Академический Документы
Профессиональный Документы
Культура Документы
CONTENTS
FROM THE EDITOR'S DESK 175
Journal Office: Indian Journal of Practical Pediatrics, IAP-TNSC Flat, F Block, Ground Floor, Halls Towers,
56, Halls Road, Egmore, Chennai - 600 008. INDIA. Tel.No. : 044-28190032 E.mail : ijpp_iap@rediff mail.com
Address for ordinary letters: The Editor-in-Chief, Indian Journal of Practical Pediatrics, Post Bag No.524,
Chennai 600 008.
Address for registered/insured/speed post/courier letters/parcels and communication by various authors:
Dr. A. Balachandran, Editor-in-chief, Indian Journal of Practical Pediatrics, F Block, No. 177, Plot No. 235,
4th Street, Anna Nagar East, Chennai - 600 102. Tamil Nadu, INDIA.
1
Indian Journal of Practical Pediatrics 2005; 7(3) : 174
- Editorial Board
Published and owned by Dr. A. Balachandran, from Halls Towers, 56, Halls Road, Egmore,
Chennai - 600 008 and printed by Mr. D. Ramanathan, at Alamu Printing Works,
9, Iyyah Mudali Street, Royapettah, Chennai - 600 014. Editor : Dr. A. Balacnadran.
2
2005; 7(3) : 175
Greetings from the Journal Committee of of metabolism, though a rare disorder is still
IJPP! In this issue we focus on some of the posing a problem in the diagnosis and
common as well as interesting topics in the field management. Dr.Mamta Muranjan discusses an
of Neonatology. This issue is compiled and overview on this complex subject in detail. Hope
edited Dr.Durai Arasan, Dr.V.Lakshmi and this article will be an academic feast to all
Dr.S.Lakshmi. They have carefully chosen the postgraduates and neonatologists. Dr.Muralinath
topics and authors for this issue, with the focuses the role of plain X-ray in neonatal chest
concurrence of the Journal Committee of IJPP. diseases. With years of experience in the field
Birth asphyxia - Definition and concepts of pediatric radiology, he has emphasized how
in the management is written by Dr.Vishnu Bhat, the plain x-ray plays a vital and key role in the
et al. They have given a detailed account on this evaluation of RDS in infants with illustrative
topic and also mentioned that prevention of chest skiagrams. We hope the FAQs in neonatal
asphyxia is important in bringing down neonatal office practice will be useful for the practitioners.
mortality and morbidity. Respiratory distress in Dr.S.Criton has discussed in detail the
newborn is a symptom complex consisting of Cutaneous viral infections in children and
various clinical entities. Dr.Arvind Saili has highlighted the common viral exanthems in
given a vivid picture on the Approach to children. Dr.Panna Choudhury, et al in their
respiratory distress in newborn. We hope this article on Prevention of adult diseases in
article will benefit both postgraduates and children: Nutrition perspective, stressed the
pediatricians while dealing with neonatal crucial role of pediatricians in identification of
problems. Surfactant deficiency is the main children at risk of obesity. In the Radiologist
contributor for respiratory distress in newborn. talks to you column, Dr.Vijayalakshmi, et al
The introduction of Surfactant therapy in infants have discussed the role of ultrasonogram in the
with low birth weight and prematurity has been diagnosis of renal cystic disease. Persistent cough
cost effective in developing countries. in children is well narrated by Dr. Paramesh.
Dr.Namasivayam Ambalavanan stressed that They conclude that ultrasonogram is the only
surfactant should be administered early and more investigation necessary to diagnose and follow-
than one dose is occasionally required in neonates up polycystic kidney disease. We thank all the
with RDS. contributors for the column on Case study. The
Journal Committee of IJPP once again thank all
The article on Necrotizing enterocolitis the contributors in this issue. The next issue will
(NEC), which is one of the most common medico also cover some more interesting topics related
surgical emergencies in neonates is contributed to neonatology.
by Dr.Arvind Shenoi, et al. He has discussed the
pathophysiology, management and outcome of Dr. A.Balachandran
NEC in NICU in Indian scenario. Inborn errors Editor-in-Chief
3
Indian Journal of Practical Pediatrics 2005; 7(3) : 176
INSTRUCTIONS TO AUTHORS
General
Print the manuscript on one side of standard size A4, white bond paper, with margins of at least 2.5 cm (1)
in double space typescript on each side.
Use American English using Times New Roman font 12 size. Submit four complete sets of the manuscript.
They are considered for publication on the understanding that they are contributed to this journal solely.
All pages are numbered at the top of the right corner, beginning with the title page.
All manuscripts should be sent to: The Editor-in-Chief, Indian Journal of Practical Pediatrics
Manuscript
1st Page
Title
Name of the author and affiliation
Institution
Address for correspondence (Email, Phone, Fax if any)
Word count,
No. of figures (colour / black and white)
No. of references
Authors contribution
2nd Page
Abstract (unstructured, not exceeding 100 words) with key words (not exceeding 4)
3rd Page -
Text
Points to remember (not more than 5 points)
Acknowledgement
References
Tables
Figures should be good quality, 4 copies black & white / colour,*
Legends
(4 x 6 inches Maxi size) Glossy print
* Colour images will be charged separately
Text
Only generic names should be used
Measurements must be in metric units with System International (SI) Equivalents given in parentheses.
References
Recent and relevant references only
Strictly adhere to Vancouver style
Should be identified in the text by Arabic numerals in parentheses.
Type double-space on separate sheets and number consecutively as they appear in the text.
Defective references will entail rejection of article
Tables
Numbered with Roman numerals and typed on separate sheets.
Title should be centered above the table and explanatory notes below the table.
4
2005; 7(3) : 177
NEONATOLOGY
BIRTH ASPHYXIA DEFINITION Birth asphyxia: Apgar score of less than 7 at one
AND CURRENT CONCEPTS IN minute of age
MANAGEMENT Moderate asphyxia: Apgar score between 4 to 6
* Vishnu Bhat B at one minute of age or slow gasping breathing
** Narayanan P at one minute of age
Abstract: Birth asphyxia is an important cause Severe asphyxia: Apgar score of 3 or less at one
of mortality and morbidity in India. Improved minute of age or no breathing at one minute of
antenatal care will definitely bring down its age.
incidence. Once the cerebral injury has occurred, The overall incidence of perinatal asphyxia
the management is mainly supportive. Newer is around 0.5 to 2 % but is significantly more
cerebroprotective therapies are being tried. The when the gestational age is below 36 weeks3. It
outcome depends on various factors. Most of the is the leading cause of neonatal mortality in India.
severely affected babies do not survive and the
ones who do not have multisystem involvement Ninety percent of insults due to asphyxia
usually do well with excellent outcome. occur in the antepartum or intrapartum period and
Key words: Birth asphyxia, definition, the rest occur in the immediate postpartum
management, outcome. period4. Antepartum causes include impaired
maternal oxygenation (maternal hypertension,
Perinatal asphyxia is defined as an insult to diabetes, vascular disease, drug use or other
the fetus or newborn due to lack of oxygen and systemic disease), decreased blood flow from the
or perfusion to various organs. It is characterized mother to the fetus (placental infarction or
by presence of profound metabolic or mixed fibrosis, placental abruption and cord accidents),
acidemia with a pH of less than 7.1 on an impaired gas exchange across the placenta and
umbilical cord arterial blood sample, persistence increased fetal oxygen requirement, other causes
of an Apgar score of 0-3 for more than 5 minutes, include birth trauma, failure to initiate respiration,
presence of clinical and neurologic sequelae in severe respiratory diseases and congenital heart
the immediate neonatal period and evidence of diseases etc. The response to mild and moderate
multi organ system dysfunction1. asphyxia differs from that to severe asphyxia. The
The two working definitions of the National fetus and the neonate are more resistant to
Neonatal and Perinatal Database network are as asphyxia than an adult because of a lower rate of
follows: 2 metabolism and presence of more glycogen
reserves5.
* Professor
** Senior Resident, An increase in the PCO2 and a fall in the
Department of Pediatrics, PO2 produces a diving reflex wherein there is a
JIPMER, Pondicherry shunting of blood towards vital organs i.e. the
6
2005; 7(3) : 179
brain, heart and adrenals due to vasodilatation in paralysed child, 3. Decision on stopping
these organs and flow of blood away from the anticonvulsants and 4.Predicting long term
viscera, bone, muscle and skin due to neurological outcome.
vasoconstriction caused by an increased
Limitations: 1.Subtle seizures arising from sub
chemoreceptor and sympathetic activity. 6
cortical focus are not associated with EEG
Hypoxia also results in energy being produced
changes and 2. Technically difficult to obtain
by anaerobic glycolysis which leads to metabolic
EEG in newborns due to movement artefacts.
acidosis due to accumulation of pyruvate and
lactate. There is an overall reduction in body Neuroimaging
movements to minimize oxygen consumption. USG: The anterior fontanelle approach is used
When severe asphyxia occurs (defined as a to detect injury to the basal ganglia, thalamus and
reduction of oxygen content of the blood to less periventricular leukomalacia. The characteristic
than 1 nmol/L) all the adaptive and protective evolution of echo densities of periventricular
mechanisms mentioned above are completely leukomalacia is the initial formation of small
overwhelmed; there is a failure of the cerebral echolucent cysts to final swiss cheese appearance.
auto regulation and hence the cerebral blood flow
decreases, there is a drastic fall in the cardiac CT scan: It provides important information in
output and in the blood pressure and ultimately the diagnosis of diffuse cortical injury in severe
mechanical asystole and cardiac electro- selective neuronal necrosis. The value in
mechanical dissociation and renal tubular assessment is evident only several weeks after
necrosis occurs. the injury.
8
2005; 7(3) : 181
9
Indian Journal of Practical Pediatrics 2005; 7(3) : 182
monitoring of blood pressure and respiration. A is 40%. The recurrence is 20-30% with asphyxia
dose of 20 mg/kg achieves a blood level of and 100% corticol dysgenesis. Metabolic seizures
20 g/ml which is needed to achieve have the lowest recurrence rates.
anticonvulsant effect. If seizures are not
9. Other system management
controlled, administer additional doses of
5 mg/kg every 15 minutes till seizures are A. Management of cardiac effects: Adequate
controlled or a total dose of 40 mg /kg is reached. ventilation with correction of hypoxemia, acido-
Total dose in excess of 40 mg/ kg does not sis and hypoglycemia can reduce myocardial
provide additional anticonvulsant effect. In damage. Volume overload must be avoided.
severely asphyxiated infants with hepatic or renal Diuretics may be ineffective if there is
dysfunction, higher blood levels are reached and concomitant renal failure. If there is cardiac
last longer with 40mg/kg dose resulting in collapse, inotropic drugs like dopamine and
sedation and hypotension for several days. Hence dobutamine have to be started. Epinephrine
after first 20mg/kg dose, some clinicians go for should be avoided as it causes vasoconstriction
20mg/kg phenytoin with cardiac monitoring. If and fall in perfusion and acidosis. Some infants
still there is no response, i.v. Lorazepam is given in great distress may require afterload reduction
at dose of 0.05- 0.1 mg / kg as often as needed. It with a peripheral beta agonist like Isoproterenol
is better to use phenytoin when the baby is or peripheral alpha-blocker like phentolamine,
comatosed or has respiratory depression. A tolazoline or nitroprusside10.
combination of phenytoin with phenobarbitone B. Management of renal effects: Two main
often controls convulsions better with lesser side problems are Acute tubular necrosis (ATN) and
effects. Other drugs used for acute seizures are Syndrome of inappropriate anti diuretic hormone
primidone, lidocaine, thiopentone, paraldehyde secretion (SIADH), which are managed mainly
and valproate where experience in newborns is by fluid restriction. Oliguria must not be at-
lacking. Once levels of conventional tributed to SIADH or ATN unless prerenal
anticonvulsants are maximized to 40 g/ml for etiologies such as hypovolemia or vasodilation
phenobarbitone and 20 g/ml for phenytoin, there have been ruled out. Dopamine at 1.25-2.5
is little reason to eliminate every twitch11. g/kg/min may aid renal blood flow. Dialysis is
Maintenance therapy is with phenobarbitone at the treatment for severe cases, but not offered to
dose of 3-5 mg / kg day in 2 divided doses IV or many babies because of high mortality associated
orally and / or phenytoin at 5-8 mg/kg/day in 2 with such cases10.
divided doses IV. Oral absorption of phenytoin C. Gastrointestinal effects: There is increased risk
is poor. When infants condition is stable for 3-4 for bowel ischemia and necrotizing enterocolitis.
days, anticonvulsants arc weaned of gradually. So infants with asphyxia must not be fed for 2-3
days or till good bowel sounds are heard and
Duration of treatment and indications for
stools are negative for blood or reducing
stopping anticonvulsant: Optimum duration of
substance10.
therapy relates to the likelihood of recurrence of
seizures if the drugs are discontinued. The three D. Hepatic effects: Since there may be bleeding
main determinants include neurological status, due to hepatic dysfunction clotting factors and
cause of seizures and EEG. If neurological fresh frozen plasma may be given. Blood sugar
examination is abnormal, 50% will have should be maintained at 75-100 mg/dL and drugs
recurrence, while if interictal EEG is abnormal it metabolized by liver should be avoided10.
10
2005; 7(3) : 183
E. Pulmonary effects: Adequate oxygenation and cells in response to asphyxia. Superoxide and NO
ventilation with possibly mild alkalinisation may combine to form Peroxynitrite which decomposes
be helpful. Method of ventilation is different if releasing oxidants. Inhibition of NO synthesis
the primary problem is hyaline membrane with L-NAME - (Nitro L arginine methyl ester)
disease, primary pulmonary hypertension of has been tried. It prevents secondary brain injury
newborn or meconium aspiration syndrome. High by suppression of NO production during
frequency ventilation and ECMO can be tried in recovery. But inhibition during hypoxic insult
selected cases6. could be deleterious.
Potential new therapies of cerebroprotection7: Vitamin E (alpha-tocopherol) - membrane bound
It is very difficult to predict during the neonatal chain breaking anti oxidant prevents chain
period which neonates will suffer the most elongation in free radical damage.
profound damage after an insult to the central
nervous system, since more than 30 percent of Lazeroids-non-glucocorticoid 21 aminosteroid
neonates presenting with moderate prevents iron dependent lipid peroxidation by
encephalopathy have normal outcome. scavenging peroxyl radicals16.
11
Indian Journal of Practical Pediatrics 2005; 7(3) : 184
hypoxic damage by multiple mechanisms. outcomes at 18 months than did newborns in the
Calcium channel blockers, which cross the blood normothermic group18.
brain barrier like flunarizine and nimodipine are
tried. But the neuroprotective effect is not Hypoxic Preconditioning: Immature rats
impressive. subjected to cerebral hypoxia sustain less damage
if exposed to hypoxia alone compared to animals
Platelet-activating factor antagonist BN 52021 not exposed previously to hypoxia. The
attenuates hypoxic damage. mechanism is by induction of genes or proteins
that influence metabolic events during insult or
2. Other drugs reperfusion.
Monosialogangliosides are important constituent Prognosis of perinatal asphyxia
of nerve cell membrane. It gives neuroprotection
by incorporation into cell membrane. The degree of asphyxia necessary to cause
permanent brain damage in experimental animals
Growth factors: Nerve Growth Factor has been is quite close to that which causes death (> 25
shown to reduce severity of hypoxic damage in minutes of total asphyxia). Survival with brain
immature rat. The neuroprotective effect of damage is actually uncommon in this model. The
exogenously administered erythropoietin has extremes of death or intact survival are the most
received much attention for ischemic disease, and likely outcome. Likewise in humans, birth
promising data are emerging for the newborn. asphyxia severe enough to damage fetal brain
usually kills before or soon after birth, the
Glucocorticoids: Dexamethasone given
remainder survive and are normal. The only
immediately before hypoxic insult does not give
groups with significant neurological impairment
protection. But if administered > 24 hrs before
are those who were severely asphyxiated yet
insult, there is improved neuronal outcome.
narrowly escaped death. Any infant severely
3. Non-pharmacological interventions asphyxiated to result in neurological sequelae
would have other organ system severely affected.
Hypo / Hyperglycemia : Blood glucose level Full term asphyxiated infants have mortality of
of >600 mg/dL is shown to protect the brain. 10-20% and neurological sequelae in survivors
Similarily prolonged fasting induced will be 20-45 % (40% mild 60% severe)
hypoglycemia (>12 hrs) has been shown to be (Table 2).
neuroprotective.
Within the first two weeks, it is very difficult
Carbondioxide: Premature babies ventilated to offer a prognosis because the present methods
for RDS are at increased risk for hypoxic damage of prognostication are very unreliable.
if they develop hypocapnia. Unfavorable signs are:
Hypothermia: Preliminary results of two 1) Severe prolonged asphyxia, 2) Sarnat Stage
randomized clinical trials of either systemic III encephalopathy, 3) Multiorgan system
cooling or selective head cooling in involvement, 4) Elevated intracranial pressure
encephalopathic neonates suggest that moderate more than 10 mm Hg, 5) Persistence of abnormal
hypothermia is safe in the high risk newborn. In neurological signs at discharge especially absence
at least one study, newborns with moderate of Moro reflex., 6) Persistence of extensive hypo
encephalopathy had better neurodevelopmental densities (cystic encephalomalacia) on CT scan
12
2005; 7(3) : 185
Table 2. Sarnat staging and outcome of cerebral palsy. Obstet Gynecol 1988, 71;
899-905.
Stage Outcome
6. Volpe JJ. Hypoxic ischaemic encephalopathy:
1 100 % normal neurological outcome
Biochemical and Physiological Aspects. In:
Volpe JJ.Neurology of the newborn. 4th edn,
I1 80 % normal (if symptoms persist for Philadelphia, WB Saunders Company: 2001;
<5 days) pp 217-276.
111 50% die; 50 % have severe sequelae 7. Obrien P, Lawrence SM, Kohl M, Intrapartum
(mental retardation, epilepsy, fetal cerebral oxygenation measured using
microcephaly) intensity modulated optical spectrometry
(IMOS). Br J Obstet Gynaecol 1995; 103:
1166-1170.
at least 4 weeks after the insult, 7) Abnormalities 8. Griesen G, Trojagorg W. Cerebral blood flow,
on brain scan and 8) Persistent oliguria less than paCO2 changes, and visual evoked potentials
1 ml/kg/hour for the first 36 hours of life19. in mechanically ventilated, preterm infants.
Points to remember Acta Pediatr Scand 1987; 76;394-398.
9. Fernandez F, Verdu A, Quero J. Cerebrospinal
1. Birth asphyxia is an important cause of
fluid lactate levels in term infants with perinatal
neonatal mortality and morbidity
hypoxia. Pediatr Neurol 1986;2:39-45.
2. Severe asphyxia results in death and most 10. Volpe JJ. Hypoxic Ischaemic Encephalopathy:
of the survivors may be normal. Clinical aspects. In: Volpe JJ. Neurology of the
3. Persisting neurological abnormality and newborn. 4th edn, Philadelphia, WB Saunders
abnormal brain scan indicate poor Company: 2001; pp 331-394.
outcome. 11. Volpe JJ Perinatal hypoxic ischaemic brain
injury. Paediatr Clin N Am 1976; 23:383-397.
4. Prevention of asphyxia is important.
12. Devane, Simkins J, Stout S. Distribution of
References Phenobarbital and phenytoin in pregnant rats
1. Gilstrap LC, Lcvono KL, Burris I, Diagnosis and their fetuses. Epilepsia 1991; 32: 250-256.
of birth asphyxia on the basis of fetal pH, Apgar 13. Palmer C, Vanucci RW, Towfighti J. Reduction
score and newborn cerebral dysfunction. Am J of perinatal hypoxic ischaemic brain damage
Obstet Gynaecol 1989;161: 825-830. with allopurinol. Pediatr Res 1990;27:332-336
2. National Neonatal- Perinatal Database Report 14. Patt A, Honesh IR, Erger EM, Iron depletion
2002-2003. NNPD network, National or chelation reduces ischemic brain damage
neonatology forum, New Delhi. with allopurinol in gerbil brains. J Pediatr Surg
3. Thornberg E, Thringer K, Odeback A, 1990; 25: 224-228.
Milsom I. Birth asphyxia incidence, clinical 15. Sarco D, Becker J, Palmer C, Sheldon RA,
course and outcome in a Swedish Population. Ferriero DM. The neuroprotective effect of
Acta Paediatr 1995;84:927- 932. deferoxamine in the hypoxic-ischemic
4. Ross MG, Gala R. Use of umbilical artery base immature mouse brain. Neurosci Lett 2000;
excess: algorithm for the timing of hypoxic 282:113-118.
injury. Am J Obstet Gynaecol 2002; 187: 1-9.
16. Jacobson EJ, Mc Call JM, Ayer De. Novel
5. Shields JR, Schifrin BS. Perinatal antecedents 21-amino steroids that inhibit iron dependent
13
Indian Journal of Practical Pediatrics 2005; 7(3) : 186
lipid peroxidation and protect against CNS 18. Donna MF. Neonatal Brain Injury. N Engl J
trauma. J Med Chem 1990; 33: 1145-1151. Med 2004;351:1985-1995.
17. Church J, Zeman S, Lodge D. The
19. Sarnat HB, Sarnat MS. Neonatal
neuroprotective action of ketamine and
encephalopathy following fetal distress. Arch
MK 801 after transient cerebral ischemia in
Neurol 1976;33:696-702.
rats. Anaesthesiology 1988;69:702-709.
14
2005; 7(3) : 187
NEONATOLOGY
15
Indian Journal of Practical Pediatrics 2005; 7(3) : 188
16
2005; 7(3) : 189
Management
1. Warmth and humidity : The temperature decrease in surfactant synthesis and
of the baby should be maintained between increased risk of persistent pulmonary
36.50C to 37.50C and the humidity should hypertension. The oxygen tension should be
be above 60%. The baby can be nursed in between 60-90 mm Hg and the oxygen
the incubator or under a radiant warmer. saturation on pulse oxymetry between
Safe measures to keep the baby warm must 90-95%. Cyanosis is not an early clinical
be used. sign for hypoxemia since it appears very late
2. Oxygenation : The neonate must be well in the course of illness due to presence of
oxygenated. Hypoxemia can lead to fetal hemoglobin in neonates which has high
acidemia, patency of the ductus arteriosus, affinity to oxygen.7
17
Indian Journal of Practical Pediatrics 2005; 7(3) : 190
18
2005; 7(3) : 191
19
Indian Journal of Practical Pediatrics 2005; 7(3) : 192
NEONATOLOGY
21
Indian Journal of Practical Pediatrics 2005; 7(3) : 194
administration of surfactant in the delivery room Infants on the ventilator: Kendig et al,
may result in unilateral administration (if there administered rescue surfactant if the fractional
is endotracheal tube displacement into a main inspiratory oxygen concentration (FiO2) was at
bronchus) or in pharyngeal/esophageal least 0.40 or if the mean airway pressure was at
administration (if endotracheal tube dislodgement least 0.686 kPa (7 cm H2O), or both.15 Dunn et
occurs). al, used chest radiographs consistent with RDS,
as well as supplemental oxygen with a mean
Early selective use of surfactant (neonates airway pressure of at least 7 cm H2O.16 Egberts
< 2 hours of age, intubated for RDS) is better et al, used a FiO2 of > 0.60 while on mechanical
than delayed selective use of surfactant as it may ventilation as an indication for surfactant.17 There
reduce pneumothorax (RR 0.70, 95%CI 0.59, have been no studies comparing the effectiveness
0.82), pulmonary interstitial emphysema (RR of surfactant administration at each of these
0.63, 95%CI 0.43, 0.93), neonatal mortality (RR thresholds.
0.87, 95%CI 0.77, 0.99), chronic lung disease
(RR 0.70, 95%CI 0. 55, 0.88), and chronic lung In neonates with (or at risk for) RDS, early
disease or death at 36 weeks (RR 0.84, 95%CI surfactant replacement therapy with extubation
0.75, 0.93).13 Therefore, the current clinical to nasal CPAP is associated with a reduced need
practice in many referral centers is to administer for mechanical ventilation and increased
rescue surfactant early, once it is clear that the utilization of exogenous surfactant therapy, when
infant has RDS and requires intubation for compared with later selective surfactant
mechanical ventilation. replacement and continued mechanical
ventilation.18 Before administration of surfactant,
Indications for surfactant it probably does not matter whether nasal CPAP
is initiated in a prophylactic (immediately after
Different studies have used different criteria birth regardless of clinical status) or in a rescue
as indications for administration of surfactant. manner (requiring FiO2 > 0.40).19
Infants on CPAP: Verder et al, evaluated early Method of administration
versus late treatment of RDS in preterm babies
<30 weeks gestation receiving nasal CPAP.14 Surfactant is administered by bolus
Early-treated neonates (arterial to alveolar oxygen administration through the endotracheal tube. It
tension ratio or a/APO2 of 0.22 to 0.35; mean, is important not to shake the vial and cause
0.26) had a lower incidence of mechanical frothing. Each dose is often given over a few
ventilation (main indications for mechanical minutes as two to four aliquots into the
ventilation being a/A PO2 <0.15 or severe apnea) endotracheal tube. These doses may be given
or death (21%) than did late-treated neonates either directly with a syringe into the endotracheal
(63%), who did not receive surfactant treatment tube, or via a side-port adapter. Changes in
(Curosurf) until the a/APO2 was <0.22 (0.15 to position of the baby to ensure adequate spreading
0.21; mean, 0.16). This study demonstrates that has not been shown to be useful. Slow
although half the neonates <30 weeks gestation administration by an infusion pump through an
with RDS can be treated with nasal CPAP alone, endotracheal catheter has also not shown to
early treatment with surfactant when the a/APO2 improve results.20 Opened vials can be kept in
is 0.22 to 0.36 may reduce the need for mechanical the refrigerator at 2-8oC for up to 12 hours, and
ventilation.14 should not be frozen. It is necessary to rapidly
22
2005; 7(3) : 195
wean off from the ventilator if the clinical indications for re-dosing are variable. In general,
response is quick. most of the benefit occurs with the first dose,
with declining benefit from subsequent doses.
Pilot trials have examined the feasibility of Most infants do not need more than two doses.
the laryngeal mask airway (LMA) for surfactant Infants with very severe RDS or a persistently
administration 21 and of intrapartum high oxygen requirement may occasionally
nasopharyngeal instillation of surfactant after receive up to four doses.
delivery of the head but before delivery of the
shoulders 22, but the effectiveness of these In neonates of 30-36 weeks gestation with
techniques has not yet been determined. The RDS, Dunn et al, showed that surfactant
administration of surfactant by nebulization does improved oxygenation by 10 minutes
not appear to have any advantages, and may not postinstillation, and better oxygenation with
be as effective as direct endotracheal instillation. lower ventilatory parameters was maintained
over the first 24 hours, despite deterioration in
When do we give additional doses? oxygenation and ventilatory requirements starting
6 to 12 hours after the first dose. 24 The
Kattwinkel et al, compared the relative
deterioration in oxygenation could be minimized
efficacy of administering second and subsequent
by the use of multiple doses; however, extra doses
doses of Infasurf surfactant (not the initial dose)
had no effect on diminishing ventilatory
at a low threshold (FiO2 >30%, still requiring
requirements or time to extubation. Multiple
endotracheal intubation) versus a high threshold
doses of surfactant may have a greater effect on
(FiO2 >40%, mean airway pressure >7 cm H2O)
sustaining improvements in oxygenation than on
of respiratory support.23 There was no difference
ventilatory requirements.24
in the number receiving mechanical ventilation
at 72 hours or in the secondary respiratory Speer et al, evaluated in a randomized
outcomes (BPD at 28 days or 36 weeks). European multicenter trial whether the beneficial
However, there was a significantly higher effects of a single large dose of Curosurf in babies
mortality for infants with complicated RDS (with with severe RDS could be enhanced by using
perinatal compromise or sepsis) who had multiple doses of surfactant. Both the single dose
received retreatment according to the high- and multiple dose groups had a rapid
threshold strategy.23 The dosing interval usually improvement in oxygenation and a decline in
ranges from 6-12 hours between doses, and varies ventilatory requirements, but diminished
with the characteristics of the surfactant. The ventilatory requirements were noted in the
usual dosing frequency of Survanta is 4 mL/kg multiple dose group 2-4 days after
at least six hours apart. For Curosurf, the initial randomization.25
dose is 2.5 ml/kg, with up to two subsequent
doses of 1.25 mL/kg at 12-hour intervals. Each Surfactant in term infants and older
dose of Infasurf is 3 mL/kg, which can be given children
every 12 hours for a total of up to 3 doses. The Surfactant therapy has been used in
older synthetic surfactant Exosurf was given at 5 situations other than the premature infant with
mL/kg every 12 hours. RDS, such as in term infants with meconium
aspiration syndrome. 26 A multicenter
How many doses? randomized, double-blind, placebo-controlled
As stated in the previous paragraph, the trial was conducted on term infants (>2000g, >36
23
Indian Journal of Practical Pediatrics 2005; 7(3) : 196
compares favourably with cost per QALY of recommendations appear relevant to most
several forms of adult health interventions.39 institutions around the world:
Natural surfactants improve oxygenation 1. Surfactant replacement therapy should be
faster and lead to slightly better outcomes as directed by physicians qualified and trained
compared to the older synthetic surfactants, in its use and administration. Qualifications
although even these synthetic surfactants show should include experience in management
marked improvement in clinical outcomes of the respiratory care of low birth weight
compared to no surfactant. In many developing neonates, particularly those on mechanical
countries, the natural surfactants may be more ventilation.
expensive and harder to obtain as compared to
2. Nursing and respiratory therapy personnel
locally produced synthetic surfactants. Clinicians
experienced in the management of low birth
have to weigh the relative benefits and
weight neonates, including mechanical
disadvantages and individualize their approach.40
ventilation, should be available within the
With increasing use of surfactant in unit at the bedside when surfactant therapy
developing countries, an increase in the is administered.
prevalence of bronchopulmonary dysplasia41 as
3. Equipment necessary for managing and
well as associated morbidities such as retinopathy
monitoring the condition of low birth weight
of prematurity and long-term handicap may be
neonates, including that needed for
observed in infants who may otherwise have died
mechanical ventilation, should be available
without the use of surfactant. Surfactant alone
on-site when surfactant therapy is
will not prevent or treat RDS. Skilled nursing care
administered. Radiology and laboratory
and physician intervention is essential, with close
support to manage a broad range of needs of
emphasis placed on minimizing mechanical
these neonates should be available.
ventilation, improving nutrition, and preventing
infection. Therefore, surfactant should only be 4. More important, surfactant therapy should
used in referral centers and by personnel with be used only in institutions in which facilities
expertise in the care of critically ill neonates. It and personnel are available for the
is necessary to remember that antenatal steroids management of multisystem disorders and
are probably more important in developing low birth weight neonates.
countries they are far cheaper, safer, and more
5. An institutionally approved surfactant
effective in reducing mortality and morbidity due
therapy protocol, which is a mandatory
to RDS and other illnesses in premature infants.
component of the quality assurance program
The use of antenatal steroids must be optimized
for neonates, should exist.
before surfactant is used extensively. The benefits
of surfactant will not be observed unless optimal 6. In the institutions not satisfying
CPAP/ventilatory management is used, and recommendations 2 through 5, and when
overall supportive care is excellent. timely transfer to an appropriate institution
cannot be achieved, surfactant therapy may
Recommendations be given, but only by a physician skilled in
The Committee of the Fetus and Newborn endotracheal intubation. Under these
of the American Academy of Pediatrics has made circumstances, consultation with a
the following recommendations 6 and these subspecialty center should be obtained.
25
Indian Journal of Practical Pediatrics 2005; 7(3) : 198
Neonates should be transferred from such on Fetus and Newborn. Surfactant replacement
institutions if appropriate and when feasible therapy for respiratory distress syndrome.
to a center with appropriate facilities and staff Pediatrics. 1999;103:684-685.
trained to care for multisystem morbidity in 7. Soll RF, Blanco F. Natural surfactant extract
low birth weight neonates. versus synthetic surfactant for neonatal
respiratory distress syndrome. Cochrane
Points to remember: Database Syst Rev 2001; (2):CD000144.
8. Soll RF. Synthetic surfactant for respiratory
1. Surfactant reduces death and death/
distress syndrome in preterm infants. Cochrane
bronchopulmonary dysplasia in premature Database Syst Rev. 2000;(2):CD001149.
neonates with respiratory distress
9. Speer CP, Gefeller O, Groneck P, et al. Arch
syndrome. Dis Child Fetal Neonatal Ed. 1995; 72: F8-F13
2. In neonates requiring mechanical 10. Ramanathan R, Rasmussen MR, Gerstmann
ventilation for respiratory distress DR, Finer N, Sekar K. North American Study
syndrome, surfactant should be Group. A randomized, multicenter masked
administered early, and more than one dose comparison trial of poractant alfa (Curosurf)
is occasionally required. versus beractant (Survanta) in the treatment of
respiratory distress syndrome in preterm
3. The use of surfactant is cost-effective in infants. Am J Perinatol 2004;21:109-119.
developing countries, but it is also essential 11. Bloom BT, Kattwinkel J, Hall RT, et al.
to optimize the use of antenatal steroids, Comparison of Infasurf (calf lung surfactant
CPAP/ventilatory management, and overall extract) to Survanta (Beractant) in the treatment
supportive care in order to observe the and prevention of respiratory distress
benefits of surfactant and improve syndrome. Pediatrics 1997; 100: 31-38.
outcomes. 12. Soll RF, Morley CJ. Prophylactic versus
selective use of surfactant in preventing
References morbidity and mortality in preterm infants.
1. Pattle RE. Properties, function and origin of the Cochrane Database Syst Rev. 2001; (2):
alveolar lining layer. Nature 1955, 175: 1125- CD000510.
1126. 13. Yost CC, Soll RF. Early versus delayed
2. Clements JA. Dependence of pressure-volume selective surfactant treatment for neonatal
characteristics of lungs on intrinsic surface respiratory distress syndrome. Cochrane
active-material. Am J Physiol 1956, 187: 592. Database Syst Rev. 2000;(2):CD001456.
3. Avery ME, Mead J. Surface properties in 14. Verder H, Albertsen P, Ebbesen F, et al.. Nasal
relation to atelectasis and hyaline membrane continuous positive airway pressure and early
disease. Am J Dis Child 1959; 97: 517-523. surfactant therapy for respiratory distress
4. Fujiwara T, Maeta H, Chida S, Morita T, syndrome in newborns of less than 30 weeks
Watabe Y, Abe T. Artificial surfactant therapy gestation. Pediatrics 1999;103(2):E24.
in hyaline-membrane disease. Lancet 15. Kendig JW, Notter RH, Cox C, et al. A
1980;1(8159):55-59. comparison of surfactant as immediate
5. Morley C, Davis P. Surfactant treatment for prophylaxis and as rescue therapy in newborns
premature lung disorders: A review of best of less than 30 weeks gestation. N Engl J Med.
practices in 2002. Paediatr Respir Rev 2004; 1991; 324:865-871.
5(SupplA).S299-S304. 16. Dunn MS, Shennan AT, Zayack D,
6. American Academy of Pediatrics. Committee Possmayer F. Bovine surfactant replacement
26
2005; 7(3) : 199
therapy in neonates of less than 30 weeks with respiratory distress syndrome. Pediatrics
gestation: a randomized controlled trial of 1990;86:564-571.
prophylaxis versus treatment. Pediatrics. 25. Speer CP, Robertson B, Curstedt T, et al.
1991;87:377-386. Randomized European multicenter trial of
17. Egberts J, de Winter JP, Sedin G, et al. . surfactant replacement therapy for severe
Comparison of prophylaxis and rescue neonatal respiratory distress syndrome: single
treatment with Curosurf in neonates less than versus multiple doses of Curosurf. Pediatrics
30 weeks gestation: a randomized trial. 1992;89:13-20.
Pediatrics. 1993;92:768-774. 26. Soll RF, Dargaville P. Surfactant for meconium
18. Stevens TP, Blennow M, Soll RF. Early aspiration syndrome in full term infants.
surfactant administration with brief ventilation Cochrane Database Syst Rev 2000;(2):
vs selective surfactant and continued CD002054.
mechanical ventilation for preterm infants with 27. Lotze A, Mitchell BR, Bulas DI, Zola EM,
or at risk for respiratory distress syndrome. Shalwitz RA, Gunkel JH. Multicenter study of
Cochrane Database Syst Rev. 2004;(3): surfactant (beractant) use in the treatment of
CD003063. term infants with severe respiratory failure.
Survanta in Term Infants Study Group. J
19. Sandri F, Ancora G, Lanzoni A, et al.
Pediatr. 1998;132:40-47.
Prophylactic nasal continuous positive airways
pressure in newborns of 28-31 weeks gestation: 28. Moller JC, Kohl M, Reiss I et al. Saline lavage
multicentre randomised controlled clinical trial. with substitution of bovine surfactant in term
Arch Dis Child Fetal Neonatal Ed. 2004;89: neonates with meconium aspiration syndrome
F394-398. (MAS) transferred for extracorporeal
membrane oxygenation (ECMO): a pilot study.
20. Segerer H, van Gelder W, Angenent FW, et al.
Crit Care 1999;3:19-22.
Pulmonary distribution and efficacy of
exogenous surfactant in lung-lavaged rabbits 29. Lam BC, Yeung CY. Surfactant lavage for
are influenced by the instillation technique. meconium aspiration syndrome: a pilot study.
Pediatr Res. 1993;34:490-494. Pediatrics. 1999;103:1014-1018.
30. Herting E, Gefeller O, Land M, van Sonderen
21. Trevisanuto D, Grazzina N, Ferrarese P,
L, Harms K, Robertson B. Surfactant treatment
Micaglio M, Verghese C, Zanardo V. Laryngeal
of neonates with respiratory failure and group
Mask Airway Used as a Delivery Conduit for
B streptococcal infection. Members of the
the Administration of Surfactant to Preterm
Collaborative European Multicenter Study
Infants with Respiratory Distress Syndrome.
Group. Pediatrics. 2000;106:957-964
Biol Neonate. 2005;87:217-222
31. Van Meurs K. Congenital Diaphragmatic
22. Kattwinkel J, Robinson M, Bloom BT, Delmore Hernia Study Group. Is surfactant therapy
P, Ferguson JE. Technique for intrapartum beneficial in the treatment of the term newborn
administration of surfactant without infant with congenital diaphragmatic hernia? J
requirement for an endotracheal tube. J Pediatr. 2004;145:312-316.
Perinatol. 2004;24:360-365.
32. Willson DF, Thomas NJ, Markovitz BP, et al.
23. Kattwinkel J, Bloom BT, Delmore P, et al. Pediatric Acute Lung Injury and Sepsis
High-versus low-threshold surfactant Investigators. Effect of exogenous surfactant
retreatment for neonatal respiratory distress (calfactant) in pediatric acute lung injury: a
syndrome. Pediatrics 2000;106:282-288. randomized controlled trial. JAMA. 2005;293:
24. Dunn MS, Shennan AT, Possmayer F. Single- 470-476
versus multiple-dose surfactant replacement 33. Luchetti M, Casiraghi G, Valsecchi R, Galassini
therapy in neonates of 30 to 36 weeks gestation E, Marraro G. Porcine-derived surfactant
27
Indian Journal of Practical Pediatrics 2005; 7(3) : 200
treatment of severe bronchiolitis. Acta 37. Moya FR, Gadzinowski J, Bancalari E, et al.
Anaesthesiol Scand 1998;42:805-810. International Surfaxin Collaborative Study
34. Davis JM, Rosenfeld WN, Richter SE, et al. Group. A multicenter, randomized, masked,
Safety and pharmacokinetics of multiple doses comparison trial of lucinactant, colfosceril
of recombinant human CuZn superoxide palmitate, and beractant for the prevention of
dismutase administered intratracheally to respiratory distress syndrome among very
premature neonates with respiratory distress preterm infants. Pediatrics 2005;115:1018-
syndrome. Pediatrics 1997;100:24-30. 1029.
35. Davis JM, Parad RB, Michele T, Allred E, Price 38. al Umran K, Yaseen H. Cost-effectiveness of
A, Rosenfeld W; North American Recombinant surfactant replacement therapy in a developing
Human CuZnSOD Study Group. Pulmonary country. J Trop Pediatr 1997;43:167-169.
outcome at 1 year corrected age in premature 39. Pejaver RK, al Hifzi I, Aldussari S. Surfactant
infants treated at birth with recombinant human replacement therapyeconomic impact. Indian
CuZn superoxide dismutase. Pediatrics. J Pediatr 2001;68:501-505.
2003;111:469-476. 40. da Costa DE, Pai MG, Al Khusaiby SM.
36. Sinha SK, Lacaze-Masmonteil T, Valls i Soler Comparative trial of artificial and natural
A, et al. Surfaxin Therapy Against Respiratory surfactants in the treatment of respiratory
Distress Syndrome Collaborative Group. A distress syndrome of prematurity: experiences
multicenter, randomized, controlled trial of in a developing country. Pediatr Pulmonol
lucinactant versus poractant alfa among very 1999;27:312-317.
premature infants at high risk for respiratory 41. Narang A, Kumar P, Kumar R. Chronic lung
distress syndrome. Pediatrics 2005;115: disease in neonates: emerging problem in India.
1030-1038. Indian Pediatr 2002;39:158-162.
Registration Fee Before 31st July 2005 After July Spot Registration
Workshop (28-30 Sept.) Rs. 2500 Rs. 3000 Nil
Symposium (1t & 2d Oct.) Rs. 1000 Rs . 1500 Rs 2000
Workshop + Symposium Rs. 3000 Rs . 4000
Send your registration fees as a demand draft in the name Sir Ganga Ram Hospital at the following address:
Dr. IC Verma, Department of Genetic Medicine, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi -
110060 Tele: 52251382, Tel. and fax: +91-11-25861767, Email:dr_icverma@yahoo.com
28
2005; 7(3) : 201
NEONATOLOGY
29
Indian Journal of Practical Pediatrics 2005; 7(3) : 202
There are also reports of preterm infants Published data from Chandigarh suggests
developing NEC following the use of mydriatic that prefeed residue, abdominal distension,
eye drops during ophthalmologic examinations5. lethargy were the commonest presenting signs6.
Race/Sex: Most studies show no difference in Early surgical consultation is mandatory,
the incidence based on race. Male and female especially if abdominal signs are present as
babies are affected equally. transfer to a tertiary care facility for appropriate
Gestational age: The incidence of NEC varies surgical care may be required.
inversely in relation to birth weight and
gestational age. The attack rates are as high as Laboratory investigations
40% in those weighing less than 1000g at birth, 1. Complete Blood count, 2. Blood culture - to
falling dramatically to just 3.8 per 1000 lives rule out sepsis mimicking NEC, 3.Serum
births for infants weighing between 1501 and electrolytes and 4. Serum bicarbonate.
2500g at birth. The average age of onset is related
to the post-conceptional age, with those more An extremely ill baby may also need an
premature developing NEC at a later date. arterial blood gas to rule out impending
respiratory failure.
Clinical features
NEC is more common in the preterm Characteristic abnormalities include.
infants and there is a significant difference in the 1. Thrombocytopenia (<100,000/ cu.mm) is
antecedent history between term and preterm usually associated with NEC. It may be
infants. The affected term baby has a median age worsened by a consumption coagulopathy
of onset between 1-3 days of life and is usually (raised PT, raised aPTT, low fibrinogen,
systemically ill with asphyxia, respiratory distress elevated fibrin degradation products).
and sepsis or has a history of intrauterine growth
retardation. Maternal cocaine abuse is a 2. Hyponatremia due to a developing capillary
significant risk factor for the term baby. leak.
Preterm babies have usually achieved full- 3. Metabolic acidosis: Persistently low platelet
volume feeds or are advancing on enteral feeds counts and sodium levels, and persistent
when symptoms develop. metabolic acidosis despite treatment may be
Gastrointestinal symptoms include: 1.Feed an indication for laparotomy in an ill infant,
intolerance characterized by abdominal distention even in the absence of signs of perforation.
and vomiting, 2. Increased abdominal girth, Imaging studies:Antero-posterior and left lateral
3. Gastric residuals, 4. Decreased bowel sounds, decubitus radiographs are essential for the initial
5. Visible intestinal loops or a palpable abdominal evaluation and for monitoring any baby with
mass, 6. Blood-streaked stools (the presence of abdominal signs, and may be needed as
occult blood in stools is not a specific marker of frequently as every 6 hours. The abdominal
NEC) and 7. Erythema of the abdominal wall. radiograph may reveal an abnormal gas pattern,
Systemic signs and symptoms include:1.Lethargy dilated loops and thickened bowel walls. A fixed
and temperature instability, 2. Apnea and dilated loop that does not change position on
bradycardia, 3. Poor peripheral perfusion and serial radiographs may indicate a gangrenous
shock, 4. Bleeding diathesis and 5.Cardiovascular loop. Pneumatosis intestinalis is pathognomoic
collapse. of NEC and represents intramural air extravasated
30
2005; 7(3) : 203
from the intestinal lumen. It appears as a nutrition. Parenteral nutrition may be needed
characteristic train track lucency within the bowel till enteral feeds can be restarted. At our
wall. Portal gas, is air present in the portal unit, we have found a combination of lipids
venous system, appears as hypodense branching and amino acids infused through an
areas over the liver shadow. Abdominal free air aseptically placed peripheral venous canula
indicates a perforation and it mandates immediate and changed every three days, to be adequate
surgical intervention. The football sign for intravenous alimentation.
represents the oblong lucency over the liver
3. Broad spectrum parenteral antibiotic
shadow due to intraperitoneal free air on a supine
therapy, after collection of blood and urine
film.
cultures, should be initiated without delay.
Abdominal ultrasonography may reveal At our unit we use a combination which
(a) Ascites (b) Portal air (Champagne flute) provides coverage for gram-positive, gram-
sign (c) A doppler of the orientation of the negative and anaerobic organisms, till
superior mesenteric artery to the superior cultures become available.
mesenteric vein may help rule out a malrotation 4. Extremely ill babies in impending
and volvulus. (d) Recent studies demonstrate a respiratory failure require endotracheal
markedly increased peak flow velocity in the intubation and ventilation.
celiac and superior mesenteric arteries in early
NEC. 5. Immediately consult a pediatric surgeon and
organize a laparotomy if indicated.
An upper GI barium study with a small Abdominal decompression with a large bore
bowel follow through and a water-soluble catheter, paracentesis to drain an ascites
contrast enema may definitely rule out volvulus causing respiratory embarrassment, and
and Hirschsprungs disease. placing an intra-abdominal drain are
alternatives to laparotomy in babies who are
Based on the systemic, gastrointestinal and too sick for surgery.
radiological signs NEC has been staged according
to the Modified Bells criteria (Table 1). Complications
Complications are related to the disease or
Treatment
the therapy. To name a few
Early or suspected NEC is often difficult to
diagnose as the clinical signs and symptoms are 1. Intestinal strictures, short-gut syndrome and
often non-specific, as are the radiological and malabsorbtion following extensive surgery and
laboratory findings. All babies with definite NEC resection, 2. Centrally placed catheters are a risk
should be transferred to a level III unit. factor for staphylococcal and fungal sepsis and
3. Prolonged parenteral nutrition may be
Management varies according to the stage of associated with cholestasis and direct
NEC hyperbilirubinemia.
1. Cease all enteral feeds.
Mortality
2. Secure intravenous access. Central venous
access through percutaneously inserted It ranges from 10-44% in infants weighing
central venous catheters or surgically placed less than 1500g compared to 0-20% in those more
central lines may be required for parenteral than 2500g.
31
Indian Journal of Practical Pediatrics 2005; 7(3) : 204
Prevention
Cochrane Collaboration in 1999 reported no
1. Breast fed babies have a lower incidence of effect on NEC of rapid feeding advancement
NEC compared to formula fed babies. for low birth weight infants.
2. Systematic review published by the 3. High clinical suspicion of NEC in premature
32
2005; 7(3) : 205
babies and early surgical consultation do Newborn. 7th edn. Philadelphia, Pa: WB
help reduce the morbidity and mortality. Saunders Co; 1998: pp 965-970.
4. In pregnancies at risk for fetal growth 2. Kennedy KA, Tyson JE, Chamnanvanakij S.
Rapid versus slow rate of advancement of
restriction, abnormal antenatal doppler
feedings for promoting growth and preventing
velocimetry in the form of Absent or Reverse necrotizing enterocolitis in enterally fed low-
End Diastolic Frequencies (A/R EDF) in the birth-weight infants. Cochrane Database Syst
umbilical arteries is a useful guide to predict Rev 2000; (2): CD001241
NEC and mortality in the early neonatal
3. Eyal F, Sagi E, Arad I. Necrotising enterocolitis
period7.
in the very low birthweight infant: expressed
Points to Remember breast milk feeding compared with parenteral
feeding. Arch Dis Child 1982; 57(4): 274-276.
1. NEC is the most common GI emergency in
4. Lucas A, Cole TJ. Breast milk and neonatal
neonates.
necrotising enterocolitis. Lancet 1990; 336:
2. NEC can present late in the smallest babies. 1519-1523.
5. Nair AK, Pai GM, Da Costa DE, Al Khusaiby
3. Early NEC is difficult to diagnose if in
SM: Necrotising Enterocolitis Following
doubt treat early and conservatively (cease
Ophthalmological Examination in Preterm
feeds and start broad spectrum antibiotics). Neonates . Indian Pediatr 2000;37:417-421
4. Early surgical consultation is a must, and 6. Narang A, Rao R, Bhakoo ON. Neonatal
babies with definite NEC should be necrotising enterocolitis : a clinical study.
referred to a NICU. Indian Pediatr 1993; 30: 1417-1422.
33
Indian Journal of Practical Pediatrics 2005; 7(3) : 206
NEONATOLOGY
34
2005; 7(3) : 207
35
Indian Journal of Practical Pediatrics 2005; 7(3) : 208
and the focus of this paper is on diagnosis and GM1 gangliosidosis, MPS Type IV and VII,
management of acute neonatal IEM. Farbers disease, red cell enzymopathies
(glucose-6-phosphate dehydrogenase deficiency,
Often, the first hint of an IEM is a family pyruvate kinase deficiency), congenital disorders
history of neonatal deaths, similarly affected of glycosylation, neonatal hemochromatosis and
siblings or sudden infant death syndrome (SIDS); glycogen storage disorder type IV. Development
though most newborns with inborn errors have of cardiac failure or arrhythmias in respiratory
no family history. Affected males on the mothers chain disorders can also result in hydrops. 5,11
side of the family should raise suspicion of X-
linked recessive disorder. Parental consanguinity B. At birth: IEM like energy deficiency disorders
is a risk for autosomal recessive disorders. cause in-utero metabolic derangements leading
to disruption of normal fetal development.
The onset of symptoms depends on nature Consequently, dysmorphisms and malformations
of the molecular defect, environmental factors are characteristically noted in such disorders. The
and possibly other genetic factors 6 . An manifestations and differential diagnosis of
environmental trigger provoking acute metabolic disorders presenting at birth are described in
crisis can often be identified (Table 2) 7 . Table 3.5,6,11,12
Mutations leading to complete lack of enzyme
synthesis produce severe disease with early onset. C. After birth
An example is methylmalonic acidemia with a i. Sudden death: Death in a neonate without a
Mut 0 phenotype. The mutation causes near previous illness, following a
complete deficiency of methylmalonyl-CoA disproportionately mild illness or in a family
mutase. On the other hand Mut-phenotype has with a history of unexpected deaths should
residual enzyme activity. Mut0 causes severe raise the suspicion of an IEM. Defects of
neonatal disease with 80% developing symptoms FAO and respiratory chain disorders lead to
in the first week of life 8. sudden death. Medium chain acyl CoA
dehydrogenase (MCAD) deficiency
Modes of presentation
typically presents with sudden death and has
A. During pregnancy: Some metabolic diseases been proved by post-mortem investigations
cause maternal complications during pregnancy in 1% of infants with SIDS 13. Respiratory
carrying affected fetuses. Acute fatty liver of arrest or cardiac arrhythmia is usually
pregnancy (AFLP) and hemolysis elevated liver responsible for sudden death in such cases11.
enzymes and low platelets (HELLP) syndrome Other disorders causing apparently sudden
are known to be associated with fetal long chain death like UCD, organic acidemias,
acyl Co-A dehydrogenase (LCHAD) deficiency, biotinidase deficiency or pyruvate
an inborn error of fatty acid oxidation.7,9,10 A fetus dehydrogenase (PDH) deficiency usually
affected by non-ketotic hyperglycinemia or cause acute illness with obvious clinical
pyridoxine dependency could develop symptoms that precede death by hours to
intrauterine seizures in late pregnancy perceived days 7.
by the mother as abnormal fetal movements 6. Any unexpected death should be probed by
Non-immune fetal hydrops is a presenting feature autopsy. Autopsy should be performed within 4
of IEM like Gauchers disease type II, sialidosis to 6 hours of death 14. Unfortunately, in India such
type II, galactosialidosis, mucolipidosis type II, deaths are seldom investigated, not even in
36
2005; 7(3) : 209
37
Indian Journal of Practical Pediatrics 2005; 7(3) : 210
teaching institutions. Physicians are disinclined In the rare event of autopsy being performed,
to motivate the family and parents refuse consent findings that should raise suspicion of an
for autopsy. Thus, an opportunity for establishing IEM are cardiomyopathy, dilatation of the
diagnosis and offering genetic counseling is lost heart (especially if endocardial thickening
until the next affected child is born. is detected), pale flabby muscles, enlarged
38
2005; 7(3) : 211
39
Indian Journal of Practical Pediatrics 2005; 7(3) : 212
liver or spleen, microvesicular fatty liver, and thrombocytopenia which are markers of
fibrosis or cirrhosis of the liver and edema neonatal sepsis are also seen with diseases
of the brain 13. In most cases there is dearth like propionic and methylmalonic
of gross findings, but if IEM is suspected acidemia 7,8. Furthermore, disorders like
gross autopsy must be complemented by galactosemia predispose to gram-negative
biochemical investigations (Table 4) sepsis 12 . Ostensible illnesses like
5,11,12,13,14
pneumonia, adrenal crisis, shock,
ii. Deterioration after a symptom-free interval: dehydration, congestive heart failure, bowel
Most neonates with IEM are typically born obstruction, intracranial bleed and neonatal
healthy. They deteriorate after a variable diabetes should raise doubt of an IEM 7,15.
symptom-free interval ranging from hours In fact, a respiratory disease with tachypnea
to weeks after feeds are commenced. in absence of cough, retractions and
However, catabolism occurs even in the auscultatory signs is likely to be an IEM.
absence of oral feeds. Progressive
Patterns of deterioration
accumulation of toxic metabolites results in
symptoms. Physical signs like cataracts and 1) Acid-base disturbances: An IEM is
unusual odours immediately raise suspicion suspected in a neonate with metabolic
of an IEM. Most symptoms however are acidosis when it is persistent or unexplained
relatively non-specific and do not despite normal tissue perfusion, associated
discriminate metabolic disorders from other with increased anion gap and not easily
insults as manifestations in neonates are corrected by sodium bicarbonate
stereotypic. Therefore high index of administration. Another disturbance that
suspicion, clinical acumen and experience arouses suspicion of IEM is respiratory
are the keys to correct diagnosis. Clues to alkalosis which is an early finding in UCD.
suspect IEM are mysterious onset of illness Both will be clinically apparent as tachypnea.
after a variable interval in a previously Blood gas analysis will identify the nature
healthy full term baby born without antenatal of defect and should be performed in any
or perinatal risk factors. The usual course is tachypneic baby with paucity of respiratory
to investigate and treat for sepsis, but when findings. However, blood gas analysis may
investigations for sepsis yields no result and not reflect presence of lactic acidosis.
the baby relentlessly deteriorates despite Significant lactic acidosis can be present
ongoing therapy, an alternative diagnosis is with a normal pH, as the lactate level should
suspected. This strategy delays onset of exceed 5 mM/L before blood pH is altered7.
therapy to a stage where death is imminent It is therefore essential to measure serum
or significant neurological damage has set lactate and pyruvate when congenital lactic
in which predicts permanent neuro- acidosis is suspected. IEM associated with
developmental disability. It is therefore lactic acidosis are disorders of pyruvate
prudent to perform screening tests for IEM metabolism, FAO defects, mitochondrial
simultaneously with investigations for diseases, organic acidurias and UCD.
sepsis 11 . It must be remembered that Technique of sample collection for lactate
documentation of sepsis does not exclude estimation is of utmost importance as
IEM as such infants rapidly become applying tourniquet, squeezing the
debilitated and develop sepsis. Neutropenia extremity, crying or breath holding elevate
40
2005; 7(3) : 213
lactate level. Lactic acidosis is significant boxing, pedaling, slow limb elevations and
when associated with ketosis and in large amplitude tremors may be noted.
the absence of shock, infections and Seizures, apnea, stupor and coma occur late
seizures, as all these cause secondary lactic in the course of the disease 7,11. When
acidosis 5. Estimation of ketones in blood or seizures occur, neonates are usually
urine should always accompany determina- comatose. Seizures may be associated with
tion of acid-base status. hypoglycemia. Cerebral edema with signs
of raised intracranial pressure can be present,
2) Metabolic encephalopathy: The pointers to
especially in disorders like galactosemia
a metabolic cause of neurologic symptoms
which is known to give rise to pseudotumor
are altered neurologic status disproportionate
cerebri11,12. The manifestations of some of
to systemic signs and symptoms. Early
the disorders causing metabolic
symptoms are poor feeding, vomiting,
encephalopathy are summarized below.
lethargy, irritability, breathlessness and
abnormalities of tone. Abnormality of tone, MSUD: Opisthotonus, abnormal limb
especially generalized hypertonic episodes movements, abnormal urine odor (burnt
and opisthotonus are characteristic, whereas sugar or curry-like), DNPH positive
non-metabolic causes of coma usually cause UCD: Reye-like disease, hypotonia, coma,
hypotonia. Abnormal limb movements like anicteric hepatomegaly, hyperammonemia,
41
Indian Journal of Practical Pediatrics 2005; 7(3) : 214
42
2005; 7(3) : 215
43
Indian Journal of Practical Pediatrics 2005; 7(3) : 216
mechanical ventilation. Infants with organic 10% dextrose. Dextrose is infused at the rate of
acidemia are dehydrated and require fluid at least 5 mg/kg/min (3 ml/kg/hr of 10%
replacement with volumes one and a half to twice dextrose)16. Infusion through an umbilical venous
the maintenance with an electrolyte solution in catheter is necessary if concentration to maintain
44
2005; 7(3) : 217
Genes
Proteins
A B C D
Co- factor
H ypoglycem ia
45
Indian Journal of Practical Pediatrics 2005; 7(3) : 218
diseases, 8th Edn, Scriver CR, Beaudet AL, Sly 12. Burton BK. Inborn errors of metabolism in
WS, Valle D (Eds) Mc-Graw Hill, New York, early infancy: Clinical diagnosis, Pediatrics
2001; pp 1327-1329. 1998; 102: 1-9.
8. Haas RH, Marsden DL. Disorders of organic 13. Emery JL, Howat AJ, Variend S, Vawter GF.
acids, In: Principles of child neurology, 1st Edn, Investigation of inborn errors of metabolism
Berg BO (Ed), McGraw Hill, New York, 1996; in unexpected infant deaths, Lancet 1988; 29-
pp 1049-1089. 31.
9. Innes AM, Seargent LE, Balachandra K, Roe
14. Steiner RD, Cederbaum SD. Laboratory
CR, Wanders RJA, Ruiter JPN, et al; Hepatic
evaluation of urea cycle disorders, J Pediatr
carnitine palmitoyltransferase I deficiency
(Suppl) 2001; 138: S21 S29.
presenting as maternal illness in pregnancy,
Pediatr Res 2000; 47: 43-45. 15. Burton BK. Inborn errors of metabolism: The
10. Ibdah JA, Bennett MJ, Rinaldo P, Zhao Y, clinical diagnosis in early infancy, Pediatrics
Gibson B, Sims HF, et al. A fetal fatty-acid 1987; 3: 359-369.
oxidation disorder as a cause of liver disease in 16. Metabolic disease, a neonatal approach,
pregnant women, N Eng J Med 1999; 340: Neonatal handbook, Newborn emergency
1723-1731. transport service (NETS), Victoria, URL: http:/
11. Leonard JV, Morris AAM. Inborn errors of /www.netsvic.org.au/nets/handbook/
metabolism around time of birth, Lancet 2000; index.cfm?doc_id=895, accessed April 15,
356: 583-87. 2005, updated November 30, 2004
47
Indian Journal of Practical Pediatrics 2005; 7(3) : 220
NEONATOLOGY
X-RAY CHEST AND THE meticulous and systematic. One such approach
NEONATE to the neonatal chest radiograph is listed in
Table 1.
* Muralinath
Table I. Interpretative approach to Neonatal
Abstract: This article is about the role of plain chest x-ray
x-ray in the evaluation of neonatal chest.
Essential features to note in an x-ray chest along Technique
with an interpretative approach are dealt with. Penetration
The focus is on the evaluation of the respiratory Rotation
distress in the newborn, where plain x-ray plays
Inspiration
a vital and key role. Basic pathology is
emphasized, and how, the x-ray findings are but Motion
a reflection of the basic structural changes Systematic approach
ensuing from the pathology is stressed and stated. Extrathoracic
Key words:Neonate, X-ray chest, Interpretative Abdomen
approach, Respiratory distress. Neck
Tubes, catheters
Plain x-ray of the chest plays a pivotal role
in the evaluation of the newborn chest. Swischuk Soft tissues
(1979) calls the neonatal radiograph the right Bony thorax
arm of the clinician. Hence it is mandatory that Mediastinum
a clinician caring for the newborn has a basic Thymus
understanding of this vital tool x-ray chest
Trachea and bronchi
which will provide the clinician with a wealth of
information. It is a simple and cost-effective Great vessels
imaging modality and above all the examination Heart
can be conducted at the bedside without altering Diaphragm
the conditioned environment of the critically ill Lungs
newborn in whom examination is often required.
To begin with, evaluate the technical
In reading the x-ray of the chest, it is
adequacy of the chest radiograph. It should be
essential that one develops a rational and
adequately penetrated so that the pulmonary
interpretative approach. The approach should be
details are well brought out; which is essentially
* Consultant Radiologist the vascular markings. When the penetration is
Kanchi Kamakoti CHILDS Trust Hospital and adequate, the intervertebral disc spaces and the
Dr.Mehtas Hospital Pvt Ltd, Chennai. vessels posterior to the heart are seen well. The
48
2005; 7(3) : 221
Table 2. Features to assess on x-ray chest in then be thoroughly evaluated. Various tubes and
infant with suspected cardiac disease catheters when present should be scrutinized for
their appropriateness. For example endotracheal
Feature Comment tube when present should be 1 to 2 cms above
Quality of film Adequate inspiration the carina or approximately at the level of T1-
Normal penetration T2.
Centred on mid chest
The routine view is the supine (AP) view of
Not rotated the chest. Lateral views are taken when required
Abdominal situs Normal/inverted/ambiguous (eg. anterior pneumothorax).
Bronchial situs
Aortic arch side Left or right X-ray of the chest is excellent for the
evaluation of lungs, bones and soft tissues. When
Heart Side
it comes to the heart per se its role is rather
Direction of apex limited. As far as imaging of the heart is
Size concerned, fetal and neonatal echocardiography
Contour are the mainstay in the antenatal detection and
Lung vasculature Plethora postnatal evaluation of cardiac disease.
Oligaemia However, the plain x-ray is excellent in the
Pulmonary venous evaluation of the pulmonary status in cardiac
engorgement disease. An approach to the evaluation of the
Diaphragm Distinct chest x-ray in cardiac disease is appended in
Side of apex should be more Table 2. Through the Plain x-ray the common
caudal observations made are:
Lung fields Any pathology 1. The cardiac size through the CT ratio (55 to
Musculoskeletal Vertebral / rib abnormalities 60%). This is not very precise; the subjective
Fractures evaluation through experience is a better
option.
degree of rotation is evaluated by noting the
distance between the centre of the vertebral 2. Gross cardiac anatomy.
bodies and the lateral aspect of the ribs thereby 3. Pulmonary status.
evaluating the bilateral symmetry. Classically, 4. Situs.
aeration or volume of the lungs is assessed by
Respiratory distress
noting the level of the diaphragm; in an adequate
inspiration the diaphragm should be at the level Respiratory distress is a symptom, not a
of the 6th rib anteriorly or the 8th rib posteriorly. disease. Respiratory symptoms of tachypnea,
[Evaluation of the degree of inspiration in infants retractions, nasal flaring, grunting and cyanosis
often is more a matter of experience than science]. in a neonate can be caused by diverse diseases
Motion artefacts creep in if the exposure time is such as sepsis, acidosis, anemia, central nervous
not short enough; either patient or respiratory system and cardiac diseases, short rib skeletal
motion will cause blurring of the diaphragmatic dysplasias and thoracic anomalies. The first chest
contour and pulmonary vascular markings. Each radiograph is crucial for defining whether the
anatomic portion of the chest radiograph should lesion is of pulmonary, nonpulmonary
49
Indian Journal of Practical Pediatrics 2005; 7(3) : 222
Fig 2. Transient tachypnoea of newborn Fig 3. TTN: Clear lungs after 24 hours
Transient Tachypnea of the Newborn (TTN): upon site and nature of obstruction - complete or
TTN is the most common cause of respiratory incomplete). Because of distal airway obstruction
distress in the newborn. Basic pathology is air trapping and airleak are common. Meconium
delayed clearance of pulmonic fluid. This leads in addition to the mechanical obstruction also
to normal or large volume lungs. The fluid is produces chemical inflammation (pneumonitis)
drained through lymphatics and venous channels and tends to inactivate surfactant. This further
in the interstitium giving raise to stiff / less complicates the issue; the resulting ventilatory
compliant lungs with streaky interstitial / vascular and vascular alterations and airleak result in
densities. hypoxaemia and acidosis. This leads to persistent
pulmonary hypertension (PPHN). There are no
The radiographic features are: 1. Normal / large
specific imaging findings for PPHN. Since the
volume lungs, 2. Parahilar / perihilar radiating
severity of PPHN is the major prognostic
streaky densities and 3. Minimal fluid in pleural
determinant, it is no surprise that the radiographic
space / fissures (Fig 2). These changes usually
severity of the disease may not correlate with the
resolve in 24-72 hrs (Fig 3).
clinical picture.
Meconium Aspiration Syndrome (MAS):
Meconium aspiration is the most common cause The radiographic picture in MAS is 1.Bilateral
of neonatal respiratory distress in mature / hyperaeration, 2. Uneven aeration (because of
postmature infants. This is essentially due to atelectasis and focal hyperaeration) leading to
aspiration of meconium in to the airway and its heterogeneous opacities (Fig 4) and 3. Airleak
attendant sequelae. The effect will depend on the (Commonly pneumothorax).
nature of the matter (large or small particles) and
Neonatal pneumonia
the extent of involvement; which will depend on
the amount and particle size - large volume, small Here a high index of clinical suspicion
particles will produce marked damage as they is the key to the diagnosis. The radiographic
can impact distal airways to a greater extent. The findings are quite varied and often non-specific.
result will be hyperaeration (due to compromised The radiographic signs of neonatal pneumonia
and narrow airway), uneven aeration (depending are quite non-specific and tend to mimic or blend
51
Indian Journal of Practical Pediatrics 2005; 7(3) : 224
The radiographic picture is that of cystic mimic a diaphragmatic hernia. The differentiating
lucencies in the hemithorax. Radiographic feature is defined diaphragm and normal
findings in CCAM are cystic mass (90%), single complement of bowel loops / gas in the abdomen
lobe and unilateral (>95%). It is rare in right (Fig 11). Type III may present as opaque
middle lobe. When CCAM is large it produces hemithorax.
contra lateral shift of medaistinum. This may
55
2005; 7(3) : 229
V NATIONAL CONFERENCE
OF
ADOLESCENT PEDIATRIC CHAPTER OF IAP AT KOLKATA (ADOLECON 2005) ON
5TH & 6TH NOVEMBER, 2005 AT SCIENCE CITY.
Theme: Importance of Adolescent Health in Clinical Practice
Scientific: Your will have a different experience here-in. Few of regular lectures; more sessions devoted on Panels
e.g. Medico-legal issues in adolescent clinical practice.
Meet the Experts sessions on issues of day-to-day adolescent case management. WHO and UNICEF faculties are
added attractions. Every where you will get opportunities to interact and get your query answered by the experts.
Registration: Delegates Rs.1000/- upto 31.08.05; Rs.1200/- upto 31.10.05; Rs.1500/- thereafter. PG students
Rs.200 less at every stage (certificate from HOD). Send draft in favour of Adolecon 2005 payable at Kolkata.
Correspondence: Dr.Sukanta Chatterjee, HOD Ped. CMC Kolkata, Organizing Secretary, Adolecon 2005, 889A,
Lake Town, Kolkata 700 089. Tel-fax 033-22198118(O), 25345909 , 09830275685 (M). Email:
adolecon2005@rediffmail.com
57
Indian Journal of Practical Pediatrics 2005; 7(3) : 230
NEONATOLOGY
FREQUENTLY ASKED QUESTIONS baby loses weight for the first few days.
IN NEONATAL OFFICE PRACTICE Weight loss is usually 4-7% and should not
exceed 10-12% of the birth weight. From
1. What is the normal pattern of urination 1 week of age a normal baby should gain
and passage of stools in the newborn? weight at the rate of 20-30 g/day in the initial
Babies pass urine immediately after birth and three months.
a little urine in the next 24-36 hours.
4. What is the best advice for mother
Thereafter they pass 40-60 ml of urine/kg/
regarding feeding ?
day or a minimum of 6 times per day.
Babies usually pass meconium immediately Mother is motivated and encouraged to give
after birth, which is dark, sticky green exclusive breast-feeding only. She is also
material composed of bile, intestinal advised not to give pre-lacteal feeds,
secretions and amniotic debri. Most of them pacifiers, bottles or other indigenous
pass meconium within 24 hours (but this may preparations and to exclusively breast feed
be delayed in preterm babies). By 2-3 days on demand for 6 months. Successful breast-
transitional stools, which is a mixture of feeding prevents hypoglycemia and other
meconium and normal stools are passed. metabolic problems in the babies
Once breast feeding is established they pass
5. How frequently should a baby be fed?
golden yellow, soft stools with every feed.
2. How long can a newborn sleep? Can he Generally newborns have to be fed on
recognize the mother when awake? demand. Healthy neonates feed 10 or more
times in a day. Two or three hourly feeding
Baby has irregular sleep wake cycles and schedule should not be imposed. Topping
sleeps for up to 18 hours in a day with with other feeds before the next feeding time
50-60% of sleep being REM sleep. Circadian will result in failed lactation.
rhythm is detectable in heart rate and body
temperature by 1 month of age. 6. How long should the baby be fed?
A neonate prefers familiar face of a human Baby should be put to the breast until he has
being to scrambled shapes or structure. He completed and is satisfied. This usually
recognises his mother using the sense of takes 7-10 minutes. Once lactation is
hearing and smell. established a baby gets most of the milk in
the first 4-6 minutes. Sucking longer than
3. How to assess the adequacy of weight gain
this is therefore is of non-nutritive value. The
in the newborn?
baby should be offered the other breast once
All babies should be weighed at birth. The a breast is completely empty
58
2005; 7(3) : 231
7. How do we assess if the baby is getting Relaxed mother, proper positioning of the
sufficient milk? baby, prokinetics and antispasmodics have
been advocated.
A baby who sleeps for 2 hours at a stretch,
has well formed golden yellow semisolid 11. Whydo babies have hiccups?
stools, voids urine at least 6 times a day, It occurs due to rhythmic clonic contraction
appears content and gains adequate weight of the diaphragm. It usually occurs
is considered to have adequate breast milk. immediately after a feed due to distension
Babies on breast milk judge their own intake of stomach and irritation of diaphragm.
and only if the weight gain is unsatisfactory Faulty feeding technique and aerophagy
should some assessment of intake be often produce hiccup. Burping the baby and
attempted. proper advice regarding feeding must be
8. What are the reasons for a baby not imparted to all mothers.
feeding well? 12. When does the umbilical cord fall? How
If the baby is well, the common causes are do you take care of the umbilicus of a
prematurity, difficult delivery, sedated due baby?
to intrapartum or postnatal sedation. It may The umbilical cord usually falls in one week
also be due to poor attachment (Latching) at and epithelializes by 2 weeks. The umbilical
breast and due to poor positioning. stup should be kept clean and dry without
9. What are the common causes for frequent any local applications either indigenous or
crying in the newborn? commercial. Scanty bloody discharge for a
day or two is common. Persistent bleeding
Persistent crying in the neonate is usually should be evaluated for coagulation
due to hunger but can also be due to pain, disorders, while persistent discharge should
boredom and discomfort. Painful conditions be evaluated for patent vitello intestinal duct
include otitis media, intussusception, bone or urachus. If a granuloma is present, it can
and joint infection and incarcerated hernia. be cauterized by topical coppersulphate
The common myth of wind or insufficient crystals or the commonly available rock salt.
milk should not be accepted.
13. When a baby feels warm, does it mean he
10. Does passing of wind indicate colic? is febrile? What is the approach to a
The bottle fed baby will always swallow febrile neonate?
some air with each feed compared to the If the body feels warm it need not be fever,
breast fed baby. Positioning the baby upright however if the measured body temperature
helps to burp the baby. shows a rise, it could be either due to
Infantile colic occurs in the late neonatal infection or dehydration secondary to
period. Its etiology remains a mystery environmental causes. Inadequate intake
although food allergy, lactose intolerance with a weight loss of more than 10%
and GERD are thought to be predisposing resulting in dehydration may result in fever.
factors. Maternal stress may play a role. If dehydration is the cause, serum osmolality,
Switching over to bottle feeds will not help. is increased to 310 mOsm/L. This should be
Reassuring the mother regarding the benign managed by increasing oral feeds and
nature of the condition is helpful. nursing the baby in a cool environment.
59
Indian Journal of Practical Pediatrics 2005; 7(3) : 232
14. Is vaginal bleed in the newborn normal? 17. How to treat noisy nasal breathing in
newborn?
Vaginal bleeding is common and it occurs
in 25% of female neonates and Snuffles (makes sniffing sounds / breaths
macroscopically visible in 3.3% of babies. noisily). A nasal discharge following a spell
It is due to maternal hormonal withdrawal of crying is common in early infancy. For
and needs to be investigated when persistent. unknown reasons, some babies in the first
2 to 3 months have a mucoid nasal discharge,
15. What are the common eye changes seen which, although unpleasant to see, is
in the newborn following vaginal harmless. It is apparently non infective and
delivery? non allergic. No treatment is required as it
Retinal and subconjunctival hemorrhages are clears up spontaneously.
commonly seen after vaginal delivery. They 18. How to manage enlargement of breast in
result from increased venous congestion and neonates?
pressure during delivery. Retinal
hemorrhages usually resolve within 1-5 Breast enlargement of varying degrees is
days. Subconjunctival hemorrhages resolve seen in 80% or more of full term infants of
within 1-2 weeks. both sexes, starting 2 or 3 days after birth
and reaching a peak in the second week. It
16. What is the management for the watering may be asymmetrical. Milk secretion may
of eyes in the Newborn? occur by 7 days of age. The breast
It is enough to instruct the mother to massage enlargement is presumably related to the
the duct by firm pressure (several times a estrogen received from the mother via the
day) over the medial angle of eye (Lacrimal placenta. No treatment is indicated and
duct area). If infection occurs, it can be kept massage of the breast should be avoided.
under control by antibiotic eye drops or Prolonged enlargement could be due to
ointment. exposure to estrogenic substances.
60
2005; 7(3) : 233
DERMATOLOGY
61
Indian Journal of Practical Pediatrics 2005; 7(3) : 234
entire body is involved. Pruritus is not a 1-5 days prior to onset of rash. Prodromal
prominent symptom. Usually by 4th day the rash symptoms are more common in adolescents and
begins to fade, in the same order as it appeared. young adults.
Fever persists through the second or third day of
the rash and then falls. Persistence of fever after The exanthem in rubella is a generalized,
the onset of exanthem may suggest erythematous macular and papular eruption with
complications1. Associated with these findings a variable progression1. It usually progresses
generalized lymphadenopathy and splenomegaly downwards to the trunk and then the extremities.
can occur. The full expression is usually apparent by 24
hours after its onset and begins to fade in a day
Modified measles occurs in individuals with or two in the same order of distribution in which
pre existing partial immunity. This is usually seen it appeared. The eruption is completely absent
in infants less than 1 year who possess maternal by third day. Generally the rash consists of
antibody to measles and those who have received discrete pink macules and papules which may
exogenous immunoglobulin. The symptoms of become confluent with a morbilliform
this clinical syndrome are characterized by appearance or it may at times appear
shortened prodrome, less severe symptoms and scarletiniform. An erythema infectiosum like rash
prolonged incubation period2,3. The presence of is also described in rubella 5,6. An exanthem
Kopliks spot is variable and skin eruption is characterized by erythematous and petechial
usually less confluent. macules on the soft palate (Forscheimers spots)
may also be present7.
Atypical measles has been reported in
recipients of killed measles vaccine, which was Occipital, posterior auricular and posterior
used from 1963 to 1968, who later come in cervical lymphadenopathy is a consistent finding
contact with wild type measles virus. This is in rubella. It appears during the prodromal period
characterized by high fever, myalgia, cough, and become prominent during the period of
headache and abdominal pain. Coryza and exanthem. The complications are not usual.
conjunctivitis are absent. The rash begins more However, joint involvement as evidenced by
distally, concentrated on ankles, wrist and arthralgia and arthritis can occur in majority.
creases. The morphology of exanthem is variable Other less common complications include
including vesicular, purpuric, petechial and encephalitis, myocarditis, pericarditis, hemolytic
scarletiniform lesion4 Sometimes there may be anaemia, thrombocytopenic purpura and
haemorrhagic lesions. hepatitis.
Following measles vaccination a less Treatment is supportive. Prevention is best
severe exanthem similar to classical measles achieved by vaccination.
exanthem may develop in certain people and
known as measles vaccination exanthema. Congenital rubella syndrome (CRS): The
Management is mainly supportive. features in CRS may be grouped into three such
as (1) transient, (2) permanent and (3)
Rubella
developmental. The transient abnormalities
Rubella also known as German measles, disappear in a few months from birth, such as
may be asymptomatic in majority. In others, thrombocytopenic purpura or hepatitis, the
disease presents with a mild prodrome occurring permanent defects persist and include congenital
62
2005; 7(3) : 235
heart disease, cataract, hearing loss and the acral purpuric erythema, occasionally associated
developmental group will have defects appearing with fever and oral lesions. The rash starts as
later in life such as behavioural disorders and symmetric erythema and edema of the hands,
endocrine malfunction. fever with gradual progression to petechiae and
purpura. One of the clinical hall marks of the
There are a few cutaneous findings as well. rash is the sharp demarcation on the wrists and
These include Cranberry muffin lesions ankles. The rash is typically painful. Mucosal
characterized by soft 2 to 20 mm raised, involvement such as oral erosions, petechiae and
erythematous, spongy lesions which later become edema of lips, buccal mucosa and palate can also
more classical Blueberry muffin. In addition occur.
petechiae, purpura, morbilliform rash, reticulate
erythema of face and acral areas, facial The treatment of EI is mainly symptomatic.
seborrhoea, hyperpigmentation of face and other One advance in the treatment of EI in
parts of body, cyanosis, dermatologlyphic immunocompromised patient is the use of
changes, leucocytoclastic vasculitis, localized intravenous immunoglobulin (IVIG).
scleroderma are some other not so common
manifestations8. Roseola (Exanthem Subitum)
Roseola is a common exanthematous illness
No specific treatment exists for rubella
of infancy and young child. It is characterised
infection during pregnancy; so also for CRS1.
by high fever of 3-5 days and the appearance of
Hence it is important to prevent rubella infection
skin rash after defervesence. Roseola is caused
by proper immunisation.
by HHV-6, a double stranded DNA Virus.HHV-
Erythema infectiosum 7 is also implicated in the etiology of this disease9.
Majority contracts infection during the infancy;
Erythema infectiosum (EI) is otherwise between 6 months to 3 years of age.
known as fifth disease, slapped cheek disease.
It is caused by human parvovirus B191. Hand-foot- and- mouth disease
(HFMD)
The most well known dermatologic
manifestation is described as slapped cheek. This is caused mostly by coxasakie A1b infection.
This is characterized by bright red macular But it may also be due to a variety of other entero
erythema on either or both cheeks. There is a rim viruses such as coxasakie virus A 5,A7, A9, A10,
of sparing around mouth. As the disease B1, B2, B3, B5 and enterovirus 71 10,11. The
advances, a generalized eruption occurs. It incubation period is 4-6 days and is highly
appears first on proximal extremities and then contagious12. After a brief period of prodrome,
spreads to the trunk. This is characterized by lacy, the characteristic enanthem develops which is
reticulate erythema. The palms and soles are followed shortly by exanthem.
spared. Pruritus is also present along with rash.
The enanthem of HFMD consists of vesicles
This rash lasts for 3 to 4 weeks with waxing and
that rapidly rupture to leave behind erosions and
waning in intensity.
ulcers superimposed on an erythematous base.
Papular purpuric glove and socks syndrome They are usually 4-8 mm in size and occur most
is another characteristic rash seen in infection commonly on buccal mucosa and tongue, as well
with parvovirus B19. The typical features include as palate, uvula, and anterior tonsillar pillar12.
63
Indian Journal of Practical Pediatrics 2005; 7(3) : 236
The exanthem is vesiculopustule ranging may persist for 2-7 days and ulcers recover
from 3 to 7mm. They are characteristically seen completely in 2-3 weeks.
on palms and soles. It is also seen on the buttocks
and perineum. This may be associated with Recurrent herpetic gingivostomatitis: The
submandibular or cervical lymphadenopathy12. lesions are seen on the lips. The commonest
There is no specific treatment for HFMD. affected site is the mucocutaneous junction of
lips. The recurrent lesions are less severe, more
Herpes simplex virus (HSV) infec- localized and heal rapidly.
tions
Herpes genitalis: This is usually caused by type
The name herpes is derived from the 2 HSV, transmitted through sexual route. Most
Greek word meaning to creep13. There are two children with HSV genital infection are
antigenic types of HSV, type 1 and 2. Though adolescents and acquire it after the onset of sexual
HSV1 and 2 can affect any cutaneous site, HSV2 activity 14 . Younger children may acquire
is more frequently associated with genital infection through autoinoculation, exogenous
infection. inoculation from care given, usually a parent,
close non sexual physical contact and sexual
The highest rate of HSV infection is in the abuse15,16,17.
first 5 years of life. Most children will be
asymptomatic or have a trivial illness following In HSV seronegative individuals primary
exposure to HSV infection. About 50% of HSV infection is severe. Symptoms may be more
children will develop HSV antibody by the age in females than in males due to the wider area of
of 5 and 95% will develop antibody by 10 years involvement in the former. Initially one or more
of age. prutitic papules develop and then it turns into
vesicles which in turn form shallow ulcers which
Clinical features: The clinical features depend crust. The symptoms include fever, malaise,
on whether the infection is primary or recurrent. dysuria, discharge per vaginum, etc. The illness
The primary infection includes herpetic lasts for 2-3 weeks and settles on its own provided
gingivostomatitis, herpes genitalis, there is no secondary bacterial infection.
keratoconjunctivitis and inoculation herpes
simplex. Recurrent infection occurs in orolabial Recurrent herpes genitalis: This is not very
and perilabial sites as well as in genitalia. common in children. They are of shorter duration
and less severe. The lesion is heralded by prutitus
Primary herpetic gingivostomatitis: This is the or tingling sensation at the site of involvement,
commonest clinical manifestation of primary which is soon followed by vesicles. These
HSV infection in children. The infection starts vesicles rupture easily and crust and then heal in
with fever and malaise which is followed by 5 to 7 days.
appearance of vesicles. The fever is high grade.
The vesicles occur on the lips, gingivae, palate, Keratoconjunctivitis: Primary infection of the
buccal mucosa, pharynx, larynx and tonsils. eye causes severe and often purulent
These vesicles later transform into shallow ulcers conjunctivitis with opacity and superficial
with yellow exudative base and an erythematous ulceration of the cornea 18. The eye lids are
halo. The lesions may coalesce also. Associated edematous and there may be vesicles on the
tender lymphadenopathy is also present. The surrounding skin 18. The preauricular gland
gingiva may be swollen and may bleed. Fever enlarges and becomes tender.
64
2005; 7(3) : 237
Inoculation herpes simplex: Direct inoculation infection. The newer drugs like imiquimod and
of the virus into an abrasion or into normal skin resiquimod, which cause local release of
gives rise to indurated papules, large bullae or cytokines and enhances antigen presentation,
irregularly scattered papules and vesicles. The have shown promise in treatment of herpes
regional nodes are enlarged and tender but fever genitalis19. A 10 minute application of zinc
and constitutional features are usually mild. sulphate 0.025 0.05% in water to the expected
Inoculation of finger tip usually results in herpetic site of the herpes, repeated 2 to 4 times per month,
whitlow. has been reported to prevent recurrent eruption
previously associated with erythema
Complications: A number of complications are multiforme20.
seen following HSV infection. These include
eczema herpeticum, erythema multiforme, Bells Eczema herpeticum (EH): EH may be defined
palsy, recurrent lymphocytic meningitis and as an acute disseminated herpes simplex virus
encephalitis. infection in a patient with atopic dermatitis. EH
is usually a primary infection in children. It
Diagnosis: The history and physical examination
occurs in all age group of children but more
is often sufficient for making a diagnosis.
common with children of age 2-3 years. There
However in atypical forms a clinical diagnosis is
is no seasonal variation in the incidence of EH.
often difficult. The gold standard of diagnosis is
viral culture. Tzanck smear examination is Clinical features: Usually presents as sudden
another method for diagnosis in which multi deterioration of childs eczema. Vesicles are
nucleated giant cells are seen in the smear. the most common lesion; but papules, crusted
Detection of viral DNA by PCR is also useful lesions and punched out ulcers can also occur.
but not commonly used in clinical practice. Lesions may be either discrete or confluent and
Serological testing for type specific antibodies tends to occur in crops. Any cutaneous site may
is another useful method of diagnosis. be affected; some of the vesicles rupture and
ooze. The signs of EH are usually subtle and
Treatment: Early diagnosis and rapid initiation
include fever, vomiting, anorexia, diarrhea, etc.
of antiviral therapy are essential for effective
Secondary bacterial infection may occur.
treatment of HSV infection. Mild uncomplicated
Treatment should start early to avoid serious
eruptions need no treatment. In severe primary
complications. Here again treatment is with anti
infection and frequent recurrences antiviral
viral agents such as acyclovir and valaciclovir.
therapy is instituted.
Severe cases are best treated with intravenous
The antiviral drugs used in the treatment of acyclovir. The undercurrent bacterial infection
HSV infection are acyclovir, valaciclovir and must be tackled in its own merit, so also the
famciclovir. All these drugs are effective and underlying eczema.
safe in the treatment of HSV infection. The virus
Neonatal HSV infection: Neonatal HSV
is now showing significant resistance to
infection occurs in three clinically recognizable
acyclovir. However, in case of viral resistance
syndromes such as 1. disseminated infection 2.
foscarnet may be used. Cidofovir is another
infection localized to skin, eye or mouth and 3.
alternative.
CNS infection. All these will have skin
Other than antiviral agents, immune involvement which may be minimal or severe.
modulators are promising in the treatment of HSV Neonatal HSV infection tends to manifest within
65
Indian Journal of Practical Pediatrics 2005; 7(3) : 238
the first four weeks of life and most commonly The incubation period of varicella is
within the first week21. Upto 30% of infected 14-17 days. The infection starts with fever and
new borns will have symptoms on the first day malaise. This is followed by the development of
of life itself22. papules which rapidly turn into vesicles. The
contents become turbid within few hours. Then
The infection may manifest with lesions are surrounded by an erythematous halo.
cutaneous or mucosal lesions, with or without In 2-4 days dry crust forms which separate leav-
signs of sepsis or encephalitis23. The skin lesions ing no scar. The vesicles appear in crops and
appear as small, 2 to 4 mm vesicles, with usually three to five crops are seen. These le-
surrounding erythema, often in herpetiform sions are mostly seen on the trunk and then on
clusters. The skin lesions usually occur on the face and scalp and on the limbs. A characteristic
part of the body in prolonged contact with cervix. feature of varicella is the presence of lesions at
These lesions either disseminate or settle by itself. different stages of evolution in any given time.
These vesicles may become necrotic and ulcerate.
Skin lesions are present in most neonates with Zoster: The first manifestation of zoster is pain.
disseminated disease (77%) and in 60% of infants The pain has varying intensity and sharply
who present with CNS disease23. The treatment localized in the dermatome affected. It may be
of choice in neonatal herpes infection is acyclovir diffuse and less severe also. The eruption then
administered intravenously, regardless of clinical appears. They start as grouped erythematous
presentation 24 But oral acyclovir will be papules which rapidly become vesicular and then
sufficient for disease limited to skin alone pustular. New vesicles continue to appear for
(personal data). several days. In children the presence of a
prodrome is unusual. The usual site of
Varicella and zoster infections involvement in children is the thoracic region.
Involvement of the nasociliary branch of the
Varicella and zoster are caused by the same trigeminal nerve leads to appearance of the
virus, herpes virus varicella. Varicella occurs vesicles at the tip of the nose. This is described
throughout the world and transmitted by droplet as Hutchinsons sign. The recognition of this sign
infection. Patients are infectious from about 2 is important because it usually indicates
days before to 5 days after the onset of the rash. involvement of the cornea and conjunctiva. In
Varicella infection confer lasting immunity and immunocompromised patients the disease may
second attack is uncommon. Maternal varicella become disseminated forming disseminated
in the first 20 weeks of pregnancy is associated herpes zoster or it may appear at different
with an approximate 2% risk of fetal damage, dermatomes (multidermatomal involvement).
including death of the fetus25. Maternal zoster The lesions may become necrotic and take more
during pregnancy is not associated with time to heal.
intrauterine infection26,27. Zoster in infancy has
followed maternal varicella and the primary Treatment: Varicella in healthy child requires
infection has occurred in utero28,29,30. If mother only symptomatic treatment with analgesics and
has varicella within 4 days before to 2 days after other supportive measures. Some advocate anti
term, the neonate would have no maternal viral treatment. In immuno compromised
antibody and is at a risk of severe varicella, with individuals anti viral drug must be given at the
a mortality rate of upto 30% in the absence of earliest. The drugs used in the treatment are
treatment31,32. acyclovir or valaciclovir.
66
2005; 7(3) : 239
CMV infection in immunosuppressed can Treatment: Most CMV infections do not require
be severe and even fatal. The dermatological treatment but in life threatening or vision
features include a wide spread eruption that may threatening as on CMV retinitis, ganciclovir and
become papular and purpuric with foscarnet have been used.
vesiculobullous and pustular lesions. There may
Human Papilloma virus
be indurated pigmented nodules or plaques37. In
AIDS, keratotic skin lesions40 and severe oral41 Papilloma viruses are small DNA viruses
and skin ulcerations42 have been reported. that infect squamous epithelia, causing cell
67
Indian Journal of Practical Pediatrics 2005; 7(3) : 240
proliferation. The commonest effect of this to HPV-1, while the mosaic warts are caused by
infection is the development of warts (verrucae). HPV-2. At first it appears as a small, shiny deep
seated papule and later assumes the well defined
Warts: Human papillomavirus (HPV) can infect
rounded shape. Surrounding the papule is a collar
any site with stratified squamous epithelium. The
of hyperkeratotic epithelium. Most plantar warts
usual clinical presentation can be divided into
are seen over pressure areas such as over the
cutaneous warts, genital warts, oral warts and
heads of metatarsals, heel and lateral aspect of
laryngeal warts. The tissue specificity is mostly
foot.
governed by the type of HPV eg. Nongenital
plantar wart is caused by HPV 1; oral lesions are In most cases pain is a common symptom;
caused by HPV 13,32,5751. however, sometimes it may be absent. Plantar
warts are commonly confused with callosities.
Warts occur at any age but are unusual in
The differentiation can be made by noting the
infancy and early childhood. The incidence
interface between the epidermis and wart as well
increases during the school years and peaks in
as by noting bleeding points on paring. Another
adolescences and early adulthood52,53,54.
useful sign may be application of pressure from
Modes of transmission: Warts spread by direct sides which causes pain in plantar warts.
or indirect contact. Trauma and maceration
predisposes the entry of virus into the skin. Plane warts: Plane warts are mainly due to HPV-
3 and HPV-10. They are smooth, minimally
Anogenital warts are uncommon among children. elevated, brownish or hyperpigmented papules.
In them, infection from mothers genital tract at It may be rounded or polygonal and there will
delivery is considered as a frequent source of not be any scaling on the surface. The usual sites
infection at this site. However sexual abuse may of involvement are face and dorsum of hands.
also be considered if anogenital infection is seen The number may range from a few to many.
in children. Postnatally, transmission from adults These warts are relatively less common in
with genital warts may occur non-sexually such children.
as sharing a bath with an infected adult55.
Filiform warts: These are usually seen in face
Common warts: These are found on all body and neck. It can also occur in hairy regions. They
surfaces and are commonly associated with HPV appear as slender verrucous papules and the
2; it is also associated with HPV-57, 1 and HPV- number may range from a few to many.
4. Clinically characterized by firm papules with
verrucous surface of size 1mm to 1cm. Anogenital warts: These are variously termed
Sometimes it may reach larger sizes. Usually as condyloma acuminatum, genital warts or
these are located over extremities. In children venereal warts. Anogenital warts are caused
the other favoured site is around knees. In mainly by HPV-6, -11, -16 and 18 55,56. In
habitual nail biters warts may be located children HPV-2 and -4 are also isolated 57.
periungually Common warts are sessile in most Oncogenic progression occurs with infection due
of the times; however small pedunculated warts to HPV-16 and 18.
may also seen (filiform warts). Common warts
The typical anogenital warts are soft,
can also occur on genitalia.
hyperpigmented elongated and sometimes
Plantar warts: Plantar warts are caused by HPV- pedunculated. The lesions are usually multiple.
1, -2, -4 or 57. The deep myrmecia form is due They are classically distributed around anal
68
2005; 7(3) : 241
orifice and may extend to the contiguous anal patterns are also observed61. The lesions are seen
mucosa. The other areas could be frenulum, on face, neck, trunk and limbs. The lesions may
corona and glans penis as well as posterior be macular or plaque like. In children, the lesions
fourchette. These warts may persist for a variable spread fast. The colour of the lesion may be
period from a few weeks to many years58. In some hypopigmented or brownish. Dysplasia and
situations, anogenital warts are associated with malignant changes occur in sun exposed skin. The
other sexually transmitted infections. When these effective treatment for EV is still to be found out.
lesions are present, a careful history must be However, etritinate in the dose of 1mg/Kg is
obtained from child and parents for possible found to be useful. The effect is dose dependent
sexual transmission and the child must be and relapse occurs if the drug is stopped.
evaluated for any other signs of abuse. The usual
differential diagnosis includes condylomata lata, Poxvirus infections
anogenital mollusca, skin tags and rarely skin
lesion of Crohns disease. The poxvirus family consists of DNA
viruses that can infect animals and human beings.
Treatment: Being self limited disease, warts They are brick - or oval shaped and are generally
require a balanced approach for treatment. The large enough to be seen by light microscopy.
agents used for topical application are salicylic There are four genera of pox viruses and
acid, gluteraldehyde, podophyllin and molluscum contageosum virus is the most
podophyllotoxine, formalin, 5-flurouracil and commonly encountered one.
retinoic acid. Surgical methods include excision,
curettage and cautery, cryotherapy and laser Molluscum contagiosum: Molluscum
ablation. Intra lesional injections with interferon contageosum (MC) is a benign self limiting
and bleomycin are also advocated as treatment infection of skin caused by Molluscum
for warts. Anti viral drug cidofovir applied contageosum virus (MCV)
topically as 1% gel or by intra lesional injection
The individual lesion is a shiny, pearly
is effective. Plantar, anogenital and laryngeal
white, hemispherical, umbilicated papule. The
warts resolve completely59. Cimetidine given in
size may vary from 1 mm to 1cm. In certain
a dose of 30-40mg/Kg daily for a prolonged
situations it may become more than one cm and
period may be effective. In a placebo controlled
is known as giant molluscum. These are usually
study there is not much of difference in the
seen in immuno compromised individuals. The
outcome 60. Topical immunomodulation is a
number of lesions is also variable; usually in the
promising new treatment for warts. Imiquimod
range of 10-20. But innumerable lesions are seen
5% cream is currently used as a topical therapy
in immunosuppressed individuals. Even though
for warts.
it can occur at any site, the usual sites of
Epidermodysplasia verruciformis (EV): EV is involvement are trunk and limbs. The genitals
a genetic disease characterized by HPV infection are also affected. The lesions resolve
giving rise to characteristic combination of plane spontaneously with or without inflammation.
warts, pityriasis versicolor like lesions and Occasionally, an eczematous reaction around a
reddish plaques. Malignant change is common. molluscum papule occurs, termed as molluscum
Susceptibility to virus is inherited. The common dermatitis. This reaction usually resolves on its
mode of inheritance is autosomal recessive; own62 when molluscum is treated or regresses.
however X-linked or autosomal dominent Periocular molluscum may be associated with
69
Indian Journal of Practical Pediatrics 2005; 7(3) : 242
70
2005; 7(3) : 243
10. Cherry JD. Contemporary infectious 24. Whittley R, Arvin A, Prober C, et al. A
exanthema. Clin infect Dis 1993;16: 199-207. controlled trial comparing vidarabine with
11. Lendenbaum JE, Van Dyck PC, Alten RG. acyclovir in neonatal herpes simplex virus
Hand foot and month disease associated with infection. N Engl J Med 1991;324-444.
Coxsakie virus group B. Scand J Infect Dis 25. Essex Cater A, Heggarty H. Fatal congenital
1975;7:161-163. varicella syndrome. J Infect 1983;7:77-78.
12. Maneini AJ. Viral exanthema in Paediatric 26. Enders G, Miller E, Cradock Watson J et al.
dermatology. 3 rd Edn. Ed. Schachner LA, Consequences of varicella and herpes zoster in
Hausen RC, Mosby, 2003; pp 1059-1092. pregnancy. Prospective study of 1739 cases.
Lancet 1994;343:1548-1551.
13. Snavely SR, Lin C. Clinical spectrum of herpes
simplex virus infection. Clin Dermatol 1984; 27. Pastuszak AL, Levy M, Schick B, et al.
2: 8-22. Outcome after maternal varicella infection in
the first 20 weeks of pregnancy. N Engl J Med
14. Chang T-W. Herpes simplex. Clin Dermatol 1994; 330:901-905.
1984; 2:5-7.
28. Lewkonia IK, Jackson AA. Infantile herpes
15. Jaffe AC. Sexual abuse and herpetic genital zoster after intra uterine exposure to varicella.
infection. J Pediatr 1976; 89:338. Brt Med J 1973; iii; 149.
16. Gardner M, Jone JG. Genital herpes acquired 29. Laude TA, Rajkumar S. Herpes zoster in a 4
by sexual abuse of children. Pediatrics month infant. Arch Dermatol 1980;116:160.
1984;104:243-244.
30. Helander I, Arstila P, Terho P. Herpes zoster
17. Kaplan KM, Fleischer GR, Paradix JE, et al. in a 6 month old infant. Acta Derm Venereol
Social relevance of genital herpes simplex in (Stockh) 1983; 63:180-181.
children. Am J Dis child 1984; 138:872-874.
31. Meyers TD. Congenital varicells in term
18. Sterling JC. Virus infections In: Rooks infants: risk reconsidered of Infect Dis
textbook of dermatology. 7th Ed, Eds. Burns 1974;129:215-217
T, Breathnach S, Cox N, et al Blackwell
32. Miller E, Cradock Watson JE, Ridehalgh
publishing, 2004; 25.1-25-83.
MKS Outcome in new born babies given anti
19. Miller RL, Tomai MA, Harrison CJ, et al. varicella zoster immunoglobulin after
Immunomodulation as a treatment strategy for perinatal maternal infection with varicella
genital herpes: review of the evidence. Int zoster virus. Lancet 1989;ii 371-3.
Immunopharmacol 2002 2:443-451.
33. Weibel RE, Neff BJ Kuter BJ, et al. Live
20. Brody I. Topical treatment of recurrent herpes attenuated varicella vaccine. N Engl J Med
simplex and post herpetic erythema multiforme 1984; 310:1409-1415.
with low concentration of zinc sulphate
34. Gershon AA, Steinberg SP. Persistence of
solution. Br J Dermatol 1981:104;191-194.
immunity to varicella in children with leukemia
21. Kohl S. Neonatal herpes simplex virus infection immunized with live attenuated varicella
Clin Perinatol 1997; 24:129-150. vaccine. N Engl J Med 1989; 320:892-897.
22. Riley LE. Herpes simplex virus. Sem Perinatol 35. Centres for Disease control. Varicells zoster
1998:22:284-292. immuneglobulin for prevention of chicken pox.
Am Intern Med 1984;100: 859-865.
23. Friedlander SF, Bradley JS. Viral infections In:
Textbook of Neonatal dermatology, Ed 36. Blatt J, Kastner O, Hods DS. Cutaneous vesicle
Eichenfield LF, Friedman IJ, Esterly NB, WB in congenial cytomegalovirus infection. J
Saunders Company, 2001; 201-222. Pediatr 1978;92:509.
71
Indian Journal of Practical Pediatrics 2005; 7(3) : 244
37. Sterling JC. Virus infection. In: Rooks in disseminated cytomegalovirus infection J
textbook of dermatology. 7th Ed, Ed. Burns T, Am Acad Dermatol 1983;9:937-946.
Breathnach S, Cox N, et al Blackwell 49. Bhawan J, Gellis S, Ucci A, et al. Vesiculo-
publishing, 2004; 25.1- 25.83. bullous lesion caused by cytomegalovirus
38. Humphreys DM, Myers A. Cytomegalovirus infection in an immunocompromised adult. J
mononucleosis with urticaria . Postgrad Med J Am Acad Dermatol 1984;11:743-747.
1975;51:404-406. 50. Carraseosa JM, Bielsa I, Ribera M, et al Papular
39. Weigand DA, Burgdorf WHC, Tarpay MM, purpuric glove and- socks syndrome related
Vasculitis in cytomegalovirus infection Arch to cytomegalovirus infection. Dermatology
Dermatol 1980; 116:1174-1176. 1995;191:269-270.
40. Bourncrias I, Boisnic S, Patey O et al. Unusual 51. Brentjens MH, Yeung Yue KA, Lee PC, et
cutaneous cytomegalovirus involvement in al. Human papilloma virus: A review
patients with acquired immunodeficiency Dermatology Clin 2002; 20:315-331.
syndrome. Arch Dermatol 1989;125:1243- 52. Kilkenny M, Marks R. The descriptive
1246. epidemiology of warts in the community. Aust
41. Andriolo M, Wolf JM, Rosenberg JS. AIDS and J Dermatol 1996;37 80-86.
AIDS related complex: oral manifestations 53. Barr A, Coles RB Plantar warts: a statistical
and treatment. J Am Dent survey. Trans St.Johns Hosp Dermatol Soc
Assoc.1986;113:586-589. 1966; 52: 226-233.
42. Colsky AS, Jagasothy SM, Leonardi C, et al. 54. Van Casse JT, Muller RF. Incidence of
Diagnosis and treatment of a case of cutaneous verrucca plantaris (Plantar warts) in a school
cytomegalovirus infection with a dramatic population. Arch Pediatr 1958;75:279-284.
clinical presentation J Am Acad Dermatol
55. Stumpf PC. Increasing occurrence of
1998;38:349-351.
condycomata acuminata in premenarchal
43. Drago F, Aragon MG, Lugani C, Rebora A. children. Obstet Gynaecol 1980;56:262-4.
Cytomegalovirus infection in normal and
56. Beutner KR, Tyring S. Human papilloma virus
immuno compromised humans. Dermatology
and human disease. Am J Med 1997:102:9.
2000; 200:189-95.
57. Gree M, Husnjak K, Skerlev M, et al. Detection
44. Vilmer C, Perof Y, Manifestation cutaneous
and typing of human papilloma viruses by
des infections a cytomegalovirus - Am
means of polymerase chain reaction and
Dermatol venereal 1984;111:119-25. Quoted
fragment length polymorphism in male genital
in Dermatology Clinics.
lesions. Anticancer Res 2000;20:2097.
45. Lin CS, :Penha PD, Krishnan MN, et al.
58. Bodemer C. Human papilloma virus. In:
Cytomegalovirus inclusion disease of the skin.
Pediatric dermatology, 3rd Edn. Ed Schachner
Arch Dermatol 1981;117:282-284.
LA, Hansen RC Mosby, 2003; pp 1087-1092.
46. Bowenerias I, Boisinic S, Patey O, et al.
59. Van Cutsem E, Snoeck R, Van Ranst, et al.
Unusual cutaneous cytomegalovirus
Successful treatment of a squamous papilloma
involvement in patients with acquired
of the hypopharynx-esophagus by local
immunodeficiency syndrome Arch Dermatol
injection of (S) 1 (3 hydroxy 2
1989;125:1243-1246.
phophosnylmethoxypropyl) cytosine. J Med
47. Horn TD, Hood AF. Clinically occult Vir 1995;45:230-235.
cytomegalovirus present in skin biopsy
60. Yilmaz E, Alpsoy E, Basaren E. Cimetidine
specimens in immunosuppressed hosts. J Am
therapy for warts: a placebo-controlled, double
Acad Dermatol 1989;21:781-784.
blind study J Am Acad Dermatol
48. Pariser RJ. Histologically specific skin lesions 1995;34:1005-1007.
72
2005; 7(3) : 245
61. Kanerva LO, Johnsson E, Niemi K-M et al. with HIV/AIDS A pilot study J Eur Acad
Epidermodysplasia verruciformis. Clinical and Dermatol Venereol 2000; 14: 484-488.
light and electron microscopic observation 65. Hengge VR, Esser S, Schultewolter T et al.
during etretinate therapy. Arch Dermatol Res Self administered topical 5% imiquimod for
1985;278:153-160. treatment of common warts and molluscum
62. Diven DG. An overview of Poxvirus. J Am contageosum Br J Dermatol 2000;143:1026-
Acad Dermatol 2001; 44:1-14. 1031.
66. Liota E, Smith KJ, Buckley R, et al. Imiquimod
63. Jang KA, Kim S.H, Choi JH et al Viral
therapy for molluscum contageosum. J Cutan
folliculitis on the face Br J Dermatol
Med Surg 2000;4:76-82.
2000;142:555-559.
67. Dohil M, Prendiville JS Treatment of
64. Calista D. Topical Cidofovir for severe molluscum contageosum with oral cimetidine:
cutaneous human papillomavirus and clinical experience in 13 patients. Pediatr
molluscum contageosum infections in patients Dermatol 1996;13:310-312.
LUDHICON 2005
Date : September 18, 2005.
Host : IAP-Ludhiana district Branch, In association with NNF Punjab state and
IAP-Intensive care chapter, Punjab state branch
Contact : Dr Harinder Singh, Organizing secretary, 8-A, Model town extension, Ludhiana.
Email:harinder_dr@rediffmail.com, Ph: 0161-2450074, 9814117501.
Website: www.geocities.com/iapludhiana
73
Indian Journal of Practical Pediatrics 2005; 7(3) : 246
NUTRITION
fighting undernutrition and infectious diseases. randomized trial that a Mediterranean diet (twice
Adverse health consequences of positive nutrition the amount of fiber, 49 times more antioxidants,
transition in children were undermined as these three times the amount of polyunsaturated and
were seemingly remote and therefore omega-3 fatty acids) when given for four weeks
relatively invisible. However these are now in a cross over design with the normal Swedish
gaining prominence with early markers of diet caused approximately 20 % reduction in total
atherosclerosis like endothelial dysfunction and LDL (low-density lipoprotein)-cholesterol,
becoming evident in early adolescence. Further triacylglycerols (triglycerides) and apo B
late childhood and early adolescence remains the (apolipoprotein B). The absence of a carry-over
ideal age group for establishment of healthy effect on plasma lipids between the arms of the
lifestyle and dietary patterns (and modifications study suggests such dietary interventions need
where necessary). Thus, if the epidemic of adult to be maintained to sustain the changes in lipid
metabolic diseases is to be controlled, it is actually profile. Similarly in children (9-12 years)
the pediatricians who will now have to perform improvement in cholesterol levels and endothelial
a crucial role by looking after children and function was documented after six weeks of a
adolescents more meaningfully, as intervention diet providing 900-1200 kcal/day (Low in fat (20-
must commence early in life. 25%); high in complex carbohydrate (50-60%);
The beneficial effects of exercise and and sufficient in protein (25-30%) over 6 weeks10.
lifestyle modification in decreasing the risk for Data is also available of single step dietary
developing coronary artery disease and diabetes interventions such as the introduction of soy
is well established in adults. Data also suggests protein and/or flavonoids in adults . Soy is a rich
that exercise6 and dietary modifications7 improve source of polyphenolic isoflavones genistein and
the fore-bringers of atherosclerosis like diadzein. These are structurally similar to
endothelial dysfunction. A Western diet high in estradiol and genistein in particular has several
saturated fat, simple sugars and salt and low in cellular activities (inhibition of tyrosine kinase
fiber, fish oils and antioxidants has been activity, decreased smooth muscle cell
associated with an increased risk of proliferation and nitric oxide dependent
atherosclerosis, an effect which is likely to be relaxation) which may influence vascular tissue
mediated through elevations in orthodox risk metabolism. Steinberg et al11 in a randomized,
factors and possibly also through pro- double blind cross over study enrolled 28 healthy
inflammatory, pro-oxidant and prothrombotic post menopausal women and they consumed 25
mechanisms. Populations from Southern Europe, grams/day of the 3 products for 6 weeks each
who consume a Mediterranean-style diet low in with intervening washout periods. The products
saturated fat, rich in oleic acid and antioxidants, were isolated soy protein with isoflavones,
have a lower incidence of cardiovascular disease ethanol washed soy protein with trace isoflavones
as do populations, such as the Greenland Inuit, and total milk protein which supplied 107, 2 and
who consume diets rich in omega-3 0 isoflavone units per day. Improvement was
polyunsaturated fatty acids derived from oily documented in endothelial function independent
fish8. of the anti-oxidant and lipid effects. Similar data
These observations have led to prospective is however not available in children.
randomized control trials based on a variety of Many epidemiological studies have
dietary combinations in at risk adult populations. investigated the relationship between flavonoid
Ambring et al9 has recently documented in a and cardiovascular disease risk. The subject has
75
Indian Journal of Practical Pediatrics 2005; 7(3) : 248
been reviewed; overall the evidence suggests that inactivity, sedentary behaviour (like >2 hrs
individuals with highest flavonoid intake have TV viewing);
moderately reduced risks for cardiovascular
b) Family history of early hypertension,
disease. Tea, apples, onions and red wine are
coronary artery disease and diabetes.
particularly rich in flavonoids with particularly
strong evidence in favor of tea with a meta- ii) Physical examination:
analysis by Peters et al12 suggesting an overall a) Linear growth should be assessed by
reduction in cardiovascular disease ~11% with yearly growth (height, weight and weight for
consumption of 3 cups per day. height / BMI) charting 3 to 6 monthly from
Further, in a recent study from low birth to 5 years of age and 6 to 12 monthly
socioeconomic stratum residing in urban slums thereafter. Any accelerated weight gain
of New Delhi, cardiovascular risks like should be considered as risk factor. If
hypertension and hypertriglyceridemia were feasible, multiple skin fold thickness (biceps,
noted in a significant number of cases even with triceps, subscapular, suprailiac), waist
BMI and waist circumference (WC) values circumference should be measured.
considered normal. The data suggested that b) All Indian children >10 years in age who
definitions of normal ranges of BMI and WC are overweight (BMI >85th centile for age
need to be revised for Asian Indians 13. The or weight >120% of the 50th centile weight
International Obesity Task Force (IOTF) has for height by national standards), and have
proposed the standards for adult obesity in Asia any one of the following risk factors: family
and India as BMI >23 as overweight and BMI history of type 2 diabetes in first or second
>25 as obesity14. degree relative, polycystic ovaries,
acanthosis nigricans, dyslipidemia or
To create awareness among pediatricians of
hypertension. Pending the availability of
their role in the prevention of these metabolic
good Indian National representative
conditions, and to provide clear guidelines for
standards for BMI in childhood, the NCHS/
actions to be taken by them, the Indian Academy
CDC BMI chart may be followed at present.
of Pediatrics established a National Task Force
on Childhood Prevention of Adult Diseases. The c) To regularly monitor blood pressure in
Task Force had recently published its all children from age 3 years and to look for
recommendations in a series of articles15-17. It is acanthosis nigricans and polycystic ovaries
important that the pediatricians integrate these from 10 years of age.
recommendations in their routine daily clinic iii) Investigations:
practices. The salient features of these
recommendations are summarized here. a) Blood glucose screening should be done
once in 2 year for children at risk after 10
Important Features of Recommen- years of age. Diabetes is diagnosed if fasting
dations plasma glucose is >126 mg/dL and or 2 hour
1. Identifying Cases at riskby Orienting post prandial plasma glucose value is >200
Routine Clinical Practices mg/dL.
b) Lipid profile should be done in children
i) History:
age > 2 years with family history of
a) Personal history of fattening diet, physical dyslipidemia or premature cardio-vascular
76
2005; 7(3) : 249
77
Indian Journal of Practical Pediatrics 2005; 7(3) : 250
Lebovitz HE. Body composition, visceral fat, Kumar K, Murray MJ. Soy protein with
leptin and insulin resistance in Asian Indian isoflavones has favorable effects on endothelial
men. J Clin Endocrinol Metab 1999; 84: 137- function that are independent of lipid and
144. antioxidant effects in healthy postmenopausal
4. Bhargava SK, Sachdev HPS, Fall CHD, women Am J Clin Nutr 2003; 78:12330.
Osmond C, Lakshmy R, Barker DJP, et al. 12. Peters U, Poole C, Arab L. Does tea affect
Relation of serial changes in childhood body- cardiovascular disease? A meta-analysis. Am
mass index to impaired glucose tolerance in J Epidemiol 2001;154:495503.
young adulthood. N Engl J Med 2004; 350:
13. Vikram NK, Pandey RM, Misra A, Sharma R,
865-875.
Ramadevi J, Khanna N. Non-Obese (Body
5. Kapil U, Singh P, Pathak, Dwivedi SN. Mass Index < 25 kg/m2) Asian Indians with
Prevalence of obesity amongst affluent normal waist circumference have high
adolescent school children in Delhi. Indian cardiovascular risk. Nutrition 2003; 19:503
Pediatr 2002 ; 39 : 449-452. 509.
6. Clarkson P, Muntgomery HE, Mullen MJ, et 14. WHO/IASO/IOTF. The Asia Pacific
al. Exercise training enhances endothelial Perspective: Redefining Obesity and its
functions in young men. J Am Coll Cardiol treatment. Health Communications Australia
1999 ; 33 : 1379-1385. Pty Ltd. 2000.
7. Fuentes F, Lopez Miranda J, Sanchez E, et al. 15. Kurpad AV, Swaminathan S, Bhat S. IAP
Mediterranean and low fat diets improve National Task Force for Childhood Prevention
endothelial function in hyper cholestrolemic of Adult Diseases: The effect of childhood
men. Ann Intern Med 2001; 134: 1115-1119. activity on prevention of adult diseases. Indian
8. Hingorani AD. Diet, the endothelium and Pediatr 2004; 41:37-62.
atherosclerosis. Clinical Science 2004; 106, 16. Bhatia V. IAP National Task Force for Child-
447448. hood Prevention of Adult Diseases: Insulin
9. Ambring A, Friberg G, Axelse, M. et al. Effects resistance and type 2 diabetes mellitus in child-
of Mediterranean-inspired diet on blood lipids, hood. Indian Pediatr 2004; 41: 443-457.
vascular function and oxidative stress in healthy
17. Bhave S, Bavdekar A, Otiv M. IAP National
subjects. Clin Sci 2004; 106:519525.
Task Force for Childhood Prevention of Adult
10. Woo KS, Chook P, Yu CW, Sung RY, Qiao Diseases: Childhood obesity. Indian Pediatr
M, Leung SS et al. Effects of diet and exercise 2004; 41: 559-575.
on obesity-related vascular dysfunction in
18. Inamdar S. Ten commandments for child
children. Circulation. 2004;109:1981-1986.
friendly school initiative. Indian Pediatrics
11. Steinberg FM, Guthrie NL, Villablanca AC, 2005;42: 269-272.
PALS COURSE
Date: October, 1-2, 2005 Venue: Delhi
Contact: Dr.K.K.Jani, Cell: 98103 40599, Email: jkk00001@yahoo.co.in
Dr.Alok Kumar Agarwal, Cell: 98181 09691, Email: alokkragarwal@hotmail.com
78
2005; 7(3) : 251
RENAL CYSTIC DISEASE not symptomatic till adulthood and that cysts take
a long time to develop. Ultrasound may be used
* Vijayalakshmi G to screen these children though they can be
** Natarajan B declared free of disease only if they have not
*** Ramalingam A developed any cysts by thirty years of age. CT
and MRI can also detect these cysts, but are not
One of the common finding in any
required as ultrasound provides adequate
ultrasound report of adults is the simple renal cyst.
This is a normal consequence of aging. More than information.
fifty percent of people over the age of fifty years In the adult type of polycystic disease both
have renal cysts. This is rare in a child. The kidneys are symmetrically involved and are
pathogenesis is uncertain. Focal tubular enlarged to the same degree with cysts of varying
obstruction, past trauma or ischemia followed by sizes. In the initial stage two or more cysts in
necrosis have been proposed. any kidney should raise the suspicion of the
disease. In the fully developed stage ultrasound
The ultrasound criteria for a simple cyst are
shows multiple cysts filling the entire kidney (Fig
that it should be unilocular, have a smooth wall
2). In contrast to polycystic disease the
and have no communication with the collecting
involvement is usually unilateral in multicystic
system. It may involve the right or left kidney
kidney disease. Exceptionally it may be bilateral
but the upper pole is frequently involved.(Fig.1a).
but the kidneys are asymmetrically involved. A
When you see an upper pole cyst make sure you
multicystic kidney disease is not inherited and
are not dealing with an adrenal cyst (Fig. 1b) or
has a sporadic occurrence. Patients with the adult
the upper moiety of duplication. Once diagnosed
type of polycystic disease also develop cysts in
as a simple renal cyst no further investigation is
other organs like liver and pancreas.
necessary.
The recessive type of congenital polycystic
Congenital polycystic disease is an inherited
disease is a more serious entity associated with
disorder. There are two types, the dominant
poor renal function. It manifests in the
(ADPKD) and the recessive(ARPKD). The
intrauterine period itself as oligohydramnios. In
dominant type or the adult type is rarely
this, both the kidneys are involved symmetrically.
recognized in the child. This is because they are
The cysts are too tiny to be resolved by
* Addl Professor, Dept. of Radiology ultrasound. But the innumerable cyst walls reflect
Chenglepet Medical College and Hospital. almost all the ultrasonic waves so that the kidneys
** Lecturer appear bright. Bilateral, symmetrically large,
*** Reader bright white kidneys seen in the neonate or the
Dept. of Radiology fetus points to a diagnosis of autosomal recessive
ICH & HC., Egmore, Chennai. polycystic disease (ARPKD) (Fig 3).
79
Indian Journal of Practical Pediatrics 2005; 7(3) : 252
Fig 1a. Simple cyst in the upper pole of the Fig 1b. Adrenal hemorrhage in a newborn
kidney
Sometimes these children have enough renal These cysts are not large. Some may be too tiny
function to survive a few years. Renal failure to be seen in ultrasound. Hepatic fibrosis may
may manifest only at the end of the first decade also be present. A similar picture is also seen in
or in the second decade. In such cases also the Jeunes syndrome, Ellis Van Creveld and
kidneys are large and bright. The liver also shows Laurence Moon Biedle syndromes.
multiple cysts (Fig. 4). These are due to cystic
dilation of malformed biliary ducts. In the initial Finally a word about medullary sponge
stage the liver is normal in size or enlarged with kidney. The condition is characterized by cystic
a normal echotexture and a few cysts. Later dilations of the collecting tubules in the medullary
fibrosis sets in and the echotexture becomes pyramids. Stasis calculi form in these and may
patchy. Liver shrinkage continues with cause hematuria. The calculi may be picked up
deteriorating liver function and the child by ultrasound as nephrocalcinosis. The IVU is
succumbs to hepatic failure rather than renal specific and shows an enlarged papilla with tiny
failure. calculi resembling a bunch of grapes.
Medullary cystic disease is another spectrum To sum up, ultrasound is the only
of inherited renal cystic disease where there is a investigation necessary to diagnose polycystic
reduction of renal parenchyma due to fibrosis. disease. Early dominant polycystic disease can
In ultrasound, the kidneys are either normal sized be followed up with serial scans. In medullary
or moderately reduced in size. Corticomedullary cystic disease also, ultrasound will be
differentiation is lost. Parenchymal echotexture confirmative except when cysts may be too tiny
is increased. Cysts are present in the medullary to be visualized. The kidneys are then contracted
region or in the corticomedullary area (Fig 5). as in any end stage renal disease.
CONGRATULATION
Dr.Bharat R Agarwal, Mumbai has been elected as the Honorary Secretary General of SIOP for a
period of 3 years (2006-2008). SIOP did not have a general secretary from any continent other than Europe
or North America in the past. This election of an Indian for the first time in the history of SIOP promises to
bring hope to a large pool of children with cancer from our region.
SIOP is the major global organization concerned with the issues of children and young people who
have cancer. The official name of this society is the Societe Internationale dOncologie Pediatrrique with
the acronym SIOP. It is also known by the English translation; namely, the International Society of Paediatric
Oncology (Website: www.siop.nl).
Beginning with a few members in the late 1960s, the Society has now grown to + 1,150 members living
and working all over the world. For the past 40 years it has brought together doctors of many different
disciplines to develop better care for this disease. SIOPs mission is to bring the best possible care for
children with cancer to the farthest corners of the globe. SIOP aims to bring together all of those concerned
with the care of children with cancer.
81
Indian Journal of Practical Pediatrics 2005; 7(3) : 254
PRACTITIONERS COLUMN
Nocturnal :
Soon after going to bed Post nasal drip , sinusitis
1AM to 3 AM Gastroesophageal reflux disease
3AM to 5AM Asthma
While arising in moring Bronchietesis, cystic fibrosis
Related to feeding Pharyngeal incoordination, tracheoesophageal
fistula, mass in hypopharynx
Winter / Rainy Season Allergic cough, reactive airway disease
Absent at night Psychogenic , habit tic
During exercise , crying , laughing Exercise induced, emotional stress induced
asthma
respiratory disorders. ACE inhibitors used in with any respiratory infections and activity but
treating hypertension causes exaggeration of disappears during quite breathing .
cough which is dry, throaty, nocturnal in supine
position, often leads to change in tone of voice . Foreign body aspiration is common in the
The reflex is mediated via alteration of age group of 1-5 years of age. One has to have
neurohumoral regulatory chains 8 . While high index of suspicion since nearly 40 percent
evaluating the child with persistent cough any of the time there is no history of foreign body
child shows any of the serious clinical finding as aspiration. Majority are vegetable foreign bodies
mentioned in Table 4 needs admission for proper like ground nut, arecanut, seeds, dal and melon
management9. seeds and often they are treated as asthma .
The possible causes for persistent cough fall Small infants who suck vigorously have
into five categories: Anamolies, aspiration, small aspiration and cough without producing
infection, tumors or allergic causes either in upper any pneumonia and they do thrive very well
airway, lower airway or parenchyma as in without any problem . They are grouped as
Table 5. fatigue aspiration10.
barking or honking nature, dry variety, isolated vocal cords during inspiration resisting in cough.
and explosive, significantly absent during sleep These children have a negative result in
and most noticeable when the child is under stress methacholine challenge study and normal
or when the attention is drawn to the cough. pulmonary function testing. Bronchoscopy
including upper airway examination for dynamic
The following are few findings of vocal cord movement can diagnose the laryngeal
psychoganic cough. Over protective parents, dyskinesia.
stress at school, not able to cope with school
work, sibling rivalry and parental comparison The physician should investigate in an
with other sibling. organized manner to arrive at or ruling out the
diagnosis.
Further personality analysis revealed that
attention seeking, psychological insecurity, The routine investigations are complete
unable to face competition, hypersensitivity to blood count, an erythrocyte sedimentation rate
criticism were some other causes. absolute eosinophil count, IgE level .
Sometimes laryngeal dyskinesia can mimic Eosinophils in the nasal smear and sputum
asthma or labelled as psychogenic cough . In this is a simple test indicative of allergic rhinitis and
situation there is paradoxic movement of the asthma respectively .
85
Indian Journal of Practical Pediatrics 2005; 7(3) : 258
Peak flow values before and after capacity by 20 percent can be diagnostic of cough
bronchodilators in older children compared with variant asthma.Chang AB has observed that
local standards will give additional information11. children with cough alone are usually less atopic
less responsive to usual challenge tests but more
Inspiratory and expiratory chest films are responsive to cough receptor challenge test with
needed to delineate foreign body in the lower capsaicin. There is a small group of children with
airway . Chest X-ray can be normal in 15-20% persistent cough who are non responsive to usual
of children with bronchial foreign body and is bronchodilator therapy, grouped under
61% of laryngeal and tracheal foreign body. Hypersensitive cough receptor syndrome12,13.
C.T.Scan is great help in identifying the Treatment
mediastinal and carinal lymph models .
In general, regardless of duration, a
In general, the investigations contribute only productive cough should not be suppressed.
8 percent in establishing the diagnosis. However a productive cough with hemoptysis or
Serological test does help in specific dry cough in influenza and convalescent phase
diagnosis. We need acute and convalescent phase of pertussis can be suppressed by central
serum to see the rising titre ;however in infectious antitussive agents . Treatment of persistent cough
mononucleosis single titre is sufficient. is summarized in Table 6.
PCR is the most sensitive test where The two most commonly used central
specific nucleic acid probes are used . antitussive agents are codeine and
dextromethorphan. Dextromethorphan will be a
When indicated, bronchial provocative substitute for opiates dependent individuals.
challenge tests can be done in a special research Dosage is similar to codeine, the safe close range
laboratory using histamine, methacholine, appears to be considerably higher than codeine.
exercise, hypertonic saline, cold air, distilled Diphenhydramine hydrochloride was considered
water and observing the drop in forced vital to be effective to some extent.
86
2005; 7(3) : 259
No improvement Improvement
87
Indian Journal of Practical Pediatrics 2005; 7(3) : 260
CME PROGRAMME
ON
PEDIATRIC DERMATOLOGY
AT
CHENNAI
ORGANIZED BY IAP - DERMATOLOGY GROUP
Date : 6th November, 2005
Venue : Savera Hotel, Chennai
Time : 9.00 am to 4.30 pm
Tentative : Eczema
Programme Infections
Drug reaction
Urticaria in children
Cutaneous markers of Genetic disorders
Fever with rash
Panel discussion - Life threatening dermatoses
Registration : Delegates - Rs. 300/-, PG students - Rs. 250/- (Certificate from HOD).
Send DD in the name of IAP Dermatology Group payable at Chennai.
Last date for registration on or before 15th October 2005.
No spot registration
Correspondence: Dr. C. Vijayabhaskar, Door # 4, Gandhi Street, SS Nagar Extension,
Thirumullivoyal, Chennai 600 062, Tamilnadu. Ph:044-28190032
Email:iapdermatology@yahoo.co.in
88
2005; 7(3) : 261
CASE STUDY
90
2005; 7(3) : 263
OBITUARY
Dr.N.Sundaravalli is one of the very few pediatricians with AB pediatrics to come back to
serve our nation in those days. She had contributed her service to the development of pediatrics,
Madras Medical College, ever since it was functioning at the Government General Hospital,
Chennai, as well as after moving in to the campus as separate institution, the Institute of Child
Health and Hospital for children. Dr.N.Sundaravalli, as an individual was a soft spoken, simple
to move with and kind hearted doctor. She had done yeomen service to the downtrodden by
virtue of her various positions in lioness club. She had been a key person in organizing health
check up and immunization camps in Tamilnadu and neighbouring states. She was promoting
research in Protein Energy Malnutrition, Infectious Diseases and Liver Disorders especially
Indian Childhood Cirrhosis. Her contribution along with Dr.V.Balagobalraju in the field of
Indian Childhood Cirrhosis in yester years is commendable. She was an active member of
Indian Academy of Pediatrics and was known all over India. She was the Executive Board
Member of IAP for the year 1976, 1980 and 1981. She was the President of IAP for the year
1986 and Ex-officio Member for the year 1987. She was one the popular presidents of IAP
elected from Tamilnadu. She was also conferred with FIAP. We pray the almighty to rest her
sole in peace.
91
Indian Journal of Practical Pediatrics 2005; 7(3) : 264
CASE STUDY
Fig.1-Well defined septated, left ovarian cyst Fig.2- Left ovary is normal. Previous cyst
measuring 3.4 by 2.8 cm is seen. Please note has completely regressed.
an additional small cyst within the cyst.
hormonal tests were requested. The serum T4 vaginal bleeding, her TSH was 3.2 mIu/ml and
was 0.80 g/dL (range-7.3 to 15.0), thyroid T4 was 12 g/dL (both normal).
stimulating hormone (TSH) was 41mIU/ml
(range-0.60-6.30), the serum follicle stimulating Discussion
hormone was 11.6 mIU/ml (range-<1 mIU/ml), Majority of ovarian cysts in the pediatric
the leutinising hormone was 0.55mIU/ml (range population develop as a result of perturbed
-<1 mIU/ml), the serum prolactin was 138 ngm/ hormonal stimulation of the ovary and are likely
ml (range-<20 ngm/ml) and serum estradiol (E2) to occur in the first year of life or around
was 57.50 pgm/ml (range-<20 pgm/ml). Thyroid menarche. The development of an ovarian cyst
antibodies were tested and found to be strongly at other times should raise suspicion of aberrant
positive. hormonal release as is seen in severe
The patient was started on 50 micrograms hypothyroidism 1 . In severe juvenile
of thyroxine per day. A repeat thyroid function hypothyroidism large multicystic ovaries may
test and ultrasound examination was performed develop in response to hormonal overlap from
after 6 weeks. The T4 was 12mcg/dl and the TSH or prolactin2.
TSH was 0.629mIU/ml (both normal). The
It is suggested that the pseudoprecocious
abdominal and pelvic ultrasound showed the size
puberty seen in girls with hypothyroidism occurs
of the uterus to be 4 by 1.8 cms, and the
because TSH shares a common alpha-subunit
endometrium was 1mm thick.
with the gonadotrophins, and this results in
The left ovary was normal and the cyst had hyperstimulation of the ovaries and cyst
completely regressed (fig.2). One year follow up formation. The second mechanism suggested for
showed that she had caught up growth in terms pseudoprecocious puberty is that the elevated
of her height, she has had no further episodes of TRH (Thyrotropin releasing hormone) drive
93
Indian Journal of Practical Pediatrics 2005; 7(3) : 266
Clinical experience in children shows that 6. Chitkara AJ, Singh JP, Khalil A, Mittal SK,
ovarian cysts usually regress without treatment Sharma D. Sexual precocity in primary
and are seldom associated with malignancy9. This hypothyroidism. Indian Pediatr 1986; 23(9):
case demonstrates the importance of assessing 737-740.
thyroid function in girls with cystic ovaries, and
awareness of this association can avoid 7. Dhanwal D, Tandon N. Isolated menarche and
multicystic ovaries in a 7 1/2 year girl with
unnecessary surgery and improve ovarian
hypothyroidism. Indian Pediatr.2001; 38(4):
preservation rates. 432-433.
Acknowledgment: We are grateful for the
8. Gordon CM, Austin DJ, Radovick S, Laufer,
valuable guidance by Dr.A.S. Kinnare for helping
MR. Primary hypothyroidism presenting as
with the ultrasonographic pictures. severe vaginal bleeding in a prepubertal girl.
References J.Pediatr.Adolesc.Gynecol. 1997; 10(1): 35-38.
1. Helmrath MA, Shin CE, Warner BW. Ovarian 9. Strickland JL. Ovarian cysts in neonates,
cysts in the pediatric population. Semin Pediatr children and adolescents. Curr Opin Obstet
Surg 1998; 7(1):19-28. Gynecol 2002; 14(5): 459-465.
94
2005; 7(3) : 267
PRACTICAL GUDIELINES
ON FLUID THERAPY
Second Edition by Dr. Sanjay Pandya - Nephrologist
*
* First, handy, (390 pages), practice oriented, user friendly,
complete book in simple language
* For quick reference and easy use, separate chapters on
fluid therapy in children
* Addition of New chapter on Total parenteral nutrition
* Provides easy approach to fluid, electrolytes, acid base
disorders and parenteral nutrition
* Essential for all paediatrician, PG students, ICUs and
Hospitals
*
Send draft of Rs. 285/- to Dr/ Sanjay Pandya HUF
payable at Rajkot, Samarpan Hospital,
Bhootkhana Chowk, Near ST, Rajkot (Gujarat) - 360 002
Mobil : 098250 79122 E-mail : fluidtherapy2002@yahoo.co.in
Distributor : Bhalani Medical Book House, opp. KEM, Parel, Mumbai - 400 012.
Name ..................................................................................................................................
Address ................................................................................................................................
...............................................................................................................................................
Signature
Subscription rate
Individual Annual Rs.300/- Send your subscription, only by crossed demand draft,
Ten Years Rs.3000/- drawn in favour of INDIAN JOURNAL OF PRACTICAL
PEDIATRICS, payable at Chennai and mail to
Institution Annual Rs.400/-
Dr.A.BALACHANDRAN, Editor-in-Chief, F Block,
Ten Years Rs.4000/-
No.177, Plot No.235, 4th Street, Anna Nagar East, Chennai
Foreign Annual US $ 50/- - 600 102, Tamilnadu, India.
97
2005; 7(3) : 269
Signature
Kinldy send your payment by crossed demand draft only drawn in favour of
Indian Journal of Practical Pediatrics and art work / matter to
MANAGING EDITOR
Indian Journal of Practical Pediatrics
IAP-TNSC Flat, Ground Floor,
F Block, Halls Towers,
56 (Old No.33), Halls Road,
Egmore, Chennai - 600 008. India
Phone : 2819 0032
Email : ijpp_iap@rediffmail.com
98
Indian Journal of Practical Pediatrics 2005; 7(3) : 270
Indian Journal of
Practical Pediatrics IJPP
Subscription Journal of the
Indian Academy of Pediatrics
Indian Academy
of Pediatrics
IAP Team - 2005 Kailash Darshan,
Kennedy Bridge,
Mumbai - 400 007.
President Karnataka
Dr.Raju C Shah Dr.M.Govindaraj
President-2006 Dr.Santosh T Soans
Dr.Nitin K Shah Kerala
President-2004 Dr.T.M.Ananda Kesavan
Dr..M.K.C.Nair Dr.M.A.Mathew
Dr.T.U.Sukumaran
Vice President Madhya Pradesh
Dr.Anoop Kumar Verma Dr.M.L.Agnihotri
Secretary General Dr.Chandra Has Sharma
Dr.Bharat R. Agarwal Maharashtra
Treasurer Dr.Pramod Jog
Dr.Deepak Ugra Dr.Rajendra V Kulkarni
Dr.Sandeep Bapu Kadam
Editor-in-Chief, IP Dr.Yashwant Patil
Dr.Panna Choudhury Manipur
Editor-in-Chief, IJPP Dr.K.S.H.Chourjit Singh
Dr.A.Balachandran Orissa
Dr.Gadadhar Sarangi
Joint Secretary
Punjab
Dr.A.K.Dutta
Dr.Harmesh Singh
Members of the Executive Board Rajasthan
Andhra Pradesh Dr.B.D.Gupta
Dr.V.Ram Narsimha Reddy Tamilnadu
Dr.P.Venkateshwara Rao Dr.D.Gunasingh
Assam Dr.K.Meer Mustafa Hussain
Dr.Garima Saikia Dr.P.Velusamy
Bihar Uttar Pradesh
Dr.Radha Krishna Sinha Dr.Ashok Kumar Rai
Chandigarh Dr.V.N.Tripathi
Dr.R.K.Marwaha Dr.Vineet K Saxena
Delhi West Bengal
Dr.Ajay Gambhir Dr.Debasis Biswas
Dr.Anupam Sachdeva Dr.Sukanta Chatterjee
Gujarat Services
Dr.Baldev S Prajapati Col.M.K.Behera
Dr.Satish V Pandya Presidents Spl. Representative
Haryana Dr.Rajesh Mehta
Dr.Dinesh Khosla A.A.A.
Jharkhand Dr.Tanmay Amladi
Dr.Brij Bhushan Sahni