new indian journal of pediatrics - pediatrics association of india |...

Editor- in- Chief: Dr Satish Tiwari

Managing Editors: Dr Amar Varma, Dr Jayant Vagha,

Associate Editors: Dr Utpal kanta Singh, Dr Asok Kr. DattaDr Prasanth Saboth

Ethical Issues: Dr Vishesh Kumar

Legal Issues: Dr Balraj Yadav

Executive Members: Dr Sukanto ChattarjeeDr Arun ThakurDr Jyanindranath BeheraDr Satish AgrawalDr Ranbir LaishramDr Nimain Mohanty

International Members:Dr Pushpa Chaturvedi (UAE)Dr Sudipta Misra (USA)Dr Salma S. Syed (USA)

New Indian Journal of PediatricsNIJP: ISSN no. 2277-9507

Editorial Team

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Volume 3 Jan.-Mar. 2014 H

Contents Page No

From the desk of editor-in-chief Editorial:Childhood obesity: A preventable calamity Dr Kritika Malhotra, Dr Pratibha Kale

Research Study: Utility of Cerebrospinal Fluid C-reactive Protein in the Diagnosis of Bacterial Meningitis: Dr Shelly Singla, Dr. Sunita Vagha, Dr. Jayant Vagha, Dr. Amit Nagpal

Clinico-pharmacological profile of scorpion envenomation in children: A retrospective studyDr Vivekanand Paul, Dr C B Kumar, Dr (Prof.) Sanjata R Chaudhary

Extended family screening in thalassimic subject by cost effective approach: Dr. Nandini Bhaduri, Dr.AdityaPrasad Sarkar, Dr. Debasish Guha, Dr. Tapankumar Ghosh

Prevalence of Neurologic symptoms in children of agricultural workers exposed to organophosphate pesticides in rural India: Dr Neelam D Sukhsohale, Dr Prachi R Sawant, Dr Sanket Pande, Dr Sushma Pande

Case Reports:1. Ultrasound Signs of Hydatid Liver Cyst:

Dr Maunil Bhuta, Dr.Vivek Ukirde, Dr.Kishor Rajpal, Dr.Ajita Nawale

2. Aplasia Cutis Congenita: Dr Shaifali Patil, Dr. Nimain Mohanty, Dr. Vidhya Kamble, Dr. Mugdha Bhamre

3. Collodion baby: Dr K. Sunilbala, Dr Amita M, Dr Abhijit Datta, Dr Raghavendra P, Dr. Mrinal Das, Dr Prof. L. Ranbir Singh

Media Watch / Around the World: Dr Anil Lohar, Dr Satish AgrawalManuscript Preparation: Guidelines for AuthorsMembership forms

Dr Satish Tiwari,

B Published by:Pediatrics Association of IndiaCuttack, Odisha

B Editorial office:Dr Satish TiwariEditor-in-chief, Professor of PediatricsMedical College Amravati

B Address for correspondence:Yashodanagar no 2 Amravati, 444606Maharashtra, IndiaPh: 0721-2541252, 9422857204E-mail: [email protected], [email protected]

B Disclaimer:Views expressed in the articles or letters are of individual

writers. Publisher or editor may not necessarily agree with the same.

All efforts have been taken not to include any unethical or unlawful advertisements in this journal. Publisher or editor may not necessarily agree with the advertisements or exaggerated claims in any particular advertisements.

Important information: All possible care has been taken to ensure accuracy of the

material, but, the editor, printer or publisher shall not be responsible for any inadvertent error(s) or consequences arising out of it.

All rights reserved:Any part of these publications can't be reproduced or transmitted

in any form, by any means or otherwise without the permission of the editor, printer or publisher

NIJP: ISSN no. 2277-9507

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Volume 3 Jan.-Mar. 2014 H

Dear all, warm regards

Our journal is now entering the third year of its publication. The baby who was born two years back is now becoming a toddler. The first two years of this publication saw many critical hurdles, obstructions and hiccoughs. But, all these ultimately resulted in strengthening and building our self confidence and removing the feelings of inferiority complex. The journal is already registered with the ISSN and the Registrar of the Newspaper of India. We are now planning for the indexing of this journal at National and International level.

This year we had the privilege of first National conference of Pediatric Association of India. This event was held at Bhubaneshwar in a well organized manner, Kudos to Dr Gadadhar Sarangi and his ever enthusiastic and over- zealous team. We now look forward to the PAICON 2014 at Burdwan under the guidance and directions of Dr Nabendu Choudhary.

There was immense support, cooperation and guidance from various parts throughout the country. Many articles, case reports, writes – up started pouring in. The support from reviewers was also good and encouraging though many of them have taken their own time and preferences.

We expect similar cooperation, support and guidance for the future issues or volumes. We hope to continue this venture with new zeal and zest in the coming years. We hope that in the coming years, we will receive more and more contributions from different parts of the country on various hot topics, current issues, recent advances and latest developments.

Wishing you all a very happy, prosperous and glorious new year…….

Yours

Dr Satish Tiwari

Editor- in- Chief

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Volume 3 Jan.-Mar. 2014 001

From the desk of editor-in-chief:

Editorial:Childhood obesity: A preventable calamityDr Kritika Malhotra, Dr Satish Tiwari, Dr Pratibha Kale

* Dept of Pediatrics, Dr PDMMC Amravati E-mail [email protected]

Childhood obesity is one of the most serious public health challenges of the 21st century. The problem is global and is steadily affecting many low- and middle-income countries, particularly in urban settings. The prevalence has increased at an alarming rate. Globally, in 2010 the number of overweight children under the age of five is estimated to be over 42 million. Close to 35 million of these are living in developing countries.

Historically, a heavy child meant a healthy child and the concept “bigger is better” was widely accepted. Today, this perception has drastically changed on the basis of evidence that obesity in childhood is associated with a wide range of serious health complications and an increased risk of premature illness and death later in life.(1) This problem is of a larger magnitude in developing countries like India. Overweight and obese children are likely to stay obese into adulthood and more likely to develop non-communicable diseases like diabetes and cardiovascular diseases at a younger age.

Obesity is a condition characterised by excessive accumulation of fat, mainly under the skin (subcutaneous), but also on various organs of the body (visceral). The most common cause of obesity is the imbalance between daily energy intake and energy expenditure. When energy intake is higher compared to energy expenditure, the excess energy is stored in the form of adipose tissue. Overweight and obesity are defined using the Body Mass Index (BMI) which is considered to be a direct measurement of body fat. Children >2

thyears of age with BMI ≥ 95 percentile are considered obese and those with a BMI between

th th85 and 95 percentiles fall in the overweight range. Overweight and obesity, as well as their related diseases, are largely preventable. Prevention of childhood obesity therefore needs high priority. The obesity is of multi-factorial origin and includes factors like:

Nutritional imbalances:

Overfeeding in a child, more so, a bottle-fed child definitely takes in more milk as compared to a breast-fed infant. Excessive milk intake with little solids has been associated with over-weight babies.

Another problem is the increasing number of commercial baby foods that are being marketed. The media portrays a 'healthy baby' on such products, so the parents are lured to feed their child with them. No doubt they taste good due to the variety of flavours available, but are consumed in excess and for prolonged periods. It is easy for the mother to mix and feed rather than make an effort to prepare home-based diets and feed. They also contain excess of sugar and salt which further increases the chances of increase in the weight.

One of the most important factors leading to obesity is consumption of junk food. The variety of such products being manufactured and heavily advertised through the media makes the young child compel the parents to procure these items and he keeps munching them anytime and anywhere. Thus, the child misses regular meals. The temptation of little surprise gifts with the products traps children. Most of these items are high on calories or even “empty calories” since they are devoid of other important nutrients. It is postulated that consumption of extra 100 calories per day will result in 5 kg weight gain in one year time.

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Sweetened beverages containing fructose lead to a further increase in obesity.

Social factors:

Increasing per capita income of the middle income groups has led to an increase in the trend of social gatherings, functions, and celebrations. In school, children celebrate their birthdays by getting sweets, pastries or savouries (that are often high in calories) for their classmates. In a class, average 40-50 children, there would be an equal number of such occasions spread out not so far apart.

A child's health is a direct reflection of the lifestyle of the family. In certain families, the eating pattern itself is such that meals are rich in fats and consumption of desserts is regular feature. Most often, children are given pacifiers in the form of chocolates, biscuits, noodles etc by parents who leave them back home with the care of baby sitters to make up for the guilt of not being able to devote adequate time to them.

Also, children have unlimited access to video games and computers nowadays. Mushrooming cyber and video game parlours have made these accessible. This contributes to the child becoming a 'couch potato' rather than spending that time in outdoor activity. Consequently, children are gaining more weight than they should. Parents also tend to exploit availability of video games and television in order to meet their own commitments of partying, socializing, etc. by leaving the children at the mercy of the small screen. This lack of exercise is augmented by the fact that earlier, children had more time to play, run about or work out compared to the children of this generation. Long school hours, tuitions and pressure to excel in academics increases inactivity. Also, due to unsafe roads (traffic, crime) children are discouraged from walking or cycling to school. Motorized vehicles are popular and they are perceived to be quicker and safer for transport. Erosion of open spaces for exercise and lack of parental time to supervise play are all part of new lifestyles. Without activity, even the recommended calories lead to a positive energy balance, which accumulates as body fat

contributing to obesity.

Endocrine and Genetic causes of Obesity (2):

More than 600 gene, markers and chromosomal regions have been associated with obesity. Rare single gene disorders like FTO (fat mass and obesity) and INSIG2 (insulin- induced gene2) mutations result in obesity. Genetic diseases like Alstrom syndrome, Bardet-Biedl syndrome, and many others have associated obesity. Endocrine disorders that are associated with obesity are Cushings syndrome, growth hormone deficiency, hyperinsulinism, hypothyroidism, pseudohypoparathyroidism.

Other factors:

Many other factors like parental obesity correlates with a higher risk for obesity in children. Perinatal factors including weight gain during pregnancy, high birth weight, and gestational diabetes in mother are associated with increased risk for later obesity. Paradoxically intrauterine growth restriction with early infant catch-up growth (Barker's hypothesis) is associated with the development of centra l adiposi ty and cardiovascular risk.

Altered sleep patterns or chronic partial sleep loss can increase the risk for obesity. Recently, children and adults have decreased the amount of time spent sleeping. Reasons for these changes may relate to increased time at work, increased time watching television, and a generally faster pace of life.(2)

Obesity related co-morbidities

Obesity is associated with multiple co-morbidities such as type 2 diabetes mellitus, dyslipidemia, polycystic ovarian disease, hypertension and the metabolic syndrome which are increasingly seen among children and urban adolescents. Most importantly childhood obesity has been associated with higher risk of morbidity and mortality in adult life.

As childhood overweight increases, its medical complications are becoming more common and more frequently recognized. For

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example, the prevalence of type 2 diabetes has risen dramatically among adolescents in the past 20 years. Studies suggest that a substantial percentage of overweight children and adolescents may be afflicted with the metabolic syndrome because many have one or more of the following; an elevated triglyceride level, a low HDL cholesterol level, and high blood pressure. Many overweight children also have elevated insulin levels, indicating an increase in insulin resistance.(3) Studies have revealed that overweight in adolescence is associated with accelerated coronary atherosclerosis.

Overweight and obesity are associated with increased risk for many types of cancer, including cancer of the breast, colon, endometrium, esophagus, kidney, pancreas, gall bladder, thyroid, ovary, cervix, and prostate, as well as multiple myeloma and Hodgkin 's lymphoma.(4) Other diseases like asthma, non-alcoholic fatty liver disease, musculoskeletal problems, behavioural abnormalities and obstructive sleep apnea are also associated with obesity.

Preventive measures:

Considering all the grave implications that childhood obesity has on public health, preventive measures should be taken right from the beginning. Prevention of obesity is a holistic approach, requiring equal contribution from parents, school authorities and teachers, community, health care providers and government and regulating bodies. It starts right from the pre-pregnancy state when BMI should be normalised and moderate exercise should be maintained. Exclusive breast-feeding should be done for 6 months and continued at least up-to two years.

Family plays the most important role. Parents should ensure fixed meal timings and place that is away from television and fatty foods and soft drinks should be avoided. Children's natural inclination to be active should be encouraged, not restricted.

The next most influential places are schools. Hours of physical education should be increased

and benefits of physical activity should be taught. Canteens should be discouraged from selling unhealthy and high-calorie junk food and cold drinks.

The health care providers should ensure proper growth and BMI monitoring to pick up risk of obesity early and impart proper and essential health education which will include appropriate dietary advice and counselling of parents.

As far as the government is concerned, their role should be to regulate advertisements and make sure they do not mislead the children. There should be programs in place for prevention of childhood obesity and implementation of them should be ensured. More and more play grounds and stadiums should be constructed to provide children with a safe play area.

Thus, combined efforts of the society in an appropriate manner should successfully reduce the global burden of the disease leading to a healthier childhood and a safer adulthood.

References

1. William H. Dietz. Health consequences of obesity in youth: Childhood predictors of adult disease. Pediatrics, 1998, 101, pp.518–25.

2. Sheila Gahagan. Overweight and Obesity. In: R. M. Kliegman, B.F. Stanton, J.St. Geme, N.F. Schor, R.E. Behrman (eds.). Nelson Textbook of Pediatrics Nineteenth Edition: Saunders Philadelphia;2012,pp.179-187

3. Misra A, Vikram NK Insulin resistance syndrome (metabolic syndrome) and obesity in Asian Indians: evidence and implications. Nutrition 2004, 20(5) pp 482–491

4. LH, Byers T, Doyle C, Bandera EV, McCullough M, Gansler T. American Cancer Society guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA: A Cancer Journal for Clinicians 2006;56:254–281.

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EeE

Utility of Cerebrospinal Fluid C-reactive Protein in the Diagnosis of Bacterial Meningitis * Dr. Shelly Singla, *Dr. Sunita Vagha, **Dr. Jayant Vagha, **Dr. Amit Nagpal

*Department of Pathology, JNMC Sawangi(Meghe) Wardha, **Department of Pediatrics, JNMC Sawangi(Meghe) Wardha. E-mail: [email protected]

Key Words - Cerebrospinal fluid, C-reactive protein, Bacterial meningitis

Abstract-Objective -

The present study was undertaken to evaluate the utility of Cerebrospinal fluid C-reactive protein in the diagnosis and differentiation of bacterial meningitis from non bacterial meningitis in comparison to routine CSF analysis.

Introduction

Among the various central nervous system infections, bacterial meningitis is commonest infection in infants and children. It is a potentially devastating illness and arouses tremendous anxiety in both the patients and physician.

No single test or battery of tests can replace the clinical acumen of the physician in identifying the children with early signs of bacterial meningitis. The diagnosis and treatment of acute bacterial meningitis is a challenge for the primary care physician.

Delay in distinguishing bacterial infection from other infections of central nervous system may have irrevocable consequence, as the regenerative capacity of central nervous tissue is limited, so prompt and correct diagnosis to select appropriate therapy is required.

Besides routine cerebrospinal fluid analysis (protein, glucose and cell count), other additional tests l ike Latex agglut inat ion, Counter- immuno electrophoresis, Radio-immunoassay and measurement of cerebrospinal fluid lactate have been utilized with varying degrees of success for the diagnosis of bacterial meningitis. The limitation of these options is however considerable as some require specific antisera and some are too slow and laborious procedures.

The culture of cerebrospinal fluid (CSF) which gives a definite diagnosis and most importantly the antibiotic sensitivity pattern of the infecting organism, takes longer time. Moreover, CSF culture for pyogenic

,organisms is positive only in 30%-60% cases.

Attention was recently drawn to the importance of Cerebrospinal fluid C-reactive protein (CSF CRP) measurement in differentiating bacterial and other conditions of central nervous system. CRP in CSF has been reputed to be one of the most reliable and early indices for differentiating bacterial from non-bacterial

,meningitis.

C-reactive protein (CRP) an acute phase protein is a globulin formed by the body in response to various non-specific stimuli such as infection, tissue necrosis or neoplasm. Microbial infection stimulates hepatocytes in

,the liver to produce CRP.

Method of study -

A prospective analytical study included 50 infants and children between 0 and 12 years of age suspected of having meningitis admitted to Department of Paediatrics JNMC, Sawangi (Meghe), Wardha. The subjects had a blood test and routine cerebrospinal fluid (CSF) analysis which included CSF cell count with differential count, sugar, protein, gram stain and culture. Qualitative latex agglutination test for C - reactive protein (CRP) was done in all cases. Diagnosis of meningitis was made on basis of history, clinical examination and CSF analysis.

Conclusion -

CSF CRP has highly significant positive co-relation with routinely used CSF parameters. CSF CRP is an easy, quick to perform, reliable, highly sensitive and specific diagnostic test than other routinely used CSF parameters (cell count, glucose, protein and culture). It should be routinely performed as a bed side

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Research Study :

procedure along with CSF analysis in suspected meningitis patients for differentiating bacterial meningitis from non bacterial meningitis..Material and Methods

This study was a prospective analytical study carried out in the Department of Paediatrics and Department of Pathology, Jawaharlal Nehru Medical

st st College, Sawangi between 1 August 2011 to 31 July 2013. 50 cases of infants and children between 0 and 12 years age with suspected signs of meningitis were included in the study group. Relevant history and details of treatment (antibiotics) taken prior to admission were recorded and thorough examination was done in each case.

Blood and CSF samples were collected as a part of diagnostic work up. CSF sample was divided into 3 tubes- first tube for Chemistry (glucose and protein), second tube for Microbiology examination (Gram's stain, Bacterial culture and sensitivity), third tube for Total Cell count and Differential count.

A qualitative latex agglutination test was done at bed side to determine CRP in CSF. Commercially prepared kit available from Pathozyme Diagnostics was used. The major advantage of test is its rapid two minute reaction time. It indicates the CRP concentration equal or greater than 6 mg/L.

CSF Gram stain and culture were taken as gold standard test in diagnosing bacterial meningitis. In cases where the staining results were negative, CSF cytology and glucose and protein levels were considered. CSF CRP was then evaluated against these routinely used CSF parameters. All 50 patients were divided into 4

,groups based on clinical and CSF cyto-chemistry.

Group I - Bacterial meningitis(BM) was defined by a 3

C S F c e l l c o u n t > 5 0 0 c e l l s / m m w i t h polymorphonuclear neutrophils (PMNs) of >60%, CSF Glucose <40 mg/dL or reduced significantly to below the 50% of blood sugar and a CSF protein level of >100 mg/dl.

Cases with history of previous antibiotics intake were included in the group.

Group II - Viral meningitis(VM) was defined as those 3with a CSF Cell count between 10-100 cells/mm with

lymphocyte predominance, CSF glucose >50 mg/dL, protein levels between 50-100 mg/dL and a negative

bacterial culture and Gram stain.

Group III - Tuberculous meningitis(TBM) was defined as those with a history of contact with a sputum positive tuberculosis case, clinico-radiological findings consistent with TB and CSF Cell count between 100-

3500 cells/mm with predominant lymphocytes, CSF glucose < 45 mg/dL or below 50% of blood sugar, high CSF protein between 100-500 mg/dL or in cases where a CSF culture and/or Ziehl-Neelsen staining have revealed acid-fast bacilli.

Group IV - No meningitis(NM) was defined as those 3

with CSF Cell count <5 cells/mm , CSF glucose >50 mg/dL, CSF protein between 20-40 mg/dL, negative Gram stain and Ziehl Neelson stain and no growth on culture

Statistical Analysis

The Statistical software namely SPSS 17.0, Graph PAD prism 5.0 was used for the analysis of the data. Significance is assessed at 5% level of significance. Sensitivity, Specificity, Positive Predictive Value, Negative Predictive value and Accuracy were calculated to know the diagnostic performance of CRP in various types of meningitis. Analysis of variance (ANOVA) has been used to find the significance of study parameters between three or more groups of patients. Chi-square has been used to find the significance of study parameters on categorical scale between groups.

Results

Out of 50 cases, 19 cases (38%) were of bacterial meningitis, 23 cases (46%) of viral meningitis, 5 cases (10%) of tuberculous meningitis (all 5 were ZN stain positive) and 3 cases (6%) of no meningitis group.

Male to Female ratio was 1.08:1.

Results -

Of 50 cases, 19 cases (38%) were of bacterial meningitis, 23 cases (46%) of viral meningitis, 5 cases (10%) of tuberculous meningitis and 3 cases (6%) of no meningitis group. CSF culture was positive in only 13 cases (68.4%) of bacterial meningitis. Predictive values of CSF parameters (CSF total cell count with neutrophil count, sugar, protein and culture) in diagnosing bacterial meningitis were calculated. CSF CRP was positive in 18 (94.7%) cases in bacterial meningitis, 1(20%) case in tuberculous meningitis and was negative in all 23 cases

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of viral meningitis and 3 cases of no meningitis. CSF CRP showed sensitivity 94.7%, specificity 96.7%, and positive predictive value 94.73%, negative predictive value of 96.7% and accuracy of 0.96 in differentiating bacterial meningitis from non bacterial meningitis.

The maximum numbers of cases (28 cases i.e. 56%) were present in age group 2 month-5 yr with bacterial meningitis also predominating in same age (table no 1)

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Age BM(n=19) VM(n=23) TBM(n=5) NM (n=3) Total (n=50)

0-2 months 4(21.05%) 6(26.10%) 0 0 10(20.00%)

2month -5 yr 11(57.90%) 12(52.17%) 3(60.00%) 2(66.66%) 28(56.00%)

5-12 yr 4(21.05%) 5(21.73%) 2(40.00%) 1(33.34%) 12(24.00%)

Total 19(100.00%) 23(100.00%) 5(100.00%) 3(100.00%) 50(100.00%)

Mean age ±S.D 3 ± 3.65 3± 3.24 5.05± 5.18 4.83±4.80 3.0±3.58

Table no 1: Distribution of cases according to age

CSF parameter BM(n=19) (n=23) (n=5) (n=3) p value

Total cell 582 ± 299.89 94 ± 135.50 296± 139.37 4.33 ± 0.577 <0.0001count(cells/mm3)

Neutrophils % 67.48 ± 10.63 2.05 ± 2.24 17.6 ± 23.90 0 <0.0001

Lymphocytes % 32.52 ± 10.63 97.95 ± 2.24 82.4 ± 23.90 100 ± 0.0 <0.0001

Glucose(mg/dl) 35 ± 11 55 ± 7.40 39.60 ± 8.87 57.3 ± 5.03 <0.0001

Protein(mg/dl) 142 ± 47.85 66 ± 11.71 257.6 ± 2.10 37.3 ± 3.05 <0.0001

VM TBM NM

Table 2: CSF parameters in different types of meningitis

CSF CRP CSF parameter Positive Negative -value p-value

(n=19) (n=31)

CSF Cell <100 2 20

count /mm3 100-500 4 7 13.66 0.0002

>500 13 4

CSF glucose <40 13 5

mg/dL >40 6 26 13.98 0.0002

CSF Protein >100 16 6

<100 3 25 20.11 <0.0001

CSF Culture Positive 12 1 18.80 <0.0001

Negative 7 30

Table 3 : Co-relation between CSF CRP and other CSF parameters

CSF gram stain was positive in 5(26.3%) cases and culture was positive in 13 (68.4%) cases of bacterial meningitis (n=19). Among the organisms isolated E.Coli was leading pathogen in 0-2 month age, Haemophilus Influenzae was most common organism in 2 month-5years age and predominance of Streptococcus pneumoniae was seen in 5-12 years age.

Out of total 50 cases, 18 cases (94.7%) of bacterial meningitis group (n=19) and 1 case (20%) of tuberculous meningitis (n=5) were positive for CSF CRP (Qualitative test indicating levels > 6 mg/L). 4 cases (80%) in tuberculous meningitis (n=5), all 23 cases (100%) of viral meningitis and all 3 cases (100%) of no meningitis group were negative for CSF CRP.

Prior antibiotics were given to 8 cases (these cases were included in bacterial meningitis as they met the inclusion criteria for bacterial meningitis group), all these cases showed altered CSF picture with low CSF count (Mean CSF count of 347 ±

3273.10 cells/mm ), negative gram stain and negative culture but these cases were CRP positive indicating that antibiotic use can alter routinely used CSF parameters but doesn't alter CRP response.

There was positive co-relation of CSF count and CSF CRP, with number of positive cases increasing with increased CSF count.

Out of 19 CSF CRP positive cases, 13 cases (68.4%) of bacterial meningitis had CSF glucose< 40 mg/dL. There was positive and significant co-relation between decreasing CSF glucose and positive CSF CRP.

CSF CRP was positive only if CSF protein was >45 mg/dL and maximum positivity was noted in range of 101-200 mg/dL. Out of 19 cases of CSF CRP positive, 14 cases (73.6%) had CSF protein in range of 101-200 mg/dL and all these were diagnosed as bacterial meningitis indicating significant co-relation between CSF CRP and CSF protein.

Of 19 cases of bacterial meningitis, 13 cases were culture positive and out of these 12 (92.3%) cases were CSF CRP positive, indicating highly significant co-relation.

Predictive values for CSF parameters in differentiating bacterial meningitis from non bacterial meningitis were calculated based on various cut off values (table 4)

Discussion

Meningitis is one of the common clinical problems during infancy and childhood. It often presents as a medical emergency, which requires rapid and prompt diagnosis with aggressive management to select appropriate therapy to prevent mortality and long-

,term morbidity associated with the disease.

The etiological diagnosis of meningitis remains a problem as the clinical and biochemical picture is often masked because of prior antibiotic use. This becomes

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Table 4 : Predictive value of CSF parameters in differentiating bacterial meningitis from non bacterial meningitis

CSF parameter Criteria for Sensitivity Specificity PPV NPV Accuracydiagnosis

Cell count >500 73.68 % 90.32 % 82.35 % 84.84% 0.84cells/mm3

Neutrophil >60% 78.94% 96.77 % 93.75 % 88.23 % 0.90

Glucose <40 mg/dL 68.42% 83.87% 72.22% 81.25% 0.78

Protein >100 mg/dL 84.21% 80.64% 72.72% 89.28% 0.82

CRP Positive 94.73 % 96.77 % 94.73 % 96.77 % 0.96

Gram stain Positive 26.31 % 100 % 100 % 68.18 % 0.72

Culture Positive 68.42 % 100 % 100 % 83.78 % 0.88

even more difficult in a population like ours where patients first attend a private practitioner and receive a course of antibiotic. They then come to our hospital when they do not improve. In such a scenario, it becomes impossible to isolate the organisms from blood

, or CSF. Moreover, CSF cultures for pyogenic organisms are positive in only 30–60% of cases.

In spite of glorious medical advancement and discoveries, bacterial meningitis remains one of the most challenging emergencies of medical sciences. Early diagnosis and treatment is essential to avoid poor outcome and long term sequelae.

A quick and sensitive test is therefore, required for rapid bedside diagnosis.

In present study, meningitis most commonly affects children between ages 2 month - 5 years. Prior antibiotic use can alter routinely used CSF parameters like cell count, biochemical values, staining results and culture, but doesn't alter CRP response as the underlying disease activity persists.

CSF analysis in bacterial meningitis shows increased cell count with predominance of neutrophils, decreased glucose levels and increased protein levels, but sensitivity of these parameters alone is low in diagnosing bacterial meningitis. These findings were similar with findings of Kumar et al, Oostenbrink et al, Jadali et al, Abro et al, Uddin et al, Khanam et al and Malla et al

Although CSF culture is the gold standard for diagnosis of bacterial meningitis for direct evidence of the organism, it has sensitivity of 68.42%.Prior antibiotic reduces the rate of culture positivity. It was

also reported in study of Gaur et al, Jadali et aland Uddin et al

CRP in CSF is positive in maximum no of cases of bacterial meningitis and it has high sensitivity, specificity, negative predictive value and positive predictive value in diagnosing bacterial meningitis. Findings were in hand to hand with findings observed in

lstudy of Singh et a , Pemde et al, Hemvani et al, Gaur et al, Prasad et al, Uddin et al and Patel et al.

The reason for significantly higher positivity of CSF CRP in bacterial meningitis could be as CRP production is non specific response to tissue damage and the greater destruction of tissue caused by bacteria than by viruses explains higher positivity of CSF CRP.

In the present study, 1 case was negative for CSF CRP in bacterial meningitis and reason that can be offered is that CRP response varies enormously and minimal CSF inflammation is present very early in course of disease leading to decreased CRP levels, which may be less as to be detected by qualitative method.

1 case was positive for CSF CRP in tuberculous meningitis. It can be due to either CRP is acute phase reactant so can be positive in acute stages of tuberculous meningitis or simultaneous occurrence of tuberculous meningitis and bacterial meningitis can occur in occasional cases. Similar findings were also reported by Gaur et al, Prasad et al and Patel et al.

CSF CRP positivity increases with increasing cell count, decreasing CSF glucose levels, increasing CSF protein levels and positive culture. CSF CRP has highly significant positive co-relation with routinely used CSF parameters indicated for diagnosis of bacterial meningitis. Findings of present study were in accordance with Uddin et al, Patel et al and Sadat et al.

Conclusion

CSF CRP has highly significant positive co-relation with routinely used CSF parameters. CSF CRP is an easy, quick to perform, reliable, highly sensitive and specific diagnostic test than other routinely used CSF parameters (cell count, glucose, protein and culture). It should be routinely performed as a bed side procedure along with CSF analysis in suspected meningitis patients for differentiating bacterial meningitis from non bacterial meningitis.

References

1) Patel N, Patel U, Nagpal AC, Jain RK. Evaluating Utility of C- Reactive Protein in Differentiating Bacterial from Non- Bacterial Meningitis in Tertiary care Hospital, in Central India. Int J Med Res Rev. 2013; 1(2): 47-55

2) Pemde HK, Harish K, Thawrani YP, Shrivastava S, Belapurkar BM. C-reactive Protein in Childhood Meningitides. Indian J Pediatr. 1996; 63: 73-77

3) Ribeiro MA, Kimura RT, Irulegui I et al. Cerebrospinal fluid levels of lysozyme, IgM and C-reactive protein in the identification of

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bacterial meningitis J Trop Med Hyg. 1992 Apr; 95(2) : 87-94

4) Kumar L, Chitlangiya S, Ayyagari A. The current status of Pyogenic Meningitis. Indian Pediatr. May 1980; 17(5):438-444

5) Stearman M, Southgate HJ. The Use of Cytokine and C - react ive protein Measurements in Cerebrospinal Fluid during Acute Infective Meningitis. Ann Clin Biochem. 1994 May; 31(3): 255-61

6) Singh UK. Cerebrospinal fluid C-reactive protein in the diagnosis of meningitis in children. Indian Pediatr. August 1994; 31(8):939-942

7) John M, Raj IS, Macaden R, Raghuveer TS, Yeswanth M, Meundi DM. Cerebrospinal Fluid C - reactive protein Measurement-A Bedside Test in the Rapid Diagnosis of Bacterial Meningitis. J Trop Pediatr. 1990; 36(5): 213-217

8) Singh UK, Sinha RK, Suman S, Singh VK. C-Reactive protein as an indicator of complications in bacterial meningitis. Indian Pediatr. May 1996; 33(5): 373-376

9) Venkatesh B, Scott P, Ziegenfuss M. Cerebrospinal Fluid in Critical Illness. Critical Care and Resuscitation. 2000; 2: 42-54

10) Marx GE, Chan ED. Tuberculous Meningitis: Diagnosis and Treatment Overview. Tuberc Res Treat. 2011: 798764

11) Singh N, Arora S, Kahlon PS. Cerebrospinal fluid C-reactive protein in meningitis. Indian Pediatr. June 1995; 32(6): 687-688

12) Kumar R, Singh S N, Kohli N; A diagnostic rule for tuberculous meningitis, Arch Dis Child. 1999; 81: 221-224

13) Oostenbrick R, Moons KGM, Twinstra MJ, Grobbee DE, Moll HA. Children with meningeal signs. Arch Pediatr Adolesc Med. 2002; 156: 1189-1194

14) Jadali F, Sharifi M, Jarollahi A, Nahidi S. C-Reactive Protein And Lactate Dehydrogenase In Serum And Cerebrospinal Fluid In Rapid And Early Diagnosis Of Childhood Meningitis. IJCN. Jan 2009; 1(4): 37-46.

15) Abro AH, Abdou AS, Ali H, Ustadi AM, Hasab AAH. Cerebrospinal fluid analysis – acute bacterial versus viral meningitis. Pak J Med Sci. 2008; 24(5): 645-50

16) Uddin M B, Rahman M, Siddique A B. Usefulness of CSF C-Reactive Protein in Differentiating Pyogenic and Aseptic Meningitis. TAJ 2009; 22(1): 78-81

17) Khanam R, Hanif M, Hoque M, Tawfique, Ahmed U. Role of CSF C-Reactive Protein for the Differentiation of Bacterial Meningitis from Aseptic Meningitis in Children. Bangladesh J Child Health. 2012; 36(3): 126-132

18) Malla K.K, Malla T, Rao K.S., Basnet S, Shah R. Is Cerebrospinal Fluid C-reactive Protein a Better Tool than Blood C-reactive Protein in Laboratory Diagnosis of Meningitis in Children?. Sultan Qaboos Univ Med J. February 2013; 13(1): 93-99

19) Gaur A, Seshan S.V. CSF C-Reactive Protein Estimation for Bedside Diagnosis of Pyogenic Meningitis. Indian Pediatr. 2004; 41: 1073-1074

20) Hemvani N, Chitnis DS, Joshi SP. C- Reactive Protein in Cerebro-spinal fluid and its role in differentiation of meningitis. Indian J Med Microbiol. 2001; 19(1): 26-29

21) Prasad R, Kalra K, Mathur P.P, Singh M, Kalra A, Dayal R et al. Study on outbreak of meningococcalmeningitis. Indian Pediatr. April1985; 22(4)

22) Sadat P, Patel SV, Shah K. Role of CSF-CRP as a Bedside Diagnostic Test in Children with Meningitis. NHL Journal of Medical Sciences. Jan 2013; 2(1): 54-56.

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Clinico-pharmacological profile of scorpion envenomation in children with outcome: A retrospective studyDr Vivekanand Paul, Dr C B Kumar, Dr (Prof.) Sanjata R Chaudhary

Department of Pediatrics, Patna Medical College & Hospital, Patna, Bihar 800004, India. Email [email protected]

Keywords: Scorpion Sting, Prazosin, Sympathetic storm

Abstract :

Scorpion sting is an acute life threatening, medical emergency. Most of the victims are toddlers and young children of rural areas. Pediatric age group especially infants and young children are more vulnerable to toxic effects of scorpion sting envenomation due to high concentration of venom per square body surface area . The usefulness of Prazosin (Alpha1blocker) therapy in this condition was scientifically established in mid-eighties in India. The time lapse between the sting and administration of Prazosin for autonomic storm determines the outcome. We have done this retrospective study in our Upgraded department of Pediatrics, PMCH, Patna. It was noted that none of the referral slips mentioned Prazosin in the initial treatment given before referring the patient. This indicates that there is still a lack of awareness among doctors posted in the peripheries about the use of Prazosin in the management of Scorpion sting cases in our state. There should be initiative by various medical bodies in the state for the awareness of the working doctors in the peripheries for the right approach towards management of Scorpion Sting cases which could save many lives.

Introduction:

Scorpion sting is an acute life threatening 1

medical emergency . It is commonly seen in rural areas of tropical and sub-tropical region especially in summer and rainy season. Most of the victims are toddlers and young children of rural areas where they are barefooted and used to sleep on the ground and also because of their irresistible desire to explore hidden objects. We encounter scorpion sting cases in our Paediatrics emergency quite often mostly referred from various

Primary Health Centres of adjoining areas.

Pediatric age group especially infant and young children are more vulnerable to toxic effects of scorpion sting envenomation. This is due to larger venom dose to body size ratio than older children and adults. Most of the fatal envenomation due to scorpion sting occurs in

2Paediatric age group .The usefulness of Prazosin therapy in this condition was scientifically established in mid-eighties in India. The experimental evidence of Gueron confirmed the clinical experience of Bawaskar

3and Bawaskar . It is however not clear as to why the use of Prazosin was not put into practice at all centres. The reasons for this may be many viz., lack of awareness, lack of availability or lack of published data from different settings. Most of the cases are dealt by the general practitioners who are generally not aware about the recent treatment guidelines. It is to be noted that guidelines for the management of snake bite has become universal whereas treatment guideline for scorpion sting has not been popularised.

In the pre-Prazosin era (before 1983), 25-30% fatality due to pulmonary edema was reported in scorpion victims from Western India. Since the use of Prazosin (1984 onwards) the mortality in these victims

3was reduced to less than 1% . Clinical acceptance of Prazosin for scorpion sting now exists. There must be no delay in administration of Prazosin.Prazosin is available as 1mg tablet. Loading dose of Prazosin is 50mcg/kg stat and 20mcg/kg every 4 hourly (generally six doses required).Pediatricians should also not hesitate to treat pulmonary edema effectively with isosorbidedinitrate, sodium nitroprusside or nitroglycerininfusate and

4dobutamine support wherever appropriate .

The time lapse between the sting and administration of Prazosin for autonomic storm determines the outcome.

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Research Study :

Recent studies have proved that previously used drugs like steroids have no role, instead have adverse effects.Steroids might enhance the necrotizing effects of circulating catecholamines on myocardium resulting in

5clinical deterioration .

Atropine should also not be given routinely for profuse perspiration, vomiting, and increased salivation because it may aggravate the tachycardia and other sympathetic effects of venom. It also aggravates hypertension and the severity of pulmonary edema.

Insulin glucose potassium drip and lytic cocktail also do not reduce the cardiovascular morbidity and mortality in scorpion sting victims.

Aims & Objectives:

This study will emphasize upon the need to train doctors posted in rural setup and Primary Health Centres about the rational management of Scorpion Sting cases.

Materials & Methods:

This is a Retrospective study done in the Upgraded department of Pediatrics, PMCH, Patna. All the scorpion sting cases referred to PMCH during the

st thstudy period (1 January 2013 to 30 June 2013) were included. The prescription and referral slips having initial treatment were recorded and interpreted. Drugs prescribed in those referral slips were:

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S/n Drugs Total= 204

1 InjDexona (Dexamethasone) 200 (98%)

2 Lytic cocktail (Pethidine + Chlorpromazine + Promethazine) 4 (1.9%)

3 InjOndem (Ondensetron) 97 (47.5%)

4 Inj Atropine 118 (57.8%)

5 Inj Ceftriaxone 168 (82.4%)

6 InjTetvac 196 (96%)

7 IVF DNS, RL 96 (47%)

8 Anti Scorpion Venom 3 (1.4%)

9 Inj Ranitidine 18 (8.8%)

10 Lignocaine 2% for local infiltration 54 (26.4%)

11 Inj Hydrocortisone 38 (18.62%)

12 Inj Insulin 6 (2.9%)

13 InjAvil 198 (97%)

14 Tab Inderal 11 (5.3%)

Table 01 :

Table 02 : Number of cases admitted and death (Month wise)

Cases admitted Deaths

January 36 0

February 39 1

March 50 4

April 29 3

May 17 4

June 33 2

It was observed that in all cases of death the time elapsed between Scorpion Sting and Prazosin administration was long (average >24 hours) and there was history of intravenous fluid administration outside.It was also noted that none of the referral slips had mentioned Prazosin in the initial treatment given before referring the patient.

Results:

It was clear from the study of referral slips that none of the physicianshave prescribed Prazosin. Majority of patients came here having features of cardiac failure compounded by irrational intravenous fluid administration.

Children who came late had the features of excessive sympathetic activity (tachycardia, intense vasoconstriction and carditis). Those children who presented immediately after the sting (within 30 minutes) had the features of parasympathetic hyperactivity (i.e. sweating, salivation bronchospasm, priapism in males and vomiting). All these symptoms indicated the autonomic storm at presentation. The most common presenting symptoms were irritability and profuse sweating, hurried breathing and cold extremities followed by an altered sensorium. The most common clinical signs were tachycardia, tachypnoea, cold extremities and perspiration [Table No.03]. A majority of the cases approached the hospital after 6-12 hours of the scorpion sting.

Table No. 03

The time gap between the scorpion sting and presentation to the hospital is one of the significant risk factors which determine better outcomes and mortality. Children who presented after 6 hours of the sting had a significantly higher mortality rate, as was also reported

6.by Biswal et al

Themortalitywhichwasobservedinthisstudywasseenin 14(6.8%) cases, ascomparedtothe1% to 10.7% whichwas reported by various authors from different

1,3,7. places The causes for highermortality may be late presentation, theuse of intravenous fluids, dexamethasoneand antihistamines and associated m u l t i p l e s y s t e m i c i n v o l v e m e n t s . Dexamethasonealoneorin combinat ion with antihistaminesis known to potentiatethe effect of catech olamineonthe cardiovascular system and the CN Sand to

worsen the encephalopathy, as wasalso observed by 6other authors .

Conclusion:

Scorpion sting envenomation is an acute life threatening emergency in children and timely referral and early therapy with Prazosin may be lifesaving. The presence of metabolic acidosis, myocarditis, encephalopathy and acute pulmonary oedema are important determinants of the mortality and morbidity in children. Treatment with steroids and antihistamines before admission was associated with a poor outcome. There is still a huge lack of awareness among doctors posted in periphery aboutthe use of Prazosin in the management of Scorpion sting cases in our state. There should be initiative by various medical bodies around the state for the awareness about the right approach towards management of Scorpion Sting cases which will be vital in saving many lives of our children

Discussion:

Scorpions live in warm dry regions throughout India. They inhabit commonly the crevices of dwellings, underground burrows, under logs or debris, paddy husk, sugarcane fields, coconut and banana plantations. Their distribution is more in regions with abundant red soil.

The Indian red scorpion's (Mesobuthus 8

tamulus') venom is a potent sodium channel activator , resulting in the stimulation of the autonomic nervous system, which in turn leads to the sudden release of

9endogenous catecholamines into the circulation . The venom initially leads to a transient cholinergic phase, followed by sustained adrenergic hyperactivity, which

10. is a venom dose dependent phenomenon The clinical manifestations depend upon the dose of the venom, the age of the child, the season of the sting and the time lapse

11between the sting and hospitalization .

Of the 204 cases, 143 (70%) were boys and 51 (30%) were girls. Peripheral circulatory failure cases with cold extremities were seen in 152 (74.5%) of the cases.This is due to early stage of compensated shock due to excessive catecholamine, resulting in peripheralvasoconstriction, but without significant myocardial dysfunction.

Scorpion antivenom is considered as the specific treatment of scorpion envenomation. However, the benefit of scorpion antivenom has been seriously

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challenged by recent randomised placebo controlled 12. trial

Insulin glucose potassium drip and lytic cocktail also do not reduce the cardiovascular morbidity

13, 14. and mortality in scorpion sting victims As scorpion venom acts indirectly through the release of auto-pharmacological agents, the aim of the treatment should be to counteract the effects of these agents.

Alpha receptor stimulation plays important role in the pathogenesis of pulmonary edema. Prazosin, a post synaptic alpha blocker, reverses both inotropic and hypokinetic phases and reverses the metabolic effects

15.caused by depressed insulin secretion Oral Prazosin is fast acting, relatively cheap, free from any anaphylaxis and highly effective. Early intervention with oral Prazosin and appropriate use of dobutamine with avoidance of atropine, excessive diuretics, steroids, and antihistamines might help to hasten the recovery in severe scorpion sting victims.

References:

1. Bawaskar HS. andBawaskar PH. Prazosin in management of cardiovascular manifestations of scorpion sting. Lancet,1986; 510-11.

2. San thakr i shnan BR, Rangana than G, Ananthasubramanian P. cardiovascular man i f e s t a t i on o f s co rp ion s t i ngs i n children.Indian Pediatr 1977; 14: 353-356.

3. Bawaskar HS, Bawaskar PH. Indian red scorpion envenoming. Indian J Pediatr 1998;65: 383-391

4. Mahadevan S. Scorpion sting. Indian pedatre 2000;27.504-514.

5. Oliver MF, Kurien VA, Greenwood TW. Relation between serum fatty acids and arrhythmias and death after acute myocardial infarction. Lancet 1968; II: 710-715.

6. Biswal N, Bashir RA, MurmuUday C, Mathai B, Balachander J, Srinivasan S. Outcome of scorpion sting envenomation after a protocol

guided therapy. Indian J Pediatr 2006; 73: 577-582.

7. Prasad R, Mishra OP, Pandey N, Singh TB. Scorpion sting envenomation in children: Factors affecting the outcome. Indian J Pediatr 2011; 78(5): 544-548.

8. Vasconcelos F, Lanchote VL, Bendhack LN, et al. Effects of voltagegated Na+ channel toxin from Tityusserrulatus venom on rat arterial blood pressure and plasma catecholamines . CompBiochemPhysiol C ToxicolPharmacol. 2005; 141: 85-92.

9. Ismail M. The scorpion-envenoming syndrome. Toxicon 1995; 3: 825-858.

10. Bawaskar HS, Bawaskar PH. Management of cardiovascular manifestations of poisoning by the Indian red scorpion (Mesobuthustamulus). Br Heart J 1992; 68: 478-480.

11. Bawaskar HS, Bawaskar PH. Cardiovascular manifestations of scorpion sting in India (Review of 34 children). Ann Trop Pediatr 1991; 11: 381-387.

12. Abroug F, Elatrous S, Nouria S, Haguiga H, Touzi N, Bouchoucha S. Serotherpy in scorpion envenomation: a randomised controlled trial. Lancet 1999; 354: 906-909.

13. Mahadevan S, Choudhary P, Puri RK, Srinivasan S. Scorpion evenomation and the role of Lytic cocktail in its management. Indian J Pediatr 1981;48:757-761.

14. Murthy KRK, Joshi AG. Reduced insulin secretion in acute myocarditis produced by scorpion venom injected in rabbits. Indian Heart J 1986; 38: 467-469.

15. Bawaskar HS, Bawaskar PH. Vasodilators: Scorpion envenoming and the heart (An Indian experience). Toxicon1994; 32: 1031-1040.

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Extended family screening in thalassimec subject by cost effective approach: *Dr. Nandini Bhaduri, *Dr.AdityaPrasad Sarkar, **Dr. Debasish Guha, *Dr. Tapankumar Ghosh

*Department of Pediatrics, Burdwan Medical College, ** Department of Pediatrics, R.G.Kar Medical Coollege E-mail:[email protected]

Keywards : Screening thalassemia, Carrier detection Hemoglobinopathy

Abstract :

Dichlorophenolindophenol precipitation test (DCIP) and Naked eye single tube osmotic fragility test (NESTROFT) tests.

Total 309 subjects who are the family members of thalassemia patients have been tested. The prevalence groups are selected because of the possibility of passivity of the tests so that authenticity of the test can be better judged.

All the subjects are divided into 4 groups. Group i)117 subjects had both tests positive , Group ii) 66 subjects had DCIP test negative and NESTROFT TEST positive Group iii) 12 subjects had DCIP test positive and NESTROFT test negative and Group iv)114 subjects had both tests negative .

Out of 309 subjects 195 showed positive results with either or both the tests who also revealed abnormalities in HPLC. 114 subjects showed negative results with both DCIP and NESTROFT who were also normal in HPLC. The sensitivity of the combined tests is 100 percent and specificity is 92.68 percent.

Predictive value of positive test is 95.38 percent and Predictive value of negative test is 100 percent.

Introducation :

Hemoglobinopathy is one of the major problems in Indian scenario.About 2-17% of Indian population with an average of 3% in the general population are

1Thalassemia carriers .The people during the carrier state usually looks normal and leads almost normal life. This is manifested when two carriers get married and give birth to a child with thalassemia major. There is still no definite curative treatment for thalassemia.Stem cell transfusion has been done with controversial results in regard to long term prognosis. Genetic study is still at an

experimental level and will remain within the reach of only a few affluent people. Those who are born with major hemoglobinopathy are treated with regular blood transfusion and chelation therapy. Regular blood transfusion is hazardous and painful affair for the child. When the child develops iron over load he is to be treated with chelation therapy. The treatment regime is very costly and beyond the reaches of the common people .The way to prevent the occurrence of the disease is the identification of the carrier and pre marital counselling.

India is a rural based country where 76%of total population reside in rural areas. Screening is done by cell counter and HPLC.Both these methods are very costly. These facilities are available in apex hospitals and district hospitals. This is beyond the reach of the common people. Therefore mass screening cannot be done in such a way. Thus the primary screening should be done by very low cost, easily available methods. These tests are to be done free of cost. The sample is to be collected from the door steps. Those who are primary screening test positive, their samples are to be re tested by cell counter and HPLC.

Thus screening should be done at the level of colleges, schools and different rural areas at the panchayat level. The samples need to be collected from the doorsteps of the public without waiting for them to reach apex centres. The blood samples are to be screened by simple process and finally go for final analysis by cell counter and High Performance Liquid Chromatography(HPLC).

Modified Dichlorophenolindophenol(DCIP) test and Naked Eye Single Tube Osmotic Fragility Test(NESTROFT) are simple screening procedures for thalassemias which can have great importance in Indian senario.

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Research Study :

The purpose of this study is to evaluate a simple screening strategy to detect the carrier of thalassemia and other hemoglobinopathy carrier at community level.

Objective :

To evaluate a simple screening strategy for detection of Thalassemia at the level of rural areas with limited laboratory services.

Materials & Methods :

Blood samples were collected from 309 subjects who were attending the Thalassemia clinic at Burdwan Medical College for extended family screening. The samples were t es ted by us ing combined Dichlorophenolindophenol precipitation test (DCIP) and NESTROFT tests. The final confirmation of the results was done by cell counter and High Performance Liquid Chromatography (HPLC).

Study technique :

(1) DCIP Precipitation test – 20 microlitre of fresh blood collected in EDTA vials was mixed with 2ml of DCIP solution. The mixture is incubated at 37°C for 15 minutes. Test is interpreted as negative or positive by visualisation. Negative sample are clear and positive samples are cloudy.

(2) NESTROFT TEST – 2ml of 0.36% saline in a glass tube was mixed with 20 micro litre of fresh blood collected in EDTA. The contents were mixed by inverting the tube and allowed to stand at room temperature for 30 min. The results were interpreted as positive or negative by visualization of sharp black line on a paper held not more than 1 cm behind the tube.

All 309 cases were evaluated by cell counter and HPLC.

Results and analysis

The results of the combined tests on the blood samples of 309 subjects have been evaluated by reports of cell counter (Hb%, MCV, MCH, RDW) and HLPC (area curve of HbA2, HbF, HbA). The evaluation has been compiled in tables.

Number (%) DCIP NESTROFT

117 (37.86) + +

66 (21.36) - +

12 (3.88) + -

114 (36.89) - -

Table -1 : Table showing distribution of study subjects according to test results. (n=309).

Out of 309 study subjects 117 (37.86%) were positive for both the tests. 66 (21.36%) were only NESTROFT test positive, 12(3.88%) were only DCIP test positive. Thus 114(36.89%) subjects were negative for the tests. Thus, either one or both of the tests were positive in 195 (63%) subjects.

Hb g/dl level +/+ -/+ +/- -/-

6-8 2 2 1 7

>8-10 75 22 5 37

>10 40 42 6 70

Total 117 66 12 114

Table - 2 : Table showing distribution of haemoglobin levels according to test results (DCIP/NESTROFT). (n=309).

The table shows that large number of the carriers have haemoglobin level <10 g/dl. Thus the thalassemic family has high percentage of anemia in comparisons to normal population.

+/+ -/+ +/- -/-

MCV<80fl 96 59 8 11(82%) (89.39%) (66.66) (9.64%)

MVC>80fl 21 7 4 103(17.94%) (10%) (33.33%) (90.35%)

Total 117 66 12 114

Table-3 : The table shows relation between MCV level and test results. (DCIP/NESTROFT). (n=309).

The table shows that majority of thalassemia carriers have MCV levels less than80fl.

MCV levels are less than 80fl in 82% cases who are positive for both the tests.

MCV level less than 80fl in 89.39% subjects who are only NESTROFT test positive.

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MCV level less than 80fl in 66.66% subjects who where only DCIP test positive.

Whereas 90.35% of normal population had MCV levels more than 80fl.

+/+ -/+ +/- -/-

MCH<27pg 100 61 10 50(85.54%) (92.42%) (83.33) (43.85%)

MCH>27pg 17 5 2 64(14.52%) (7.57%) (16.66%) (56.14%)

117 66 12 114

The table shows that majority of thalassemia carriers have MCH levels less than 27pg.

MCH levels are less than 27pg. in 85.54% subjects who were positive for both the tests.

MCV level less than27pg.in 92.42% subjects who were only NESTROFT test positive.

MCV level less than 27pg. in 83.33% subjects who where only DCIP test positive.

Whereas 56% of normal population had MCH levels more than 27pg.

+/+ -/+ +/- -/-

RDW 36 21 8 48(11.5-14.5) (30.76%) (31.81%) (66.66)\%) (42.21%)

RDW 81 45 4 66>14.5 (69%) (68%) (33.33%) (57.89%)

117 66 12 114

The table shows that the percentage of subjects with high RDW (>14.5) are more in those who are

Table - 4 : The table shows relation between MCH level and test results. (DCIP/NESTROFT). (n=309).

Table - 5 : The table shows relation between RDW value and test results. (DCIP/NESTROFT). (n=309).

positive for the combined tests and positive for NESTROFT test. Thus RDW is high in case of thalassemia carriers. Low MCH and high RDW is very much suspicious of hemoglobinopathy.

No. of Subjects No. of Subjects with without Total

Thalassemia Thalassemia

DCIP(+) 129 0 129

DCIP(-) 66 114 180

195 114 309

Sensitivity is 66.15%

Specificity is 100%

Predictive value of positive test is 100%

Predictive value of negative test is 63.33%

No. of Subjects No. of Subjectswith without Total

Thalassemia ThalassemiaCarrier Carrier

NESTROFT(+) 183 0 183

NESTROFT(-) 12 114 126

195 114 309

Sensitivity is 93.84%

Specificity is 100%

Predictive value of positive test is 100%

Predictive value of negative test is 90.47%

It is observed from table no.6 & table no.7 that the sensitivity and Predictive value of negative test are higher for NESTRFOT test than that of DCIP test.

Table - 6 : Results of DCIP test and statistical analysis of data (n=309) After confirmation by HPLC

Table - 7 : Results of NESTROFT test and statistical analysis of data (n=309) After confirmation by HPLC

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Table - 8 : Results of combined tests and statistical analysis of data (n=309) After confirmation of by HPLC.

Combined tests No. of Subjects No. of Subjects with Thalassemia without Thalassemia Total

carrier state carrier state

Both tests or either 195 0 195test positive

Both tests negative 0 114 114

195 114 309

Sensitivity is 100% Specificity is 100% Predictive value of positive test is 100% Predictive value of negative test is 100%

The study had 195 carriers out of 309 screened subjects. All the carriers had either both (NESTROFT and DCIP) tests positive or any one of the tests positive (NESTROFT/DCIP).

Discussion

This study has been done to find out a simple and inexpensive methodology for primary screening of thalassemia carrier in urban and rural areas where the health facilities are limited and also been utilised in vast population survey. The families of thalassemia carrier and wide spectrum of their families are purposely included so that the positivity of the test will be more and the authenticity of the test will be better judged.NESTROFT is positive in thalssemia and thalassemia carriers whereas DCIP is positive in E thalassemia or any unstable hemoglibinopathy. Thus combinations of two tests will help to detect the thalssemia carrier and associated any unstable hemoglobinopathy or carriers.

309 subjects who came from families of thalassemia cases and their relatives of 4th generation have been tested with both NESTROFT and DCIP tests. Then the results have been compared with different aspects of electronic cell counter, like haemoglobin profile, MCV, MCH, RDW followed by subsequent confirmation by HPLC.

Conventionally primary screening for all forms of thalassemia relies on haematological index cut-offs which involves an electronic cell counter. Individuals with MCV less than 80fl needs further investigation to exclude thalassemia disease or carrier. In the present study MCV level less than 80fl in cases of positive NESTROFT is 89.39% whereas in cases of positive DCIP is 66.66%. But in combination tests it is 82%.

There is high positivity of NESTROFT test because this test is positive in any hemoglobinopathy whereas DCIP is positive only in E hemoglobinopathy or any unstable hemoglobinopathy. Thus in present series sensitivity of DCIP test is less.

MCH below 27pg. should be examined further to confirm or exclude the diagnosis of á and â

thalassemia3. In the present study MCH level is less than 27pg. in 92.42% of NESTROFT positive subjects, 83.33% of DCIP positive subjects. But in combination tests it is 85.54%, the combined percentage is less because the positivity of DCIP is less because of the same reasons described before.

In case of hemoglobinopathy RDW is usually more than normal. In the present study, RDW is high in 33.33% of DCIP positive cases, 68% of NOSTROFT positive cases, and 69 % of cases with both tests positive. If any individual has low MCV and high RDW, he always needs thalassemia screening.

In the present study there is high percentage of low MCV and increase value of RDW in case of NESTROFT and combined tests positive subjects but not in case of DCIP positive subjects. It is due higher haemoglobin level and less number of cases in this group.

A simple visual test for the detection of haemoglobin E has been proposed, based on a observation when a blue dye, 2, 6-dichlo ropheno lindophenol (DCIP) was used in testing for red cell enzyme deficiencies4, 5. It was noted that solutions containing haemoglobin E (from patients with either haemoglobin E heterozygosity or homozygosity) became turbid when exposed to this dye. This test has been used in Thailand for antenatal screening in under-resourced areas6, 7, but there are other countries with a high prevalence of haemoglobin E where routine antenatal screening for this variant haemoglobin is not carried out. The test as initially described has been modified and is now available in kit form8.

Microcytic hypochromic red cells of thalassemia trait are more resistant to lysis in 0.36% saline solution than normal normochromic normocytic red cells. This test is called NESTROFT Test. This test is being widely used in India and other developing countries in thalassemia screening programmes9

In a study conducted on 301Thai-Khmer participants, who were screened for thalassemia and HbE using combined OF and modified DCIP tests. Sensitivity, specificity, positive and negative predictive values for the combined tests were 100%, 69.8%, 77.2% and 100%10.

Our study however had higher values for

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specificity and positive predictive values. The rates for sensitivity and specificity in present study are higher because the samples are from the extended family members. It is very good observation that the family with thalssemia is tobe screened before marriage.

Another study was conducted on 587 HbE and 280 reference subjects in a study conducted in Thailand. In this study combined osmotic fragility and modified DCIP tests had sensitivity, specificity, positive and negative predictive values as 99.43%79.29%, 90.03% and 96.67%11.

In the present study DCIP sensitivity is 66.15% specificity is 100%

Predictive value of positive test is 100% predictive value of negative test is 63.33% whereas in case of NESTROT sensitivity is 93.84% specificity is 100%, predictive value of positive test is 100%

Predictive value of negative test is 90.47%.

In case of combined tests sensitivity is 100%, specificity is 100%,

Predictive value of positive test is 100%, predictive value of negative test is 100%. In the present study there is higher percentage of positive value because the subjects are taken from extended thalassemia families.

Conclusion

NESTROFT and DCIP are good preliminary tests for screening of thalassemia carriers. The final confirmation should be done by HPLC.This tes is very and cost effective approach can be done in rural areas and mass screening before going for highly costly HPLC method.

Reference

1. Choudhury V. P, Saxena R, Pari HP. Recent Advances In Hematology 2.India: Jaypee Brothers;2006.page-221-226.

2. Kumar V, Abbas KA, Fausto. N, Aster.CJ, Editors. Robins and Cortan Pathologic Basis of disease. Eighth edition. Philadelphia; Elsevier; 2010. Page 648.

3. Ravindran M, Patel Z, KKhatkhatey M, Dandekar S. â Thalassemia Carrier detection by ELISA: a simple screening strategy for developing countries. J clin Lab Anal. 2005;(191):p.22-25.

4. Frischer H, Carson P E, Bowman J E. et al Visual test for erythrocytic glucose-6-phosphate d e h y d r o g e n a s e , 6 - p h o s p h o g l u c o n i c dehydrogenase, and glutathione reductase deficiencies. J Lab Clin Med 1973. 81613–624.

5. Frischer H, Bowman J, Hemoglobin E. An oxidatively unstable mutation. J Lab Clin Med 1975. 8

6. Wiwanitkit V, Suwansaksri J, Paritpokee N. Combined one-tube osmotic fragility test and dichlorophenol-indolphenol test screening for hemoglobin disorders, an experience in 213 Thai pregnant women. Clin Lab 2002. 48525–528.

7.. Winichagoon P, Thitivichianlert A, Lebnak T. et al Screening for the carriers of thalassemias and abnormal hemoglobins at the community level. Southeast Asian J Trop Med Public Health 2002. 33(suppl)145–150.

8. Fucharoen G, Sanchaisuriya K, Sae-ung N. et al A simplified screening strategy for thalassaemia and haemoglobin E in rural communities in south-east Asia. Bull World Health Organ 2004. 82364–372.

9. SinghT, Atlas and text of hematology.First edition: Avichal publishing company; 2010.p 86.

10. Fucharoen G, Sanchaisuriya K, Sac-ung N, Dangwibul S, Fucharoen S. A simplified screening strategy for thalassemia and haemoglobin E in rural communities in South-East Asea. Bulletin of the World Health Organisation. May 2004; 82 (5): 364 – 72.

11. Prayongratana K, Raungrongmorakot K, Polprasert C, Tatone K,Santiwatanakul S. Low cost combination of DCIP and MCV was better than that of DCIP and OF in the screening for H e m o g l o b i n E . J M e d A s s o c T h a i 2008;91(10):1499-504.

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Prevalence of Neurologic symptoms in children of agricultural workers exposed to organophosphate pesticides in rural India: *Dr Neelam D Sukhsohale, *Dr Prachi R Sawant, **Dr Sanket Pande , ***Dr Sushma Pande

* Dept. of Community Medicine, IGGMC, Nagpur, **Dept. of Pediatrics, MVPS Dr.Vasantrao Pawar Medical College, Nashik, ***Dept. of Physiology, Dr. PDMMC, Amravati. E mail: [email protected]

Key Words: Organophosphate (OP) pesticides, neurological symptoms, children of agriculture workers, rural India.

Abstract

A community based descriptive cross-sectional study was carried out in 100 rural children of agricultural workers in adjoining villages (Khedgaon, Mehunbare, Khedi khurd) of Taluka Chalisgaon, district Jalgaon, Maharashtra. Children were in the age group of 8-15 years and were divided into study group (n=50) exposed to Organophosphate pesticides (OP) and control group (n=50) not exposed to OP pesticides. Various neurological symptoms like muscarinic (diarrhea, urinary incontinence, lacrimation, excessive salivation), nicotinic (tremors, muscle weakness, tachycardia) and general symptoms (headache, insomnia, numbness in legs, fatigue, anorexia, nausea, vomiting, dizziness, lethargy) were assessed by a standard Q 16 questionnaire.

Our observations revealed that high prevalence of muscarinic and general symptoms was found in study group i.e. children exposed to OP pesticides as compared to control group i.e. children not exposed to OP pesticides. On chi square analysis, a statistically significant difference was found between study group and control group for muscarinic and general symptoms (p<0.05). Thus high prevalence of neurologic symptoms found among the children of agricultural workers (exposed to OP pesticides) as compared to unexposed group could be attributed to chronic exposure to OP pesticides.

Introduction

Pesticides are used extensively throughout the world in agriculture and in pest control as well as for community health purposes.

Pesticides are a broad range of substances most commonly used to control

insects, weeds, and fungi (plant diseases). They are frequently classified by target organism or mode of use as insecticides, herbicides, fungicides, or fumigants. Insecticides are often sub-classified by chemical type as organophosphates (OPs), organochlorines, carbamates, and pyrethroids. Individuals are frequently exposed to many different pesticides or mixtures of pesticides,

1either simultaneously or serially.

Organophosphate (OP) pesticide self-poisoning is an important clinical problem in rural regions of the developing world that kills an estimated 200,000 people every year. Unintentional poisoning kills far fewer people but is an apparent problem in places where highly toxic OP pesticides are available. The best-documented health effects involve the nervous system. The neurotoxic consequences of acute high-level pesticide exposure are well established: Exposure is associated with a range of symptoms as well as deficits in neurobehavioral performance and abnormalities in nerve function. Adverse effects of OP pesticides have been reported in most type of pesticides, including organophospate (OP), carbamate, organochlorine, and pyrethroid insecticides, herbicides, fungicides, and fumigants. Acute OP pesticide exposure can involve in wide range of both central and peripheral neurologic symptoms. Increased neurologic symptom prevalence may provide early evidence of neurologic dysfunctions,

2before clinically measurable signs are evident.

Children of agricultural families in rural areas of developing countries like India appear to have a high potential for pesticide exposure, particularly when their parents are engaged in activities such as pesticide mixing, application, and intensive hand labor in treated fields. Pesticide exposure may produce well-defined muscarinic, nicotinic and cholinergic neurosymptoms

3, involving both central and peripheral nervous systems.4 With this background, we performed a comparative

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Research Study :

study of children of agricultural workers exposed to organophosphate pesticides in rural India.

Material and methods

A community based cross-sectional study was carried out in 100 children in the age group 8-15 years [study group (n=50) and control group (n=50)] in the adjoining villages (Khedgaon, Mehunbare, Khedi khurd) of Taluka Chalisgaon, district Jalgaon, Maharashtra.

Selection of study group:

Fifty rural children in the age group of 8-15 years exposed to organophosphate pesticides were included.

Selection of control group:

Fifty rural children in the age group of 8-15 years never involved in pesticide handling (neither outdoor nor indoor) belonging to similar socio-economic strata

Duration of the study: 6 months (April - September 2012).

and have no family history of pesticide exposure were included.

The study was approved by Institutional Ethics Committee IGGMC. After obtaining written informed consent from the parents of children, various neurological symptoms like muscarinic (diarrhea, urinary incontinence, lacrimation, excessive salivation), nicotinic (tremors, muscle weakness, tachycardia) and general symptoms like headache, insomnia, numbness in legs, fatigue, anorexia, nausea, vomiting, dizziness and lethargy were assessed. The questions on the symptoms were based on an established questionnaire Q16 that was used to evaluate the effects of occupational exposure to neurotoxicants

5by Lundberg et al. In addition complete clinical

Exclusion criteria:

1. Children aged < 8 years and > 15 years

2. Children suffering from congenital neurological impairment/ diseases.

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Muscarinic symptoms Study group (n= 50) Control group (n = 50) x2 df p value

Present 22 (44) 10 (20) 6.61 1 *0.01

Absent 28 (56) 40 (80)

Table 1: Distribution of children according to muscarinic symptomsFigures in parentheses indicate percentages.*statistically significant df : degrees of freedom

Nicotinic symptoms Study group (n= 50) Control group (n = 50) x2 df 1 p value

Present 19 (38) 22 (44) 0.37 1 0.54

Absent 31 (62) 28 (56)

Table 2: Distribution of children according to nicotinic symptomsFigures in parentheses indicate percentages.df: degrees of freedom

General symptoms Study group (n= 50) Control group (n = 50) x2 df 1 p value

Present 40 (80) 31 (62) 3.93 1 *0.04

Absent 10 (20) 19 (38)

Table 3: Distribution of children according to general SymptomsFigures in parentheses indicate percentages.*statistically significant df: degrees of freedom

examination including general and systemic examination was done.

Statistical analysis:

Data analyses (differences between categorical variables tested with chi-square test) were conducted by means of statistical software Open Epi Info version 2.3 year 2009. P values less than 0.05 were considered as statistically significant.

Results:

Table 1 shows the distribution of children according to muscarinic symptoms. More number of children from the study group i.e. 22 (44%) suffered from muscarinic symptoms as compared to 10 (20%)

2 from control group. On applying test, the difference between the study and control group was found to be

2 statistically significant ( 6.61 df 1 p<0.05).

As far as nicotinic symptoms are concerned, maximum number of children from control group 22 (44%) had suffered from nicotinic symptoms than study group 19 (38%). The difference between them was not found to be statistically significant (p>0.05) as shown in Table 2.

Table 3 shows the distribution of children according to general symptoms.

Moreover, general symptoms were also found to be significantly more in study group 40 (80%) as compared to 31 (62%) in control group on statistical chi

2 square analysis ( 6.61 df 1 p<0.05). The findings are summarized in Table 3.

Discussion:

In the present study, we compared the children of agricultural workers exposed to organophosphate (OP) pesticide in rural areas. We found the high prevalence of muscarinic and general symptoms in study group exposed to OP pesticides study group as compared to control group. However no significant difference was noted in nicotinic symptoms.

Our study findings conform to the findings of 6-8other investigators.

The important neurologic manifestations in the form of muscarinic, nicotinic and general symptoms may be attributable to the chronic effects of most of the OP pesticides on theperipheral and central nervous

9systems. The pesticide-related neurologic symptoms, muscarinic symptoms observed in this study could be

due to the inhibition of red blood cells, acetyl cholinesterase, as well as plasma butyryl cholinesterase recorded in the study group and reported in earlier

10,11 12studies by the authors. Lotti, observed that the association between OP pesticide exposure and

13neurotoxic effects are well known. Farhat et al also studied the association between pesticide exposure and neurologic endpoints and concluded that environmental and occupational exposure to OP pesticides leads to neurodegenerative functions in agricultural workers. Studies on neurologic symptoms among Sri Lankan farmers showed that 24% of the neurologic symptoms resulted from occupational exposure to AChE-

14inhibiting OP insecticides.

Thus we infer that the knowledge and understanding of neurological symptoms among exposed children of agricultural workers will be useful in creating awareness and imparting knowledge (regarding use of personal protective equipments, improved eye safety, hand washing, balanced diet) among agricultural workers of rural India.

Conclusions

Thus the high prevalence of neurologic symptoms found among the children of agricultural workers (exposed to OP pesticides) as compared to unexposed group could be attributed to chronic exposure to OP pesticides.

Acknowledgement:

Our sincere thanks to Indian Council of Medical Research (ICMR) for approving our project work.

References:

1. Jaga K, Dharmani C. Sources of exposure to and public health implications of organophosphate pesticides. Rev Panam Salud Publica. 2003;14(3):171-85.

2. Rastogi SK, Tripathi S, Ravishankar D. A study of neurological symptoms on exposure to organophosphate pesticides in the children of agricultural workers. Indian Journal of occupational and environmental medicine. 2010;14:54-57.

3. Kamel F, Engel LS, Gladen BC, Hoppin JA,

Future research studies are needed to improve assessment of pesticide exposure in children as well as in adults and consider the role of genetic susceptibility.

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Alavanja MC, Sandler DP. Neurologic symptoms in licensed private pesticide applicators in the Agricultural Health Study. Environ Health Perspect 2005;113:877-82.

4. Kamel F, Hoppin JA. Association of pesticides exposure with neurologic dysfunction and disease . Environ Health Perspect 2004;112:950-8.

5. Lundberg I, Hogberg M. Evaluation of the Q16 questionnaire on neurotoxic symptoms and review of its use. Occup Environ Med. 1997;54:343–350.

6. Gomes J, Lloyd O, Revitt MD, Basha M. Morbidity among farm workers in a desert country in relation to long-term exposure to pesticides. Scand J Work Environ Health 1998;24:213-9.

7. Strong LL, Thompson B, Coronado GD, Griffith WC, Vigoren EM, Islas I. Health symptoms and exposure to organophosphate pesticides in farmworkers. Am J Ind Med 2004;46:599-606.

8. Bazylewicz-Walczak B, Majczakowa W, Szymczak M. Behavioural effects of occupational exposure to organophosphorus pesticides in female greenhouse planting workers. Neurotoxicology 1999;20:819-26.

9. Savitz DA, Sonnenfeld NL, Olshan AF. Review of epidemiologic studies of paternal occupational exposure and spontaneous abortions. Am J Ind Med. 1994;25:361–83.

10. Rastogi SK, Singh VK, Kesavachandran C, Jyoti, Siddiqui MK, Mathur N, et al. Monitoring of plasma butyrylcholinesterase activity and hematological parameters in pesticide sprayers. Indian J Occup Environ Med. 2008;12:29–32.

11. Rastogi SK, Satyanarayna PV, Ravishanker D, Tripathi S. A study on oxidative stress and anti-oxidant status of agricultural workers exposed to organophosphate insecticides during spraying. Indian J Occup Environ Med. 2009;13:131–4.

12. Lo t t i M. Expe r imen ta l and c l in i ca l neurotoxicology. New York:Oxford University Press;2000.p.911-8.

13. Farhat TM, Abdelrasoul GM, Amir MM, Shebi MM, Farhat FM, anger WK. Neurobehavioural effects among workers occupationally exposed to organophosphorus pesticides. Occup Environ Med 2003;60:279-86.

14. Peiris-John RJ, Ruberu DK, Wickremasinghe AR, Smit LA, vander Hoek W. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. J Occup Environ Med 2002;44:352-7.

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Case Report :Ultrasound Signs of Hydatid Liver Cyst: Dr Maunil Bhuta, Dr.Vivek Ukirde, Dr.Kishor Rajpal, Dr.Ajita Nawale

Department of Radio-Diagnosis, L.T.M.M.C and L.T.M.G.H, Sion, Mumbaie-mail: [email protected]

Keywords : Hydatid disease, Ultrasonography Findings , Double membrane sign, Hydatid sand, Floating membrane sign, Water lily sign, Snowstorm sign, Wheel spoke sign

Introduction :

Hydatid disease is a worldwide zoonosis produced by the larval stage of the Echinococcus tapeworm. The two main types of hydatid disease are caused by E granulosus and E multilocularis. The former is the most frequently encountered type of hydatid disease in human.

Organism Definitive Hosts Intermediate Hosts

E. granulosus dogs and sheep, goats,swine,other canidae kangaroos, and

other wild herbivores

E. multilocularis foxes, dogs, other small rodentscanidae and cats

E. vogeli bush dogs and dogs rodents

E. oligarthus wild felids small rodents

Case History:

A female patient, presented to the surgery O.P.D. with complaints of pain in the right hypochondrium with few episodes of mild fever since 2 months. The pain was not responding to analgesics and antacids. The patient was advised to get an ultrasonography of the abdomen.

Ultrasonography Findings:

The USG revealed presence of a well-defined hypo-echoic lesion in the liver. The lesion showed presence of a well-defined double membrane (1) with echogenic debris (2) within. There were also few similar but smaller anechoic cystic lesions adhered to the inner aspect of the wall of the lesion (3). Few crumpled hyper-echoic structures are also noted in the lesion (4).

On correlation with the USG findings and clinical history, the diagnosis of Hydatid Liver Cyst was made.

Patho-physiology of Hydatid Liver Cyst:

The life cycle of Echinococcus granulosus involves two hosts. The definitive host is usually a dog but may be some other carnivore. The adult worm of the parasite lives in the proximal small bowel of the definitive host, attached by hooklets to the mucosa. Eggs are released into the host's intestine and excreted in the feces.

Sheep are the most common intermediate hosts. They ingest the ovum while grazing on contaminated ground. The ovum loses its protective chitinous layer as it is digested in the duodenum. The released hexacanth embryo, or oncosphere, passes through the intestinal wall into the portal circulation and develops into a cyst within the liver.

When the definitive host eats the viscera of the intermediate host, the cycle is completed. Humans may become intermediate hosts through contact with a definitive host (usually a domesticated dog) or ingestion of contaminated water or vegetables.

Once in the human liver, cysts grow to 1 cm during the first 6 months and 2–3 cm annually thereafter depending on host tissue resistance.

Ultrasound signs of Hydatid Liver Cyst:

The ultra-sonographic (US) appearance of hydatid cysts may vary. Several classification schemes based on cyst appearance have been proposed. The cyst wall usually manifests as double echogenic lines separated by a hypo-echogenic layer which is the “double membrane sign”. Simple cysts do not demonstrate internal structures, although multiple echogenic foci due to hydatid sand may be seen within

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the lesion by repositioning the patient. The echogenic foci quickly fall to the most dependent portion of the cavity without forming visible strata. This finding has been referred to as the “snowstorm sign”.

Detachment of the endocyst from the pericyst is probably related to decreasing intracystic pressure, degeneration, host response, trauma, or response to therapy. The cyst may appear as a well-defined fluid collection with a localized split in the wall and “floating membranes” inside the cavity. Complete detachment of the membranes inside the cyst has been referred to as the USG “water lily sign” because of its resemblance to the radiographic water lily sign in pulmonary cysts. USG is the most sensitive modality for the detection of membranes, septa, and hydatid sand within the cyst.

Multi-vesicular cysts manifest as well-defined fluid collections in a honeycomb pattern with multiple septa representing the walls of the daughter cysts. “Daughter cysts” appear as cysts within a cyst. When daughter cysts are separated by the hydatid matrix (a material with mixed echogenicity), they demonstrate a “wheel spoke” pattern. The matrix represents hydatid fluid containing membranes of broken daughter vesicles, scolices, and “hydatid sand”. Membranes may appear within the matrix as serpentine linear structures, a finding that is highly specific for hydatid disease.

When the matrix fills the cyst completely, a

mixed echogenic pattern is created that mimics a solid mass. Because differentiation of this lesion from other hepatic masses or abscesses is usually difficult, it is important to look for daughter vesicles or membranes within the lesion that may help in making a correct diagnosis.

Cyst calcification usually occurs in the cyst wall, although internal calcification in the matrix may also be seen. USG demonstrates a hyper-echoic contour with a cone-shaped acoustic shadow. When the cyst wall is heavily calcified, only the anterior portion of the wall is visualized and appears as a thick arch with a posterior concavity. As stated earlier, partial calcification of the cyst does not always indicate the death of the parasite; nevertheless, densely calcified cysts may be assumed to be inactive.

USG signs of Hydatid Liver Cyst:

Double membrane sign

Hydatid sand

Daughter cysts

Floating membrane sign

Water lily sign

Snowstorm sign

Wheel spoke sign

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1) DOUBLE MEMBRANE SIGN

2) HYDATID SAND

3) DAUGHTER CYSTS

4) FLOATING MEMBRANE SIGN

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Management of Hydatid Liver Cyst:

For simple cases of hepatic echinococcosis, the most common form of treatment is surgical removal of the cysts combined with chemotherapy using albendazole and/or mebendazole before and after surgery. However, if there are cysts in multiple organs or tissues, or the cysts are in risky locations, surgery becomes impractical. For inoperable cases such as these, chemotherapy and/or PAIR (puncture-aspiration-injection-reaspiration) become alternative options of treatment. In the case of alternative treatment using just chemotherapy, albendazole is preferred with an adult dosage of 400 mg orally, twice a day for 1–5 months and a pediatric dosage of 15 mg/kg/day (max. of 800 mg) for 1–6 months. An alternative to albendazole is mebendazole at a dosage of 40 to 50 mg/kg/day for at least 3 to 6 months. The other alternative to surgery is PAIR with chemotherapy. PAIR is a minimally invasive procedure that involves three steps: puncture and needle aspiration of the cyst, injection of a scolicidal solution for 20-30 min, and cyst-re-aspiration and final

irrigation. Patients who undergo PAIR typically take albendazole or mebendazole from 7 days before the procedure until 28 days after the procedure. While surgery still remains as the standard for cystic echinococcosis treatment, there have been a number of studies that suggest that PAIR with chemotherapy is more effective than surgery in terms of disease

]recurrence, and morbidity and mortality. In addition to the three abovementioned treatments, there is currently research and studies looking at new treatment involving percutaneous thermal ablation (PTA) of the germinal layer in the cyst by means of a radiofrequency ablation device. This form of treatment is still relatively new and requires much more testing before being widely used. Another treatment that is also currently being looked into is laparoscropy hydatid liver surgery, whose efficacy is still controversial even though studies have suggested that it has clear benefits.

Note: This is a case from adult patient, but similar findings can be observed or seen in children also.

5) WATER LILY SIGN 6) SNOW-STORM SIGN

REFERENCES :

1) Hydatid liver disease. Jean-Luc Jourdan, M.D. and David L Morris, M.D..

2) www.ncbi.nlm.nih.gov › NCBI › Literature

3) Tappe, Dennis, August Stich, and Matthias Frosch. "Emergence of Polycystic Neotropical Echinococcosis." Emerging Infectious Disease 14.2 (2008): 292-97. Web. 21 February 2010.

4) Singh M, "Anaphylactic Shock After Traumatic Rupture of a Splenic Echinococcal Cyst." Harefuah 122.4 (1992): 226-28. Web. 24 February 2010.

5) Sharma, Deborshi, "Laparoscopy for Liver Hydatid Disease: Where Do We Stand Today?" Surgical Laparoscopy, Endoscopy & Percutaneous Techniques 19.6 (2009): 419-23. Web. 23 February 2010.

6) Mandell, Gerald L. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 7th ed. Philadelphia, PA: Elsevier Inc., 2010. Ch. 290. Print.

7) Budke, Christine M., Peter Deplazes, and Paul R. Torgerson. “Global Socioeconomic Impact of Cystic Echinococcosis.” Emerging Infectious Disease (2006). Web. 15 February 2010

8) Images & Diagrams : Department of Radio-Diagnosis , Division of Ultrasonography , LTMMC and LTMGH , Sion , Mumbai - 12 and Vanders textbook on hydatid.

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Pic -1 : Puncture aspiration injection re-aspiration

Pic -2 : Post - op specimen of hydatid liver cyst

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Case Report :Aplasia Cutis Congenita *Dr Shaifali Patil, **Dr. Nimain Mohanty, *Dr. Vidhya Kamble, *Dr. Mugdha Bhamre

*Dept of Obstetrics & Gynecology and ** Dept of Pediatrics, MGM Medical College Hospital for Women and Children, Kalamboli, Navi Mumbai, e-mail: [email protected]

Keywords : Aplasia cutis congenita

Abstract

Aplasia cutis congenita is characterized by and diagnosed at birth by simple observation of a clean, sharply demarcated, and non-inflammatory lesion of an

1area of skin similar to the lesion described in our case.

We describe a neonate with this uncommon disease born to a 27 year old G P L A with 38 weeks of 3 1 1 1

gestation diagnosed with oligohydramnios and gestational hypertension.In prenatal visits and investigations it remained undiagnosed during routine ANC care and TVS scan but was identified postnatally after a caesarean section.

It occurs most often sporadically though 2

autosomal recessive and dominant inheritance .The etiology is uncertain but suggested hypotheses include ectodermal arrest during embryogenesis, vascular anomalies in the fetus, intrauterine trauma, amniotic bands and hereditary factors. The reported incidence is one in 10,000 births. The most common cause of Aplasia Cutis Congenita is the teratogenic effects of antithyroid drugs taken in first trimester of gestation, it was reported.

3Frieden has classified aplasia cutis into nine

types.It is also associated with various syndromes and congenital anomalies which accounts for the poor prognosis. But in this case no such anomalies or syndromes were identified. The neonate succumbed on post operative day 15 due to sepsis.

Introduction

Aplasia cutis congenita (ACC) is a rare, etiologically heterogeneous condition characterized by congenital absence of skin and encompasses a spectrum of subtypes where either localized or widespread areas of skin are affected. The condition is rare with scalp ACC affecting 0.03% of the newborns . The lesion is

solitary in 75% of cases, most commonly located at the parietal hair whorl. Only 8% of those lesions have associated congenital defects.

Heredity has been predominantly autosomal dominant, but recessive inheritance has also been implicated. Although the majority of these scalp defects occur sporadically, many familial cases have been reported.

Etiology :

Genet ic causes include chromosomal aberrations,namely trisomy 13 and deletion (4p) syndromes and single gene mutations such as Goltz syndrome.Other syndromes include Adams-Oliver syndrome, Setleis syndrome, Anderson-Hollister-Szalay syndrome, Johanson-Blizzard syndrome and a familial syndrome of 46,XY gonadal dysgenesis with multiple anomalies. Also teratogenic causes include intrauterine infection (i.e., VZV, HSV), fetal exposure to drugs of abuse (i.e. cocaine, heroin, marijuana, alcohol), or the antithyroid drugs.

Several classification systems for ACC have been 3

proposed. In 1986, Frieden categorized ACC by presence or absence of associated anomalies , the location and number of lesions. There are 9 sub-types .

Case history

A 27 year old lady ,a G P L A with 38 weeks of 3 1 1 1

gestation reported with complaints of pain in abdomen since one hour with no other associated complaints.

She has a history of D & C 4 years back i/v/o spontaneous abortion. She underwent LSCS three years back for breech presentation when she delivered a female child with no congenital abnormalities.

In present pregnancy, she was registered with at 26 weeks of her gestation. She bared a USG of 18 weeks and had no anomaly scan.

On examination , her general condition was

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fair,with pulse of 84/min and BP of 140/104 mm of hg. She had facial puffiness with bilateral pedal oedema grade III.

On per abdomen examination, her uterine size was full term with cephalic presentation and longitudinal lie. Pfannensteil's scar of previous LSCS was present. Scar tenderness was not elicited.

On per speculum examination ,nitrazine test was negative.

On per vaginal examination, cervix was mid-posterior and closed.

Her blood investigations revealed Hb of 9 g/dL and other blood counts being normal. Her urine report showed trace albumin. Her LFT, RFT, coagulation profile were within normal limits.

Her USG revealed SLIUG of 38 weeks with oligohydramnios with AFI of 2.5cm. Also USG obs-doppler showed normal study.

She was posted for LSCS i/v/o severe oligohydramnios and a female child of 2.1kg was born. The baby had clean and sharply demarcated non-inflammatory lesions on lower extremities extending

from mid thigh to feet and also on flexor aspect of left wrist.

Aplasia cutis congenita (ACC) type-6 is characterized by epidermolysis bullosa (EB) in

4,5association with aplasia of skin .This condition may be associated with other malformations like low set abnormal ears, duodenal atresia, trachea-esophageal fistula, large fontanelle, narrow palpebral fissures, micrognathia, cleft palate, hypoplasia of nose, joint contractures, rocker bottom feet, genito-urinary malformations which were not diagnosed in this case.

The present case did not have any bullae at birth but features like dystrophy of nails, positive Nikolsky's sign suggests the diagnosis of epidermolysis bullosa causing intrauterine blistering and a presentation like aplasia cutis. Bullae started appearing later which resulted in extensive lesions. It led to the sepsis and subsequently loss of the baby.

Membranous, also known as bullous ACC is a subtype of ACC that is distinguishable from non-membranous ACC by its sharp borders and scaly

6surfaces .This distinction is useful because unlike non-membranous ACC, membranous ACC does not have a

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Type Sites Transmission Associated malformations

Type 1 Scalp(Usually vertex) Autosomal dominant Nil

Type 2 Scalp(usually midline) Autosomal dominant Limb reduction anomalies

Type 3 Scalp Sporadic Epidermal naevi(asymmetrical)

Type 4 Any Sporadic /multifactorial Gastro intestinal (omphalocele, gastroschisis), CNS(encephalocele, spinal dysmorphism, prosencephaly)

Type 5 Limbs / trunk Unknown Twin pregnancy; Other sibling usually fetuspapyraceous.

Type 6 Extremities Autosomal recessive Duoenal/pyloric atresia , narrow palpebral fissures,or dominant nasal hypoplasia, low set ears, micrognathia,

syndactyly, hypoplastic nails, overlapping of fingers, simian crease

Type 7 Scalp/ limbs/trunk Sporadic Methimazole induced

Type 8 Linear unilateral Sporadic Due to herpes/varicella infection

Type 9 Scalp Sporadic/ Autosomal Trisomy 13,4 p-syndrome

TABLE 1 - Classification and Salient Features of Aplasia Cutis

familial inheritance pattern and is unlikely to be associated with other non-neuroectodermal anomalies. Membranous ACC has been reported in association with other dermatologic lesions, hydrocephalus, and

7holoprosencephaly .

Approximately 20 case reports of membranous ACC are available in the literature. In a review of 17 cases, 5 were associated with additional skin lesions, including alopecia, nevi, hemangiomas and port wine stains.

Four cases were complicated by hydrocephalus, 8and 1 case had a large meningeal arteriovenous fistula .

The epithelial covering of membranous ACC histologically resembles that of encepholoceles and meningoceles, driving the hypothesis that membranous

6ACC is a mild form of a neuroectodermal defect .

The recognition of ACC on prenatal sonography should prompt a careful family history (ie, autosomal dominant inheritance) and pregnancy history (ie, teratogens including HSV, VZV & exposure to methimazole or valproic acid). In addition, detailed sonography must be done to exclude associated major fetal anomalies and complications of the placenta and

membranes including placental infarcts, amniotic bands, and fetus papyraceous, which have also been associated with certain types of ACC.

In most cases, when in isolation, ACC is a benign condition of only minor cosmetic importance. Further imaging of the fetal brain by MRI is useful for evaluation of underlying cranial defects and to exclude the possibility of an encephalocele.

9Cambiaghi et al provided the only previous case report of membranous ACC visualized on prenatal sonography. The lesion was visualized sonographically in the antepartum period, and ACC was diagnosed clinically in the neonate. Membranous ACC has yet to be diagnosed prenatally. The prenatal sonograms

9presented by Cambiaghi et al , suggesting that a prenatal diagnosis of membranous ACC should be strongly considered when such a lesion is visualized on prenatal sonography. The lesion can be recognized as a smooth cystic lesion isolated to the scalp without Doppler flow or underlying cerebral abnormalities.

References:

1. Campbell W. Case of congenital ulcer on the

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Pic 1 : iscussion

cranium of a fetus terminating in fatal hemorrhage, on 18th day after birth. Edinb J Med Sci 1826; 2:82–84

.

3. Frieden IJ. Aplasia cutis congenita: a clinical review and proposal for classification. J Am Acad Dermatol 1986;14:646–660.

2. Levin DL, Nolan KS, Esterly NB. Congenital absence of skin. J Am Acad Dermatol 1980; 2: 203-206

4. McCarthy MA, Clarke T, Powell FC. Epidermolysis bullosa and aplasia cutis. Int J Derm 1991; 30: 481-484.

5. Atherton DJ, Naewi and other developmental defects. In: Rook/ Wilkison/Ebling Textbook of Dermatology, Vol. 1 Eds. Champion RH, Burton JL, Ebling FJG. London, Blackweli Scientific Publication, 1992, pp 518-524.

6. Drolet B, Prendiville J, Golden J, Enjolras O, Esterly NB.“Membranous aplasia cutis” with hair collars: congenital absence of skin or neuroectodermal defect? Arch Dermatol1995; 131:1427–1431.

7. Tiang MM, Lau BH, Lee TX, Ling MI. Holoprosencephaly presenting as membranous aplasia cutis and diabetes insipidus: report of one case. Acta Paediatr Taiwan 2004;45:181–183.

8. Colon-Fontanez F, Fallon Friedlander S, Newbury R,Eichenfield LF. Bullous aplasia cutis congenita. J Am Acad Dermatol 2003; 48(suppl):S95–S98.

9. Cambiaghi S, Gelmetti C, Nicolini U. Prenatal findings in membranous aplasia cutis. J Am Acad Dermatol 1998;39:638–640.

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Case Report :Collodion babyDr K. Sunilbala, Dr Amita M, Dr Abhijit Datta, Dr Raghavendra P, Dr. Mrinal Das, Dr Prof. L. Ranbir Singh

Department of Pediatrics, Regional Institute of Medical Sciences, Imphal, Manipur, India E-mail: [email protected]

Key words : Collodion, ectropion, ichthyosiform erythroderma

Abstract

Collodion baby is a rare manifestation of nonbullous congenital ichthyosiform erythroderma (NBCIE) or lamellar icthyosis. We report here one such

rdcase in a full term, male baby born to a 3 gravid mother with no history of consanguinity and no family history of congenital anomalies. At birth, the baby was covered by a shiny, tight membrane all over the body. He had weak neonatal reflexes, fed poorly, had ectropion of the upper eyelids, flattening of the ears and nose, eversion of upper lips and fixed, semiflexed attitude of limbs. The baby was managed conservatively and discharged in a stable condition after two weeks of uneventful stay in the hospital and was doing well at follow up.

Introduction

Collodion baby is usually a manifestation of nonbullous congenital ichthyosiform erythroderma or lamellar icthyosis. It is very difficult to predict the prognosis of the underlying ichthyoses phenotype at birth. Skin biopsy at birth will not help in distinguishing the different conditions leading to development of collodion membrane. Observation over a period of time

1will reveal the ultimate fate of the skin.

Case Report :

A male baby, weighing 3 kg, born to a 27-year-old rd 3 gravida mother at term gestation following

uneventful vaginal delivery was immediately admitted in pediatric ward for abnormal appearance of skin. There was no history of consanguinity and family history was unremarkable.

On examination, the baby was covered by a shiny, tight membrane resembling oiled parchment or collodion [Figure 1]. The baby had weak neonatal reflexes, fed poorly, had ectropion, flattening of the ears

and nose, and lips were also everted giving a fish mouth configuration. He was also having fixed, semiflexed attitude of limbs due to limited range of motion in all joints because of the taut collodion membrane. The hair was sparse. No other associated congenital anomalies could be detected. Systemic examination was essentially unremarkable.

The baby was placed in an incubator and nasogastric feeding with expressed breast milk was started. It was supplemented with parenteral fluid assuming high transcutaneous fluid loss and a 7 day course of IV antibiotics was given prophylactically. Emollient cream in the form of liquid paraffin was applied all over the body 3-4 h. Lubricating eye drops and antibiotic eye ointment were also administered to keep cornea moist and to prevent infection of the eyes. During 2nd week, shedding of the membrane started and was completed after two weeks revealing normal raw skin underneath. On day 18, the patient was discharged in a stable condition . On follow up at 3 months, the baby was found to have normal skin and he was gaining weight and had normal development.

Discussion

Collodion baby is a rare congenital disorder. The frequency is estimated to be 1:300,000 newborns

2worldwide. It appears to be one phenotype for several

3 genotypes. Due to mechanical compression, features of the face and extremities in such babies may be distorted. The membrane in such collodion babies cracks with initial respiratory efforts and shortly after birth begins to desquamate in large sheets. Complete shedding may take several weeks and a new membrane may

3occasionally form in localized areas.

Approximately 75% of collodion babies will go on to develop a type of autosomal recessive congenital ichthyosis, either lamellar ichthyosis or congenital

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4ichthyosiform erythrodema.

In another 10% of cases the baby sheds this layer 2of skin and has normal skin for the rest of its life. This is

known as self-healing collodion baby. The remaining 15% of cases could stem from variety of diseases involving keratinization disorders like Harlequin fetus, ichthyosis vulgaris, X-linked ichthyosis, Sjogren-

5 Larsson syndrome, Netherton syndrome. In our case, as the skin was normal on follow up at 3 months we feel that our case belongs to self healing collodion baby. Extracutaneous symptoms of such disorder could be helpful for diagnosis. Neonatal complications can occur in 45% of all collodion babies leading to a mortality rate

2of approximately 11% in the first few weeks of life. Neonatal morbidity and deaths may be due to cutaneous infection, aspiration pneumonia, hypothermia or hypernatremic dehydration from excessive transcutaneous fluid losses as a result of increased skin permeability. Constrictive bands in extremity can result

7,8in vascular compromise and edema.

The management of such babies is a challenging task. Transcutaneous water loss in such babies may be 6-7 times more than normal skin. Placement of the baby in

humidified incubator with prophylactic antibiotics and emollients will help to reduce mortality in such babies. Application of non-occlusive lubricants may facilitate shedding of the membrane. Urea containing agents should be avoided, as there may be toxicity due to

1,9absorption of urea.

References

1. Akiyama M, Sawamura D, Shimizu H. The clinical spectrum of nonbullous congenital ichthyosiformerythroderma and lamellar ichthyosis. ClinExpDermatol 2003;28:235-40.

2. Van Gysel D, Lijnen RL, Moekti SS, de Laat PCJ, Oranjet AP. Collodion baby: a follow-up study of 17 cases. J Eur Acad DermVenereol 2002; 16:472-75

3. Judge MR. Collodion baby and harlequin ichthyosis. In: Harper J, Oranje A, Prose N,

ndeditors. Textbook of Pediatric Dermatology. 2 ed. USA: Blackwell, Malden, Mass; 2006. p. 118-25.

4. Dermatology at the Millennium, By Delwyn Dyall-Smith, Robin Marks, Page 586, Published by Informa Health Care, 1999, ISBN 1-85070-005-2

5. Taïeb A, Labrèze C. "Collodion baby: what's new". J Eur Acad Dermatol Venereol 2002; 16: 436–7

6. Larregue M, Bressieux JM, Fournet JP. Collodion baby. Mod ProblPaediatr 1976;20:40-9.

7. Roberts JB, Adelson D. Case report: Prolonged collodion membrane causing constrictive bands of the digits and treatment. Dermatol Online J 2010;16:15.

8. Sandler B, Hashimoto K. Collodion baby and lamellar ichthyosis. J CutanPathol 1998;25:116-21.

9. Buyse L, Graves C, Marks R, Wijeyesekera K, Alfaham M, Finlay AY. Collodion baby dehydration: The danger of high transepidermal water loss. Br J Dermatol 1993;129:86-8.

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Pic.1: Showing collodion baby with everted eyelid.

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Media Watch / Around the World : *Dr Anil Lohar, **Dr Satish Agrawal

* Senior Resident, Dr.PDMMC Amravati. ** Practicing Pediatrician, Amravati.E-mail : [email protected]

Role of Bottle Feeding in the Etiology of Hypertrophic Pyloric Stenosis

Hypertrophic pyloric stenosis (HPS) is an idiopathic thickening of the circular smooth muscle layer of the pylorus typically occurring within the first several weeks of life. Despite the frequency with which HPS occurs, its etiology remains unknown. It is known to be more common among firstborns, males, and white individuals, and although most cases are sporadic, the disease tends to cluster in families. The biological factors driving these patterns, however, remain elusive.

Because of its almost exclusive occurrence within the first 2 months of life, early environmental exposures have been a natural focus of inquiry. Bottle feeding has been implicated in the etiology of hypertrophic pyloric stenosis (HPS).

Population-based case-control study of births from January 1, 2003, to December 31, 2009, using Washington State birth certificates linked to hospital discharge data. Cases included all singleton infants born within the study period and subsequently admitted with both a diagnostic code for HPS and a procedure code for pyloromyotomy (n?=?714). Controls were randomly chosen among singleton infants who did not develop HPS and were frequency matched to cases by birth year. Feeding status (breast vs bottle) was coded on the birth certificate as the type of feeding the infant was receiving at birth discharge.

Main Outcome and Measure is Diagnosis of HPS. Results are Hypertrophic pyloric stenosis incidence decreased over time, from 14 per 10?000 births in 2003 to 9 per 10?000 in 2009. Simultaneously, breastfeeding prevalence increased from 80% in 2003 to 94% in 2009. Compared with controls, cases were more likely to be bottle feeding after birth (19.5% vs 9.1%). After adjustment, bottle feeding was associated with an increased risk of HPS (odds ratio [OR], 2.31; 95% CI, 1.81-2.95). This association did not differ according to

sex or maternal smoking status but was significantly modified by maternal age (<20 years OR, 0.98; 95% CI,

0.51-1.88; ≥35 years OR, 6.07; 95% CI, 2.81-13.10) and parity (nulliparous OR, 1.60; 95% CI, 1.07-2.38; multiparous OR, 3.42; 95% CI, 2.23-5.24).

Conclusions is bottle feeding is associated with an increased risk of HPS, and this effect seems to be most important in older and multiparous women. These data suggest that bottle feeding may play a role in HPS etiology.

Source : JAMA Pediatr. 2013;167(12):1143-1149

Comments : Further investigations required to elucidate the mechanisms underlying the observed effect modification by age and parity.

Sleep Inducing for EEG Recording in Children: A Comparison between Oral Midazolam and Chloral Hydrate

Performing procedures in children are difficult due to no cooperation and fear of procedures. Therefore, sedation and sleep are frequently induced using some agents as pre procedure medication in children. Electroencephalography (EEG) recording is a long duration procedure and needs patient cooperation for device setup and performing the procedure. Because of long duration of the EEG recording, many children lose their cooperation and begin to move or cry during the procedure and due to lack of cooperation, EEGs are recorded poorly and are difficult to interpret by neurophysiologists.

This study aimed to compare the sedative effects of oral midazolam versus chloral hydrate before the procedure along with their impacts on EEG recording in children.

Chloral hydrate is a sedative and hypnotic medication. Chloral hydrate has two active metabolite, Trichloroethanol (TCE) and Trichloroacetic acid

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(TCA). By an unknown mechanism, TCE exerts sedative and hypnotic effects of chloral hydrate on the CNS. Midazolam is a sedative, hypnotic, and anticonvulsant agent, which has been used as a pre medication agent in many procedures in children (5-10). Recently, oral solution of this medication has been available in Iran , and anecdotal reports have proposed its efficacy as a pre medication in intubation and endoscopy. However, to the best of our knowledge, no study has yet been performed to show the superiority of oral midazolam as a pre medication for EEG recording in children. Therefore, they have carried out a randomized trial to compare the sedative effects of oral midazolam versus chloral hydrate and their impacts on EEG recording in children.

This study was conducted between May 2010 and May 2011 in a major University Paediatric Hospital in Tehran, Iran. they enrolled children aged between one month and ten years who were referred for EEG recording and were uncooperative with the device setup or were referred to our center for sleep EEG recording, We excluded children if they had hypersensitivity to midazolam or chloral hydrate, hepatic disease, peptic ulcer, respiratory disease or received medications that had dangerous interactions with midazolam or chloral hydrate. 198 Consecutive patients were enrolled and randomly assigned to receive either oral moidazolam (midazolam group, n=100) or chloral hydrate (chloral group, n=98). Parents were asked to awaken their children at 6.00 am and not to let them fall asleep until the time of EEG recording.

Midazolam was given at a dose of 0.5 mg/kg and Chloral hydrate 5% was given at a dose of one ml/kg of

body weight orally, one hour before EEG recording.

A trained staff filled out a questionnaire for each patient to collect the following data: neurological diagnosis, sleep onset latency, sleep duration, drowsiness time, and adverse events that occurred in the first 24 h after EEG recording. They used an analogue EEG machine (Nihon Kohden) in our center for EEG recording, and EEG was recorded using 21 scalp electrodes based on the standard international 10 20 system. A trained and skilled child neurophysiologist interpreted the recorded EEGs.

The midazolam group consisted of 47 boys and 53 girls, with the median age of 4 years and a range from 2 month to 9 years. The chloral hydrate group consisted of 48 boys and 50 girls with the median age of 4 years with a range of 3 months to 10 years. In the midazolam group, 80 children were referred for EEG recording due to seizure disorders, 15 because of developmental delay, and five due to autistic feature. In the chloral hydrate group, 79 children were referred for EEG recording due to seizure disorders, 13 for developmental delay, and six due to autism. No significant difference was seen between two groups concerning referral etiologies (x2 = 0.22, df=2; p=0.896).

The results of this study showed that both chloral hydrate 5% (one ml/kg) and oral midazolam (0.5 mg/kg) could be administered as a pre medication agent for EEG recording in children. However, oral midazolam at this dose had no advantage compared with chloral hydrate.

Source : Iran J Child Neurol. 2013 winter;7(1):15-19

Comment : Further studies are required with large number of patients to reach the conclusion.

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Table : Sleep Characteristics Between Groups of Chloral Hydrate and Oral Midazolam

Sleep p- Sleep p- Drowsiness p-onset value duration value time valuelatency a b a b a b

Chloral Midazolam Chloral Midazolam Chloral Midazolamhydrate range hydrate range hydrate rangerange (median) range (median) range (median)(median) (median) (median)

20-95 45-98 (58) <0.001 56-98 12-38 <0.001 21-36 2-9 <0.001(32) (66.5) (25.5) (32) (6)

a : Values are expressed in minutes b : P-value using Mann-Whitney U test

Vitamin D status in diabetic Egyptian children and adolescents: a case–control study

Type 1 (insulin-dependent) diabetes mellitus (T1DM) is an auto immune disease that results in the destruction of beta cells in the pancreas as a result of interactions between different susceptibility genes and environmental exposures .

Peak incidence occurs around puberty, and the disease is usually diagnosed before age 30. It is estimated that, by the time the DM1 is diagnosed, 80–90% of the beta cells are lost .

Recent studies suggest that vitamin D deficiency may increase the risk of developing autoimmune diseases including type 1 diabetes (T1DM) . This occurs partly through loss of vitamin D modulation of the immune and inflammatory reaction in diabetes .

At the level of the immune system, 1, 25(OH) D 2 3

inhibits the differentiation and maturation of dendritic cells and promotes their apoptosis , thus preventing their transformation into antigen presenting cells which is the first step in the initiation of an immune response.

Before conducting a clinical trial of supplementing patients with T1DM, it is required to assess the existing status. In this study, aim was to estimate vitamin D status in Egyptian children and adolescents with T1DM.

This was a case control study performed in Zagazig University hospital from January to December 2012. The study included 80 children and adolescents diagnosed as T1DM cases (34 males and 46 females) while attending Pediatric outpatient endocrine clinic in Zagazig University Hospital. The age of the patients ranged from 6 to 16 years (mean, 11.4 years). Forty healthy children of comparable age and gender served as a control group. Subjects were excluded from the study if they had consumed cholecalciferol, calcium, multi-vitamin or mineral supplementation, vitamin D-fortified foods during the previous 3 months, or any medical co-morbidities or any other major chronic disease.

All patients and controls included were subjected to proper history taking, thorough clinical examination, including anthropometric measurements (weight, height and BMI).

For all subjects, serum 25 (OH) D levels were measured by ELISA, Serum parathyroid hormone

(PTH) and serum insulin were measured by an electrochemiluminesce immunoassay. Serum glucose, Glycosylated hemoglobin (HbA1c) levels and homeostasis model assessment of insulin resistance (HOMA-IR) were also assessed.

SPSS version 19 was used for data analysis. The data are expressed as the mean?±?SD or median (min-max) where appropriate.

Compared to the control group, serum vitamin D levels were not significantly lower in diabetic subjects (24.7?±?5.6 vs 26.5?±?4.8 ng/ml; P?>?0.05). Among diabetic cases 44(55%) were vitamin D deficient; meanwhile 36(45%) cases had normal vitamin D level (P?<?0.01). In addition, 26(32.5%) diabetic cases had secondary hyperparathyroidism and 54(67.5%) cases had normal parathyroid hormone level; meanwhile, none of the control group had 2ry hyperparathyroidism (P?<?0.01). Furthermore, we found a significant difference between vitamin D deficient diabetic cases and those with normal vitamin D level as regards HOMA-IR and diabetes duration (P?<?0.01).

Source : Italian Journal of Pediatrics 2013, 39:73 doi:10.1186/1824-7288-39-73

Comment : Health message on the importance of vitamin D status; especially in diabetic children and adolescents, should be disseminated to the public.

Background changing patterns of neonatal fungal sepsis in a developing country

Fungal sepsis (FS) is an important problem in sick newborn infants, with a mortality rate between 21% and 76% . FS should be suspected in the critically ill neonate with negative blood cultures . Risk factors include very low birth weight, gestational age <30 weeks, intravenous hyperalimentation, exposure to H2 receptor antagonists, lack of antenatal care, use of central catheters, prolonged hospitalization, mechanical ventilation, endotracheal intubation, use of broad-spectrum antibiotics/steroids and previous colonization with Candida albicans.

Early diagnosis and aggressive treatment improves the outcome of FS . Definite diagnosis of neonatal FS is difficult and pathogens take time to isolate, so babies with suspected FS are treated with empiric antifungal therapy while awaiting culture r e s u l t s . S i g n s o f s u s p e c t e d F S i n c l u d e

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thrombocytopenia, lethargy, glucose instability, increasing ventilation requirements and apnea

Routine use of empiric fluconazole as first-line therapy may therefore be inappropriate. It is thus important to have current data on neonatal fungal isolates and their antimicrobial susceptibility patterns to guide empiric antifungal therapy.

The aim of this study was to review the characteristics of neonates with fungal bloodstream isolates and to determine the different fungal pathogens and review their sensitivity patterns.

This is a review of neonates with fungal BSI at the neonatal unit of Charlotte Maxeke Johannesburg Academic Hospital (CMJAH) between 1 January 2007 and 31 December 2011. A neonate was considered to be any patient admitted to the neonatal unit within 28 days of birth or those neonates who were born in the hospital and had not ever been discharged, e.g. a preterm infant now 40 days old would still be included in the study.

All neonates with a fungal organism isolated on blood culture were included in the study. The duration of incubation, identification of the organism and mean inhibitory concentrations (MICs) of fluconazole and voriconazole were obtained from the culture result. The different

Candida species isolated were classified as resistant based on species-specific MIC cut-off levels for fluconazole or voriconazole Patients were started on empiric antifungal therapy at the discretion of the attending physician. Treatment was adjusted according to the fungal isolate and sensitivity pattern, as soon as this information was available. Fluconazole was used as

first-line empiric antifungal therapy. This did not change during the whole study period, and amphotericin was not used in any patient as empiric therapy. There was no prophylactic use of fluconazole in the neonatal unit at the time of the study.

Statistical analysis was done using IBM SPSS statistics version 20.

There were 63 patients with fungal BSI in the CMJAH neonatal unit during the study period. Adequate clinical data could not be obtained on four patients, so these were excluded from the study. The final sample therefore comprised 59 neonates. Candida parapsilosis (54.2%) was isolated in majority of the cases, followed by C. albicans (27.1%). Fluconazole resistance was present in 16 of 32 cases of C. parapsilosis versus 1 of 16 cases of C. albicans (P=0.003). Mortality rate was 45.8%. Surgical problems were present in 55.9%. Death was significantly associated with lower birth weight (P=0.046) and necrotizing enterocolitis (P=0.034).

The use of prophylactic fluconazole in this setting is questionable, and empiric antifungal therapy with fluconazole may not be effective.

Fungal BSI isolates and their sensitivity must be monitored on an ongoing basis.

Source : journal of tropical pediatrics, vol. 59, no. 6, 2013

Comment : The increase in neonatal fungal BSI and resistant organisms highlights the need to review use of routine empiric fluconazole and to implement preventive measures.

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From journals:

Mahesh Baldawa, Satish Tiwari: Legal issues and preventable medical errors, New Indian Journal of Pediatrics 2012, 1: 8-12.

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Bhattacharya A, Mishra S. DNR, Euthanasia and Life support systems; In: Tiwari S, Baldwa M, Tiwari M, Kuthe A editors; Text Book on medico-legal issues related to various medical specialties: 1st edition, Jaypee brothers medical Publishers, New Delhi 2012; 179-185

From Newspapers:

Aamir ko ho raha pachhatava. Dainik Bhaskar th

(Hindi), 2011; 4 December. Nagpur p.5 (Col.3)

From internet:

Harms Roger W. Breast-feeding while pregnant: Is it safe? http://www.mayoclinic.com/health/breast-feeding-while-pregnant/AN01840

thAccessed on 16 Oct 2011.

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