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Efficacy of clonidine in hyperammonemia induced hyperexcitability syndrome

and patient was discharged home a week later. Because of the large head, a pressure gradient exists between the heart and the veins of the head in infants predisposing them to VAE (1). We hypothesize that the sudden decrease in raised ICP upon CSF drainage led to rupture of a bridging vein or emissary veins, resulting in venous air embolism (VAE). The reappearance of signs of air embolism after the reintroduction of nitrous oxide was probably because of the expansion of the air which was still present in the circulation (2). Change in position from supine to prone might have played a role in the recurrence of VAE symptoms as well. The change in position could have caused the air bubbles present in the upper part of the right atrium to have floated into the right ventricular out flow tract and subsequently to the pulmonary arteries and pulmonary arterioles producing the symptoms of the second VAE. As compared with hypoxia, tachycardia and hypotension are the most common initial signs of VAE (3). An episode of VAE severe enough to cause hypoxia is likely to be preceded by hemodynamic instability, which was conspicuously absent during the first episode. We suspect pulmonary hypertension following air entrainment resulted in shunt reversal causing hypoxia. Absence of tachycardia and hypotension during the first episode was most likely because of the preservation of sufficient blood flow from right to left atrium preserving adequate cardiac output (4). During the second episode of VAE, the occurrence of hypoxia preceding fall in EtCO2 was most likely because of the persisting pulmonary hypertension. Readministration of the nitrous oxide at this stage aggravated the preexisting pulmonary hypertension resulting in the reappearance of the right to left shunt before the increase in dead space. In presence of right to left shunt, fall in EtCO2 normally seen with VAE, may be absent due to the relatively well preserved left heart filling (4). PFO is very common in newborns and infants (5). Our case emphasizes that because of the high prevalence of PFO in newborn and infants, the signs of VAE in this group may be unusual and a high index of suspicion is needed for timely diagnosis. The increased chance of shunt reversal following hypoxia, hypercarbia, and acidosis predisposes them to the development of paradoxical air embolism with grave consequences. In light of this experience, we also caution the readers against the reintroduction of N2O when a VAE has been suspected earlier, even when all symptoms have abated.