Ajpp April-June 2013

Page 1

Volume 16, Number 4



Online Submission

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

Asian Journal of

Paediatric Practice Volume 16, No. 4, 2013

Dr Deepak Chopra Chief Editorial Advisor

Padma Shri and Dr BC Roy National Awardee

Dr KK Aggarwal

FROM THE DESK OF EDITOR

Group Editor-in-Chief

Dr Veena Aggarwal

MD, Group Executive Editor

5

Swati Y Bhave

Anand Gopal Bhatnagar Editorial Anchor

AJPP Speciality Board Chief Editor Dr Swati Y Bhave Editorial Board National Dr Alagiriswamy Parthasarathy Dr Ajay Kalra Dr K Nedunchelian Dr Yagnesh Popat Dr Chhaya Prasad Dr Atul Agarwal Dr Anoop Verma Dr Vijay Zawar Dr J S Tuteja Dr Surekha Joshi Editorial Board International Dr Professor Antonio An Tung Chuh Dr Jay E Berkelhamer Dr Neil Wigg Professor Andreas Konstantopoulos Ahmaduddin Maarij Professor Leyla Namazova-Baranova Dr Angelo Neeneo Dr Yoshikatsu Eto Dr Peter Cooper

IJCP Editorial Board

FROM THE DESK OF GROUP EDITOR-IN-CHIEF 6 Bihar Children Death after Eating Mid-day Meal Update

KK Aggarwal

REVIEW ARTICLE 7 Diagnosis and Management of Dehydration in Children

Amy Canavan, Billy S Arant

Obstetrics and Gynaecology Dr Alka Kriplani, Dr Thankam Verma, Dr Kamala Selvaraj Cardiology Dr Praveen Chandra, Dr SK Parashar Paediatrics Dr Swati Y Bhave Diabetology Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty ENT Dr Jasveer Singh Dentistry Dr KMK Masthan, Dr Rajesh Chandna

ORIGINAL STUDY 12 Cord Blood Nucleated RBC as a Predictor of Perinatal Asphyxia, Severity and Outcome

Gastroenterology Dr Ajay Kumar

Anil Kumar Mohanty, Leena Das, Subal Pradhan, Bijay Meher, Siba Shankar Beriha

Dermatology Dr Hasmukh J Shroff Neurology Dr V Nagarajan Orthopedics Dr J Maheshwari Journal of Applied Medicine and Surgery Dr SM Rajendran, Dr Jayakar Thomas Advisory Bodies Heart Care Foundation of India Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

CLINICAL STUDY 16 Etiological Determinants of Rhesus Isoimmunization and its Perinatal Outcome

Neetu Singh, Kiran Pandey, Preeti Dubey, Yashwant Rao


CLINICAL STUDY

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

20 Serum IgE Levels and Absolute Eosinophil Count in Children with Bronchiolitis

Rugmini Kamalammal, PJ Parameswari

Printed at SR Offset Art Printers, Chennai © Copyright 2013 IJCP Publications Ltd. All rights reserved. The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

24 Impact of Overweight/Obesity on Emotional Health of Adolescents: A Cross-sectional Study

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

Shweta Pathak, Anjoo Bhatnagar, Sanjeev Dutta, Bindu Dhingra

PHOTO QUIZ 31 Rash and Fever in an Ιll-Appearing Child

RESEARCH REVIEW 35 From the Journals...

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

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FROM THE DESK OF EDITOR

Dr Swati Y Bhave

Chief Editor Executive Director, AACCI, (Association of Adolescent and Child Care in India) Senior Visiting Consultant Indraprastha Apollo Hospitals, New Delhi

Dear Readers Energy Drinks - Harmful to Children. Energy drinks are under-studied, overused and can be dangerous for children and teens. The potential harms, caused mostly by too much caffeine or similar ingredients, include heart palpitations, seizures, strokes and even sudden death, according to a study published in the journal Pediatrics. “Surveys show that 30-50% of teens and young adults consume energy drinks, but we didn’t find any evidence that drinks have beneficial effects in improving energy, weight loss, stamina, athletic performance and concentration”, said study author Steven Lipshultz, chair of Pediatrics at the University of Miami School of Medicine.

Address for correspondence IJCP Group of Publications E - 219, Greater Kailash, Part - 1, New Delhi - 110 048

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

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FROM THE DESK OF GROUP EDITOR-IN-CHIEF

Dr KK Aggarwal

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

Bihar Children Death after Eating Mid-day Meal Update Food poisoning epidemic keep occurring now and then and it is unfortunate that children or people die every year because of these instances which can occur in school mid-day meal, marriage functions, religious functions, etc. Possible ways of food poisoning, one is, pre-formed toxin in the food like staph and bacillus cereus. Both poisoning occur when someone eat partially cooked food including rice and vegetables. When the partially cooked food is kept at room temperature overnight toxins can form from the bacteria. The key point is food should not be kept for more than two hours at room temperature at no cost. Even if this food is reheated and served it can still cause poisoning as most of the toxins are heat stable. In mid-day school meal or in marriage functions, this is very likely that the food is served at 11 am. The food either might have been prepared in night before or early in the morning and then it stays at a room temperature for hours together. Another is poisoning because of insecticides and pesticides. The classical toxic oil syndrome, a name given to spain epidemic in 1981, which killed over 600 people was linked to either adulterated coiza oil, which had been intended for industrial rather than food use. In the same epidemic some people linked the poisoning because of organophosphorus compound, which is often used as an insecticide. In the present epidemic till the final report comes possibility of all three will remain. Preformed toxin usually cannot cause deaths in such a large number. Canned food can cause such epidemic because of botulism. But is unlikely in the present epidemic. The basic precautions are:

6

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Food should be properly cooked for the right time and at the right temperature

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Food should be properly hot when eaten

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Vegetables should be properly washed in running water for 15 minutes

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Egg and meat should be properly and fully cooked

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Half cooked rice can be dangerous

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Water should be boiled before used

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All liquids should be boiled

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Eating fruits which can be pealed by hand are safe.

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013


REVIEW ARTICLE

Diagnosis and Management of Dehydration in Children AMY CANAVAN, BILLY S ARANT

ABSTRACT The most useful individual signs for identifying dehydration in children are prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern. However, clinical dehydration scales based on a combination of physical examination findings are better predictors than individual signs. Oral rehydration therapy is the preferred treatment of mild to moderate dehydration caused by diarrhea in children. Appropriate oral rehydration therapy is as effective as intravenous fluid in managing fluid and electrolyte losses and has many advantages. Goals of oral rehydration therapy are restoration of circulating blood volume, restoration of interstitial fluid volume, and maintenance of rehydration. When rehydration is achieved, a normal age-appropriate diet should be initiated. Keywords: Dehydration, oral rehydration therapy, interstitial fluid volume, diarrhea, electrolyte loss

C

linical dehydration scales based on a combination of physical examination findings are the most specific and sensitive tools for accurately diagnosing dehydration in children and categorizing its severity. Overdiagnosis of dehydration may lead to unnecessary tests and treatment, whereas underdiagnosis may lead to increased morbidity (e.g., protracted vomiting, electrolyte disturbances, acute renal insufficiency). Among children in the United States, fluid and electrolyte disturbances from acute gastroenteritis result in 1.5 million outpatient visits, 200,000 hospitalizations, and 300 deaths per year.1 Additionally, children may become dehydrated because of a variety of other illnesses that cause vomiting, diarrhea, or poor fluid intake. DIAGNOSIS

Parental Observation Parental report of vomiting, diarrhea, or decreased oral intake is sensitive, but not specific, for identifying AMY CANAVAN, MD, FAAP, is a pediatric hospitalist at Inova Fairfax Hospital for Children, Falls Church, Va., and an assistant professor in the Department of Pediatrics at Virginia Commonwealth University School of Medicine in Falls Church. At the time this article was written, Dr. Canavan was a pediatric hospitalist at T.C. Thompson Children’s Hospital, Chattanooga, Tenn., and an assistant professor in the Department of Pediatrics at the University of Tennessee College of Medicine Chattanooga. BILLY S. ARANT, JR., MD, FAAP, is a pediatric nephrologist at T.C. Thompson Children’s Hospital and a professor in the Department of Pediatrics at the University of Tennessee College of Medicine Chattanooga. Source: Adapted from Am Fam Physician. 2009;80(7):692-696.

dehydration in children. If parents report that the child does not have diarrhea, has normal oral intake, and has normal urine output, the chance of dehydration is low. Likewise, when parents are asked about physical signs of dehydration, a number of positive answers suggest dehydration. However, if the parents report normal tear production, the chance of dehydration is low.2,3

Physical Examination Comparing change in body weight from before and after rehydration is the standard method for diagnosing dehydration.4 To identify dehydration in infants and children before treatment, a number of symptoms and clinical signs have been evaluated and compared with this standard method. Physical examination findings during dehydration represent desiccation of tissue, the body’s compensatory reaction to maintain perfusion, or both. The most useful individual signs for identifying dehydration are prolonged capillary refill time, abnormal skin turgor, and abnormal respiratory pattern.5 However, clinical dehydration scales based on a combination of physical examination findings are much better predictors than individual signs.5 In one study, four factors predicted dehydration: capillary refill time of more than two seconds, absence of tears, dry mucous membranes, and ill general appearance; the presence of two or more of these signs indicated a fluid deficit of at least 5%.6 In a similar validated scale, general appearance, degree of sunken eyes, dryness of mucous membranes, and tear production were associated with length of hospital

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

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REVIEW ARTICLE stay and need for intravenous fluids in children with acute gastroenteritis.7 Capillary refill time is performed in warm ambient temperature, and is measured on the sternum of infants and on a finger or arm held at the level of the heart in older children. The measurement is not affected by fever and should be less than two seconds.8 Assessment of skin turgor is performed by pinching skin on the lateral abdominal wall at the level of the umbilicus. Turgor (i.e., time required for the skin to recoil) is normally instantaneous and increases linearly with degree of dehydration.9 Respiratory pattern and heart rate should be compared with agespecific normal values.

Laboratory Assessment Unlike in adults, calculation of the blood urea nitrogen (BUN)/creatinine ratio is not useful in children. Although the normal BUN level is the same for children and adults, the normal serum creatinine level changes with age (0.2 mg per dL [17.68 μmol per L] in infants to 0.8 mg per dL [70.72 μmol per L] in adolescents). BUN alone and urine specific gravity also have poor sensitivity and specificity for predicting dehydration in children.10 In combination with a clinical dehydration scale, a serum bicarbonate level of less than 17 mEq per L (17 mmol per L) may improve sensitivity of identifying children with moderate to severe hypovolemia.11 Additionally, a serum bicarbonate level of less than 13 mEq per L (13 mmol per L) is associated with increased risk of failure of outpatient rehydration efforts.12 TREATMENT

Pathophysiology Most of the volume loss in dehydration is extracellular fluid. The extracellular fluid space has two components: plasma and lymph as a delivery system, and interstitial fluid for solute exchange.13 The goal of rehydration therapy is first to restore the circulating blood volume, if necessary; then to restore the interstitial fluid volume; and finally to maintain hydration and replace continuing losses, such as diarrhea and increased insensible losses caused by fever.

Oral Rehydration Therapy The American Academy of Pediatrics recommends oral rehydration therapy (ORT) as the preferred treatment of fluid and electrolyte losses caused by diarrhea in children with mild to moderate dehydration.14

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ORT is as effective as intravenous fluid in rehydration of children with mild to moderate dehydration—there is no difference in failure rate or hospital admission rate between the two treatments.15 Additionally, ORT has many advantages compared with intravenous fluid therapy. It can be administered at home, reducing the need for outpatient and emergency department visits; requires less emergency department staff time; and leads to shorter emergency department stays. Parents are also more satisfied with the visit when ORT had been used.16 With ORT, the same fluid can be used for rehydration, maintenance, and replacement of stool losses; and ORT can be initiated more quickly than intravenous fluid therapy.17 The principles of ORT to treat dehydration from gastroenteritis apply to the treatment of dehydration from other causes. Altered mental status with risk of aspiration, abdominal ileus, and underlying intestinal malabsorption are contraindications. Cost to the family may be a deterrent to home ORT; therefore, ORT solution provided by the physician’s office or emergency department increases the likelihood that parents will use ORT and reduces unscheduled followup visits.16 Nasogastric rehydration therapy with ORT solution is an alternative to intravenous fluid therapy in patients with poor oral intake. Nasogastric hydration using oral rehydration solution is tolerated as well as ORT. Failure rate of nasogastric tube placement is significantly less than that of intravenous lines, and significant complications of nasogastric tube placement are rare. Nasogastric rehydration therapy is also less expensive than intravenous fluid therapy.18 As soon as children with acute gastroenteritis are rehydrated, a regular age-appropriate diet should be initiated. This does not worsen the symptoms of mild diarrhea, and may decrease its duration.14 Preparations Use of an appropriate ORT solution, such as commercial electrolyte solutions for children (e.g., Pedialyte), corrects and helps prevent electrolyte disturbances caused by gastroenteritis.17-19 The World Health Organization ORT solution contains 90 mEq per L of sodium, mimicking the sodium content of diarrhea caused by cholera. Commercial ORT preparations typically contain around 50 mEq per L of sodium, which is more consistent with the sodium content of diarrhea caused by rotavirus.20 Commercial ORT solutions contain 25 g per L of dextrose, which


REVIEW ARTICLE Table 1. Approximate Electrolyte Composition of Clear Liquids Type of liquid

Carbohydrates (g per L)

Sodium (mEq per L)

Potassium (mEq per L)

Base (mEq per L)

Osmolality (mOsm per L)

Commercial electrolyte solutions for children (e.g., Pedialyte)*

140

45 to 50

20

30

250

Sports drinks (e.g., Gatorade)

255

20

3

2

360

Juice

690

2

30

0

730

Soda

700

3

0

13

750

*Only clear liquid recommended for oral rehydration in children with dehydration. Clear sodas and juices are not recommended because hyponatremia may occur.

helps prevent hypoglycemia without causing osmotic diuresis,21 and 30 mEq per L of bicarbonate, which leads to less vomiting and more efficient correction of acidosis.19 Commercial ORT solutions are recommended over homemade solutions because of the risk of preparation errors.22 Clear sodas and juices should not be used for ORT because hyponatremia may occur. Table 1 compares the electrolyte composition of commercial electrolyte solutions with other clear liquids. Administration For mild dehydration, 50 mL per kg of ORT solution should be administered over four hours using a spoon, syringe, or medicine cup14; this can be accomplished by giving 1 mL per kg of the solution to the child every five minutes. Patients may be treated at home.14 If the child vomits, treatment should be resumed after 30 minutes.15 After the four-hour treatment period, maintenance fluids should be given and ongoing losses assessed and replaced every two hours. Maintenance therapy includes providing anticipated water and electrolyte needs for the next 24 hours in the child who is now euvolemic with expected normal urine output. The Holliday-Segar method (Table 223) is a simple, reliable formula for estimating water needs.24 Based on average weights of infants and children, this method can be further simplified to provide maintenance ORT at home: 1 oz per hour for infants, 2 oz per hour for toddlers, and 3 oz per hour for older children. To replace ongoing losses, 10 mL per kg for every loose stool and 2 mL per kg for every episode of emesis should be administered. For moderate dehydration, 100 mL per kg of ORT solution should be given over four hours in the physician’s office or emergency department.14 If treatment is successful and ongoing losses are not excessive, the child may be sent home. At home, caregivers should provide maintenance therapy and replace ongoing losses every two hours as described

for mild dehydration. ORT is considered to be unsuccessful if vomiting is severe and persistent (i.e., at least 25 percent of the hourly oral requirement) or if ORT cannot keep up with the volume of stool losses.17 Severe dehydration should be treated with intravenous fluids until the patient is stabilized (i.e., circulating blood volume is restored). Treatment should include 20 mL per kg of isotonic crystalloid (normal saline or lactated Ringer solution) over 10 to 15 minutes.25 No other fluid type is currently recommended for volume resuscitation in children.26 Treatment should be repeated as necessary, with monitoring of the patient’s pulse strength, capillary refill time, mental status, and urine output. Stabilization often requires up to 60 mL per kg of fluid within an hour.25 Electrolyte measurement should be performed in all children with severe dehydration and considered in those with moderate dehydration because it may be difficult to predict which children have significant electrolyte abnormalities.27 After resuscitation is completed and normal electrolyte levels are achieved, the patient should receive 100 mL per kg of ORT solution over four hours, then maintenance fluid and replacement Table 2. Holliday-Segar Method for Determining Maintenance ORT in Children Body weight

Daily water requirement

Hourly water requirement

≤ 23 lb (10 kg)

100 mL per kg

4 mL per kg

24 to 44 lb (11 to 20 kg)

1,000 mL, plus 50 mL 40 mL, plus 2 mL per kg for each kg per kg for each kg between 11 and 20 kg between 11 and 20 kg

> 44 lb (20 kg)

1,500 mL, plus 20 mL per kg for each kg over 20 kg

60 mL, plus 1 mL per kg for each kg over 20 kg

Note: This method can be further simplified to provide maintenance ORT at home: 1 oz per hour for infants, 2 oz per hour for toddlers, and 3 oz per hour for older children. ORT = Oral rehydration therapy.

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REVIEW ARTICLE of ongoing losses. If ORT fails after initial resuscitation of a child with severe dehydration, intravenous fluid therapy should be initiated. First, 100 mL per kg of isotonic crystalloid should be administered over four hours, followed by a maintenance solution. This method also may be used when a child with moderate dehydration fails ORT. The electrolyte content of intravenous maintenance fluid for infants and children with normal serum electrolyte levels should be 5 percent dextrose and 25 percent normal saline, plus 20 mEq per L of potassium.23,28,29 Intake, output, and vital signs must be checked every four hours, and adjustments made to the therapy as necessary (e.g., in the setting of ongoing losses, such as excessive stool output, or persistent fever). If stool output exceeds 30 mL per kg per day, it should be replaced in an equal volume every four hours with an intravenous solution comparable in electrolytes with the stool (50 percent normal saline plus 20 to 30 mEq per L of potassium), in addition to the volume of maintenance fluid, until ORT can be tolerated. Children with persistent fever may require 1 mL per kg per degree centigrade every hour, in addition to the calculated maintenance therapy. Postoperatively and in children with central nervous system infection or injury, 20 to 50 percent less fluid and fluid with higher sodium content may be needed because of abnormal antidiuretic hormone secretion.28 These adjustments in fluid rates are guided by regular measurement of urine output and vital signs.

Medications Pharmacologic agents are not recommended to decrease diarrhea because of limited evidence and concern for toxicity. Although Lactobacillus has no major toxic effects, its effectiveness in patients with diarrhea has not been demonstrated.14 A single dose of ondansetron has been shown to facilitate ORT by reducing the incidents and frequency of vomiting and, therefore, reducing the failure of ORT and the need for intravenous fluid therapy.30 Recurrent dosing of ondansetron has not been studied. COMPLICATIONS Hypernatremia, hyponatremia, and hypoglycemia occasionally complicate dehydration. Serum electrolyte levels should be measured in children with severe dehydration and in those with moderate dehydration that presents in atypical ways.

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Hypernatremia (serum sodium level of greater than 145 mEq per L [145 mmol per L]) indicates water loss in excess of sodium loss. Because sodium is restricted to the extracellular fluid space, the typical signs of dehydration are less pronounced in the setting of hypernatremia, and significant circulatory disturbance is not likely to be noted until dehydration reaches 10 percent. Findings that may aid in the diagnosis of hypernatremia in children include a “doughy� feeling rather than tenting when testing for skin turgor, increased muscle tone, irritability, and a highpitched cry.31 Hyponatremia is often caused by inappropriate use of oral fluids that are low in sodium, such as water, juice, and soda. If severe dehydration is present, a child with hypernatremia or hyponatremia should receive isotonic crystalloid until stabilized. If after initial volume repletion, hyponatremia or hypernatremia remains moderate to severe (serum sodium level of less than 130 mEq per L [130 mmol per L] or greater than 150 mEq per L [150 mmol per L]), replacement of the remaining fluid deficit should be altered, with a principal goal of slow correction. In one study, blood glucose levels of less than 60 mg per dL (3.33 mmol per L) were detected in 9 percent of children younger than nine years (mean age 18 months) admitted to the hospital with diarrhea.27 History and physical examination findings did not indicate that these children were at risk; therefore, blood glucose screening may be indicated for toddlers with diarrhea. REFERENCES 1. King CK, Glass R, Bresee JS, Duggan C, for the Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16. 2. Porter SC, Fleisher GR, Kohane IS, Mandl KD. The value of parental report for diagnosis and management of dehydration in the emergency department. Ann Emerg Med. 2003;41(2):196-205. 3. Armon K, Stephenson T, MacFaul R, Eccleston P, Werneke U. An evidence and consensus based guideline for acute diarrhoea management. Arch Dis Child. 2001;85(2):132-142. 4. Friedman JN, Goldman RD, Srivastava R, Parkin PC. Development of a clinical dehydration scale for use in children between 1 and 36 months of age. J Pediatr. 2004;145(2):201-07. 5. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated? JAMA. 2004;291(22):2746-754. 6. Gorelick MH, Shaw KN, Murphy KO. Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics. 1997;99(5):E6.


REVIEW ARTICLE 7. Goldman RD, Friedman JN, Parkin PC. Validation of the clinical dehydration scale for children with acute gastroenteritis. Pediatrics. 2008;122(3):545-49. 8. Gorelick MH, Shaw KN, Murphy KO, Baker MD. Effect of fever on capillary refill time. Pediatr Emerg Care. 1997;13(5):305-07. 9. Laron Z. Skin turgor as a quantitative index of dehydration J in children. Pediatrics. 1957;19(5):816-22. 10. Teach SJ, Yates EW, Feld LG. Laboratory predictors of fluid deficit in acutely dehydrated children. Clin Pediatr (Phila). 1997;36(7):395-400. 11. Vega RM, Avner JR. A prospective study of the usefulness of clinical and laboratory parameters for predicting percentage of dehydration in children. Pediatr Emerg Care. 1997;13(3):179-82. 12. Reid SR, Bonadio WA. Outpatient rapid intravenous rehydration to correct dehydration and resolve vomiting in children with acute gastroenteritis. Ann Emerg Med. 1996;28(3):318-23. 13. Holliday MA, Friedman AL, Wassner SJ. Extracellular fluid restoration in dehydration: a critique of rapid versus slow. Pediatr Nephrol. 1999;13(4):292-97. 14. Practice parameter: the management of acute gastroenteritis in young children. American Academy of Pediatrics, Provisional Committee on Quality Improvement, Subcommittee on Acute Gastroenteritis. Pediatrics. 1996;97(3):424-35. 15. Atherly-John YC, Cunningham SJ, Crain EF. A randomized trial of oral vs intravenous rehydration in a pediatric emergency department. Arch Pediatr Adolesc Med. 2002;156(12):1240-1243. 16. Duggan C, Lasche J, McCarty M, et al. Oral rehydration solution for acute diarrhea prevents subsequent unscheduled follow-up visits. Pediatrics. 1999;104(3):e29. 17. Spandorfer PR, Alessandrini EA, Joffe MD, Localio R, Shaw KN. Oral versus intravenous rehydration of moderately dehydrated children: a randomized, controlled trial. Pediatrics. 2005;115(2):295-301. 18. Nager AL, Wang VJ. Comparison of nasogastric and intravenous methods of rehydration in pediatric patients with acute dehydration. Pediatrics. 2002;109(4):566-72.

19. Islam MR, Ahmed SM. Oral rehydration solution without bicarbonate. Arch Dis Child. 1984;59(11):1072-1075. 20. Molla AM, Rahman M, Sarker SA, Sack DA, Molla A. Stool electrolyte content and purging rates in diarrhea caused by rotavirus, enterotoxigenic E. coli, and V. cholerae in children. J Pediatr. 1981;98(5):835-38. 21. Rahman O, Bennish ML, Alam AN, Salam MA. Rapid intravenous rehydration by means of a single polyelectrolyte solution with or without dextrose. J Pediatr. 1988;113(4):654-60. 22. Meyers A, Sampson A, Saladino R, Dixit S, Adams W, Mondolfi A. Safety and effectiveness of homemade and reconstituted packet cereal based oral rehydration solutions: a randomized clinical trial. Pediatrics. 1997;100(5):E3. 23. Holliday MA, Segar WE. The maintenance need for water in parenteral fluid therapy. Pediatrics. 1957;19(5):823-32. 24. Holliday MA, Ray PE, Friedman AL. Fluid therapy for children: facts, fashions and questions. Arch Dis Child. 2007;92(6):546-50. 25. Boluyt N, Bollen CW, Bos AP, Kok JH, Offringa M. Fluid resuscitation in neonatal and pediatric hypovolemic shock: a Dutch Pediatric Society evidence-based clinical practice guideline. Intensive Care Med. 2006;32(7):995-1003. 26. Pediatric Advanced Life Support Provider Manual. Dallas, Tex.: American Heart Association; 2006:232. 27. Wathen JE, MacKenzie T, Bothner JP. Usefulness of the serum electrolyte panel in the management of pediatric dehydration treated with intravenously administered fluids. Pediatrics. 2004;114(5):1227-1234. 28. Friedman AL, Ray PE. Maintenance fluid therapy: what it is and what it is not. Pediatr Nephrol. 2008;23(5):677-80. 29. Assadi F, Copelovitch L. Simplified treatment strategies to fluid therapy in diarrhea [published correction appears in Pediatr Nephrol. 2004;19(3):364]. Pediatr Nephrol. 2003;18(11):1152-1156. 30. Freedman SB, Adler M, Seshadri R, Powell EC. Oral ondansetron for gastroenteritis in a pediatric emergency department. N Engl J Med. 2006;354(16):1698-1705. 31. Conley SB. Hypernatremia. Pediatr Clin North Am. 1990;37(2): 365-72.

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Clinical and Laboratory Profile of Enteric Fever in Children in Northern India The diagnosis of enteric fever poses several problems due to the nonspecific and wide array of clinical features. A five-year retrospective study enrolling 136 culture-proven cases of enteric fever was undertaken in order to estimate the clinical and laboratory characteristics, fever clearance time and outcome. The common symptoms and signs were: Fever, vomiting, cough, anorexia, diarrhea, abdominal pain, hepatomegaly, splenomegaly and coated tongue. Enteric fever should be considered in the differential diagnosis of febrile patients with abdominal symptoms. Source: Dheer G, Kundra S, Singh T. Trop Doct 2012;42(3):154-6.

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ORIGINAL STUDY

Cord Blood Nucleated RBC as a Predictor of Perinatal Asphyxia, Severity and Outcome ANIL KUMAR MOHANTY*, LEENA DAS**, SUBAL PRADHAN†, BIJAY MEHER†, SIBA SHANKAR BERIHA†

ABSTRACT Objective: To study the correlation of cord blood nucleated red blood cell (NRBC)/100 white blood cell (WBC) count with perinatal asphyxia in terms of severity and short-term outcome. Subject and method: A prospective, comparative case-control study was undertaken in a tertiary care hospital from January 2011 to December 2012, which included a total of 200 neonates with 100 asphyxiated babies (case group) and 100 normal babies (control group). The cord blood was collected immediately after delivery for measurement of NRCB/100 WBC, and pH. Early neonatal outcome of both groups was also evaluated in relation to the NRBC/100 WBC count. Statistical analysis was performed with chi-square and student t-test. Results: The mean NRBC/100 WBC count was 50.82 ± 23.85 (range from 5 to 106) in case group and 1.67 ± 1.005 (range from 0 to 13) in control group (p < 0.001). Also a statistically significant correlation existed between severity of asphyxia (stage of hypoxic-ischemic encephalopathy [HIE]), poor outcome and higher number of NRBC/100 WBC count (p < 0.001). Conclusion: It is an inexpensive and easily available procedure to evaluate perinatal asphyxia, specially in a resource poor country like ours, where blood gas analysis facilities are not available in majority of places. Also, it is a good predictor of short-term outcome of asphyxiated babies. Keywords: Cord blood, nucleated red blood cells, perinatal, asphyxia

P

erinatal asphyxia is a major cause of acute mortality and chronic neurologic disability amongst survivors, and is a complication that occurs between 2-10% of deliveries.1 No single parameter can define perinatal asphyxia, rather a combination of parameters like fetal distress, meconium-stained liquor, low Apgar score, umbilical cord blood pH and clinical features of hypoxic-ischemic encephalopathy (HIE) can predict it. The 1996 guideline from the American Academy of Pediatrics (AAP) and American College of Obstetricians and Gynecologists (ACOG)2 for HIE indicate that all of the following must be present for designation of perinatal asphyxia severe enough to result in acute neurological injury: ÂÂ

Profound metabolic or mixed academia (pH <7) in an umbilical blood sample and persistence of an Apgar score of 0-3 for longer than 5 minutes

*Professor **Associate Professor †Assistant Professor Dept. of Pediatrics SCB Medical College, Cuttack, Odisha Address for correspondence Dr Anil Kumar Mohanty Professor, Dept. of Pediatrics Duplex-31, Bhawani Construction, Sector-6, CDA, Cuttack - 753 014 E-mail: ctcanil55@gmail.com

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

ÂÂ

Neonatal neurologic sequelae (e.g., seizure, coma, hypotonia)

ÂÂ

Multiple organ involvement (e.g., kidney, lungs, liver, heart and intestines).

But, as per Cloherty et al 3 perinatal asphyxia is defined as a condition of fetal hypoxia and hypercarbia, identified by fetal acidosis as umbilical artery pH <7. The condition can be diagnosed by fetal distress, meconium aspiration, low Apgar score <6 by five minutes, umbilical cord blood pH <7. Recent studies on hematological variations in asphyxiated neonates as a predictor of neonatal asphyxia have suggested that number of nucleated red blood cells (NRBCs) in cord blood of asphyxiated neonates help in identifying birth asphyxia. The number of NRBC/100 white blood cells (WBC) is quite variable but is rarely >10.4-7 The instances, where number of NRBCs exceed 10/100 WBC are asphyxia, prematurity, Rh-sensitization, maternal diabetes mellitus and intrauterine growth retardation. Considering the hematopoietic response to hypoxia in utero the elevated NRBC/100 WBC count is being hailed as the marker for not only perinatal asphyxia but also the chances of the neonates to develop neurological sequelae.4, 7-10 The present study was undertaken to evaluate the cord blood NRBC/100 WBC count as a marker of perinatal


ORIGINAL STUDY asphyxia in conjuction with other clinical markers and its ability as a predictor of perinatal asphyxia, its severity and short-term outcome. SUBJECT AND METHOD A prospective, case-control study was conducted in the Dept. of Pediatrics, SCB Medical College and Hospital, Cuttack, Odisha from January 2011 to December 2012. In this study, hematological profile of a total number of 200 neonates were evaluated (100 asphyxiated/case group and 100 nonasphyxiated/control group). The case group included the mothers in labor between 38-42 weeks of gestation with singleton pregnancies. They were observed during labor for development of signs of fetal distress, thick meconium-staining of liquor, Apgar at one minute and five minutes <6 and umbilical arterial pH <7.0. Control group included nonasphyxiated newborns with appropriate for gestational age (neonates from 38 to 42 weeks gestation), birth weight >2,500 g, Apgar score >7 at both one and five minutes, normal intrapartum fetal heart rate (FHR) pattern, clear amniotic fluid, normal neurologic evaluation during the 1st week. Neonates born to mothers with pre-eclamptic toxemia (PET), diabetes mellitus, Rh-sensitization, multiple pregnancies, born by breech presentation, born before 37 weeks gestation and birth weight <2.5 kg were excluded from the study. Immediately after birth of baby, 1 ml of blood was collected in heparinized syringe from doubly clamped segment of umbilical cord for pH estimation and another 2 ml blood collected in ethylenediaminetetraacetic acid (EDTA) vial from which hemoglobin (HB), total leukocyte count (TLC) were estimated. Along with it a thin blood film was prepared on a glass slide, which was dried and stained with Leishman’s stain. The slide was first examined with low power objective to screen the whole slide to assess the adequacy of cell distribution quality of staining: Subsequently, the slide was examined with oil immersion lens (90 or 100 x 10 = 900 or 1,000 magnification) to examine the red cells for deviation from normal. These NRBCs/100 WBC was counted. Asphyxiated baby was shifted to neonate intensive care unit (NICU) after resuscitation and normal baby to Obstetrics ward. Detailed clinical examination including anthropometric measurement and gestational age was recorded in all cases. Daily evaluation for detection of abnormal symptoms and signs and neurological examination were done at birth, 24 hours after birth and every day thereafter

till discharge/death. Grading of neonates was done according to Sarnat and Sarnat staging for HIE. Correlation of cord blood NRBC/100 WBC count with clinical condition at different stages of HIE during hospital management was observed until discharge or death. Adverse, or poor short-term outcome was diagnosed as the presence of at least one of the following condition death, hemiplegia, hypertonicity or significant hypotonia, unreliable sucking, seizures resistant to phenobarbital and sensorineural hearing loss. Controls were followed up in the same manner. Statistical analysis was done with Chi-square (χ2) analysis (for quantitative analysis), student t-test (comparing mean NRBC in different stages) by SPSS version 20 software for biostatistics. RESULTS Both the case group and control group were similar in terms of gestational age, birth weight, sex of baby, maternal parity and maternal age. However, there was a statistically significant difference in both one minute and five minutes Apgar score and cord blood pH leading to HIE (p < 0.001) (Table 1). The NRBC/100 WBC count for case group was 50.82 ± 23.85 with a range from 5 to 106, whereas, it was 1.67 ± 1.05 with range from 0 to 13 in normal babies (control, group). T value was 20.32 and p value was <0.001, which was statistically significant (Table 2). The NRBC/100 WBC count correlated with degree of asphyxia and staging of HIE. The NRBC count was found to be 15.88 (range 5-28) in Stage Ι HIE, 46.5 (range 6-89) in Stage ΙΙ HIE and 77.12 (range 8-106) in Stage ΙΙΙ HIE. There was a significant relationship between NRBC/100 WBC and HIE staging (p < 0.001) (Table 3). Table 1. Various Parameters of Study Population Parameters Sex (M/F) Maternal age

Asphyxia

Control

p value

56/44

58/42

>0.05

24.3 ± 6

23.6 ± 5

>0.05

Parity (p/m)

47/53

38/62

>0.05

Mode of delivery (ND/CS)

46/54

81/19

>0.05

Birth weight (gr) Gestational age (weeks) Apgar score 1 minute

2,865 ± 404 2,776 ± 405 >0.05 38.4 ± 1.4

37.6 ± 1.3

>0.05

4 ± 1.2

8.6 ± 0.5

<0.001

Apgar score 5 minute

5.4 ± 1.4

9.0 ± 0.4

<0.001

Cord pH

7.0 ± 1.4

7.34 ± 0.1

<0.001

Data presented as mean ± SD; ND = Normal delivery, CS = Cesarean section.

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ORIGINAL STUDY Table 2. Distribution of NRBCs in Both Groups NRBC/100 WBC

Asphyxiated group n (%)

Control n (%)

0-10

4 (4%)

98 (98%)

11-50

55 (55%)

2 (2%)

51-100

38 (38%)

nil

101-150

3 (3%)

nil

100

100

50.82 ± 23.85

1.67 ± 1.05

5-106

0-13

Total Mean + SD Range

Table 4. HIE Staging and Outcome p value

<0.001

Clinical staging

Cases

Death/Disability n (%)

Stage Ι

25

3 (12%)

Stage ΙΙ

50

16 (32%)

Stage ΙΙΙ

25

18 (72%)

Total

100

37 (37%)

Table 5. Relation of NRBC/100 WBC Count with Outcome.

Values expressed as mean ± SD, NRBC = Nucleated red blood cell; WBC = white blood cell.

Mean NRBC/100 WBC with range

Outcome

65.44 (32-106)

Death/Disability

T = 20.32, p value <0.001

42.14 (5-104)

Survived with normal neurodevelopment

P value <0.001

Table 3. NRBC in Different Stages of HIE Stage of HIE Stage Ι

NRBC range

Mean

5-28

15.88

Stage ΙΙ

6-89

46.5

Stage ΙΙΙ

8-106

77.125

NRBC = Nucleated red blood cell; HIE = Hypoxic-ischemic encephalopathy. P value <0.001.

Among asphyxiated group 63 (63%) had good outcome (survived with normal neurologic development), whereas remaining 37 (37%) had poor outcome (either death or disability like neurological sequelae) (Table 4). The NRBC/100 WBC count was significantly higher in babies with adverse outcome, than the babies with good outcome, 65.44 (range 32-106) versus 42.14 (range 5-104) (p < 0.001) (Table 5). Cord blood NRBC count was found to be a good predictor of perinatal asphyxia with sensitivity of 96%, specificity of 98%, positive predictive value of 97.9% and negative predictive value of 96%. DISCUSSION In the present study attempt has been made to evaluate the relation of cord blood NRBC/100 WBC in predicting perinatal asphyxia and its immediate outcome. In our study, the NRBC/100 WBC count for normal newborn was 1.67 ± 1.05, and in the case group it was 50.82 ± 23.85. Several studies have reported an increased NRBC in neonatal cord blood following perinatal asphyxia.5,6,9,11-13 Gupta et al14 in their study had found out NRBC/100 WBC count of 5.7 ± 2.33212 in control group and 10.34 ± 3.87883 in asphyxiated group.

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

Previous studies suggested that erythropoietin increases erythroid production and release of erythrocytes into the peripheral circulation in response to hypoxia.5,10 NRBC/100 WBC count was also related to Sarnat and Sarnat’s grading of HIE. We found out the higher value of NRBC/100 WBC count, in higher degree of severity of HIE; 15.88 in Stage Ι, 46.5 in Stage ΙΙ and 77.12 in Stage ΙΙΙ of HIE. This is statistically significant, as p value is <0.001. Hermansen et al,9 Phelan et al13 and Hanlon-Lundberg et al15 had found higher number of cord blood NRBC in severe asphyxia cases. Boskabadi et al16 in their study had found NRBC as follows, 11.94 in Grade Ι HIE, 21.08 in Grade ΙΙ HIE and 29.18 in Grade ΙΙΙ HIE cases. In our study, among the asphyxiated babies, 37% had poor outcome (either death or survived with sequelae) and in these babies NRBC count was higher, 65.44 (range 32-106), whereas in babies with good outcome the count was less, 42.14 (range 5-104), which is statistically significant (p value <0.001). Other authors like Boskabadi et al16 and Fern et al17 had found similar observations in their study and reported that rate of erythropoiesis was related to degree of asphyxia, which in term influenced the neurological impairment. CONCLUSION In our study, the cord blood NRBC count was shown to be a good predictor of perinatal asphyxia with sensitivity of 96%, specificity of 98%, positive predictive value of 97.9% and negative predictive value of 96%. Since, it is cost-effective and does not require any special expertise or any high-tech facilities, it may


ORIGINAL STUDY be a useful, reliable, inexpensive and easily available marker to evaluate perinatal asphyxia, specially in a resource poor country like ours, where blood gas analysis facilities are not available in majority of place. REFERENCES 1. Low JA. The role of blood gas and acid-base assessment in the diagnosis of intrapartum fetal asphyxia. Am J Obstet Gynecol 1988;159(5):1235-40. 2. Use and abuse of the Apgar score. Committee on Fetus and Newborn, American Academy of Pediatrics, and Committee on Obstetric Practice, American College of Obstetricians and Gynecologists. Pediatrics 1996;98(1): 141-2. 3. Cloherty JP, Eichenwald EC, Hansen AR, Stark AR. Perinatal asphyxia and hypoxic-ischemic encephalopathy. (Chapter 55). In: Manual of Neonatal Care. 7th edition, Wolter Kluwer, Lippincott Williams & Wilkins: Philadelphia USA 2011:p.713-26. 4. Green DW, Mimouni F. Nucleated erythrocytes in healthy infants and in infants of diabetic mothers. J Pediatr 1990;116(1):129-31.

8. Ghosh B, Mittal S, Kumar S, Dadhwal V. Prediction of perinatal asphyxia with nucleated red blood cells in cord blood of newborns. Int J Gynaecol Obstet 2003;81(3):267-71. 9. Hermansen MC. Nucleated red blood cells in the fetus and newborn. Arch Dis Child Fetal Neonatal Ed 2001;84(3): F211-F215. 10. Saraçoglu F, Sahin I, Eser E, Göl K, Türkkani B. Nucleated red blood cells as a marker in acute and chronic fetal asphyxia. Int J Gynaecol Obstet 2000;71(2):113-8. 11. Naeye RL, Localio AR. Determining the time before birth when ischemia and hypoxemia initiated cerebral palsy. Obstet Gynecol 1995;86(5):713-9. 12. Phelan JP, Korst LM, Ahn MO, Martin GI. Neonatal nucleated red blood cell and lymphocyte counts in fetal brain injury. Obstet Gynecol 1998;91(4):485-9. 13. Thilaganathan B, Athanasiou S, Ozmen S, Creighton S, Watson NR, Nicolaides KH. Umbilical cord blood erythroblast count as an index of intrauterine hypoxia. Arch Dis Child Fetal Neonatal Ed 1994;70(3): F192-F194. 14. Sikarwar S, Gupta S. The correlation of clinical perinatal asphyxia with counts of NRBC/100 WBC in cord blood. Webmed Central Obstet Gynaecol 2011;2(1):WMC001511

5. Phelan JP, Ahn MO, Korst LM, Martin GI. Nucleated red blood cells: a marker for fetal asphyxia? Am J Obstet Gynecol 1995;173(5):1380-4.

15. Hanlon-Lundberg KM, Kirby RS. Nucleated red blood cells as a marker of acidemia in term neonates. Am J Obstet Gynecol 1999;181(1):196-201.

6. Philip AG, Tito AM. Increased nucleated red blood cell counts in small for gestational age infants with very low birth weight. Am J Dis Child 1989;143(2):164-9.

16. Boskabadi H, Maamouri G, Sadeghian MH, GhayourMobarhan M, Heidarzade M, Shakeri MT, et al. Early diagnosis of perinatal asphyxia by nucleated red blood cell count: a case-control study. Arch Iran Med 2010;13(4):275-81.

7. McCarthy JM, Capullari T, Thompson Z, Zhu Y, Spellacy WN. Umbilical cord nucleated red blood cell counts: normal values and the effect of labor. J Perinatol 2006;26(2):89-92.

17. Ferns SJ, Bhat BV, Basu D. Value of nucleated red blood cells in predicting severity and outcome of perinatal asphyxia. Indian J Pathol Microbiol 2004;47(4):503-5.

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Acute Disseminated Encephalomyelitis (ADEM): A Rare Complication of Falciparum Malaria A 4-year-old girl was admitted with fever and altered sensorium. Peripheral blood smear and quantified buffy coat test showed Plasmodium falciparum infection. She received antimalarial therapy and got discharged on seventh day without any neurological deficit. Seven days later she was readmitted with fever and disorientation. Neurological examination revealed coma and decerebration. The deep tendon reflexes were exaggerated and babiniski response was positive in the right lower limb. Magnetic resonance imaging (MRI) of brain revealed multifocal asymmetrical T2W/FLAIR hyperintensities in cerebral hemispheres, subcortical white matter and midbrain.

There was minimal patchy enhancement on contrast study. Any feature of grey matter involvement was not observed. The child improved remarkably after the treatment with methyl prednisolone. A follow-up MRI after one year showed a complete resolution of demyelinating lesions. Diagnosis of acute disseminated encephalomyelitis (ADEM) as a complication of falciparum malaria was made based on sudden onset of neurological events, MRI findings and prompt response to corticosteroid therapy. Source: Rachita S, Satyasundar M, Mrutunjaya D, et al. Indian J Pediatr 2013;80(6):499-501.

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

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CLINICAL STUDY

Etiological Determinants of Rhesus Isoimmunization and its Perinatal Outcome NEETU SINGH*, KIRAN PANDEY**, PREETI DUBEY†, YASHWANT RAO‡

ABSTRACT Aims and objectives: To evaluate the etiological determinants of Rh-isoimmunization and to study the prevalence of perinatal mortality and morbidity in Rh-isoimmunization. Material and methods: This retrospective study was carried out in the Dept. of Obstetrics and Gynecology, UISEMH, Kanpur from November 2007 to November 2010. All cases were thoroughly studied, especially their history, examination, investigation, mode of delivery, passive immunization and their perinatal outcome. Results: We found an increased rate of isoimmunization with increasing parity. Most of our patients (44%) were gravida 4. In our study, we found that 84% of isoimmunized patients had a history of previous delivery in which there must have been a large fetomaternal hemorrhage (FMH). It was found that 80% did not receive anti-D while 20% received it. Rh-isoimmunization in 20% of those who received anti-D could be explained due to inadequate dosage. The major cause of perinatal morbidity was hyperbilirubinemia followed by anemia. Conclusion: Rh-isoimmunization is a persistent problem in developing countries. As Rh-immunizing stimulus occurs late in pregnancy and most often at delivery, a successful program for Rh-immunoprophylaxis with Rh-Ig, prevents not only fetal death but also sensitizing prospects. Early reference of affected patients with early assessment and judicial interventions as well as intensive neonatal care is essential in ensuring satisfactory results. Keywords: Retrospective study, Rh-isoimmunization, Rh-immunoprophylaxis

A

bout 5-10% of Indian population is Rh-negative. The Rh gene is located on the short arm of chromosome-1. In utero the Rh-antigens are well-developed by Day 38. Rh-isoimmunization is a major problem in developing countries like India. Rh-stimulus occurs late in the course of pregnancy mostly at the time of delivery. It should be kept in mind that 1-2% of Rh-negative mothers become sensitized to the Rh-antigen during pregnancy by what is known as ‘silent bleeds’. There are many causes of Rh-isoimmunization such as fetomaternal hemorrhage (FMH) during delivery, medical termination of pregnancy (MTP), abruption, placenta previa (PP), bleeding in first trimester, external cephalic version, etc. So, in the present day practice, utilization of antibody mediated immune-suppression in order to assure a more effective disappearance of Rh-disease, is needed and will require a timely antepartum and postpartum

*Assistant Professor **Professor and Head †Professor Dept. of Obstetrics and Gynecology ‡Assistant Professor, Dept. of Pediatrics GSVM Medical College, Kanpur Address for correspondence Dr Neetu Singh Assistant Professor, Dept. of Obstetrics and Gynecology GSVM Medical College, Kanpur E-mail: drneetusingh73@gmail.com

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

prophylaxis to reduce perinatal morbidity and mortality. The relationship between hemolytic disease of newborn (HDN) and Rh-sensitization was wellestablished by Levine et al, in 1941. An approach to prevention and eradication of this disease has been developed by techniques of preventing immunization in mothers. The development of real time ultrasound and Doppler not only helped us to understand fetal anatomy but also physiological states and dynamics of blood flow in fetal circulation. Intrauterine transfusions have become routine to treat fetal anemia. Several recent improvements like phototherapy, fiber-optic delivery system and intravenous immunoglobulin (IV-IG) have revolutionized the management of hemolytic disease of newborn. Anti-D prophylaxis has been a remarkable step to prevent Rhisoimmunization. Despite such progress in prevention, Rh-isoimmunization is still widespread. Cases of Rhisoimmunization still occur at increased rates in India and this urgently called for re-evaluation of the cases of anti-D prophylaxis. AIMS AND OBJECTIVES To evaluate the etiological determinates of Rhisoimmunization and to study the prevalence of perinatal mortality and morbidity in Rh-isoimmunization.


CLINICAL STUDY MATERIAL AND METHODS This retrospective study was carried out on 96 patients in the Dept. of Obstetrics and Gynecology, UISEMH, GSVM Medical College, Kanpur, from November 2007 to November 2010. All cases were thoroughly studied especially their history, examination, investigation, mode of delivery, passive immunization and their perinatal outcome. OBSERVATIONS During the 3-year study period, 7,920 deliveries occurred in UISE Maternal Hospital. Out of 7,920 deliveries, 560 patients were Rh-negative giving an incidence of 7%. Out of 560 Rh-negative women, 96 were isoimmunized patients according to their Coomb’s titer status. Of these 96 cases, 69 women (72%) were unbooked while 27 women (28%) were booked. Table 1 shows that majority of the women were between age group 26-30 years (64%). We found an increased rate of isoimmunization with increasing parity. Most of our patients (44%) were gravida 4.

It also shows the correlation of outcome of the babies with their respective gestational age. Our study showed that 90% of the preterm babies required treatment while only 27% of term babies required treatment showing that preterm babies are more susceptible. Table 2 shows the etiological determinants. In our study, we found that 84% of isoimmunized patients had a history of previous delivery in which there must have been a large FMH. Ten percent had a history of APH (abruption - 6%; PP - 4%). Table 3 shows that 58% were complicated deliveries and 22% had a history of cesarean. Twenty percent of patients who had a normal delivery also had FMH. Table 4 shows relation of isoimmunization with history of anti-D received. It was found that 80% did not receive anti-D while 20% received it. Rh-isoimmunization in 20% of those who received anti-D could be explained due to inadequate dosage. Table 5 shows the clinical outcome of Rh-positive babies; 45% had hyperbilirubinemia, 28% were anemic while kernicterus, hypoglycemia, hydrops and IUD were

Table 1. Demographic Profile of Rh-immunized Pregnancies Age in years

No. of cases/ (percentage) (n = 96)

Parity

No. of cases/ (percentage) (n = 96)

GA

Incidence of babies affected (n = 86)*

1 (1%)

G1

1 (1%)

< 34 weeks

24 (28%)

< 20 21-25

21 (22%)

G2

13 (14%)

34-37 weeks

20 (24%)

26-30

61 (64%)

G3

15 (16%)

37-40 weeks

37 (42%)

31-35

10 (10%)

G4

43 (44%)

>40 weeks

05 (06%)

36-40

2 (2%)

G5

18 (19%)

>40

1 (1%)

G6

6 (6%)

* Excluding IUD

Table 2. To Evaluate the Etiological Determinants of FMH Leading to Rh-isoimmunization

Table 3. Association of Mode of Delivery of Previous Pregnancy with FMH

Sensitizing events

Mode of Delivery

Bleeding in first trimester

Incidence (n = 81)

Percentage (%)

Normal

16

20

1

Forceps

10

12

8

10

No. of cases (n = 96)

Percentage (%)

1

MTP

4

3

Ventouse

Abortion

1

1

LSCS

18

22

Breech

15

19

IUD

14

17

Ectopic

Nil

Nil

H. mole

Nil

Nil

Abruption

5

6

PP with bleeding

4

4

Table 4. History of Anti-D Received

ECV

1

1

Received

20%

Delivery

81

84

Not received

80%

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CLINICAL STUDY Table 5. Clinical Outcome of Rh-positive Babies Clinical outcome

No. of cases

Percentage (%)

Hyperbilirubinemia

43

45

Anemia

27

28

Kernicterus

8

8

Hypoglycemia

6

7

Hydrops fetalis

2

2

IUD

10

10

Table 6. Perinatal Outcome in Rh-sensitized Pregnancy Perinatal outcome

No. of cases

Percentage (%)

NICU admission  Expired

11

12

Recovered

36

38

IUD

10

10

No treatment required

39

40

found in 8%, 7%, 2% and 10% cases, respectively. The major cause of perinatal morbidity was hyperbilirubinemia followed by anemia. As regards the perinatal outcome 40% required no treatment while 50% required treatment out of which 12% expired. Recovery was noted in 38% of cases (Table 6). DISCUSSION

to his study, 84% of patients had history of delivery while 16% cases were associated with antenatal FMH in our study. In one case, primigravida was noted to be isoimmunized. After a proper evaluation, she had no history of any FMH or any blood transfusion. This may be explained by silent FMH occurring throughout pregnancy. Frigoletto et al (1983) showed in his study that 1-2% of cases may have FMH known as ‘silent bleeds’. The majority of the cases had no history of anti-D after delivery (80%), it was found that 60% patients with previous history of complicated vaginal delivery and cesarean section had larger number of FMH leading to isoimmunization. This was supported by Mehta et al (1979) who showed that complicated or instrumental deliveries increase the risk of FMH to around 80%. Rh-isoimmunization causes significant perinatal mortality and morbidity. This was shown by Diamond et al (1932) and Levine et al (1941). The clinical outcome varied, out of which, the most common morbidity was hyperbilirubinemia followed by anemia. Our study reported a perinatal mortality of 22% (including IUD) and perinatal morbidity of 38%. Higher perinatal mortality in our study may be due to 72% of unbooked cases, which did not receive any antenatal care and were referred to our tertiary care center with antepartum and intrapartum complications. Our results for perinatal morbidity show that 40% required no treatment, 38% recovered after treatment while there were 22% deaths despite treatment due to severe disease. Our outcomes were comparable to Alvin et al (1995) who during their study noted that 51% required no treatment and 31% required treatment after term delivery. Ashma Madan et al (2004) also showed that 25% had severe disease, 20% had no apparent disease.

One would expect the incidence of Rh-isoimmunization to be low but this does not appear to be the case due to lack of anti-D prophylaxis and inadequate dosage of anti-D given after delivery. Therefore, the exact incidence is probably unknown due to failure to diagnose or under reporting as stated by Mandeep et al. The prevalence of Rh-isoimmunization in our study was 15% out of those who were Rh-negative.

CONCLUSION

According to Lau et al (1995) external cephalic version (ECV) caused FMH in 2-6% cases, though in our study only 1% had a history of ECV. Reddy et al (1999), reported incidence of FMH in first, second and third trimester as 6.7%, 13.9% and 29%, respectively which was similar in our study, which reported the incidence of 4.5%, 9.5% in first and second trimester. In our study, majority of the patients had a previous history of delivery; 84% of those who were isoimmunized.

Rh-isoimmunization is a persistent problem in developing countries. As the Rh-immunizing stimulus occurs late in pregnancy and most often at delivery, a successful program for Rh immunoprophylaxis with Rh-IgG, prevents not only fetal death but also sensitizing prospects. Early reference of affected patients from periphery to higher center, with early assessment and judicial interventions as well as intensive neonatal care are essential in ensuring satisfactory results.

Bowman et al (1998) found that the major cause FMH was at delivery 90% and antenatally 10%; in accordance

Future challenges such as spreading awareness of the need of antenatal prophylaxis, routine postpartum

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013


CLINICAL STUDY prophylaxis is to be emphasized. Advanced method for increasing safety of anti-D preparations, use of monoclonal Rh-D antibodies and newer future test for FMH will need future researches. SUGGESTED READING 1. Alvin: Avery’s textbook of neonatalogy. Isoimmune HD. Alvin Zipursky, John M, Bowman 1995:44-66. 2. Ashma Avery’s textbook of neonatalogy. 79. Neonatal Hyperbilirubinemia. 8th edition 2004:1231.

5. Frigoletto FD Jr (Ed.). Antepartum administration of Rh-immune globulin: a guide to office procedure. Ortho Diag Syst. Inc., New Jersey, 1983. 6. Lau TK, Stock A, Rogers M. Fetomaternal haemorrhage after external cephalic version at term. Aust N Z J Obstet Gynaecol 1995;35(2):173-4. 7. Levine P, Burnham L. The role of isoimmunization in the pathogenesis of erythroblastosis fetalis. Am J Obstet Gynecol 1941;42:825-7. 8. Mandeep et al FOGSI FOCUS. 2006;11

3. Bowman JM. The prevention of Rh-immunization. Transfus Med Rev 1988;2(3):129-50.

9. Mehta DM, Gupta SC, Bhatia HM. Transplacental haemorrhage and maternal isoimmunisation. J Post Grad Med 1979;25(2):75-80.

4. Diamond LK, Blackfan KD, Baty JM. Erythroblastosis fetalis and its association with universal edema of fetus, icterus gravis neonatorum and anemia of the newborn. J Pediatr 1932;1:269-309.

10. Reddy U, Witter F. Isoimmunization. In: Johns Hopkins Manual of Gynecology and Obstetrics. Lambrou N, Morse A, Wallach EE (Eds.), Lippincott Williams and Wilkins 1999:p106.

mmmmm

Epidemiology of Pandemic H1N1 Strains in a Tertiary Hospital of Maharashtra Swine-flu is a viral fever caused by a new mutated strain influenza A virus subtype H1N1, which infects humans. Pandemic H1N1 (pH1N1/2009) virus was detected in the first quarter of 2009 in the west coastal region of North America and spread very rapidly to the other countries during April-June, 2009. This study was conducted to assess the epidemiology of pandemic H1N1 strains using a cross-sectional study design in a tertiary hospital. The symptomatic patients attending the flu outpatient department (OPD)/emergency from August 2009 to April 2011 at Indira Gandhi

Government Medical College, Nagpur were included using a standard case definition. A total of 67 (27.01%) samples from 247 patients were pandemic influenza A/H1N1 positive. None of the patients had a history of foreign travel, whereas 23.88% of the patients gave history of travel to an endemic area. Overall, 22.38% of the patients came in contact with proven cases of pandemic H1N1. pH1N1 transmission activity has increased since May 2010. Source: Shrikhande S, Bhoyar SK, Tenpe SH, et al. Indian J Public Health 2012;56(3):242-4.

Novel Mutations Causing Hyperimmunoglobulin D and Periodic Fever Syndrome Hyperimmunoglobulin D and periodic fever syndrome (HIDS) is a rare, hereditary autoinflammatory condition characterized by recurrent inflammatory episodes. We report a 9-year-old boy, diagnosed with HIDS due to two novel mutations, c.62C>T (p.Ala21Val) and c.372-6T>C (probable splicing defect), in the mevalonate kinase (MVK) gene. The pathogenicity of these mutations was confirmed

by measurement of low MVK enzyme activity in cultured primary skin fibroblasts of the patient. The symptoms have been refractory to therapy with steroids and non steroidal anti-inflammatory drugs. This report expands the genetic and ethnic spectrum of HIDS. Source: Sinha A, Waterham HR, Sreedhar KV, et al. Indian Pediatr 2012;49(7):583-5.

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

19


CLINICAL STUDY

Serum IgE Levels and Absolute Eosinophil Count in Children with Bronchiolitis RUGMINI KAMALAMMAL*, PJ PARAMESWARI**

ABSTRACT Bronchiolitis is considered to be viral in origin but the possibility of allergic sensitization after an episode of bronchiolitis still exists. Allergic sensitization occurs here due to an imbalance between Th1 cytokine pathway and Th2 cytokine pathway leading to activation of Th2 cytokine. Total serum IgE is an indirect marker for activation of Th2 cytokine and absolute eosinophil count (AEC) is another marker for allergy. Study design: Serum IgE estimation and absolute eosinophil count was done in 30 infants admitted with bronchiolitis and were compared with serum IgE levels and absolute eosinophil counts in 15 controls. Statistical analysis: SPSS 15.0 was used for analysis and the observed findings were tested at 10% level of significance. Results: A significant increase in serum IgE level and an insignificant change in absolute eosinophil count was observed among children in the acute phase of bronchiolitis, compared to controls. Conclusion: Findings suggest that allergic sensitization as evidenced by increase in serum IgE levels occurs in children with bronchiolitis possibly through the activation of Th2 cytokine. Keywords: Bronchiolitis, allergic sensitization, serum IgE, absolute eosinophil count

B

ronchiolitis is an acute inflammatory disease of lower airway characterized by tissue necrosis with sloughing of the epithelium of the small airways, edema, increased mucus secretion and bronchospasm. The clinical hallmarks of bronchiolitis are hyperinflation, atelectasis and wheezing. It is a seasonal infection with peak incidence in the winter months and is considered to be due to respiratory syncytial virus (RSV) in 75% of cases. Around 70% of all infants will be infected with RSV in their first year of life.1

Bronchiolitis accounts for 30.8 hospitalizations/1,000 infants below one year of age for lower respiratory infections. The rate of intensive care admission related to RSV infections is 2.7% and the observed mortality is 0.2%.2 There is a relationship between the occurrence of bronchiolitis, allergic sensitization and the development of asthma later in life as suggested in a study by Sigurs.3 In this study, a multivariate analysis for risk factors for

*Assistant Professor Dept. of Pediatrics **Assistant Professor (Biostatistics) Dept. of Community Medicine Sree Balaji Medical College and Hospital, Chrompet, Chennai Address for correspondence Dr Rugmini Kamalammal D-97, Sunnyvale Apartments, 351, Konnur High Road Ayanavaram, Chennai - 23 E-mail: rugminirao@yahoo.com

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

these diseases showed RSV bronchiolitis had the highest independent risk ratio for asthma and a significantly elevated independent risk ratio for allergic sensitization and the study concluded that RSV bronchiolitis in infancy severe enough to cause hospitalization was highly associated with the development of asthma and allergic sensitization upto age 7. RSV influences the mechanisms involved in the development of asthma and allergy in children. For a normal infant at birth the inflammatory response is mediated by Th2 cells. This later on switches over to a response-mediated by Th1 cells as a result of stimulation by multiple viral infections early in life.4 Th1 cells secreteinterleukin (IL)-2, interferon-γ (IFN-γ).5 Th1 cell response provides protection against the development of wheezing through production of IFN-γ.4 Children having a genetic predisposition for Th2 responses are at risk for development of allergic sensitization and asthma. In these children, instead of the Th1 response, Th2 response is triggered during the first exposure to viral infections.4 Th2 cells secrete IL-4, -5, -6, and -10. IL-4, and IL-5 promote immunoglobulin E (IgE) production and eosinophilia. The Th2 cells have a predominant role in immediate type hypersensitivity, and produce IL-4, which switches IgE production.6 Thus, it can be hypothesized that significant increase in serum IgE in the acute phase of bronchiolitis may be an indirect marker of Th2 activation. The Th2 cytokine, IL-4 is one of the cytokines that may play a role in the pathogenesis of asthma and allergic sensitization.4


CLINICAL STUDY The gene for IL-4 is located in the Th2 cytokine cluster on human chromosome 5q31.1. IL-4 or nearby gene in 5-q31.1 regulates IgE production in a nonantigenspecific (noncognate) fashion. This chromosomal area is linked with total IgE concentration.5 IL-4 plays an important role in the stimulation and differentiation of Th2 cells. It promotes the proliferation and differentiation of activated B cells, which produces IgE.

answering the above question by estimating, whether there is an increase in total serum IgE levels in infants in acute phase of bronchiolitis, as IgE antibodies are indirect markers of Th2 cytokine pathway and IgE and absolute eosinophil counts (AEC) are simple indirect markers of type 1 hypersensitivity.

According to some studies Th2 cytokine responses were noted in children who developed RSV bronchiolitis,6,7 whereas in other studies, such a shift towards a Th2 response was not found.8 The possible skewing of the Th1/Th2 cytokine balance was investigated in this study by calculating IL-4/IFN-Îł ratios. IL-4/IFN-Îł ratios were normal in the acute and convalescent phase in both RSV infected and noninfected patient groups.

The study was a prospective clinical study in which 30 children below the age of one year admitted in our hospital for treatment of first episode of bronchiolitis were included. Fifteen normal children belonging to the same age group were taken as controls for the study.

One meta-analysis9 had quoted a study by Welliver et al,10 which concluded that the RSV IgE titer in nasopharyngeal secretions were predictive of the risk for developing wheezing from all causes later in life upto age four years. More frequent and severe wheezing has been correlated with elevated levels of specific IgE antibody. RSV IgE at time of bronchiolitis is useful indicator of recurrent wheezing. This is supported by studies in serum IgE by Sigurs.3 All these reports are contradicted by a few studies.11 Mean serum IgE levels did not show any difference in acute or convalescent phase of RSV infection.11 In a study, it was seen that peripheral blood eosinophil counts were suppressed in all infected infants > 2 months of age but eosinophil counts in patients with bronchiolitis were found to be significantly greater than in those with URI alone.12 In bronchiolitis, there will be recruitment of T cells and eosinophils and the release of histamine, kinins and other leukotrienes. In another study, eosinophilia at the time of bronchiolitis demonstrated a statistically significant relationship to the presence of wheezing at seven years of age13 suggesting an immunological remodeling happening during the time of bronchiolitis. Eosinophils and eosinophil activity during RSV LRTI have been studied in relation to the development of recurrent wheeze. Reijonen14 found that eosinophilic cationic protein (ECP) levels during bronchiolitis in nasopharyngeal secretions (NPS) and serum, respectively, were associated with recurrent wheezing in the first year of life. Thus, various studies done raise the question, whether the bronchiolitis triggers allergic sensitization by Th2 cytokine production or not. This study is focused on

MATERIAL AND METHODS

Diagnosis of acute bronchiolitis should be considered in an infant with nasal discharge and a wheezy cough, in the presence of fine aspiratory crackles and/or high pitched expiratory wheeze.2 Signs of respiratory infection taken into consideration were increase in respiratory rate, tachycardia, increased work of breathing, fine crackles and wheeze.2 Severity was assessed by SpO2 on admission, lowest O2 saturation and X-ray findings. Admission and management was decided by the emergency physician using the Respiratory Distress Assessment Instrument (RDAI) score.15 Children with moderate and severe bronchiolitis according to the score were admitted. Patients were excluded from the study for a variety of reasons including previous wheezing, previous history of any atopic diseases, regular use of bronchodilator or anti-inflammatory medications, any pre-existing lung disease, chronic lung disease of prematurity/bronchopulmonary dysplasia or cystic fibrosis; congenital anomalies of the chest, lung or heart. In addition to the routine complete blood count, these children underwent a total serum IgE estimation. Total serum IgE levels and absolute eosionophil count were estimated in all the 15 controls. Informed consent was taken before the said investigations from the parents or caregivers. Serum IgE was estimated using electrochemiluminescence method. Ethical committee clearance was obtained from Institutional Ethical Committee before starting the study. STATISTICAL ANALYSIS SPSS 15.0 was used for analyzing the information obtained from the 45 children. The findings are presented in Table 1 as descriptive frequency, range, median, mean, standard error of Mean along with the inferential statistics - Pearsons coefficient of

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

21


CLINICAL STUDY correlation and students t-test for independent groups. The observed findings were tested at 10% level of significance. Values within parentheses represent percentages. RESULTS In the present study, 23 female and 22 male children with age group ranging from 1 to 12 months with a mean age of 7.7 months were included. There was no significant difference in age group between the study population and the controls. Table 1 highlights the descriptive analysis for 30 cases and 15 controls. AEC was ranging from 0 to 854 with mean ± SE (mean) as 280.6 ± 40.0 for cases and 47.8 to 650 with 288.3 ± 38.9 for controls and an insignificant difference was observed statistically with t = 0.123 (p = 0.903). The statistically significant difference for serum IgE between mean ± SE (mean) as 149.1 ± 35.5 for cases and 49.4 ± 15.6 for controls with t = 1.927 and p = 0.061 is presented as Box plot in Figure 1. The Pearson coefficient of correlation between IgE and AEC was observed to be statistically insignificant negligible positive correlation with r = 0.278 and p = 0.137 for 30 cases.

and half months, a significant elevation in IgE antibodies for common food, and inhalant antigens were noted in RSV children than in children in the control group (p = 0.002). The meta-analysis, by Sigurs3 reveals that specific IgE titers were elevated in bronchiolitis and it is predictive of wheeze later in life. Even though all these studies are in accordance with our own results, it is prudent to note that there are some other studies, which showed no increase in serum IgE levels. In a study17 it was shown that serum IgE levels were normal in 90% of children at the time of bronchiolitis and in another study11 there were undetectable levels of IgE in both nasopharyngeal secretions and sera in children positive for respiratory syncytial virus infection. Study by Polmar et al,18 in which 30 infants with bronchiolitis were studied, also supports that there is no increase in serum IgE in cases with bronchiolitis, which occurred as an epidemic but he observed an increase in IgE in sporadic cases of bronchiolitis. Another study19 showed that total serum IgE levels were generally low, and values from wheezing and control subjects overlapped considerably in children <3 years of age. In the meta-analysis mentioned earlier by Sigurs9 there are two studies, which showed no increase in IgE levels in bronchiolitis.

DISCUSSION

1000

As explained earlier the aim of our study was to test the hypothesis that there occurs an imbalance in immune mechanism-mediated through cytokine production favoring increased production of IL-4, which in turn increases serum IgE in children with bronchiolitis. The study result agrees with this, as the study showed a significant increase in serum total IgE levels in children with bronchiolitis when compared to normal children of same age group. Significance at 10% level is acceptable for a clinical study. Our result concurred with the results of following studies.

*

800 600 IgE

30 23 26

400

4,537

200 0

Sigurs,16

In a study conducted by which included 47 infants who had experienced RSV bronchiolitis severe enough to cause hospitalization at a mean age of three

25

Case

Control

Figure 1. Significant difference for serum IgE.

Table 1. Descriptive and Inferential Statistics for Parameters Variables

Cases (n = 30)

Controls (n = 15)

T value

Range

Median

Mean ± SE (Mean)

Range

Median

Mean ± SE (Mean)

(p value)

AEC

0-854

232

280.6 ± 40.0

47.8-650

240

288.3 ± 38.9

0.123 (0.903)

IGE

10-876

66.4

149.1 ± 35.5

11-182

15

49.4 ± 15.6

1.927 (0.061)*

*Significant at 10% level

22

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013


CLINICAL STUDY Our study did not reveal any eosinophilia in accordance with studies quoted earlier,12,13 which showed eosinophils during bronchiolitis or infectioninduced changes in eosinophils were not associated with subsequent wheezing/asthma at any age during the follow-up. RSV bronchiolitis patients had lower eosinophils on admission than non-RSV cases, but the changes induced by RSV or other infections did not differ significantly. CONCLUSION This study shows that there is definite increase in IgE concentration in sera of children suffering from bronchiolitis especially in acute phase of the illness. The effect of the viral infection later on leading to allergic sensitization and asthma, attributed mainly to immune imbalance in Th2 cell pathway and cytokine IL-4 production is reinforced. It can be hypothesized that the virus, rather than causing damage to respiratory epithelium, causes immune imbalance, which acts as a mechanism of developing allergic sensitization. Limitation of the study is that total serum IgE level, which is only an indirect marker of Th2 cell-cytokine pathway was used as the predictive outcome, it will be useful if IL-4 level is used as marker in further studies. Further studies with specific IgE antibodies for food and inhalant allergens and also long-term followup of same cohort is indicated. Eosinophil count in nasopharyngeal secretions would have been a better option and further studies in nasopharyngeal secretions are strongly advocated. REFERENCES 1. Bronchiolitis in children - a national clinical guideline. Nov 2006 1.1 Scottish Intercollegiate Guidelines Network. ISBN 1 (10) 905813 01 5, ISBN (13) 978 1 2. Deshpande SA, Northern V. The clinical and health economic burden of respiratory syncytial virus disease among children under 2 years of age in a defined geographical area. Arch Dis Child 2003;88(12):1065-9. 3. Sigurs N, Bjarnason R, Sigurbergsson F, Kjellman B. Respiratory syncytial virus bronchiolitis in infancy is an important risk factor for asthma and allergy at age 7. Am J Respir Crit Care Med 2000;161(5):1501-7.

6. Román M, Calhoun WJ, Hinton KL, Avendaño LF, Simon V, Escobar AM, et al. Respiratory syncytial virus infection in infants is associated with predominant Th-2-like response. Am J Respir Crit Care Med 1997;156(1):190-5. 7. Bendelja K, Gagro A, Bace A, Lokar-Kolbas R, KrsulovicHresic V, Drazenovic V,et al. Predominant type-2 response in infants with respiratory syncytial virus (RSV) infection demonstrated by cytokine flow cytometry. Clin Exp Immunol 2000;121(2):332-8. 8. Bont L, Heijnen CJ, Kavelaars A, van Aalderen WM, Brus F, Draaisma JT, et al. Peripheral blood cytokine responses and disease severity in respiratory syncytial virus bronchiolitis. Eur Respir J 1999;14(1):144-9. 9. Sigurs N. Clinical perspectives on the association between respiratory syncytial virus and reactive airway disease. Respir Res 2002;3 Suppl 1:S8-14. 10. Welliver RC, Sun M, Rinaldo D, Ogra PL. Predictive value of respiratory syncytial virus-specific IgE responses for recurrent wheezing following bronchiolitis. J Pediatr 1986;109(5):776-80. 11. Toms GL, Quinn R, Robinson JW. Undetectable IgE responses after respiratory syncytial virus infection. Arch Dis Child 1996;74(2):126-30. 12. Garofalo R, Dorris A, Ahlstedt S, Welliver RC. Peripheral blood eosinophil counts and eosinophil cationic protein content of respiratory secretions in bronchiolitis: relationship to severity of disease. Pediatr Allergy Immunol 1994;5(2):111-7. 13. Ehlenfield DR, Cameron K, Welliver RC. Eosinophilia at the time of respiratory syncytial virus bronchiolitis predicts childhood reactive airway disease. Pediatrics 2000;105(1 Pt 1):79-83. 14. Reijonen TM, Korppi M, Kuikka L, Savolainen K, Kleemola M, Mononen I, et al. Serum eosinophil cationic protein as a predictor of wheezing after bronchiolitis. Pediatr Pulmonol 1997;23(6):397-403. 15. Lowell DI, Lister G, Von Koss H, McCarthy P. Wheezing in infants: the response to epinephrine. Pediatrics 1987;79(6):939-45. 16. Sigurs N, Bjarnason R, Sigurbergsson F, Kjellman B, Björkstén B. Asthma and immunoglobulin E antibodies after respiratory syncytial virus bronchiolitis: a prospective cohort study with matched controls. Pediatrics 1995;95(4):500-5. 17. Renzi PM, Turgeon JP, Marcotte JE, Drblik SP, Bérubé D, Gagnon MF, et al. Reduced interferon-gamma production in infants with bronchiolitis and asthma. Am J Respir Crit Care Med 1999;159(5 Pt 1):1417-22.

4. Hall CB. Respiratory syncytial virus and parainfluenza virus. N Engl J Med 2001;344(25):1917-28.

18. Polmar SH, Robinson Immunoglobulin E in 1972;50(2):279-84.

LD Jr, Minnefor AB. bronchiolitis. Pediatrics

5. Marsh DG, Neely JD, Breazeale DR, Ghosh B, Freidhoff LR, Ehrlich-Kautzky E, et al. Linkage analysis of IL4 and other chromosome 5q31.1 markers and total serum immunoglobulin E concentrations. Science 1994;264(5162):1152-60.

19. Heymann PW, Carper HT, Murphy DD, Platts-Mills TA, Patrie J, McLaughlin AP, et al. Viral infections in relation to age, atopy, and season of admission among children hospitalized for wheezing. J Allergy Clin Immunol 2004;114(2):239-47.

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

23


CLINICAL STUDY

Impact of Overweight/Obesity on Emotional Health of Adolescents: A Cross-sectional Study SHWETA PATHAK*, ANJOO BHATNAGAR*, SANJEEV DUTTA*, BINDU DHINGRA**

ABSTRACT Objective: To study the impact of obesity on emotional health of obese/overweight children. Design: Cross-sectional study. Setting: Randomly selected public and private sector schools. Participants: School-going children aged 12-17 years. Main outcome measures: Rate of depression and low self-esteem derived from Center for Epidemiologic Studies Depression (CES-D) and Rosenberg scale, respectively. Secondary outcome measure was prevalence of obesity and overweight-based on body mass index (BMI) categories. Results: The prevalence rate of obesity was found to be 7.33% and 10.17% for overweight among adolescents in 12-17 years age group. The prevalence of obesity and overweight was higher among 15-17 years adolescents at 8% and 11.11%, respectively; in comparison to 6.81% and 9.42% among 12-14 years adolescents indicating increasing rate of obesity and overweight with growing age among adolescents. Similarly, male population had higher observed prevalence rate of obesity and overweight at 10.91% and 8.10%; in comparison to 9.09% and 6.22% in female population, respectively. The observed rate of depression was higher amongst obese females in 12-14 years age group at 8.3% versus 7.3% in normal females (p = 0.019). However, this difference in depression rate was not significant among male population in the 12-14 years age group (7.4% in obese vs 6.7% in normal [p = 0.053]). Similar observation was there for 15-17 years age group, with obese females having significantly higher depression rate than normal females (7.1% vs 6.8% [p = 0.002]). Males in 15-17 years age groups didn’t exhibit significant difference in depression rate in relation to obesity and overweight. The observed rate of low self-esteem was significantly higher amongst abnormal BMI (obese and overweight) group in comparison to normal population across all age groups. In 15-17 years, it was 9.1% versus 8.1% (p = 0.037), whereas in 12-14 years it was 6.5% versus 5.7% (p = 0.028). Among males, the significant difference in the low self-esteem rate among normal versus abnormal BMI population was only observed in 15-17 years group at 7.5% versus 7.4% (p = 0.002). Conclusion: The prevalence rate of overweight and obesity is higher among males. It was also found that with increasing age, the percent of children with overweight and obesity also increase in both the sexes. Higher BMI has a direct correlation with depression among females and leads to lower self-esteem among adolescent both male and female. Keywords: Adolescent, obesity, emotional health, depression, self-esteem

T

oday, approximately one-fifth of the world’s population is of adolescents (10-19 years of age). More than four-fifth of these are in developing countries. Adolescence is a period of transition between childhood and adulthood. It occupies a critical position in the life of human beings, which prepares a child for adulthood. There is an all round rapid phase of emotional, intellectual and sexual development during this period. The National Health and Nutrition Examination Surveys (NHANES Cycles I, II and III) have been surveying the prevalence of obesity in American children and youth since 1971. The 1988-91

NHANES Cycle III study identified 21% of adolescents 12-19 years of age as being overweight (using, BMI or body mass index as criteria)-up from 15% in the 1966-80 NHANES II study.1 In India, several studies to identify the prevalence of obesity in adolescents have been conducted. These studies reveal that the prevalence of overweight in affluent adolescents varies from 22% to 31% in Indian urban areas.2,3 The need for present study was realized as the burden of obesity is increasing. Though, the prevalence of obesity is known, little is known about its effect on emotional health of adolescents in our country. METHODS

*Dept. of Pediatrics and Neonatology **Child Psychology Fortis Escorts and Research Centre, Faridabad, Haryana Address for correspondence Dr Shweta Pathak, Dept. of Pediatrics and Neonatology Fortis Escorts and Research Centre, Faridabad, Haryana E-mail: dr.shwetapgupta@gmail.com

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

This was a cross-sectional study using a pre-tested questionnaire (Center for Epidemiologic Studies Depression (CES-D) scale and Rosenberg self-esteem scale) for assessing the emotional health of adolescents aged 12-17 years. The schools in which the study


CLINICAL STUDY was conducted were randomly selected amongst the private and public schools in the district of Faridabad (Haryana). The study was conducted from February 2008 to March 2010. The clearance was obtained from the Institute’s Ethical Committee. Proforma along with the questionnaires were distributed to the children, weight and height were recorded, after a week the proforma and the questionnaire were collected. ÂÂ

ÂÂ

ÂÂ

Anthropometric measures: All the students were weighed without shoes and heavy clothing, using a electronic weighing scale with an error of 100 g. The weighing scale was regularly checked with known standard weights. A portable anthropometric rod was used for measuring height, with an error to the nearest of 0.1 cm, using standard procedures. The World Health Organization reference charts were used to define overweight and obesity in this study. WHO guidelines for obese (BMI) ≥95th percentile for the age and sex) and overweight (BMI ≥ 85th percentile and BMI < 95th percentile for the age and sex) were used. Sample size: The sample size of 1,023 adolescents was achieved after applying the inclusion and exclusion criteria on the targeted population. Sample size was determined according to Hopkins formula, N = 32/ES2, where ES is the smallest effect size worth detecting (smallest difference worth noticing divided by standard deviation, expressed in the same units). With type 1 error of 0.05 and type 2 error of 0.2, the sample size was calculated as 1,000. Exclusion criteria: Children submitting invalid questionnaire were excluded from the study (for example-unanswered questions, more than one answer to same question, etc.)

Statistical Analysis The data was analyzed using SPSS version 12.5. The frequency distribution technique was used to analyze the prevalence of obesity, low self-esteem and depression. Pearson’s Chi-square test was used to assess the statistical difference in the evaluated parameters across different demographic groups. RESULT The observations in this study are based on survey done on 1,052 adolescents studying in Standards VII to XII across various schools in Faridabad, during the study period of 20 months (February 2008 to September 2009). Of these 1,052 adolescents, 29 were excluded from the study due to invalid answers given by them in the survey (Fig. 1). Among the sample population of 1,023 adolescents, the indication of obesity and overweight (based on BMI) was found in 75 adolescents and 104 adolescents, respectively. This results in the prevalence rate of 7.33% for obesity and 10.17% for overweight. The prevalence of obesity and overweight was higher among

4 schools randomly selected for study (2 private and 2 public) Estimated sample size - 1,000 using Hopkins formula Survey participants - 1,052 adolescents (12-17 yrs) Total exclusion - 29 reason (s): Invalid responses - 29 1,023 eligible participants

Data Collection The data was collected by conducting a survey amongst adolescents aged 12-17 years studying in the randomly selected private and public schools. A pre-designed proforma and pre-tested questionnaires (CES-D and Rosenberg self-esteem scale) were distributed to the subjects. The completed questionnaires were collected and the information was validated to reject any incomplete or invalid questionnaires. The data was compiled using Microsoft Excel 2007 and was imported to SPSS version 12.5 for further detailed data analysis.

15-17 years 450 participants

12-14 years 573 participants

Males 349 participants

Females 224 participants

Males 256 participants

Females 194 participants

Figure 1. Study flowchart.

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

25


CLINICAL STUDY

PROFORMA Personal Details Name: _________________________________________________________________________________ Age: ________________ Years: _________________

Sex: M

F

Class:______________ School: __________________Contact Number : _____________________________ Contact Address:__________________________________________________________________________ Anthropometry Weight: __________________ Kgs

Height:__________________cm

BMI: _____________________

Birth Details (To be filled by Parents) Birth Weight: ____________________Kgs

Term/Preterm:______________________________

Medical History On any Medication: Y __ N __ . If Yes then Specify, _____________________________________________ Any Established Endocrine Disorder: __________________________________________________________ Center for Epidemiologic Studies Depression Scale (CES-D) Week Rarely or none of the time (< 1 day)

1. I was bothered by things that usually don’t bother me. 2. I did not feel like eating; my appetite was poor. 3. I left that I could not shake off the blues even with help from my family or friends. 4. I felt I was just as good as other people. 5. I had trouble keeping my mind on what I was doing. 6. I felt depressed. 7. I felt that everything I did was an effort. 8. I felt hopeful about the future. 9. I thought my life had been a failure. 10. I felt fearful. 11. My sleep was restless. 12. I was happy 13. I talked less than usual. 14. I felt lonely. 15. People were unfriendly. 16. I enjoyed life. 17. I had crying spells. 18. I felt sad. 19. I felt that people dislike me. 20. I could not get ‘going’.

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

Some or a little of the time (1-2 days)

During the Past Occasionally or a moderate amount of time (3-4 days)

Most or all of the time (5-7 days)


CLINICAL STUDY Scoring Scoring for all except Questions 4, 8, 12 and 16

Scoring for Questions 4, 8, 12 and 16

Options

Options

Points

Interpretation of Scores

Points

Score ranges

Interpretation

Rarely or none of the time (<1 day)

0

Rarely or none of the time (<1 day)

3

<15

No depression

Some or little of the time (1-2 days)

1

Some or little of the time (1-2 days)

2

15-21

Occasionally or moderate amount of time (3-4 days)

2

Occasionally or moderate amount of time (3-4 days)

1

>21

Most or all of the time (5-7 days)

3

Most or all of the time (5-7 days)

0

Mild to moderate depression Possibility of major depression

Rosenberg’s Self-Esteem Scale The Rosenberg’s Self-Esteem Scale17 is a 10 item Likert scale with items answered on a 4 point scale - from strongly agrees to strongly disagree. The original sample for which the scale was developed consisted of 5,024 High School Juniors and Seniors from 10 randomly selected schools in New York State 1. On the whole, I am satisfied with myself.

SA

A

D

SD

2.* At times, I think I am no good at all.

SA

A

D

SD

3. I feel that I have a number of good qualities

SA

A

D

SD

4. I am table to do things as well as most other people.

SA

A

D

SD

5. I feel I do not have much to be proud of.

SA

A

D

SD

6.* I certainly feel useless at times.

SA

A

D

SD

7. I feel that I am a person of worth, at least on an equal plane with others.

SA

A

D

SD

8.* I wish I could have more respect for myself.

SA

A

D

SD

9.* All in all, I am inclined to feel that I am a failure.

SA

A

D

SD

10. I take a positive attitude toward myself.

SA

A

D

SD

Scoring Scoring for Questions 1, 3, 4, 7 and 10

Scoring for Questions 2, 5, 6, 8 and 9

Options

Options

Points

Points

Interpretation of Scores Score ranges

Interpretation

SA (Strongly Agree)

3

SA (Strongly Agree)

0

<15

Low self-esteem

A (Agree)

2

A (Agree)

1

≥ 15

Normal self-esteem

D (Disagree)

1

D (Disagree)

2

SD (Strongly Disagree)

0

SD (Strongly Disagree)

3

15-17 years adolescents at 8% and 11.11%, respectively, in comparison to 6.81% and 9.42% among 12-14 years (Fig. 2). In our study, depression was found to be higher in females as compared to males, which were placed at 7.2 and 6.4%, respectively across both the age groups (Table 1). For the adolescents in the age group 12-14 years statistically significant difference in the depression rate between normal BMI and obese population was found

among females (p = 0.019), but not among the male population (p = 0.053). The results of the Chi-square test for the adolescents in the age group 15-17 years showed statistically significant difference in the depression rate between normal BMI and obese population among females (p = 0.002) but not significant among the male population (p = 0.176). The data obtained from the present study demonstrate a significant relationship between obesity and changes

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

27


CLINICAL STUDY in self-esteem during early adolescence. In our study, the prevalence of low self-esteem among overweight and obese subjects was respectively 6.73 and 10.67 %, as compared to a rate of 7.11% in the general population (Table 2). Among the 12-14 years old group overweight and obese females had significantly low self-esteem as compared to male children of the same age group (p value 0.028). The results were different in 15-17 years old aged children, the overall prevalence of low self-esteem was 9.1 and 7.5% in females and males,

Overall

12-14 yrs 20%

40%

60%

80%

100%

12-14 yrs

15-17 yrs

Overall

Normal

83.77%

88.89%

82.50%

Overweight

9.42%

11.11%

10.17%

Obese

6.81%

8.00%

7.33%

DISCUSSION To our knowledge, this is the first comprehensive study in the Indian subcontinent attempting to document the prevalence of overweight and obesity, and emotional health of adolescents that covered an adequate sample of urban adolescents. In our study, we considered two outcomes, depression and self-esteem, as measures of emotional health of obese adolescents. So, the data were stratified into two groups 12-14 years (mid adolescent) and 15-17 years old (late adolescent) to know the trends in these groups. It was found that the prevalence of obesity and overweight was higher among 15-17 years in comparison to 12-14 years adolescents, indicating an increase in rate of obesity and overweight with growing age among adolescents. This can be explained by the fact that once the vicious cycle (excessive TV watching, sedentary

15-17 yrs

0%

respectively. In this group, obese and overweight children had statistically significant decrease in selfesteem both in males (p value 0.002) and females (p value 0.037).

Figure 2. Prevalence of obesity and overweight by age.

Table 1. Results of Statistical Test to Assess Difference between Observed Rate of Depression Across BMI Groups Female Normal

With depression

179

14

92.75%

7.25%

Male P value (Pearson Chisquare test)

Normal

With depression

249

18

93.26%

6.74%

P value (Pearson Chisquare test)

12-14 years Normal

Count % within BMI category

Overweight

Count % within BMI category

Obese

Count % within BMI category

Obese/

Count

Overweight

% within BMI category

18

1

94.74%

5.26%

11

1

91.67%

8.33%

29

2

93.55%

6.45%

148

13

91.93%

8.071%

NA 0.104 0.019 0.026

33

2

94.29%

5.71%

25

2

92.59%

7.41%

58

4

93.55%

6.45%

189

14

93.10%

6.90%

NA 0.017 0.053 0.003

15-17 years Normal

Count % within BMI category

Overweight

Count % within BMI category

Obese

Count % within BMI category

Obese/

Count

Overweight

% within BMI category

28

18

1

94.74%

5.26%

12

2

85.71%

14.29%

30

3

90.91%

9.09%

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

NA 0.346 0.002 0.209

29

2

93.55%

6.45%

21

1

95.45%

4.55%

50

3

94.34%

5.66%

NA 0.008 0.176 0.104


CLINICAL STUDY Table 2. Results of Statistical Test to Assess Difference between Observed Rate of Low Self-esteem Across BMI Groups Female Male Normal

With depression

P value (Pearson Chisquare test)

Normal

With depression

P value (Pearson Chisquare test)

12-14 years Normal

Count % within BMI category

Overweight

Count % within BMI category

Obese

Count % within BMI category

Obese/

Count

Overweight

% within BMI category

182

11

94.30%

5.70%

18

1`

94.74%

5.26%

11

1

91.67%

8.33%

29

2

93.55

6.45%

148

13

91.33%

8.07%

18

1

94.74%

5.26%

12

2

85.71%

14.29%

NA 0.006 0.142 0.028

266

21

92.68%

7.32%

32

3

91.43%

8.57%

24

3

88.89%

11.11%

56

6

92.32%

9.68%

188

15

92.61%

7.39%

29

2

93.55%

6.45%

20

2

90.91%

9.09%

NA 0.071 0.503 0.398

15-17 years Normal

Count % within BMI category

Overweight

Count % within BMI category

Obese

Count % within BMI category

Obese/

Count

Overweight

% within BMI category

30

3

90.91%

9.09%

lifestyle and food faddism) sets in, it is increasingly difficult to get out of it. Eighty percent of overweight adolescents become overweight adults.4 Boys were found to have higher prevalence of overweight and obesity than girls across both the subgroups. In India, this could be attributed to gender bias and child rearing practices with preferential treatment being given to the male child, especially prevalent in northern part of India. Previous research has attempted to assess the impact of overweight on children’s physical and psychosocial outcomes. Traditionally, these studies examined one outcome (e.g. self-esteem, glucose intolerance) in isolation from others.5-12 Previous research on the relationship between childhood overweight and psychosocial outcomes has been inconsistent, finding either no association or a small inverse relationship. The association between overweight and physical health has been much more consistent. Overweight has been linked to multiple physical health problems in children and adolescents, including glucose intolerance and risk factors for cardiovascular disease as have been documented by Erickson et al in his study.13 In our study, depression was found to be higher in females

NA 0.187 0.634 0.037

49

4

92.45%

7.55%

NA 0.035 0.082 0.002

as compared to males across both the age groups. These results imply that obese females are more likely to be depressed than their male counterparts irrespective of period of adolescence. The stigma related to obesity is thought to be higher in females, because of cultural expectations of thinness in females.14-15 Epidemiological research shows a recent increase in the incidence of anorexia nervosa over the last two decades. These changes are interpreted in the light of recent changes in the concept of female beauty with an increased emphasis on thinness. Dieting and weight control measures have become common pre-occupations, evidenced by the number of lowcalorie diet foods, in the market and proliferation of commercial establishments for losing weight and many articles and advertisements on dieting and slimming in women’s magazines and the media. Obsession with thinness not only prevails in western world, but also exists in the developing world.16 The data obtained from the present study demonstrate a significant relationship between obesity and changes in self-esteem during early adolescence. In our study, the prevalence of low self-esteem among overweight

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CLINICAL STUDY and obese subjects was found to be higher as compared to that in the general population. As negative weight perceptions are fairly common amongst females so, it is not surprising that adolescent females have a higher percentage of low self-esteem. Nevertheless, negative perceptions of obesity also exist among adolescent boys.17-21 Low self-esteem in adolescents has been associated with a number of risk and protective factors in previous studies, but results have been mixed. Recent study done in New Hampshire, USA, published in Acad Pediatric in July 2010, examined the characteristics associated with low self-esteem in a large national sample of young adolescents.17 They found that female gender Hispanic race, overweight and obesity, sensation seeking rebelliousness and daily TV time were each associated with lower self-esteem. Teens of black race, with higher parental responsiveness and, better school performance or involvement in team sports were less likely to report low self-esteem. Low self-esteem has been associated with a lot of modifiable risk factors including obesity, TV time, team sports participation, school performance and parenting styles that should be discussed with teens and parents at health supervision visits. Further research examining race and gender specific factors that serve-to-moderate risk for poor self-esteem in adolescents is warranted. There is no data available in India to define the magnitude of poor emotional health associated with overweight and obesity and related factors. Research needs to be carried out in this field to know the burden of disease and various factors affecting it. REFERENCES 1. Centers for Disease Control and Prevention (CDC). Prevalence of overweight among adolescents-United States, 1988-91. MMWR Morb Mortal Wkly Rep 1994;43(44):818-21. 2. Ramachandran A, Snehalatha C, Vinitha R, Thayyil M, Kumar CK, Sheeba L, et al. Prevalence of overweight in urban Indian adolescent school children. Diabetes Res Clin Pract 2002;57(3):185-90. 3. Bhave S, Bavdekar A, Otiv M; IAP National Task Force for Childhood Prevention of Adult Diseases: Childhood

Obesity. IAP National Task Force for Childhood Prevention of Adult Diseases: Childhood Obesity. Indian Pediatr 2004;41(6):559-75. 4. Dietz WH. Overweight in childhood and adolescence. N Engl J Med 2004;350(9):855-7. 5. Strauss RS. Childhood obesity and self-esteem. J Pediatr 2000;105(1):e15. 6. Kaplan KM, Wadden TA. Childhood obesity and selfesteem. J Pediatr 1986;109(2):367-70. 7. French SA, Story M, Perry CL. Self-esteem and obesity in children and adolescents: a literature review. Obes Res 1995;3(5):479-90. 8. Dietz WH. Health consequences of obesity in youth: childhood predictors of adult disease. Pediatrics 1998;101(3 Pt 2):518-25. 9. Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K, et al. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med 2002;346(11):802-10. 10. Trent ME, Ludwig DS. Adolescent obesity, a need for greater awareness and improved treatment. Curr Opin Pediatr 1999;11(4):297-302. 11. Barlow SE, Dietz WH. Obesity Evaluation and Treatment: Expert Committee Recommendations. Pediatrics 1998;102(3):e29. 12. Garner DM, Garfinkel PE, Schwartz D, Thompson M. Cultural expectations of thinness in women. Psychol Rep 1980;47(2):483-91. 13. Brownell KD. Dieting and the search for the perfect body: Where physiology and culture collide. Behav Ther 1991;22(1):1-12. 14. Freedman DS, Dietz WH, Srinivasan SR, Berenson GS. The relation of overweight to cardiovascular risk factors among children and adolescents: the Bogalusa Heart Study. Pediatrics 1999;103(6 Pt 1):1175-82. 15. Erickson SJ, Robinson TN, Haydel KF, Killen JD. Are overweight children unhappy?: Body mass index, depressive symptoms, and overweight concerns in elementary school children. Arch Pediatr Adolesc Med 2000;154(9):931-5. 16. McCarthy M. The thin ideal, depression and eating disorders in women. Behav Res Ther 1990;28(3):205-15. 17. McClure AC, Tanski SE, Kingsbury J, Gerrard M, Sargent JD. Characteristics associated with low selfesteem among US adolescents. Acad Pediatr 2010;10(4):238-44.e2.

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013


PHOTO QUIZ

Rash and Fever in an Ιll-Appearing Child

A

seven-year-old girl with a three-day history of fever as high as 40°C (103°F) came to an urgent care clinic located in the Central Valley area of California. Twelve hours after the onset of fever, she started to have flank and abdominal pain. She had no complaints of cold or influenza symptoms; no cough; and no diarrhea, nausea, or vomiting. Her parents reported no known drug allergies. Her fever was reduced by acetaminophen. Her only antibiotic exposure was amoxicillin as an infant. She had no recent travel history and no pets at home. The urgent care physician started her on trimethoprim-sulfamethoxazole for possible urinary tract infection.

Approximately 12 hours after receiving her first antibiotic dose, she started to have red spots on her trunk and extremities. These spots later became confluent, with some central clearing and a purple hue (Figures 1 and 2). Ulcerations appeared on her lips, but she was still able to eat and drink. Her parents brought her back to the urgent care clinic. On repeat evaluation, she was ill-appearing but was in no respiratory distress. Her white blood cell count was 7,700 per mm3 (7.7 × 109 per L), with a differential that showed 80 percent polymorphonucleocytes (with no bands), 12 percent lymphocytes, 8 percent monocytes, and no eosinophils. Serum chemistries and urinalysis were normal. Clinical chest examination was normal, but a chest radiograph demonstrated right lower lobe pneumonitis (Figure 3).

Figure 1.

QUESTION Based on the patient’s history and physical examination, which one of the following is the correct diagnosis? A. Kawasaki disease. B. Bacterial pneumonia with allergy to sulfa medication. C. Valley fever (coccidioidomycosis). D. Rocky Mountain spotted fever. E. Measles. Source: Adapted from Am Fam Physician. 2004;70(2):361-363.

Figure 2.

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PHOTO QUIZ The fever, rash, and mucosal changes in this patient could be consistent with Kawasaki disease. However, this disease typically occurs in children younger than five years, is more common in boys, and does not include pneumonitis as a typical finding. The criteria for Kawasaki disease include fever lasting more than five days (often as high as 40 to 41°C [104 to 105°F], with poor response to antipyretics) and four of the five following clinical findings: conjunctivitis, oropharyngeal changes (e.g., fissured lips, injection, strawberry tongue), peripheral extremity changes (e.g., edema, desquamation, erythema), exanthem, and cervical lymphadenopathy.3,4

Figure 3.

DISCUSSION The answer is C: Valley fever. Coccidioidomycosis is endemic to dry, arid areas of the Western Hemisphere, including the southwestern United States. It is particularly common in the Central Valley of California where this patient lived. Only 40 percent of persons who are infected become symptomatic. Of these, most have a self-limited infection. Pregnant women and immunocompromised patients (e.g., those with human immunodeficiency virus infection) are at increased risk for disseminated infection. If the infection is symptomatic, it often presents with chest pain, cough, and fever. Several different types of immune-mediated rashes may occur, including erythroderma, macular exanthem, erythema multiforme (as in this patient), or erythema nodosum. Arthralgias also can occur with primary infection. Disseminated disease, which occurs in about 1 percent of patients, can affect the skin (e.g., granulomas, abscesses, pustules), joints, or the central nervous system. Serologic testing for IgM antibody is positive in most, but not all, cases within one to three weeks of symptom onset. If initial antibody testing is negative, but clinical suspicion of coccidioidomycosis is high, repeat testing is indicated because it may take a month or more to develop measurable antibody titers. Cases that are not self limiting are treated with antifungals, and occasionally surgery is necessary for persistent focal lesions.1,2

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

Multiple medications, including those containing sulfa, can cause erythema multiforme. Erythema multiforme can be divided into minor and major types. The major type also is known as a StevensJohnson reaction, which is associated with a greater number and severity of skin lesions and affects the mucous membranes. When a medication causes erythema multiforme, it usually occurs two to three weeks after exposure,3 not hours after the first dose, as occurred in this case. An allergic reaction could have happened within this 12 hour timeframe, but it would have caused hives or a morbilliform rash, sometimes with associated wheezing or even circulatory collapse from anaphylaxis. Table 1. Selected Differential Diagnosis of Rash and Fever in an Ιll Child Condition

Characteristics

Kawasaki disease

Fever lasting longer than five days, conjunctivitis, mucosal changes, edema, desquamation, and cervical lymphadenopathy

Bacterial pneumonia with allergy to sulfa medication

Systemically ill, raised plaque-like hives in response to allergy to antibiotic, subacute rash may be morbilliform

Valley fever (coccidioidomycosis)

Endemic to Southwest United States, influenza-like illness, pneumonitis, several types of rash possible, another great imitator

Rocky Mountain spotted fever

Fever, malaise, headache, thrombocytopenia, hyponatremia, and petechial rash

Measles

Cold-like symptoms, Koplik spots (white spots with red halo) on buccal mucosa, then rash starts on head, quickly spreads, confluent, all areas maximal intensity simultaneously


PHOTO QUIZ Rocky Mountain spotted fever has been diagnosed all across the United States, but the highest incidence occurs in a band from Oklahoma to North Carolina. It is caused by infection with Rickettsia rickettsii, an intracellular bacterium transmitted by ticks that are found on wild animals and domestic dogs. Infection in humans can occur at any age, but more serious sequelae may develop in young children. The prodrome starts with fever, malaise, and severe headache. Blanching macules or papules on the extremities (especially palms and soles) appear two to three days later, which may then progress to palpable purpura or necrotic ecchymoses. Associated laboratory findings may include thrombocytopenia, hyponatremia, and liver function test abnormalities. Rocky Mountain spotted fever is fatal in 2 to 7 percent of cases, primarily because of the delay in diagnosis and initiation of treatment with doxycycline.3–5 Measles begins with a typical viral prodrome, followed by prominent cough, coryza, and conjunctivitis, which

did not occur in this patient. The maculopapular rash that occurs with measles begins at the face, then spreads to the trunk and extremities, and may become confluent. Children who lack proper immunization are at risk of measles. REFERENCES 1. Deresinski SC. Coccidioides immitis. In: Gorbach SL, Bartlett JG, Blacklow NR, eds. Infectious diseases. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2004:2227-45. 2. Goldman M, Johnson PC, Sarosi GA. Fungal pneumonias. The endemic mycoses. Clin Chest Med. 1999;20:507-19. 3. Gable EK, Liu G, Morrell DS. Pediatric exanthems. Prim Care. 2000;27:353-69. 4. McKinnon HD Jr, Howard T. Evaluating the febrile patient with a rash [published correction appears in Am Fam Physician 2001;64:220]. Am Fam Physician. 2000;62: 804-16. 5. Dumler JS. Rocky Mountain spotted fever. In: Gorbach SL, Bartlett JG, Blacklow NR, eds. Infectious diseases. 3d ed. Philadelphia: Lippincott Williams & Wilkins, 2004:1473-80.

mmmmm

Intraventricular Chordoid Meningioma in a Child: Fever of Unknown Origin, Clinical Course and Response to Treatment The authors present the case of an 11-year-old boy with an intraventricular chordoid meningioma, which is a rare presentation of prolonged fever of unknown origin due to a rare tumor in a rare location. The fever resolved after excision of the lesion. Subsequent imaging revealed recurrence at one year. After a repeat excision and fractionated radiotherapy, the patient has remained disease free five years after the first surgery. Very few cases of intraventricular chordoid meningioma have been reported to date. The pathological features and clinical course are described. A review of the literature describing management options for this tumor type, recently found to have a higher recurrence rate, is described herein. Source: Nambiar A, Pillai A, Parmar C, et al. J Neurosurg Pediatr 2012;10(6):478-81.

Validation of A New Serology-based Dipstick Test for Rapid Diagnosis of Typhoid Fever Currently, no reliable diagnostic test is available for typhoid fever. One serology-based dipstick test, developed indigenously, was validated in this study. Preserved sera from 336 fever patients with known culture results for Salmonella typhi were blindly tested by the Widal test and the new assay. Analytical sensitivities, specificities, and efficiencies for the new assay versus the Widal test were 68.8% versus 62.5%, 71.1% versus 37.1% and 70.5% versus 43.2%, respectively (p < 0.001), considering S. typhi-positive samples as gold standards. Thereafter, fresh sera from 102 hospital-attending children with clinical typhoid fever (including 20 confirmed nontyphoidal cases as control) were tested by both methods and analyzed statistically. The diagnostic sensitivity, specificity, and efficiency were 51.2%, 85% and 57.8% for the new assay, and 43.9%, 65%, and 48% for the Widal test, respectively. Overall performance ability of the new assay was not better than the Widal test (p > 0.5). Further improvement of the new point-of-care typhoid assay is recommended before implementation in the field setup. Source: Das S, Rajendran K, Dutta P, et al. Diagn Microbiol Infect Dis 2013;76(1):5-9.

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

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RESEARCH REVIEW

From the Journals...

Duration of Fever and Course of Symptoms in Young Febrile Children Presenting with Uncomplicated Ιllness Purpose: It is important to advise parents when to consult a doctor when their child has fever. To provide evidencebased, safety-net advice for young febrile children, we studied the risk of complications, the occurrence of alarm symptoms, the duration of fever.Methods: In a seven day prospective follow-up study, we included 463 consecutive children aged three months to six years who presented with fever at a general practitioner out-of-hours service. We excluded 43 children with complicated illnesses at presentation. In a structured assessment, the duration of fever before presentation was noted and a physical examination was performed. Parents reported alarming symptoms and rectal temperature in a diary for one week. The total duration of fever included its duration before presentation. Median duration of fever was

estimated using the Kaplan-Meier test. Results: During follow-up, 3.2% of the children with uncomplicated illness at presentation developed a complicated illness. The presence of alarming symptoms dropped from 79.3% at day 2 of the fever episode to 36.7% at day 9. The estimated median duration of the total fever episode was four days (95% confidence interval, 3.6-4.4). Conclusions: In children with uncomplicated illnesses, the daily occurrence of alarming symptoms reported by parents was high. The median duration of fever was four days. The predictive value of alarming symptoms reported by parents for complicated illness should be reconsidered. Source: Kool M, Elshout G, Moll HA, et al. J Am Board Fam Med 2013;26(4):445-52.

Acute Kidney Injury in Dengue Fever Using Acute Kidney Injury Network Criteria: Incidence and Risk Factors The aim of this study was to assess incidence and risk factors for acute kidney injury (AKI) in patients with dengue fever (DF). A total of 223 patients (males 130; females 93; mean age 26.2 Âą 18.2 years) from a tertiary care centre in southern India were retrospectively analyzed. Acute renal failure (ARF) developed in 24 (10.8%) patients. Based on the Acute Kidney Injury Network (AKIN) criteria, the results revealed that: 12 (5.4%) had mild AKI; seven (3.1%) had moderate AKI; and five (2.2%) had severe AKI. A further 54 (24%) were diagnosed with dengue hemorrhagic fever (DHF); 11 (5%) were coinfected with leptospirosis; thrombocytopenia was present in 157 (70%) and 64 (29%) were hypotensive. Patients were divided into either group A (with AKI) or group B (without AKI), and group A was divided into mild (A1), moderate (A2) and severe (A3) subgroups. We recorded: a higher total white count (A = 9824; B = 6706; p = 0.001); serum

glutamic pyruvic transaminase (SGPT; A = 450; B = 144; p = 0.001); alkaline phosphatase (ALP) levels (A = 207; B = 42; p = 0.001); lower albumin (A = 2.65; B = 3.09; p < 0.001) and serum bicarbonate (A = 20.57; B = 23.21; p = 0.009). Hypotension (p = 0.001); coexisting viral hepatitis (p < 0.001); sepsis (p < 0.001); multiple organ dysfunction syndrome (MODS; P < 0.001) and the need for inotropes (p < 0.001); were associated with DF. Total white count (p = 0.038); glomerular filtration rate (GFR) on discharge (p = 0.034); specific gravity of urine (p = 0.006); ALP (p = 0.013); SGPT (p = 0.042); MODS (p = 0.05) and use of platelet fresh frozen plasma (FFP; p = 0.007) were significantly different between mild, moderate and severe AKI subgroups. Twentytwo (9%) died. AKI is associated with an increased mortality in DF (p = 0.005). Source: Mehra N, Patel A, Abraham G, et al. Trop Doct 2012; 42 (3):1602.

Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

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Asian Journal of

Paediatric Practice Information for Authors Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767). Asian Journal of Paediatric Practice strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so. The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript. Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper.

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

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Results

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

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

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Articles

Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes. Q. J. Expt. Physiol. 1955;40:89-111.

Books

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

Articles in Books

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

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

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Asian Journal of Paediatric Practice, Vol. 16, No. 4, 2013

For Editorial Correspondence: Dr KK Aggarwal Group Editor-in-Chief

Asian Journal of Paediatric Practice E- 219, Greater Kailash, Part - 1, New Delhi - 110 048, Tel: 40587513 E-mail: editorial@ijcp.com Website: www.ijcpgroup.com




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