Friday, April 24, 2015

Thompson Scoring in HIE : Severity and Prognostic grading

Thompson Score 


Score                  0                  1                                2                                     3
Tone              normal            hyper                           hypo                          flaccid
LOC                normal         hyper alert, stare       lethargic                        comatose
Fits                 none              < 3 per day                 > 2 per day
Posture         normal            fisting, cycling            strong distal flexion       decerebrate
Moro              normal          partial                        absent
Grasp             normal          poor                          absent
Suck              normal           poor                          absent ± bites
Respir            normal          hyperventilation         brief apnea                     IPPV (apnea)
Fontanel       normal            full, not tense               tense              













Maximum Score = 22
Infants scoring 1–10 are considered to have
mild HIE, 11–14 have moderate HIE and
15–22 are considered to have severe HIE

Thompson CM, Puterman AS, Linley LL, Hann FM, van der Elst CW, Molteno CD, Malan AF. The value of a scoring system for hypoxic ischaemic encepha­lopathy in predicting neurodevelopmental outcome. Acta Paediatr 1997; 86: 757-61

Tuesday, April 14, 2015

Case of Cyanotic CHD : PGE1 saves life

A Single Male baby was born at 38 weeks of gestation with birth weight of 3.1 kg through Normal vaginal delivery. At birth the child cried immediately. At 15 minutes of life, the child had central cyanosis. There was no respiratory distress and heart rate was normal range.

Child was shifter immediately to NICU. Saturation was 70% and with oxygen reached up to 84%. On auscultation, chest was normal and there was a faint murmur on heart auscultation. Hyperoxia test was also performed, the baby failed the test.

Immediately Echo screening was done to see if there was any duct dependent circulation. ECHO showed large VSD with over-riding of Aorta with severe pulmonary stenosis. PDA was seen with 

Left to right shunt measuring 3mm. It was case of TOF with PDA (Duct-dependent ) as baby had severe PS.

Chest Xray was ordered. Xray showed oligemic lung fields with upturned apex of cardiac silhouette. 
In any scenario, Prostene would have been started but since ECHO showed patent PDA, it was with holded and monitoring was planned. On the second day, the baby was deteriorating, saturation was not maintained, reached upto 60%. Generally SpO2 above 75% is adequate for Cyanotic heart diseases. ECHO was reassessed and PDA was still patent at 2-3mm.  The desaturation was not explained by CHD. So child was kept under CPAP and finally intubated for drop in saturation.

After intubation, the problem was the SpO2 got worse to 30-40%. Since cardiologist was at the spot, reassessment was done with ECHO. PDA was patent with 2 mm size. A trial of PGE1-Prostene was given.
After 5 minutes the SpO2 came to 60%, heart rate improved from 100 to 120 and by 10 minutes SpO2 was 87% under MV and baby looked much better.


It was a case of closure or narrowing of PDA in duct depended circulation. The child was saved by PGE1 which keeps the PDA open, until the definitive management- BTS Blalock Taussing Shunt.

Saturday, February 21, 2015

Final MD Past Questions in Pediatrics, IOM

Either I was too lazy to type or wanted it like this, here are the past papers of MD pediatrics collection. Hope this will be helpful.

Thursday, February 5, 2015


The perfect smile on a parent’s face rotates to a frown when they are informed that their child may have less number of teeth than normal. The total number of teeth in the primary dentition is 20 and that in the adult dentition is 32. The parents may not be more worried about losing a tooth to dental decay than they are to know that the teeth are missing congenitally. So when we break the news to parents about these missing teeth, they question …Where? When? How? And now what?

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Dental Terminologies:
  • Hypodontia: 1 to 6 teeth missing
  • Oligodontia:more than six teeth missing
  • Anodontia: complete absence of teeth

How common is it?
Congenitally missing teeth are one of the most common dental findings and is even more common than having extra tooth. It is reported to vary from 2.6 to 11.3% (excluding third molars) in permanent dentition. It is more commonly seen in permanent dentition and only about 0.5 to 0.9% baby tooth may be missing.

GENETIC: The cause may be genetic and the condition may run in the family. Studies have shown that in many cases, multiple genetic and environmental factors act together.
SYNDROMIC: in certain cases it may be found clubbed other medical conditions in the form of a syndrome. E.g. Down’s syndrome, Ectodermal dysplasia
The most common permanent teeth to be congenitally missing are:
  • Wisdom Teeth
  • Second Premolars
  • Upper Lateral Incisors
  • Lower Central Incisors

In the developmental phase of child (up to the age of 15 to 16 years) the missing tooth space is maintained by giving removable or fixed partial space maintainers are given and no permanent treatment is done
Permanent treatment is as follows:
Replacement of the missing teeth can be done by removal dentures, fixed partial dentures (bridge) or implants
  1. Removable Partial Denture is an appliance that can be put in and taken out of the mouth.  It consists of an acrylic plate that holds the missing teeth.
  2. Bridge: it uses two or three adjacent teeth for support and replaces the missing teeth. The missing as well as supporting teeth are given crowns which are interconnected like a bridge. 
  3. Implant: An implant replaces the missing tooth with a metal root like structure that integrates with the jaw bone and a crown is put on top for a natural tooth like appearance.

Congenitally missing teeth is not as rare as you may have guessed.  The causes are varied, but there are multiple treatment options available. So if you or your near ones are facing such a problem, please visit a dentist as soon as possible.

You can contact with your queries at

Dr. Parajeeta Dikshit is an Assistant Professor, Dept of Pedodontics and Preventive Dentistry (Pediatric Dentistry) at Kantipur Dental College teaching hospital and research center Basundhara , Kathmandu and Consultant Pediatric Dentist at Smile Square Dental Care Center, Maharajgunj, Kathmandu.

Sunday, January 11, 2015

Lung Surfactant and Factors affecting its maturation

Origin- Type II alveolar cells and Lamellar bodies

Recycling- 90% is reprocessed, average time for turnover is around 10 hours.
CPAP can prevent excessive loss of surfactant drainage into airways by decreasing depth and length of respiration.

Phophatidylcholine ( 70-80%) and phosphatidylglycerol (5-10%)
Phosphatidylinositol, Phosphatidylserine,Phosphatidylethalomine - 10%
Other lipids- 10%, 2% surfactant lipids
Surfactant Proteins- SP-A, SP-B, SP-C, SP-D (5-10%)

Decreases surface tension of alveoli in Laplace equation ie P= 2 gamma/ r

Factors Affecting Surfactant maturation-

1. Glucocorticoids- Intrinsic cortisol accelerates surfactant maturation. Dexamethasone administered increases expression of beta-adrenergic receptors with resultant increase in surfactant production.

2.Beta- adrenergic Drugs- Terbutalline, Formeterol increase cAMP and increase production and secretion of Surfactant

3. Thyroid Hormones- T4 has enhancing property on lung maturation and surfactant secretion however, it does not cross placenta.

4.Prolactin is under study. However low prolactin has been seen in infants with RDS.

5.Epidermal growth factor- Has shown to increase SP-A and L:S ratio in non-human models.

6. Fibroblast pneumocyte factor- under study

7. Insulin- delays the maturation of alveolar type II cells and decrease production of saturated Phosphatidylcholine. It inhibits the expression of SP-A gene.

8, Testosterone- delays the lung maturation through its action on lung fibroblast.

Errors of Surfactant Metabolism-
Polymorphism of SP-A expression- predisposition to sever RSV infection and increase risk for BPD.
SP-B polymorhism- RDS 
SP-C deficiency- Interstitial Lung disease
SP-D- Alveolar accumulation of lipids and proteins.