INDIAN JOURNAL OF

PRACTICAL PEDIATRICS
• IJPP is a quarterly subscription journal of the Indian Academy of Pediatrics committed
to presenting practical pediatric issues and management updates in a simple and clear
manner
• Indexed in Excerpta Medica, CABI Publishing, Scopus

Vol.19 No.4 OCT.- DEC. 2017

Dr.N.C.Gowrishankar Dr.S.Thangavelu
Editor-in-Chief Executive Editor

CONTENTS
TOPIC OF INTEREST - “IAP - IJPP CME 2017”
Growth charts and monitoring 319
- Hemchand K Prasad, Vaman Khadilkar
H1N1 revisited 327
- Vidya Krishna
Sedation and analgesia in office practice 332
- Mullai Baalaaji AR
Financial literacy for doctors 337
- Thirumalai Kolundu S
Thrombocytopenia 338
- Janani Sankar
Late talking toddler - When to worry? 342
- Somasundaram A
Elevated transaminases in a child - Approach 347
- Malathi Sathiyasekaran
Hypopigmented skin lesions - What a pediatrician should know? 353
- Madhu R
Early childhood caries - Causes and management 361
- Muthu MS, Ankita Saikia

Journal Office and address for communications: Dr. N.C.Gowrishankar, Editor-in-Chief, Indian Journal of Practical
Pediatrics, 1A, Block II, Krsna Apartments, 50, Halls Road, Egmore, Chennai - 600 008. Tamil Nadu, India.
Tel.No. : 044-28190032 E.mail : ijpp_iap@rediffmail.com
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Indian Journal of Practical Pediatrics 2017;19(4) : 316

Head injury in children - Triaging and imaging 366

- Leema Pauline C, Viveka Saravanan, Ravi LA
Ten pitfalls in management of urinary tract infection 374
- Sudha Ekambaram, Vaishnavi Raman
DRUG PROFILE
Antiarrhythmic agents 378
- Jeeson C Unni, Ranjit Baby Joseph, Sajana TM
SURGERY
Mediastinal tumours in children - An insight 386
- Senthilnathan R, Vijay Raj S, Hariharan G
RADIOLOGY
Torticollis 390
- Vijayalakshmi G, Natarajan B, Abirami K, Thangalakshmi A, Raveendran J
CASE REPORT
Recurrent vaginal foreign body - Two much prank 392
- Udayakumar N, Abhinayaa J, Balamourougane P, Priyadharshini R
ADVERTISEMENTS 352,394,397
CLIPPINGS 336,352,377,385,391,394
NEWS AND NOTES 331,341,346,373,377
AUTHOR INDEX 395
SUBJECT INDEX 396

FOR YOUR KIND ATTENTION

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"Acknowledgement" to "Indian Journal of Practical Pediatrics" without prior permission.
- Editorial Board

Published by Dr.N.C.Gowrishankar, Editor-in-Chief, IJPP, on behalf of Indian Academy of Pediatrics, from 1A, Block II,
Krsna Apartments, 50, Halls Road, Egmore, Chennai - 600 008. Tamil Nadu, India and printed by Mr. D.Ramanathan,
at Alamu Printing Works, 9, Iyyah Street, Royapettah, Chennai-14.

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Indian Journal of Practical Pediatrics 2017;19(4) : 317

INSTRUCTIONS TO AUTHORS

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Indian Journal of Practical Pediatrics 2017;19(4) : 318

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should therefore ensure that they retain at least one copy and the illustration, if any.

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Indian Journal of Practical Pediatrics 2017;19(4) : 319

IAP - IJPP CME 2017

GROWTH CHARTS AND MONITORING systemic diseases, early. Normal growth occurs only if the
child is healthy.
*Hemchand K Prasad
**Vaman Khadilkar Growth standard and reference - Difference

Abstract: Growth is a measure of well being in a given A growth reference is a descriptive chart prepared
child. All pediatricians should follow the growth monitoring from a population which is believed to be growing under
guidelines released in 2007. Measured growth should be optimal health and nutrition. A growth standard is a
plotted on IAP modified WHO charts in children less than prescriptive standard prepared from a population where
5 years and on IAP 2015 charts above 5 years. all possible environmental and nutritional variables are
Standard guidelines of WHO and IAP should be used to controlled. It is a sole independent instrument upon which
measure and plot growth measures. The redefined target decisions are made. The various growth charts that are
range, short stature and overweight cut-offs must be used available today are given in Box 1.
to diagnose growth problems early. The new charts allow
a pediatrician to plot the growth in accurate months. It is
Box 1. Growth charts
also colour coded to diagnose and alert families of children
with obesity. The definitions of stunting, wasting, National
overweight and obesity in different ages are presented.
Early recognition of these growth abnormalities is crucial i. Old IAP charts (K N Agarwal charts)1,2 (descriptive)
for the long term health of the child. ii. Charts from Khadilkar, et al (descriptive)
Keywords: Growth charts, Growth monitoring, Adult iii. Charts from Marwaha, et al3 (descriptive)
equivalent. iv. New IAP 2015 charts (descriptive for height and
Growth and development are complementary weight, prescriptive for BMI)4
processes. Growth indicates the quantitative changes in International
the body-height and weight. The basic pre-requisites for
optimal assessment of childhood growth are reliable growth i. Centre for disease control (CDC) charts (descriptive)
parameter, reliable reference population, reliable cut-off ii. WHO 2006 standards 0-5 years (prescriptive)
and reliable calibrated instrument.
iii. WHO 2007 charts(descriptive)5
Importance of monitoring growth of a child
iv. International Obesity Task Force (IOTF) cut-offs for
Growth is a measure of well being in a given child. body mass index (BMI)6 (prescriptive)
Pediatric care consists of two important components:
curative and preventive care. Vaccinations, growth
monitoring and developmental assessments are important Interpretation of growth measures
pillars of preventive care. Growth monitoring helps a
Percentiles and Z–scores are the two ways of
pediatrician not only to reassure normalcy but also to
interpreting a growth measure. Percentiles and z-scores are
identify growth disorders, nutritional disorders and
interchangeable. On a practical note, it is suggested that
* Consultant, Department of Pediatric Endocrinology, pediatricians adhere to percentiles for common
Dr.Mehta’s Hospital, Chennai. anthropometric measures and Z-scores be used in diseased
** Consultant Pediatric Endocrinologist, children with severe growth abnormalities (e.g. severe
Growth and Pediatric Endocrine unit, chronic diarrhea and growth hormone deficiency).
Hirabai Cowasji Jehangir Medical Research Institute, Pune. The equivalent percentiles and z-scores are shown in
email : hemchan82@gmail.com Table I.
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Indian Journal of Practical Pediatrics 2017;19(4) : 320

Table I. Anthropometric measures interpre- d) Normal BMI – CDC, Marwaha references or

tation - Equivalent percentiles and Z-scores7 Khadilkar 2007 references
Z-score Percentile This ultimately results in ambiguity on the intervention
warranted for the child and compromises care for the child.
0 50
Anthropometric measures to be recorded in
-1 15 office practice

-2 3 The IAP has come out with growth monitoring

guidelines for pediatricians to adopt in office practice in
-3 1 2007. 8 The same guidelines are applicable today.
The measurements should be made as per the
+1 85
recommendations of the WHO.9 The recommendations
+2 97 depend on the age of the child:
a) 0-2 years - length, weight and head circumference at
+3 99
0, 6, 10 and 14 weeks, 6, 9, 15 and 18 months (every
vaccination visit),
Need for using the same chart and cut-offs b) 2-5 years – height, weight and head circumference
for interpretation every 6 months and
The usage of different growth charts and different c) Beyond 5 years – height, weight, BMI (every 6 months
cut-offs lead to different interpretation of the same till 9 years and annually there after); SMR every year.
anthropometric measure. Consider a 10 year old boy with
Growth charts preferred in office practice
a height of 124 cm and a BMI of 19.1 kg/m2. If different
growth charts are used he can be labelled as The growth charts committee of the IAP recommends
that the following growth charts be used in pediatric office
a) Stunted – CDC or WHO 2007 charts practice - IAP modified WHO charts in children less than
b) Normal stature – IAP 2015 chart (3rd percentile to 5 years and IAP 2015 5-18 years charts for children aged
diagnose short stature) 5-18 years. Combined IAP - WHO charts from birth to
18 years (0-5 WHO and 5-18 IAP) are also made available
c) Overweight – IAP 2015 charts, IOTF charts and for continuous growth monitoring. The similarities between
WHO 2006 charts the two charts are summarised in Table II.

Table II. Comparison of the similarities in the WHO 2007 standards and IAP 2015 references
WHO 2006 standards10 IAP 2015 references
Nature Prescriptive - described how children should grow Prescriptive for BMI; descriptive for other
aspects of growth (height and weight)
Norm Breast feeding established as a biological norm Good nutrition and health are a biological
norm
Statistical methods LMS (lambda-mu-sigma) method of statistics11 LMS method of statistics
Exclusion of Excluded weight for height more than +2 SD in Excluded weight for height more than +2
obese subjects cross sectional component and +3SD in SD; detects both malnutrition and
longitudinal component; detects both malnutrition overweight
and overweight
Study sample Pooled sample from 6 countries Pooled sample from 13 studies (nationally
(internationally representative sample) representative sample)
BMI – Body mass index; LMS– Power in the Box - Cox transformation (L), Median (M), Coefficient of variation and
skewness (S).
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Indian Journal of Practical Pediatrics 2017;19(4) : 321

Method of plotting on growth chart rate of growth being high in infancy and slower beyond
infancy. One must remember that movement towards the
Using a growth chart begins with entering the name 50th percentile is a good sign and away from the median
and date of birth on the chart. Growth is marked with a dot should be viewed suspiciously. The new charts allow a
(not circle or cross) at point of intersection of measure pediatrician to plot at accurate months (i.e there are
(on the y-axis) and the chronological age (on x-axis). 12 divisions between two consecutive years) thus making
The target height is calculated as below and marked with the concept of decimal age obsolete.
a horizontal arrow at 18 years. Target range is marked as
6 cm above and below the target height. New charts - More user friendly and parent
friendly
Father’s height + mother’s height + 13
Target height in boys =
2 The new charts are very user friendly. The IAP
Father’s height + mother’s height – 13 modified WHO charts allows one to plot - weight, height
Target height in girls = and head circumference on a single page and at convenient
2
15 day intervals. The weight, height (0-18) and BMI
When subsequent measurements are made on the same (5-18) measurements can be plotted at 6 monthly intervals
chart, the points are joined by a line. It is necessary to on the 0-18 year charts (Fig.1). The BMI and weight for
explain the findings to the parents, reassure them and height charts in 0-18 charts and 0-5 charts respectively are
remind them of the next growth measurement. colour coded - red colour indicating obesity. This is in
The following common errors are to be avoided. All girls principle with the idea of Prof David Morley - the founder
must have their growth plotted on pink chart and boys on of growth charts who intended that the charts should either
the blue chart. Plotting growth on the chart for opposite reassure or alert the mother.
sex is not acceptable. Weight should not be measured more
than once in 15 days and 30 days - during and beyond Figure 1(b) IAP 2015 charts for children 5-18 years
infancy, respectively. This is to avoid unnecessary anxiety. and combined WHO IAP 2015 charts for 0-18 years.

Changes in the current recommendations Recognition of abnormal growth using

growth chart
The following aspects are new in the current
recommendations (Table III). The target range has been The cut-offs and terminologies to be used are
lowered (from ±8 cm to ±6 cm) in line with the other summarised in Table IV. One must note the following:
international guidelines to facilitate early recognition of
abnormal growth. The threshold for abnormality picked a) It is preferred to interpret weight in conjunction with
up by crossing of percentiles varies with age owing to the height and not in an isolated perspective. This is on
Table III. Modifications in current recommendations of IAP growth charts
Previous Current
What chart should be WHO 2007 standards IAP modified WHO charts
used in a child <5 years
What chart should be Old IAP charts Combined WHO-IAP2015 charts
used in a child >5 years
Definition of short stature <3rd percentile in IAP chart constructed for the <3rd percentile on the new IAP chart
growth monitoring guideline or <5th percentile
on IAP charts
Overweight >85th percentile >23rd adult equivalent
Obesity >95th percentile >27th adult equivalent
Plotting age Decimal age On accurate months
Target range 8 cm above and below target height 6 cm above and below target height
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Height, weight and head circumference (boys) Weight for height chart 0-5 years (boys)

Height, weight and head circumference (girls) Weight for height chart 0-5 years (girls)

Fig.1(a) IAP modified WHO charts for children 0-5 years

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Indian Journal of Practical Pediatrics 2017;19(4) : 323

Weight and height 5-18 years (boys) BMI 5-18 years (boys) Weight and height 0-18 years (boys)

Weight and height 5-18 years (girls) BMI 5-18 years (girls) Weight and height 0-18 years (girls)

Fig.1(b) IAP 2015 charts for children 5-18 years and combined WHO IAP 2015 charts for
0-18 years

the lines of WHO recommendations. Hence, BMI or Weight for height charts and BMI for age assessments
weight for height is more useful than isolated weight often complement each other.
(especially in >5 years) in diagnosing wasting or
obesity. The term ‘Severe Acute Malnutrition (SAM)’ was
defined by WHO for health workers based on weight for
b) Crossing of percentile lines should be interpreted height Z-score of less than -3 should be used beyond
carefully. Although crossing of percentiles have to be 6 months.
viewed carefully, one must keep in mind certain
clinical situations where crossing of percentiles may Recognition of abnormal growth - Actions
be physiological: SGA trying to catch up; a child with On recognition of abnormal growth, a pediatrician
familial short stature catching down on height should check the accuracy of measurement/ plotting, look
percentiles. at the trend of deviation (a single cross sectional measure
c) The growth charts committee recommends weight for has limitations and growth does not always follow a smooth
height to diagnose wasting and obesity in the under curve) and plan further evaluation. Once abnormal growth
5 age group. This is purely for logistic reasons as errors is recognised, a step wise analysis of anthropometry in the
are minimal on weight for height versus BMI. background of clinical scenario is necessary for further
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Indian Journal of Practical Pediatrics 2017;19(4) : 324

Table IV. Abnormal growth parameters – Current acceptable terminologies

<5 years >5 years
Height Stunting <3rd percentile <3rd percentile
Severe stunting <0.1 percentile
Weight Underweight <3rd percentile
Severe underweight <0.1 percentile
BMI Wasting <3rd percentile <3rd percentile
or Severe wasting <0.1 percentile
weight for height Overweight >2SD from mean >23rd adult equivalent
Obese >3SD from mean >27th adult equivalent
Crossing of Abnormal growth 2 major percentiles in 2 major percentiles in
percentiles 6 month period a one year period

elucidation. The measures can be interpreted by either

calculation of height age and weight age or by calculation
of Z scores.
Calculation of height age and weight age
The appropriate anthropometric measure is plotted on
the correct growth chart. A line is drawn from the plotted
point to the 50th percentile and then vertically downwards
from the 50th percentile to touch the X- axis which is the
corresponding height age and weight age as depicted in
Fig.2. A child who has:
a) CA = HA = WA : is a normal child
b) CA > HA > WA : has nutritional deprivation or
systemic disease
c) CA > WA > HA : has endocrine disease Fig.2. Calculation of height age and weight
age
d) HA > WA > CA: has precocious puberty
e) WA > CA > HA : has endocrine obesity The same Z scores may be calculated by downloading
f) WA > HA > CA : has nutritional obesity the WHO anthro software (for WHO standards) or LMS
data can be procured for the authors for usage on their
It would be appropriate to remember that addition of personal computer. A child with:
accurately assessed bone age to the above equations in
specialised units adds more value. But the above equations a) Height Z score less than -2 is stunted
guide the pediatrician to rationalise and plan investigations
(Fig.3). b) Height Z score more than +2 (5-18 years) and more
than +3 (0-5 years) is tall stature
Calculation of Z scores
c) BMI or weight for height Z score less than -2 is wasted
Z score is a measure of deviation from the mean for
the reference population. The Z score for a given d) Height Z score more than +1.32 for boys and more
anthropometric measure is calculated as follows: than +1.64 for girls on IAP 2015 charts and more than
+3 (0-5 years) is obesity.
Measure – mean for age and sex
Z score = The etiology can be derived based on the child’s
SD for age and sex (reference population) growth (Table V).

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Indian Journal of Practical Pediatrics 2017;19(4) : 325

Fig.3. Summary of growth charts and growth monitoring in office practice

Growth of a LBW preterm baby – Assessment achondroplasia, Russell Silver syndrome and
hypochondroplasia. Such usage is mandatory to recognise
The growth curves for preterm babies have been
co-morbidities to the pathologies e.g. usage of Down’s
developed similar to the WHO 2007 standards - intergrowth
syndrome chart will facilitate early recognition of
21st post natal standards.12 These standards must be used
hypothyroidism in these children.
in preterm babies till they reach term gestational age.
Specialised growth charts Conclusion
The growth of certain genetic and skeletal pathologies Reliable growth markers, reliable references and cut-
are varied from normal children and these conditions have offs for usage have been summarised. It is of pivotal
specialised growth charts. Special growth charts are importance that all health professionals involved in the care
available for: Down syndrome, Turner syndrome, of children equip their units with reliable calibrated
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Indian Journal of Practical Pediatrics 2017;19(4) : 326

Table V. Growth parameters – Inference

Growth parameters Etiology
Stunted and wasted Stunting more than wasting Endocrinopathy
Wasting more than stunting Systemic or nutritional disorder
Obese child With tall stature Nutritional obesity
With short stature Endocrine obesity
Tall child With normal BMI Precocious puberty
measurement devices and assess the growth of children as 2. Agarwal DK, Agarwal KN. Physical growth in Indian
per laid down guidelines and contribute to preventive care affluent children (Birth - 6 years). Indian Pediatr 1994;
of children. 31:377-413.
3. Marwaha RK, Tandon N, Ganie MA, Kanwar R,
Points to Remember Shivaprasad C, Sabharwal A, et al. Nationwide Reference
• A ‘growth reference’ is a comparison of the given Data for Height, Weight and Body Mass Index of Indian
Schoolchildren. Natl Med J India 2011; 24(5):269-277.
child’s growth to the local population. A ‘growth
standard’ is a concept of “what should be the growth 4. Khadilkar V, Yadav S, Agarwal KK, Tamboli S,
in optimal conditions”. Banerjee M, Cherian A, et al. Revised IAP growth charts
for height, weight and body mass index for 5- to 18-year-
• Usage of different growth charts and different cut- old Indian children. Indian Pediatr 2015; 52(1):47-55.
offs lead to different interpretation of the same
5. de Onis M, Onyango AW, Borghi E, Siyam A, Nishida C,
anthropometric measure.
Siekmann J. Development of a WHO growth reference
• All pediatricians should follow the IAP growth for school-aged children and adolescents. Bull World
monitoring guidelines published in 20078. Health Organ 2007; 85:660-667.

• IAP recommends - IAP modified WHO charts in 6. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing
children less than 5 years and IAP 2015 growth a standard definition for child overweight and obesity
charts in children more than 5 years. worldwide: International survey. Br Med J 2000; 320:1240-
1243.
• Key modifications in the new recommendations
7. Khadilkar V, Khadilkar A. Growth charts: A diagnostic tool.
include - Lowered target range to ± 6 cm; new Indian J Endocr Metab. 2011; 15(Suppl 3):S166-171.
definition of overweight and obesity to 23 rd and
27th adult BMI equivalent and definition of short 8. Khadilkar V, Khadilkar A, Choudhury P, Agarwal A,
stature to height < 3rd percentile. Ugra D, Shah N. IAP Growth Monitoring Guidelines for
Children from Birth to 18 Years. Indian Pediatr 2007;
• The new charts are user friendly - Colour coding for 44:187-197.
obesity; plotting can be done in accurate months 9. World Health Organization, Physical Status: The Use and
(not decimal age). Interpretation of Anthropometry. Report of a WHO Expert
• Once abnormal growth is recognised, calculating Committee. Technical Report Series No. 854. Geneva:
height and weight age or calculation of Z scores must WHO; 1995.
be done for further evaluation. 10. Onis M, Garza C, Onyango AW, Martorell R. WHO Child
growth standards. Acta Pediatr 2006; 95(Suppl 450):S1-
• Specialised growth charts - Intergrowth and
101.
syndrome specific charts must be used in preterms
and syndromic children, as appropriate. 11. Cole T, Green P. Smoothing reference centile curves:
The LMS method and penalized likelihood. Stat Med 1992;
References 11:1305-1319.
1. Agarwal DK, Agarwal KN, Upadhyay SK, Mittal R, 12. Villar J, Giuliani F, Fenton TR, Ohuma EO, Ismail LC,
st
Prakash R, Rai S. Physical and sexual growth pattern of Kennedy SH. INTERGROWTH-21 Consortium.
st
affluent Indian children from 6-18 years of age. INTERGROWTH-21 very preterm size at birth reference
Indian Pediatr 1992; 29:1203-1282. charts. Lancet 2016; 387:844-845.
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Indian Journal of Practical Pediatrics 2017;19(4) : 327

IAP - IJPP CME 2017

H1N1 REVISITED shift” refers to abrupt and major antigenic changes in HA

or NA due to genetic re-assortment with animal strains
*Vidya Krishna and is responsible for pandemics.
Abstract: Seasonal influenza is an acute febrile respiratory Seasonality
illness caused predominantly by Influenza type A (H1N1).
Influenza, traditionally an under recognised disease, Influenza A (H1N1) and A (H3N2) are the circulating
gained notice after the 2009 pandemic. In children, it can seasonal influenza A virus subtypes, with majority of
cause asymptomatic infection to severe illness and even infections caused by A (H1N1) this season. Influenza A
death, particularly in infants and those with co-morbid (H1N1) virus is the same virus that caused the 2009
conditions. This article will focus on the epidemiology of influenza pandemic. The two type B viruses also circulating
influenza and clinical aspects including clinical features, as seasonal influenza viruses, are named after the areas
complications, diagnosis, treatment and prevention where they were first identified, Victoria lineage and
including chemoprophylaxis, vaccination and infection Yamagata lineage.4 Influenza occurs year-round in the
control measures. tropics and during winters in the temperate countries.
Influenza peaks in India typically occur with the monsoons-
Keywords: Influenza, H1N1, Children. North, northeast and southwest regions get their peaks in
July-September whereas Southeast (Chennai and Vellore)
Influenza is an important cause of acute respiratory has its peak in October-November. Srinagar (Northern most
infections worldwide and is associated with more severe city) has its peak in January-March during the winter
disease and mortality especially in children under 5 years months.5
of age. Influenza accounts for 10% of hospitalisation due
to respiratory illness in children less than 18 years of age.1 Disease burden and transmission
Various studies have shown that influenza accounts for
It is estimated that influenza results in approximately
15% - 20% outpatient cases in children.2,3
374,000 hospitalizations in infants, (228,000 in children
Epidemiology under 6 months of age) and 870,000 hospitalizations in
children <5 years globally per year. Hospitalization rates
Classification are three times higher in the developing countries.1
Influenza viruses belong to the Orthomyxoviridae and Significant morbidity and mortality can occur in children
have 3 distinct types-A, B and C. The differences between under 5 years of age (especially under 2 years), children
the 3 viruses are given in Table I. They are enveloped single with chronic cardio-pulmonary diseases including asthma,
stranded RNA viruses. Influenza A viruses are further renal, hematologic, hepatic or metabolic conditions
subtyped based on their hemagglutination (HA) and including diabetes mellitus, neuromuscular disorders,
neuraminidase (NA) antigens (Fig.1). immunosuppressed and those on long term aspirin therapy
who have a risk of Reye’s syndrome. Other high risk groups
The influenza viruses undergo continuous changes and include pregnant women, obese individuals and the elderly
hence, the vaccine strains must be updated every year. (>65 years of age).
“Antigenic drift” refers to the minor antigenic changes in
the HA or NA or both resulting in new strains of the virus These viruses are transmitted from person to person
and cause seasonal outbreaks or epidemics. “Antigenic via the droplets generated by coughing and sneezing,
generally within 3 feet distance. Transmission can also
* Assistant Professor, occur through contact with infected surfaces like tables,
Department of Pediatrics, toys, door handles, etc. Viral shedding typically peaks at
Sri Ramachandra Medical College and the onset of illness and lasts for 4-5 days. It is typically
Research Institute, Chennai. longer in infants (up to 7-10 days, maximum 21 days) and
email: docvidyakrishna@gmail.com in the immunosuppressed (weeks-months).6
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Indian Journal of Practical Pediatrics 2017;19(4) : 328

Table I. Influenza virus types

Influenza A Influenza B Influenza C
Natural host Humans, birds, swine, equine, Humans only Humans and swine
marine mammals.
Epidemiology Antigenic shift and drift Antigenic drift only Antigenic drift only
Clinical Can cause large pandemics with significant Severe disease in the Mild disease without
manifestations mortality in young individuals elderly or patients seasonality.
with co-morbidities

NEP (nuclear export protein)

Fig.1.Structure of the influenza virus
(Source: http://www.virology.ws/2009/04/30/structure-of-influenza-virus)

Clinical features secondary bacterial pneumonia (typically with

Streptococcus pneumoniae, Staphylococcus aureus -both
Asymptomatic infections can occur in about 30%-60%
MSSA and MRSA and Streptococcus pyogenes) and
of the children.6 Symptomatic patients, after an incubation
ARDS.
period of 1-4 days, typically develop an abrupt onset of
high grade fever, usually with chills. They can also have Non-respiratory complications include myocarditis,
non-productive cough, rhinorrhea, myalgia, headache and pericarditis, febrile seizures, status epilepticus,
sore throat. Nausea, vomiting, diarrhea and abdominal pain encephalopathy, encephalitis, myositis, rhabdomyolysis,
can occur in about 30% especially with Influenza B.6 mild-moderate transaminitis, Reye’s syndrome with
Fever may sometimes be absent in young infants and salicylate exposure and sudden death.6 Influenza associated
neonates. Young infants can present as bronchiolitis, encephalopathy (IAE) is more common in children than
pneumonia, croup or sepsis like syndrome and neonates adults and is typically associated with diffuse cerebral
can have apnea or respiratory failure. Children with asthma edema on neuroimaging.7 Associated fever or respiratory
may present with an acute exacerbation. symptoms may be absent in up to 40% of the children with
IAE.8 CSF is usually normal or has mild pleocytosis.7
Complications
The pathogenesis is believed to be cytokine dysregulation
Complications are especially common in the high-risk and not direct viral invasion. Severe necrotising
groups mentioned above. The common respiratory encephalopathy with bilateral thalamic necrosis is known
complications include otitis media, sinusitis, viral and to occur.9 Milder forms of encephalitis with reversible
14
Indian Journal of Practical Pediatrics 2017;19(4) : 329

lesions (MERS) in the splenium of corpus callosum is also infants are appropriate respiratory specimens for testing.
known.10 Swabs should have a plastic shaft and dacron tips. Wooden
shafts, cotton or calcium alginate tips must be avoided.
Categories In hospitalised and intubated children, lower respiratory
Ministry of Health and Family Welfare (MOHFW) tract should be tested if upper respiratory specimens are
of India has issued guidelines on clinical categorisation of negative as the virus is shed longer in the lower respiratory
patients for testing, treating and isolation puposes.11 tract.12 Specimens should be transported in viral transport
medium and should be kept at 4°C for no longer than
Category A 72 hours before testing and ideally should be tested within
24 hours of collection.
Influenza like illness (ILI): Mild fever plus cough or
sore throat with or without body ache, headache, diarrhea Molecular assays like RT-PCR or multiplex respiratory
and vomiting. For patient in category A, no testing or viral panels (like the Film Array respiratory panel,
treatment is required. Patients should confine themselves Biomerieux) are reliable for the diagnosis of influenza with
at home and avoid mixing up with public and high risk a good sensitivity (86%-100%) and specificity.
members in the family. False negatives may occur especially later in the disease
(> 3-4 days). Turnaround time (TAT) is around 6-8 hours.
Category B
Antigen based tests like rapid influenza diagnostic
(i) Category A plus high grade fever and severe sore throat tests (RIDTs) and direct or indirect fluorescent antibody
(DFA/IFA) staining have shorter TATs and good specificity
(ii) Any mild ILI in (>95%) but have low sensitivity and cannot distinguish
• Pregnant women Influenza A and B. These tests are not recommended in the
diagnosis of influenza by MOHFW.12 Viral cultures have a
• Lung/ heart / liver/ kidney / neurological disease, blood longer TAT of 1-3 days for shell vial culture and 3-10 days
disorders/ diabetes/ cancer / HIV-AIDS for tissue culture and hence, may not be clinically relevant.
• Patients on long term steroids/aspirin.
Treatment
• Children with mild illness but with predisposing risk
Oseltamivir is approved by FDA for treatment in
factors.
babies and children >14 days of life for treatment and
• Age greater than 65 years. children >1 year of age for chemoprophylaxis. Centers for
No testing for H1N1 is required for category-B Disease Control and Prevention (CDC) and the American
(i) and (ii) and they can be managed at home. All patients Academy of Pediatrics (AAP) approve use of the drug for
of category-B (i) and (ii) should receive treatment with treatment in babies less than 14 days of life and for
oseltamivir and should be followed up for improvement. chemoprophylaxis above 3 months of age.13 The dose of
oseltamivir in the various weight bands is given in
Category C Table II. Dose in infancy is 3mg/kg BD. Duration of
treatment is 5 days in uncomplicated cases and can be
• Breathlessness, chest pain, drowsiness, fall in blood extended to 10 days.14 Dosing adjustments need to be made
pressure, hemoptysis, cyanosis. for those patients with renal failure. Adverse events with
• Children with ILI (influenza like illness) with red flag oseltamivir include nausea, vomiting, serious skin reactions
signs: Somnolence, high/persistent fever, inability to and sometimes transient neuro-psychiatric manifestations.
feed well, convulsions, dyspnea /respiratory distress, Chemoprophylaxis is recommended in high risk
etc. contacts at the above doses for 7 days.13 Oseltamivir is safe
• Worsening of underlying chronic conditions. in pregnancy and should be administered irrespective of
the trimester. Severe complications are known to occur to
All these patients mentioned above in category - C
mother in pregnancy though no vertical transmission is
require testing, immediate hospitalization and treatment.
noted.6 Resistance to oseltamivir is rare but can occur in
Diagnosis the immunocompromised host.13
Nasopharyngeal (preferable) or throat swabs from Other drugs: Inhaled zanamivir is approved but not for
older children and nasal or nasopharyngeal aspirates from children with asthma / respiratory diseases. Dose for

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Indian Journal of Practical Pediatrics 2017;19(4) : 330

Table II. Oseltamivir dose

Weight band Treatment dose of oseltamivir Chemoprophylaxis dose
<15 kg 30mg BD 30mg OD
15-23 kg 45mg BD 45mg OD
24-40 kg 60mg BD 60 mg OD
>40 kg 75mg BD 75 mg OD

treatment (>7 years) is 5 mg in each nostril twice a day for Table III. Vaccination dosage and schedule
5 days and for prophylaxis (>5 years) is 5 mg once a day
for 7 days. Intravenous peramivir is not approved in age Age 6-35 months 3-8 years From 9 years
<18 years and is not found to be effective in severe disease. Dose 0.25 ml 0.5 ml 0.5 ml
Both these drugs are not available in India. Amantadine
and rimantadine have high resistance rates and are not No. of 2* 2* 1
useful in the treatment of influenza. doses
*For previously vaccinated children, one dose should
Vaccination
be sufficient.
There are many types of influenza vaccines- trivalent
split virion inactivated vaccine, live attenuated influenza Infection control
vaccine, adjuvanted trivalent influenza vaccine, Non-hospitalised patients: They should be advised to
recombinant vaccine and quadrivalent influenza vaccine. avoid crowded enclosed spaces and close contact with high
The trivalent split virion vaccine is available and risk groups. They should be encouraged to practise cough
recommended in India. The vaccine is approved for age etiquette (maintain distance, cover coughs and sneezes with
> 6 months and in pregnancy. Children under 5 years, high disposable tissues or clothing or cough in the crook of the
risk groups including pregnancy and all healthcare workers elbow) and wash hands frequently.
(HCWs) should be vaccinated annually, ideally in
September-October in Tamil Nadu.15 Protective antibody Hospitalised patients: They should be placed in droplet
levels are known to drop to 50% by 6 months after and contact precautions. Healthcare workers (HCWs)
vaccination and hence, it is mandatory to repeat vaccine should use hand hygiene, gloves and surgical mask and
annually. The vaccine is safe and the risk of Guillaine- will require N-95 mask during suctioning and
Barre syndrome (GBS) is 1 in 1 million recipients and is bronchoscopy. Isolation should be continued for the 7 days
the same as the risk of GBS in the general population. after the onset of illness or until 24 hours after the resolution
The vaccine should be administered with caution in patients of fever and respiratory symptoms, whichever is longer.17
with history of severe egg allergy only if expected benefits If resources are limited, patients can be cohorted and
outweigh risks.16 isolation rooms can be prioritized for those in the early
phase of illness. A minimum distance of 3 feet between
Dosage and schedule the beds with physical barriers like curtains or partitions
The dosing and schedule of influenza vaccines in will help to prevent the transmission in resource limited
children is given in Table III. The 2016-17 influenza settings. Isolation precautions for longer periods should
vaccines contain HA derived from the following: be considered in the case of young children or severely
(a) A/California/7/2009 (H1N1)-like virus, (b) A/Hong immunocompromised patients, who may shed influenza
Kong/ 4801/2014 (H3N2) – like virus, and (c) a B/Brisbane/ virus for longer periods of time and also, might be shedding
60/2008–like virus (Victoria lineage). The 2016–17 antiviral resistant virus. Cough after influenza infection
quadrivalent vaccines will contain the same three antigens may be prolonged and may not be an indicator of viral
and an additional influenza B virus HA, derived from a B/ shedding.
Phuket/3073/2013–like virus (Yamagata lineage). Points to Remember
The composition for 2016–17 represents a change in the
influenza A (H3N2) virus and a switch in lineage for the • Influenza A (H1N1) is the major seasonal influenza
influenza B viruses. virus.
16
Indian Journal of Practical Pediatrics 2017;19(4) : 331

• High risk groups include children under 5 years, 7. Surtees R, DeSousa C. Influenza virus associated
immunosuppressed, those with chronic medical encephalopathy. Arch Dis Child 2006; 91(6):455-456.
conditions, obesity, pregnancy and those aged doi:10.1136/adc.2005.092890
>65 years. 8. Khandaker G, Zurynski Y, Buttery J, Marshall H, Richmond
PC, Dale RC, et al. Neurologic complications of influenza
• Testing for influenza is mandatory only for the A(H1N1)pdm09: surveillance in 6 pediatric hospitals.
hospitalized patients. Neurology 2012; 79(14): 1474–1481. doi: 10.1212/
WNL.0b013e31826d5ea7.
• Treatment should be started without delay in the 9. Ormitti F, Ventura E, Summa A, Picetti E, Crisi G. Acute
high-risk groups and the complicated cases. necrotizing encephalopathy in a child during the 2009
influenza A(H1N1) pandemia: MR imaging in diagnosis
• Vaccination of the high-risk groups and healthcare and follow-up. AJNR Am J Neuroradiol 2010; 31(3):396-
workers should be done in September - October each 400. doi: 10.3174/ajnr.A2058.
year. 10. Tada H, Takanashi J, Barkovich AJ, Oba H, Maeda M,
References Tsukahara H, et al. Clinically mild encephalitis/
encephalopathy with a reversible splenial lesion.
1. Lafond KE, Nair H, Rasooly MH, Valente F, Booy R, Neurology 2004; 63(10):1854–1858.
Rahman M, et al. Global Role and Burden of Influenza in 11. Ministry of Health and Family Welfare. Guidelines on
Pediatric Respiratory Hospitalizations, 1982–2012: categorization of Influenza A H1N1 cases during screening
A Systematic Analysis. PLoS Med. 2016; 13(3): e1001977. for home isolation, testing, treatment and hospitalization.
doi: 10.1371/journal.pmed.1001977. Available from: www.mohfw.nic.in/WriteReadData/l892s/
2. Poehling KA, Edwards KM, Griffin MR, Szilagyi PG, 804456402Categorisation.pdf
Staat MA, Iwane MK, et al. The burden of influenza in 12. Ministry of Health and Family Welfare. Clinical
young children, 2004–2009. Pediatrics 2013; 131(2):207- Management Protocol for Seasonal Influenza. Available
216. doi:10.1542/peds.2012-1255. from: http://mohfw.gov.in/showfile.php?lid=3626
13. Centers for Diseases Control and Prevention. Influenza
3. Zhang T, Zhang J, Hua J, Wang D, Chen L, Ding Y, et al.
Antiviral Medications: Summary for Clinicians. Available
Influenza-associated outpatient visits among children less
from: https://www.cdc.gov/flu/professionals/antivirals/
than 5 years of age in eastern China, 2011–2014. BMC
summary-clinicians.htm
Infect Dis 2016; 16:267. doi:10.1186/s12879-016-
1614-z. 14. Interim Guidance on the Use of Antiviral Medications for
Treatment of Human Infections with Novel Influenza A
4. World Health Organisation. Influenza virus infections in Viruses Associated with Severe Human Disease. https://
humans (February 2014). Available from:http://who.int/ www.cdc.gov/flu/avianflu/novel-av-treatment-
influenza/human_animal_interface/virology_ guidance.htm accessed on 16th August, 2017.
laboratories_and_vaccines/influenza_virus_ infections_
15. Vashistha VM, Kalra A, Choudhury P. Influenza
humans_feb14.pdf.
vaccination in India: position paper of Indian Academy
5. Chadha MS, Potdar VA, Saha S, Koul PA, Broor S, Dar L, of Pediatrics, 2013. Indian Pediatr 2013; 50(9):867-874.
et al. Dynamics of influenza seasonality at sub-regional 16. Vashishtha VM, Choudhury P, Bansal CP, Yewale VN,
levels in India and implications for vaccination timing. Agarwal R. Influenza vaccines. IAP Guidebook on
PLoS One 2015; 10(5): e0124122. doi: 10.1371/ Immunization 2013–14. Indian Academy of Pediatrics,
journal.pone.0124122. National Publication House, Gwalior 2014; pp291-302.
6. Gail JJC. Demmler-Harrison, Kaplan SL Steinbach WJ, 17. Centers for Diseases Control and Prevention. Prevention
Feigin PH Influenza Viruses .In: Cherry’s Textbook of Strategies for Seasonal Influenza in Healthcare Settings.
th
Pediatric Infectious Diseases. 7 ed. Philadelphia: Elsevier Available from: https://www.cdc.gov/flu/professionals/
Saunders, 2014; pp2326-2358. infectioncontrol/healthcaresettings.htm.

NEWS AND NOTES

Recent Advances in Paediatric Neurology
Theme: Treatable Disorders Date: 28th January, 2018 Venue: The RainTree, Teynampet, Chennai - 35
Registration Free but mandatory, on or before 20th January, 2018
Contact
Dr.K.Lakshminarayanan email: dr_kln@yahoo.co.in
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Indian Journal of Practical Pediatrics 2017;19(4) : 332

IAP - IJPP CME 2017

SEDATION AND ANALGESIA IN OFFICE a particular procedure depends not only on the
PRACTICE chronological age but also on cognitive and emotional
development. The vulnerability of children’s airway and
*Mullai Baalaaji AR protective reflexes makes them at risk for serious
complications while administering sedative agents.
Abstract: The number of diagnostic and therapeutic
procedures performed outside the operating room are Levels of sedation
increasing. Sedation and analgesia is required to control
child’s behaviour during the safe execution of an Sedation occurs as a continuous state from minimal
unpleasant procedure. The physiological characteristics sedation to general anesthesia depending on the drug, route,
of children make them vulnerable to the potential side dosage used and patient characteristics. It is important to
effects of sedative agents. The key to provide safe know the intended level of sedation to assess the level of
procedural sedation involves choosing the right agent and care that is required (Table I).1
anticipatory preparedness for any untoward event. Topical
Pre-sedation assessment
and locally acting agents along with non-pharmacologic
interventions are useful adjuncts and help in reducing the A focussed history and physical examination are
sedative requirements. helpful to identify those who are ‘at risk’ for potential
complications arising from sedative agents. SAMPLE is a
Keywords: Pain management, Anesthesia, Analgesia.
mnemonic used for focussed history – S: signs and
Children undergo a variety of diagnostic and minor symptoms, A: allergy, M: medications used, P: past history,
therapeutic procedures outside the traditional operating L: last meal, E: events. Pre-existing medical problems, prior
theatres and it is imperative for the practicing pediatrician adverse events to procedures/sedative agents and history
to have a knowledge of the unique needs of children, of snoring also have to be detailed. Fasting
commonly used drugs, systematic pre-sedation assessment, recommendations before an elective sedation are shown
intra-procedural monitoring and post procedural care. in Table II.2

Goals of sedation Assessment of airway is a key component of

examination prior to PSA. Adequacy of visualisation of
Procedural sedation and analgesia (PSA) is the posterior oropharynx has been shown to correlate with
technique of administering sedatives or dissociative agents visualisation of glottis during laryngoscopy. A modification
with or without analgesics to induce a state that allows of the original Mallampati score with child in supine
safe execution of unpleasant procedures while maintaining position has been suggested in children. Other parameters
cardiorespiratory function. The process is a continuous one, to evaluate the child’s airways include evaluation of
involving titrating the doses of agents to the desired effect mandible size, adequacy of mouth opening, size of tongue
while monitoring for the adverse effects resulting from drug in relation to oral cavity, dentition, tonsillar enlargement,
overdosage. The goals of sedation are to control child’s anatomical abnormalities of neck and neck mobility.3
behaviour to allow safe completion of the procedure,
minimise physical discomfort, anxiety and pain and return Preparation for sedation
the child to a safe physiological state that allows for
Preparation for procedural sedation involves
discharge/transfer. The ability of a child to co-operate for
identifying the right patient, informed written consent,
arranging necessary equipments, medications and
* Consultant Pediatric Intensivist, personnel. The acronym SOAPME is useful in planning
Kovai Medical Center and Hospital, for a procedure (Box 1). The procedure should be
Coimbatore. performed in the designated areas such as pediatric
email: drmullaibaalaaji@gmail.com emergency department or intensive care unit.
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Indian Journal of Practical Pediatrics 2017;19(4) : 333

Table I. Comparison of different levels of sedation continuum

Physiologic Minimal sedation/ Moderate sedation/ Deep sedation/ General
function Anxiolysis analgesia analgesia anesthesia
Responsiveness Normal response to Purposeful response to Purposeful response Unarousable
verbal stimulus verbal/tactile stimulus following repeated/
noxious stimulus
Airway Unaffected No intervention needed Intervention may be Intervention often
needed needed
Spontaneous Unaffected Adequate May be inadequate Often inadequate
Ventilation
Cardiovascular Unaffected Usually maintained Usually maintained May be impaired
function

Box 1. Preparation for sedation (SOAPME) Box 2. Selection of PSA drugs

S - Suction: Size appropriate suction catheters and a) Intended purpose – Anxiolysis vs analgesia vs
functioning suction apparatus movement control
O - Oxygen: Supply/ delivery devices and flowmeter b) Desired route of administration
A - Airway: Age appropriate bag valve mask, c) Pre-existing medical conditions
oropharyngeal airways, laryngoscope blades, d) Familiarity of use
endotracheal tubes, stylets
e) Availability/Cost
P - Pharmacology: Sedation, analgesic, antiemetic,
resuscitation and reversal medications
profile of different classes of agents help in choosing the
M - Monitoring: SpO2, ECG, blood pressure, end-tidal
appropriate drug for a given clinical scenario. It is also
carbon-dioxide
important to adminster the right dosage at the right time,
E - Equipment/drugs for a particular case so that the effect peaks at the time of the unpleasant stimulus
(e.g. defibrillator) (Table III). The choice of drug depends upon the factors
given in Box 2 and Table IV.
Table II. Fasting recommendations before
Benzodiazepines: They are one of the commonly used
elective sedation
sedative agents in clinical practice. They are extremely
Ingested food Minimum fasting period (hours) potent amnestics, sedative hypnotics, but donot have
analgesic properties. These agents act by augmenting
Clear liquids 2 γ-aminobutyric acid and glycine transmission. Midazolam
is the prototype drug and can be administered transmucosal
Human milk 4
(buccal, rectal, nasal), intramuscular and intravenous
Infant formula 6 routes. There is a dose-dependent depression of breathing
that is potentiated with concomitant opioid administration.
Nonhuman milk 6 Significant hypotension can occur especially when
administered as a rapid bolus injection in the setting of
Light meal* 6
hypovolemia.
*The amount and type of food must be considered to
Opioids: Opioid analgesics are commonly used in
determine the fasting period
combination with sedative agents during PSA. They act
Choice of agents on mu (μ), kappa (κ) and delta (δ) opioid receptors and
decrease the release of excitatory neurotransmitters from
Knowledge about the pharmacokinetics, side effect terminals carrying nociceptive stimulus. Morphine is the
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Indian Journal of Practical Pediatrics 2017;19(4) : 334

Table III. Dose, onset and duration of action of commonly used sedative/analgesic agents
Drug Dosage* Onset of action Duration of action
Midazolam 0.05-0.1 mg/kg 1-4 minutes At least 30 minutes
Morphine 0.05-0.1 mg/kg 1-3 minutes 2-7 hours
Ketamine 0.5-2 mg/kg 1-2 minutes 30-60 minutes
Propofol 2-3 mg/kg 15-30 seconds 5-10 minutes
Dexmedetomidine 0.3-1 mcg/kg 10-15 minutes At least 30 minutes
Etomidate 0.1-0.3 mg/kg 15-20 seconds 5-10 minutes
Triclofos 20-50 mg/kg (Oral) 30 minutes 8-10 hours
* Dosage is for intravenous route unless specified otherwise

Table IV. Choice of agents for common procedures

Procedure type Procedure Goals of PSA Choice of agents
Painless diagnostic ECHO, USG, EEG, Only sedation and motion control Triclofos, midazolam
CT, MRI
Painful diagnostic FNAC, lumbar puncture, Sedation, analgesia, anxiolysis and Topical / local anesthetics +
thoracentesis,paracentesis movement control midazolam / morphine /
ketamine
Painful therapeutic Incision and drainage, Sedation, analgesia, anxiolysis, Topical / local anesthetics +
intercostal tube drainage, movement control, amnesia midazolam and morphine /
percutaneous nephrostomy and muscle relaxation ketamine

prototype drug and has analgesic, sedative properties inotropic effect and vasodilation. The risk of bacterial
without producing amnesia. Fentanyl is about 100 times contamination of solution can be prevented by strict aseptic
more potent than morphine and is devoid of sedative/ precautions and avoiding multiple use of opened vial.
hypnotic action. All opioids produce side effects such as Prolonged infusions are not recommended due to the risk
pruritus, nausea, vomiting, constipation, tolerance and of fatal propofol infusion syndrome.
dependence.
Dexmedetomidine: It is an α2-adrenergic receptor agonist
Ketamine: It is a N-methyl-D-aspartate (NMDA) that acts on locus ceruleus, producing a state similar to
antagonist that produces dissociative anesthesia, amnesia natural sleep.5 The sedative and analgesic property without
and analgesia. The minimal respiratory depressant effect significant respiratory depression has made it a popular
and stable hemodynamic profile makes it an attractive agent agent for procedural sedation, nevertheless cost is a
in PSA. The side effects are hallucinations, myoclonic deterrent to its widespread use in our settings. The side
movements and excessive salivation. Other adverse effects effects include bradycardia and hypotension.
that remain controversial include apnea in infants,
laryngospasm and possible increase in intracranial pressure. Etomidate: It is an imidazole derivative that acts by
potentiating GABA inhibitory neurotransmission. It is
Propofol: It is an alkylphenol general anesthetic which generally devoid of adverse effects on cardiac and
acts by potentiating GABA-mediated synaptic inhibition. hemodynamic function, making it a promising agent in
It has a rapid onset of action, dose-proportionate sedative PSA. However, the concerns on suppression of endogenous
effect without analgesia and rapid recovery time.4 corticosteroid production have led to widespread restriction
The side effects include pain on injection, negative on its use in pediatric clinical practice.6

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Indian Journal of Practical Pediatrics 2017;19(4) : 335

Triclofos: It is an oral non-barbiturate sedative hypnotic Monitoring during sedation

that lacks analgesic properties. Oral usage and minimal
respiratory depression have made it an ideal agent for The practitioner responsible for providing PSA should
outpatient use for non-painful procedures. Side effects be skilled in resuscitation and trained in providing advanced
include clumsiness, nausea, vomiting and skin rash. pediatric airway support [certified in Pediatric Advanced
Life Support (PALS)]. There should be supporting
Combination agents personnel trained in PALS to assist during resuscitation
measures. The practitioners must be equipped with skills
A combination of drugs from different classes is
to rescue the child from a deeper level of sedation than
commonly employed during PSA. While using more than
that is intended. The name, dosage, route, time of
one drug, titration of drug with lowest effective doses is of
administration of all drugs administered have to be
paramount importance but the potential for increased side
documented by a designated person.
effects have to be kept in mind. Midazolam and morphine,
midazolam and ketamine are popular drug combinations Baseline vital signs have to be recorded prior to
during PSA. administration of sedative medications. During the
Local anesthetics procedure, there should be a continuous monitoring of
airway patency, respiratory rate, heart rate and oxygen
Local anesthetics reversibly block conduction of saturation, which have to be documented at frequent
impulses along peripheral and central neural pathways and intervals. Monitoring of ventilation using capnography is
are useful adjuncts to sedative/analgesics for painful recommended especially in situations where purposeful
procedures. Lignocaine is a commonly used local verbal communication between the patient and provider is
anesthetic, administered in a dose of 5-7 mg/kg. not possible. The child’s head and neck position should be
Vasoconstrictor, particularly epinephrine is frequently monitored to ensure airway patency. During restraint, care
added to limit systemic absorption and lengthen the should be taken to avoid airway obstruction or chest
duration of sensory blockade. Care should be taken to avoid restriction.2,9
intravenous injection of local anesthetic agents. All local
anesthetics are not only cardiac depressants but may also Special situations
cause central nervous system excitation or depression.
Neonates and former premature infants have immature
Topical agents hepatic and renal functions that alter drug metabolism,
necessitating drug dosing modifications and extended post-
Topical creams such as eutectic mixture of lidocaine procedure monitoring. 10 The increased risk of
and prilocaine produce effective skin anesthesia and can postanesthesia apnea in former preterm infants has to be
be applied under occlusive dressing one hour prior to borne in mind.
procedures such as intravenous cannulation and lumbar
puncture. Topical vapocoolant sprays delivered onto the Children with anatomic malformations such as Pierre-
skin just before needle insertion offers pain relief during Robin sequence, Treacher Collins syndrome, Apert
intravenous cannulation.7 syndrome, Crouzon syndrome, Down syndrome,
micrognathia, macroglossia, tonsillar enlargement may
Non-pharmacologic interventions
need the help of advanced providers expertise in managing
Non-pharmocologic interventions such as distraction difficult airway.
helps in reducing the procedure time as well as the number
of staff required for a procedure.8 The interventions that Superior mediastinal syndrome needs special mention,
can be used to minimise pain are as follows: least invasive diagnostic techniques need to be employed
with avoidance of general anesthesia for diagnostic
a) Cognitive interventions: They are used in older procedures. Personnel and equipment for emergency
children to direct attention away from the painful airway management including rigid bronchoscopy and
procedure. Examples include imagery, preparation and tracheostomy should be available beforehand.
education of the child in an age-appropriate manner,
coping statements, video games and television. Post-procedure care
b) Behavioral interventions: The techniques include Children have to be monitored in a suitably equipped
breathing exercises, positive reinforcement, coping recovery area till they become awake. Continuous
behaviours, desensitisation and parental coaching. monitoring of vital signs is recommended till discharge

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Indian Journal of Practical Pediatrics 2017;19(4) : 336

criteria are met. The goals during post-procedure period American Academy of Pediatric Dentistry. Guidelines for
are stable vital signs, intact protective airway reflexes, Monitoring and Management of Pediatric Patients before,
ability to communicate at baseline, tolerate oral fluids and during, and after sedation for diagnostic and therapeutic
absence of pain. procedures: Update 2016. Pediatrics 2016; 138(1):
e20161212
Points to Remember 3. Gorelick M, Nagler J, Losek JD, Bajaj L, Green SM,
Luhmann J, et al. Pediatric sedation pearls. Clin Ped Emerg
• Procedural sedation and analgesia (PSA) is a Med 2007; 8:268-278.
continuous process and involves titration of agents 4. Denny MA, Manson R, Della-Giustina D. Propofol and
to the desired effect. etomidate are safe for deep sedation in the emergency
• Pre-sedation assessment includes focussed history department. West J Emerg Med 2011; 12:399-403.
and physical examination of the child’s airways. 5. Afonso J, Reis F. Dexmedetomidine: Current role in
anaesthesia and intensive care. Rev Bras Anestesiol 2012;
• The goals during PSA include sedation, anxiolysis, 62(1):118-133.
analgesia, motion control, amnesia and muscle 6. Tobias JD. Etomidate in pediatric anaesthesiology: Where
relaxation and the choice of agents depends on the are we now? Saudi J Anaesth 2015; 9(4):451-456.
type of procedure and the intended need.
7. Griffith RJ, Jordan V, Herd D, Reed PW, Dalziel SR.
• Careful monitoring is vital during and after sedation Vapocoolants (cold spray) for pain treatment during
with appropriate documentation. intravenous cannulation. Cochrane Database of Systematic
reviews 2016; 4:CD009484.
References
8. Srouji R, Ratnapalan S, Schneeweiss S. Pain in Children:
1. American Society of Anaesthesiologists [Internet] Assessment and Nonpharmacological Management.
Continuum of depth of sedation: Definition of General International Journal of Pediatrics, vol. 2010, Article ID
Anaesthesia and Levels of Sedation/Analgesia. c2014 474838, 11 pages, 2010. doi:10.1155/2010/474838
[updated 2014 October 15; cited 2017 July 15].Available 9. Mahajan C, Dash HH. Procedural sedation and analgesia
from: http://www.asahq.org/quality-and-practice- in pediatric patients. J Pediatr Neurosci 2014; 9(1):1-6.
management/standards-and-guidelines accessed on 10. Allegaert K, van den Anker JN. Clinical pharmacology in
th
5 September, 2017. neonates: small size, huge variability. Neonatology 2014;
2. Cote CJ, Wilson S. American Academy of Pediatrics, 105(4):344-349.

CLIPPINGS

Long-term effects of glucocorticoids on function, quality of life, and survival in patients with Duchenne
muscular dystrophy: a prospective cohort study.
A 10 year follow up study of 440 subjects was conducted to determine the long-term impact of glucocorticoids
on milestone-related disease progression across the lifespan and survival in patients with Duchenne muscular
dystrophy.The results are as follows: In patients treated with glucocorticoids for 1 year or longer vs in patients
treated for less than 1 month or never treated (log-rank p<0·0001), time to all disease progression milestone
events was significantly longer.Compared with treatment for less than 1 month, glucocorticoid treatment for
1 year or longer was associated with increased median age at loss of mobility milestones by 2.1-4.4 years and
upper limb milestones by 2.8-8.0 years. In comparison with prednisone or prednisolone, deflazacort was related
to increased median age at loss of three milestones by 2.1-2.7 years (log-rank p<0·012).
McDonald CM, Henricson EK, Abresch RT, Duong T, Joyce NC, Hu F, et al. Long-term effects of
glucocorticoids on function, quality of life, and survival in patients with Duchenne muscular dystrophy:
a prospective cohort study. Lancet 2017 Nov 22. pii: S0140-6736(17)32160-8. doi: 10.1016/S0140-
6736(17)32160-8.

22
Indian Journal of Practical Pediatrics 2017;19(4) : 337

IAP - IJPP CME 2017

FINANCIAL LITERACY FOR DOCTORS after getting married and make the policy as family
floater.
Thirumalai Kolundu S
5. Invest 6 months equivalent of your expenses in liquid
Doctors vulnerability funds as emergency money which can be withdrawn
within 24 hours. This will earn double the interest
Due to our hectic work schedule, lack of time to read
when compared to SB account.
financial magazines and reluctance to discuss financial
matters with peers, doctors seldom possess adequate 6. Percentage of saving equivalent to your age should be
financial knowledge. in fixed-income instruments like debt funds, PPF, tax
free bonds and fixed deposits (last).
Moreover we easily succumb to the pressure of the
bank people and investment agents who are mostly our 7. For income tax exemption under 80c, best options are
patients or relatives and take wrong financial calls resulting Equity linked savings schemes (ELSS) and Public
in huge loss. provident fund (PPF).
In order to avoid this, we must take basic training to 8. Only 5% of portfolio should be gold and that too only
become financially literate and can also engage a financial as gold exchange traded fund (ETF). Jewels will have
adviser registered under Securities and Exchange Board only ornamental value and will not serve as good
of India (SEBI) to manage our finance. investment.
Need for financial prudence 9. Buy first flat without any hesitation but think twice
before buying second one. Most of the time good
Due to extended period of education, we settle very mutual fund earns more than the real estate.
late in our life and start to earn only at the age of 30 to 35
years. Marriage and having a child are also delayed because 10. Investment in mutual funds are very important and
of this. Even then when we start our life, we go for loans should make up 50% of our portfolio. Instead of
to buy a car, house, to set up a clinic and to buy instruments investing in multiple mutual funds, choose 4 or 5
leading to heavy debt trap which takes away most of our mutual funds and invest under systematic investment
income as interest. To overcome all these things, we must plan (SIP). Our spread in mutual funds can be like
have adequate financial knowledge to optimise our this - Large cap funds 2 numbers, diversified funds
investments to get good returns. 2 numbers and one mid cap fund.

Finance advice in a nutshell 11. Investment in shares requires lot of knowledge. When
we don’t have time to read financial magazines, we
1. Start financial planning and retirement planning at an can choose best 20 to 30 top performing companies in
early age as soon as we start earning and not very late various sectors and buy 1 or 2 shares during every fall
in life. of SENSEX by 500 to 1000 points. Similarly we can
2. Save with discipline and innovation. buy Nifty BeES also during every fall of SENSEX.
This will give a decent return of at least 15%.
3. Take term insurance up to 8 to 10 times of your annual This will make us rich in a long time horizon.
income.
12. Try to avoid high cost loans.
4. Take health insurance for Rs 5 lakhs immediately after
starting to earn and increase it to minimum of 10 lakhs 13. Try to use debit cards instead of credit cards. Credit
cards favour uninhibited spending.
* President, Indian Academy of Pediatrics, It is ideal to attain financial independence by the age
Tamilnadu. of 55, so that we can enjoy life in travel, reading, writing
email : iap_tvl@yahoo.co.in and spending time with our family and lead a peaceful life.
23
Indian Journal of Practical Pediatrics 2017;19(4) : 338

IAP - IJPP CME 2017

THROMBOCYTOPENIA ITP. A MPV that is considerably higher than normal

suggests one of the macro thrombocytopenia syndromes
*Janani Sankar (eg, Bernard-Soulier syndrome or MYH9-related
Abstract: In an infant or child thrombocytopenia can occur disorders). A low MPV (3 to 5 fL) is typically seen in
due to large spectrum of illness ranging from tropical patients with Wiskott–Aldrich syndrome (WAS) and
infection to malignancy or bone marrow failure. it is X-linked thrombocytopenia. These abnormalities should
important recognize signs and symptoms to identify the be further evaluated by visual examination of the peripheral
underlying illness which caused thrombocytopenia. blood smear as since both platelet counts and calculated
Laboratory evaluation is essential to reach the diagnosis. MPV from automated cell counters can be inaccurate when
Management is decided by the severity of platelet size is outside the reference range.
thrombocytopenia, associated risk factors and underlying The peripheral blood smear must be carefully
illness. examined to estimate the platelet number, determine the
Keywords: Platelets, Bleeding. platelet morphology presence or absence of platelet
clumping and also to assess if there are associated white
Thrombocytopenia, defined as a platelet count of less and red blood cell abnormalities.
than 150,000/μL, is clinically suspected when there is a
history of easy bruising or bleeding in a child. It may also Circulating blast cells suggest a leukemic process.
present as an incidental finding during routine evaluation Blast cells on the peripheral blood smear may be difficult
or during investigations performed for other reasons. to distinguish from atypical lymphocytes that are
sometimes present in a postviral case of ITP.
The etiology for thrombocytopenia can be broadly
divided as decreased production and increased destruction Fragmented erythrocytes (schistocytes) suggest a
(Table I). microangiopathic process, such as disseminated
intravascular coagulation (DIC), hemolytic-uremic
Thorough history about the duration, severity and site syndrome, or thrombotic thrombocytopenic purpura.
of bleeds, associated systemic symptoms like fever, bone Spherocytes may suggest autoimmune hemolytic anemia
pains if any, previous history of transfusions, drug intake coupled with autoimmune-mediated thrombocytopenia
and family history are very vital to the etiological diagnosis. (Evans syndrome) In these patients, the direct antiglobulin
Clinical examination should focus on anthropometry, test (DAT, also known as the Coombs test) will be positive.
dysmorphic features and cutaneous markers which narrow Less commonly, autoimmune-mediated neutropenia may
down the etiology to bone marrow failure syndromes and also occur.
findings such as lymphadenopathy and organomegaly
points to an infiltrative disorder. Bone marrow examination

Lab investigations In most cases of isolated unexplained

thrombocytopenia in children, a bone marrow examination
In the complete blood count not only the platelet count is not required in the initial evaluation unless there are
and mean platelet volume (MPV) but also evidence of any clinical features that suggest bone marrow infiltration or
other cytopenias (ie, anemia and leukopenia) should be failure.
noted. In a child with thrombocytopenia, a mildly elevated
MPV is consistent with a destructive etiology, including A bone marrow examination is indicated if any of the
following findings, which are suggestive of either marrow
* Senior consultant, infiltration with abnormal cells or marrow hypocellularity
Kanchi Kamakoti CHILDS Trust Hospital,
are present -
Chennai.
email : janani.sankar@yahoo.com (i) Evidence of involvement of other blood cell lines
24
Indian Journal of Practical Pediatrics 2017;19(4) : 339

Table I. Thrombocytopenia in children - Etiology

Destructive Thrombocytopenias Decreased platelet production
Immune mediated Infection: Epstein bar virus, cytomegalo virus, varicella,
Immune thrombocytopenia (ITP)* bacterial infection.
Drug-induced thrombocytopenia Nutritional deficiencies (Folate, B 12, Iron)
Systemic lupus erythematosus (SLE)
Infection such as malaria, scrub typhus, leptospirosis Acquired bone marrow failure
Neonatal immune thrombocytopenias Aplastic anemia, drugs, viral infections, Chemotherapy,
Post-transplant thrombocytopenia radiation myelodysplastic syndromes
Non-immune Infiltrative bone marrow diseases
Hemolytic-uremic syndrome Acute leukemias, lymphoma, metastatic cancers,
Thrombotic thrombocytopenic purpura infectious granulomas, storage diseases
Extracorporeal therapies (eg, cardiopulmonary bypass)
Congenital or acquired heart disease Genetic causes of impaired thrombopoiesis
Disseminated intravascular coagulation Wiskott-Aldrich syndrome/X-linked thrombocytopenia
Kasabach-Merritt syndrome Inherited bone marrow failure syndrome
Hypersplenism Fanconi anemia
Hypothermia Dyskeratosis congenita
Type 2B Von Willebrand disease Swachmann Diamond syndrome
Congenital amegakaryocytic thrombocytopenia (CAMT)
Thrombocytopenia with absent radii (TAR) syndrome
Congenital amegakaryocytic thrombocytopenia with
radioulnar synostosis
Familial platelet disorder with predisposition to myeloid
malignancy
Bernard-Soulier syndrome
MYH9-related disorders
Paris-Trousseau syndromeX-linked thrombocytopenia
with dyserythropoiesis
Source : Donald LY, Donald HM, Leung LLK, Armsby C. Approach to the child with unexplained thrombocytopenia.
UpToDate. Topic 5939 Version 19.0 last updated: Jul 10, 2015.

(e.g. anemia or leukopenia) in the absence of a likely cells. In bone marrow failure syndromes there is marrow
alternative explanation. hypocellularity, with decreased megakaryocytes.
(ii) Presence of blasts on peripheral blood smear. Other tests
(iii) Chronic, stable thrombocytopenia even when the For children with evidence of hemolytic anemia on
presumed diagnosis is ITP as it is a diagnosis of the peripheral blood smear (eg, spherocytes or
exclusion. schistocytes), the additional test are required. A direct
(iv) Systemic symptoms (e.g. fever, weight loss, bone pain) antiglobulin (DAT, also known as a direct Coombs test) is
that are consistent with an underlying malignancy done to detect an autoimmune hemolytic anemia. D-dimer
and fibrinogen levels are useful for diagnosis of
In patients with ITP, the bone marrow will be cellular, intravascular coagulation in children with schistocytes on
and the erythroid and myeloid precursors normal in number the peripheral blood smear and/or vascular tumors on exam.
and appearance. The megakaryocytes are typically normal Other tests to evaluate for a microangiopathy include serum
or increased in number, and may appear large and/or lactic dehydrogenase, creatinine and ADAMTS13 activity.
immature. By contrast, in patients with leukemia the normal
cellular components of the bone marrow are partially or Children with chronic thrombocytopenia or with
almost totally replaced by immature or undifferentiated features suggesting inherited bone marrow failure
25
Indian Journal of Practical Pediatrics 2017;19(4) : 340

syndromes (e.g. pancytopenia with short stature, café au catheterization to maintain a safer count of 50,000.
lait spots) should undergo specific testing for these c) In an asymptomatic child when the platelet count is
disorders in addition to a bone marrow biopsy. For example, <10,000 where there is a risk of spontaneous bleed. Here
the presence of increased chromosomal breakage in again transfusion is not given if the child is
lymphocyte cultures with DNA cross-linking agents such hemodynamically stable and in the recovery phase.
as mitomycin C is diagnostic of Fanconi anemia.
2. In leukemia: Transfusion threshold is lower in a sick
Reticulated platelets - Although not yet widely child with acute leukemia and there is a risk of spontaneous
available in clinical laboratories, many reports indicate that bleed.
quantification of reticulated platelets (RP) may provide
useful information for differentiating between disorders 3. Immune thrombocytopenic purpura: Acquired
of platelet destruction and production. Analogous to red thrombocytopenias usually respond to intravenous gamma
blood cell reticulocytes, RP consist of the larger, younger, globulin and sometimes steroids in select situations. Clear
more recently released platelets containing mRNA and protocols are available for the management of a child with
reflect increased platelet turnover. RP measurem ITP. It is decided by the severity of bleeding and degree of
thrombocytopenia, individual patient characteristics and
End methods have not been standardized, but usually
associated risk factors.
have involved flow cytometric techniques utilizing
fluorescent dyes such as thiazole orange to stain mRNA. In the presence of life threatening bleeding such as
Successful validation and standardization of reliable, cardiopulmonary compromise or intracranial bleed,
automated methods for measuring RP are anticipated as a resuscitation and immediate intervention is needed
future aid in the evaluation of thrombocytopenia. including one or the combination of the following - platelet
Management transfusion, intravenous immunoglobulin or anti D
immunoglobulin.
Bleeding risk and thrombocytopenia: Risk of spontaneous
bleeding is high when the platelet count is < 10,000. In non life threatening bleeding: There is no role of platelet
For the same count risk is higher in thrombocytopenia due transfusion. IVIG can be safely used in an emergency if
to decreased production as in bone marrow failure or bone marrow examination is not planned as it does not
leukemia. But the risk is less when it is caused by peripheral affect the bone marrow findings in leukemia. Anti D
destruction because of the presence of younger healthy Immunoglobulin is used as an alternative in a child with
circulating platelets as in ITP. rhesus positive blood group. Steroids, Dexamethasone or
prednisolone is used when bone marrow examination is
Once the etiological diagnosis is made the treatment normal.
becomes individualised.
General measures to reduce bleeding: Restriction of Low bleeding risk: Children with only skin bleed or no
activities, avoiding contact and collision sports, avoiding bleeding may not need any pharmacologic intervention and
trauma, wearing helmets in ambulant children and avoiding watchful waiting is the plan.
drugs like NSAID are advocated. Antifibrinolytics and 4. Inherited bone marrow failure syndromes are usually
hormone therapy are used in adolescent girls to prevent treated with stem cell transplantation.
blood loss due to menstrual bleed. Monitoring and
educating the parents is an important component. Points to Remember
The management of thrombocytopenia is dependent on
etiology. Platelet concentrates are usually reserved for • Thrombocytopenia is defined as a platelet count of
children with either severe thrombocytopenia or a bleeding less than 150,000/microL. Spontaneous bleeding
sick child. The management of commonly encountered four does not usually occur until the platelet count is less
disorders are discussed. than 20,000/microL.
1. Dengue: Thrombocytopenia in dengue is not aggressively • Clinical presentation with cutaneous (eg, petechiae,
corrected. Platelet transfusion is often not decided on non-palpable purpura, ecchymoses) and/or mucosal
platelet count alone. It is indicated only in three situations. (eg, epistaxis, gingival bleeding, bullous hemorrhage,
a) Adolescent girl with thrombocytopenia and menstrual menorrhagia) bleeding are common while
bleed, b) Prior to procedures like central venous intracranial hemorrhage (ICH) is rare.

26
Indian Journal of Practical Pediatrics 2017;19(4) : 341

• Thrombocytopenia with systemic symptoms and/or 6. Balduini CL, Savoia A, Seri M. Inherited
the presence of lymphadenopathy or thrombocytopenias frequently diagnosed in adults.
hepatosplenomegaly should raise suspicion for J Thromb Haemost 2013; 11:1006-1019.
malignancy or and should be evaluated expeditiously. 7. Drachman JG. Inherited thrombocytopenia: when a low
platelet count does not mean ITP. Blood 2004; 103:390-
• Peripheral blood smear must be carefully examined 398.
for estimation of platelet number, morphology, 8. Alter BP. Diagnosis, genetics, and management of inherited
presence or absence of platelet clumping and bone marrow failure syndromes. Hematology Am Soc
evaluation for associated white and red blood cell Hematol Educ Program 2007; 29-39.
abnormalities. 9. Israels SJ, Kahr WH, Blanchette VS, Luban NL,
Rivard GE, Rand ML. Platelet disorders in children:
• Bone marrow examinations generally are not
A diagnostic approach. Pediatr Blood Cancer 2011;
required for the initial evaluation in most cases of 56:975-983.
unexplained isolated thrombocytopenia in children.
10. Moake JL. Thrombotic micro angiopathies. N Engl J Med
Bibliography 2002; 347:589-600.
11. Mathew P, Chen G, Wang W. Evans syndrome: results of a
1. Rodeghiero F, Stasi R, Gernsheimer T, Michel M, national survey. J Pediatr Hematol Oncol 1997; 19:433-
Provan D, Arnold DM, et al. Standardization of 437.
terminology, definitions and outcome criteria in immune
12. Miller BA, Schultz Beardsley D. Autoimmune
thrombocytopenic purpura of adults and children: report
pancytopenia of childhood associated with multisystem
from an international working group. Blood 2009;
disease manifestations. J Pediatr 1983; 103:877-881.
113:23862393.
13. Savoia A, De Rocco D, Panza E, Bozzi V, Scandellari R,
2. Lusher JM. Clinical and laboratory approach to the patient Loffredo G, et al. Heavy chain myosin 9-related disease
with bleeding. In: Nathan and Oski’s Hematology of (MYH9 -RD): neutrophil inclusions of myosin-9 as a
th
Infancy and Childhood, 6 edn, Nathan DG, Orkin SH, pathognomonic sign of the disorder. Thromb Haemost
Ginsburg D and Look AT (Eds), Saunders, Philadelphia, 2010; 103:826-832.
2003; p1449-1486.
14. Balduini CL, Pecci A, Savoia A. Recent advances in the
3. Vesely S, Buchanan GR, Cohen A, Raskob G, George J. understanding and management of MYH9-related
Self-reported diagnostic and management strategies in inherited thrombocytopenias. Br J Haematol 2011;
childhood idiopathic thrombocytopenic purpura: results 154:161-174.
of a survey of practicing pediatric hematology/oncology 15. Monteagudo M, Amengual MJ, Muñoz L, Soler JA,
specialists. J Pediatr Hematol Oncol 2000; 22:55-61. Roig I, Tolosa C. Reticulated platelets as a screening test
4. Crosby WH. Editorial: Wet purpura, dry purpura. JAMA to identify thrombocytopenia aetiology. QJM 2008;
1975; 232:744-745. 101:549-555.
5. Kumar R, Kahr WH. Congenital thrombocytopenia: 16. Donald LY, Donald HM, Leung LLK, Armsby C. Approach
clinical manifestations, laboratory abnormalities, and to the child with unexplained thrombocytopenia.
molecular defects of a heterogeneous group of conditions. UpToDate. Topic 5939 Version 19.0 last updated: Jul 10,
Hematol Oncol Clin North Am 2013; 27:465-494. 2015.

NEWS AND NOTES

43rd ANNUAL CONFERENCE OF IAP – TNSC

and
32nd SOUTH ZONE CONFERENCE
Date: 9th - 12th AUGUST, 2018
Venue: Sangam Hotels, Tiruchirappalli, Tamil Nadu.
Conference Secretariat
Dr. K Senthilkumar MD DM
Organizing Secretary
Website: www.trypedicon2018.com

27
Indian Journal of Practical Pediatrics 2017;19(4) : 342

IAP - IJPP CME 2017

LATE TALKING TODDLER-WHEN TO Box 1. Late talkers – Synonyms

WORRY?
Children with expressive language delay (It is delay not
*Somasundaram A disorder)
Abstract: Late talkers are children who exhibit delay in Late language learners
language onset with no other diagnosed disabilities or Late language emergence (LLE)
developmental delays in other cognitive or motor domains.
The primary objective is to differentiate them from other Maturational speech delay
causes of speech and language delay. They may present Einstein syndrome
with expressive language delay only or mixed expressive
and receptive delay. Family history, male gender, lack of Normal language development trajectory
communicative interaction between parents and children
All human languages have rules which determine their
are the known risk factors for late talking. It is appropriate
grammar, tune or music (“prosody”) and the range of
to adopt ‘watchful waiting’ strategy with late talkers who
sounds used. Babies absorb these rules through a natural
have good comprehension and without any family history
process of hearing and learning. How infants and children
of language problems.
master the rules of language is one of the miracles of nature
Keywords: Late talkers, Expressive speech delay. which is still not understood well till now. The normal
language developmental milestones are summarized in the
‘Late talkers’ is a term used in the scientific field of Table I.2 The red flag signs suggesting a need for immediate
atypical language development to describe toddlers who evaluation are given in Table II.3
exhibit delay in expressive language skills, although they
do have intact receptive skills with no other deficits, such Risk factors
as cognitive, neurological, socio-emotional or a sensory
i) Male gender: A large-scale study by Zubrick, Taylor,
deficit.1 Late talking does not define a clinical disorder,
Rice, and Slegers (2007) found that male children are three
but may be a stage in the language development of a child
times more likely to have language delay compared with
or a symptom of an evolving disorder.
females. Horwitz et al. (2003) found that males between
Late talking may be an early or secondary sign of 12 and 17 months tend to have statistically significantly
disorders, such as specific language impairment, social lower expressive language performance than girls.
communication disorder, autism spectrum disorder,
ii) Heritability: Family history of language impairments
learning disability, attention deficit hyperactivity disorder,
appears to be one of the main risk factors for the presence
intellectual disability or other developmental disorders.
of delayed language emergence in children.
In order to make a differential diagnosis, it is critical to
monitor the global development of a child in domains that iii) Communicative interaction between parents and late
include, but are not limited to, cognitive, communication, talkers: Parental language input to late talkers is
sensory and motor skills. The synonyms of ‘late talkers’ is quantitatively similar to input to children with typical
given in Box 1. Some researchers distinguish a subset of language development. Parents of children with typical
children with LLE as “late bloomers”. They infer that late language development and parents of children with
bloomers catch up to their peers in language skills by 3 to language delay produce similar language in terms of the
5 years of age. number of utterances and the number of words.
* Consultant - Developmental and Behavioural Pediatrics, Nevertheless, in terms of quality of interaction, it seems
Kanchi Kamakoti CHILDS Trust Hospital, that parents of late talkers respond less often to their
Chennai. children compared to parents of children with typical
email : drsoma2001@yahoo.com language development.
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Indian Journal of Practical Pediatrics 2017;19(4) : 343

Table I. Speech and language - Developmental milestones

Age Receptive Expressive
0-2 months Turns to sound Cries
Prefer voices
Interested in faces
2-4 months - Coos
6 months Responds to name Babbles
9 months Understands verbal routines Points
12 months Follows a verbal command Jargon
First words
15 months Points to body parts by name Learning new words slowly 10-20 words
18-24 months Understands sentences Learning new words quickly 50-100 words
Uses two-word phrases
24-36 months Answers questions Uses three-words phrases
Follows two-step commands Asks “what” questions 50% intelligible
36-48 months Understands much of what issaid Ask “why” questions 75% intelligible
48-60 months Understands much of what issaid, Creates well-formed sentences Tells stories
commensurate withcognitive level 100% intelligible

Table II. Red flags suggesting need for immediate speech-language evaluation
Age Receptive Expressive
12 months - Does not babble, point, or gesture
15 months Does not look at or point to 5 to 10 objects Does not use at least three words
or persons when named by parents
18 months Does not follow one-step directions Does not say “mama,” “dada,” or other names
2 years Does not point to pictures or body parts Does not use at least 25 words
when named
2.5 years Does not verbally respond or nod/shake Does not use unique two-word phrases, including
head to questions noun-verb combinations
3 years Does not understand prepositions or Does not use at least 200 words
action words
- Does not follow two-step directions Does not ask for things by name
- - Repeats phrases in response to questions
(echolalia)
At any age - Has regressed or lost previously acquired speech/
language milestones

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Indian Journal of Practical Pediatrics 2017;19(4) : 344

iv) Parental stress: Children growing in an environment Primary

characterized by high levels of parental stress concerning
a child’s language difficulties are more likely to exhibit Developmental speech and language delay: Speech is
poor expressive language. It is worth noting here that delayed. Children have normal comprehension,
mothers of late talkers in their reports evaluate their intelligence, hearing, emotional relationships and
relationship with their late talking child as very stressful. articulation skills.
Expressive language disorder: Speech is delayed.
v) Socio-economic status of the family: Children who come
Children have normal comprehension, intelligence,
from families characterized by a low educational level and
hearing, emotional relationships, and articulation skills.
poverty are more likely to experience delays and difficulties
Expressive language disorder is difficult to distinguish at
in expressive language. Highly educated mothers are more
an early age from the more common developmental speech
likely to use rich vocabulary and speak in longer utterances
and language delay.
when interacting with their children. It is evident that
factors such as mother’s education, socioeconomic status, Receptive language disorder: Speech is delayed and
parental occupation, parenting style or even parental mental also sparse, agrammatic and indistinct in articulation.
health issues (for example, maternal depression) have an Children may not look at or point to objects or persons
impact on a child’s likelihood of being a late talker. named by parents (demonstrating a deficit in
comprehension).Children have normal responses to
Language profile of late talkers nonverbal auditory stimuli.
Vocabulary: Late talkers appear to delay about 12 months Secondary
in lexical acquisition compared to typically developing
children. It has been known that late talkers actually use Autism spectrum disorder: Children have a variety of
more communicative gestures than their typically speech abnormalities, including speech delay (especially
developing peers. This is probably because late talkers with concurrent intellectual disability), echolalia (repeating
cannot temporarily rely on their expressive language skills, phrases) without generation of their own novel phrases,
and thus prefer using communicative gestures. difficulty initiating and sustaining conversations, pronoun
reversal and speech and language regression. Children have
Linguistic outcome of late talkers impaired communication, impaired social interaction, and
repetitive behaviors/circumscribed interests.
Some children recover and have comparable
expressive language skills with their same-age typically Cerebral palsy: Speech delay in children with cerebral palsy
developing peers. A significant number of children are may be due to difficulty with coordination or spasticity of
expected to perform within the mean or above the 10th tongue muscles, hearing loss, coexisting intellectual
percentile on expressive language measures, whereas a disability or a defect in the cerebral cortex.
smaller number of children continue to experience Childhood apraxia of speech: Apraxia of speech is a
expressive language difficulties. They are at high risk for physical problem in which children have difficulty making
language disorders, learning disabilities, poor academic sounds in the right order, making it hard for their speech to
outcomes, social or behavioural problems and declining be understood by others.Children communicate with
IQ as the child ages.4 gestures but have difficulty with speech (demonstrating
motivation to communicate, but lack of speech ability).
Language delay-How to identify from other
causes?2 Dysarthria: Dysarthria is a physical problem in which
children can have speech difficulties ranging from mild,
The causes of speech and language delay can be with slightly slurred articulation and low-pitched voice, to
primary or secondary. Primary speech and language delay profound, with an inability to produce any recognizable
include developmental speech and language delay, words. Children communicate with gestures but have
expressive language disorder and receptive language difficulty with speech (demonstrating motivation to
disorder. Secondary speech and language delay are communicate, but lack of speech ability).
attributable to other conditions such as hearing loss,
intellectual disability, autism spectrum disorder, physical Hearing loss after spoken language established: Speech
speech problems or selective mutism. and language are often gradually affected, with a decline

30
Indian Journal of Practical Pediatrics 2017;19(4) : 345

in the precision of speech articulation and a lack of progress Box 3. 4S strategy

in vocabulary acquisition. Parents may report that the child
does not seem to be listening, or describe the child speaking (i) Say less
better than listening. Short sentences
Hearing loss before onset of speech: Speech is delayed. Simplify messages
Children may have distortions of speech sounds and
(ii) Stress
prosodic patterns (intonation, rate, rhythm, and loudness
of speech). Children may not look at or point to objects or Emphasize key words
persons named by parents (demonstrating a deficit in Vary and exaggerate tone of voice
comprehension). Children have normal visual
communication skills. Repeat
(iii) Go slow
Intellectual disability: Speech is delayed. Use of gestures
is delayed, and there is a generalized delay in all aspects Speak slowly
of developmental milestones. Children may not look at or
Use longer pauses between words
point to objects or persons named by parents, demonstrating
a deficit in comprehension. (iv) Show

Selective mutism: Children with selective mutism show a Talk about familiar things / here-and-now
consistent failure to speak in specific social situations in Use objects or point to the object
which there is an expectation for speaking [e.g., at school]
despite speaking in other situations. Screening and assessment
Parents of children with symptoms of delayed speech
Box 2. Interaction and information and language development usually approach a clinician
strategies when the child is 18-36 months old. In such cases any
concern that something may be wrong with the child should
A) Interaction strategies be taken seriously, as parents’ observations of abnormal
behaviour in children at this age are quite accurate.
• Be face-to-face (Don’t be an arm chair parent). Being
at your child’s level means he/she can see your face History should include information about
and mouth when you speak consanguinity, family history of hearing loss, family history
• Establish eye contact of late talking, birth history including prenatal
(medications, radiation, TORCH), natal (gestation, weight,
• Observe and listen APGAR) and neonatal history (NICU stay,
• Wait - to see the child’s interest hyperbilirubinemia, seizures, meningitis, ototoxic drugs),
environmental factors (e.g., amount of language
• Allow your child to lead stimulation), trauma to ear / ear discharge and
developmental milestones history.
• Take a turn
B) Information strategies During examination the child should be observed
while interacting with parents and also when the child plays.
• Talk slowly Dysmorphic features, growth abnormality, neurocutaneous
markers should be noted. ENT examination along with
• Short sentences
neurological examination including cranial nerves, motor
• Repeat and/or emphasize key words system and reflexes should be done.
• Modelling Diagnostic workup includes audiometry, MRI/CT
• Expansion - Use the REPEAT + 1 WORD rule brain, karyotyping, IQ assessment and screening and
(repeat the word the child has said and add another subsequent assessment for language using standardised
word to it) tools. Screening for speech and language delay can be done
using early language milestone scale 0-3 years or Language
• Asking questions Evaluation Scale Trivandrum (LEST). LEST 0-3 and 3-6
31
Indian Journal of Practical Pediatrics 2017;19(4) : 346

years is a simple tool developed by CDC Kerala. • A family history of language/literacy problems is a
Receptive–Expressive Emergent Language Scale (REELS) risk factor for persisting problems.
is designed to identify receptive and expressive language
• A good clinical evaluation of the central nervous
problems in children up to 3 years.
system, ear, nose and throat and audiometry are
Interventions for late talkers mandatory in all cases of suspected speech and
language delay.
Delay in speech and language development in children
• Almost all kids with autism are late talkers - but not
should be detected as early as possible to ensure optimal
all late talkers have autism.
treatment and to prevent psychiatric problems later in life.
This process of detection and treatment should be • ‘Watchful waiting’ strategy can be adopted in late
multidisciplinary, involving the parents, school teacher, talkers who have good comprehension and without
pediatrician, pediatric neurologist, ear, nose, and throat family history of language problems.
specialist, child psychiatrist, child psychologist, linguist
References
and speech pathologist.5
1. Hawa VV, Spanoudis G. Toddlers with delayed expressive
Interaction and information strategies help stimulate language: An overview of the characteristics, risk factors
speech and language (Box 2) and to make the language and language outcomes. Res Dev Disabil 2014; 35:400–
easy to understand one needs to use the “4S” (Box 3). 407.
2. McLaughlin MR. Speech and Language Delay in Children.
Late talking toddlers can create anxiety to parents.
Am Fam Physician 2011; 83(10):1183-1188.
In the majority of cases, there’s no need for alarm. It is the
3. Schum RL. Language screening in the pediatric office
duty of the paediatrician to examine the child in detail and
setting. Pediatr Clin North Am 2007; 54(3):425–436.
ensure that there are no red flags needing immediate speech
and language evaluation. Most children do develop 4. Irwin JR, CarterAS, Briggs-Gowan MJ. The Social-
Emotional Development of “Late-Talking” Toddlers,
language at their own pace.
J Am Acad Child Adolesc Psychiatry 2002; 41(11):1324–
Points to Remember 1332.
5. Jamiu O Busari, Nielske M Weggelaar. How to investigate
• Majority of late talkers do not have later language and manage the child who is slow to speak. Brit Med J
difficulties. 2004; 328:272–276.

NEWS AND NOTES

Pediatric Conference of North India 2017

&
1st National Conference on Research in Child Health
Organized by
IAP Delhi State Branch
Date: 22nd – 24th December, 2017
Venue: Hotel Pullman, Aerocity, New Delhi
Further details contact
IAP Delhi State Branch, 113-114 First Floor, (Punjab & Sind Bank Building)
21 Rajendra Place, New Delhi-110008.
Tel:+91 11 25811029, M: +91 8447441560
Email: iapdelhi2@gmail.com, info@pcni2017.com; Web: www.pcni2017.com

32
Indian Journal of Practical Pediatrics 2017;19(4) : 347

IAP - IJPP CME 2017

ELEVATED TRANSAMINASES IN A CHILD and erythrocytes. In the hepatocyte, SGOT is present

- APPROACH mainly in the mitochondria (80%) and only 20% in the
cytosol. When both enzymes are elevated and if SGPT is
*Malathi Sathiyasekaran more than SGOT it would indicate cytosol injury as seen
in viral hepatitis. Whereas if SGOT is more than SGPT,
Abstract: Elevated transaminases or transferases implies
it may indicate mitochondrial injury as seen in drug induced
that the levels of serum glutamic pyruvic transaminase
or toxic hepatitis. Isolated elevation of SGOT may be due
(SGPT) or alanine aminotransferase (ALT) and serum
to muscle disorders or cardiac disease. Transaminases are
glutamic oxaloacetic transaminase (SGOT) or aspartate
considered as elevated when they are more than twice the
aminotransferase (AST) are more than twice the upper limit
upper limit of normal (ULN). In a child with jaundice the
of normal and indicate hepatocyte injury. This may be
term hepatitis is used only when the transaminases are
detected incidentally in an asymptomatic child or be
elevated.
present in a symptomatic child with liver disease. The level
of transaminases may be elevated both in acute and chronic Transaminase levels
hepatitis but is not an index of prognosis. In acute hepatitis
the level may indicate the etiology and recovery whereas The normal level of transaminases varies with age,
in chronic hepatitis it is used as a surrogate marker to gender, BMI, exercise and even the time of collection.
monitor therapy. The usual lab value ranges between 0-40 U/L and in day to
day practice if the value is more than twice ULN, it is
Keywords: Transaminases, Transferases, Hepatocyte considered as elevated. However, several population based
injury. studies have documented that the upper limit of normal is
Transaminases or aminotransferases are catalyst much lower than 40 U/L. A landmark study done in 2002
enzymes which are detected normally in low levels in the by Prati et al., in 6835 adult blood donors have reported
serum (1-40U/L). The two transaminases are serum the 95th centile for SGPT in male donors as 30 U/L and for
glutamic-pyruvic transaminase (SGPT) and serum glutamic female donors as 19 U/L.1 If this value is accepted as the
oxaloacetic transaminase (SGOT) which are now upper limit of normal then even 40 U/L would be
designated as alanine aminotransferase (ALT) and aspartate considered as elevated. In children and adolescents, studies
aminotransferase (AST) respectively. These enzymes help have shown different values. England et al., have reported
in the transfer of the α amino groups of alanine and aspartic that in 1293 HCV uninfected children, the 95th centile in
acid to the α-keto group of ketoglutaric acid resulting in boys was 60 U/L and in girls 55U/L below 18 months of
the formation of pyruvic and oxaloacetic acid (Box 1). age.2 In the above 18 months group the 95th centile in boys
was 40 U/L and in girls 35U/L. The SAFETY (Screening
The transaminases or transferases are sensitive ALT for Elevation in Today’s Youth) study in
indicators of hepatocyte injury. Though they are grouped 982 adolescents of 12-17 years by National Health and
as liver function tests it is a misnomer since they do not Nutrition Examination Survey (NHANES) was published
detect functions of the liver. in 2010 by Schwimmer et al where the 95th centile for SGPT
Significance of SGOT and SGPT in boys was 25.8 and in girls 22.1U/L.3 Since the value
differs in the various studies, the normal range in the
SGPT is more liver specific and is present in the laboratory where the blood is tested is taken to determine
cytosol of the hepatocyte. SGOT is not liver specific and the cut off value.
is present in several tissues such as liver, cardiac muscle,
skeletal muscle, kidney, brain, pancreas, lung, leukocyte Elevated transaminases - Approach
* Consultant Pediatric Gastroenterologist, Children with elevated transaminases- SGPT more
Kanchi Kamakoti CHILDS Trust Hospitals, Chennai. than twice ULN on two occasions 4 weeks apart should be
email: mal.bwcs@gmail.com subjected to detailed evaluation. Elevated SGPT may be
33
Indian Journal of Practical Pediatrics 2017;19(4) : 348

Box 1. Transaminases and transfer of α amino group

Alanine + ketoglutaric acid SGPT L–glutamic acid + pyruvic acid
(ALT)
L-aspartic acid + ketoglutaric acid SGOT L-glutamic acid + oxaloacetic acid
(AST)

Box 2. Elevated transaminases in II. Symptomatic child with elevated

asymptomatic children - Common causes transaminases

• Chronic hepatitis - HBV, HCV The same approach to elevated transaminases as in

an asymptomatic child should be done for a symptomatic
• Non alcoholic fatty liver disease (NAFLD)
child.
• Wilson disease
Detailed history: A detailed history should be elicited
• Glycogen storage disorder regarding fever, nausea, vomiting, jaundice, duration of
• Drug induced liver disease (DILI) illness, itching, stool and urine color, abdominal pain, fluid
retention, urine output, loss of appetite, gastro intestinal
• Autoimmune hepatitis
bleed, altered sensorium, similar history in family or
neighbourhood, blood transfusion, needle pricks, past
seen in an asymptomatic child (incidentally detected) or
history of jaundice, school performance, medications, rash
symptomatic child. It is essential that a detailed history,
and joint problem will give a clue to the type of jaundice
a complete clinical examination, careful perusal of
as to whether it is hepatocellular or cholestatic. The duration
available reports is done before subjecting asymptomatic
of illness if more than 6 months is usually considered as
or symptomatic child to further investigations.
chronic. But in children 3 months is accepted as cut off for
I. Asymptomatic child with elevated chronicity.
transaminases4
Clinical examination: Icterus, scratch marks, liver size
Detailed history: A detailed history regarding jaundice in
and consistency, presence of free fluid and splenomegaly
the past, blood transfusions, recurrent needle pricks,
should be looked for. Eyes should be examined for KF
medications, family history of liver disease and dietary
ring. Presence of firm liver with or without splenomegaly
habits should be noted in detail.
is a marker for chronic liver disease.
Examination: The child’s weight, height and BMI should
be recorded. Acanthosis nigricans, if present, indicates Investigations: All available investigations should be
insulin resistance and is seen in non-alcoholic fatty liver carefully scrutinized. A low hemoglobin may indicate blood
disease (NAFLD) whereas Kayser-Fleischer ring is an loss or nutritional deficiency. A low platelet count may be
excellent clue for Wilson disease. The abdomen should be a feature of cirrhosis. Bicytopenia or pancytopenia may
examined in detail and the size of the liver and its give a clue to hemophagocytic lymphohistiocytosis (HLH).
consistency should be noted. Splenomegaly is usually not Serum bilirubin with fractionation, alkaline phosphatase,
a finding in NAFLD and GSD I but may be present in all albumin, gamma glutamyl transpeptidase and prothrombin
the other conditions listed in Box 2. time should be studied. A low albumin and prolonged
prothrombin time may indicate chronic liver disease with
Investigations: Careful perusal of available investigations impaired function. All symptomatic children should have
is essential before performing new tests. Biochemical tests an ultrasound of abdomen and the details of liver
of the liver-serum bilirubin, alkaline phosphatase, gamma echotexture and presence of ascites should be noted.
glutamyl transpeptidase and prothombin time are done.
All children should have an ultrasound of the abdomen to Specific investigations: Viral serology-HBsAg should be
check the liver size, echotexture and the grading of fatty done and if positive anti HBc IgM has to be done in those
liver. Specific investigations are shown in Table I. with acute hepatitis. If the history and clinical findings are
These conditions require definitive treatment even if the suggestive of chronic hepatitis HBsAg, HBeAg, anti HBe
child is asymptomatic but presents with elevated and HBV DNA, anti HCV and HCV RNA should be done.
transaminases. A simplified treatment protocol is shown If there are features of infective non viral hepatitis, work
in Table II. up for typhoid, rickettsia and leptospirosis should be done.

34
Indian Journal of Practical Pediatrics 2017;19(4) : 349

Table I. Investigations in asymptomatic children with elevated transaminases

Disease Investigations
Chronic HBV infection HBsAg, HBeAg, anti HBe, HBV DNA (viral load), liver biopsy
Chronic HCV infection Anti HCV, HCV RNA (Viral load)
NAFLD Blood sugar, lipid profile, fibroscan, liver biopsy
Wilson disease Serum ceruloplasmin, 24 hour urine copper and liver biopsy
Glycogen storage disease Fasting blood sugar, triglycerides, lactate, uric acid, liver biopsy
Autoimmune liver disease ANA, ASMA, globulin profile, IgG, liver biopsy
ANA – Antinuclear antibody; ASMA – Anti smooth muscle antibody

Table II. Treatment in asymptomatic children with elevated transaminases

Disease Treatment
Chronic HBV infection Peg IFN and antivirals entecavir, tenofovir
Chronic HCV infection Peg IFN + ribavirin or oral direct acting antivirals (DAAs)
NAFLD Regular exercise, weight reduction, vitamin E
Wilson disease D pencillamine
Glycogen storage disease Uncooked corn starch
Autoimmune liver disease Steroids / azathioprine
Peg IFN – Pegylated interferon

Table III. Elevated trasaminases in symptomatic children - Etiology

Acute Chronic
I. Infective hepatitis: viral (HAV, HEV, HBV, HCV, EBV, CMV) I. Infections: HBV, HCV
bacterial (typhoid), spirochetal (leptospirosis), protozoal (malaria)
II. Non infective II. Non infective
Medications Metabolic: Wilson’s
Metabolic: Wilson’s, glycogen storage disease Autoimmune hepatitis
Autoimmune: Type I, 2 Medications
Vascular Vascular
Malignancy Malignancy
Hemophagocytic lymphohistiocytosis
35
Indian Journal of Practical Pediatrics 2017;19(4) : 350

Fig.1. Approach to a symptomatic child with acute hepatitis

Table IV. Etiology according to level of transaminases

Mild (2-3 elevation) >3-20 elevation)
Moderate (> >20 elevation)
Marked (>
Viral infection Bacterial hepatitis(typhoid) Viral (hepatotrophic virus)
Sepsis Spirochetal (leptospirosis) Hypoxic (DSS, CCF)*
Cholestasis Metabolic (Wilson,GSD)* Drug induced hepatitis*
Liver abscess Biliary obstruction Autoimmune hepatitis
Non alcoholic steato hepatitis Autoimmune hepatitis
GSD: Glycogen storage disease, DSS: Dengue shock syndrome, CCF: Congestive cardiac failure
* Mitochondrial injury: SGOT > SGPT

Autoantibodies, ceruloplasmin etc., may be necessary to or marked as mild 2-3 ULN, moderate >3-20 ULN, marked
exclude autoimmune hepatitis (AIH) and Wilson disease >20ULN. The various causes of hepatitis can be arbitrarily
(WD). Upper GI endoscopy should be done in a child with categorized into the three groups as shown in Table IV.
features of chronic liver disease to exclude portal Marked elevation of transaminases is seen in viral hepatitis
hypertension. If there is ascites a diagnostic tap and analysis due to the hepatotrophic viruses, toxic hepatitis as seen in
is necessary. drug induced liver injury (DILI) and hypoxic hepatitis as
seen in dengue shock syndrome. In the latter there is a
The hepatic causes of elevated transaminases in a
simultaneous increase in LDH and the transaminases which
symptomatic child which may be due to acute hepatitis or
will decrease as soon as the child is stabilized which is not
chronic hepatitis as shown in Table III. The important non
a feature in viral hepatitis.
hepatic causes of elevated transaminases in a child are
celiac disease and muscular dystrophy. Ratio of SGOT /SGPT: The normal SGOT /SGPT ratio
is 1 and if it is more than 2, a mitochondrial injury should
a) Acute hepatitis
be suspected as seen in dengue shock, metabolic liver
Level of transaminases: According to the level of enzymes disease e.g. Wilson disease and drug induced hepatitis
elevated transaminases can be divided as mild, moderate (paracetamol). This change in ratio is not a feature in the
36
Indian Journal of Practical Pediatrics 2017;19(4) : 351

Table V. Usefulness of elevated transaminases in acute and chronic liver disease

Acute liver disease Chronic liver disease
Diagnosis Confirms hepatitis Confirms hepatitis
Levels and SGOT / SGPT ratio may give Levels and SGOT / SGPT ratio do not help in
clue in etiological diagnosis etiological diagnosis
Monitoring Decreases with recovery; beware may also Helps in monitoring therapy
indicate massive necrosis
Prognosis No No
Therapy Specific treatment for underlying etiology. Specific treatment for underlying etiology.
Fall in levels supports response to therapy. Fall in levels supports response to therapy

classical viral hepatitis where the SGPT is markedly The transaminases therefore are good surrogate marker for
elevated because the injury is more in the cytosol. response to therapy in chronic HBV infection and
The level of transaminases and the SGOT / SGPT ratio autoimmune hepatitis. In end stage liver disease the
may give some clue to the etiology which can then be pediatric end-stage liver disease (PELD) score is used for
confirmed with definitive tests as shown in Fig.1 and registering for liver transplant which does not include these
Table IV. enzymes as indices.
Serial transaminases in acute hepatitis: In a child with In conclusion, the role of elevated transaminases in
acute viral hepatitis a fall in the transaminases may indicate acute or chronic liver disease in relation to four parameters-
recovery if the serum bilirubin is also decreasing and the diagnosis, monitoring, prognosis and therapy are shown
prothrombin time is normal. However, a rapid fall in in Table V.
transaminases with rising serum bilirubin and prolonged
prothrombin time may indicate hepatocellular necrosis and Points to Remember
acute liver failure. Therefore the level of transaminases is • Elevated transaminases are markers of hepatocyte
not a useful prognostic index in acute hepatitis and is not injury and do not indicate liver function.
included in the prognostic indices of acute liver failure.
• A child with elevated transaminases whether
b) Chronic hepatitis asymptomatic or symptomatic needs to be evaluated
in detail.
The causes of chronic hepatitis are shown in Table III.
• In acute hepatitis elevated transaminases may give
Level of transaminases: In chronic hepatitis there is a some clue to etiology and indicate recovery when the
mild or moderate elevation of transaminases. In the level decreases.
majority they are usually 3 to 5 times the ULN. A value
more than 5 times ULN with elevated bilirubin more than • Transaminases are not a marker for prognosis in
5 mg /dL may indicate acute on chronic liver failure. either acute or chronic liver disease.
In cirrhosis the transaminases may be normal indicating • In chronic hepatitis B elevated transaminases helps
that the level of transaminases does not help in in initiating therapy.
prognostication in acute as well as in chronic liver disease.
In chronic HBV infection the elevated transaminases helps • Transaminase levels are used as a surrogate marker
in classifying the phase of chronic infection. for monitoring therapy in both chronic hepatitis B
The transaminases are normal in immune tolerance and and autoimmune hepatitis.
inactive HBsAg carrier phase. References
Level of transaminases and therapy: In chronic HBV 1. Prati D, Taioli E, Zanella A, Della Torre E, Butelli S, Del
infection at present only those with elevated transaminases Vecchio E, et al. Updated definitions of healthy ranges for
more than twice ULN should be treated. In chronic HCV, serum alanine aminotransferase levels. Ann Intern
the transaminases may be normal and child is treated based Med 2002; 137(1):1-10.
on the HCV RNA and the fibrosis score on fibroscan. 2. England K, Thorne C, Pembrey L, Tovo PA, Newell ML.
37
Indian Journal of Practical Pediatrics 2017;19(4) : 352

Age- and sex-related reference ranges of alanine detection of pediatric chronic liver disease.
aminotransferase levels in children: European paediatric Gastroenterology 2010; 138(4):1357–1364.e2. doi:10.
HCV network. J Pediatr Gastroenterol Nutr 2009; 49:71- 1053/j.gastro.2009.12.052.
77. [PMID: 19465871 DOI: 10.1097/MPG.0b013e 4. Vajro P, Maddaluno S, Veropalumbo C. Persistent
31818fc63b] hypertransaminasemia in asymptomatic
3. Schwimmer JB, Dunn W, Norman GJ, Pardee PE, children: A stepwise approach. World J Gastroenterol
Middleton MS, Kerkar N, et al. SAFETY study: Alanine 2013; 19(18): 2740-2751. doi: 10.3748/wjg.v19.
aminotransferase cutoff values are set too high for reliable i18.2740.

CLIPPINGS

Positive and Negative Themes Found in Superhero Films.

Superhero films have become incredibly popular. The objective of this study was to determine the positive and
negative themes found in a select number of superhero films. A total of 30 superhero films were analyzed.
The average numbers of positive and negative themes were 19.4 and 29.5 mean events per hour for all included
films, respectively. The most common positive themes were “assisting others/protecting the public,” “positive
relationships with family/friends,” and “teamwork/collaboration.” The most common negative themes were
“acts of violence/fighting,” “use of guns/knives/lethal weapons,” and “bullying/intimidation/torture.” Based on
the superhero films included in our study, the number of negative themes, especially acts of violence, outweighs
positive themes. Although an exposure to positive themes found in superhero films may be beneficial to the
development of children, pediatric health care providers should counsel children and their families in an attempt
to limit their exposure to violence.
Bauer M, Georgeson A, McNamara C, Wakefield BH, King TS, Olympia RP. Positive and Negative Themes
Found in Superhero Films. Clinical Pediatrics 2017; 56(14): 1293-1300.

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CONTACT NUMBERS: 8185935783, 9030213662

38
Indian Journal of Practical Pediatrics 2017;19(4) : 353

IAP - IJPP CME 2017

HYPOPIGMENTED SKIN LESIONS – WHAT of Ito in the decreasing order of frequency to be the common
A PEDIATRICIAN SHOULD KNOW? congenital disorders of pigmentation in a study done at
Rajasthan.1 A south Indian study observed the frequency
*Madhu R of hypopigmentary disorders among children to be 3.28
per 1000 children attending the dermatology outpatient
Abstract: Hypopigmentation in a child, is of deep concern
department. Pityriasis alba, vitiligo, leprosy, nevus
to the parents mainly owing to the social stigmatization
depigmentosus and pityriasis versicolor were the most
and the belief that all hypopigmented lesions are either
common hypopigmentary disorders observed in this study.2
due to leprosy or vitiligo. Hypopigmentation may be
congenital or acquired, localized or generalized, Approach to a hypopigmented lesion
circumscribed or diffuse and may be due to infectious or
non-infectious causes, with or without scales. It becomes First and the foremost factor to be considered is
important for the pediatrician to be well versed with the whether the lesion is congenital or acquired. Congenital
clinical presentation of the various common conditions hypopigmented lesion may be localized, circumscribed
associated with hypopigmentation. Four congenital causes hypomelanosis or associated with extracutaneous, systemic
of hypomelanosis and few acquired causes of manifestations. Congenital, localized hypomelanosis
hypopigmentation such as pityriasis alba, pityriasis without systemic involvement include nevus achromicus
versicolor, polymorphic light eruption, vitiligo, post or nevus depigmentosus and nevus anemicus. Those with
inflammatory hypopigmentation and leprosy will be systemic involvement are Hypomelanosis of Ito, tuberous
discussed in this article. sclerosis and nevoid hypomelanosis. Common acquired
hypopigmented conditions in children may be classified
Keywords: Hypopigmentation, Congenital, Acquired. as those associated with the presence of scales such as
Hypopigmented skin lesion in a child is a cause of pityriasis versicolor, pityriasis alba and polymorphic light
mighty concern to the parents who always think that it is eruption and those without scales such as vitiligo, Hansen
either vitiligo or leprosy, both of which carry a strong social disease, lichen striatus and post inflammatory
stigma. It becomes a difficult task for the pediatrician, many hypopigmentation. Other less common conditions in office
a times to arrive at the correct diagnosis due to the close practice include kwashiorkor, lichen sclerosus,
resemblance of these lesions and to address the anxious onchocerciasis and post kala azar dermal leishmaniasis.
parents and at times the children too. Hypopigmentation Approach to hypopigmented skin lesions is depicted in the
may be congenital or acquired, localized or generalized, Fig.1.
circumscribed or diffuse and may be due to infectious or Congenital hypomelanosis
non-infectious causes, with or without scales. A well
elicited history and an astute clinical examination will aid Nevus achromicus / Nevus depigmentosus
in clinical diagnosis. Dermatological examination of a
hypopigmented skin lesion is incomplete if one does not Nevus achromicus also known as nevus
use a magnifying lens to look for the border (well defined depigmentosus (ND)3 occurs in 1.6% to 4.7% of children.4
or well to ill-defined), surface, shape, presence of scales, It may be present at birth or may occur during the early
atrophy and distribution of hair. Raghavendra,et al observed infanthood.3 Clinical diagnostic criteria proposed by Coupe
nevus depigmentosus, nevus anemicus, halo nevus, in 1976 include the presence of leukoderma at birth or
tuberous sclerosis complex, piebaldism and Hypomelanosis during early childhood with no alteration in the distribution,
texture or sensation over the lesion throughout life and
* Senior Assistant Professor, absence of hyperpigmented border around the achromic
Department of Dermatology (Mycology), lesion. Nevus achromicus, a non-familial well
Madras Medical College, Chennai circumscribed hypomelanosis is said to occur probably due
email: renmadhu08@gmail.com to a developmental defect in the fetal melanocyte.
39
Indian Journal of Practical Pediatrics 2017;19(4) : 354

Fig.1. Approach to hypopigmented skin lesions

Melanocytes are normal in number, while the melanosomes concern could be addressed by procedures such as blister
are found to be abnormally small, reduced in content and roof grafting or cultured epidermal grafting.5
scattered.5 There are autophagosomes and aggregation of Nevus anemicus
melanosomes within the stubby dentrites of melanocytes
along with a defective transfer of melanosomes to the Nevus anemicus (NA) is a vascular developmental
keratinocytes. ND usually occurs as a solitary lesion but anomaly, often present since birth, but may present in
may be focal, segmental or multiple following the infancy or early childhood. NA occurs as a result of neurally
Blaschko’s lines.6Multiple nevus depigmentosus along the mediated vasoconstriction. There is a localized vascular
Blaschko’s lines associated with systemic involvement is hypersensitivity response to catecholamines which implies
referred to as Hypomelanosis of Ito.3 ND is typically that there is only a functional abnormality while the number
characterized by the presence of hypopigmented rather than of melanocytes and melanosomes are normal. It is
depigmented macules or patches of variable sizes with characterized by the presence of well demarcated,
regular or serrated borders. Lesions usually do not cross hypopigmented patches with serrated margins most
the midline and are seen on the trunk, neck, face and commonly seen on the trunk. Diascopy of the adjacent skin
proximal part of the extremities. However, ND may occur (pressing the skin with a glass slide) results in blanching
in any site of the body. and merging with the nevus anemicus lesion). On firm
stroking of the lesion, wheals appear without erythema.
Treatment: Reassurance should be given as there is no Nevus anemicus may be associated with capillary vascular
effective treatment for ND. Camouflage could be suggested malformation, phakomatosis pigmento vascularis and
for children and adolescents. Subsequently, cosmetic neurofibromatosis.6,7,8
40
Indian Journal of Practical Pediatrics 2017;19(4) : 355

Treatment: Camouflage may be helpful to address the and the skeletal system. Cutaneous manifestations of
cosmetic concern of the individual and that of the parents. tuberous sclerosis include hypopigmented macules,
angiofibroma, fibrotic plaques or nodules, fibrous tumours,
Hypomelanosis of Ito Shagreen patch, ungual or periungual fibroma, gingival
Hypomelanosis of Ito (HI) is characterized by the fibroma and Confetti skin lesions. Presence of three or more
presence of multiple nevus depigmentosus following hypopigmented macules of size more than 5 mm is
Blaschko linear pattern in association with extra-cutaneous considered as one of the major features in the diagnostic
involvement. HI has been reported to occur in 1in 8000 to criteria for tuberous sclerosis complex. These lesions may
10,000 cases. Familial tendency with autosomal dominant be present in about 97% of patients at birth or a little later
or autosomal recessive pattern of inheritance has been in life and are found to be the most common clinical feature
reported. Though both ND and HI are due to mosaicism, in these children. They are most commonly seen on the
type of mutation and the timing of mutation during the trunk with the size ranging from few millimeters to
development of embryo determines the pattern, number centimeters. Shape of these hypopigmented macules may
and the association of extracutaneous involvement. be oval, linear, round (thumb-print), confetti-like or the
Mosaicism is considered to be most likely due to most characteristic lance- ovate shape, commonly referred
chromosomal non-dysjunction during embryo to as the ash leaf spots or ash leaf macules . Wood lamp
development. Short arm of the X-chromosome, the short examination will aid in better visualization of the
arm of chromosome 12 and chromosome 18 are more hypopigmented macules and differentiation from vitiligo.
commonly involved, although many chromosomes that Histopathological examination of the hypopigmented
cause disruption of either the expression or function of lesions reveals a normal number of melanocytes with a
pigmentary genes can be affected.3 reduction in the number, size and melanization of
melanosomes.4.10, 11
Clinical features: HI is characterized by the presence of
well demarcated, hypopigmented patches with regular or Treatment: Reassurance and camouflage are the options
irregular border occurring in multiple segments along the for hypopigmented lesions. Usually patients with tuberous
Blaschko linear pattern or block pattern, which may become sclerosis complex tend to more concerned about the
systematized. Systemic associations are seen as mainly disfigurement due to the facial angiofibromas than about
neurological, ocular and musculoskeletal involvement. the hypopigmented macules which are more often present
Neurological manifestations include developmental delay, in the trunk.
mental retardation, seizures, microcephaly, deafness, Acquired hypopigmented skin lesions
hypotonia, ataxia and hyperkinesia. Ophthalmic
involvement may present as micropthalmia, corneal Acquired hypopigmented skin lesions, although may
opacity, cataract, nystagmus, strabismus, myopia, be classified based on the infective etiology, is best
ambylopia and retinal degeneration. Skeletal abnormalities approached on the basis of the presence or absence of
that may occur are facial and limb asymmetry, short stature, scales. Among those disorders associated with the presence
thoracic deformity, syndactyly, brachydactyly and of scales, common conditions such as pityriasis versicolor,
polydactyly.3, 6,9 pityriasis alba and polymorphic light eruption would be
discussed.
Treatment: There is no specific treatment available for
HI, though the use of 308-nm Excimer laser has been Acquired hypopigmented disorders
reported in literature.6 associated with scaling
Tuberous sclerosis complex Pityriasis versicolor: Tinea versicolor (Misnomer),Tinea
flavea, Dermatomycosi furfuracea, Liver spots,
Tuberous sclerosis complex also known as Chromophytosis.12
Bourneville’s disease is a hereditary disorder with
autosomal dominant inheritance with variable expressivity. Pityriasis versicolor (PV) is a chronic, recurrent,
This disorder which occurs in 1 in 6000 to 1 in 10,000 asymptomatic superficial fungal infection caused by
population results due to mutation of either TSC 1 gene Malassezia which are lipophilic yeasts. The word,
encoding hamartin or TSC 2 gene encoding tuberin. “Pityriasis” is derived from a Greek word which means
Multiple system involvement is seen in the form of “bran like” and “versicolor” means varied colour to denote
hamartomas of the skin, eye, brain, heart, lungs, kidneys the achromic (hypopigmented) and chromic

41
Indian Journal of Practical Pediatrics 2017;19(4) : 356

(hyperpigmented) forms of PV. Wilan first described the

Box 1. Therapy of Pityriasis versicolor14,17
lesions of pityriasis versicolor in 1801.13 Malassezia forms
a part of the normal flora of the skin in more than 90% of Localised lesions
normal adults. In infants, colonization has been observed
by 40 days of life.14 It affects about 30%-40% of population Clotrimazole, miconazole, ketoconazole, sertaconazole,
in temperate climate. In a study conducted in Rajasthan, eberconazole creams twice daily Terbinafine cream
this infection was reported in 21% of the study population twice daily
comprising of children and adolescents.1Study by Reddy Extensive lesions
VS, et al done at Kerala observed pityriasis versicolor to
be the second common fungal infection (39.4%) next to Ketoconazole lotion / shampoo – short contact for 10
dermatophytosis (48.5%).15 Pityriasis versicolor is more minutes before bath x 10 days (to be applied over the
common in adolescents and young adults compared to neck, trunk, arms and forearms)
younger children.16 A positive family history has been
reported, especially in first degree relatives. Infection Selenium sulfide shampoo daily – short contact for 10
results due to the shift from the commensal yeast phase to minutes before bath (Cosmetically unacceptable)
the mycelia phase under certain predisposing conditions Systemic therapy - Tab Fluconazole 400 mg stat dose
such as hot and humid tropical climate, individual host Tab Fluconazole 300 mg once a
susceptibility, malnutrition, hyperhidrosis, occlusive week x 2 weeks
clothing, increased sebum production, corticosteroid Itraconazole 200 mg x 5 days
therapy, immunosuppression and Cushing’s disease.17
Among the 13 species of genus, pityriasis versicolor is Recurrence
usually caused by Malassezia globosa and less often by M
sympodialis and M furfur. The causative organism does Itraconazole 400 mg od monthly once x 6 months
not affect the nails, mucous membrane or hair shaft, but
may cause pulmonary and systemic infections in infants
on intravenous lipid therapy.12 Depressed or altered cell or has undergone treatment. Scaling can also be observed
mediated immunity may be considered as a factor in the by stretching the skin and this is termed as, “Zireli’s sign”.17
development of this infection.14 Common sites of involvement include chest, upper back
and arms. Lesions may be less often seen on the face, neck,
There have been varied mechanisms postulated for forearms, thighs, scalp and rarely over the palms and
the hypopigmented and hyperpigmented lesions of dorsum of fingers. Face is the most frequently affected
pityriasis versicolor. Malassezia species produce azalaic site in infants and children, with the forehead, temple,
acid which competitively inhibits tyrosinase, resulting in medial canthi of eyes and paranasal area being involved.2,14
hypopigmentation. Scales produce a sunscreen effect. Extensive lesions and recurrent episodes are usually seen
Azelaic acid is also said to have a direct cytotoxic effect in the adolescents. Wood’s lamp examination of the scaly
on the hyperactive melanocytes. Electron microscopic lesions reveals a pale yellow fluorescence. Diagnosis is
studies have revealed that there were smaller than normal usually clinical, in the presence of the characteristic clinical
melanosomes in achromic pityriasis versicolor features. When there is a clinical suspicion, scraping of
(hypopigmented type) while, there were abnormally large the scales could be done using a blunt scalpel and examined
melanosomes in chromic (hyperpigmented) type. Stratum in 10% potassium hydroxide for hyaline, short, aseptate,
corneum is found to be thicker in the hyperpigmented angulated hyphae, spherical yeast cells either as isolated
lesions.12,14 ,17 or in groups and blastospores (budding yeast cells). This
characteristic appearance of the hyphae and the yeast cells
Clinical features: Characteristic lesions are in clusters has been referred to as “Spaghetti and meat ball”
hypopigmented or pigmented macules and patches with or “banana and grapes appearance”.
well defined border and fine branny or furfuraceous scales
over the sebum rich areas. When the scales are not visible, Treatment: Localised lesions may be treated with topical
scratching with a finger nail causes loosening of the scales azole antifungal agents or topical terbinafine cream for a
making it perceptible, which is termed as, “Scratch sign or period of 4 to 6 weeks. Extensive lesions over the trunk
Coup d’Ongle sign or Besnier’s sign” and this is considered have to be treated with short contact therapy for 10 minutes
as an important diagnostic feature of pityriasis versicolor.18 before bath with azole lotions or shampoo once a day for
Scratch sign would be negative if a patient has taken bath 10 days. Details of treatment is given in Box1.

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Indian Journal of Practical Pediatrics 2017;19(4) : 357

Pityriasis alba going children who are more vulnerable due to prolonged
hours of playing in the sun. Episodes of PMLE occur during
Pityriasis alba (PA) is an asymptomatic, non-specific spring (March) and early summer. Sharma, et al reported a
eczematous dermatitis of unknown etiology, commonly high incidence of PMLE during March and September in
seen in children in the age group between 3-16 years with a study done at Varanasi. PMLE may also occur due to
equal sex predisposition. It is said to affect 1.9% to 5.25% penetration of ultraviolet radiation through window glasses
of preadolescent children.19 PA results in post inflammatory or even during winter at high altitudes. Lesions are of acute
hypopigmentation and is said to be more common in nature and may develop within hours to days after sun
children with darker skin types. Though it is often exposure and last for one to two weeks after cessation of
associated with atopic dermatitis, PA can occur in the sun exposure. However, there may be persistence of lesions
unaffected children. Dry skin, exposure to sunlight or wind for weeks in the presence of continued exposure to sun,
and soap can affect the outcome of pityriasis alba. There is after which lesions may improve with reduction in
no definite association between bacterial, fungal or parasitic frequency and severity due to the phenomena of hardening
infections and PA. Electron microscopy revealed a normal which occurs as the summer progresses. Hardening refers
number of melanocytes with a reduction in the number to the increased tolerance of skin with continued exposure
and size of the melanosomes.20 to sun. PMLE has been postulated to be due to delayed
hypersensitivity reaction to endogenous cutaneous
Clinical features: PA is characterized by the presence of
photoantigen of unknown nature induced by exposure to
round or irregular hypopigmented patches with ill-defined
ultraviolet (UV) radiation. In normal individuals, UV light
borders and fine scales. Initial phase of erythema is most
induced immunosuppression prevents the autoimmune
often not made out and children are brought for consultation
reactivity that may result due to UV radiation. There is
when the hypopigmentation and scaling have set in. Usually
resistance to this UV induced immunosuppression in those
PA gets noticed in children after prolonged sun exposure
with PMLE. Hereditary form of PMLE with autosomal
during sports activities when the surrounding skin gets sun
dominant inheritance has been reported in native
tanned but not the PA affected skin. Lesions range in size
Americans.23-29
from 0.5cms to 2 cms in size and are most commonly seen
on the face, especially the cheeks, perioral area and chin. Clinical features: PMLE is seen more often on the face
They may also occur on the neck, upper arms and upper and ears in children, when compared to adults. Usually
trunk. Two uncommon variants namely extensive and affected sites are the malar areas of the cheek, bridge of
pigmenting pityriasis alba have been reported. PA runs a the nose, forehead, chin, ‘V’ area and nape of the neck,
chronic and recurrent course in children, sometimes extensor aspect of the forearms and arms, dorsum of the
extending up to 1 year duration.21, 22 hands and upper back. Pruritic skin lesions develop on the
sun exposed sites, within minutes to hours to days after
Treatment: Parents need to be counseled about the post
sun exposure depending on the individual susceptibility.
inflammatory hypopigmentation that takes a long time to
Though the lesions are polymorphic, in any single
repigment. General measures such as reduction of sun
individual, lesions are always monomorphic and even
exposure and regular use of sunscreens should be
during the recurrent episodes, lesions are of the same
advocated. Topical application of emollients is the first
morphology. Various lesions of PMLE are erythematous
line of management. Mild topical corticosteroids such as
to skin coloured grouped papules, plaques, vesicles,
hydrocortisone cream or desonide cream are useful. Topical
papulovesicles, hypopigmented or eczematous patches and
tacrolimus and pimecrolimus may be effective in the
nodules, of which the papular type is the most common.
persistent lesions.20
Hyperpigmentation is often observed within the
Polymorphic light eruption hypopigmented patches. Lesions tend to be symmetrical
in distribution. A pinpoint papular variant with lesions
Polymorphic light eruption (PMLE), an idiopathic resembling lichen nitidus has been described in individuals
immune mediated photosensitive disorder, is the most with dark skin colour. Rarely erythema multiforme like or
common photosensitive dermatoses seen in children. It is urticarial lesions may occur. Hypopigmented patch of
characterized by the occurrence of pruritic, polymorphic PMLE could be differentiated from pityriasis alba
lesions in the sun-exposed sites of the body, on exposure and pityriasis versicolor by the presence of itching after
to ultraviolet radiation. PMLE is more common in children sun exposure and symmetrical distribution when
with Fitzpatrick’s skin types I – IV, especially in the school present.23,25, 26

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Indian Journal of Practical Pediatrics 2017;19(4) : 358

Treatment: Children with PMLE should be advised to limit children. At this stage of early manifestation of infection,
exposure to sunlight from 9 am to 4 pm. General preventive lesion heals without leaving any sequel if the host immunity
measures such as use of long sleeved shirt, broad brimmed is good. Children with indeterminate leprosy present with
hat and umbrella should be strictly followed. Broad one or few asymptomatic, ill-defined hypopigmented
spectrum sunscreen that will offer protection against UVA macules with normal sensation. Lesions are commonly seen
and UVB is preferable. Sunscreen is to be applied 20 on the face, buttocks and extremities. Peripheral nerve
minutes before sun exposure and is to be reapplied every examination is normal. It is very difficult to make a
3-4 hours. In addition, some children may require the diagnosis at this stage as biopsy may not be a feasible option
application of low potent topical steroid such as in children, especially if the lesion is on the face and hence,
hydrocortisone cream on the face or mid potent steroids may require observation over a period of time with regular
such as fluticasone or mometasone for lesions on the follow up. Lesions in indeterminate leprosy may undergo
forearms or back. spontaneous resolution or may evolve into a more definite
spectrum of leprosy.
Common hypopigmented disorders without
scaling True tuberculoid (TT) leprosy: TT leprosy is
characterized by the presence of 1 to 3 well defined,
Among those hypopigmented disorders that are not anesthetic macules or plaques with dry surface. Trophic
associated with scales, leprosy, vitiligo and post changes such as loss of sweating and loss of hair are present.
inflammatory hypopigmentation would be discussed. Asymmetrical thickening of the peripheral nerves in the
Leprosy (Hansen’s disease) region may be present. Sites of predilection in TT leprosy
are similar to indeterminate leprosy.
Childhood leprosy is considered to reflect the burden
of leprosy in the community. Studies have shown that boys Borderlne tuberculoid ( BT) leprosy: Patients with BT
are affected more than the girls. Children in the age group leprosy may present with 3-10 well to ill defined
of 10-12 years are most commonly affected. Index case is hypopigmented, hypoanestheic patches with trophic
most often a close family member or a neighbor with changes. Satellite lesions are present in the periphery of
multibacillary disease. Hypopigmented macules and the lesion. There is asymmetric thickening of the peripheral
patches are the most common skin lesions seen in children nerves.
with leprosy. In a clinic based epidemiological study of Borderline lepromatous leprosy: Multiple
pediatric leprosy done at Kerala, Nair observed hypopigmented patches and plaques with a tendency
hypopigmented macule to be the most common primary towards symmetrical distribution are seen. Sensation may
skin lesion in 71.66% of patients.30 Hypopigmented macule vary. Peripheral nerve thickening may also show tendency
or patch is usually a feature of indeterminate leprosy, towards symmetry.
tuberculoid or borderline tuberculoid leprosy. Borderline
tuberculoid leprosy is the most common type of childhood Lepromatous leprosy: Lepromatous leprosy is rare in
leprosy, followed by indeterminate leprosy and tuberculoid children. Characteristic skin lesions include multiple
leprosy. Borderline lepromatous leprosy and lepromatous macules, infiltrated plaques and nodules in a symmetrical
leprosy are rare in children. distribution.
Clinical features: Indeterminate leprosy, considered as the Treatment: Treatment is based on the classification into
first sign of leprosy is the most common presentation in paucibacillary and multibacillary leprosy. Paucibacillary

Table I.Treatment schedule in children 10 – 14 years31

Drug Paucibacillary - 6 months Multibacillary - 1 year
Monthly supervised dose Daily dose Monthly supervised dose Daily dose 2- 28 days
2- 28 days
Rifampicin 450 mg — 450 mg —
Dapsone 50 mg 50 mg 50 mg 50 mg
Clofazamine — — 150 mg 50 mg alternate days
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Indian Journal of Practical Pediatrics 2017;19(4) : 359

leprosy refers to the presence of 1 to 5 lesions including Post-inflammatory hypopigmentation

single nerve involvement with negative slit skin smear
(SSS). Multibacillary leprosy is inclusive of six and more Many inflammatory disorders such as infections,
skin lesions or more than one nerve involvement burns, bullous disorders, psoriasis, pityriasis rosea,
irrespective of the number of skin lesions and a positive pityriasis alba, pinta, sarcoidosis etc are associated with
SSS. Treatment schedule for children between the age post-inflammatory hypopigmentation. Exact mechanism of
group of 10-14 years is given in Table I. hypopigmentation in these disorders is not clear. It has been
postulated that the keratinocytes that are injured due to
In children younger than 10 years, drug dose may be inflammation are not in a position to accept the
calculated based on the body weight 31 melanosomes that are being transferred from the dendrites
of the melanocytes temporarily. Post-inflammatory
i) Rifampicin - 10 mg /kg body weight once a month, hypopigmentation takes months to years to repigment.4
ii) Dapsone - 2mg/ kg body weight / day
Conclusion
iii) Clofazamine - 2-3 mg/kg body weight once a month
Hypopigmented skin lesion in a child even if single,
and 1 mg/kg body weight on alternate day.
is worrisome to the entire family, which makes it difficult
Early vitiligo for the attending physician, be it a pediatrician or a
dermatologist, as one has to not only make a correct
Vitiligo is an acquired, autoimmune disorder diagnosis and start treatment, but in addition has to offer
characterized by the presence of well demarcated proper counseling and reassurance to the parents. Proper
depigmented macules and patches that occur due to elicitation of history and astute clinical examination will
progressive loss of melanocytes. This is considered to be a aid in correct diagnosis of these lesions.
result of cytotoxic activity of autoreactive T cells against
the melanocytes. Studies have detected autoantibodies Points to Remember
against melanocyte specific antigens that destroy the
• Hypopigmentation may be due to infections or non-
melanocytes. Vitiligo occurs in 1% of the world population
infectious causes, with or without scales. It can be
and can affect any age group. Among these patients, 50%
congenital or acquired, localized or generalized,
of them have their onset before 20 years of age, while in
circumscribed or diffuse.
25% of patients, vitiligo develops before 8 years of age.
Vitiligo is said to have a polygenic inheritance. • Reassurance, camouflage and masterly inactivity are
Monozygotic twins have been reported to have a prevalence the options in children with localised congenital
of 23%, siblings 6% and first–degree relatives 7%-12%. hypomelanotic conditions - Nevus depigmentosus
Classical vitiligo lesions are seen as well demarcated, and nevus anemicus.
depigmented ivory white macules and patches, which pose • Children with Hypomelanosis of Ito and tuberous
no difficulty in diagnosis. However, an early vitiligo lesion sclerosis complex require evaluation for systemic
may appear hypopigmented due to the partial loss of associations.
pigmentation and hence may be confused with pityriasis
alba or pityriasis versicolor. In this scenario, it is noteworthy • Common acquired hypopigmented conditions with
that an early vitiligo lesion appears as a well defined patch scaling includes pityriasis versicolor, pityriasis alba
without scales, whereas pityriasis alba is characterized by and polymorphic light eruption.
ill-defined borders and pityriasis versicolor by well defined • Hypopigmented patch of PMLE could be
macules and patches with fine branny scales. Wood’s lamp differentiated from pityriasis alba and pityriasis
examination provides a good delineation between the versicolor by the presence of itching after sun
normal skin and the vitiligenous lesion.4, 32 exposure and symmetrical distribution when present
Treatment: Early vitiligo could be treated by application • Common acquired hypopigmented conditions
of topical corticosteroids such as fluticasone, mometasone without scaling includes leprosy, vitiligo and post-
or betamethasone valerate once daily for a period of 3-4 inflammatory hypopigmentation.
weeks, followed by intermittent application. Combination
References
of topical corticosteroid with topical calcineurin inhibitor
such as tacrolimus and pimecrolimus, has been found to 1. Soni B, Raghavendra KR, Yadav DK, Kumawat P,
effective in producing repigmentation. Singhal A. A clinico-epidemiological study of

45
Indian Journal of Practical Pediatrics 2017;19(4) : 360

hypopigmented and depigmented lesions in children and 17. Gupta Ak, Bluhm R, Summerbell R. Pityriasis versicolor.
adolescent age group in Hadoti region (South East J Eur Acad Dermatol Venereol 2002; 16:19-33.
Rajasthan). Indian J Paediatr Dermatol 2017; 18:9-13. 18. Kangle S, Amladi S, Sawant S. Scaly signs in dermatology.
2. Sori T, Nath AK, Thappa DM, Jaisankar TJ. Indian J Dermatol Venereol Leprol 2006; 72:161-164.
Hypopigmentary disorders in children in South India. 19. AlShahwan MA. Pigmenting pityriasis alba: Case report
Indian J Dermatol 2011; 56:546-549. and review of the literature. Journal of the Saudi Society
3. Baselga E. Disorders of hypopigmentation. In: Schachner of Dermatology & Dermatologic Surgery 2012;16: 31-
th
LA, Hansen RC, (eds). Pediatric dermatology, vol.1, 4 33.
edn. Philadelphia: Mosby Elsevier; 2011; pp719–734. 20. Ingram JR. Eczematous disorders. Griffiths CEM, Barker
4. Disorders of pigmentation. In: Paller AS, Mancini AJ (eds). J, Bleiker T, Chalmers R, Creamer D (eds). Rook’s
th
Hurwitz Clinical Pediatric Dermatology. 5th edn. New Textbook of Dermatology. 9 edn. West Sussex: Wiley
Delhi: RELX India Pvt Ltd with Elsevier Inc; 2011; pp245- Blackwell; 2016; pp1221-1256.
278.
21. Eczematous eruptions in childhood. In: Paller AS, Mancini
th
5. Hewedy ES, Hassan AM, Salah EF, Sallam FA, NM AJ (eds). Hurwitz Clinical Pediatric Dermatology. 5 edn.
Dawood, Al-Bakary RH, et al. Clinical and ultrastructural New Delhi: RELX India Pvt Ltd with Elsevier Inc; 2011;
study of nevus depigmentosus. J Microsc Ultrastruct 2013; pp38-72.
22-29.
22. Sarifakioglu E. Extensive pityriasis alba in a nonatopic
6. Kumaran SM, Prasad D. Depigmentary and hypopigentary child. Pediatr Dermatol 2007; 24: 199-200.
disorders. In: Sacchidanand S, Oberoi C, Inamdar AC
th
(eds). IADVL Textbook of Dermatology. 4 edn. Mumbai: 23. Photosensitivity and photoreactions. In: Paller AS, Mancini
th
Bhalani Publishing House; 2015; pp1295-1326. AJ (eds). Hurwitz Clinical Pediatric Dermatology. 5 edn.
New Delhi: RELX India Pvt Ltd with Elsevier Inc; 2011.
7. Orchard D, Burden D. Vascular reactions. In: Schachner
th pp245-278.
LA, Hansen RC, (eds). Pediatric dermatology, vol.1, 4
edn. Philadelphia: Mosby Elsevier; 2011; pp1120-1121. 24. Ling TC, Gibbs NK, Rhodes LE. Treatment of polymorphic
light eruption. Photodermatol Photoimmunol Photomed
8. Sethi A, Kaur T, Puri KJPS. Giant nevus anemicus: A rare
2003; 19:217-227.
case report. Indian J Paediatr Dermatol 2013; 14:39-40.
25. Ferguson J. The Idiopathic photodermatoses. Irvine AD,
9. Bodemer C. Incontinentia pigmenti and hypomelanosis of
Hoeger PH, Yan AC, Editors. Harper’s Textbook of
Ito. Handb Clin Neurol 2013; 111:341-347. rd
pediatric dermatology vol 1. 3 ed. West Sussex: Wiley
10. Korf BR. Tuberous sclerosis complex and Blackwell; 2011; pp106.1-106.10.
neurofibromatosis. In: Schachner LA, Hansen RC, (eds).
th
Pediatric dermatology, vol.1, 4 edn. Philadelphia: Mosby 26. Rogers M, McCuaig, Pruksachatkun C, Jeffries M, Duante
Elsevier; 2011; pp481-484. Am, Cocca G et al. Physical injury and environmental
hazards. In: Schachner LA, Hansen RC, (eds). Pediatric
11. Rodrigues DA, Gomes CM, Costa IM. Tuberous sclerosis th
dermatology, vol.2, 4 edn. Philadelphia: Mosby Elsevier;
complex. Ann Bras Dermatol 2012; 87:184-196.
2011; pp1642-1697.
12. Hay RJ, Ashbee HR. Fungal infections. Griffiths CEM,
27. Madhu R. Polymorphic light eruption. Indian J of Pract
Barker J, Bleiker T, Chalmers R, Creamer D (eds). Rook’s
th Pediatr 2013; 15(3): 220-224.
Textbook of Dermatology. 9 edn. West Sussex: Wiley
Blackwell; 2016; pp932-935. 28. Sharma L, Basnet A. A clinicoepidemiological study of
13. Morais PM, Cunha Mda MGS, Frota MZ. Clinical aspects polymorphic light eruption. Indian J Dermatol Venereol
of patients with pityriasis versicolor seen at a referral center Leprol 2008; 74(1):15-17.
for tropical dermatology in Manaus, Amazonas, Brazil. 29. Inamadar AC, Palit A. Photosensitivity in children: An
An Bras Dermatol 2010; 85:797-803. approach to diagnosis and management. Indian J Dermatol
14. Lam JM, Rios HWC, Friedlaner SF. Fungal, protozoal and Venereol Leprol 2005; 71:73-79.
helminthic infections. In: Schachner LA, Hansen RC, (eds). 30. Nair SP. A clinico-epidemiological study of pediatric
th
Pediatric dermatology, vol.2, 4 edn. Philadelphia : Mosby leprosy in the urban leprosy center of a tertiary care
Elsevier; 2011;pp1487-1491. institute. Indian J Paediatr Dermatol 2017; 18:24-27.
15. Reddy VS, Anoop T, Ajayakumar S, Bindurani S, Rajiv S, 31. Kumar J, Ramesh V. Leprosy in Children. In: Sacchidanand
Bifi J. Study of clinical spectrum of pediatric dermatoses S, Oberoi C, Inamdar AC (eds). IADVL Textbook of
th
in patients attending a Tertiary Care Center in North Kerala. Dermatology. 4 edn. Mumbai: Bhalani Publishing House;
Indian J Paediatr Dermatol 2016; 17:267-272. 2015; pp3136-3141.
16. Ghosh SR, Dey SK, Saha I, Barbhuiya JN, Ghosh A, Roy 32. Jain M, Jain SK, Kumar R, Mehta P, Banjara N, Kalwaniya
AK. Pityriasis Versicolor: A Clinicomycological and S. Clinical profile of childhood vitiligo patients in Hadoti
Epidemiological Study from a Tertiary Care Hospital. region in Rajasthan. Indian J Paediatr Dermatol 2014;
Indian J Dermatol 2008; 53(4):182-185. 15:20-23.

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Indian Journal of Practical Pediatrics 2017;19(4) : 361

IAP - IJPP CME 2017

EARLY CHILDHOOD CARIES - CAUSES Consequences of ECC

AND MANAGEMENT ECC is a serious health problem in very young
*Muthu MS children. Though it is not life threatening, if left untreated
*Ankita Saikia it may lead to pain, swelling, compromised chewing ability
and bacteremia. It may be followed by malocclusion in
Abstract: Early childhood caries is a disease affecting permanent dentition, phonetic problems, suboptimal health,
the primary dentition of children below six years of age. sleep disturbances, lower self-esteem and failure to thrive.2,3
Previously, termed as ‘nursing caries’ or ‘baby bottle Consequences of ECC include a higher risk of new carious
caries’, this disease has become endemic in all developed lesions in both the primary and permanent dentitions,4,5
as well as developing countries. Although, there are hospitalizations and emergency room visits,6,7 increased
numerous factors associated with this disease, night time treatment costs,8 risk for delayed physical growth and
feeding practices are strongly associated. This disease not development,9,10 loss of school days and days with restricted
only affects the child’s teeth but also affects the overall activity,11,12 diminished ability to learn13 and diminished
health. Children with early childhood caries have been oral health-related quality of life. It has been demonstrated
associated with poor quality of life. This disease is that dental caries can gradually reduce a child’s ability to
completely preventable when intervened by the first year gain weight, which may get reversed after complete oral
of life. rehabilitation.14

Keywords: Caries, Children, Full mouth rehabilitation, Etiology and risk factors
Prevention. The etiology of ECC is multi-factorial. Risk factors
The disease of early childhood caries (ECC) is defined associated with ECC include early colonization of mutans
by the American Academy of Pediatric Dentistry (AAPD) streptococci (MS) through vertical and horizontal
as the presence of one or more decayed (non cavitated or transmission, low salivary flow at night, the presence of
cavitated lesions), missing (due to caries) or filled tooth plaque, poor oral hygiene, frequency and timing of
surfaces in any primary tooth in a child 71 months of age consumption of sugar-containing drinks.15–18 Other reported
or younger. In children younger than 3 years of age, any associated factors are nocturnal breastfeeding19 and
sign of smooth-surface caries is indicative of severe early prolonged duration of breastfeeding,20 presence of enamel
childhood caries (S-ECC). From ages 3 through 5, one or hypoplasia,21 molar-incisor hypomineralisation22 and the
more cavitated, missing (due to caries), or filled smooth child’s socioeconomic status.23 There are controversies
surfaces in primary maxillary anterior teeth or a decayed, regarding breast milk and bottle milk as etiological factors
missing, or filled score of >4 (age 3), >5 (age 4), or >6 for dental caries.24 A large randomized trial in the area of
(age 5) surfaces is diagnosed as S-ECC.1 In simple words, human lactation provides no evidence of beneficial or
the presence of any decayed tooth or teeth in children below harmful effects of prolonged and exclusive breast-feeding
6 years of age is diagnosed as early childhood caries. on dental caries at early school age.Though it was a large
The presence of any decay in the front teeth in children scale RCT, there were few limitations on these trials in
less than 3 years is diagnosed as severe early childhood terms of measuring the outcome at 6 years of age, lack of
caries. pediatric dentists involvement in the study (public health
dentists recorded the caries status), not scoring or
* Professor and Head, documenting non cavitated lesions. To understand the role
Department of Pediatric Dentistry, of night time feeding practices, further research is needed
Sri Ramachandra University, Porur, Chennai. in the age group of 1-3 years, as during later stage of
email: muthumurugan@gmail.com development (after 2.5- 3 years) multiple other factors play
** Consultant Pediatric Dentist, a greater role and make the etiology of the caries process
Chennai. complex and difficult to understand. Many maternal factors
47
Indian Journal of Practical Pediatrics 2017;19(4) : 362

Table I. Factors found to be significantly related to the prevalence and/or incidence of

deciduous caries in children age 6 years and under
Socio- demographic Dietary factors Oral hygiene Factors related to Oral bacterial
factors breast/bottle feeding flora
Gender of child (male), High frequency, Daily tooth-brushing, Bottle as opposed to Presence of strep.
public rather than high sugar foods/day, frequency of tooth- breast fed, duration of mutans, presence of
private school, family high number of brushing: more often breast feeding, lactobacilli, strep.
income, father between meals sugary & less often, age at nocturnal breast mutans count, rare
unemployed, food/drink, no set time which brushing started, feeding, night-time transfer of maternal
low parental education, for snacks, cariostat visible plaque, bottle use, use of saliva to baby
low maternal education, score, high pocket combined frequency sugar/cereal in the
single mother, money for sweets, brushing and parental bottle, frequency of
occupation of head delayed of weaning, supervision, adults breast feeding, bottle
of household, not eating fruit as a involved in brushing, with sugary drink at
high number children snack, high sugar / lack of use of fluoride bed-time, bottle/breast
per family, 3+ adults fat snacks, 5xdaily toothpaste, not having fed to stop baby crying
in household, sweet snacks, teeth cleaned at at night, duration of
mother with non candy >1x/week, bed-time, bottle feeding with
full-time jobs, low magnesium intake, high gingival score fruit juice, breast fed
birth order, high iron intake, high or plain milk in bottle
immigrant background, cariogenicity score, at night, still bottle /
mother’s young age, high daily frequency breast fed at
2+ children living of sugar intake at 18 months, bottle at
household,cohabitation nursery, high daily night >24mths,
of parents, ethnicity, weight of sugar intake duration of breast or
parental occupation at nursery, >6 eatings bottle feeding, if child
/ drinkings per day, slept with bottle or
food before sleeping, breast at 12 months,
fruit juice at bed-time, bottle carried around
sugary bed-time drink, during the day
carbonated drinks at
bed-time, daily sucrose
intake, night-time
meals/drinks,
night-time juice,
frequency of
consumption of
diluted syrup, milk
intake score, dates
eaten daily, frequent
consumption of sugary
drinks, frequent
consumption of
carbonated drinks,
amount and frequency
of sweet consumption

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Indian Journal of Practical Pediatrics 2017;19(4) : 363

that may predispose children to ECC are bad infant-feeding general anesthesia, children were reported to have better
practices, poor maternal knowledge of oral perceived quality of life. Thus, ECC has a tremendous,
hygiene practices, maternal nutrition and maternal stress but almost invisible, impact on society and the health care
(Table I).25-31 Additionally, newly-erupted teeth, because system.36
of immature enamel and teeth with enamel hypoplasia may
be at higher risk of developing caries32. In 2004, Rebecca Management
Harris conducted a systematic review and concluded that Due to the aggressive nature of ECC, cavities can
there are 106 risk factors associated with ECC.33 develop quickly and if untreated, can infect the tooth’s
Microbial risk markers pulpal tissue. Such infections may result in a medical
emergency that could require hospitalization and the
Microbial risk markers for ECC include mutans extraction of the offending tooth.37 Managing ECC is
streptococci (MS) and lactobacillus species.34 However, challenging task for even a trained pediatric dentist. In ECC
new tools for bacterial identification (e.g., polymerase management, treating dental pain is very important. Pain
chain reaction (PCR) techniques, 16s rRNA gene is difficult to measure due to its subjectivity. Children may
sequencing) are revealing the complexity of the oral not have the language skills to communicate the level of
microbiome and other bacterial species that may be pain they are feeling and assessing pain levels often
associated with ECC.35 depends on the report of parents or pain scale indicators.38
As a result, it’s possible to undertreat or overtreat pain,
ECC and quality of life each of which carries its own set of health risks.36 Since,
Several studies have addressed the effects that ECC ECC mostly affects very young age-group comprising
has on a child’s and their family’s quality of life (QoL). children lacking cooperative ability, the treatment is done
Quality of life factors frequently associated with poor oral mostly under sedation, general anesthesia, etc. Whenever,
health were tooth aches, having trouble eating certain foods, a need for multiple dental procedures like pulp therapy,
missing school, difficulty to brush the teeth, frequent stainless steel crowns and deep caries management are
episodes of fever, cough and cold and poor self-image required, full mouth rehabilitation under general anesthesia
(Fig.1). Studies have also investigated the potential positive is the best way as it allows the pediatric dentist to provide
effect of treatment intervention on QoL for children with the highest quality of dental care (Fig.2 & 3). However,
severe caries. These studies demonstrate improved oral the benefits and the risks involved should be weighed for
health-related QoL following treatment under general each patient and a decision should be taken accordingly.
anesthesia. One to four weeks following treatment under For children with mild ECC (children with white spot

Fig.1. Early childhood caries – Progression

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Indian Journal of Practical Pediatrics 2017;19(4) : 364

Points to Remember
• Presence of caries in children below 6 years of age
can be diagnosed as early childhood caries.
• First dental visit of a child must be as soon as the
Fig.2.Full mouth rehabilitation. first milk tooth erupts or on their first birthday,
(Pre and Post-operative) whichever is the earliest.
• Early childhood caries can result in poor quality of
life for the child. This can be reversed by full mouth
rehabilitation. Consequences of not treating can lead
to damage to permanent teeth as well as increased
caries risk on permanent teeth.
• Full mouth rehabilitation under general anesthesia
is one of the best method for rehabilitation of multiple
caries in children of pre cooperative age.
• Measures like good oral hygiene practices, periodic
fluoride application and periodic dental check up
every 6 months can possibly prevent early childhood
Fig.3.Full mouth rehabilitation - Restoration caries.
of maxillary teeth using strip crowns
References
(Pre operative, after caries removal and post
operative) 1. Policy on Early Childhood Caries (ECC): Classifications,
Consequences, and Preventive Strategies. AMERICAN
lesions or one or two small cavities), chairside treatment ACADEMY OF PEDIATRIC DENTISTRY ORAL
is attempted. Caries removal is done by a slow-speed HEALTH POLICIES 59 Review Council Council on
(micromotor) followed by restoration.39 Clinical Affairs Latest Revision 2016.
Prevention http://www.aapd.org/search/? Keywords=Definition% 2 0
of % 20 Early % 20 Childhood % 20 Caries. % 20
Preventive measures can be categorized into American % 20 Academy % 20 of % 20 Pediatric %20
st
community based measures, professional measures and Dentistry. %20 2015-16 % 3a % 2015 accessed on 1 June,
home care methods. Community-based measures are 2017.
community water fluoridation and education programs 2. Kagihara LE, Niederhauser VP, Stark M. Assessment,
organized at the community level, professional measures management, and prevention of early childhood caries.
are steps taken at the dental office by a dentist to prevent J Am Acad Nurse Pract 2009; 21:1–10.
ECC. These measures include teaching appropriate oral 3. Casamassimo PS, Thikkurissy S, Edelstein B, Maiorini E.
hygiene measures, regular fluoride application, recall visits, Beyond the dmft: The human and Economic cost of Early
childhood caries. J Am Dent Assoc 2009; 140:650–657.
etc. Home care methods are efforts taken by the parents in
relation to dietary habits, feeding habits and oral hygiene 4. O’Sullivan DM, Tinanoff N. The association of early
childhood caries patterns with caries incidence in pre-
measures. Prevention of transmission of mutans
school children. J Public Health Dent 1996; 56(2):81-83.
streptococci from mothers with high counts of mutans
streptococci can be achieved by use of xylitol containing 5. Al-Shalan TA, Erickson PR, Hardie NA. Primary incisor
decay before age 4 as a risk factor for future dental caries.
chewing gum after? delivery. Studies have shown
Pediatr Dent 1997; 19(1):37-41.
significantly lower def index in children whose mothers
6. Ladrillo TE, Hobdell MH, Caviness AC. Increasing
have used xylitol chewing gums from 3-24 months after
prevalence of emergency department visits for pediatric
delivery. Dental education to improve the habits of parents dental care 1997-2001. J Am Dent Assoc 2006;
or caregivers through anticipatory guidance and infant oral 137(3):379-385.
health care measures for ECC prevention can be promoted.
7. Griffin SO, Gooch BF, Beltran E, Sutherland JN,
If the oral hygiene practices are established early this Barsley R. Dental services, costs, and factors associated
disease can be prevented. This can be achieved by with hospitalization for Medicaid-eligible children,
promoting first dental visit at the age of one or after the Louisiana 1996-97. J Public Health Dent 2000; 60(3):
eruption of the first milk tooth whichever is earlier.40 21-27.
50
Indian Journal of Practical Pediatrics 2017;19(4) : 365

8. Kanellis MJ, Damiano PC, Monamy ET. Medicaid costs children. ASDC J Dent Child 1977; 44 :192–193.
associated with the hospitalization of young children for 25. Derkson GD, Ponti P. Nursing bottle syndrome; prevalence
restorative dental treatment under general anesthesia. and etiology in a non-fluoridated city. J Can Dent Assoc
J Public Health Dent 2000; 60(1):28-32. 1982; 48: 389–393.
9. Acs G, Lodolini G, Kaminsky S, Cisneros GJ. Effect of 26. Brams M, Maloney J. Nursing bottle caries in breast-fed
nursing caries on body weight in a pediatric population. children. J Pediatr 1983; 103:415–416.
Pediatr Dent 1992; 14(5):302-305.
27. Kramer MS, Vanilovich I, Matush L, Bogdanovich N,
10. Ayhan H, Suskan E, Yildirim S. The effect of nursing or Zhang X, Shishko G, et al. The Effect of Prolonged and
rampant caries on height, body weight, and head circum- Exclusive Breast-Feeding on Dental Caries in Early
ference. J Clin Pediatr Dent 1996; 20(3):209-212. School-Age Children. Caries Res 2007;41:484–488.
11. Reisine ST. Dental health and public policy: The social 28. Finlayson TL, Siefert K, Ismail AI, Sohn W. Maternal self-
impact of disease. Am J Public Health 1985; 75(1):27-30. efficacy and 1-5-year-old children’s brushing
12. Gift HC, Reisine ST, Larach DC. The social impact of habits. Community Dent Oral Epidemiol 2007; 35:272–
dental problems and visits. Am J Public Health 1992; 281. 29. Leong PM, Gussy MG, Barrow SY, de Silva-
82(12):1663-1668. Sanigorski A, Waters E. A systematic review of risk factors
13. Blumenshine SL, Vann WF Jr, Gizlice Z, Lee JY. Children’s during first year of life for early childhood caries. Int J
school performance: Impact of general and oral health. Paediatr Dent 2013; 23:235–250.
J Public Health Dent 2008; 68(2):82-87. 30. Moynihan PJ, Holt RD. The national diet and nutrition
14. Acs G, Shulman R, Ng MW, Chussid S. The effect of dental survey of 1.5 to 4.5 year old children: summary of the
rehabilitation on the body weight of children with early findings of the dental survey. Br Dent J 1996; 181:328–
childhood caries. Pediatr Dent 1999; 21:109–113. 332.
15. Benjamin RM. Oral health: the silent epidemic. Public 31. Finlayson TL, Siefert K, Ismail AI, Sohn W. Psychosocial
Health Rep 2010; 125:158-159. factors and early childhood caries among low-income
16. Reisine S, Douglass JM. Psychosocial and behavioural African-American children in Detroit. Community Dent
issues in early childhood caries. Community Dent Oral Oral Epidemiol 2007; 35:439–448.
Epidemiol 1998; 26:32–44. 32. Caufield PW, Li Y, Bromage TG. Hypoplasia-associated
17. Tinanoff N. Introduction to the early childhood caries severe early childhood caries: A proposed definition. J Dent
conference: initial description and current Res 2012; 91(6):544-550.
understanding. Community Dent Oral Epidemiol 1998; 33. Harris R, Nicoll DA, Adair MP, Pine MC. Risk factors for
26:5–7. dental caries in young children: a systematic review of the
18. Declerck D, Leroy R, Martens L, Lesaffre E, Garcia-Zattera literature. Community Dent Health 2004; 21(1):71-85.
MJ, Broucke VS, et al. Factors associated with prevalence 34. Kanasi E, Johansson I, Lu SC, Kressin NR, Nunn ME,
and severity of caries experience in preschool Kent R Jr, et al. Microbial risk markers for childhood caries
children. Community Dental Oral Epidemiol 2008; in pediatrician’s offices. J Dent Res 2010; 89(4):378-383.
36:168–178. 35. Li Y, Tanner A. Effect of antimicrobial interactions on the
19. van Palenstein Helderman WH, Soe W, van ‘t Hof MA. oral microbiota associated with early childhood caries.
Risk factors of early childhood caries in a Southeast Asian Pediatr Dent 2015; 37(3):226-244.
population. J Dent Res 2006; 85:85–88. 36. Muthu MS, Sivakumar N. Early childhood caries. In:
20. Folayan MO, Sowole CA, Owotade FJ, Sote E. Impact of Muthu MS, Sivakumar N. Pediatric Dentistry-Principles
nd
infant feeding practices on caries experience of preschool and Practice. 2 ed. Delhi: Elsevier; 2009; pp209-217.
children. J Clin Pediatr Dent 2010; -34:297–301. 37. Sheller B, Williams BJ, Lombardi SM. Diagnosis and
21. Oliveira AF, Chaves AM, Rosenblatt A. The influence of treatment of dental caries-related emergencies in a
enamel defects on the development of early childhood children’s hospital. Pediatr Dent 1997; 19(8):470-475.
caries in a population with low socioeconomic status: a 38. Barrêtto Ede P, Ferreira e Ferreira E, Pordeus IA.
longitudinal study. Caries Res 2006; 40:296–302. Evaluation of toothache severity in children using a visual
22. Elfrink ME, Schuller AA, Veerkamp JS, Poorterman JH, analog scale of faces. Pediatr Dent 2004; 26(6):485-491.
Moll HA, ten Cate BJ. Factors increasing the caries risk 39. Thikkurissy S, Allen P, Smiley M, Casamassimo PS.
of second primary molars in 5-year-old Dutch children. Int Waiting for the Pain to Get Worse: Caregiver Behaviors
J Paediatr Dent 2010; 20:151–157. and Knowledge Toward Pain Medication and Acute Dental
23. Hallett KB, O’Rourke PK. Social and behavioural Pain in Children. Pediatr Dent 2011; 34:289-294.
determinants of early childhood caries. Aust Dent J 2003; 40. Guideline on Perinatal and Infant Oral Health Care.
48:27–33. Reference Manual. American Academy of Pediatric
24. Kotlow LA. Breast feeding: a cause of dental caries in Dentistry. 2016-17; 38 (6):150-154.
51
Indian Journal of Practical Pediatrics 2017;19(4) : 366

IAP - IJPP 2017

HEAD INJURY IN CHILDREN - TRIAGING AND and injuries during sports and games in school aged
IMAGING children and road traffic accidents in adolescents.
*Leema Pauline C Significance
**Viveka Saravanan
**Ravi LA It takes a second to injure the brain but it takes weeks,
months to years to recover. There has been a general view
Abstract: Head injury in infancy and childhood differ that young children can bounce back from any insult.
significantly from adults in the modes of injury, mechanisms There is a common belief that a younger brain is more
of damage and the management of specific problems. Fall plastic and is better able to find new ways of doing things.
from height forms the most important cause of pediatric It is true that children fare better than their adult
head injury. The overall outcome for children with head counterparts in the immediate post traumatic period.
injury is better than that of adults with the same injury However, the neuro-cognitive impairments they face in the
score but recovery takes a longer time. domains of attention, concentration, social skills, executive
skills, communication and learning are often ignored.
Keywords: Head injury, Assessment, Management. Hence, it is very important to prevent head injury in children
Traumatic brain injury (TBI) is a major cause of and treat aggressively if it happens.
disability and death in children and young adults Pediatric uniqueness
worldwide. It is considered a “silent epidemic” because
the general public are mostly unaware of the scale of the Children have a larger head to body surface area -
problem.1 Head injury is one of the most common injuries 18% versus 7% in adults which makes them prone for head
in childhood comprising about 84.3% of all injuries of injury.5 The compliant skull of a child is easily deformed
which isolated head injury constitutes (78.9%) and and so impacts on the brain produce coup injury in contrast
polytrauma including head injury about 5.4%. It is one of to adults in whom the brain is forced against bony
the most frequent reasons for a visit to the emergency prominences to produce countercoup injury. Pediatric brain
department.2 No age is exempt from head trauma with has a higher water content 88% versus 77% in adults which
nearly 25%-27% of all victims being less than 16 years of makes the brain softer and prone for acceleration-
age. deceleration injury. The water content is inversely
proportional to myelination and the unmyelinated brain is
Fall from height such as from unprotected roof tops more susceptible to shear injuries.
or balconies while playing (56.5%) remains the most
common cause of head trauma followed by road traffic Children have a soft cervical vertebra and supple neck
accidents (21%), simple fall from chair or bed (17.5%) which increase their susceptibility for injuries of upper
and fall of heavy objects on the head.3 Boys are more prone cervical spine. They also have a smaller airway
for head trauma than girls with ratio being 1.6:1.4 compromised by large tonsils, adenoid and anteriorly
placed larynx which is more compromised when neck is
The common modes of injury in different age groups flexed or extended. Infants, in general, are more vulnerable
vary - non accidental trauma in infants, falls in toddlers to abusive trauma due to their size, dependency on
caretakers and their inability to report abuse. Premature or
* Professor, disabled children are also more likely than other children
** Assistant Professor, to suffer this type of trauma, perhaps because their
Dept. of Pediatric Neurology, caretakers may feel additionally burdened.6 Children are
Institute of Child Health & Hospital for Children, dependent on the caregiver for supervision and safety and
Madras Medical College, Chennai. ironically often the care givers are the perpetrators of child
email: leemapauline@rediffmail.com abuse.
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Indian Journal of Practical Pediatrics 2017;19(4) : 367

Types of injury by sand bags and towel rolls in younger children as up to

10% of children can have associated cervical spine injury.
There are two types of injury namely the primary
TBI patients should be considered to have a full stomach.
injury which is the direct consequence of the initial physical
In children with suspected basilar skull fracture, orogastric
insult. It comprises irreversible cell damage that is the main
and not nasogastric tube should be passed, as there is a
determinant of clinical outcome. In the secondary injury,
possibility that the tube may enter the cranial cavity through
inflammatory and neurotoxic responses triggered by the
the fractured site.
primary injury induce edema, hypoperfusion, hypoxia and
ischemia.7 These changes often lead to raised intracranial Spinal immobilization: Spinal immobilization should be
pressure (ICP), temperature dysregulation, loss of maintained during intubation since cervical injury cannot
autoregulation and seizures. Much of these secondary be excluded. Full spinal immobilization is indicated in
injuries may be amenable to intervention and left untreated children whose GCS<15 (Table I) with neck pain and
can significantly increase morbidity and mortality tenderness, focal neurological deficit and paresthesia in
associated with TBI. extremities.
Assessment Breathing: When pediatric GCS is less than or equal to 8,
endotracheal intubation with rapid sequence induction
Assessment begins with primary survey which is a
(RSI) with cervical spine protection should be done.
focused physical examination to identify and treat life
Oro tracheal intubation is indicated in suspected basilar
threatening injuries and prevent or minimize secondary
skull fracture. Rapid sequence intubation (RSI) technique
brain injury.8
involves pretreatment with lidocaine which minimizes
Airway: Airway should be stable to provide oxygenation increase in ICP that can be associated with airway
and ventilation. Head and neck should be kept in neutral manipulation and sedation which can be provided by
position. Airway is cleared by a jaw thrust maneuver instead etomidate and thiopental which are neuroprotective.
of head tilt chin lift. Cervical spine should be protected by Paralysis can be induced by non depolarising agents such
a cervical collar of appropriate size in older children and as vecuronium or rocuronium. Succinyl choline is

Table I. Glasgow coma scale (GCS)

Activity Best Response
Adults/Older Children Infants (modified GCS) Score
Eye opening(E) Spontaneous Spontaneous 4
To speech To speech 3
To pain To pain 2
None None 1
Verbal(V) Appropriate speech Coos, babbles 5
Confused speech Irritable, cries but consolable 4
Inappropriate words Cries, Inconsolable 3
Incomprehensible or Moans to pain 2
none specific sounds None 1
None
Motor(M) Obeys Normal spontaneous movement 6
Localizes pain Withdraws to touch 5
Withdraws to pain Withdraws to pain 4
Decorticate to pain Decorticate to pain 3
Decerebrate to pain Decerebrate to pain 2
None None 1

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Indian Journal of Practical Pediatrics 2017;19(4) : 368

contraindicated in neuromuscular disorders as it can cause Head, neck, eyes, ears, nose, mouth and motor function
malignant hyperthermia. Ketamine is contraindicated in should be examined methodically (Table II and Fig.1a, 1b,
patients with significant eye injuries as it can increase both 1c).
ICP and intra ocular pressure.9 Oro-tracheal route is the
preferred one for intubation. It is ideal to ventilate with History
100% oxygen to maintain normocapnia. A proper history is crucial in the management of head
Circulation: Hemodynamic instability is unlikely to be trauma. Historical features regarding the mechanism of
caused by an isolated traumatic brain injury except in case injury (witnessed / unwitnessed), time of injury,
of large scalp laceration which can cause severe bleeding circumstances of injury for e.g. accident, non accidental
in an infant. Hence, if the child presents with shock, other trauma, unexplained fall (seizure or arrhythmia to be
sources of blood loss such as intra abdominal injuries considered) and state in which child was found (LOC,
should be ruled out. There is no single best fluid for children seizures) are important. Presenting symptoms such as loss
with traumatic brain injury, but isotonic crystalloids are of consciousness, repeated vomiting, worsening headache,
widely used and have good scientific basis. Normal saline ear, nose, throat bleed and their duration, condition prior
or lactated ringer’s solution should be the standard to consultation (stable, deteriorating, improving), past h/o
resuscitation fluid. Fluid restriction is no longer bleeding diathesis and medication use such as
recommended.10 Dextrose containing fluids should be anticoagulants should be sought for.
avoided in the correction of shock as the resulting Parents provide the most reliable and trust worthy
hyperglycemia is associated with a poor outcome. 11 information. However if the history is inconsistent and does
Similarly even brief periods of hypotension is associated not match with the physical findings, then the possibility
with poor outcome and hence should be treated of inflicted injury (child abuse) should be thought of.
aggressively. Since children have a large body surface area, Unless a high index of suspicion is maintained, much of
hypothermia poses a real danger. Under stress, hypothermia these can go unrecognized. Presence of fundal
causes acidosis and worsening of metabolic status. hemorrhages, fractures of various ages on skeletal survey,
Disability: Levels of consciousness is assessed by AVPU
(alert, responds to verbal stimuli, responds to painful
stimuli, unresponsive) scale in the emergency department
and by modified Glasgow Coma Scale further (Table I).
Secondary survey: Secondary survey aims at detailed
examination and assessment of individual systems,
identifying all injuries and directing further treatment.
Table II. Head injury site and signs
Site Signs
Head Bruising, laceration, swelling, depression,
Fig.1a.Raccoon eyes Fig.1b.Battle sign
Neck Deformity, tenderness, muscle spasm
Eyes Raccoon eyes, pupil - size, equality,
reactivity, retinal hemorrhage
Ears CSF otorrhea, Battle sign (ecchymosis over
mastoid)
Nose CSF rhinorrhea, deformity, swelling,
bleeding
Mouth Soft tissue injuries, dental trauma
Motor Lateralizing signs
functions Fig.1c.Retinal hemorrhages
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Indian Journal of Practical Pediatrics 2017;19(4) : 369

Table III. Various grades of head injury- Clinical features

Mild head injury Moderate head injury Severe head injury
PGCSs 13-15 PGCSs 9-12 PGCSs 3-8
No LOC Brief LOC at injury, drowsy/alert currently Responds to pain
Up to one episode of vomiting Two / more episodes of vomiting Unresponsive
Alert, stable Persistent headache Localizing signs
Scalp bruising/laceration present Up to a single brief seizure Signs of increased ICP
Normal examination Large scalp hematoma/laceration Penetrating head injury
CSF leak from nose / ear

subdural hematoma in neuro imaging are clinical clues to growing evidence demonstrating that observation before
suspect non accidental trauma. CT is safe in a large majority of patients, especially among
those who present with mild symptoms.17,18 The optimal
Classification duration of observation after head injury is however yet to
Head injury in children can be classified into mild be well-defined and more study is needed in this area.
(score 13-15), moderate (score 9-12) and severe (score 3- The indications for neuro imaging are given in Box 1 and
8) head injury based on Pediatric Glasgow Coma Scale the common findings in CT is given in Fig.3a, 3b, 3c &
(PGCS) scores and their clinical features is given in 3d.
Table III. Indications for skull X-ray
Investigations Skull X- rays do not give any direct information about
Blood investigations such as complete blood count, intracranial injury, hence the indications are limited.
blood sugar, grouping and typing, coagulation profile Whenever there is a suspicion of non accidental trauma,
should be carried out. Non contrast CT brain with bone skull radiograph is done as a part of skeletal survey. Rarely
window is the most useful imaging study in patients with it is done to screen for fractures in selected asymptomatic
head trauma.7 Head CT is the imaging modality of choice patients of 3 to 24 months age with scalp hematomas
in children with severe traumatic head injury. By definition, (Fig.4a & 4b).
all children with moderate to severe head injury have an
abnormal neurologic evaluation and should have a head Box 1. Neuro imaging indications
CT. In mild head injury whether to do CT or not is a • PGCS < 14
dilemma. There are decision rules that can assist the
clinician to decide about neuro imaging in children with • Suspicion of open or depressed skull fracture
minor head trauma. The three of the largest derived rules • Signs of basilar skull fracture
include Canadian Assessment of Tomography for
• Dangerous mechanism of injury
Childhood Head rule (CATCH).12 Childrens Head Injury
(fall from height > 3feet or 5 steps, RTA)
Algorithm for prediction of Important Clinical Events
(CHALICE)13 and Pediatric Emergency Care Applied • Large, boggy scalp hematoma especially non frontal
Research Network (PECARN) rules.14 Only PECARN • Persistent vomiting (3 or more discrete episodes)
has been derived and validated among the three (Fig.2).
• Worsening headache
A period of observation may allow the physician to
make a more informed decision on neuroimaging in a • Irritability at the time of examination
majority of the head-injured children. Studies have shown • Focal neurological deficit
that a delayed presentation of severe head injury is very
• Suspicion of abusive head trauma
uncommon in children who present with only mild
symptoms from minor head injury. 15, 16 There is also • Bleeding diathesis or on anticoagulants

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Indian Journal of Practical Pediatrics 2017;19(4) : 370

Fig.2.Decision on ordering CT based on Pediatric Emergency Care Applied Research Network

(PECARN) rules.

Cervical spine X-ray - indications: X-ray cervical spine Management

is taken whenever there is neck pain or tenderness, Increased intracranial pressure
dangerous mechanism of injury such as fall from a height
Neuro observation: Level of consciousness, pupil size and
of > 3 feet or 5 stairs and high speed motor vehicle
reactivity, vitals such as heart rate, respiratory rate, blood
accidents.
pressure, temperature and oxygen saturation should be
CT cervical spine - indications: CT cervical spine is monitored in every child with traumatic brain injury.
indicated in children with GCS less than 13, In children whose GCS score is less than 15, it has to be
focal neurological signs, paresthesia in upper or done on half hourly basis till GCS becomes 15. In children
lower limbs, significant bony injury in plain X rays, whose GCS is equal to 15, monitoring has to be done on
strong clinical suspicion of cervical injury despite normal half hourly basis for 2 hours, hourly for 4 hours and
X-rays. 2 hourly thereafter.
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Indian Journal of Practical Pediatrics 2017;19(4) : 371

Fig.3a.Extradural Fig.3b.Subdural Fig.3c.Contusion Fig.3d. Diffuse

hemorrhage hemorrhage axonal injury

Fig.4a. Linear skull fracture Fig.4b.Depressed fracture

Indications for neurosurgical consultation: Significant confirmed in multicentric trials. Moreover it causes
abnormality in neuro imaging, persistent coma, rebound rise in ICP during rewarming. Careful monitoring
deterioration in GCS score, progressive neurological signs, of ICP during nursing care, clustering the nursing activities
seizures, penetrating injury and CSF leak are the indications and limited handling of the patient are essential.
for neurosurgical referral in children with head injury. As suctioning can increase ICP, it is better to suction only
Maintaining the head and neck in midline to avoid when needed. Pre-oxygenation before suctioning and use
the kinking and compression of the jugular vein and of lidocaine intravenously or intratracheally are simple
elevating the head end to 30 degrees to improve the venous measures to prevent increase in ICP when suctioning is
return are useful. Hyperosmolar therapy with intravenous done.
hypertonic saline or mannitol are useful to bring down the Seizures: Post traumatic seizures occur in about 10% of
increased intracranial pressure. Hyperventilation as an anti children with head trauma. They affect the outcome by
edema measure should be used carefully as it decreases increasing the ICP, metabolic demand, leading to hypoxia
the ICP by vasoconstriction which can worsen already and hypoventilation. Short acting benzodiazepines are used
existing cerebral ischemia. Hence, it is recommended only for immediate control of seizures followed by phenytoin
in emergency situations such as herniation. or phenobarbitone for maintenance. The former is preferred
Steroids have no effect and are not recommended in as it does not produce CNS depression. Though not
children with head injury.7 However, in the presence of indicated in all patients, prophylactic treatment with
spinal cord injury, prompt use of intravenous methyl phenytoin or fosphenytoin may be given in children with
prednisolone is indicated. Barbiturates decrease ICP, severe TBI, intracranial hemorrhage, depressed skull
provide cerebral protection and decrease the metabolic fracture to prevent early post traumatic seizures.7
demand, but can cause severe hemodynamic compromise.
Hence barbiturates are used as rescue therapy in refractory Disseminated intra vascular coagulation (DIVC):
cases. Decompressive craniectomy with duraplasty is life Thromboplastin from the injured brain can initiate the
saving in refractory cases.7 Hypothermia decreases ICP, coagulation cascade and cause DIVC as early as 1-2 hours
metabolic demand and seizures. However, benefits are not after surgery. Profuse bleeding can occur which is difficult

57
Indian Journal of Practical Pediatrics 2017;19(4) : 372

to control. One third of children with severe TBI can have • Maintenance of adequate airway, breathing and
DIVC. circulation would minimize the secondary brain
injury.
Neurogenic pulmonary edema: Neurogenic pulmonary
edema can occur 2-12 hours after head injury characterized • Prompt management of increased intracranial
clinically by hypoxia, hypoventilation, hypercarbia, pressure, hypothermia, seizures and neurogenic
bilateral fluffy infiltrates in X-ray chest. Medullary pulmo nary odema would significantly reduce the
ischemia causes sudden massive surge in the sympathetic morbidity.
activity which increase the pulmonary venous pressures • The overall outcome for children with head injury is
and shifts the blood from systemic circulation into better than that of adults with the same injury scores.
pulmonary circulation leading onto transduction of fluid
into the alveoli. High levels of PEEP may be needed to References
overcome pulmonary odema. However it can interfere with 1. Langlois JA, Marr A, Mitchko J, Johnson RL. Tracking
cerebral venous drainage and can cause increased ICP. the silent epidemic and educating the public: CDC’s
traumatic brain injury-associated activities under the TBI
In cases of skull fractures with CSF leakage, Act of 1996 and the Children’s Health Act of 2000. J Head
pneumococcal vaccination in unvaccinated children and Trauma Rehabil 2005; 20:196-204.
prophylactic antibiotics should be administered.19 2. Adirim TA, Wright JL, Lee E, Lomax TA, Chamberlain
JM. Injury surveillance in a pediatric emergency
Outcome
department. Am J Emerg Med 1999; 17:499-503.
The overall outcome for children with head injury is 3. Bhargava P, Singh S, Sinha R. Pediatric head injury:
better than that of adults with the same injury score.20 An Epidemiological study. J Pediatr Neurosci 2011; 6(1):
Recovery in children takes longer- months to sometimes 97-98.
years whereas adults reach maximum recovery by about 6 4. Hu CF, Fan HC, Chang CF, Chen SJ. Current approaches
months following the injury. Poor prognosticating factors to the treatment of head injury in children. Pediatr
include low GCS, prolonged altered level of consciousness, Neonatol 2013; 54(2):73-81.
persistent hyperglycemia, presence of subarachnoid 5. Sookplung P, Vavilala MS. What is new in pediatric
hemorrhage, diffuse axonal injury. Evidence of traumatic brain injury? Curr Opin Anesthesiol 2009;
parenchymal damage is an independent poor 22(5):572-578.
prognosticating factor. Early sequelae include transient 6. Timothy J. Titchner, Mara Aloi, Pritika Gupta, Kirsten
cortical blindness, seizures, cranial nerve palsy, diabetes Bechtel, Monograph on Pediatric Head Injury. Trauma
insipidus, syndrome of inappropriate ADH secretion, reports. Issue date: September 1, 2015.
cerebral venous sinus occlusion and hemiparesis. Late 7. Kochanek PM, Carney N, Adelson PD, Ashwal S, Bell
sequelae include post traumatic epilepsy, head ache, MJ, Bratton S, et al. Guidelines for the acute medical
management of severe traumatic brain injury in infants,
aneurysm, meningitis, memory loss and behavioral
children, and adolescents—second edition. Pediatr Crit
problems. Care Med 2012; 13 Suppl 1:S1-82.
Points to remember 8. George A Alexiou, George Sfakianos, Neofytos
Prodromou. Pediatric head trauma. J Emerg Trauma Shock
• Head injury remains the leading cause of death and 2011; 4(3):403-408.
disability in pediatric trauma victims. 9. Ben YahudaY, Watemberg N. Ketamine increases opening
• Fall from height is the most common cause of head pressure in children undergoing lumbar punture. J Child
Neurol 2006; 21(6):441-443.
trauma in children.
10. Agrawal S, Branco RG. Neuroprotective measures in
• Presence of fundal hemorrhages, fractures of various children with traumatic brain injury. World J Crit Care Med
ages on skeletal survey, subdural hematoma in neuro 2016; 5(1):36-46.
imaging are clinical clues to suspect non accidental 11. Elkon B, Cambrin JR, Hirshberg E, Bratton SL.
trauma. Hyperglycemia: an independent risk factor for poor
outcome in children with traumatic brain injury. Pediatr
• It is very important to prevent head injury in children
Crit Care Med 2014; 15:623-631.
and if it occurs, should be treated aggressively.
12. Osmond MH, Klassen TP, Wells GA, Correll R, Jarvis A,
• Non contrast CT brain with bone window is the most Joubert G, et al. Pediatric Emergency Research Canada
useful imaging study in patients with head trauma. (PERC) Head Injury Study Group. CATCH: a clinical
58
Indian Journal of Practical Pediatrics 2017;19(4) : 373

decision rule for the use of computed tomography in 16. Beaudin M, Saint-Vil D, Ouimet A, Mercier C, Crevier L.
children with minor head injury. CMAJ 2010; 182(4):341- Clinical algorithm and resource use in the management of
348. children with minor head trauma. J Pediatr Surg 2007;
13. Dunning J, Daly JP, Lomas JP, Lecky F, Batchelor J, 42:849-852.
Mackway-Jones K. Children’s head injury algorithm for 17. Schonfeld D, Fitz BM, Nigrovic LE. Effect of the duration
the prediction of important clinical events study group. of emergency department observation on computed
Derivation of the children’s head injury algorithm for the tomography use in children with minor blunt head trauma.
prediction of important clinical events decision rule for Ann Emerg Med 2013; 62:597-603.
head injury in children. Arch Dis Child 2006; 91:885-891. 18. Crowe L, Anderson V, Babl FE. Application of the
14. Kuppermann N, Holmes JF, Dayan PS, Hoyle JD, Atabaki CHALICE clinical prediction rule for intracranial injury
SM, Holubkov R, et al. Identifi cation of children at very in children outside the UK: impact on head CT rate. Arch
low risk of clinically-important brain injuries after head Dis Child 2010; 95:1017-22.
trauma: a prospective cohort study. Lancet 2009; 374:1160- 19. Paul SP, Barratt F, Homer S. Treatment and management
1170. of head injuries in children. Emerg Nurse 2011; 18 (10):23-
15. Hamilton M, Mrazik M, Johnson DW. Incidence of delayed 26.
intracranial hemorrhage in children after uncomplicated 20. Iranmanesh F. Outcome of head trauma. Indian J Pediatr
minor head injuries. Pediatrics 2010; 126:e33-39. 2009; 76(9): 929-931.

NEWS AND NOTES

22nd Edition of International Conference on Neonatology and Perinatology

May 07-08, 2018
Frankfurt, Germany
Meet World leading Academic and Industry Leaders from
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CME
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59
Indian Journal of Practical Pediatrics 2017;19(4) : 374

IAP - IJPP CME 2017

TEN PITFALLS IN MANAGEMENT OF wheezing, diarrhea or skin rash suggestive of a viral

URINARY TRACT INFECTION infection need not be investigated for UTI.

*Sudha Ekambaram Lower urinary tract infection can present with or

**Vaishnavi Raman without low grade fever. Cystitis occurs mainly in post-
pubertal girls presenting as dysuria and increased urinary
Abstract: Urinary tract infection (UTI) is a common frequency. Fortunately for cystitis a 2-4 day course of oral
disease in infants and young children. Infants present with antibiotic based on local community-acquired
fever. Children have associated urinary symptoms. E.coli susceptibility is likely to be effective.6
Immediate diagnosis and appropriate therapy prevents
Is bag sample the ideal method of collecting urine in
renal scarring, hypertension and reduced renal function.
children?
This presentation will assist the treating pediatrician to
identify top clinical pitfalls in managing UTI. A sample collected from urinary bag can be used for
routine urinalysis but should not be used for urine culture.
Keywords: UTI, pyuria, uroprophylaxis, investigations, The only utility of this method is that a negative culture in
antibiotics. bag urine sample rules out UTI. A midstream clean catch
Urinary tract infection (UTI) is relatively common in urine sample should be collected for culture in toilet-trained
children, with 8.4% of girls and 1.7% of boys having at children; while others should have urine collected by
least one episode by 7 years of age.1 The most common catheter or suprapubic aspirate.7
pathogen is Escherichia coli, accounting for approximately Does a cloudy or smelly urine indicate UTI?
79% of UTIs in children.2 UTI if missed or untreated can
lead to renal damage/scars that can progress later to Urine colour, clarity or odour alone should not be used
hypertension, preeclampsia, proteinuria and renal to diagnose or start antibiotic therapy. Foley et al., in their
insufficiency.3 It is the duty of primary care pediatrician to study concluded that visual inspection of urine was not
diagnose and treat UTI appropriately in children. The 10 accurate to rule out UTI after testing 100 urine samples
pitfalls outlined below are common fallacies related to the for clarity by determining if newsprint could be legibly
management of UTI seen in day to day practice. read through them.8 Foul-smelling urine is an unreliable
indicator of infection and is usually dependent on patient’s
Are the symptoms of UTI similar in all age groups? hydration status and concentration of urea in the urine.9
Symptoms of childhood UTI differ depending on the Can absence of pyuria exclude urinary tract infection
age. Fever is a common feature. Newborns can present in febrile infant with urine culture positivity?
with non-specific systemic symptoms such as hypo/ The absence of pyuria in urine sediments does not
hyperthermia, vomiting, refusal of feeds, jaundice, lethargy, rule out UTI. One needs to look for other evidences.
poor weight gain and abdominal distension while infants A small percentage (9%) of children with acute
can additionally have vomiting, poor feeding and lethargy.4 pyelonephritis (APN) can have absence of pyuria and is
Children usually present with typical urinary symptoms more common in neutropenic febrile children 10 (Reference
like dysuria, increased frequency, urgency, cloudy urine, needed). Conditions in which urine contains a significant
hematuria, renal angle and suprapubic tenderness5 Note amount of pus cells but without bacterial growth (sterile
that fever associated with symptoms of rhinitis, cough, pyuria) are glomerulonephritis, renal stone disease, renal
* Consultant Pediatric Nephrologist. tuberculosis, dehydration and vaginits/urethritis.11
** Fellow - Pediatric Nephrology, Does bacteria in the urine culture always indicate UTI?
Dr. Mehta’s Hospitals,
Chennai. The presence of bacteria on microscopic examination
email: docsudha80@yahoo.co.in in the urine or a positive urine culture without UTI
60
Indian Journal of Practical Pediatrics 2017;19(4) : 375

symptoms is not an indication of UTI. It could be due to What is the greatest risk factor for recurrent UTI in
contamination or asymptomatic bacteriuria which needs children?
no treatment.7 Common reasons for false positive urine
cultures are inappropriate urine collection method in a Bowel bladder dysfunction (BBD) is the most
female child, infant with diarrhoea, child with tight prepuce common risk factor for UTI seen in children nowadays.
and poor hygiene, and adolescent girl during post BBD presents with a broad spectrum of manifestation
menstruation days. When in doubt these children must be which includes lower urinary tract symptoms like
followed up for a few months. frequency, urgency and dysuria associated with bowel
dysfunction in the form of constipation / encopresis.
What is the significant number of bacteria per ml of Correction of voiding dysfunction and constipation leads
urine that indicates UTI? to a decrease in UTI recurrence.13

Infection of the urinary tract is identified by growth When is circumcision indicated in children with UTI?
of a significant number (105 CFU/mL) of organism of a
According to AAP Task Force, circumcision is
single species in the midstream clean catch urine, in the
indicated in children with recurrent UTI or vesicoureteric
presence of symptom(s).
reflux (VUR).15
According to American Academy of Pediatrics (AAP) Young infant with grade IV reflux. Is prophylaxis
guideline, significant bacteriuria in infants and children indicated? What is the drug of choice?
is the presence of at least 5 x 104 CFU/mL of a single
urinary pathogen in midstream clean catch urine. 12 In view of the Randomized Intervention for Children
According to Indian Society of Pediatric Nephrology with Vesicoureteral Reflux (RIVUR) trial results, the debate
(ISPN) guideline urine culture is considered positive on antimicrobial prophylaxis has moved from “no
even if it demonstrates growth of a single bacterium with prophylaxis” to “selective prophylaxis” in children with
the following colony counts: (i) any growth by suprapubic VUR. 16 The decision to give antibiotic prophylaxis in
aspiration (ii) >5 x 104 CFU/mL by urethral catheterization children with reflux still remains a clinical dilemma.
or (iii) >105 CFU/mL by midstream clean catch.13 But Emerging evidence indicates that not all children diagnosed
a count of even 104 CFU/mL with symptoms is considered with VUR require antibiotic prophylaxis. Neonates with
significant especially if the child has had antibiotics antenatally diagnosed hydronephrosis, infants with all
prior to culture.14 grades of VUR, low-grade (I or II) VUR with recurrent
febrile UTIs, children with high-grade (III–V) VUR, BBD,
Should we delay treatment in UTI until urine culture or renal cortical abnormalities can be given antibiotic
report is available? prophylaxis (Table I). Afebrile grade I or II VUR can be
observed for spontaneous resolution without prophylaxis.
Fever with no apparent source with two or more
positive rapid urine tests (positive nitrite test, positive Drugs used for prophylaxis in recurrent UTI should
leukocyte esterase test, pyuria (>5 pus cells/HPF) and even have low serum and high urinary level, wide spectrum
one bacteria in a Gram’s stain) is a strong indicator of activity, least effect on fecal flora, minimal side effects
UTI and antibiotics can be introduced after sending urine and low bacterial resistance. Ampicillin, amoxicillin and
culture. As E. coli is sensitive to 3 rd generation cephalexin are appropriate prophylactic drugs in children
cephalosporins (ceftriaxone, cefixime) or amikacin, these less than 3 months. The typical dose is one fourth of the
would be the ideal empirical drugs of choice. Antibiotics therapeutic dose given once daily in the evening to
should be changed based on subsequent culture sensitivity
pattern. A normal renal function needs to be documented Table I. VUR prophylaxis–A practical approach
when on amikacin.7 as per ISPN guidelines

Oral antibiotics is indicated in stable children above VUR - Grades Uroprophylaxis

3 months of age. Parenteral therapy is indicated in
I, II 6 months – 1 year
urosepsis, bacteremia, newborns and infants less than
3 months of age, noncompliance, associated congenital III, IV, V Till 5 years of age
anomalies of kidney and urinary tract (CAKUT) and acute
kidney injury. Duration of treatment is 7–14 days depending Associated BBD Till BBD normalizes
on clinical condition.13 irrespective of grade
61
Indian Journal of Practical Pediatrics 2017;19(4) : 376

Points to Remember
• Early diagnosis and prompt treatment of UTI will
reduce renal damage.
• Bag sample is not the method of choice for urine
culture.
• Diagnosis of UTI is not based on a single factor but
collective factors like symptoms, pyuria and urine
culture.
• BBD is the common risk factor noted for
Fig.1. Evaluation following initial UTI as per
breakthrough UTI.
ISPN guidelines
• Uroprohylaxsis is not a universal therapeutic choice.
maximize overnight drug levels in the bladder. References
Nitrofurantoin (NFT), cotrimoxazole and cephalexin are
appropriate drugs in children older than 4 months. 1. Hellstrom A, Hanson E, Hansson S, Hjalmas K, Jodal U.
The discontinuation of NFT by parents is a possibility in Association between urinary symptoms at 7 years old and
view of its gastrointestinal complications. Ampicillin and previous urinary tract infection. Arch Dis Child 1991; 66:
232-234.
amoxicillin, because of increasing antimicrobial resistance,
are not recommended as the first choice and beyond 2. Edlin RS, Shapiro DJ, Hersh AL, Copp HL. Antibiotic
resistance patterns of outpatient pediatric urinary tract
2 months of age.
infections. J Urol 2013; 190: 222–227.
Yet another clinical dilemma is about imaging 3. Mattoo TK. Medical management of vesicoureteral reflux.
protocol. Renal ultrasonogram evaluation is the standard Pediatr Nephrol 2007; 22:1113–1120.
tool for evaluating children with a first febrile UTI as per 4. Lin CW, Chiou YH, Chen YY, Huang YF, Hsieh KS, Sung
ISPN guidelines (Fig 1). It could identify obstructive PK. Urinary Tract Infection in Neonates. J Clin Neonatol
uropathy, hydronephrosis, high grade VUR, dilated 1999; 6:1-4.
collecting systems and anomalies of the kidneys. Second 5. Tsai JD, Lin CC, Yang SS. Diagnosis of pediatric urinary
is the voiding cystourethrogram (VCUG) for diagnosing tract infections. Urol Science 2016; 27:131-134.
VUR and for assessing the degree of VUR and posterior 6. Michael M, Hodson EM, Craig JC, Martin S, Moyer VA.
urethral valve in male children. Third is dimercatosuccinic Short versus standard duration oral antibiotic therapy for
acid (DMSA) scan which can diagnose acute pyelonephritis acute urinary tract infection in children. Cochrane Database
during acute illness and renal scars when performed Syst Rev 2003. DOI: 10.1002/14651858.CD003966.
3 months following the acute illness. Recently there are 7. Saadeh SA, Mattoo TK. Managing urinary tract infections.
suggestions to do DMSA earlier than VCUG. A VCUG Pediatr Nephrol 2011; 26:1967–1976.
can be avoided if the DMSA shows no nucelopenic areas 8. Foley A, French L. Urine Clarity Inaccurate to rule out
indicating pyelonephritis or scars. This can avoid urinary tract infection in women. J Am Board Fam Med
unnecessary exposure to radiation as in VCUG. In recurrent 2011; 24 :474-475.
UTI at any age we need to evaluate with USG, DMSA and 9. Struthers S, Scanlon J, Parker K, Goddard J, Hallett R.
VCUG. Parental reporting of smelly urine and urinary tract
infection. Arch Dis Child 2003; 88:250–252.
Conclusion 10. Yamasaki Y, Uemura O, Nagai T, Yamakawa S, Hibi Y,
Yamamoto M, Nakano M, Kasahara K, Bo Z. Pitfalls of
Pediatricians are the primary care physicians involved diagnosing urinary tract infection in infants and young
in the diagnosis and management of children with UTI. children. Pediatr Int. 2017 ;59:786-792. doi: 10.1111/
There are many pitfalls in the interpretation of patient’s ped.13292.
symptom, lab values and treatment that leads to either over 11. Hodson EM, Craig JC. Urinary tract infections in children.
th
or under treatment of UTI. Not only a good clinical history In: Avner ED (ed.), Pediatric Nephrology. 7 edn,
and supportive laboratory data but also clear understanding Heidelberg, Germany: Springer, 2016; pp1695-1714.
about the common pitfalls will help the treating doctor to 12. Subcommittee on Urinary Tract Infection, Steering
manage UTI in children better and prevent the Committee on Quality Improvement and Management,
complications associated with it. Roberts KB. Urinary Tract Infection: Clinical Practice
62
Indian Journal of Practical Pediatrics 2017;19(4) : 377

Guideline for the Diagnosis and Management of the Initial Urol 2015; 67:546-558.
UTI in Febrile Infants and Children 2 to 24 Months. 15. Blank S, Brady M, Buerk E, Carlo W, Diekema D,
Pediatrics 2011; 128:595-610. Freedman A, Maxwell L, Wegner S, LeBaron C,
13. Vijayakumar M, Kanitkar M, Nammalwar BR, Bagga A. Atwood L, Craigo S, Flinn SK, Janowsky EC,
Revised statement on management of urinary tract Zimmerman EP. American Academy of Pediatrics Task
infections. Indian Pediatr 2011; 48:709-717. Force on Circumcision. Male circumcision. Pediatrics
14. Stein R, Dogan HS, Hoebeke P, Koèvara R, Nijman 2012; 130:e756-785.
RJ, Radmayr C, Tekgül S. European Association of 16. Cara-Fuentes G, Gupta N, GarinEH. The RIVUR study:
Urology; European Society for Pediatric Urology. Urinary a review of its findings. Pediatr Nephrol 2015; 30:
tract infections in children: EAU/ESPU guidelines. Eur 703-706.

CLIPPINGS

Impact of the US Maternal Tetanus, Diphtheria, and Acellular Pertussis Vaccination Program on Preventing
Pertussis in Infants <2 Months of Age: A Case-Control Evaluation.
A total of 240 cases and 535 controls were included; 17 (7.1%) case mothers and 90 (16.8%) control mothers
received Tdap during the third trimester of pregnancy. The multivariable Vaccine effectiveness (VE) estimate
for Tdap administered during the third trimester of pregnancy was 77.7% (95% confidence interval [CI],
48.3%-90.4%); VE increased to 90.5% (95% CI, 65.2%–97.4%) against hospitalized cases.Vaccination during
pregnancy is an effective way to protect infants during the early months of life. With a continuing resurgence in
pertussis, efforts should focus on maximizing Tdap uptake among pregnant women.
Skoff TH, Blain AE, Watt J, Scherzinger K, McMahon M, Zansky SM, et al. Impact of the US Maternal
Tetanus, Diphtheria, and Acellular Pertussis Vaccination Program on Preventing Pertussis in Infants
<2 Months of Age: A Case-Control Evaluation. Clin Infect Dis. 2017 Nov 29;65(12):1977-1983. doi: 10.1093/
cid/cix724.

NEWS AND NOTES

PEDIATRIC PULMONOLOGY UPDATE - 2018

Pediatric Pulmonology Foundation Chennai & Indian Academy of Pediatrics National Respiratory Chapter
Date: 25th March, 2018 Venue: Accord Metropolitan, T-Nagar, Chennai

Delegate fees Upto February10th Upto February 28th

Post Graduates Rs.1000 Rs.1200
Delegates Rs.1200 Rs.1400
Spot Rs.1500

(As Cash/Cheque/DD, drawn in favour of “Pediatric Pulmonology Foundation Chennai”, payable at “Chennai”.
CME Secretariat
Dr.N.C.Gowrishankar
Organising Secretary,
1A, Block II, Krsna Apartments, 50, Halls Road, Egmore, Chennai – 600 008.
Ph: 044-28190032, 42052900 Email:ijpp_iap@rediffmail.com

63
Indian Journal of Practical Pediatrics 2017;19(4) : 378

DRUG PROFILE

ANTIARRHYTHMIC AGENTS iii) ventricular arrhythmias (Table II). The negative

inotropic effect of these agents tends to be additive. Hence,
*Jeeson C Unni special care should be taken if two or more drugs are
**Ranjit Baby Joseph prescribed especially if myocardial function is impaired.
*** Sajana TM Most of the antiarrhythmic drugs can provoke arrhythmias
Abstract: Symptomatic cardiac arrhythmias are relatively especially when there is an underlying hypokalemia.3
uncommon in childhood, accounting for about 5% of the Class I A agents
emergency hospital admissions. Atrial tachyarrhythmias
are the most common rate and rhythm disturbance in this This group of drugs impair the entry of sodium into
population. With the advent of effective ablation therapy, the cells and exert a membrane stabilizing effect which
management of arrhythmia has undergone dramatic ultimately slows the rate of depolarization causing
change. A clear understanding of the mechanisms that reduction in the excitability of atrial and ventricular tissue,
initiate the rhythm disturbances and the various allowing the SA node to regain dominance of the cardiac
pharmacological agents that are used would enable rhythm. It also prolongs the effective refractory period and
optimal management of arrhythmias. Some of the agents abolishes the impulse re-entry by blocking the cardiac
that are licensed for use in children are discussed in this potassium channels and thus delaying repolarization.
article. The resultant QT prolongation can be pro-arrhythmic and
can sometimes precipitate Torsade de Pointes. The negative
Keywords: Arrhythmias, Action potential, inotropic effects make it unsafe for use in patients with
Supraventricular tachycardia, Ventricular tachycardia. structural heart disease. Quinidine, procainamide and
disopyramide are the drugs which belong to this class.4
Cardiac rhythm is maintained with the help of cardiac
action potential. The resting membrane potential of cardiac Quinidine
cells is maintained mainly by potassium ions. Complex
interplay of various cations like sodium, potassium and It is derived from cinchona. It delays depolarization
calcium results in generation of action potential. 1 and repolarization by Na+ channel and inward rectifier
Any deviation in the normal pattern of cardiac rhythm potassium (IKi) channel blocking effects respectively. It is
results in arrhythmia. The various drugs used in the effective in atrial arrhythmias such as atrial flutter and
management of cardiac arrhythmia focus on stabilisation fibrillation, re-entry SVTs and ventricular arrhythmias such
of cardiac action potential by acting at different levels. In as VT. Oral and IV formulations are available and ideally
general, antiarrhythmic drugs are classified into four needs a test dose to assess for idiosyncratic reaction.
categories based on their mechanism of action (Vaughan Dosage5: IV- As quinidine gluconate: 2-10mg/kg/dose
Williams classification) but this classification is not of great 3-6 hourly. PO- As quinidine sulphate: 15-60mg/kg/day in
clinical relevance (Table I).2 divided doses 6th hourly. Toxicity is indicated by increase
Antiarrhythmic drugs can also be classified clinically in QRS interval by>0.02 sec.Therapeutic levels: 3-7mg/L.
as those acting on i) supraventricular arrhythmias, Side effects include GI symptoms, hypotension,
ii) supraventricular and ventricular arrhythmias and tinnitus, TTP, rash, heart block and blood dyscrasias. When
used alone, it may cause 1:1 conduction in atrial flutter
* Editor-in-Chief, leading to ventricular fibrillation. It can also cause
IAP Drug Formulary idiosyncratic ventricular tachycardia with low levels,
** Senior Specialist in Pediatrics, especially when initiating therapy. Its use has declined
*** Specialist in Pediatrics, because of the potent side effects mainly thrombocytopenia,
Aster Medcity, Kochi. hemolytic anemia, abdominal cramps, diarrhea, decreased
email: jeeson1955@gmail.com hearing and tinnitus, QRS widening and proarrhythmia.6
64
Indian Journal of Practical Pediatrics 2017;19(4) : 379

Table I. Anti-arrhythmic drugs - Vaughan Williams classification

Class Mechanism of action Drugs
I Fast sodium channel blockers
Ia Prolong repolarization Quinidine, procainamide, disopyramide
Ib Shorten repolarization Lidocaine, mexiletine, phenytoin, tocainide
Ic Little or no effect on repolarization Flecainide, encainide, moricizine, propafenone
II Beta blockers Propranolol, esmolol, metoprolol
III Potassium channel blockers Amiodarone, sotalol, dofetilide, ibutilide
IV Slow calcium channel blockers Verapamil, diltiazem
V Miscellaneous drugs Digoxin, adenosine, magnesium

Table II. Anti-arrhythmic drugs - Clinical Disopyramide

classification
This has similar action as quinidine without the
Type of arrhythmia Drugs preferred adrenergic effects. It is effective in refractory vasodepressor
syncope. 16 The negative inotropic effect inhibits the
Supraventricular Adenosine, digoxin, verapamil ventricle from becoming hypercontractile which is the
Supraventricular Amiodarone, beta blockers, trigger for the vasodepressor reflex. The dose used is
and ventricular flecainide, procainamide 20-30 mg/kg/day in 3-4 divided doses. Side effects include
anticholinergic effects such as urinary retention,
Ventricular Lidocaine constipation, blurred vision and dry mouth. Renal clearance
may be affected by betablockers.
Procainamide
Class 1B
Procainamide has both Na+ and K+ channel blocking
effects. The onset of action is between 10 to 30 minutes.7 These drugs shorten action potential duration and
It is usually given as several small slow intravenous boluses, repolarization by blocking the fast Na channel activity.
with close monitoring for hypotension and cardiac It includes lidocaine, mexilitine, phenytoin, tocainide and
depression. It is the drug of choice in the treatment of post- moricizine.
operative junctional ectopic tachycardia (JET).8,9 It is Lidocaine
reported to be more effective than amiodarone in a pediatric
cohort with a variety of SVT including orthodromic It may be used in cardiopulmonary resuscitation in
reciprocating tachycardia, intra-atrial re-entrant tachycardia children with ventricular fibrillation especially in Torsade
(IART) and ectopic atrial tachycardia (EAT). 10 Other de Pointes or pulseless ventricular tachycardia
indications include atrial flutter, atrial fibrillation and AV unresponsive to DC. shock, but only if amiodarone is not
nodal re-entrant tachycardia (AVNRT).11-13 available. Dose needs to be reduced in children with
persistently poor cardiac output and hepatic or renal
Dosage: PO: 20–100 mg/kg/day in 6 divided doses. failure.17
Maximum: 4 g/24 hour. IV: 3–6 mg/kg/dose IV over 5 min
and can be repeated every 5 min to a maximum of Dosage: 18 IV/IO: Neonates and children 1 month-12 years:
15 mg/kg. Maintenance: 20–80 mcg/kg/min as IV infusion. 0.5-1mg/kg as bolus followed by infusion of 0.6-3mg/kg/
hour.
Side effects include hypotension, arrhythmias (including
QT prolongation and Torsades des Pointes), lupus-like Side effects include CNS effects like dizziness, confusion,
syndrome (usually reversible upon discontinuation) and paresthesia, altered sensorium, respiratory depression,
blood dyscrasias (e.g. agranulocytosis).11,14,15 convulsions, hypotension and bradycardia.

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Indian Journal of Practical Pediatrics 2017;19(4) : 380

Contraindications include all sinoatrial disorders, all Class I C

grades of atrio ventricular block, severe myocardial
These agents are potent in blocking Na and affecting
depression and acute porphyria.
repolarization. They also have an effect on inward K
Mexiletine channel and the slow inward Ca current. They include
flecanide, propafenone and encanide.
This drug, the oral form of lidocaine with similar Na
channel effects, is effective in chronic therapy of some Flecainide
VTs and also long QT syndrome (LQTS [type III]).19 It prolongs the QRS duration by acting on the bundle
The safety and efficacy in children are not well of His, purkinje system and ventricular myocardium. It has
documented. The most common side effects associated with a negative inotropic action and may induce ventricular
mexiletine therapy have been gastrointestinal and nervous arrhythmia in patients with significant myocardial
system effects but is usually well tolerated. dysfunction.
Dosage: 1.4 to 5 mg/kg/dose given every 8 hours. It is ideal Flecainide can be used for termination of acute SVT
to begin with lower initial dosages and titrated to desired as well as can be used for prophylaxis of SVT in cases
effects and serum concentrations.20 refractory to conventional drugs like digoxin, betablockers
and calcium channel blockers. It is particularly useful for
Mexiletene is an useful drug for the long term control of treatment of automatic atrial tachycardia, JET, atrial flutter,
ventricular arrhythmias in children with congenital heart postoperative intra-atrial re-entrant tachycardia and VT.1
disease; much less effective in the settling of
cardiomyopathy and least effective in those with normal Dosage3: In cases of resistant re entry supraventricular
heart. Contraindications to its use are congestive heart tachycardia, ventricular ectopics or ventricular tachycardia,
failure (CHF), hypotension and a history of seizures. arrhythmias associated with accessory conduction
Its use is not recommended in less severe arrhythmias like pathways (WPW syndrome), paroxysmal atrial fibrillation-
asymptomatic ventricular premature contractions or Oral: Neonate- 2 mg/kg 2-3 times daily. Dose to be adjusted
conduction disturbances. Side effects are minimal and according to response and plasma flecainide levels.
mild.21 Child 1month to 12 years: 2 mg/kg 2-3 times daily.
Dose to be adjusted according to response and plasma
Phenytoin flecainide levels (maximum 8 mg/kg/day or 300 mg/day).
Child 12-18 years: initially 50-100 mg twice daily;
It has similar effects as lidocaine on the Na channel maximum 300 mg/day.
but also has Ca channel blocking and sinus node and AV
node effects in higher concentrations. Its effect of By slow IV injection/ infusion in cases of acute episode of
depressing phase 4 depolarization is used in treatment of SVT: Neonate- 1-2 mg/kg over 10-30 minutes. If necessary
digoxin toxicity. It is used in some forms of refractory followed by continuous infusion at the rate of
ventricular arrhythmias. It crosses the placental barrier and 100-250 mcg/kg/hour until arrhythmia is controlled. Child
is known to have a potent teratogenic effect on fetus.22 1month- 12 years: 2 mg/kg over 10-30 minutes. If necessary
can be followed by continuous infusion at the rate of
Dosage23: Loading dose (all ages): 1.25mg/kg IV every 5 100-250 mcg/kg/hour until arrhythmia is controlled. Child
minutes up to a total of 15mg/kg. Maintenance dose: Child 12-18 years- 2 mg/kg (maximum 150 mg) over 10-30
(IV/PO): 5-10mg/kg/day in 2-3 divided doses. minutes. If necessary it has to be followed by continuous
infusion at a rate of 1.5 mg/kg/hour for 1 hour, then reduced
Side effects include hypotension, nystagmus, ataxia,
to 100-250 mcg/kg/hour until arrhythmia is controlled.
gingival hyperplasia (on prolonged use) and skin rash (may
progress to Steven Johnson’s syndrome). It is Flecainide is safe and effective in children with
contraindicated in patients with heart block or sinus supraventricular tachycardia. The drug was found to be
bradycardia. Sudden death late after surgery for congenital very effective for treatment of fetal tachyarrhythmias.
heart disease is usually attributed to ventricular It may not be safe for children who have structurally
dysrhythmias, which may be difficult to suppress. abnormal heart and atrial flutter or ventricular arrhythmias.
Phenytoin orally was found to be effective in suppressing The safety of flecainide for patients with ventricular
ventricular dysrhythmias especially VPCs after surgery for arrhythmias and normal heart requires further
congenital heart disease.24 investigation.25

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Indian Journal of Practical Pediatrics 2017;19(4) : 381

Side effects include body ache, asthenia, tremors, headache, enzymes, edema, and rarely agranulocytosis.
fatigue, agitation and gastrointestinal upset. Electrophysiologic adverse effects include QRS and
The most dreaded side effect is proarrhythmia, seen in 7%- PR widening, sinus node dysfunction, AV block,
8% of cases which is more likely if there is myocardial bradycardia, arrhythmias and QT prolongation.
ischemia or ventricular dysfunction.1 In children it has
also been reported to cause incessant supraventricular Class II agents
tachycardia26,27,28 cardiac arrest or sudden death27,28 and non- Class II drugs reduce sympathetic activity which are
sustained ventricular tachycardia.29 The incidence of known to be pro-arrhythmic and also propagate re-entry
arrhythmogenesis is said to be lower in children than in mechanisms. Beta blockade reduces the spontaneous firing
adults.30 Though the arrhythmogenic effects of flecainide rate of the SA node and ectopic pacemakers, prolongs intra
(and encainide) in children is to be reported in 5%-7%28 nodal conduction and the refractory period of AV node.
and found to be equally common in those with and those This results in a negative chronotropic effect reducing
without structural heart disease,29 in further review it has cardiac work. Beta blockers are effective in prophylaxis
been suggested that flecainide is effective and probably of SVT by inhibiting the initiating atrial ectopic beat.
safe in children with supraventricular tachycardia and Class II drugs include beta-1 cardiac selective (atenelol,
structurally normal hearts. metoprolol), non selective (propranolol, nadalol) and drugs
Contraindications include heart failure, abnormal LV that have intrinsic sympathomimetic activity (Pindalol).
function, long standing atrial fibrillation where conversion Propranolol
to sinus rhythm is not attempted, hemodynamically
significant valvular heart disease, sinus node dysfunction Propranolol is the drug of choice in LQTS and also
and atrial conduction defects. the most common beta blocker used for chronic prophylaxis
of SVT, the first line drug in re-entry SVT of all ages
Monitoring: Flecainide should be started in a hospital (including newborn), some ventricular arrhythmias
setting. The QRS duration needs to be monitored (especially catecholamine sensitive).32 It has membrane
meticulously. A 10% increase is expected. An increase in effects on Na+ channel and weak Ca++ channel effects with
QRS duration of more than 25% during flecainide therapy higher doses. Though there is little effect on the action
is a sign of potential risk of proarrhythmia and the drug potential duration, it prolongs intranodal conduction
should be stopped or the dose reduced. Plasma levels of (increases AH interval and Wenckebach block).
flecainide should be monitored ideally, especially in hepatic
or renal impairment, but this facility is not yet available in Dosage3: Oral: Neonates- 250-500mcg/kg 3 times daily,
India. adjusted according to response. Child 1month - 18years:
250-500 mcg/kg 3-4 times daily, adjusted according to
Propafenone response to a maximum of 1 mg/kg 4 times a day, total
In addition to blocking Na+ channels, propafenone also daily dose not exceeding 160 mg daily.
has β adrenergic blocking and weak Ca2+ channel blocking
IV: By slow injection, with ECG monitoring: Neonate: 20-
activities resulting in prolongation of the refractory periods
50 mcg/kg repeated if necessary every 6-8 hours. Child 1
in the atrium and ventricle as well as slowing conduction
month - 18 years: 25-50 mcg/kg repeated every 6-8 hours
at the AV node. It is effective in the treatment of JET, EAT,
if necessary.
AVNRT, atrial flutter, AV reciprocating tachycardia
(AVRT) and chaotic atrial tachycardia, but is generally used Side effects include GI disturbances, bradycardia, heart
as a second line agent after other therapies have failed.31 failure, hypotension, conduction disorders, peripheral
vasoconstriction and bronchospasm.
Dosage: Oral: 200 mg/M2 /day or 7-10 mg/kg/day in
3 divided doses. The dose is increased every 3 days by It is contraindicated in children with asthma,
20%–30% if needed to a maximum of 500 mg/M2/day or uncontrolled heart failure, marked bradycardia,
18-20 mg/kg/day. IV: 0.2 mg/kg/dose every 10 minutes to hypotension, sick sinus syndrome, second or third degree
a maximum of 2 mg/kg followed by infusion at 4–7 mcg/ AV block, cardiogenic shock, metabolic acidosis, severe
kg/min. peripheral arterial disease and pheochromocytoma.
Side effects include hypotension with intravenous Esmolol
administration, vomiting and unpleasant taste with oral
administration, transient blurred vision, elevations in liver Esmolol is a relatively cardioselective beta blocker
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Indian Journal of Practical Pediatrics 2017;19(4) : 382

with a very short duration of action, used intravenously in combination with flecainide33 and propranolol34 for
for short term treatment of supraventricular arrhythmias refractory tachyarrhythmias in infants and children.
and sinus tachycardias particulary in the perioperative
period. Contraindications and the side effects are similar Dosage1: IV - Loading dose is 5 mg /kg given over 20- 30
to that of propranolol. min, followed by 5-15 mcg/kg/min infusion. In rare cases,
a higher loading dose, up to a maximum of 15 mg/kg, can
Dosage3: IV: Child 1 month – 18 years: 500 mcg/kg through be given. Oral - Loading dose is 5 mg/kg given 2-3 times a
a central venous catheter over 1 minute followed by day (maximum 200 mg/dose) for 5 days followed by
infusion of 50 mcg/kg/min for 4 minutes. If inadequate 5 mg/kg/day as a single dose.
response, the loading dose is repeated, maintenance
infusion increased by increments of 50 mcg/kg/min until Side effects: IV amiodarone may result in hypotension,
effective or maximum infusion of 200 mcg/kg/min is nausea, sweating and hot flushes. Chronic use of oral
reached. amiodarone can cause cardiac effects like bradycardia,
prolongation of QT interval, myocardial depression,
Metoprolol endocrine effects like hypothyroidism or hyperthyroidism,
pulmonary complications like pulmonary alveolitis,
Though Metoprolol is not considered as a first line
pneumonitis and fibrosis, neurological effects like
beta blocker, it can also be used in selected patients.
peripheral neuropathy, vertigo, headache, insomnia and
Dosage: Oral: Child 1 month- 12 years: 1 mg/kg twice daily, dermatological effects like rashes, photosensitivity etc.,
increase if necessary to 8 mg/kg/day (maximum 400 mg) Other side effects seen occasionally are ocular changes
in 2-4 divided doses. Child 12-18 years: initially like corneal deposits, optic neuritis and hepatic dysfunction.
50-100 mg daily increased if necessary to 200 mg daily in Amiodarone decreases the clearance of digoxin, flecainide,
1-2 divided doses; maximum 400 mg daily.3 procainamide and warfarin. There is increased risk of
ventricular arrhythmias when given with erythromycin.
Class III agents
Monitoring: BP monitoring is mandatory when using IV
Class III agents prolong the repolarisation phase by
amiodarone, especially in patients with ventricular
reducing the K+ efflux out of the cells. The time interval
dysfunction. Periodic ECGs must be done to look for QT
required for re-excitation is prolonged and hence
interval changes. Testing for thyroid functions (before
arrhythmias are suppressed. The predominant advantage
starting amiodarone, after loading dose and 6 monthly),
is that it can be used even in the presence of left ventricular
liver functions (before, after loading and 6 monthly),
dysfunction. Significant QT prolongation and attendant risk
pulmonary functions, chest X-ray (before and 3-6 monthly
of Torsades des Pointes is an adverse effect to be watched
later) and slit lamp examination of the eyes should be
for.1 Amiodarone, sotalol, ibutalide and dofetalide belong
carried out periodically. Amiodarone, though a very
to this class.
effective antiarrhythmic agent, is not really recommended
Amiodarone especially for chronic use. Unfortunately due to difficulties
in procuring other, safer antiarrhythmics, amiodarone is
Amiodarone has been described as close to being the being widely used in India. It should ideally be reserved
ideal antiarrhythmic agent in SVT and VT in children. Even for refractory arrhythmias which are not responding to
though it is primarily a class III anti-arrhythmic drug, it simpler medications.1
has other class effects also. The predominant effect after
IV administration is due to its betablocking and calcium Sotalol
channel blocking actions. The onset of action depends on
It is a non- cardioselective betablocker with additional
the route of administration. As interactions with numerous
class III anti-arrhythmic activity. Thus it is a K+ channel
drugs are known, careful monitoring is required.1
blocker as well as non-selective â adrenergic blocker.
It is commonly used as first line therapy to manage At lower doses the β adrenergic effects predominate
JET and other supra ventricular arrhythmias, particularly whereas the K+ channel effects predominate at higher
in patients with structural cardiac abnormalities or doses.31 It can suppress ventricular ectopic beats and non-
decreased cardiac output. It is also indicated for difficult sustained ventricular tachycardia. It prolongs action
to control SVT, which may be due to AVRT, AVNRT, atrial potential duration and results in lengthening of QTc
flutter or AF, automatic EATs and life threatening interval. It also exerts a negative inotropic and chronotropic
ventricular arrhythmias. It has also been successfully used effect and reduces AV nodal conduction.

68
Indian Journal of Practical Pediatrics 2017;19(4) : 383

The pro-arrhythmic effects of sotaolol may prolong the Ca channel activity and has predominant effect on sinus
QT interval and induce Torsade de Pointes especially in and AV node. It has been used predominantly in the control
children with sick sinus syndrome.1, 3 of hypertension and acute treatment of SVT. Its use is
similar to verapamil and dosing recommendations are
Sotalol is indicated for refractory atrial 0.5-2 mg/kg/day in 2-3 divided doses. Side effects include
tachyarrhythmia and arrhythmias in postoperative patients. bradycardia and postural hypotension.
It is superior to class I agents for ventricular arrhythmias
and preferred over amiodarone due to less serious side Class V agents (Miscellaneous)
effects. It is also safe to use in fetal arrhythmias.1
These include miscellaneous drugs like digoxin,
Dosage: Sotalol is given orally in a dose of 2-4 mg/ kg/day adenosine and magnesium which act by various
in two divided doses. Doses up to 8 mg/kg/ day have been mechanisms as anti arrhythmics.
used. Body surface area is reported to be a better predictor
for sotalol dosing; the recommended dose is 30-70 mg/ Digoxin
M2/day.1
Digoxin has both cholinergic and anti adrenergic
Side effects: Sotalol is a relatively safe drug apart from its effects which serve to slow the sinus rate and AV node
proarrhythmic effect seen in 3%-5%, due to prolongation conduction by prolonging the effective refractory period.
of QTc interval. Bronchospasm may occur in predisposed It also blocks Na +/K + adenosine triphosphatase and
patients, due to its beta blocking effect. Sotalol has also increases intracellular Ca2+, which likely is responsible for
been associated with proarrhythmia, including bradycardia, its inotropic properties but may also contribute to its
QT prolongation, and Torsade de Pointes.35 proarrhythmic effects.36
Class IV agents Oral administration of digoxin slows the ventricular
rate in atrial fibrillation and in atrial flutter. However,
These agents block the cardiac Ca2+ channels and
intravenous infusion is rarely effective for rapid control of
decreases cardiac conduction velocity by prolonging
ventricular rate. Now a days it is not commonly used in
repolarization at the AV node. They are contraindicated
SVT where adenosine is used more frequently.
when preexcitation is manifest, as they can facilitate
antegrade conduction during atrial fibrillation leading to Adenosine
ventricular fibrillation and arrest. Verapamil and diltiazem
are drugs in this group. Adenosine is the drug of choice for terminating supra
ventricular tachycardias including those associated with
Verapamil accessory conducting pathways like WPW syndrome.
Verapamil is the most selective agent for the It does not cause significant hypotension. It can be used
myocardial Ca2+ channels. It is used to treat atrial flutter, safely in children with impaired cardiac function or post-
atrial fibrillation and AVNRT in children. It can also be operative arrhythmias. The injection should be rapidly
used as a second line agent for SVT unresponsive to first administered into a central or a large peripheral vein.1
line therapies. Verapamil is contraindicated in infants less
It is effective in the termination of sinus node re-entry
than one year old because it has been associated with
tachycardia and in re-entrant tachycardias that use the AV
increased apnea, bradycardia, hypotension and cardiac
node as a part of the re-entrant mechanism.
arrest in this age group. It should not be used in patients
Tachycardias originating in the atrium (e.g. atrial
with decreased cardiac function or in those receiving
fibrillation, atrial flutter, EAT, IART) do not rely on the
β-blockers because of the risk of bradycardia and AV
SA or AV node and thus are not typically terminated by
block.3, 29
adenosine. EAT has a variable response to the
Dosage: In Supra ventricular arrhythmias: IV over 2-3 administration of adenosine and may produce transient
minutes: Child 1-18 years: 100-300 mcg/kg (maximum 5 termination or rate slowing, which is thought to be
mg) as a single dose, repeated after 30 minutes if necessary. secondary to adenosine’s anti adrenergic effect.37

Side effects include flushing, rash, worsening heart Dosage3 : IV/IO dose: First dose 0.1 mg/kg rapid bolus
failure, seizures, increased liver enzymes, tinnitus, vertigo, (max: 6 mg), second dose: 0.2 mg/kg rapid bolus
dyspnea and bronchospasm. Diltiazem blocks the inward (max: 12 mg).38

69
Indian Journal of Practical Pediatrics 2017;19(4) : 384

Beyond neotatal period : 150 mcg/kg, if necessary repeat Pickoff AS. Procainamide elimination kinetics in pediatric
injection every 1-2 minutes increasing dose by 50-100 mcg/ patients. Clin Pharmacol Ther 1982; 32:607-611.
kg until tachycardia is terminated or maximum single dose 8. Mandapati R, Byrum CJ, Kavey RE. Procainamide for rate
of 300 mcg/kg given. control of postsurgical junctional tachycardia. Pediatr
Cardiol 2000; 21:123-128.
Contraindications include second or third degree AV 9. Walsh EP, Saul JP, Sholler GF. Evaluation of a staged
block and sick sinus syndrome, severe hypotension, treatment protocol for rapid automatic junctional
decompensated heart failure and asthma. Side effects tachycardia after operation for congenital heart disease.
though rare but include nausea, AV block, flushing, angina, J Am Coll Cardiol 1997; 29:1046-1053.
dizziness, dyspnoea, headache and palpitations. 10. Chang PM, Silka MJ, Moromisato DY, Bar-Cohen Y.
Amiodarone versus procainamide for the acute treatment
Magnesium
of recurrent supraventricular tachycardia in pediatric
Magnesium sulphate injection is recommended for the patients. Circ Arrhythm Electrophysiol 2010; 3:134-140.
emergency treatment of serious arrhythmias, especially in 11. Luedtke SA, Kuhn RJ, McCaffrey FM. Pharmacologic
the presence of hypokalemia and when the ventricular management of supraventricular tachycardias in children.
tachycardia shows the characteristic twisting wave front Part 2: atrial flutter, atrial fibrillation and junctional and
known as Torsade de Pointes.3 atrial ectopic tachycardia. Ann Pharmacother 1997;
31:1347-1359.
Dosage: IV-Over 10-15 minutes. Child 1 month- 18 years: 12. Bouhouch R, El Houari T, Fellat I, Arharbi M.
0.1-0.2 mmol/kg (25-50 mg/kg magnesium sulphate Pharmacological therapy in children with nodal reentry
heptahydrate); maximum 8 mmol (2 gm magnesium tachycardia: when, how and how long to treat the affected
sulphate heptahydrate); dose repeated once if necessary. patients. Curr Pharm Des 2008; 14:766-769.
13. Fengler BT, Brady WJ, Plautz CU. Atrial fibrillation in
Conclusion the Wolff–Parkinson–White syndrome: ECG recognition
Pharmacotherapy of arrhythmias in children is very and treatment in the ED. Am J Emerg Med 2007; 25:576-
583.
effective in situations where ablation is not preferred. Side-
effects of different drugs and combinations, drug 14. Bink-Boelkens MT. Pharmacologic management of
arrhythmias. Pediatr Cardiol 2000; 21:508-515.
interactions and patient compliance need to be taken into
consideration and monitored during treatment. Initiation 15. Luedtke SA, Kuhn RJ, McCaffrey FM. Pharmacologic
management of supraventricular tachycardias in children.
of the drug should always be done in a hospital setting,
Part 1: Wolff-Parkinson-White and atrioventricular nodal
preferably by a pediatric cardiologist who is well
reentry. Ann Pharmacother 1997; 31:1227-1243.
acquainted with these drugs.
16. Milstein S, Buetikofer J, Dunnigan A, Benditt DG,
References Gornick C, Reyes WJ. Usefulness of disopramide for
prevention of upright tilt-induced hypotension-bradycardia.
1. Indian Pediatrics Working group on Management of Am J Cardiol 1990; 65:1339-1344.
Congenital Heart Disease in India. Drug therapy for
17. Sonnenblick EH. Symposium: Esmolol: An ultrashort-
congenital disease in children, Drug therapy of cardiac
acting intravenous beta blocker. Am J Cardiol 1985; 56:1F–
diseases in children. Indian Pediatr 2009; 46:310-338.
62F.
2. Nattel S. Antiarrhythmic drug classifications. A critical
18. Joint Formulary Committee. British National Formulary
appraisal of their history, present status and clinical
for children. London: BMJ Group and Pharmaceutical
relevance. Drugs 1991; 41(5):672-701.
Press, 2013-2014: 85-86.
3. Joint Formulary Committee. British National Formulary
19. Schwartz PJ, Priori SJ, Locati EH, Napolitano C, Cantù F,
for children. London: BMJ Group and Pharmaceutical
Towbin JA, et al. Long QT syndrome patients with mutation
Press, 82:2013-2014.
of the SCNA5 and HERG genes have differential responses
4. Wang Y, Hill JA. Electrophysiological Remodelling in to Na channel blockade and to increases in heart
Heart Failure. J Mol Cell Cardiol 2010; 48(4):619–632. rate. Circulation 1995; 92:3381-3386.
5. Custer JW, Rau RE. (Eds.) The Harriet Lane handbook: a 20. Manolis AS, Deering TF, Cameron J, Mark NA. Mexiletine:
th
manual for pediatric house officers, 18 edn, Philadelphia, Pharmacology and Therapeutic Use. Clin Cardiol 1990;
PA: Mosby Elsevier, 2010;pp972-973. 13:349-359.
6. Selzer A, Wray HW. Quinidine syncope: Paroxysmal 21. Moak JP, Smith RT, Garson A. Mexiletine: An Effective
Ventricular fibrillation occurring during treatment of Antiarrhythmic Drug for Treatment of Ventricular
chronic atrial arrhythmias. Circulation 1964; 30:17–26. Arrhythmias in Congenital Heart Disease. J Am Coll
7. Singh S, Gelband H, Mehta AV, Kessler K, Casta A, Cardiol 1987; 10:824-829.
70
Indian Journal of Practical Pediatrics 2017;19(4) : 385

22. Iyer VR. Drug Therapy Considerations in Arrhythmias in 30. Hornik CP, Chu PY, Li JS, Clark RH, Smith PB, Hill KD.
Children. Indian Pacing Electrophysiol J 2008; 8(3):202– Comparative effectiveness of digoxin and propranolol for
210. supraventricular tachycardia in infants. Pediatr Crit Care
23. Custer JW, Rau RE. (Eds.) The Harriet Lane handbook: a Med 2014; 15(9):839–845.
th
manual for pediatric house officers, 18 edn, Philadelphia, 31. Escudero C, Carr R, Sanatan S. Overview of antiarrhythmic
PA: Mosby Elsevier, 2010p 948. drug therapy for supraventricular tachycardia in children.
24. Kavey RE, Blackman MS, Sondheimer HM. Phenytoin Progress in Pediatric Cardiology 2013;35:55–63.
therapy for ventricular arrhythmias occurring late after 32. Lerman BB, Belardinelli L. Cardiac electrophysiology of
surgery for congenital heart disease. Am Heart J adenosine: Basic and clinical concepts. Circulation 1991;
1982; 104(4 Pt 1):794-798. 83:1499-1509.
25. Perry JC, Garson A. Flecainide acetate for treatment of 33. Fenrich AL Jr, Perry JC, Friedman RA. Flecainide and
tachyarrhythmias in children: review of world literature amiodarone: combined therapy for refractory
on efficacy, safety, and dosing. Am Heart J 1992; tachyarrhythmias in infancy. J Am Coll Cardiol 1995;
124(6):1614-1621. 25:1195-1198.
26. Perry JC, McQuinn RL, Smith RT, Gothing C, Fredell P, 34. Drago F, Mazza A, Guccione P, Mafrici A, Di Liso G,
Garson A. Flecainide acetate for resistant arrhythmias in Ragonese P. Amiodarone used alone or in combination with
the young: efficacy and pharmacokinetics. J Am Coll propranolol: a very effective therapy for tachyarrhythmias
Cardiol 1989; 14:185-191. in infants and children. Pediatr Cardiol 1998; 19:445-449.
27. Fish FA, Gillette PC, Benson DW. Proarrhythmia, cardiac 35. Pfammatter JP, Paul T. New antiarrhythmic drug in
arrest and death in young patients receiving encainide and pediatric use: sotalol. Pediatr Cardiol 1997; 18:28-34.
flecainide. J Am Coll Cardiol 1991; 18:356-365. 36. Gbadebo TG, Mazur A, Anderson ME. Is digoxin and
28. Perry JC, Garson A. Flecainide acetate for treatment of antiarrhythmic drug? Card Electrophysiol Rev 2000;
tachyarrhythmias in children: review of world literature 4:312-315.
on efficacy, safety and dosing. Am Heart J 1992; 124:1614- 37. Wilbur SL, Marchlinski FE. Adenosine as an anti
1621. arrhythmic agent. Am J Cardiol 1997; 79:30-37.
29. Epstein AE. Flecainide for pediatric arrhythmias: do 38. Disque K. Tachycardia. In: Pediatric advanced life support,
children behave like little adults? J Am Coll Cardiol 1989; provider manual. Satori continuum publishing, Las Vegas
14:192-193. USA 2016; pp:42.

CLIPPINGS

Randomized Double-blind Trial of Ringer Lactate Versus Normal Saline in Pediatric Acute Severe Diarrheal
Dehydration.
The aim of this study was to compare the effectiveness of Ringer Lactate (RL) versus normal Saline (NS) in the
correction of pediatric acute severe diarrheal dehydration, as measured by improvement in clinical status and
pH (> 7.35).The primary outcome was an improvement in clinical status and pH (> 7.35) at the end of 6 hrs.
Secondary outcome measures were changes in serum electrolytes , renal and blood gas parameters, the
volume of fluid used for rehydration excluding the first cycle, time to start oral feeding, hospital stay and cost
effectiveness analysis.Primary outcome was achieved in 38% (relative risk=1.63, 95% confidence Interval 0.80-
3.40) in RL and NS groups, respectively. No significant difference were observed in secondary outcomes in
electrolytes , renal and blood gas parameters.Study concluded that in pediatric acute severe dehydration ,
resuscitation with RL and NS was associated with similar clinical improvement and biochemical
resolution.Hence .NS to be considered as the fluid of choice because of the clinical improvement, cost and
availability.
Kartha GB, Rameshkumar R, Mahadevan S. Randomized Double-blind Trial of Ringer Lactate Versus Normal
Saline in Pediatric Acute Severe Diarrheal Dehydration. J Pediatr Gastroenterol Nutr 2017 Dec; 65(6):621-
626. doi:10.1097/MPG.0000000000001609.

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Indian Journal of Practical Pediatrics 2017;19(4) : 386

SURGERY

MEDIASTINAL TUMOURS IN CHILDREN -

AN INSIGHT
*Senthilnathan R
**Vijay Raj S
***Hariharan G
Abstract: Common complaints for which children seek
pediatric consultation are recurrent lower respiratory tract
infection, wheeze, respiratory distress with or without fever
and pneumonia. Pediatricians should be diligent to unmask
a mediastinal tumour that may underlie a persistent or
recurrent pneumonia. Chest X-ray in these children may
give a clue for further evaluation. The earlier the diagnosis
of mediastinal tumour is made, better the long term
outcome. This review article highlights the common
presenting features of mediastinal tumours and approach Fig.1.Subdivisions of mediastinum
to their management.
Mediastinal anatomy
Keywords: Bronchopneumonia, Mediastinal tumour,
Thoracic neuroblastoma. Mediastinum is an anatomical space situated between
the thoracic inlet superiorly, the diaphragm inferiorly, hila
Mediastinal tumours in children include a wide of the lungs laterally, sternum anteriorly and vertebral
spectrum of histopathological lesions, of which 65%-72% bodies posteriorly. Mediastinum can be divided into
are malignant.1,2 Mediastinal lesions can be asymptomatic superior mediastinum and inferior mediastinum by an
or present with common respiratory symptoms like cough, imaginary line extending from the sterno-manubrial joint
wheeze, chest pain, hemoptysis, respiratory distress with anteriorly to the lower border of fourth thoracic vertebra
or without fever. Mediastinal lesions due to posteriorly (Fig.1).
lymphoproliferative diseases can present acutely with fever,
weight loss or night sweats in addition to the respiratory Superior mediastinum extends from thoracic inlet up
symptoms. to on imaginary line between angle of Louis and fourth
thoracic vertebra. Inferior mediastinum which is below the
Though pediatricians encounter these common superior mediastinum can be further divided into anterior,
respiratory symptoms in day to day practice, it is the middle and posterior mediastinum. Anterior mediastinum
persistence of these symptoms that should alert the treating extends from sternum up to the pericardium. Middle
physician to evaluate further with the help of imaging mediastinum includes pericardium, heart and hilar
facilities. structures of both lungs. Posterior mediastinum extends
between pericardium and pre vertebral fascia.
The anatomical structures located in the mediastinum
classically give rise to the lesions, which when imaged
* Professor of Pediatric Surgery
and evaluated provide the type of lesion and tumour.
** Assistant Professor of Pediatric Surgery,
This helps in the diagnosis and management (Table I).
Stanley Medical College and Hospital, Chennai.
*** Pediatric Surgeon, In children, 44% of lesions arise in the antero superior
Tamilnadu Medical Services. mediastinum as reported by Grosfeld et al.,1 and they
email: drrsnsurgeon@yahoo.in include lymphoma, teratoma, germ cell tumours and cystic
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Indian Journal of Practical Pediatrics 2017;19(4) : 387

Table I. Common mass lesions in mediastinum

Anterior Middle Posterior
Thymus Pericardial teratoma Neurogenic tumours
Hyperplasia Pericardial cyst Neurofibroma
Teratoma Neurilemmoma
Mature Neurofibrosarcoma
Immature Sympathetic origin tumours
Malignant Ganglioma
Germ cell tumours Ganglioneuroblastoma
Yolk sac tumours Neuroblastoma
Embryonal tumours Parasympathetic origin tumours
Mixed tumours Paraganglioma
(pheochromocytoma)
Lymphoma Enteric cyst (foregut duplication cyst)
Hemangioma

hygroma. In the middle mediastinum, 20% of lesions occur Neuroblastomas presenting with opsoclonus-myoclonus
which predominantly include lymphoma and also the rare syndrome due to an autoimmune mechanism are said to
pericardial cyst and cardiac tumours while 36% of lesions have better prognosis indicating a mature phenotype and
occur in the posterior mediastinum where tumours arising are more common in thoracic neuroblastomas.7 Other signs
from the neurogenic structures in para vetebral sulcus - like Horner’s syndrome by compressive effect and
ganglioneuroma, neuroblastoma and neurofibroma occur.3 paraparesis and paraplegia by dumb bell tumours extending
into spinal cord can occur in superior mediastinal and
Diagnosis posterior mediastinal tumours respectively. Germ cell
Mediastinal tumours are occasionally diagnosed tumours in mediastinum are more common in adolescent
before birth. Most cases are diagnosed following evaluation boys. These tumours can produce hormonally active
for respiratory symptoms like cough, wheeze, stridor, chest substances like beta HCG leading to precocious puberty
pain, respiratory distress with or without fever in infancy in some cases.
or early childhood period. Unusual manifestations of The evaluation of a mediastinal lesion should start
mediastinal tumours include enlarged neck veins in a crying with a simple chest X-ray. Lateral and oblique views should
child, sternal bulge due to anterior mediastinal mass, be included in the digital X-ray to localize an opacity seen
symptoms due to recurrent laryngeal nerve or phrenic nerve on a frontal projection.
palsy, Horner syndrome due to compression of nerve trunks,
Contrast enhanced computerised tomography (CECT)
opsoclonus-myoclonus syndrome and sudden weakness of
of chest is the investigation of choice for evaluation and
lower limbs or paraplegia. Phantom hernia can also be
staging of mediastinal tumours and its efficacy increases
diligently observed in the child. Hemoptysis or trichoptysis
when combined with angiography. CECT can be done
due to erosion of tumour into bronchi, rupture into pleural
rapidly without the need for anesthesia in children.
cavity, or heart failure are rare presentations.4, 5
Magnetic resonance imaging helps in characterisation
Constant chest pain in the parasternal region should of lesion but the prolonged duration of study and the noise
not be ignored as it can be a manifestation of anterior requires careful procedural sedation as the child may
mediastinal tumours. Posterior mediastinal tumours cause already have respiratory symptoms including respiratory
chest pain due to the direct compressive effect on the inter distress. Posterior mediastinal tumour with an intraspinal
costal nerves or rib erosion. extension always needs evaluation with MRI spine.
Persistent cough, wheeze, recurrent or non-resolving Tumour markers like serum alpha fetoprotein (AFP),
pneumonia can be due to the direct compression on the beta-human chorionic gonadotropin (β-hCG), urine vanillyl
bronchi by evolving posterior mediastinal tumour. 6 mandelic acid and lactate dehydrogenase are necessary for

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Indian Journal of Practical Pediatrics 2017;19(4) : 388

Table II. Approach to common mediastinal masses

General investigations Germ cell tumour Neuroblastoma Lymphoma
Chest-xray X ray chest: lesion in X-ray chest: lesion in X-ray chest Mediastinal
AP/lateral views anterior mediastinum posterior mediastinum widening. Lesion can occur
+/- coarse calcifications +/- stippled calcifications. anywhere in mediastinum.
Complete blood CECT chest: Heterogenous CECT Chest:Heterogenous CECT chest and abdomen:
hemogram. lesion with mixed fat and lesion in posterior Multiple mediastinal nodes
bone densities. mediastinum with or with or without compression
without spinal involvement. of vital structures.
Hepatosplenomegaly may be
present. LDH Bone marrow
aspiration. Peripheral node
biopsy with immunochemistry
and staining.
Peripheral smear. Alpha feto protein Beta-Hcg MRI Spine: if involvement
present.
Urine VMA, Serum ferritin,
LDH Bone marrow
aspiration.
USG / CT abdomen.
Bone scan.
Renal function test
(before contrast CT)
CECT chest +/-
angiogram.

diagnosis as well as prognostication. Other investigation In general, thoracic neuroblastoma are said to have
includes USG abdomen, bone marrow aspiration or bone good prognosis8 compared to abdominal neuroblastoma if
scan as a part of metastatic work up. PET scan though does tumour excision is complete and followed by adjuvant
not have much of a role in diagnosis, may be useful for chemotherapy (Fig.2a, 2b, 2c and 2d). Dumb bell tumours
assessing therapeutic response and recurrence in in view of intraspinal extension will require laminectomy.
lymphomas. A well structured, clinically oriented approach Germ cell tumour responds well to three drug
increases the efficiency of the investigations and eliminates chemotherapy (PEB regimen – cisplatin, etoposide and
unnecessary studies (Table II). bleomycin - four to six cycles). Total excision of germ cell
tumour with adjuvant chemotherapy makes them eminently
Management
curable.
The operability and resectability of tumours can be
assessed with the help of investigations. Mediastinal Role of surgery in mediastinal lymphoma is primarily
tumours can be approached by conventional surgical in establishing diagnosis by biopsy. Peripheral lymphnode
approach like thoracotomy or by video assisted biopsy is preferable and if indicated mediastinal biopsy
thoracoscopic surgery (VATS). Any lesion less than 6 cm can be taken thoracoscopically. Chemotherapy is the
in size can be approached by VATS. VATS can itself be a mainstay of management in these tumours.
diagnostic tool for tissue biopsy especially in a large
tumour. Preoperative anesthetic work up should include Tumours or tumour-like lesions arising from the
the assessment of tracheal compression by tumour and the thymus include thymic cysts, thymic hyperplasia,
mode of anesthesia should be well planned to avoid any thymomas and thymolipomas. Thymic hyperplasia is
intra operative catastrophe. commonly seen in antero-superior mediastinum and is often

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Indian Journal of Practical Pediatrics 2017;19(4) : 389

Points to Remember
• Persistent pneumonia in a child should be thoroughly
investigated to unmask a mediastinal lesion.
• CT chest is an important first line investigation to
evaluate a non-resolving chest opacity.
• Early diagnosis and total excision of mediastinal
tumours will have a favourable outcome.
• Video assisted thoracic surgery will play a crucial
Fig.2a. X-ray chest - 2b.Intra operative role in evaluation and management of thoracic
Homogenous opacity photograph thoracic lesions.
in right upper lobe neuroblastoma
References
1. Grosfeld JL, Skinner MA, Rescorla FJ, West KW,
Scherer LR. Mediastinal tumors in children: experience
with 196 cases. Ann Surg Oncol 1994; 1(2): 121-127.
2. Zhurilo IP, Kononuchenko VP, Litovka VK, Moskalenko
VZ, Sopov GA, Vesely- SV, Kichik DV, Litovka EV.
Mediastinal tumors and tumor-like formations in children.
Klinichna khirurhiia/Ministerstvo okhorony zdorov’ia
Ukrainy, Naukove tovarystvo khirurhiv Ukrainy 2001;
9:44-47.
3. Saenz NC, Schnitzer JJ, Eraklis AE, Hendren WH,
Fig.2c. X-ray chest - Fig.2d. MRI - Hyper- Grier HE, Macklis RM, Shamberger RC. Posterior
Non homogenous intense mass posterior mediastinal masses. J Pediatr Surg 1993; 28(2):172-176.
opacity in right mediastinum right 4. Laberge J, NguyenL, Shaw K. Teratomas, dermoids and
upper lobe side with fine other soft tissue tumors. In: Ashcraft K, Holcomb G,
calcifications (HPE Murphy J (eds) Pediatric Surgery. Philadelphia: Elsevier
neuroblastoma) Saunders, 2005; pp972–996.
5. ÖzergÝn U, Görmüs N, Kadir O, Durgut K, Yüksek T.
detected as ‘Sail sign’ in chest X-ray when evaluated for Benign mature cystic teratoma of the anterior mediastinum
pneumonia.9 Thymic hyperplasia regresses spontaneously leading to heart failure: report of a case. Surg Today 2003;
and may need steroids for remission if symptomatic. 33(7):518-520.
6. Das RR, Sami A, Seth R, Nandan D, Kabra SK, Suri V.
Primitive neuroectodermal tumour known as Askin’s Thoracic neuroblastoma presenting as recurrent empyema.
tumour is a rapidly growing tumour of the chest wall and Natl Med J India 2014; 27(2):84-85.
in a short time can invade the posterior mediastinum.
7. Rudnick C, Khakoo Y, Antunes NL. Opsoclonus-
Diagnosis can be made with VATS and follow up treatment myoclonus-ataxia syndrome in neuroblastoma: Clinical
with chemotherapy. outcome and antineural antibodies-a report from the
Children’s Cancer Group study. Med Pediatr Oncol 2001;
Conclusion
36:612-622.
Persistent or recurrent respiratory symptoms in a child 8. Altman A, Baehner RL. Favorable prognosis for survival
calls for a proactive approach with further investigation if in children with coincident opsomyoclonus and
the chest skiagram shows a non resolving opacity. neuroblastoma. Cancer 1976; 37:846-852.
If detected early and managed appropriately, mediastinal 9. Alves ND, Sousa M. Images in pediatrics: the thymic sail
tumours have a good outcome. sign and thymic wave sign. Eur J Pediatr 2013; 172(1):133.

75
Indian Journal of Practical Pediatrics 2017;19(4) : 390

RADIOLOGY

TORTICOLLIS
*Vijayalakshmi G
**Natarajan B
**Abirami K
**Thangalakshmi A
**Raveendran J
Torticollis is a symptom with many causes. Congenital
vertebral anomalies, strabismus and nystagmus, trauma,
inflammations and tumors near the cervical spine can cause
torticollis. The simplest and least alarming is the congenital
muscular torticollis that is evident from history and onset
or duration of the posture. It is the commonest cause of Fig.2.X-ray neck (lateral) - Retropharyngeal
torticollis in the infant. There may be a history of birth abscess
trauma. In utero crowding is another etiological factor
accounting for torticollis being associated with useful investigation in the presence of a palpable mass.
developmental dysplasia of the hip. It usually presents by The normal muscle is hypoechoic with short echogenic
the age of two months. The ear on the side of the contracture lines running within, representing the perimysium in
is tilted towards the ipsilateral shoulder while the chin is between bundles of muscle fibers. In Fig.1 there is a focal
rotated towards the contralateral side. Plagiocephaly with widening of the sternomastoid with loss of normal muscle
occipital flattening on the same side is seen. echogenicity (arrow) with normal thickness of the
This asymmetry is not seen when torticollis is acquired sternomastoid seen superiorly (arrowhead).
later in life. Hence, the diagnosis of congenital muscular
torticollis is essentially clinical. However, ultrasound is a The child in Fig.2 presented with acute painful
torticollis. The child had fever and pain on swallowing.
Lateral X-ray of neck shows the space between the air
column and the spine at the level of C2 and C3 is clearly
widened to more than the width of the vertebrae.
Retropharyngeal abscess is common in children and not in
older children mainly because the space involutes as they
grow older. The retropharyngeal space is the area between
the buccopharyngeal fascia (which closely invests the
pharyngeal constrictors) and the prevertebral fascia (which
borders the cervical spine). It contains loose connective
tissue and is rich in lymph nodes that can trap infective
Fig.1.Ultrasound neck- Sternomastoid tumor organisms leading on to inflammation and suppuration.
(arrow) with normal muscle thickness (arrow- Torticollis is due to irritation of inflammed, edematous neck
head) muscles that go into spasm. Mild subluxation of C1 over
C2 can also be seen in Fig.2.
* Professor
** Assistant Professor, The prevertebral fascia usually prevents the spread
Department of Radiology, of inflammation into the prevertebral space from the
Institute of Child Health and Hospital for Children, retropharyngeal space. Fig.3 is an X-ray of neck lateral
Chennai. view. The retropharyngeal soft tissue thickness is normal.
email: drviji.rad@gmail.com However, C3 vertebral body is porotic implying destruction
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Indian Journal of Practical Pediatrics 2017;19(4) : 391

Fig.3. X-ray neck Fig.4.CT neck - Lysis

lateral - (arrow points of anterior arch of C1 Fig.5.CT brain - Fig.6. CT brain -
to porotic C3) (arrow) Hyperintense Cervical cord
midline
of bone. This is spinal caries affecting the third cervical in the cerebellum just behind the fourth ventricle. Many
vertebra. There is mild narrowing of C2-3 inter space. reasons have been offered for torticollis in patients with
The torticollis in this child is due to irritation of the longus posterior fossa tumors. These include compensation for
colli and the longus capitis muscles. CT neck of the child diplopia, herniation of cerebellar tonsils, irritation of the
(Fig.4) shows the right side of the anterior arch of C1 is spinal accessory nerve because of descent and impaction
porotic compared to the left alone with rotation of C1 to of the cerebellar tonsils in the foramen magnum or just to
the right. The lysis is again due to tuberculous infection of maintain a fixed posture to avoid stretching and irritation
the vertebra. One can also see that there is no pus collection of the dura.
as yet. Inflammation and irritation of the muscles is causing
torticollis which also serves to splint and protectively Fig.6 is that of one year old child whose mother
immobilise the neck. complained of child having torticollis for an uncertain
period of time. She was sure that the child was normal at
Rarely torticollis may be the only presenting symptom birth. MRI of the cervical spine was done keeping in mind
of a posterior fossa tumor even without headache, vomiting congenital vertebral abnormalities. But the vertebral canal
or ataxia (Fig.5). This child, who came with torticollis had showed an exophytic mass from the cervical cord with
a normal neurological examination. Her neurological poorly demarcated margins. Intramedullary spinal cord
examination was normal. Power in all limbs, reflexes and tumors are rare but should be borne in mind. For these
gait were normal. The head and neck MRI revealed a reasons, torticollis should always be subjected to a full
midline, round, lobulated, hyperintense medulloblastoma neurological and radiological examination.

CLIPPINGS

Randomized trial of dexamethasone vs prednisone for children with acute asthma exacerbations.
The authors intended to analyze if 2 doses of dexamethasone were as effective as 5 days of prednisolone/
prednisone therapy in improving symptoms and quality of life of children with asthma exacerbations, admitted
to the emergency department (ED). A randomized, noninferiority trial conducted including patients aged
1-14 years who presented to the ED with acute asthma to compare the efficacy of 2 doses of dexamethasone
(0.6mg/kg/dose, experimental treatment) vs a 5-day course of prednisolone/prednisone (1.5 mg/kg/d, followed
by 1mg/kg/d on days 2-5, conventional treatment revealed the following.. 2 doses of dexamethasone could
possibly serve as an effective alternative to a 5-day course of prednisone/prednisolone for asthma exacerbations,
as estimated through the persistence of symptoms and quality of life at day 7.
Paniagua N, Lopez R, Murioz N, Tarmes M, Mojica E, Mojica E, Arana-Arri E, et al. Randomized trial of
dexamethasone vs prednisone for children with acute asthma exacerbations. J Pediatr 2017 Dec;191:190-
196.e1.

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Indian Journal of Practical Pediatrics 2017;19(4) : 392

CASE REPORT

RECURRENT VAGINAL FOREIGN BODY -

TWO MUCH PRANK
*Udayakumar N
**Abhinayaa J
***Balamourougane P
****Priyadharshini R
Abstract :Vaginal foreign body is a common cause of
vaginal bleeding in prepubertal girls. Recurrence in the
absence of abuse is rare. Examination and ultrasound-
abdomen of a six-year, eight month girl with history of Fig.1. Ultrasound abdomen showing two
two-week vaginal-bleeding and five-day fever revealed the linear streaks in vaginal area, probable
presence of vaginal foreign-body. Child reported insertion foreign body
of hairpin, diagnosed and removed. Treatment with
gynecological, psychological evaluation and follow-up was reveal signs of precocious puberty or overt signs of sepsis.
successful. Child’s developmental milestones were normal, scholastic
performance was good. She had prepubertal Tanner staging.
Keywords: Recurrent vaginal foreign body, Children, Sexual abuse was ruled out by detailed history.
Abuse, Vaginal bleeding Investigations including complete hemogram, bleeding
Vaginal foreign bodies are the cause of genital time, urine routine and urine culture were normal.
complaint in 4% of prepubertal girls. In prepubertal Ultrasound abdomen revealed two linear streaks in the
children, it is the cause of the vaginal discharge in 18% vagina, probably foreign body (Fig.1).
and upto 50%with vaginal bleeding.1 The majority of Examination by gynecologist revealed mild labial
patients are between the ages of three and nine.2 Children adhesion and intact hymen. Per rectal examination revealed
may be exploring their body out of curiosity, pruritis or two vertical ridges in the anterior wall. On vaginoscopy
behavior related to sexual abuse.3 The recurrence of vaginal under general anesthesia, two linear foreign bodies, a pencil
foreign body in the absence of child abuse makes this case measuring 5 cms (Fig.2) and a crayon measuring 4 cms
unique. (Fig.3) in length, were detected and were removed. Vaginal
Case report irrigation was done with povidine iodine solution.
The child’s symptoms settled. Before discharge both the
A 6 years 8 months old girl, who lives with her parents, child and her parents were counseled.
presented with a history of vaginal bleeding for 2 weeks
and fever for 5 days. Detailed history was taken to rule out Six months later, the child informed her mother that
various organic conditions. Clinical examination did not she had put a hair pin into the vaginal orifice. Revealed a
hair pin like structure in the pelvic area (Fig.4) and was
removed.
* Associate Professor
** Postgraduate A detailed psychological assessment of the family was
*** Associate Professor in Pediatric Surgery done. There has been no apparent emotional or
**** Senior Resident, psychological disturbance. The parents were advised to
Department of Pediatrics, provide avenues for the child to play outdoors and also
Sri Ramachandra Medical College and supervise the child when she handles certain objects.
Research Institute, Chennai. Follow-up till 12 months showed no recurrence of similar
email: drnuday@gmail.com instances.
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Indian Journal of Practical Pediatrics 2017;19(4) : 393

that symptoms exhibited for less than 1 month in 60% and

more than 1 year in 11%, prior to evaluation and treatment.4
Unfortunately, many girls may tolerate symptoms for a long
time before seeking treatment. Reasons for the delay in
diagnosis are multifactorial. It includes a poor or unclear
history, anxiety, denial, fear or embarrassment about
vaginal complaints, along with difficulty in performing a
thorough physical examination, by the pediatrician
requiring multiple evaluations before the foreign body is
found. History of self reporting of foreign body is present
in 54%.4
Fig.2. Pencil being removed
A careful history taking, high index of suspicion and
local examination, bimanual recto-abdominal palpation can
diagnose 91% of the vaginal foreign bodies. Pelvic
ultrasound, plain X-ray of pelvis and Magnetic Resonance
Imaging (MRI) are recommended to diagnose, but
vaginoscopy is confirmatory. X-ray abdomen, which can
detect radiopaque foreign bodies and pelvic ultrasound are
the initial investigations.5 MRI is the best technique in
children for evaluating nonmetallic vaginal foreign bodies
which are missed by X-ray pelvis and ultrasound.6
Self insertion of foreign body is common (75%).
Fig.2. Crayon being removed Normal masturbation or curiosity, modelling behavior or
sexual abuse believed to cause vaginal insertion of foreign
bodies.4 Children exposed to sexual abuse exhibit a number
of sexualized behaviors, including inserting objects into
the vagina or anus.4 The child and the family should be
assessed psychologically to rule out underlying emotional
and behavioral problems affecting social competence and
adaptiveness. Treatment includes timely removal and
vaginal irrigation with normal saline, or povidone-iodine
solution. Generally in older children and distally located
foreign bodies, removal is easy.7 One should be aware of
hymenal injury if the child is uncooperative or very young.
Fig.4. X-ray pelvis - Hairpin in pelvic area
The presence of any vaginal foreign body in a pre-
Discussion pubertal girl should elicit concern about sexual abuse and
thorough probing into the family dynamics and counseling
The causes for vaginal bleeding in prepubertal girls will be needed. In a developmentally normal child without
include accidental trauma, sexual abuse, vulvovaginitis, abuse, the need to stress on outdoor and recreational
endocrine abnormalities, lichen sclerosus, urethral activities are also important.
prolapse, blood dyscrasias, hemangioma and tumours. The
foreign bodies that may be found in the vagina includes Acknowledgement: We would like to acknowledge the
safety pins, hair grips, pencils and wad up pieces of toilet help from department of Obstetrics and Gynecology and
paper.2 Depending on the nature and shape of the object, it department of Psychology, Sri Ramachandra Medical
can classically result in local vaginitis, associated with College and Research Institute for helping us in the
purulent, foul smelling bloody vaginal discharge or an management of this child.
abrasion and rarely urinary and fecal fistulae.3 References
The time from insertion to symptoms and subsequent 1. Paradise JE, Willis ED. Probability of vaginal foreign body
extraction of vaginal foreign bodies varies greatly. Stricker in girls with genital complaints. Am J Dis Child 1985;
et al studied 35 girls with vaginal foreign bodies and found 139:472-476.
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Indian Journal of Practical Pediatrics 2017;19(4) : 394

2. Striegel AM, Myers JB, Sorensen MD, Furness PD, 5. Caspi B, Zalel Y, Elchalal U, Katz Z. Sonographic detection
Koyle MA. Vaginal discharge and bleeding in girls younger of vaginal foreign bodies. J Ultrasound Med 1994; 13:236-
than 6 years. J Urol 2006; 176:2632-2635. 237.
3. Simon DA, Berry S, Brannian J, Hansen K. 6. Kihara M, Sato N, Kimura H, Kamiyama M, Sekiya S,
Recurrent, purulent vaginal discharge associated with Takano H. Magnetic resonance imaging in the evaluation
longstanding presence of a foreign body and of vaginal foreign bodies in a young girl. Arch Gynecol
vaginal stenosis. J Pediatr Adolesc Gynecol 2003; Obstet 2001; 265(4):221-222.
16(6):361-363. 7. Smith YR, Berman DR, Quint EH. Premenarchal vaginal
4. Stricker T, Navratil F, Sennhauser FH. Vaginal foreign discharge: findings of procedures to rule out foreign
bodies. J Pediatr Child Health 2004; 40(4):205-207. bodies. J Pediatr Adolesc Gynecol 2002;15(4):227-230.

CLIPPINGS

Chronic cough postacute respiratory illness in children: a cohort study.

A Prospective study was undertaken among the children attending the ED with ARI with cough.Children were
followed weekly for 28 days; those with a persistent cough at day 28 were reviewed by a paediatric pulmonologist..
main outcome was cough persistence at day 28 and pulmonologist diagnosis.839 children (median age=
2.3 years, range=0.5 months to 14.7 years, 60% male) were enrolled over 2 years. Most children (n=627, 74.8%)
had cough duration of <7 days at enrolment. At day 28, 171/839 (20.4%, 95% CI 17.7 to 23.1) children had
persistent cough irrespective of cough duration at enrolment.When chronic cough develops post-ARI, clinical
review is warranted, particularly if parents report a history of prolonged or recurrent cough. Parents of children
presenting acutely to ED with cough should be counseled about the development of chronic cough, as an underlying
respiratory condition is not uncommon
O’Grady KF, Drescher BJ, Goyal V, Phillips N, Acworth J, Jason Acworth JM, et al. Chronic cough postacute
respiratory illness in children: a cohort study. Archives of Disease in Childhood 2017; 102:1044-1048.

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Indian Journal of Practical Pediatrics 2017;19(4) : 395

AUTHOR INDEX

Abhinayaa J (392) Mehul A Shah (176) Shrishu R Kamath (21)

Abirami K (390) Mullai Baalaaji AR (332) Shyamala J (5)
Aditi Sinha (140) Murari Bharadwaj (95) Smita Mishra (231)
Akila Devi V (156) Muthu MS (361) Smita Ramachandran (290)
Amzad Khan (79) Namasivayam S (183) Snehal Kulkarni (245)
Anandan V (69) Nandhini G (92, 183) Somasundaram A (342)
Anita Khalil (219) Natarajan B (72, 207, 308, 390) Sreerekha KB (62)
Ankita Saikia (361) Nirmala Dheivamani (310) Sridevi A Naaraayan (44)
Anuradha Harish (79) Nutan Singh (210) Sudha Ekambaram (92, 126, 374)
Arpana Iyengar (110) Pankaj Hari (134) Suma Balan (191)
Arpita Chattopadhyay (250) Prabha S (168) Sumathi Bavanandam (36, 310)
Arvind Bagga (140) Priyadharshini R (392) Sumitra Venkatesh (284)
Ashok Kumar (210) Raghul M (304) Suresh Goyal (79)
Balamourougane P (392) Rajakumar PS (257) Susan Uthup (119)
Dheebha V (72, 207) Rajamani G (304) Sushmita Banerjee (95)
Elamaran C (273) Rakesh Lodha (250) Tanuja Karande (245)
Gautham G (75) Ramakrishnan TCR (77) Thakur P (110)
Gnanasambandam S (273) Ramesh Chand (210) Thangalakshmi A (390)
Gowrishankar NC (16) Rani Gera (290) Thangavelu S (156)
Hariharan G (386) Ranjit Baby Joseph (62, 199, 298, 378) Thirumalai Kolundu S (337)
Hemchand K Prasad (319) Ratnakumari TL (10, 75) Udayakumar N (392)
Indira Agarwal (101) Raveendran J (390) Ujjal Poddar (58)
Janani Sankar (338) Ravi LA (366) Uthaya Kumaran (210)
Jayashree Hegde (53) Regunandan SR (304) Vaishnavi Raman (374)
Jeeson C Unni (62,199, 298, 378) Rupali Jain (79) Vaman Khadilkar (319)
Kalaivani G (168) Sajana TM (378) Vidya Krishna (327)
Kalindi R Shah (176) Saleem Akhtar (77) Vijay Raj S (386)
Kalpana S (26) Sana AMH (75) Vijayakumar M (156)
Karthik C (72, 207) Santosh T Soans (53) Vijayalakshmi G (72, 207, 308, 390)
Kavita Tiwari (79) Selvan R (49) Vindhiya K (75)
Kopika Vasan (69) Senthilnathan R (386) Vinod Choudhary (126)
Leema Pauline C (366) Shakuntala Prabhu (284) Vinod H Ratageri (294)
Liji R (119) Shanthi S (31) Viveka Saravanan (366)
Madhu R (353) Shilpa C (294) Zulfikar Ahamed (263)
Malathi Sathiyasekaran (347) Shipra Agarwal (58)
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Indian Journal of Practical Pediatrics 2017;19(4) : 396

SUBJECT INDEX

Acute intermittent peritoneal dialysis (119) Hypertension in children and adolescents (101)
Acute myocarditis and cardiomyopathy (263) Hypereosinophilic syndrome presenting as persistent
Acute pancreatitis - Management (36) pleural effusion (210)

Approach - Gross hematuria (95) Hypopigmented skin lesions - What a pediatrician should
know? (353)
Approach - Management of arrhythmias (273)
Juvenile dermatomyositis (191)
Atypical manifestations - Dengue (21)
Late talking toddler - When to worry? (342)
Bladder bowel dysfunction - Practical approach (183)
Lower gastrointestinal bleed (310)
Cardiogenic shock (250)
Media and children (53)
Cardiovascular issues in systemic conditions (284)
Nephrotic syndrome - Pathogenesis and therapy (140)
Celiac screening - Wheat eating population (58)
Nocturnal enuresis (168)
Childhood tuberculosis (26)
Pediatric pulmonary hypertension - Recent management
Common issues in office practice (49) guidelines (290)
Congenital heart defects - Non surgical management (245) Pediatric renal care - Integrated approach (92)
Congestive cardiac failure - Current concepts in Picture quiz: Sturge weber syndrome (79)
management (231)
Pneumonia - Treatment guidelines (16)
Dermatology
Radiology
- Sunscreens (69)
- Abdominal tuberculosis (308)
Disaster related injuries (294)
- Osteomyelitis - 3 (72)
Drug profile
- Osteomyelitis - 4 (207)
- Antiarrhythmic agents (378)
- Torticollis (390)
- Diuretics (199)
Recurrent vaginal foreign body - Two much prank (392)
- Pharmacotherapy - Attention deficit hyperactivity disorder
(62) Renal imaging (110)
- Pharmacotherapy of heart failure (298) Renal nutrition in chronic kidney disease (176)
Early childhood caries - Causes and management (361) Renal rickets (156)
Electrocardiogram (219) Research and paper writing (44)
Elevated transaminases in a child – Approach (347) Sedation and analgesia in office practice (332)
Extra corporeal membrane oxygenation (257) Surgery
Fetal valproate syndrome (75) - Laparoscopy (304)
Fever in newborn (5) - Mediastinal tumours in children - An insight (386)
Financial literacy for doctors (337) Ten pitfalls in management of urinary tract infection (374)
Fluid and electrolyte management in neonates (10) Thrombocytopenia (338)
Growth charts and monitoring (319) Unilateral Duane syndrome (77)
H1N1 revisited (327) Ventilation trouble shooting (31)
Head injury in children triaging and imaging (366) VUR - Scarring/hypodysplasia and antibacterial
Hypercalciuria syndrome and nephrolithiasis (126) prophylaxis for urinary tractinfection (134)
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Indian Journal of Practical Pediatrics 2017;19(4) : 398

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