Abstract 1731
Persistent apnea and bradycardia is a common problem in prematurely born infants when they reach term and are ready to be discharged home. There is controversy over the management of those infants and, moreover, there is little information concerning the risk of brain damage following repeated apnea and bradycardia. The aim of our study was to determine whether prolonged apnea, with or without bradycardia, could cause neuronal damage in brain areas known to be vulnerable to hypoxia-ischemia. We used chronically instrumented piglets at 1 (n=3), 2 (n=6), and 4-5 (n=3) weeks of age. Three consecutive apneic episodes were induced at 30 min intervals by the IV administration of propofol (20 mg/kg) either in 4 consecutive doses of 5 mg/kg (apnea alone) or in slow bolus (apnea and bradycardia). The episodes were ended after an apnea of 60 sec by stimulation or artificial ventilation (as needed). The following brain regions were examined 24-48 hours after the apneic episodes: watershed area (parasaggital cortex), hippocampus, and brainstem. 5µm paraffin sections were stained with hematoxilin-eosin. We used the following criteria for the identification of damaged neurons: increased cytoplasmic density (eosinophilia), indistinct nuclear-cytoplasmic boundaries, and retracted cells. At all ages, when bradycardia and/or hypotension were present, there was evidence of neuronal damage in the watershed area, in CA4 and/or CAl of the hippocampus and the subiculum. There was no consistent involvement of the brainstem. The age-matched control animals, and the animals having had only apnea did not show evidence of neuronal damage in those areas. We conclude that the occurrence of prolonged apnea with bradycardia leads to neuronal damage in vulnerable brain regions in young piglets. Apneic episodes accompanied with bradycardia in infants might then have the potential to induce significant brain damage, especially if the events are associated with hypotension. This deserves further investigation because measurement of blood pressure is rarely a component of continuous monitoring in those infants.
