. Childhood obesity is a global epidemic and is a complex multifactor challenging and frustrating problem that is escalating at an alarming rate in the western world and paradoxically in a developing country like India. Along with the prevalence of under malnutrition there is a paradox of increase obesity. Though the prediction of obesity has been largely in lower social economic group in western world, it is the urban effluent population effected in India. Obesity in childhood factors for obesity in adulthood. About 80% of the obese adolescents are expected to remain obese as adults. Several pathologies develop concomitantly with obesity during childhood. These include type2 diabetes, a range of respiratory problems, metabolic syndrome, liver, steaaotosis, and pseudo-tumor cerebrei. Childhood obesity is essentially an exogenous disorder, preventing intervention should focus on modifying these etiologies improve nature of childhood nutrition and its social and lucid behaviour. Epidemology: According to the American Obesity Association, 15.5% of adolescents (age 12 to 19 years) and 15.3% of children (age 6 to 11 years) are obese. There has been a 45% increase in prevalence in overweight children as reported from estimates of 11% and 16% from the NHANES 3 survey. Several studies from India too have confirmed the rising prevalence of childhood obesity and overweight in pediatric and adolescent population. Prevalence of obesity is from 5-14% and overweight 9-16% in upper social economic group. Obesity is less common in lower social economic group and in rural children varying from less than 1% to 3.6% in some of the studies. Measurement of Obesity: Obesity is measured using the Body Mass Index (BMI). BMI is calculated easily from weight and height to correlate with other measures of body fat mass in children and adolescents. The BMI changes physiologically with age and sex. At birth median BMI is low as 13kg/M2 increasing to 17kg/m2 at age 1 year, decreasing to 15.5kg/m2at age 6 years, and then increasing further to 21kg/ m2 at age 20. Age and gender specific BMI cut off points for defining overweight and obesity in children have been derived by identifying percentiles in children analogous to adult BMI are now recommended as standards for international comparison of data by the International Obesity Task Force (IOTF). Other measures like skin fold thickness, waist hip ratio and waist 3 Vol. 8, Issue 2 Jan - March 2009 circumference are also used for measuring obesity. Body fat measurements technique, DEXA, CT, MRI, and ultrasound are additional tools for quantification of body fat. Risk Factors Non-Pathological Genetic Environmental Obesity in both parents Socioeconomic deprivation, single child, single parent Bottle fed in infancy, high fat food, sugar snacks disorganized eating habits Increase inactivity, Increase TV watching

Diet related

Activity related

Pathological Syndromes Lawrence Moon Biedl Syndrome Down Syndrome, Prader Willi Syndrome Beckwith-Wiedeman Syndrome Alstrom Syndrome Cohen Syndrome Pseudohypoparathyroidism Hypothalamic Damage Trauma Tumors Craniopharyngioma Post Encephalitis Drugs Insulin Steroids Anti Thyroid Drug Sodium Valporate Thiazoldine Risperidone Single Gene Mutation Melancortin 4 Receptor (Mc4r) Propiomelancortin (POMC) Leptin, Leptin Receptor Defect Endocrine Abnormality Gh Deficiency Hypothyroidism Cushing Syndrome Hyperinsulism Insulin Resistance Klinefelter Syndrome Turner Syndrome Insulinoma PCOS Immobility Spina Biifida Cerebral Palsy Impaired Skeletal Growth Achondroplasia

IPS Kochar
Consultant Pediatrician & Adolescent Endocrinologist Fellow, Pediatric Endocrinology London

Clinical Manifestations Obesity may occur at any age, but is most common in the first year, around 5-6 years and during adolescence. Children with obesity due to excessive caloric intake are also taller for their mid-parent height and often this characteristic association of accelerated linear growth is one of the single most important clinical parameters in evaluation of children with obesity. Those with exogenous or nutritional obesity are tall and maintain significant accelerated linear growth, whereas those with endogenous pathological causes are usually short below the 25th percentile for age and sex or may have a growth rate and growth curve falling off their previous percentile on the growth curve. Overgrowth in children in children with obesity seems related to elevated insulin levels due to obesity-induced insulin resistance. Increased aromatization of adrenal androgens by fat tissue causes advancement of bone maturation, which ultimately results in normal adult height. Increased aromatization due to excess fat leading to excess production of estrogen may contribute to gynecomastia in association with lipomastia. These children have adiposity around the breast (which may mimic gynecomastia) with pendulous abdomen and fatty acids at the sides. Striae may be present if excessive or rapid weight gain occurs. In boys, external genitilia may appear disproportionately small with penis usually embedded in the fat. This is often the major reason for presentation in obese boys rather than concern about the excess body weight. Puberty may occur early affecting their ultimate height. There is genu valgum and more fat in the upper arm and thigh compared to the rest of the extremities, with small tapering fingers. Investigations Fasting sugar, total cholesterol, liver function, fasting triglycerides, low and high density lipoproteins, insulin level and glycostylated hemoglobin levels, thyroid function test, urine analysis (specific density), thyroid function test in a growing obese adolescent female. If menstrual irregularities are reported possibly combined with sign of hirsutism and/or acanthosis nigricans, investigation for PCOS may be required. Special Hormonal profile for GHD, thyroid, Parathyroidgland, IGF1, karyotype, insulin level, imaging of pituitary and adrenal area, if required. Complications The long term sequelae of childhood obesity include obesity in adulthood hypertension, insulin resistance, type 2 diabetes cholelithiasis, hyperurcemia, cardiovascular disease, dyslipidemia, early pubertal changes, menstrual irregularities orthopedic problems, sleep apnea, reparatory infections and cytological disturbances. Metabolic and Endocrine Hypernsulinemia (impaired glucose syndrome), advanced pubertal development, polycystic ovarian disease, steatohepatitis Hypertension Breathless on exertion, obstructive sleep apnea, Pickwickian syndrome

Skeletal Psychological

Knock knee or bow legs, slipped capital femoral epiphysis Poor self image, bullying, behavioral problem

Management Strategies Childhood besity s reat hallenge o ediatric ndocrinologists. o i ag c t P E Recognizing the problem, setting goals, initiating treatment strategies, proper implementation and monitoring of the therapy are the essential steps of management. Diet exercise and behavior modification are the corner stones of therapy. Anorectic drugs and bariatric surgery are to be avoided in the management of childhood obesity except in rare life threatening or very special situations. Diet Education of parents and children regarding the need for proper and adequate nutrition for normal growth and the need to avoid excess of empty calories, and other caloric advice is important. Energy-dense, high-fat, high calorie snacks and fast food and non nutritive sweetened drinks are the usual culprits. Inclusion of fruits vegetables, lentils and multi-grain breads in the diet improves the nutritive value in the fiber. Exercise Lack of exercise and sedentary lifestyles contributes more to weight gain in children than in adults. Activities like walking, cycling, tennis, aerobics, cricket, volleyball, basketball, and badminton are some of the activities that children enjoy and should be encouraged as there is greater chance of the recommendation being followed. Calisthenics and monotonous activities are found to annoy and frustrate children, leading to a negative impact on outcome. Swimming helps in weight maintenance and toning of muscle but is often associated with an increase in appetite after the swim, so care and caution must be exercised to circumvent this. School academic activities should be balanced with physical activities, playtime and family time. Health camps that educate and encourage children to lead a more active life have been found to be successful. Appetite suppressants Pharmacotherapy is not recommended for appetite suppression in children and adolescents, and the uses of these agents are strongly discouraged. New modality of leptin therapy is currently undergoing human trial and has been successful with leptin deficiency. Growth hormone is being used in patients with Prader-Willi syndrome. Batriatic surgery This is traditionally reserved for obese adults with very high BMI (>40kg/m3) or with comorbidities that are life threatening. Generally such procedures (gastric stapling/gastric/jejunoileal bypass procedures) are to be considered only in morbid obesity with complications. This modality of treatment has been used in the adolescent population where indicated, with considerable success. Prevention Childhood is a critical period for the initiation of obesity and therefore the ideal time for beginning prevention programmes. Television progammes, articles and newspapers, lecture by health care professional, health camp and health fairs are some of the ways of spreading the messages of good nutrition and active lifestyle against the problems of obesity.

Cardiovascular Respiratory

Pneumococcal Vaccination in India: Science and Commerce

Joseph L. Mathew
Introduction Much has been written and spoken about Pneumococcal vaccine for routine immunization in India. This article attempts to explore the facts with particular reference to the scientific and commercial issues behind it. As India accounts for 120 out of 478 million (25%) under-five children, developments here are closely watched all over the world. A. Science I. Burden of disease The exact number of Invasive Pneumococcal disease (IPD) is not known; even a reliable estimate is unavailable. Currently quoted figures are summarised in Table 1, from which it is clear that the calculations are neither based on robust data, nor as high as projected. However, this does not necessarily mean that IPD could not be a significant problem; a fact pointed out earlier 1. The issue can only be resolved through multi-centric population-based surveillance studies, that are cumbersome, time consuming and expensive, but inevitable. II. Significance of Pneumococcal disease Pneumococcal disease is significant for developed countries based on knowledge of (i) disease burden, (ii) serotypes causing invasive disease, (iii) control of other causes of pneumonia especially Hib and measles, (iv) increasing antibiotic resistance among S pneumoniae, (vi) pre-existing high level of hygiene, sanitation, health-care delivery etc; which cannot be significantly improved further to reduce pneumonia morbidity and mortality. Therefore, these countries have included Pneumococcal vaccine in routine immunization programmes. In developing countries, (i) burden of disease is not clear, (ii) knowledge of serotypes causing invasive disease is limited, (iii) even if IPD is a significant cause of pneumonia morbidity and mortality, it is not likely to supersede other causes including H influenzae and measles owing to poor immunization coverage, (iv) antibiotic resistance is not a significant problem yet, and (vi) there is scope for improvement in quality of life and thus morbidity/mortality. Therefore, developed country arguments cannot be extrapolated to developing countries. If the figures presented in the UNICEF report of 20062 are correct, the case fatality rate of pneumonia is 0.93% (410,000 deaths among 44 million cases). This relatively low casefatality suggests either mild disease or excellent response to therapy. However, the same document states that only two-thirds of Indian children are taken to an appropriate health5 Vol. 8, Issue 2 Jan - March 2009 care provider2, again suggesting mild disease. If this is the case, it would not merit a large-scale expensive vaccination programme. However, the document claims that pneumonia is responsible for 20% of under-five mortality, which makes it a very serious problem. This apparent paradox stems from the large denominator of 44 million that is used to demonstrate high disease burden. As this figure appears to be obviously incorrect, all the calculations based on this premise also become suspect. III. Role of Pneumococcal vaccines Since young infants are at greatest risk of IPD, vaccination should be efficacious and effective in this age-group. The 23-valent Pneumococcal polysaccharide vaccine is not recommended for young infants, hence cannot be used for routine immunization. The 7-valent Pneumococcal conjugate vaccine (PCV-7) covers only a limited proportion of serotypes causing IPD in most developing countries, hence at best would be something better than nothing. This is because PCV-7 was designed to protect children in developed countries; and hence serotype coverage is 90% for USA and Canada, 78% for Australia and 75% for Europe. It is much lower for Africa (67%) and Latin America (63%), though this is still much better than for Asia (43%) and India (53% or lower)3,4. IV. Administration and logistics The vaccination schedule of PCV can be linked with that of DPT in routine immunization programmes, making it an attractive option logistically. However, it cannot be mixed in the same syringe with other vaccines and the WHO estimates the need for a substantially increased capa 300%5. Administration would necessitate use of separate syringes and injection sites. Therefore, safety data comparing both vaccinations against DPT alone would need to be generated prior to usage. These factors make vaccination less attractive than one is led to believe. B. Commerce I. Role of industry The current heightened interest in Pneumococcal disease in India is not related to increase in scientific knowledge of the epidemiology of Pneumococcal disease or vaccine/vaccination, but the thrust by industry to increase sales of PCV-7. This is through the academic channel (organization of countless sponsored lectures on the product by experts; many of these for a fee) and the commercial channel (extensive marketing, advertising and providing the vaccine to physicians at about 20% less than the

Joseph L. Mathew
Advanced Pediatrics Centre PGIMER Chandigarh

retail price). These practices encourage physicians to be oriented in favour of a vaccine whose effectiveness is limited in the local setting. II. Role of the WHO The WHO issued a position paper5 recommending PCV-7 in developing countries, temporally coinciding with aggressive marketing of the same. This has given a substantial boost to sales of PCV-7. The WHO considers that it should be a priority to include this vaccine in national immunization programmes, particularly in countries where mortality among children aged <5 years is >50/1000 live births or where >50,000 children die annually5. However, no explanation is offered for choosing these particular cut-off criteria. The option of using either criterion (rather than both) permits the additional inclusion of seven countries that would otherwise not have been considered. These seven countries together account for 161 million underfive children, of which Brazil and China alone accounts for 104 million. As currently there is only one brand of PCV available in the world, it is obvious who will benefit the most from these statements. III. Role of the Indian Academy of Pediatrics (IAP) The recent IAP guidelines6 recommend PCV-7 in routine immunization after one-to-one discussion; this means that those who are willing to pay for a vaccine with limited effectiveness should be vaccinated. The IAP further recommends that Government of India should seriously consider PCV-7 for routine immunization. Since this is impossible owing to the huge expense involved, IAP recommends that Government could offset the cost by availing the GAVI offer of subsidized vaccine till 20156. It is not clear what the Government is expected to do when/if GAVI pulls the rug from under it after 2015. IV. Role of the Government of India The Government of India has shown unusual promptness in advocating PCV. An expert committee under the chairmanship of the DG, DBT recommended PCV for routine immunization programme within a record time of two weeks after it was set up. This is very impressive considering that a rational policy over Hib, hepatitis B and measles vaccines has not emerged over several years. Although the expert committee also recommended a vaccine covering at least 70% serotypes; since this is not available it is unclear how the recommendation will be fulfilled. Meanwhile, these actions have boosted sales of currently available PCV-7. C. What is the solution? The decision on using a vaccine (or otherwise) should be based on actual or expected burden of disease, likely effectiveness of available vaccines and existing health-care priorities; it must not be based solely on efficacy, safety, availability or affordability. Accordingly, it is possible that India needs a pneumococcal vaccine for young infants, but the currently available vaccines are not suitable. Knowledge of locally relevant serotypes and indigenous manufacture of tailor-made vaccine should be encouraged. This will make vaccination effective, affordable and sustainable in the long term. Conclusion The current hype over Pneumococcal vaccines is largely commercial in origin, boosted directly and indirectly through the loud and/or quiet acquiescence of professionals in individual, institutional and organizational capacities. The relegation of scientific considerations to the back-seat is the most unfortunate outcome of these strategies. Such events are likely to be witnessed with increasingly regularity in the future as well. 6 Vol. 8, Issue 2 Jan - March 2009

Table 1: Scientific claims on burden of Pneumococcal disease in India Published scientific claim There are 43-44 million annual childhood pneumonia cases in India 2 Comments The basis for arriving at this estimate has not been presented. The document quotes a personal communication of an unpublished paper. The subsequently published paper also does not explain the figure of 43 million predicted new cases among under five children. If this estimate and prediction are correct, it means that every third Indian child has pneumonia. This suggests gross inflation of numbers. This is a direct quote from another paper published in a developed country. As H influenzae is difficult to isolate through culture techniques, it is often not detected. The role of S aureus, Gram negative organisms, M. tuberculosis and measles virus in causation of childhood pneumonia is not even mentioned. This is lifted from Reference2 which actually states In Africa, S pneumoniae may be responsible for over 50% of severe pneumonia cases, and probably a higher proportion of fatal cases. There is no cross-reference for this claim. This range has been arrived at by applying the 15-50% calculation (unproven) to 44 million2 annual episodes (doubtful). This has been calculated by multiplying 410,000 estimated deaths in Reference2 by 50%. The basis for both these numbers is not clear.

S pneumoniae is responsible for 15-50% cases of childhood pneumonia6.

S pneumoniae is responsible for 50% childhood pneumonia mortality6.

S pneumoniae causes 6.6 to 22 million episodes of pneumonia in India annually6. S pneumoniae is responsible for 200,000 under-five deaths yearly6.

References
1. Invasive bacterial Infection Surveillance (IBIS) Group, International Clinical Epidemiology Network (INCLEN). Prospective multicentre hospital surveillance of Streptococcus pneumoniae disease in India. Lancet 1999; 353: 1216-1221 2. Kanungo R, Rajalakshmi B. Serotype distribution & antimicrobial resistance in Streptococcus pneumoniae causing invasive & other infections in South India. Indian J Med Res 2001; 114: 127-132. 3. Mathew JL. Universal Pneumococcal faccination for India. Indian Pediatr 2008; 45: 160-161. 4. No authors cited. Pneumococcal conjugate vaccine for childhood immunization WHO position paper. Wkly Epidemiol Rec 2007; 82: 93104. 5. Pneumonia: the forgotten killer of children. The United Nations Childrens Fund (UNICEF)/World Health Organization (WHO), 2006.

Diagnostic Approach to Acute Pyrexia in Young Children

Vineet Jain
Acute febrile illness in infants and children is very common in day-to-day practice and is probably the foremost reason for taking the child to a doctor. It is usually a self-limiting viral illness. Approximately 10% of children <36 months without evident source of fever have occult bacteremia and serious bacterial infection (SBI). However, there are times when it poses a diagnostic dilemma. The challenge in the evaluation of a febrile young child lies in balancing the minimization of risk to the patient with the cost of testing and treatment. Definition of fever and detection techniques The most commonly accepted definition of fever is rectal temp >380 C (100.40 F) (PCNA). For previously healthy children 3-36 month of age, rectal temp >390 C (102.20 F) warrants further evaluation. This cut off is >380 C in cases of neonates and young infants 0-3 months. A number of studies have shown that axillary and tympanic temperatures are unreliable in young children. A child with history of rectal temp higher than 380 C (100.40 F) who is afebrile at the time of presentation should be given the same level of attention as one who has fever at presentation. Parental perception of fever with the back of the hand should be considered valid and taken seriously. Risks and benefits of fever: Risks Fatigue Body aches Delirium Anorexia Tachycardia Febrile convulsion Benefits Enhanced immunological functions Some organisms die at high temperature eg Viruses - Polio and rhinovirus - Bacteria pneumococcal Children with chicken pox have prolonged crusting if treated with Paracetamol vs placebo. Antipyretics should be used judiciously for symptomatic relief, not merely to decrease temperature in an otherwise well but febrile child. Approach to a young febrile child Management of febrile young children continues to evolve. Contributing to this confusion is the 9 Vol. 8, Issue 2 Jan - March 2009 changing epidemiology of bacterial infections in young children after the advent of Hib and PCV7 vaccines in the west. Although the differential diagnosis of fever is quite broad and includes both infectious and non infectious causes, the majority of febrile children have underlying infectious causes of fever. For the purpose of this article, patients are presumed to be febrile from infectious sources. Additionally, diagnostic strategies emphasize the detection of bacterial diseases, as these are more likely to be associated with the worst outcomes. Viral infections can also be associated with significant morbidity and mortality, especially in young children. Finally most studies of febrile young children exclude patients who have potentially complicating risk factors immunocompromised, HIV, patients with indwelling medical devices, on Antibiotics or having prolonged fevers (>5 days). History and physical examination History and physical examination are invaluable in the assessment of febrile children. The duration and intensity of fever at the time of presentation does not predict whether a child has occult bacteremia. Use of antipyretics should be noted. A response (or lack thereof) to antipyretics does not predict whether underlying cause is bacterial or viral. An assessment of the childs overall appearance is critical. If the child appears to be toxic, this mandates an aggressive workup, antibiotics and hospitalization regardless of age or risk factors. Physical examination may reveal an obvious source of infection and identification of a focal infection may decrease the need for additional testing. a) Identify potentially serious illness All febrile children should be assessed for the presence or absence of symptoms and signs that predict the risk of serious illness. (Table 1) b) Look for symptoms and signs of specific illness (localization) (Table 2) c) Look for clinically recognizable viral illness Febrile patients with recognizable viral conditions (eg, croup, chickenpox, measles, stomatitis) have lower rates of bacteremia than patients with no obvious source of infection, thus decreasing the need for elaborate diagnostic workup.

Vineet Jain
Consultant Pediatrician Pushpanjali Medical Centre, Delhi Pushpanjali Crosslay Hospital, Ghaziabad, NCR

Table 1. Is it a potentially serious bacterial illness (SBI) Parameter Colour Activity appears ill Green (low risk) Normal skin/mucous membrane responds normally to social cues smiles/playful stays awake or awakens quickly strong normal cry/not crying Red (high risk) Pale /mottled skin No response to social cues Appears ill Unarousable/if aroused does not stay awake Weak/high pitched or continuous cry Grunting tachypoea RR>60/min chest indrawing

Table 2. Look for localization signs Sx and signs in conjunction with fever Non blanching rash with > of the following Ill looking child Capillary refill time >3 sec Neck stiffness Neck stiffness bulging AF Delirium /seizures Focal neurological signs Focal Seizures Decreased consciousness Possible diagnosis Meningococcal disease

Meningitis

Herpes simplex encephalitis/TBM

Respiratory

Normal breathing

Hydration

ormal kin/mucous Reduced skin turgor N s membranes Sunken eyes Normal eyes None of the red alert signs on lanching ash N b r Bulging ontanelle/ f neck stiffness Status epilepticus Focal neurological signs/focal Sz Age 0-3 mo, temp >38C Age 3-6 mo, temp >39C

Pneumonia/ bronchitis Tachypnoea - (0-6 mo >60/min - 6-12 mo >50/min - >12 mo >40/min Nasal flaring/chest indrawing/rales /rhonchi Vomiting/poor feeding Lethargy/irritability Dysuria/ frequency Offensive urine/hematuria Swelling of limb or joint Not using an extremity Non weight bearing Fever >5 d with at least 4 of the following : B/L conjuctival injection Changes in mucous membranes Changes in extremities Polymorphous rash Cervical LN UTI

Others

Septic arthritis

Kawasaki disease

Age

Others

Fever without source (FWS) Most children 0-36 months of age who have fever without an obvious source have viral infections, but certain febrile children are at higher risk for more SBI (7-13% cases). Diagnostic approach in FWS depends upon Clinical look - Well - Toxic Characterized by lethargy (absent eye contact with parents and surroundings) poor perfusion hypo / hyperventilation Age Three distinct groups: - 0-28 days - 1-3 months - 3-36 months

Neonates (0- 28 day) Neonates are at particularly high risk for SBI. Although majority of neonates are diagnosed ultimately as having a non specific viral illness, 10-12% of all febrile neonates have SBI. They are infected typically by more virulent bacteria (eg, streptococci gp B, E coli, L. monocytogenes and staph. 10 Vol. 8, Issue 2 Jan - March 2009

aureus) with high rates of meningitis, non meningeal focal infections (UTI being commonest) and occult sepsis. Studies have shown that clinical evaluation alone fails to identify neonates at risk of SBI, hence diagnostic workup is recommended if temperature >380 C irrespective of clinical wellbeing or signs of viral infection. Diagnostic workup includes: Blood C/S in all cases as CBC alone is not reliable in this age group Urine analysis>10 WBC/HPF in an uncentrifuged sample is significant but alone cannot detect all cases of UTI Urine C/S must in all cases. Catheter or suprapubic samples are preferable to avoid contamination) LP must in all cases CBC is of limited value as it cannot differentiate between SBI and non bacterial infections. WBC >15000 or < 5000 or/ and Absolute band cells >1500/mm3 may be associated with higher risk CXR only if pulmonary symptoms are observed. Hospitalization and IV Antibiotics are strongly recommended regardless of lab results or general condition. Outpatient management occurs frequently when patients present to pediatric clinics, but there are no prospective studies that address this approach.

Young infants (1-3 months) Toxic patients in this age group require the same approach as for all febrile neonates; however, patients who appear clinically well are also at high risk for SBI. Clinical evaluation alone may miss a substantial number of SBI, hence basic diagnostic workup is essential and patients are divided into two groups based on reports: Table 3. Clinically well Young infants (1-3 months) Basic diagnostic tests WBC Band neutro ratio Absolute band count Urine analysis Low risk (mostly viral) High risk (UTI and SBI)

Risk of bacteremia increases as the temperature rises, Risk of pneumococcal bacterermia increases with age Prevalence of bacteremia in well appearing older infants and young children increases with increase of WBC count. At count <15000 risk 0.5% >30,000 risk 18% Absolute neutrophil count >10,000/mm3 is a stronger predictor of bacteremia than elevated TLC of >15000/mm3 Most pediatricians use empirical antibiotics in children with high TLC. The question that needs to be addressed while doing so is - What is being treated? If it is possible occult bacteremia that is being treated in order to prevent SBI especially meningitis, then meta analysis reports are still unclear whether antibiotics reduce risk of meningitis in these older infants or toddlers. Evidence supports that clinically well infants (3-36 months) with rectal temp <390 C (102.20 F) and without an evident sources of infection can be discharged without testing and no antibiotics. They should have follow up visits if symptoms worsen. Well appearing children 3-36 months with fever>390 C but without any obvious source may have a basic diagnostic workup including CBC, and urine analysis. If TLC >15000 or ANC >10,000, then blood c/s should be obtained. Occult UTI: It is a common source of fever and may cause permanent renal damage. Symptoms are nonspecific. Identify high risk group: Female <2 years Male <6 month/ uncircumcised <12 months, Temperature >390 C with no other source of fever Urine C/S is the gold standard, but results take 48 hours, hence rapid urine analysis showing >10WBC/HPF or bacteria on gram stain in an uncentrifuged sample is taken as significant. Occult pneumonia: Most common pathogens in childhood pneumonia are viruses and S pneumoniae. The presence of any pulmonary finding on examination increases the likelihood of pneumonia and conversely the absence of these findings decreases the likelihood of pneumonia. Although chest radiograph is often believed to be gold standard, it cannot reliably differentiate between bacterial and non-bacterial causes. Some cases of pneumonia bacteria are likely to be clinically occult. Various studies have recommended that children <5 years having temp >39C, WBC count >20,000 and no other source of fever, should have chest X-ray even without pulmonary symptoms. (Table 4) Summary Most febrile illnesses (<7 days) in children 0-36 months of age turn out to be non-specific viral. However, certain febrile children are at higher risk for more serious bacterial infection. Meticulous clinical evaluation can pickup life threatening illnesses; identify potentially serious illnesses and pickup localizing signs in order to channelize investigative workup thus minimizing mortality and morbidity. However, in neonates and young children clinical evaluation alone may miss SBI in ~ 10% cases, hence the need for a diagnostic approach. 11

5000-15000 <0.2 <1500

<5000 or >15000 > 0.2 <1500

<10 WBC /HPF No organisms on gram stain OPD Mx/review in 24 h/look for red flag signs or localization No antibiotics No LP/No blood c/s

>10 WBC /HPF organisms on gram stain + Admit complete / diagnostic workup including LP/IV antibiotics

Recommended

Some studies do not mandate LP in view of rarity of meningitis in clinically well young infants with normal CBC and urine analysis. However, since the prevalence of bacterial meningitis in infant <3 month old is 4 per 1000 patients, and since clinical examination nor CBC is reliable in diagnosing meningitis in this age group; LP should be strongly considered. Older infants and toddlers (3-36 months) Physical examination is more informative in this age group, though some occult infections may still be missed. Diagnostic workup is initiated at temp >39o C (cf infants <3 months where workup is initiated at >38o C). Clinically well babies 3-36 months may have occult SBI in 1.5% cases. Three main occult SBI: Occult bacteremia Occult UTI Occult pneumonia Occult bacteremia: With widespread immunization against H influenza, streptococcus pneumoniae has become the predominant cause of SBI in infants and toddlers.(92% of all occult bacteremias in this age group), but most children in this age group clear spontaneously without antibiotics. However ~10% children with S Pneumoniae bacteremia progress to SBI and approximately 1 case per 1000 to 2500 of these febrile children progress to meningitis. (out of 100 children with S pneumoniae bacteremia -10 will have SBI and 0.5 may go on to meningitis).

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Table 4: Guidelines for evaluations Age 0- 1 months High risk for SBI at >38 C Clinically well Comprehensive workup if >38C LP Admit IV Antibiotics Basic diagnostic workup if >38C (TLC, Band cells, ANC/urine analysis) if positive high risk if negative low risk Observe Review Look for localization Clinically Toxic

ADMIT

1-3 months High risk for SBI at >39C

Comprehensive Diagnostic Workup - TLC - ANC - Bandcells - Urine analysis - Bactec c/s - Urine culture - LP

3-36 months Low risk for SBI at > 39C

Observe/review if < 39C If >39C but well No diagnostic workup Look for red signs/localizing signs No antibiotics If sick/ >39C Basic diagnostic workup if positive look for occult SBI - UTI urine c/s - Pneumonia chest X - ray - Bacteremia Bactec c/s

IV ANTIBIOTICS

References 1. Alpern ER, Alessandrini EA, Bell LM, et al. Occult bacteremia from as pediatric emergency department: current prevalence. Time to Detection and outcome, Pediatrics 2000;106(3):505-11. 2. Backur R, Perry H, Harper MB, Occult pneumonias empirics chest radiographs in febrile children with leucocytosis. Ann Emergency Med 1999;33(2):166-73. 3. Baker MD, Bell lM, Avner JR. Outpatient management without antibiotics of fever in selected infants N Engl J Med 1993,329(20):1437-41. 4. Baraff LJ. Management of fever without source in infants and children. Anm. Emerg Med 2000,36,602-14. 5. Bisgard KM, Kao A, Leak J, et al. Haemophilus influenzae invasive disease in the United States. 1994-1995: near disappearance of a vaccine preventable childhood disease. Emerg Infect Dis 1998:4(2):229-37. 6. Kuppermann N, Hersher G, Jaffa D. Predictors of occult bactermia in young febrile children. Ann Emerg Med 1998;31(6):679-87. 7. Mackowiak PA. Concepts of fever. Arch Intern Med 1998,58(17):1870-81. 8. Steere M, Sharieff GQ, Stenklyft PH. Fever in children less than 36 months of age: questions and strategies for management in the emergency department. J Emerg Med 2003:25(2):149-57. 9. Shaw KN, Gorelick M, Mc Gowan KL. et al. Prevalence of urinary tract infection in febrile young children in the emergency department Pediatrics 1998;102(2):E16. 10. Torrey SB, Henretig F, Fleisher G, et al. Temperature, response to antipyretic therapy in febrile children. Pediatr Emer Care 1987:3(4):223-7. 11. Wenger JD. Epidemiology of haemophilus influenzae typeb disease and impact of haemophilus influenzae typeb conjugate vaccines in the United States & Canada. Pediatr Infect Dis J 1998:17(9 Suppl):S132-6.

Practical recommendations All neonates and young children who appear toxic regardless of age need comprehensive workup including LP, hospitalization and parentral antiboitics in view of serious risk of SBI. Febrile children 1-3 months who are clinically well are also at risk of SBI, hence basic workup is recommended (TLC, ANC, Band cells and urine analysis). o If positive (high risk) a complete diagnostic evaluation is to be carried out, be admitted and treated with IV antibiotics. o If basic diagnostic workup is negative (low risk) they should be followed up from OPD without antibiotics, reviewed in 24 hours for developing signs of toxemia or localization and treated accordingly. Febrile older infants and toddlers (3-36 months) should be treated more selectively, observed and reviewed repeatedly for red flag signs or localization and basic workup needed if temp >39C or child appears sick to identify high risk group for occult infections especially UTI, Pneumonia and bacteremia. Finally, no single examination, no single test or combination of examinations and tests can identify all patients of SBI at the time of initial assessment, so the need for repeated evaluation cannot be over emphasized. Any diagnostic protocol can only serve as adjunct and not as areplacement for clinical judgment. 12 Vol. 8, Issue 2 Jan - March 2009

invites case studies, original, and review articles on different specialties

Please sumit your contributions by email at pmc_pub@ yahoo.co.in, pmc_pub@hotmail.com or by post at the address given below

Pushpanjali Medical Publications Pvt. Ltd.

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Celiac Disease Revisited

Manpreet Sethi
Celiac disease (CD) is an immune-mediated enteropathy that occurs in genetically susceptible individuals following the ingestion of gluten-containing storage proteins of wheat, barley and rye. Grains and genes are the two basic elements in the pathogenesis of CD. Originally considered a rare malabsorption syndrome of childhood, CD is now recognized as a common condition that may be diagnosed at any age and that affects many organ systems. Prevalence: Worldwide, the incidence is approximately 1% reported from many large population-based epidemiological studies. Few population studies have looked at the prevalence of CD in our country. In India, Lal et al have reported an incidence of 0.5-1%. Sood et al1 screened 4347 children aged 3-17 years attending different schools in the Ludhiana district of Punjab, and found an incidence of 0.32%. Most reports of CD are from northern India (Punjab, Delhi, Haryana, Rajasthan, Uttar Pradesh) where wheat is the staple cereal in the diet. It is not surprising that CD in India is under-reported. It can be attributed to various factors including low awareness levels, lack of facilities for endoscopies and biopsies and the poor availability and high costs of serological tests. Moreover, there is poor clinical suspicion in atypical cases and interpretation of histology is varied. Prevalence of CD among siblings of an index patient in our country is as high as 22%-23%.2,3 In the West, the risk of CD in first degree relatives is 13%. Pathogenesis: Gluten is digested by luminal and brush-border enzymes into amino acids and peptides. The gliadin peptides induce changes in the epithelium through the innate immune system and, in the lamina propria, through the adaptive immune system. In the epithelium, gliadin damages epithelial cells, resulting in increased expression of interleukin-15, which in turn activates intraepithelial lymphocytes. These lymphocytes become cytotoxic and kill enterocytes that express MIC-A (a stress protein) on their surface. During infections or as the result of permeability changes, gliadin enters the lamina propria, where it is deamidated by tissue transglutaminase, allowing interaction with HLADQ2 (or HLA-DQ8) on the surface of antigenpresenting cells. Gliadin is presented to gliadinreactive CD4+ T cells through a Tcell receptor, resulting in the production of cytokines that cause tissue damage. This leads to villous atrophy and crypt hyperplasia, as well as the activation and expansion of B cells that produce antibodies. Clinical Manifestations: Compared to the West, CD in India is characterized by a later onset of

Whaet Flour Gluton Glutonine Prolaminoz (Gliadin) Resistent to digestion Transported to Lamina Propria Deamidated gliadin Recognized by HLADQ2 / DQS Aetivation of T Cells Cytokines Interferon a Interulukin 4

Pathogenesis

Albumins, Glebulins

Manpreet Sethi
Consultant Pediatrics Pushpanjali Crosslay Hospital, Ghaziabad, NCR

TNF

Intestinal Mucosal Injury

13 Vol. 8, Issue 2 Jan - March 2009

disease. The mean age of onset of symptoms is 2.4 to 3 years and age at diagnosis is 6.3 to 8.6 (range 2.5 to 14) years, which indicates a delay in diagnosis by 3.4 to 5.9 years.[4],[5],[6],[7] On the other hand, children with CD in the West classically present between 9-18 months of age and the majority are diagnosed by two years of age.[8],[9] Prolonged breast-feeding and delayed introduction of gluten in the diet could be responsible for later onset of CD in Indian children. Delayed diagnosis could be due to lack of CD awareness and presence of recurrent gastrointestinal infections causing diarrhea, protein-calorie malnutrition and nutritional anemia. Over the years, the clinical picture of CD is changing. Previously, the classical form (ie, CD presenting with diarrhea and malabsorption syndrome) used to be the commonest presentation among children. However, nowadays, CD is diagnosed earlier in the silent or asymptomatic stage and also in atypical forms. As a result of this, the proportion of classical CD in the West has decreased. Diarrhea, as a presenting feature of CD, is now seen in only 25-50% of cases 9,10,11 compared to >80% of cases in the 1970s and 1980s.8 However the scene in India is different. Diarrhea (80-94%) is the most common presentation of childhood CD;4,5,6,7 anemia, failure to thrive, and stunted growth are more frequent in India than in the West, reflecting more severe disease that probably correlates with delayed diagnosis. These differences in clinical presentation also suggest that atypical CD in children in India remains undiagnosed. Clinical Manifestations GIT related Chronic diarrhea Abdominal pain Failure to thrive Anorxia Apathy Irritability Vomiting Abdominal distension Muscle wasting Pallor Constipation Non GIT Hematological Iron deficiency anemia Folate deficiency Vit. B12 deficiency

criteria13 which are listed in the table below. Histology revisited MODIFIED MARSH SCORE 0 IEL<40/100 EC & atleast 4 villi seen (<40/100 EC IEL, normal villi) 1 >40/100 EC IEL, normal villus & crypt ht 2 >40/100 EC IEL, hyperplastic crypts, normal villi 3a >40/100 EC IEL, mild villus flattening, crypt ht 3b >40/100 EC IEL, mod villus flattening, crypt ht 3c >40/100 EC IEL, total villus flattening, crypt ht 4 hypoplasia The spectrum of histological changes of CD is well recognized in the western population. In developing country settings, it is not routinely considered as a likely diagnosis in children presenting with chronic diarrhea and a mild to moderate (modified Marsh 1-3b) blunting of intestinal villi. More likely, it is assumed that such a lesion may be caused by tropical sprue, persistent enteric infection or infestation, post infectious complications, or protein energy malnutrition with associated small bowel bacterial overgrowth. Recent data have shown that among Indian children with chronic diarrhea confirmed to have CD, classical flat mucosa with crypt hyperplasia was present only in one third of children while a similar proportion had crypt hyperplasia with moderate villous blunting.14 Interestingly among children in whom the mucosal changes were limited to mild blunting of villi (equal crypt depth and villus height), at least a third were confirmed to have CD by the presence of serological antibodies, clinical response to gluten free diet and a positive gluten challenge. On the other hand, even severe villous atrophy may not always mean CD in the Indian context because such lesions are commonly seen with primary protein energy malnutrition, recurrent gastrointestinal infections including parasitic infestations and these children develop anemia, diarrhea, growth failure, vitamin deficiencies; all of which adversely affect small bowel histology. Therefore, in India, it is suggested to do CD serology at diagnosis. In a given clinical setting, antibody positivity along with typical small intestinal mucosal changes and response to GFD is helpful to establish the diagnosis. Serological Tests: The first immunological assay to be tested were the anti-gliadin antibodies (AGA) which are predominantly of the IgG and IgA class and done by solid phase ELISA. However, post infection malabsorption, Crohns disease and cows milk protein intolerance can give false positive tests for AGA. The variability and generally lower accuracy associated with the AGA tests make them unsuitable for diagnostic or screening purposes. Anti-EMA (anti-endomysial antibodies) primarily belongs to the IgA class and is directed against the intermyofibril substance of the smooth muscle. Anti-EMA is identified using indirect immunofluorescence on frozen sections of monkey esophagus or human umbilical cord sections. Positive serum samples react with the connective tissue which surrounds the smooth muscle bundles in the lamina propria, and give a characteristic lacework pattern around the unstained smooth muscles cells.15 14

Non GIT Biochemical Elevated SGOT/SGPT Elevated pancreatic enzymes Endocrine Short stature Hypogonadism Amenorrhea Neurological Seizures, peripheral neuropathy Brain white matter lesions on MRI Miscellaneous Dermatitis herpetiformis Cryptogenic hepatitis Dental enamel defects Recurrent aphthous stomatitis Osteopenia

Diagnosis Histology: At present the gold standard of diagnosing CD is the modified European Society of Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) criteria.12 Diagnostic criteria ESPGHAN 1969 3 biopsy criteria with clinical response / relapse ESPGHAN 1989 1 biopsy criteria with clinical response Positive serology helps Repeat biopsy may be required in <2 years Detailed histological evaluation should be based on Marsh

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The discovery of anti- tissue trans- glutaminase antibodies (antitTG) as the autoantigen recognized by the endomysial antibodies is seen as a major breakthrough[16].This test is carried out using the ELISA technique and substrates used include the guinea pig antigen and now even the human recombinant tTG antigen. What antibodies are most reliable?17 SENSITIVITY India Anti gliadin IgG IgA AEA tTG (g.pig) tTG (human) 75 80-94 90 76 69-85 75-90 85-98 85-98 93 78 84-92 95 94 73-90 82-90 94-100 94-95 99 West SPECIFICITY India West

3. Matrix mettaloprotienases (MMPs) 4. Plasma Nitric oxide products HLA: There is a strong genetic association of CD with HLA DR3DQ2 inherited as an extended haplotype. Patients negative for DQ2 are positive for DQ8 and therefore 90-95% of individuals with CD have an association with DQ2 or DQ8. DQ2 and DQ8 molecules bind gliadin-derived peptides, some after deamidation by tissue transglutaminase, and present them to the intestinal T lymphocytes. The activated Th1 T cells secrete proinflammatory cytokines which produce the intestinal lesions of CD.25 These findings could explain the role of HLA and tTG in the pathogenesis of the disease. However DQ2 is also present in 20-25% of the normal population as reported from the western population and North India.26 While HLA DQ2 typing is not recommended for routine diagnosis as it is cumbersome and expensive, it can be used for ruling out CD where the diagnosis is equivocal as it has a negative predictive value of greater than 95%.26 Is Gluten Challenge Necessary? Gluten challenge is not mandatory, but may be indicated when there is doubt about the diagnosis. Since cows milk sensitive enteropathy and post enteritis syndrome occur in the first two years of life, gluten challenge is usually recommended in children diagnosed within the first two years of life. It should be considered in patients with equivocal clinical response to GFD and in those who were asymptomatic at first presentation diagnosed through at risk screening programs. Wherever gluten challenge is required it should be avoided before 6 years of age to minimize risks for dental enamel defects and during periods of rapid growth like puberty. Treatment The mainstay of management in CD is life long GFD; and iron and folic supplementation for the first 3 months after diagnosis. The patient should be reassessed between 8-12 weeks after starting GFD to look for response to treatment ie, improvement of symptoms and growth parameters. This is the stage when the diagnosis is finally confirmed (as per modified ESPGHAN criteria). CD in India occurs mainly in regions where wheat is a staple diet. Families at the first contact are worried due to prolonged illness of their child despite several consultations from doctors. Parents and older children should be counseled following confirmation of diagnosis. Dietary advice of gluten avoidance and drug supplementation is readily accepted. Since we do not have marketed gluten free products available in India, each center has to devise GFD charts in local languages. A visible response is the key factor that gives parents confidence to strictly adhere to GFD despite difficulties in implementation particularly in families where other members consume wheat as a staple diet. The major hardship faced by parents is to fulfill the special needs of their CD children like birthday cakes, chocolates, ice creams, biscuits etc, and social participation on different occasions. Nonavailability of ready-made gluten-free foods (bakery products and gluten-free flour) and unlabelled food packs in India are bottlenecks in the dietary management of CD. In our country, though vegetarian symbol has been implemented, the glutenfree symbol on packed foods is not yet introduced. The reason 15

While the performance of the anti-EMA is superior to anti-tTGA, [18] interpretation of immunofluorescence assay (IFA) for antiEMA tests is operator-dependent and more liable to errors in less experienced hands. ELISA based detection of anti-tTGA is a simpler and more accessible diagnostic tool and anti-human recombinant transglutaminase antibodies is reported to perform better to the anti guinea pig transglutaminase antibodies.19 The disadvantage of the anti EMA and anti-tTGA is that they are unreliable in less than 2 years.20,21 Further they are IgA dependent antibodies and will be negative in those with selective IgA deficiency, as is seen in 3% of individuals with CD.22 In children with a high clinical and histological suspicion of CD but a negative IgA based serology, IgA deficiency needs to be excluded. The IgG AGA or the more recently evaluated IgG EMA or the IgG tTGA would be useful in these situations. Since the positive cut-offs have been designed to optimize the sensitivity of the test, it is recommended that using higher cut-off values while using these tests for screening asymptomatic individuals at risk will improve the specificity and the positive predictive value. Barker et al have shown that the sensitivity and specificity was as high as 98% and 97% respectively when cutoff values of > 100 U and <20 U were used.23 Certain caution is required while interpreting the anti tTGA ELISA assays for routine diagnostic purposes. The different source of tTG antigen, varied techniques of production i.e. genetically engineered or tissue extraction, and the use of arbitrary units by different commercial kits for defining a positive cut can influence the diagnostic accuracy of the assay. The false positivity rates have ranged from 28% to as high as 80% using the assay cut-off of four different tTG assays. 24 This variation in the assays emphasizes the need for global and national standardization among different laboratories. High false positivity has also been reported from patients with liver disease, inflammatory bowel disease and connective tissue disorder. 24 New antibodies in the pipeline (to assess disease severity and response to treatment): 1. IgA anti- actin antibodies (IgA AAA) 2. Soluble CD163

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for this is a limited number of CD cases and non-feasibility at the commercial level. In India, it is common practice for families to purchase whole grain and have the flour processed at a small neighborhood flourmill, where other cereals like corn and rice are ground separately at a different time slot after cleaning the grinding machine. These measures are inadequate, and some quantity of wheat gets mixed with other cereals27 and may be a factor of non-response in a strictly compliant patient. Therefore patients should be taught to use home grinding solely for gluten-free flour. Patients mostly adhere to follow-up visits. Noncompliance is observed by consuming toffees, sharing food with other schoolmates, or in large joint families ingestion of gluten containing domestic food items. On each follow-up visit adherence to diet must be emphasized, and growth parameters and sexual maturity monitored wherever applicable as well as a search for complications if any. Diet chart for CD patients Food Items Drinks Rice Fresh Juice Sabudana Fresh Milk Arrowroot Fresh Curd Bajra Fresh Lassi Makka Fizzy Drinks Jowar Soda Singhara atta Fresh Soup Idly Desserts Dosa Rice Kheer Vada Paneer Sandesh Mumura Caramel Custard Rice Noodles Carrot Halwa Fresh Meat Jaggery Fresh Mutton/Chicken Egg / Fish Diet chart for CD patients Food Items Drinks Atta /Maida Hot Chocolate Suji Complan Rye Horlicks Barley Boost Noodles Bottled Milk Shake Pasta/ Sphagetti Soup Powder Bread/ Bun Desserts Soup Stick Cake Sevian Pastry Dalia Ice Cream Patty/ Pizza clair Burger Chocolate Kulcha Jalebi Bhujia Gulab Jamun Upma Sevian Tinned and Canned Preparations Biscuits Preparation containing baking powder Processed meats like Sausages and Kebab Complications of Untreated CD There is a continued interest in the long term consequences of CD, which of course has particular significance in the group of silent CD individuals detected on screening, 16 Vol. 8, Issue 2 Jan - March 2009

and those that are poorly compliant with the gluten-free diet. It has been proposed that even a brief period of a GFD may confer relative protection to the sequelae of CD. Listed below are the major consequences and complications associated with untreated CD. Apart from these, delayed diagnosis and failure to adhere to a GFD has also been associated with increased prevalence of other autoimmune conditions, mortality and malignancies. Consequences of untreated CD Growth abnormalities Anemia Nutritional deficiencies Fe Folic acid B12 Zn Fat soluble vitamins Hormonal disturbances Delayed sexual maturity Infertility/recurrent abortions/low birth weight Hypothyroidism Gastrointestinal related Malignancies (small bowel lymphomas) Delayed gut transit (constipation/reflux) Refractory Celiac Disease Approximately 5% of patients may have refractory CD, defined as persistent symptoms and villous atrophy despite scrupulous adherence to a gluten-free diet28. The symptoms that usually develop in these patients include diarrhea, weight loss, recurrence of malabsorption, abdominal pain, bleeding, and anemia, and ulcerative jejunitis often arises as well. This syndrome is also known as Refractory sprue. Refractory CD may be classified as type 1, in which there is a normal intraepithelial lymphocyte phenotype, or type 2, in which there is a clonal expansion of an aberrant intraepithelial lymphocyte population and a high risk of developing intestinal T cell lymphoma. Treatment of refractory CD involves nutritional support and repletion of vitamins and minerals, together with a strict gluten-free diet. In most cases, corticosteroids induce clinical improvement29. Immunosuppressive drugs may be beneficial30 but should be used with caution, since they may promote the progression to lymphoma31. Other proposed modalities include anti-TNF alpha, and stem cell transplantation but their role in management of refractory CD needs to be evaluated further. Summary CD occurs in nearly 1% of the population in many countries. The diagnosis, which is straightforward in most cases, is usually established on the basis of serologic testing, duodenal biopsy, and observation of the response to a gluten-free diet. Increasing awareness of the epidemiology and diverse manifestations of the disease, as well as the availability of sensitive and specific serologic tests, especially among primary care physicians, will lead to more widespread screening and diagnosis, which in turn will lead to greater availability of gluten-free foods and efforts to develop drug therapies that relieve patients of the burden of a gluten-free diet. In addition, earlier diagnosis may lead to a reduction in the complications of the disease.

Key Messages Prevalence of CD is high in India. It may present with protean manifestations; atypically presenting disease must be picked up more often. Serology is helpful in screening; Confirmatory diagnosis is still by histopathology. Correct interpretation of histology is of prime importance. Management is based on strict life long gluten free diet and continuous supervision and monitoring under a pediatric gastroenterologist and nutritionist. All cases may not respond to Gluten free diet (Refractory Celiac). References 1. Sood A, Midha V, Sood N, Avasthi G, Sehgal A. Prevalence of Celiac Disease among school children in Punjab, north India. J Gastroenterol Hepatol 2006;21:1622-5. 2. Gautam A, Jain BK, Midha V, Sood A, Sood N. Prevalence of Celiac Disease among siblings of Celiac Disease patients. Indian J Gastroenterol 2006;25:233-5. 3. Goel GK, Pokharna RK, Khatri PC, Senger GS, Joshi A, Khatri M, et al . Prevalence of Celiac Disease in first-degree siblings of Celiac Disease patients. Indian J Gastroenterol 2007;26:46. 4. Mohindra S, Yachha SK, Srivastava A, Krishnani N, Aggarwal R, Ghoshal UC, et al. Celiac Disease in Indian children: assessment of clinical, nutritional and pathologic characteristics. J Health Popul Nutr 2001;19:204-8. 5. Poddar U, Thapa BR, Nain CK, Prasad A, Singh K. Celiac Disease in India: are they true cases of CD? J Pediatr Gastroenterol Nutr 2002;35:508-12. 6. Patwari AK, Anand VK, Kapur G, Narayan S. Clinical and nutritional profile of children with Celiac Disease. Indian Pediatr 2003;40:337-42. 7. Poddar U, Thapa BR, Singh K. Clinical features of Celiac Disease in Indian children: are they different from the West? J Pediatr Gastroenterol Nutr 2006;43:313-7. 8. Walker Smith JA. Celiac Disease. In: Disease of the small intestine in childhood, 3rd edn. Butterworths, London 1988; p. 88-143. 9. Bottaro G, Failla P, Rotolo N, Sanfilippo G, Azzaro F, Spina M et al. Changes in Celiac Disease behaviour over the years. Acta Pediatr 1993;82:566-8. 10. George EK, Mearin ML, Franken HCM, Houwen RH, Hirasing RA, Vandenbroucke JP. Twenty years of childhood Celiac Disease in the Netherlands: a rapidly increasing incidence? Gut 1997;40:61-6. 11. Ascher H, Holm K, Kristiansson B, Maki M. Different features of Celiac Disease in two neighboring countries. Arch Dis Child 1993;69:374-80. 12. Walker-Smith JA, Guandalini S, Schmitz J, Schmerling DH, Visakorpi JK. Revised criteria for diagnosis of Celiac Disease. Arch Dis child 1990;65:909-11. 13. Oberhuber G, Granditsch G, Vogelsang H. Histopathology of Celiac Disease: time for standardized report scheme for pathologist. Eur J Gastroenterol 1999;11:1185-94. 14. Bhatnagar S, Gupta SD, Mathur M, Phillips AD, Kumar R, Knutton S, Unsworth DJ, Lock RJ, Natchu UC, Mukhopadhyaya S, Saini S, Bhan MK. Celiac Disease with mild to moderate histologic changes is a common cause of chronic diarrhea in Indian children. J Pediatr Gastroenterol Nutr 2005 Aug; 41(2) : 204-209. 17 Vol. 8, Issue 2 Jan - March 2009

15. Bhatnagar S, Bhan MK Serological diagnosis of Celiac Disease. Indian J Pediatr 1999; 66(1 Suppl): S26-31. 16. Dieterich W, Ehnis T, Bauer M, Donner P, Volta U, Riecken EO, Schuppan D. Identification of tissue transglutaminase as the autoantigen of Celiac Disease. Nat Med 1997 Jul;3(7): 797801. 17. Bhatnagar S and Tandon N. Diagnosis of Celiac Disease. Indian J of Pediatr, Volume 73 August, 2006. 18. Rostom A, Dube C, Cranney A, Saloojee N, Sy R, Garritty C, Sampson M, Zhang L, Yazdi F, Mamaladze V, Pan I, MacNeil J, Mack D, Patel D, Moher D. The diagnostic accuracy of serologic tests for Celiac Disease: a systematic review. Gastroenterology 2005 Apr; 128(4 Suppl 1) : S38S46. 19. Sblattero D, Berti I, Trevisiol C, Marzari R, Tommasini A, Bradbury A, Fasano A, Ventura A, Not T. Human recombinant tissue transglutaminase ELISA: an innovative diagnostic assay for CD. Am J Gastroenterol 2000 May; 95(5): 12531257. 20. Agardh D, Borulf S, Lernmark A, Ivarsson SA. Tissue Garcia-Masdevall MD. Antibodies to gliadin, endomysium, transglutaminase immunoglobulin isotypes in children with and tissue transglutaminase for the diagnosis of Celiac Disease. untreated and treated Celiac Disease. J Pediatr Gastroenterol Nutr J Pediatr Gastroenterol Nutr 1999 Nov; 29(5): 571-574. 2003 Jan;36(1) : 77-82. 21. Burgin-Wolff A, Gaze H, Hadziselimovic F, Huber H, Lentze MJ, Nussle D, Reymond-Berthet C. Antigliadin and antiendomysium antibody determination for Celiac disease. Arch Dis Child 1991 Aug; 66(8): 941-947. 22. Bhatnagar S, Natchu MU. Celiac Disease in Indian children. Natl Med J India 2004 May-Jun;17(3) : 124-127. 23. Picarelli A, Sabbatella L, Di Tola M, Vetrano S, Casale C, Anania MC, Porowska B, Vergari M, Schiaffini R, Gargiulo P.Antiendomysial antibody of IgG1 isotype detection strongly increases the prevalence of celiac disease in patients affected by type I diabetes mellitus. Clin Exp Immunol 2005 Oct; 142(1): 111-115. 24. Liu E, Li M, Bao F, Miao D, Rewers MJ, Eisenbarth GS, Hoffenberg EJ. Need for quantitative assessment of transglutaminase autoantibodies for Celiac Disease in screening-identified children.J Pediatr 2005 Apr;146(4) : 494499. 25. Molberg O, Mcadam SN, Korner R, Quarsten H, Kristiansen C, Madsen L, Fugger L, Scott H, Noren O, Roepstorff P, Lundin KE, Sjostrom H, Sollid LM. Tissue transglutaminase selectively modifies gliadin peptides that are recognized by gut-derived T cells in CD. Nat Med 1998 Jun; 4(6) : 713-717. 26. Kaur G, Sarkar N, Bhatnagar S, Kumar S, Rapthap CC, Bhan MK, Mehra NK. Pediatric Celiac Disease in India is associated with multiple DR3-DQ2 haplotypes. Hum Immunol 2002 Aug; 63(8) :677-682. 27. Walker Smith JA. CD. In: Disease of the small intestine in childhood, 3rd edn. Butterworths, London 1988; p. 88143. 28. Trier JS. Celiac sprue. N Engl J Med 1991;325:1709-1719. 29. Cellier C, Delabesse E, Helmer C, et al. Refractory sprue, celiac disease, and enteropathy-associated T-cell lymphoma. Lancet 2000;356:203-208. 30. Peter H.R. Green, and Christophe C. Celiac Disease. N Engl J Med 2007;357:1731-1743.

Improving Cure Rates and reducing side-effects by modern Radiotherapy Techniques

Dinesh Singh
Radiotherapy is one of the three main treatment modalities of cancer treatment. The other two being Cancer surgery and Chemotherapy. Radiotherapy utilizes ionizing radiation to inactive DNA of cancer cells. Most common equipment used for this purpose in the western world is Linear Accelerator, but in India it is the Cobalt Machine because of cost of equipment and that of running and maintaining it.

Cobalt Machine

Linear Accelerator elivers ocused nd electable d f a s energies that help reduction of side effects and all further developments have happened in the technology of Linear Accelerator. Devices such as Multi leaf Collimator for giving irregular shapes are present like Digital Portal Imaging Device for portal verification, Computerized Treatment Planning System for fast and accurate calculation of complex plans. These help generate 3D Conformal plans for better delivery to target tissues.

IMRT or intensity Modulated Radiotherapy gives irregular plans which can treat tumor tissues accurately and spare normal tissues. Technology goes a step further where in a CT scanner is mounted on to the Linear Accelerator. Given below is a plan generated for 3D Conformal and IMRTT Technology goes a step further where in a CT scanner is mounted on to the Linear Accelerator.

Intensity Modulated RT (IMRT)

(a) 3DCRT (b) IMRT (c) IMRT (0.5 cm cord margin)

Dinesh Singh
Director, Department of Radiation Oncology Galaxy Cancer Institute Pushpanjali Crosslay Hospital Ghaziabad, NCR

19 Vol. 8, Issue 2 Jan - March 2009

This allows us to perform Image Guided Radiotherapy, when we have a CT scan mounted on the Linear Accelerator, we can actually see what we are treating. Because of this confidence, a reduction in the margins for radiation given especially when the treatment area cannot be visualized. This feature permits selective radiation to the target only, thus save normal tissues from higher radiation. This translates in High cure rates and lower side effects.

Galaxy Cancer Institute, Pushpanjali Crosslay Hospital

Brachytherapy, like external radiation has evolved tremendously. In the current updation, High Dose Rate, radiation is delivered in minutes, whereas in the earlier models it took days to deliver an equivalent dose. Brachytherapy, helps deliver very high doses precisely to the tumor site.
G alax y C anc er Ins titute @ P us hp anjali C ros s lay H os pital
W 3, S ec tor 1, Vais hali (Near G az ip ur B order)

Another complimentary technology is one in which radioactive sources are inserted into the tumor or near vicinity of this. This technology is called Brachytherapy.

In many cases, a combination of these two modalities is used to give very high dose of radiation, leading to 1) High Cure Rates 2) Low side effects of radiation. All the above techniques are available at Galaxy Cancer Institute, Pushpanjali Crosslay Hospital.

20 Vol. 8, Issue 2 Jan - March 2009

Office Management of Asthma

Deepak Pande
Asthma and wheezing disorders account for a large number of children coming to clinics. While acute asthma is attended to by virtue of the severity of symptoms, persistent asthma remains a grossly underreported, underdiagnosed and undertreated disease resulting in considerable morbidity in children. Recent developments have greatly improved the management of these disorders to a good extent. Diagnosis History of recurrent episodes of cough, breathlessness, wheezing, tightness of chest should alert the clinician. Exam may reveal rhonci, prolonged expiration, a silent chest or may even be normal. Some other features may also be suggestive of asthma. These include personal or family history of skin allergy, absence of fever in above episodes, night symptoms, symptoms induced by exercise or on exposure to specific allergens eg, pollens, house dust, food etc. Response after inhalation of bronchodilator is also a good indicator of diagnosis. Some other diseases (especially in young children) may present with features of asthma in addition to other features, which helps in exclude them. Some of these are GER, bronchiolitis, cong. defects, immunodeficiency, mucociliary defects, cystic fibrosis, adenoids, tuberculosis, foreign body, allergies to foods. Children less than 5 years age often have viral LRTI, which may be associated with wheezing and is recurrent. Although most children recover within a period of time some may continue to have recurrent wheezing in adolescence. Investigations 1. Investigations are not a must in treating asthma. 2. Hemogram and X-ray chest may be done to serve as baseline. 3. Respirometry and peak flow measurements may be used as diagnostic and monitoring tools but they have many limitations Feature Daytime Symptoms* Limitation of activity Night symptoms Reliever med. reqd. PFT (if done) Acute Exacerbations* Green (low risk) Nil (<2/wk) Nil Nil Nil (<2/wk) normal Nil and are not usually used in day-to-day practice. Tests for allergy eg, IgE, specific IgE, RAST, skin testing for allergies have a limited role.

4.

Assessing Control Degree of control achieved is used to guide the therapy. Long Term Management The goal is to reach the level of control where there are no daytime symptoms, no limitation of activity, no night symptoms, and no need for reliever medicines. Additionally, pulmonary functions are normal, and there are no exacerbations. At this time, maintenance with minimum medications should be attempted. There are five components essential to management of asthma. 1. Developing a patient/Caregivers/ Parent/ Doctor partnership: Since asthma is a chronic disease with long-term management, developing a strategy of a guided self management plan brings the best results. The goals of treatment are arrived after discussion with parents and a written plan is prepared. Patient is taught self-monitoring techniques (by symptoms or by peak flowmeter), to help adjust therapy within the parameters of the plan, recognize an exacerbation, and then followed-up every 4-8 weeks for monitoring and education. During these visits, some of the key issues to be discussed include: chronic and episodic nature of disease, ie, no cure, but control; need for compliance as drugs take time; merits and correct use of inhalation therapy 2. Prevention of asthma or its symptoms: Avoidance of smoking in pregnancy and ensuring smoke free environment for the newborn may reduce development or occurrence of symptoms. Exclusive Red (high risk) Up to 2 features deranged in a week Uncontrolled >2 features deranged in a week

Deepak Pande
Consultant Pediatrician Pushpanjali Medical Centre, Delhi Pushpanjali Crosslay Hospital, Ghaziabad, NCR

Any/yr.

Any/wk.

*Progressive in symptoms makes it exacerbated.

21 Vol. 8, Issue 2 Jan - March 2009

breastfeeding in early infancy may protect against episodes of wheezing later. Any food, drug, additive known to precipitate symptoms should be avoided. Taking reasonable precautions, helps avoid indoor and out door allergens. These involve washing bed linen every 10 days with hot water, use of plastic covered pillows and mattresses, removing dampness from walls, avoiding carpets and upholstery, vacuum cleaning, removing furred pets from home. Outdoor allergens can be avoided by staying indoors with window and doors closed during seasons, and avoiding the outdoors in dry, cold weather. Exercising after proper warming up is encouraged.

3.

Assess, Treat and Monitor: Inhalation therapy is most effective form of treatment and pressurized Meter Dose Inhalers (pMDI) are most versatile devices, which can be used across all ages. It is preferred as it reduces local and systemic side effects and makes it easier to use. A facemask is required for children less than 4 years. Nebulizers, dry powder inhalers, breath actuated inhalers are other alternatives. The technique of inhalation should be demonstrated and checked at every visit. a) Ages 5 years and above: Drug options are arranged into five steps (Table 2) of increasing efficacy. Every patient fits into one of the steps and treatment is stepped up

Table 2: Management based on control

Management Approach Based On Control For Children Older Than 5 Years, Adolescents and Adults
Level of control Controlled Partly controlled Uncontrolled Exacerbation Reduce Treatment action Maintain and find lowest controlling step Consider stepping up to gain control Step up until controlled Treat a exacerbation

Reduce Step 1 As needed rapid acting 2-agonist Select one Low-dose inhaled ICS* Step 2

Treatment Steps Step 3 Step 4

Increase

Increase Step 5

Asthma education Environmental control Select one Low-dose ICS plus long-acting 2-agonist Add one or more Medium-or high-dose ICS plus long-acting 2-agonist Add one or both Oral glucocorticosteroid (lowest dose)

Controller options****

leukotriene modifier**

Medium-or high-dose ICS

Leukotriene modifier

Anti-IgE Treatment

Low-dose ICS plus Leukotriene modifier Low-dose ICS plus sustained release theophylline

Sustained release theophylline

* ICS=inhaled glucocorticosteroids **=Receptor antagonist or synthesis inhibitors ***Preferred controller options are shown in shaded boxes Alternative reliever treatments include inhaled anticholinergics, short-acting oral _2-agonists, some long-acting _2-agonists, and short-acting theophylline. Regular dosing with short and long-acting _2-agonist is not advised unless accompanied by regular use of an inhaled glucocorticosteroid. 22 Vol. 8, Issue 2 Jan - March 2009

Table 3: Controller drugs Drug ICS: Beclometh, Budesonide, Fluticasone MOA Antiinflammatory Avail as Inhalation Low dose <200 Med dose 200400/500 High dose >400/500 Oral 4, 5, 10m g All Age Side Effects Oral thrush Growth, pub delay (High doses) Remark Used at all levels

Leukotrine modifiers, Montelucast LABA Salmeterol, Formeterol SR theophylline, Cromones SR SABA (SR salbutamol, terb, bam)

Anti leukotrines

>2 yrs

Nil

At all levels, Exercise Induced Asthma, Inferior alternatives Add-on after low dose ICS Monotherapy, Add-on, All are Inferior alternatives

Long acting brdil

Inhalation

>4-5 yrs ><5 yrs >5 yrs

Nil in comb with ICS Serum Levels (if>10 mg/kg/day) ++

Anti-inflammatory Oral Long acting brdil Oral Oral

4.

or down according to the level of control, which is assessed each time the patient reports for follow-up. An exacerbation should be actively considered for stepping up control therapy, if the preceding period shows a loss of control. Every step up requires 3 months of observation before further step up. If the patient is controlled for 3 months, consider stepping down a step at a time until the minimum required dose for maintaining control is reached. When the patient has been controlled for 1 year and is on minimum doses for 3 months, consider stopping but continue follow-up. Every patient should continuously receive asthma education, environment control and a rapid acting B2 Agonist as required. b) Ages <5 years: ICS in low-med doses is the best option for control. Leukotrine modifiers may be used >2 years. In view of good spontaneous recovery in most young children, stepping down may be considered just as control is achieved and need for therapy reviewed at 6 months of control. Manage Exacerbations: Whenever acute increase in symptoms is reported, patient is advised to take 2-4 puffs

of Rapid Acting B2 Agonist (salbutamol) every 20 minutes up to 3 times. If relief is not sustained for 4-6 hours or if risk factors (Table 4) are present, first dose of oral steroid (prednisolone 1mg/day) is started and an early appointment is scheduled. In case of severe exacerbations or if risk factors are noted any time further treatment should be carried out in an acute care facility. Table 4: Red flag signs (Risk factors) Altered sensorium, Bradycardia, low vol pulse, cyanosis, exhaustion, diaphoresis, silent chest, abnormal ABG, SpO2<92

5.

Special Situations: Special considerations are required in managing surgery, rhinitis, sinusitis, nasal polyps, respiratory infections, GER, anaphylaxis in asthmatics.

Referencs 1. GINA - the Global Initiative For Asthma - http://www. ginasthma.com

23 Vol. 8, Issue 2 Jan - March 2009

Common Drugs Acting on

Cardiovascular System and Optimal Dosing Time
Drugs Calcium channel blockers Isradipine sustained release formulation Isradipine sustained release formulation Nifedipine GITS Nifedipine GITS Amlodipine Nisoldipine extended release Cilnidipine Verapamil extended-release (marketed as Covera-HS) Diltiazem extended release (marketed as Cardizem LA) Angiotensin II receptor blockers Losartan Ibesartan Olmesartan medoxomil Valsartan Telmisartan Telmisartan Candesartan cilexetil Angiotensin-converting enzyme inhibitors Benazepril Perindopril Quinapril Ramipril Trandolapril Lisinopril Enalapril Beta-blocker Metoprolol succinate sustained release Carvedilol Carvedilol phosphate extended release Propranolol extended release Antihyperlipidaemic drugs Statins with a shorter half-life (ie, lovastatin, simvastatin and fluvastatin) Vol. 8, Issue 2 Jan - March 2009 Evening Patients with hypercholesterolaemia Morning Evening Morning Bedtime Patients with hypertension, angina pectoris or heart failure Patients who have been treated with first-line antihyperten Patients with heart failure, left ventricular dysfunction fol Patients with hypertension Morning Morning Evening Bedtime Bedtime Bedtime Bedtime Patients with primary mild-to-moderate hypertension Patients with primary mild-to-moderate hypertension Patients with primary mild-to-moderate hypertension Patients with primary mild-to-moderate hypertension Patients with primary mild-to-moderate hypertension Patients with primary mild-to-moderate hypertension Patients with primary mild-to-moderate hypertension Uncertain Regardless of time Regardless of time Bedtime Bedtime Morning Awakening Patients with uncomplicated, mild-to-moderate essential Patients with uncomplicated, mild-to-moderate essential Non-dipper hypertensive patients Non-dipper hypertensive patients Young men with mild or moderate essential hypertension Patients with mild-to-moderate essential hypertension Evening Regardless of time Bedtime Regardless of time Morning Morning Bedtime Bedtime Bedtime Hypertensive patients with chronic renal failure Patients with uncomplicated essential hypertension Patients who are non-responders to the initial 30 mg/day Hypertensive patients receiving 30 mg/day nifedipine GITS Patients with mild-to-moderate essential hypertension Patients with mild-to-moderate essential hypertension Patients with uncontrollable morning hypertension Angina or hypertensive patients Angina or hypertensive patients Optimal dosing time Patients

24

Statins with longer half-lives (ie, fluvastatin extended release, rosuvastatin and atorvastatin) Pravastatin Atorvastatin Ezetimibe Ezetimibe/simvastatin tablet Fenofibrate retard Bezafibrate retard Doxazosin GITS

Regardless of time

Patients with hypercholesterolaemia

Evening Evening Morning Evening Regardless of time Morning Morning Regardless of time

Patients with hypercholesterolaemia Patients undergoing PCI Patients with primary hypercholesterolaemia Patients with primary hypercholesterolaemia Patients with hypertriglyceridaemia Patients with hypertriglyceridaemia Patients with grade 12 essential hypertension Patients with benign prostatic hyperplasia Patients who are at risk for a cardiovascular and/or cerebrovascular event Patients with angina pectoris

Low-dose aspirin Isosorbide mononitrate sustained-release formulation (eg, Elantan LA, IMDUR) Diuretics Indapamide, hydrochlorothiazide Torasemide Once-daily hydrochlorothiazide based fixed-dose combination

Bedtime Awakening

Morning Bedtime Before 6 pm and preferably in the morning

Patients with essential hypertension Patients with essential hypertension Patients with essential hypertension

Cited in: Zhu L-L, Zhou Q, Yan X-F, Zeng S. CME - Optimal Time to Take Once - Daily Oral Medications in Clinical Practice. J Clin Pract 62(10):1560-1571, 2008.

25 Vol. 8, Issue 2 Jan - March 2009

The Role of Spirituality in Medicine

Amit Gupta
The focus of spirituality in the practice of medicine has increased to historic levels in recent years. Victor Frankl,1 a psychiatrist who wrote of his experiences in a German Nazi camp, stated: Man is not destroyed by suffering; he is destroyed by suffering without meaning. Spirituality is a personal search for meaning and purpose in life, which may or may not be related to religion. In 1992, only one medical school had a formal course in spirituality and medicine, which was an elective course. Today, more than 70 medical schools in the United States offer courses on spirituality and medicine.2 Spirituality is at the heart of the patient-centered rather than disease-centered medicine. The goal of good medical care is to act in the best interest of the patient. Religion and spiritual practices are among the resources used by the patients to cope with chronic pain. Dr. Sarah M Whitman3 said that religion and spirituality are often important to patients. She describes the way the Hindu traditions deal with pain and suffering including the concept of acceptance and she finds that these concepts will be helpful when treating not only followers of Hinduism but all patients. The results of fMRI (functional MRI) study support the notion of increased activity in the regions of amygdala and hippocampus during meditation.4 Activity of parasympathetic system would also cause a reduction in heart rate and respiratory rate. All of these physiological responses have been observed during meditation.5 Intercessory prayers and colloquial prayers were associated with higher levels of well being and life satisfaction. Meditation may decrease anxiety, depression, irritability and moodiness as well as improve learning ability, memory, self-actualization, feelings of vitality and rejuvenation, and emotional stability.6 Experiments have shown that blood lactate levels drop four times faster when subjects meditate than when subjects simply lie on 29 Vol. 8, Issue 2 Jan - March 2009 their backs.7 Yoga has shown benefit in patients with asthma, hypertension, heart failure, mood disorders, and diabetes.8 To conclude, the prevalence of spiritual and religious activities makes it important for all pain management professionals to understand and to be prepared to discuss these issues.

References 1. Frankl VE. Mans Search for Meaning. New York: Simon and Schuster;1984;1822. 2. Miriam SW, Eisenberg DM, Kaptchuk TJ. Courses Involving Complementary and Alternative Medicine at US Medical Schools. JAMA. 1998;280:784-787. 3. Whitman SM. Pain and Suffering as viewed by the Hindu Religion. The Journal of Pain, 1998; 8(8):A12-A16. 4. Lazar, Sara W. Bush G, Gollub et al. Functional brain mapping of the relaxation response and meditation. NeuroReport: 2000;11(7):1581-1585. 5. Teresa ES, DubinLF, Seeman M. Religiosity/ Spirituality and Health: A Critical Review of the Evidence for Biological Pathways. American Psychologist 2003:53 6. Harinath K, Malhotra AS, Pal K et al. Effects of Hatha Yoga and Omkar Meditation on Cardiorespiratory Performance, Psychologic Profile, and Melatonin Secretion The Journal of Alternative and Complementary Medicine. 2004,10(2):261268. 7. Delmonte MM. Meditation and anxiety reduction: A literature review. Clinical Psychology Review 1985;5(2):91-102. 8. Ramesh LB, Rama PM, Yadav RK et al. A Brief but Comprehensive Lifestyle Education Program Based on Yoga Reduces Risk Factors for Cardiovascular Disease and Diabetes Mellitus. The Journal of Alternative and Complementary Medicine. 2005,11(2):267-274.

Amit Gupta
Consultant & Head Emergency & Critical Care Pushpanjali Crosslay Hospital Ghaziabad, NCR

Clinical challenge: Acute appendicitis with pregnancy (Three case reports, one in each trimester)
AK Mittal
Introduction Acute appendicitis is most common extra uterine surgical emergency which need surgical intervention. It is a challenge for the obstetrician as well as for the surgeon. The challenge is to diagnose accurately and to intervene appropriately especially since the natural history of acute appendicitis does not change. Most pregnant women visit their obstetrician for any type of abdominal problem and subsequent treatment. In the event of acute appendicitis it is of utmost importance that the surgeon is consulted for early diagnosis and management for better prognosis of both mother and baby. It is reported that one out of 1500 pregnant mothers have an incident of acute appendicitis. Pregnancy obscures the accurate diagnosis of acute appendicitis due to gestational physiological changes. This diagnostic delay increases the incidence of complications like perforation, peritonitis, lump formation and septicemia leading to high morbidity and mortality for mother and child. Case History Presented here are three cases of acute appendicitis during pregnancy. The cases are from each trimester. Case 1: The patient was the wife of a physician who reported directly to the surgical OPD with a history of periumlical pain with vomiting and low grade fever with leucocytosis. The ultrasound showed right iliac fosse probe tenderness with 12 week size normal fetus. The diagnosis of acute appendicitis was made clinically and the decision of surgery was taken. The obstetrician was consulted and she advised the use of some tocolytic agent postoperatively. The patient was operated upon successfully and she delivered a normal baby at full term. Case 2: The second patient, five months pregnant presented to the gynaecologist with pain in lower abdomen and history of nausea without any fever. The gynecologist managed her for 24 hours prior to referring to the surgeon. Clinically the symptoms were that of acute appendicitis with localized tenderness in right iliac fossa. She was investigated for the same. 31 Vol. 8, Issue 2 Jan - March 2009 The ultrasonologist suspected an appendicular lump and the decision for surgery was taken as the patient was not responding to medical treatment and the appendix was acutely inflamed. Postoperative recovery was good, though no lump was found during surgery. A normal baby at full term was delivered. Case 3: The third patient was seven months pregnant with a history of two previous cesareans with one live child, and hence this was a precious pregnancy. She presented with acute pain in abdomen with loose motion and high grade fever to her gynecologist and then to the surgeon. On investigation, her total leucocytosis was high, and temperature between 101-102 F. On clinical examination, the right iliac fossa and right lumber region were very tender. Based on the clinical and lab findings, the patient was advised surgery for acute appendicitis. However, her relatives were reluctant due to the precious nature of this pregnancy. She was placed on a good coverage of antibiotics with other supportive treatments. She responded partially with total leukocyte count and fever receding. Even though the patient responded to medical treatment in the initial stages, on the 5th day she developed uterine contractions with severe pain in abdomen. The ultrasound indicated thin scar and the patient did not respond to medical treatment of premature contraction. After a period of 24 hours, a sessarian section was performed. A one kg female child was delivered and immediately shifted to the nursery. During the sessarian the uterus was observed to be very red, congested with pus flakes in right iliac fosse (RIF). This was explored further and an abscess with many pus flakes was found behind the uterus. The appendix was edematous and was adhered to the caecum. An appendicectomy was carried out with drainage of abscess. Peritoneal toilet was done. Post operative recovery was uneventful but the patient stayed in the hospital for eleven days. The baby was shifted to the in nursery, she developed septicemia and could not be saved. Discussion There are some conditions like acute cholecystitis, pancreatitis, acute gastroenteritis,

AK Mittal
Head of General Surgery Laproscopy and GI Surgery Pushpanjali Crosslay Hospital Ghaziabad, NCR

ureteric colic, salpingitis, threatened abortion and premature contraction, which can be considered as differential diagnosis of acute appendicitis. In such situations, the role of the obstetrician is important as all pregnant women with pain in abdomen consult only them. If the treating doctor is unable to reach a conclusive diagnosis, then cross consultation with a surgeon should be initiated to avoid any delay as it could worsen the prognosis of mother and/or child as was the outcome in Case 3. Acute appendicitis should be dealt with pregnant women as if the pregnancy itself were not present. If surgery is performed in time during pregnancy, then the outcome is usually uneventful. However, the obstetrician must be associated during surgery as well as postoperatively. Operating early is always advisable whenever the diagnosis is confirmed. An aggressive surgical approach must be adopted even though the result of appendicectomy is usually positive, but perforation and septicemia are dangerous complications. Morbidity is high because of a delay in diagnosis and as a result of the initial approach of treatment for premature contraction of uterus. Conclusion To conclude, acute abdomen with pregnancy is always a dilemma. Early diagnosis, early cross reference and early intervention is the mainstay of a successful outcome. Surgery is the treatment of choice, irrespective of the stage of pregnancy. Current modalities like MRI and diagnostic laparoscopy service as excellent aids.

References 1. Horowitz MD, Gomej GA, Santiesteban R, Burkett G. Acute appendicitis during pregnancy. Arch Surg 1985;120:1362-8 2. Robert A, DeSantis, Ernest G. Appendectomy during pregnancy. A survey of two army medical activities. Military Medicine. 1999;164:671-4 3. Mazze RI, Kallen B. Appendectomy during pregnancy. A Swedish Registry Study of 778 cases. Obstet Gynaecol 1991; 77:835-40. 4. Lim HK, Bae SH, Seo GS. Diagnosis of acute appendicitis in pregnant women: Value of sonography. Am J Roentogenol 1992;159:539-24. 5. Manmoodian S. Appendicitis complicating pregnancy. South Med J 1992;177: 371-6. 6. 6. Sharp HT. Gastrointestinal surgical conditions during pregnancy. Clin Obstet Gynaecol. 1994;37:306-15. 7. AL-Mulhim AA. Acute appendicitis in pregnancy. Int surg 1996;81:295-302. 8. Tamir IL, Bongard FS, Klein SR. Acute appendicitis in a pregnant patient. Am J surg 1990;81:295-302.

32 Vol. 8, Issue 2 Jan - March 2009

Nocturnal Enuresis
Dinesh Agarwal
Nocturnal enuresis or bedwetting is one of the most common developmental problems encountered in the day-to-day practice of both the Pediatrician and the General practitioner. It is distressing for children and their parents. If left untreated, it can lead to social isolation, loss of self esteem and parental intolerance. Nocturnal enuresis is defined as involuntary passage of urine during sleep after five years of age. It is of two types: Primary (persistent): Child never achieves dryness at night. Commonest with an incidence of 75-90% Secondary (regressive): Child achieves dryness at night but after 6 months starts bedwetting again. Its incidence is 10-25%. The prevalence of nocturnal enuresis has been difficult to estimate because of variation in its definition and in social standards. It is now accepted that 15-20% of children will have some degree of nighttime wetting at five years of age with a spontaneous resolution rate of approximately 15 per year. Therefore, at 15 years of age only 1-2% continue to wet their beds at night. Boys wet their beds more frequently than do girls. A family history of nocturnal enuresis is found in most children. If both parents had enuresis in their childhood, 77% of their children will also have enuresis. Further, if only one parent had enuresis, then 44% of their children will have enuresis. Table 1: Etiology of primary nocturnal enuresis Factors Developmental delay Antidiuretic hormone level Genetics
Dinesh Agarwal
Associate Consultant Department of Pediatrics Pushpanjali Crosslay Hospital Ghaziabad, NCR

Etiology: This remains elusive. The condition appears to be multi-factorial involving a combination of physiological, genetic and psychological causes. Possible etiologies of primary nocturnal enuresis are summarized in Table 1. Evaluation of Primary Nocturnal Enuresis The most important factors in the evaluation include the following: Age and sex, Severity of the problem, Perceived disturbance within the family, Spontaneous resolution rate, and Patients response to therapy. To achieve best results, a goal oriented and consistent approach is required. This includes a consistent method of treatment with follow up, cooperative attitude of parents and child, support and care for the child in the family social structure and home environment. A careful medical history and physical examination including urine analysis will usually provide sufficient information to arrive at a diagnosis. The history should include an assessment of the childs voiding pattern. Psychological and family histories are important as the attitudes of the child and their parents are significant in selecting proper therapy. The physical examination should include abdominal, genital and neurological assessment to obtain evidence of chronic distended bladder, epispadias and spinal lesions. Investigations

Pathophysiology Delay in functional maturation of CNS Low level of night time ADH secretion Unclear

Evidence Spontaneous cure rate as children grow older Hormonal studies Family history, Gene identification at chromosome 5, 12, 13, 22 Sleep studies Results rather than cause Normal physical examination

Sleep disorder Behavioral and Psychological disorder Anatomy

Deep sleep Unclear None found 33

Vol. 8, Issue 2 Jan - March 2009

include urine analysis for specific gravity and dipstick tests to rule out the presence of diabetes insipidus and mellitus. Urine culture is recommended only if the patient has symptoms suggestive of urinary tract infection or if the urine analysis results are positive for the presence of red and white blood cells. Treatment Table 2: Treatment choice by Age Age Educate Reassure DDAVP Alarm devices Oxybutinn Imipramine <5 + + occasionally 5-7 y + + + + >7 + + + +

Children should continue to use device after three weeks of complete dryness. Relapse occurs in 20-30% of patients. Alarm devices are generally safe. Bladder Training Exercises: In some children with a small bladder capacity, urine retention training during the day may help increase bladder capacity at night. The child is asked to hold their urine for increasing periods of time. Six months of bladder training exercises results in about 19% achieving complete resolution of symptoms, while 66% show some improvement.

Table 3: Comparative choices Modality Alarm Cure (%) 70-80 77 25 Relapse at 6 months (%) 3 24 Very high if stopped abruptly Relapse at 1 year (%) 56 10

+ +

Alarm clock DDAVP

Treatment can be divided into two broad categories: Non Pharmacological treatment: Include motivational therapy, behavior modification (conditional therapy), bladder training exercises, psychotherapy, diet therapy and hypnotherapy. Pharmacological treatment: Evolved significantly over the past 15 years, and safer, more effective medications are now available. Non Pharmacological treatment Motivational therapy: This involves both the parents and the child and works by removing the guilt associated with enuresis, providing emotional support to the child, avoiding punishment and humiliation, encouraging the child to make bedtime resolutions, maintaining a chart or diary for wet and dry nights, and a system of rewards for dry nights. The cure or resolution rate is only 25%. About 70% show marked improvement, with a relapse rate of approximately 5%. Motivational therapy is a first line approach for treatment especially in younger children. If the therapy is not successful within three to six months, a different treatment should be offered. Behavioral treatment Waking the child 2-3 hours after sleep will induce a conditional response of waking when the bladder is full. The success rate is unknown. The childs cooperation is difficult to obtain. Alarm device: An alarm is placed near the genitals. When the child voids in bed, a moisture sensing device activates and triggers an alarm. This evolves a conditional response of waking and inhibiting urination. Alarms are sound and vibratory type. Vibratory alarms have found to be more effective than sound alarm in waking children. It is recommended in children older than seven years of age. It requires a cooperative and motivated child and family. Long term success has been reported in approximately 70%. 34 Vol. 8, Issue 2 Jan - March 2009

Imipramine

25

10

Pharmacological treatment This form of therapy is usually reserved for children older than seven years of age. Two approaches are used:

Increase bladder capacity Reduce the amount of urine produced by the kidneys

Several medications are available; however, none of these medications cure enuresis. They provide a stop gap measure until the child develops their own waking habits during the night to void. Parents should not expect immediate results. Drugs have potential side effects.

Reserve for > 7 yrs Second line of treatment First line of treatment (Family circumstances or quick symptomatic relief) None of these medication cure Provide a stop-gap measure Do not expect immediate results Potential side effect

Drug therapy should be initiated only after the first live therapy has failed or quick systematic relief needed. Three groups of drugs are used:

Tricyclic Antidepressant: Imipramine has been used extensively during the past 25 years. Suggestive mechanisms alter the sleep and arousal mechanisms; alter secretion of anti-diuretic hormone, weak peripheral anticholinergic effect and effect on the sympathetic nerves in the bladder. The initial dosage is 25 mg taken one hour before bedtime. Evaluate response after two weeks. If the response is not satisfactory, the dosage can be increased to 50 mg in children 7-10 years of age and up to 75 mg in older children. Treatment should continue for three to six months and weaning by reducing the dosage in increments of 25

Table 4: Summary Medication Adjust dose every two weeks Continue therapy for 3-6 months of dry nights Wean over three to four weeks Restart if relapse occurs on stopping Consider behavioral modification in conjunction Structured withdrawal of therapy rather than tapering the doses of medications seems to improve the outcome* Combined modalities Motivation and dry bed training better (DBT) than no treatment An alarm better than DBT on its own Alarm with DBT better than alarm alone Direct contact with a therapist might enhance the effects of an intervention Combination therapy Response Cure / Resolution Only one or two wet night over three month period

Refractory primary Partial/comnocturnal enuresis plete response Alarm therapy with Treat for 3-6 Desmopressin month and ta Oxybutyrin and per gradually Desmopressin Recurrence Desmopressin and Restart same Imipramine (not therapy combined) Poor response Interchange or combine two modalities Refractory to therapy Reassess

over three to four weeks. Its use decreases because of the side effects, dry mouth, nausea, tiredness, sleep disorders, anxiety, nervousness and personality changes. Imipramine has also been associated with severe accidental overdose in both patients and their siblings. Cure rate is about 25% with this form of therapy Anti-cholinergic Therapy: Drugs eg, hyosyamine and oxybutynin have a direct effect on smooth muscle relaxation. It results in decreasing the bladders ability to contract. Experience with anti-cholinergic is limited. Oxybutynin is administered in the dosage of 5 mg at bedtime. The dosage can be increased to 10 mg in older children. Common side effects are dry mouth, constipation, facial flushing, dizziness, tremulousness, drowsiness, anthyperpyrexia during summer Desmopressin Acetate (DDAVP): A synthetic analogue of arginine vasopressin (anti-diuretic hormone), has a highly specific anti-diuretic effect, a relatively long half life and extended duration of action. The biological half life is four to six hours. It can be administered by oral and/or nasal route. The initial dose of nasal spray is 20 mg (one spray in each nostril) at bedtime. Evaluate response after two weeks of therapy and if no response seem, the dosage can be increased to 40 mg at bedtime. In children more than twelve years of age can be administered up to 60 mg intranasally. Nasal spray should be avoided in children suffering form Rhinorrhea. The tablets can be administered in the dosage of 200 microgram (0.2 mg) half an hour before or two hours after meal can increase up to 600 microgram

(0.6 mg) for desired response. Tablets are preferred over nasal spray as nasal spray can be administered in overdose. Therapy should be given for at least three to six months for a desire response. The dosage should be tapered slowly by 10 microgram per month because abrupt discontinuation of therapy can result in high replace rate. References 1. Howe AC, Walker CE. Behavioral management of toilet training, enuresis and encopresis. Pediatr Clin North Am 1992;39(3):413-32. 2. Rittig S, Knudsen UB, Norgaard JP, Peterson EB, Djurhuus JC. Abnormal diurnal rhythm of plasma vasopressin and urinary output in patients with enuresis. Am J Physiol 1989;256(4 Pt 2):664-71. 3. Marshall S, Marshall HH, Lyon RP. Enuresis: an analysis of various therapeutic approaches. Paediatrics 1973;52:813-7. 4. Rushton HG. Nocturnal enuresis: epidemiology, evaluation and currently available treatment options. J Paediatr 1989;114(4 pt 2):691-6. 5. Schmitt BD. Nocturanal enuresis. An update on treatment. Pediatr Clin North Am 1982;29:21-36. 6. Bamford MF, Cruickshank G. Dangers of intranasal desmopressin for nocturnal enuresis [Letter]. J R Coll Gen Pract 1989;39:345-6. 7. Terho P. Desmopressin in nocturnal enuresis. J Urol 1991;145(4):818-20.

A Happy and Successful First The department of Aesthetic and Plastic surgery commenced its international services with Ms. Wendy, a resident of New York State, USA. Dr. Dinesh Bhargava, head of department and director of A New Image Center for Aesthetic Surgery and Medicine performed the Ultrasonic Assisted Liposuction technique on Ms Wendy. The procedure was done as a day surgery and the patient has since returned to her home in US. The feedback is positive; and Ms. Wendy has already scheduled another procedure on her next visit to India. Congratulations to all who were involved in her care. The patient also conveys her appreciation to the hospital staff, nurses and others who made her experience a pleasant one.

35 Vol. 8, Issue 2 Jan - March 2009

Is Sunlight An Effective Treatment For Jaundice in Term Infants?

Rajiv Singh
This articles has been copied from http://www.mja.com.au/public/issues/178_08_210403/joh10652_fm.pdf History: Serum sample color change observed in icteric blood samples left in daylight. Babies lying on the side of nursery that received natural sunlight were observed to have less incidence of jaundice. Theoretically: it can be effective as it has the spectrum of 425-475 nm, known to be effective in dissolving bilirubin. Review of Literature Extensive screening of published scientific evidence, viz, Cochrane Library, Best Evidence, MEDLINE, CINAHL (Cumulative Index to Nursing and Allied Health Literature), Current Contents and Biological Abstracts was carried out. Our extensive search identified only a single original study reporting the effect of sunlight in jaundiced preterm, rather than term, infants. This widely cited and historically important article that provided the first English-language report of an association between light and a reduction in neonatal jaundice was published in 1958. The same authors then reported a case series of artificial light therapy for jaundiced preterm infants, which stimulated the subsequent volume of research articles on the effectiveness of phototherapy for neonatal jaundice in both term and preterm infants. Information analysis We found no controlled trials comparing sunlight against either no treatment or artificial light treatment for jaundice. The use of sunlight appears to have resulted from anecdotal reports of its effectiveness rather than from rigorous medical evidence. In fact, most of the time, exposure to sunlight is grossly inadequate because of fear of cold exposure. Moreover, if the effectiveness of sunlight exposure for jaundice is unknown, so too is the incidence of potential risks to the neonate, for example, undue exposure to (cold) weather (possibility of hypothermia) sunburn, photosensitivity or even skin malignancy in future. Discussion There is insufficient evidence to support exposure to sunlight for the treatment of 37 Vol. 8, Issue 2 Jan - March 2009 jaundice. The persistence of this practice 50 years after publication of a report on a single case series raises questions about the influence of evidence on the beliefs of professional healthcare workers. An Australian study reported that 36% of mothers believe that sunlight is helpful in Jaundice and the belief was communicated mostly by health workers. The study therefore identified the need to educate the Health professionals regarding the inefficacy inadvisability and potential harm of Sun therapy in NNH.

AAP Recommendation Putting your baby in sunlight is not recommended as a safe way of treating jaundice. Exposing your baby to sunlight might help lower the bilirubin level, but this will only work if the baby is completely undressed. This cannot be done safely inside your home because your baby will get cold, and newborns should never be put in direct sunlight outside because they might get sunburned. Conclusion Sunlight is not effective in NNH and it can expose the newborn to potential hazards. Additionally, hyperbilirubinemia may be missed and this could prove to be detrimental for the baby. Therefore it is strongly recommended that all physicians and pediatricians should avoid the advice of sunlight for jaundice. Instead, the parents and family members could be advised to follow up with the pediatrician for proper evaluation of the severity of jaundice.

References 1. American Academy of Pediatrics. Question and Answers: Jaundice and Your Newborn. Accessed: http://www.aap.org/ family/Jaundicefaq.htm 2. Cremer RJ, Perryman PW, Richards DH. Influence of light on the hyperbilirubinaemia of infants. Lancet 1958; i: 10941097

Rajiv Singh
Consultant Pediatrician Pushpanjali Crosslay Hospital, Ghaziabad, NCR

Rotavirus Vaccine
Anuradha
Introduction Rolavirus is the leading cause of diarrhea hospitalization among children worldwide.1 It is the single most important cause of severe dehydrating diarrhea. Development of a safe and effective rotavirus vaccine is very important. Globally every year, rotavirus is associated with nearly 25 million clinical visits, 2million hospitalization and more than 6,00,000 deaths worldwide among children younger than 5years of age.2,3 It is important to study local distribution of rotavirus strains and conduct active surveillance programs for emerging reassortant strains prior to and after the introduction of vaccines Epidemiology First described in 1973 rotavirus diarrhea occurs most commonly in winter months in temperate climates. Their clinical relevance, structural complexity and unique mode of transmission have invited extensive research on there viruses. Structure and Classification It is a double stranded RNA virus. it is grouped into groups (A-G), subgroups I & II an non I and non II - based on inner capsid protein - VP 6 (made of VP 7 and VP4) further typing schemes to describe rotavirus sprains are based on the proteins to elicit neutralizing antibodies VP7 (G serotypes) and VP4 (P serotype) G and P serotypes are defined based on reactivity to specific monoclonal antibodies (MABS). Rotavirus detection and strain characteristics ELISA is the method of choice for screening. Epidemiology in India Rotavirus epidemiology is complex due to continuous modes of transmission and strain diversity of the virus in different setting. The new hope presumption of mortality due to this agent is the use of oral vaccines which have proved to be effective in developed countries but we need evidence from developing countries with the highest disease burden.Before accepting their efficacy in our setting,we must understand the epidemiology in India .Studies done in India through 1982-1999 and 2001 to 2004 prove that the incidence of rotavirus GE requiring hospitalization ranges from 6-45% (median 20.8%). In the community the disease varies from 4%-29% (median 12.3%) most of which is symptomatic. G1 & G2 are most prevalent strains. Commonest P type was P [8]-(27%)followed by P [6]-(22%) and P [4]-(20%) In India newer strains have been discovered e.g., G-6 from Pune 5, G (8) Vellore and Kolkata 39 Vol. 8, Issue 2 Jan - March 2009 G 38 (8) from Western India and G12 from Delhi. In neonates, rotavirus causes mostly asymptomatic infection. Neonatal Rotavirus strains (attenuated) are possible candidate virus for vaccine.These include G9P[11] in Delhi4 and G10P[11] in Bangalore and Mysore5. Both symptomatic and asymptomatic infections by G10P[11] strain have been reported in Vellore6. Both neonatal strains appear to be bovinehuman reassortants. G9P[11] is a human strain with a bovine VP4 while G10P[11] is composed mainly of bovine genes and has gene segments 5 and 7, encoding NSP1 and 3, of human origin7. Vaccine Preparations Rota shield (a tetravalent rhesus- human reassortant rotavirus vaccine discovered in 1998 but was withdrawn from market due to increased incidence of intussusceptions among vaccine recipients.The estimated risk was 1 in 10,000. The risk was greatest during 3-4 day period after 1st dose and 3-7day period after 2nd dose.It was also associated with fever, vomiting, diarrhea, abdominal pain and bloody stools. Rotaeq: Oral, Live, Pentavalnt (G1, G2, G3,G4, and P(8)) human bovine (WC3) reasortant rotavirus vaccine sodium citrate and phosphate buffer at an aggregate viral type of approximately 6.7 X 107 to 12.4 X 107 infectious unit per dose. Pentavalent rotavirus vaccine was highly efficacious against severe rotavirus gastroenteritis and provided substantial protection against rotavirus gastroenteritis of any severity. Its efficacy persisted through a second rotavirus season. The immunologic mechanism by which rotavirus protect against rotavirus gastroenteritis is unclear. Efficacy The efficacy of the vaccine against G1-G4 gastroenteritis of any severity was 74.0 percent. Efficacy against hospitalization for G1-G4 rotavirus gastroenteritis was 95.8 percent..The efficacy of the vaccine against all gastroenteritisrelated hospitalizations after the first dose was shown to be 58.9 percent.R2 Adverse effects: Studies done have not demonstrated any increased risk of Intussusceptions(1.6) during a 42-day period after any dose fever, vomiting, hematochezia, were similar among vaccine and placebo recipients in study. Recommendations Three-2 ml doses starting 6wk of age 1.0 has to be completed 2, 4, 6 months of age before 6 months.

Anuradha
Consultant Pediatrician Pushpanjali Crosslay Hospital, Study Report Ghaziabad, NCR

Rotarix (GSK) A live attenuated human rotavirus vaccine containing the R1 X 4414 strain of G1 P(8) specificity has been developed 2,4,6,16,22 from the parent vaccine strain 89-12 .Two doses are well tolerated and immunogenic. Efficacy The efficacy of the vaccine against severe rotavirus gastroenteritis and against rotavirus associated hospitalization was 85 percent(P<0.001) in the large multicentric trial.,and reached 100 percent against more severe rotavirus gastroenteritis. Hospitalisation for diarrhea of any cause was reduced by 42 percent(95 confidence interval,29 to 53 percent;P<0.001).The vaccine efficacy was shown to persist through a second rotavirus season.91.0 percent efficacy was demonstrated against G1P[8] rotaviruses and 45.4 percent for G2p[4]. The vaccine was not associated with an increased risk of Adverse effects 1. Intussusceptions. Observed risk estimate of 0.32 per 10,000 infants below the initial risk increase of 4 per 10,000. 2. Diarrhea, vomiting, dehydration and hypovolaemic shock. Type of Gastroentritis Severe, as Clinical definition Rotavirus GE Severe Hospitalisation Gastroenteritis of any cause Severe Hospitalisation Severe,as Clinical definition Serotype specific gastroenteritis G1P[8] G3P[8],G4P[8], G9P[8] G2P[4] 183 145 No of Infants with>1 episode Efficacy 90.8 86.9 300 246 40 42 HRV No of Infantswith>1 episode Vaccine 12 9 Pentavalent No of infants>1 episode Placebo 77 1.5

distribution, occurrence of mixed infections, seasonality and risk of mortality can affect decisions about vaccine composition and delivery. Higher doses of vaccine or additional doses may be required to overcome the inhibitory effects of competing intestinal flora, concomitant use of oral polio vaccine and high levels of humorally transferred maternal antibodies against rotavirus. Despite a recommendation by the World Health Organization that all rotavirus vaccines be tested early in developing countries, no data from the current vaccines are available in Africa or poor Asian countries. These data will be critical to determining the probability of success of the current rotavirus vaccines and to establish requirements for vaccines in pre-clinical and clinical development. In summary, rotavirus epidemiology is complex as would be expected for a virus with multiple modes of transmission, and this complexity is amply illustrated in studies from India demonstrating the diversity of the virus in different settings. The new hope for prevention of morbidity and mortality due to this agent is the use of oral vaccines, which are effective in developed countries, but we need evidence from developing countries with the highest disease burden and virus diversity before accepting

VACCINE EFFICACY 84.7 85

Vaccine

Placebo

Vaccine Efficacy 98.0 -100%

58.9 No of infants>1 episode G1 G2 72/286 6/17 Efficacy 74.9 63.4

45.4

G3 G4 G9 N ENG J MED 354:1 JAN 5,20068

1/6 3/6 1/3

82.7 48.1 65.4

Summary The Cochrane Evidence Database analyses data from 64 trials with three kinds of vaccine, bovine, rhesus and human, and results indicate protection from rotavirus diarrhoea of any severity9. However, the important caveat to this update is that the majority of the trials were carried out in developed countries where the age of first rotavirus infection is later in childhood and where the degree of diversity of circulating strains is limited in comparison to developing countries. Rotavirus vaccines generally have yielded poor efficacy when tested in developing countries has led to concerns about the potential effectiveness of any future live, oral rotavirus vaccine in these settings64 Although rotavirus infection is universal early in childhood, the epidemiology of the disease is quite different in developed and developing countries. Differences in age of first infection, strain 40 Vol. 8, Issue 2 Jan - March 2009

their efficacy in all settings. References

1. Parashar UD, Hummelman EG, BreseeJS, Miller MA, Glass RI. Global illness and deaths caused by rotavirus disease inchildren. Emerg Infect Dis 2003;9:565-72. 2 . Parashar UD, Gibson GJ, Bresee JS, Glass RI. Rotavirus and severe childhood diarrhea. Emerg Infect Dis. 2006;12:3046. [PubMed]. 3. Bresee JS, Glass RI, Ivanoff B, Gentsc JR. Current status and future priorities for rotavirus vaccine development, evaluationand implementation in developing countries.Vaccine 1999;17:2207-22. The Journal of Alternative and Complementary Medicine. 2004,10(2):261-268.

Recent Advances in Management of Childhood Tuberculosis

Tilak Dangwal
Tuberculosis (TB) is a major public health problem worldwide. The advent of HIV infection pandemic and AIDS has resulted in the significant increase in the global burden of tuberculosis. In the developing countries, tuberculosis is a disease of the young. Childhood TB is a reflection of the ongoing transmission of the Mycobacterium tuberculosis in the community and is the result of recently acquired infection. Thus, the extent of the problem of childhood tuberculosis reflects the tuberculosis control in the given geographical area. Since there is little advance in the basic knowledge of microbiology, immunology and the pathophysiology of Mycobacterium, newer diagnostic modalities, newer drugs and newer treatment regimens need to be discussed Epidemiology Tuberculosis is leading cause of death worldwide from a single infectious disease agent. WHO estimates that up to half of the worlds population is infected .The registered number of new cases of TB worldwide roughly correlates with economic conditions. The highest incidence is seen in Africa, Asia, and Latin America ie, countries with the lowest gross national products. Around eight million people get TB every year, of whom 95% live in developing countries and around two million people die from TB every year. In India, estimated incidence/year is 1.8 million new cases out of which 0.8 million are new smear positive cases. The estimated prevalence of TB disease (in 2000) was 3.8 million bacillary cases and 1.7 million new smear positive cases and the estimated mortality is 370,000 deaths due to TB each year ie, over 1000 deaths a day. Childhood TB is a neglected aspect of the TB epidemic. Despite constituting 20% or more of
Tilak Dangwal
Consultant Pediatrician Pushpanjali Crosslay Hospital, Ghaziabad, NCR

usually smear-negative and thus is considered to make a relatively minor contribution to the spread. To redress this neglect and integrate childhood TB into the mainstream of TB control activities, it is important that research priorities be identified to assist in improving the prevention and management of childhood TB. Approach to diagnosis Diagnosis of pulmonary tuberculosis (PTB) is difficult in children aged less than 6-8 years. Contact with a smear-positive PTB case and respiratory symptoms for more than 2-3 weeks, not responding to broad-spectrum antibiotics usually raises the suspicion of the disease. Clinical signs such as erythema nodosum and phlyctenular keratoconjunctivitis, weight loss or failure to thrive may be present. The diagnosis of PTB in children is often presumptive. Various scoring systems have been produced for screening and diagnosis but their evaluation is difficult in the absence of a gold standard diagnosis. Laboratory investigations Detection of Mycobacterium: All possible efforts must be made to detect and isolate the bacteria from appropriate specimens. Gastric aspirates are used in lieu of sputum in very young children (<6 years of age) who usually do not have a cough deep enough to produce sputum for analysis. Bronchoalveolar lavage may also be used to provide bronchial secretions for detection of bacilli. Other body fluids (eg, CSF, pleural fluid, peritoneal fluid) can also be centrifuged so the sediments can be evaluated for the presence of AFB. Conventional method is Ziehl Neelsen staining and staining of the AFB provides preliminary confirmation of the diagnosis. Since it takes 6-8 weeks for bacilli to be isolated from conventional culture medium (Lowenstein-Jensen), automated radiometric culture method (BACTEC) is increasingly being used for the rapid growth of the bacteria Imaging studies: Chest X-ray is a classic

the TB case-load in many countries with high TB incidence this orphan disease exists in the shadow of adult TB and is a significant child health problem. It is neglected because it is 43

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diagnostic tool when evaluating patient for pulmonary tuberculosis. CT scan (HRCT) and MRI are not routinely indicated when CxR findings are unremarkable but in case of high suspicion these imaging studies can demonstrate hilar lymph node, endobronchial lesions, pericardial evasion and early cavitations and bronchiectasis. Mantoux test: Positive test to the standard dose of tuberculin is still the most reliable investigation of choice especially in young children but it must be remembered that with severe TB and/or advanced immunosuppression, tuberculin test may be negative. ELISA: It detects different antibodies (IgA, IgM) to different tubercular proteins. As no antigen is standardized, sensitivity, specificity, and reliability of Elisa are always doubtful. As this test is expensive, it is appropriate to say that it alleviates parent anxiety and generates funds for the laboratory performing the test. PCR: Polymerase Chain Reaction (PCR) test detects the DNA of the Mycobacterium tuberculosis complex from body fluids samples It is a highly sophisticated technology with high sensitivity (0.98) and specificity (0.7). Therefore, if PCR is negative, MTB infection is extremely unlikely, but positive PCR does not not necessarily reflect active MTB infection. QuantiFERON-TB Gold (QFT-G): Detection of IFN-gamma by ELISA is used to identify in vitro responses to ESAT-6 and CFP10 that are associated with M tuberculosis infection (substitute of TST). It detects both TB disease and LTBI (Latent TB Infection) but cannot differentiate between them. Blood must be incubated with the test antigens <12 hours after collection. Collecting the required 5-mL blood sample from younger children might not be possible or acceptable. Sensitivity of QFT-G for detecting M. tuberculosis infection in persons with untreated infection is 80% (No data is available for children<17 yrs, immunocompromised and from population of endemic areas like India). Treatment The basic principles of care

kanamycin Capreomycin p-Aminosalicylic acid (PAS) Levofloxacin Moxifloxacin Gatifloxacin

To achieve 95-99% cure rates short-course chemotherapy is recommended. INH and PAS = 24 months INH and EMB = 18 months INH and RIF = 9 months INH, RIF & PZA = 6 months As Mycobacteria grow slowly, their generation time being 1224 hours. Revised National Tuberculosis Control Programme is because Anti Tubercular Therapy (ATT) can be prescribed on intermittent basis with increased dosages and under supervision to improve the compliance with therapy. Essential Drug H R Z S E T Recommended dosage (Dose range in mg/kg) Daily 5 (4 - 6) 10 (8 - 12) 25 (20 - 30) 15 (12 - 18) 15 (15 - 20) 2.5 3 times weekly 10 (8 -12) 10 (8 - 12) 35 (30 - 40) 15 (12 - 18) 30 (20 - 35) N/A

Each patient is assigned a category according to the clinical and laboratory features and treated as per the recommendations. The parents can opt for daily regimen as per their choice and treating physician should ensure regular monitoring and compliance with the treatment Category I: 2(HRZE)3 4(HR)3

Diagnosis should be established promptly and accurately Standardized treatment regimens of proven efficacy should be used Appropriate treatment support and supervision Response to treatment should be monitored Essential public health responsibilities must be carried out.

New smear positive PTB New smear negative PTB with extensive parenchymal involvement New cases of severe forms of extra pulmonary TB.

Armamentarium 1st line drugs Isoniazid Rifampin Pyrazinamide Ethambutol 2nd line drugs Cycloserine Ethionamide Streptomycin Amikacin 44 Vol. 8, Issue 2 Jan - March 2009

Pulmonary tuberculosis (PTB) refers to disease involving the lung parenchyma. Therefore, tuberculous intrathoracic lymphadenopathy (mediastinal and/or hilar) or tuberculous pleural effusion, without radiographic abnormalities in the lungs, constitutes a case of extra pulmonary TB. A patient with both pulmonary and extra pulmonary TB should be classified as

a case of pulmonary TB. Extra pulmonary tuberculosis (EPTB) refers to tuberculosis of organs other than the lungs, eg, pleura, lymph nodes, abdomen, genitourinary tract, skin, joints and bones, meninges. Diagnosis should be based on one culturepositive specimen, or histological or strong clinical evidence consistent with active EPTB, followed by a decision by a clinician to treat with a full course of tuberculosis chemotherapy. The case definition of an extra pulmonary TB case with several sites affected depends on the site representing the most severe form of disease. Category II: 2(SHRZE)3 /1(HRZE)3 5(HRE) 3 Sputum smear positive: Relapse Treatment failure Treatment after interruption The following definitions are used: New: A patient who has never had treatment for TB or who has taken antituberculosis drugs for less than 1 month. Relapse: A patient previously treated for TB who has been declared cured or treatment completed, and is diagnosed with bacteriologically positive (smear or culture) tuberculosis. Treatment after failure: A patient who is started on a retreatment regimen after having failed previous treatment. Treatment after default: A patient who returns to treatment, positive bacteriologically, following interruption of treatment for 2 months or more. Transfer in: A patient who has been transferred from another TB register to continue treatment. Other: All cases that do not fit the above definitions. This group includes chronic case, a patient who is sputumpositive at the end of a re-treatment regimen. Category III 2(HRZ)3 4(HR)3 New smear negative PTB (other than in category I) New less severe forms of extra pulmonary TB Category IV Treatment Failure To be treated at Specialist Center with specially designed individualized regimen Actions in interruption of TB treatment Interruption for less than 1 month Trace patient Solve the cause of interruption Continue treatment and prolong it to compensate for missed doses Interruption for 12 months Action 1 Trace patient Solve the cause of interruption

Do 3 sputum smears. Continue treatment while waiting for results. Action 2 If smears Continue treatment and prolong it to negative or compensate for missed doses EPTB If one or more smears positive Treatment Continue Rx and received: <5 months prolong it to compensate for missed doses

>5 months Category I: start Categor Category II: refer (may evolve to chronic) Clinical decision on individual basis whether to restart or continue treatment, or no further treatment

Interruption for 2 months or more (defaulter) Do 3 sputum egative N smears Solve the cause of interruption, if possible results smears or EP

One or more Category I Start Category II Category II may while evolve to waiting for the chronic positive

No treatment smears

Management of children contacts of infectious adults

Screening - thorough history, clinical examination, Mx test, CXR Diagnosis of TB - Treat Symptom free & <5 years should receive prophylaxis (INH 5 mg/kg) Breastfeeding children of a sputum smear-positive mothers, a must Prophylaxis should be for at least 6 months and requires regular (eg, every 2 months) follow-up Symptom free &>5 years do not require prophylaxis Children may also be infected by smear-negative PTB cases but because transmission is less common, routine contact tracing is not recommended in this circumstance

Key Messages

An accurate and prompt diagnosis should be established All efforts should be made to isolate the bacteria Detailed clinical history, thorough physical examination and positive Mantoux test are suggestive of diagnosis of Childhood TB

In the absence of bacteriological confirmation the diagnosis is presumptive in many of the patients The newer diagnostic tests must be interpreted with great caution Standardized treatment regimens will treat most of the patients Regular monitoring, assessment of response to treatment and side effects and compliance must be ensured while prescribing the treatment.

Pushpanjali Health Care Events and Initiatives

September 14, 2008 Workshop: Level I - Infertility and Recurrent Loss of Pregnancy
Dr Sharda Jain conducted the first of a series of workshops on Infertility and Recurrent Loss of Pregnancy at the Conference Hall of Pushpanjali Crosslay Hospital. The conference was attended by over 100 Gynecologists from Delhi and adjoining NCR region. The day long conference comprised sessions by eminent speakers on different aspects of the theme. Speaking on the occasion Dr Sharda Jain informed the participants about the IVF centre being set up at PCH for the benefit of young couples requiring specialized IVF services to fulfill their dream of having children of their own. Dr Sharda Jain welcomes
the delegates

October 12, 2008 Pediatric Digest

Pediatric Digest - organized jointly by PCH, IMA-EDB and IAPEDB, on commonly occurring childhood diseases was conceived and planned by Dr SK Mittal, Director, Dept. of Pediatrics and supported by Dr PD Garg, Dr Ravi Malik, Dr Tilak Dangwal. The conference had six sessions comprising 3-4 lectures in each. Over 165 delegates attended the conference. Chief Guest Shri Ashok Pradhan, Member of Parliament, spoke on the occasion and reminisced about his school days with Dr Vinay Aggarwal and added that Dr Vinays zeal for PCH was very special. Mr Pradhan spoke of the importance of the Doctors role in society, citing in the process of his own experience when his own daughter was ill and the exemplary gentleness and care with which Dr Vijay Agarwal treated the child and the family. Several pharmaceutical and companies from allied industries participated in the conference.

September 28, 2008 1st Basic Airways Workshop

Department of Anesthesia and Department of Otorhinolaryngology under the guidance of Dr Swaraj Garg and Dr Atul Jain organized a 1-day workshop. About 125 delegates attended the lecture and 40 delegates were trained in the hands-on sessions. Delegates had come from places like Ludhiana, Muzzfarnagar, Agra, Jaipur, Hapur and Dehradun. Chief Guest Shri N Seshadri, GM, Canara Bank and Guest of Honor, Dr AK Dhaon, CMO, Ghaziabad inaugurated the workshop. Speaking on the occasion, Shri Seshadri appreciated the efforts of PCH in its regular efforts in conducting CMEs. He stated that the Canara Bank was proud to be a PCH partner. Dr AK Dhaon, in his address, thanked Dr Vinay Aggarwal for his quick response in providing a dedicated space for storage of vaccines at PCH premises and lauded the many services Dr Vinay Aggarwal and Dr Vijay Agarwal had undertaken in the area of community health.
Mr Ashok Pradhan, MP lighting the lamp

November 5, 2008 Guest Lecture on Rheumatology

Dept. of Medicine under the leadership of Dr Parkash Gera organized a Guest Lecture on Recent Advances in the Management of Rheumatic Disorders by Dr Manveen Saluja, a leading consultant in Rheumatology and Prof. Wyane University, USA. The session was by chaired by Dr YP Munjal, Director Diabetology and Life Style diseases, Banarsidas Chandiwala Institute of Medical Sciences. Speaking on the occasion, Dr Manveen emphasized the Dr Manveen making need to pay equal attention her presentation 47

Dr Basu, Dr Dhall and Dr Swaraj Garg

Vol. 8, Issue 2 Jan - March 2009

to life style management and regular counseling of patients in association with administering prescribed medications. According to Dr Saluja, the rheumatologists role was vital in the counseling process. He said that contrary to popular belief the incidence of Rheumatic Arthritis also occurs very commonly in the young and thus should not be viewed only as a consequence of old age. He pointed out that as a result it was extremely important that counseling and life style management be paid attention to in this age group as well. Dr Munjal shared with audience his professional experience and endorsed the guidelines stated by Dr Manveen. The session was attended by Physicians, Orthopedic surgeons and General Practitioners from NCR.

expressed the fact that natures law of equality must not be tempered with. She said that life was Gods gift and that the female of the species was the mother of life, therefore the act of female feticide was against this balance of nature. She expressed the view that the need of hour was to educate people about the advantage of maintaining the male-female equilibrium despite the strong public favor for a male child. She urged all present to become a vital part of the crusade against female feticide which was both a social devil and a medical vice. Dr. Jugal Kishore, Professor, Community Medicine, MAMC thanked the speakers for their thought provoking and highly enlightening words on such a burning issue and extended his services to curb the evil by educating the masses. Leading medical activists against female feticide Dr Sharda Jain and Dr Suneela Garg moderated the seminar.

November 13, 2008 Seminar on Female Feticide: Social Evil or Medical Vice
A seminar entitled Female Feticide: Social Evil or Medical Vice was organized jointly by National Medicos Organization (NMO), Delhi State, Maulana Azad Medical College (MAMC) Department of Social and Preventive Medicine, National Commission for Protection of Child Rights, Delhi Gynecologist Forum and Pushpanjali Crosslay Hospital at Maulana Azad Medical College Auditorium. The seminar was attended by over 500 persons including doctors and general public. Speaking on the occasion Dr. Vinay Aggarwal, President NMO and CMD Pushpanjali Crosslay Hospital, expressed his concerns on declining female population and the effects thereof. Dr Arun Aggarwal, Dean MAMC, during his inaugural address said that the medical fraternity and paramedics were equally responsible for the rising incidence of female feticide, which was shameful. He said that these unscrupulous persons would need to be identified and weeded out before the situation reached alarming proportions. Addressing the gathering, Ms Suman Nalwa, ACP, In-charge Crime against Women was of the opinion that the female feticide was a heinous crime and that the culprit/s should be dealt with sternly. Ms. Sandhya Bajaj, Member, National Commission for Protection of Child Right in her address stated that no human being had the right to take natures law into their own hands and that all such actions should be strongly condemned. Religious leader and activist, Didi Maa Sadhvi Ritambhara reiterated the sentiments of the previous speakers who had

November 28, 2008 Sensitizing GPs on Diabetes

A lecture session on The Right time to start insulin in a type-II Diabetes Patients by Dr Vipin Mishra, MD, PhD, DM (Endocrinology), Commonwealth Medical Fellow (UK), Sr Consultant & Head, Department of Diabetes & Endocrinology was organized at the conference hall. The lecture meeting was attended by over 50 doctors, and was appreciated and by the delegates on account of the quality of information and its use in clinical practice.

December 5, 2008 Spirometery in Clinical Practice

Dr Tilak Raj Dangwal, Consultant, Department of Pediatrics addressed pediatricians from East Delhi, Ghaziabad and NOIDA on Spirometery in Clinical Practice. The session was highly interactive, and as expressed by participants of great benefit for all.

December 20, 2008 Guest Lecture

A Guest Lecture on the Changing scenario of Healthcare was delivered by Dr Ravinder Mamtani, Diplomate of The American Board of Preventive Medicine. The lecture was attended by PCH Consultants and doctors from the NCR region.

Dr. Mamtani making a point

January 11, 2009 Workshop on Uterine Balloon Therapy

The Dept. of Gynecology in association with the Delhi Gynecologist Forum organized a workshop on DUB - Made Easy at conference hall of PCH from 9.30 am to 1.30 pm. Eminent doctors like Dr Gopinath from Chennai and Dr Sushma Chawla from Jallandher conducted sessions. 48 Vol. 8, Issue 2 Jan - March 2009

Didi Maa releasing the book

January 18-19, 2009 2nd International Temporal Bone Dissection and Live Ear Surgery Course
PCH in association with Claros Foundation, Barcelona, Spain organized the 2nd International Temporal bone dissection and Live Ear surgery course for ENT surgeons at the hospital premises on January 18 and 19, 2009. Surgeries, including cochlear implant, were performed by internationally renowned ear surgeon, Prof. Pedro Claros, Chairman of the Claros Foundation in Barcelona, Spain. Prof Claros has performed over 800 successful cochlear implants. The workshop comprised of a course on Temporal bone dissection for ENT surgeons. About 60 ENT surgeons from North India attended the course and learned the details of ear surgery from Dr Pedro Claros himself. Claros Foundation donated a cochlear implant worth Rs 10 lakh to a needy young child

Smt. Sheila Dikshit, Honble Chief Minister of Delhi thanked the organizers and reiterated that everyone - government and private sectors - needed to work conjointly to ensure that cancer treatment be made affordable for all. However, the Honble CM also said that the first line priority would have to be prevention. Dr VB Bhatnagar, former Head of the Department of Surgery, LLRM Medical College & Subharti Medical College and Guest of Honour emphasized the appropriateness of such a seminar and hoped that many more would follow to establish conclusively that cancer can and should be fought. Dr Mahesh Verma, Director Principal, Maulana Azad Dental College said that the number of cases of cancers of head and neck were on the rise because of the increased use of Gutka and Khaini. He emphasized the need for regular oral examinations so that any white/red patch could be detected before it turned cancerous. Padmashri Sh Alok Mehta, Chief Editor, Nai Dunia highlighted the role of media in the war against cancer. He said that print media because of its circulation was in Dr. Mahesh Verma addressing the a better position to reach audience the masses for cancer awareness. He also emphasized that other forms of media should also be used for cancer awareness campaign.

Workshop Captured in Camera

February 4, 2009 Symposium on World Cancer Day

Cancer is a leading cause of death around the world. WHO estimates that if no intervention measures are taken then about 84 million people will die of cancer between the years 2005 and 2015. On the occasion of World Cancer Day, 4 February, Galaxy Cancer Institute, Pushpanjali Crosslay Hospital organized a symposium on Cancer: Do not Fear it, Fight it. Chief Guest, Shiela Dikshit, Honble Chief Minister of Delhi was warmly welcomed by Dr. Vinay Aggarwal, Chairman and Managing Director of Pushpanjali Crosslay Hospital. Dr. Vinay Aggarwal spoke of the ongoing battle being fought by the medical community and highlighted the world class healthcare facilities being developed at the Pushpanjali Crosslay Hospital.

Dr Dharam Prakash, Secretary General, Indian Medical Association, highlighted the role of doctors in early diagnosis of cancer. He said that the all doctors should be trained in early diagnosis of cancer. Dr Arun Goel, Director Oncology at Galaxy Cancer Institute briefed the gathering about the Institute and spoke of the modern equipment and protocols available for the treatment and management of all types of cancers. The highlight of the center was the Linear Accelerator, which was capable of delivering Image-guided Radiotherapy and Intensity Modulated Radiotherapy. In addition, the brachytherapy facilities available at the centre with its 30 channels HDR Remote afterloading device could treat large tumors, were also appreciated. The seminar concluded with a vote of thanks by Dr. Sandeep Agarwal, Senior Consultant at Galaxy Cancer Institute, Pushpanjali Crosslay Hospital.

Honorable Chief Minister lighting the lamp

(L to R) Shri Alok Mehta, Dr. Vinany Aggarwal, Smt. Sheila Dikshit, Dr. Vijay Agarwal, Dr. Dharam Parkash on dias

49 Vol. 8, Issue 2 Jan - March 2009

February 7, 2009 Recent Advances in Prostate Surgery Dr B Sunder, an eminent Urologist from Chicago addressed a gathering of clinicians including Physicians and Surgeons on Recent Advances in Prostate Surgery. Dr Ajit Saxena, Sr Consultant, Urology chaired the session.

March 1, 2009 CME on

Tim Galekop, Director, Ahlstrom, Belgium, an expert in Global Technical support for hospitals discussed Infection Prevention - A way to early recovery and increased Patient turnover. Mr Mayank Premi, Director, Progressive Healthcare Solutions deliberated on Collective Bargaining for increasing Effectivity, Productivity and Profitability in healthcare. The CME was sponsored by Dispoline, Bangalore. Speaking on the occasion Mr Sumit Marwaha, CEO and MD, committed to providing continued support to PCH.

The lecture was attended by over 70 medical professionals from various specialties. Dr. Parkash Gera, chaired the session.

Dr. Tilak Kiran talking to the Delegates

March 22, 2009 Hearing Screening Camp

A day long hearing screening camp on the initiative of Mr Raj Sharma, Head, Audiology and Speech therapy, department of ENT and under the leadership of Dr Atul Jain, was organized. The highlight of the camp was an award of ten digital hearing aids to those diagnosed at the camp. The hearing aids costing Rs. 1 lac were arranged by Mr. Raj Sharma. A total of 57 patients were screened for their hearing of which 10 were recommended hearing aids. Since there were 10 prizes, each diagnosed patient emerged a winner.

Sumit Marwah, Tim Galekop, Dr. Vijay Agarwal and Mayank on the dies (L to R)

March 15, 2009 Health Camp

Continuing with corporate social responsibility, a health ca mp was organized in association with the Rajasthan Maheshwari Sewa Samiti at Lions Bhawan, Vivek Vihar. Senior consultants Dr Parkash Gera, Dr Vipin Mishra, Dr LD Sota, Dr Neeraj Jain, Dr BK. Gupta, Dr Dhirendra Singhania and Dr KP Singh offered free consultation to the visitors. Camp participants were also provided free investigations including Blood Sugar, Blood Pressure Checkup and ECG by the department of Lab Medicine. Yogacharya Sheshpal ji demonstrated Yogasanas. Over 250 persons benefited from the services offered at the camp.
Mr. Raj Sharma addressing patients on hearing

Training Programs Conducted

A Community CPR program was conducted to provide people with the knowledge and skill necessary in an emergency to call for help, to keep people alive, to reduce pain and minimize the consequences of injury or sudden illness until professional medical help arrives. BLS Training and Resuscitation Programme BLS training and resuscitation programme, is conducted every Wednesday of the month, from 10 am to 1 pm by Dr Amit Gupta, Consultant and Head, Emergency Medical Services, Trauma Care and Medical Intensive Care Unit. The main objective of this program is to guide people about CPR, first aid and common medical emergencies.

March 17, 2009

Honors Received
Dr Narendra Saini after been designated as President Elect, DMA was selected as the India Representative for World Hygiene Council at a glittering function at London, U.K. Dr Narinder Saini with others from 50 Vol. 8, Issue 2 Jan - March 2009

Yogacharya Sheshpal ji demonstrating Yoga

Guest lecture on Sleep Medicine

A guest lecture on Sleep Medicine was delivered by Dr. Tilak Kiran Verma, Director, Sleep Medicine, Rhode islands, USA.

Guidelines for Submission of Manuscripts

You are invited to contribute your articles, case reports, clinical experiences and any other relevant material which is for the benefit of clinical community at large. The articles/ contribution should be sent to: The Editor in-Chief Dr. Vinay Aggarwal & The Editor Dr Ashok Grover PUSHPANJALI MEDICAL PUBLICATIONS PVT. LTD. A-14, Pushpanjali, Vikas Marg Extn. Delhi 110092 E-mail : pmc_pub@hotmail.com pmc_pub@yahoo.co.in Manuscripts can be submitted by e-mail, but it is mandatory that photographs (if any) should be submitted in glossy paper by post. To maintain the uniformity the articles, authors should follow the following pattern: All Manuscripts submitted to Medi-Focus should not have been published in any form in any other publication, and become the property of the publishers. All manuscripts must be accompanied by the following written statement signed by all the authors. The undersigned author (s) certify (ies) that the article is original, is not under consideration by any other journal, and has not been previously published. All copyright ownership of the manuscript entitled (title of article) is hereby transferred to the publishers of Medi-focus. Articles will be edited for style and grammar. Technical jargon is to be kept to a minimum. American spellings are used in the Journal.

Structured Abstract. Should be a factual condensation of the entire work with objective, methods, results, conclusions and should be in one para. The abstract should state the purposes of the study or investigation, basic procedures (selection of study subjects or laboratory animal; Observational and analytical methods), main findings (giving specific data and their statistical significance, if possible), and the principal conclusion. It should emphasize new and important aspects of the study or observations. Clinical Briefs must not exceed 1000 words with one figure and 5-8 references. Text. Authors must consider and follow the format : Introduction, Material and Methods, Results, Discussion, and Conclusion (if necessary). The matter must be written in a manner which is easy to understand, and should be restricted to the topic discussed. Do not use vertical lines or underlining in the text. Acknowledgments should be placed as the last element of the text before references. Abbreviate measurements (cm, ml). Abbreviations should be used sparingly and must be preceded by the full form initially. References. In citing other work, only references consulted in the original should be included. If it is against citation by others this should also be stated. Use the Sequential numbering system. Arrange the reference list in the sequence in which the references are first cited. In the text, references cited should be superscripted and should appear on top of the line after the punctuation. Responsibility for the accuracy and completeness of references lies with the author. References should not exceed 15-20 in number. The Journal follows the Vancouver system of references. References should be numbered and listed consecutively in the order in which they are first cited in the text. Tables should be identified in the text by superior Arabic numerals. The full list of references at the end of the paper should include : names and initials of all authors (unless more than 6, when only the first 3 are given followed by et al); the title of the paper; the journal title abbreviated according to the style of Index Medicus; year of publication; volume number; first and last page numbers. References of

Preparation of Manuscripts
Format. The manuscript must not exceed 1012 pages typed in double space (including 1520 references). Number all pages in sequence, beginning with the title page. Submit a copy of all elements arranged as follows: Title Page. This should contain the title of the manuscript (5-6 words title) the names of all authors, and their affiliations, a short title (not more than 20 letters to be used as running head) and at the bottom of the page, institution where the work has been carried out, and the address for all correspondence and reprints, including Fax, Phone and E-mail. 51 Vol. 8, Issue 2 Jan - March 2009

give the book title, place of publication, publisher and year; those of multiple authorship should also include the chapter title, first and last page numbers, and names and initials of editors. 1. Mehta MN, Mehta JN. Serum lipids and ABO blood groups in cord blood of neonates. Indian J Pediatr 1984; 51 : 30-43. 2. Smith GDL. Chronic Ear Disease. Edinburgh; Churchill Livingstone, 1980 : 78-81. 3. Malhotra KC. Medicogenetic problems of Indian tribes. In Verma IC, ed. Medical Genetics in India. Vol. 2., Pondicherry; Auroma Enterprises, 1978; 51-55. Papers accepted but not yet published should be included in the references followed by In press. Those in preparation, personal communications and unpublished observations should be referred to as such in the text only. For more detailed information about the Vancouver system, authors should consult Uniform requirements for manuscripts submitted to biomedical journals (Br Med J. 1982; 284 : 1766-70). Legends. A descriptive legend must accompany each illustration and must define all abbreviations used therein. Illustrations and graphs. Submit glossy black and white photographs. The cost reproduction of colour photographs will be borne entirely by the author. Number all illustrations with Arabic numericals (1, 2).

Tables. These must be self-explanatory. The data must be clearly organized and should supplement and not duplicate the text. Explanatory matter should be given as footnotes. Statistical analyses used must be appropriate. Each table must have a title and should be numbered with Arabic numericals (1, 2).

Manuscript Submission Checklist

1. Three copies of manuscript in hard copy 2. Name and address correspondence. of author responsible for

3. Structured Abstract (150-200 words) & 3-5 key words. 4. References, cited consecutively in the text. 5. Three glossy prints for illustrations. 6. Documentation of permission to reuse any previously published material. 7. Covering letter, including statement of originality and signifying approval of final copy by all authors. 8. Upon final acceptance of the manuscript, a CD disk in MS Word should be submitted. The disk should be labeled with the title of article, file name and version used and must contain the final revised manuscript material.

52 Vol. 8, Issue 2 Jan - March 2009