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A 10-year-old girl with a lumbosacral myelomeningocele, managed withclean intermittent catheterization, presented with headache, vomiting, and lethargy. The cerebrospinal fluid (CSF) and urine cultures revealed Escherichia coli , documented to be the same subtype. The organisms were subtyped and the E. coli from both the urine and CSF were noted to be of the same strain. Management consisted of intravenous antibiotics and ultimate replacement of the ventriculoperitoneal shunt. Children with myelodysplasia and CSF shunts should be carefully monitored in a multidisciplinary fashion to anticipate, correctly diagnose, and treat CSF shunt infections associated with bacteriuria.

Hypoxanthine, the end product of purine metabolism, is usually very elevated in body fluids during severe hypoxia. We measured hypoxanthine in the cerebrospinal fluid of hydrocephalic preterm infants (12 with posthemorrhagic, one with congenital hydrocephalus) to determine whether hydrocephalus is associated with anaerobic metabolism of brain tissue. Cerebrospinal fluid hypoxanthine was undetectable in normal infants. In hydrocephalic infants, the concentration of hypoxanthine ranged from 7.5 mumol/L to 28 mumol (means = 14.3 mumol/L). The hypoxanthine concentrations fell from a mean of 12.8 mumol/L to a mean of 2.0 mumol/L (P less than 0.05) with successful treatment of the ventriculomegaly by lumbar puncture or by ventriculoperitoneal shunt. Patients with acute posthemorrhagic hydrocephalus had similar concentrations of hypoxanthine (means = 14.5 mumol/L) as patients with late or with congenital hydrocephalus (means = 13.8 mumol/L), indicating that brain hypoxia is probably a consequence of the ventriculomegaly and not of the hemorrhagic insult.

Albino rabbits with a cryogenic lesion to the left parieto-occipital cortex had cerebral blood flow studies (CBF) with the hydrogen clearance technique 24 hours after the insult. Similar subgroups were treated with DMSO (1 g/kg) bolus, DMSO (2 g/kg) infusion, indomethacin (20 mg/kg) bolus, and indomethacin followed by DMSO. Following DMSO bolus administration there was an immediate rise in CBF over both hemispheres, with a significant paradoxical decrease at 30 minutes, followed by a second smaller rise at 60 minutes. With DMSO infusion, the rise in CBF was sustained throughout the infusion period with no paradoxical decrease. With indomethacin there was an initial decrease immediately following the drug, and at 60 minutes there was a rise in the insulted left hemisphere, more than the right one. Indomethacin administration 15 minutes prior to DMSO failed to halt the immediate increase in CBF noted following DMSO bolus injection. These results, together with the changes that occurred in intracranial pressure and brain water content, are analyzed.