Abstract
Post-hemorrhagic encephalopathy is a distinct clinical condition resulting from intraventricular hemorrhage (IVH) in premature infants. Nine neonates with IVH were studied to detect possible chronic encephalopathy. Serial CSF analyses revealed persistent xanthochromia but variable RBC (679-132xK/mm3) & WBC (0-3780/mm3) counts. Protein contents were elevated (>100 mg/d1) in 7 patients (61-2420mg/d1). Hypoglycorrhachia (CSF/blood glucose ratio< 0.35) occurred in 7 cases & CSF glucose was < 10 mg/d1 in 5. Hypoglycorrhachia was not secondary to persisting cellular elements in CSF, since no correlation existed between CSF glucose level & total cell count. In addition, in vitro incubation of cellular CSF with added glucose at 37°C led to negligible rates of glucose consumption over 24 hr. Three infants manifested gross hydrocephalus documented by CAT scanning. CSF lactate in these 3 infants was increased 1-3 fold (2.3-5.5 mmol/1) above levels in non-hydrocephalic IVH neonates (1.1-1.6 mmol/1) & in patients with congenital (non-hemorrhagic) hydrocephalus (1.0-1.4 mmol/1). We speculate that IVH occurs concurrently with periventricular brain ischemia which, in turn, leads to focal anaerobic glycolysis & increased glucose requirement. With inadequate cerebral glucose delivery from blood, glucose diffuses into brain from CSF resulting in hypoglycorrhachia. Cerebral lactate production is enhanced but lactate accumulates in CSF only in the presence of an obstructed ventricular system. These metabolic alterations merit consideration of therapeutic intervention.
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Dubynsky, O., Vannucci, R. & Maisels, M. 1123 POST-HEMORRHAGIC ENCEPHALOPATHY IN PREMATURE INFANTS. Pediatr Res 12 (Suppl 4), 551 (1978). https://doi.org/10.1203/00006450-197804001-01129
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DOI: https://doi.org/10.1203/00006450-197804001-01129