Myelomeningocele: a risk factor for necrotizing enterocolitis in term infants.
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Biomedical subjects
Publications and source records attributed to J Hellmann.
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Pneumothorax has been associated with intraventricular hemorrhage in premature infants, although the mechanism for this relationship is not clear. Because alterations in cerebral blood flow are believed to be important in the pathogenesis of intraventricular hemorrhage, the effect of induced pneumothorax and subsequent evacuation on the cerebral circulation in 16 newborn dogs was evaluated. Continuous Doppler ultrasound was used to monitor changes in cerebral blood velocity. Pneumothorax was induced by slow infusion (5 cc/kg/min) or rapid infusion (5 to 10 seconds) of air to reduce mean arterial blood pressure to half of base-line levels. Both methods of pneumothorax induction resulted in significant elevations of central venous pressure and intrapleural pressure, whereas mean arterial blood pressure and cerebral blood velocity decreased significantly. In each group, the pneumothorax was evacuated either by slow withdrawal of air (10 cc/kg/min) or as rapidly as possible. Rapid evacuation of air resulted in an immediate increase in mean arterial blood pressure and cerebral blood velocity to supranormal levels. Slow evacuation led to a more gradual normalization of mean arterial blood pressure and cerebral blood velocity. It is suggested that the precipitous increases in mean arterial blood pressure and cerebral blood velocity following rapid evacuation of a tension pneumothorax may account for the observed association between pneumothorax and intraventricular hemorrhage in premature infants.
A technique employing a Doppler ultrasound probe to measure cerebral blood velocity was used to study the cerebral circulation continuously in 30 newborn mongrel dogs. Utilizing a transfontanelle approach, the probe was maintained in fixed position throughout a given experiment. In 20 animals, changes in systolic, diastolic, and mean cerebral blood velocity during hypo- and hypercarbia were directly correlated (P less than 0.01) with changes in regional cerebral blood flow (rCBF) determined in 12 regions of the brain by the [14C]iodoantipyrine autoradiography technique. In an additional 10 dogs, multiple determinations of systolic, diastolic, and mean blood velocity were made over a wide range of PaCO2 values and found to be directly related to the PaCO2 (P less than 0.001). These data suggest that changes in cerebral blood velocity are closely related to changes in cerebral blood flow. We also calculated the pulsatility index (PI) from the peak systolic and end diastolic velocities and found a poor, but direct (r = 0.28, P less than 0.05) relationship between the PI and PaCO2 rather than the indirect relationship, which has been suggested in published clinical studies. We conclude that the Doppler technique may be valuable in monitoring dynamic events of the neonatal cerebral circulation if a constant probe position is maintained. Our results suggest, however, that the PI is not a reliable index of cerebral vascular resistance.
The arteriovenous difference (A-V) method was utilized to assess the permeability of the blood-brain barrier to lactic acid in paralyzed and artificially ventilated newborn dogs. A femoral artery and the sagittal sinus were cannulated to sample arterial and cerebral venous blood simultaneously for measurements of glucose and lactate during normoglycemia, normoglycemia and hyperlactatemia insulin-induced hypoglycemia, or hypoglycemia and hyperlactatemia. During normoglycemia, arterial lactate concentrations remained less than 2 mmoles/liter for up to 2 h; mean A-V lactate was essentially zero. Arterial lactate increased up to 8 mmoles/liter during intravenous infusion of neutralized 10 mM L-lactic acid. During hyperlactatemia, the A-V lactate was directly proportional to the arterial concentration of the metabolite, a finding which is consistent with transport into brain either by simple diffusion or via a carrier with saturability greater than 8 simple diffusion or via a carrier with saturability greater than 8 mmoles/liter. During hypoglycemia (mean arterial glucose=27 mg/dl), A-V glucose was reduced by 71% with a significant increase in A-V lactate at an arterial lactate level of 1.3 mmoles/liter. Hyperlactatemia combined with hypoglycemia resulted in A-V lactate which was 2-3 fold greater than during normoglycemia at similar arterial lactate concentrations. Brain/blood lactate ratios declined by 83% during hypoglycemia compared with normoglycemic ratios, indicating that, once in brain, lactic acid was actively consumed for oxidative processes. These experimental observations may have clinical relevance in newborn human infants when concentrations of lactate in blood often approach or even exceed those of glucose.
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A total of 120 computed tomographic scans of the brain in premature and full-term infants were reviewed. Of these, 28 were judged to exhibit normal ventricular dimensions, and the bifrontal, bicaudate, and bioccipital indices of the lateral ventricles were determined. The bifrontal and bicaudate indices followed a Gaussian distribution, with mean values of 0.28 +/- 0.07 (SD) and 0.15 +/- 0.03 (SD), respectively, whereas the bioccipital index was uniform in its distribution (range, 0.13 to 0.26). For comparison, corresponding indices were determined in scans of ten infants with clinical evidence of hydrocephalus. Based on these data, guidelines are suggested to distinguish normal and abnormal ventricular dimensions in newborn infants.
Survivors of perinatal intraventricular hemorrhage often develop a distinct clinical syndrome characterized by hydrocephalus and biochemical abnormalities in cerebrospinal fluid. The authors investigated six neonates with post-hemorrhagic obstructive hydrocephalus in order to identify cerebral metabolic disturbances responsible for the hypoglycorrhachia observed in this disorder. Lactic acid concentraions and lactate/pyruvate ratios in ventricular fluid were significantly elevated in infants with post-hemorrhagic hydrocephalus compared with the values in five with congenital (non-hemorrhagic) obstructive hydrocephalus. Comparable degrees of ventricular dilatation and intracranial hypertension were present in the two groups. There is evidence that neither residual cellular elements in ventricular fluid nor a disrupted blood-CSF barrier can fully explain the observed alterations in ventricular-fluid glucose, lactate or lactate/pyruvate ratios. It is suggested that when periventricular hemorrhage occurs, the associated cerebral ischemia leads to focal anaerobic glycolysis and increased glucose requirement. With inadequate cerebral glucose glycolysis and increased glucose requirement. With inadequate cerebral glucose delivery from the blood, glucose diffuses into the brain from the ventricular fluid, resulting in hypoglycorrhachia. Cerebral lactic acid production is enhanced, which accumulates in ventricular fluid in the presence of ventricular obstruction.
Two cases of neonatal septicaemia due to group G streptococci (Streptococcus canis) are described. In one patient, infection coexisted with transient neonatal hyperthyroidism, while, in the other, concomitant group G streptococcal septicaemia and endometritis in the mother was seen. Group G streptococci are rare causes of infection, especially in the paediatric age group. Bacteria were identified by serological and biochemical methods. Both neonates responded well to penicillin therapy, but the maternal infection required combination therapy with penicillin G, gentamicin, and chloramphenicol. The literature on systemic group G streptococcal infection is briefly reviewed. With increasing use of serotyping in the identification of beta-haemolytic streptococci, non-group A organisms will probably be identified more frequently from neonatal and other infections.