Neonatal Neurologic Damage after Dehydration
Article Outline
In this issue of The Journal, Escobar et al1 present a study of neurologic damage from an episode of dehydration in term neonates. They have found no increase in neurologic damage from a carefully selected control group of infants without dehydration.
See related article, p 127
Neurologic damage secondary to dehydration occurs in one of two ways; there can be circulatory shock with hypoxic damage, or a hypernatremic state with cerebral hemorrhage and sometimes thrombosis. The shock variety is most often seen after massive water and electrolyte losses from diarrheal disease; the hypernatremic variety has also been mostly seen in diarrheal disease in which fluid intake has been prevented by vomiting. In this latter group, this rise in sodium chloride concentrations can be rapid. In some studies, neurologic damage in the hypernatremic dehydration of diarrheal disease was 4 times more likely than from isonatremic dehydration after enteritis.2, 3, 4
In the neonates reported by Escobar et al, there was no enteritis. The patients had development of hypernatremic dehydration by lack of fluid intake without concomitant pathologic losses. This problem for neonates has increased in the last two to three decades as breast-feeding has increased by mothers who frequently have not had adequate support or training. Some mothers who are having trouble initiating breast-feeding often do not recognize the degree of dehydration in their infants that will be of the hypernatremic variety because, although intake is low, water is lost through skin and lungs without the loss of electrolytes. This process will be gradual as opposed to the more abrupt process in which water curtailment is accompanied by enteric losses. The findings of Escobar et al have three probable bases: 1) Rate: When the increase in sodium chloride concentration is gradual, the capillary dilation that gives rise to rupture and hemorrhage is less likely because of the CNS internal volume and pressure adjustments; 2) Pressure: The open fontanelle and soft bony skull may compress reducing the negative pressure seen when the skull is rigid. With the rigid skull in older children or adults, the shrinking brain and sustained blood pressure gives rise to capillary dilation and subsequent hemorrhage; and 3) Population: As the authors point out, the population studied had complete medical insurance, a relatively high educational level, and assess to strong support services.
Other populations might be more vulnerable. Thus it is no surprise that no increase in neurologic damage was found in the neonates studied by Escobar et al. Nonetheless, it is important that this is documented, and it is reassuring that the findings indicate that the dehydration associated with the early days of breast-feeding are not likely to lead to permanent neurologic damage.
References
PII: S0022-3476(07)00328-9
doi:10.1016/j.jpeds.2007.03.061
© 2007 Mosby, Inc. All rights reserved.
Refers to article:
- Five-Year Neurodevelopmental Outcome of Neonatal Dehydration
