SUMMARY The detection of the onset of intraventricular haemorrhage (IVH) during life is a necessary preliminary to understanding the cause of this condition. In 10 infants of very low birthweight treated with serial transfusions of adult blood the proportions of transfused cells circulating after each transfusion were compared with the proportion of transfused cells found in the intraventricular clot at necropsy. This allowed the timing of IVH to be restricted retrospectively to the period between consecutive blood transfusions. In addition, the proportional changes of transfused cells produced by infusion of a known red cell mass allow changes in the babies' original red cell mass to be followed during life. A fall in this value occurred in 8 infants dying with IVH and was taken to indicate haemorrhage. Comparison of the two methods in 9 infants suggested that, while in some cases intraventricular bleeding occurs rapidly, in others it takes place over a period of time. The interval between birth and the onset of haemorrhage was directly proportional to the gestational age of the infant.

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SUMMARY Continuous measurements of arterial pressures, heart rates, respiratory movements, and respiratory rates were made from birth in 44 infants at risk from intraventricular haemorrhage (IVH). 17 babies died with IVH, in 10 of whom the event was timed objectively. Events in these babies were compared with survivors of similar birthweights, gestational ages, severity of birth asphyxia, and severity of hyaline membrane disease (HMD). IVH followed severe HMD and was associated with cessation of the babies' own respiratory efforts while on a ventilator and also with characteristic cardiorespiratory events. The minimum arterial pressure before IVH was lower than in comparable babies who survived. It is suggested that fluctuations of systemic blood pressure from initial low levels may be important in the pathogenesis of IVH. It is possible that changes in cerebral blood flow are of even greater significance.

Micropenis is an important sign in neonates, since it may be the only clue to the diagnosis of panhypopituitarism, a potentially lethal but eminently treatable condition. Case reportsCase 1-A boy infant was delivered at 37 weeks' gestation after an uncomplicated pregnancy. Birth weight was 2200 g. He was asphyxiated and successfully resuscitated but remained hypotonic. Jaundice developed on the third day of life and persisted. At 3 weeks of age hypothyroidism was diagnosed (plasma thyroxine concentration 54 nmol/l (4-2 /ig/lOO ml), thyroid stimulating hormone concentration 8-5 mU/l). Despite thyroxine replacement he failed to thrive and developed abdominal distension and vomiting. Laparotomy showed milk curd obstruction of the small intestine, and postoperatively he was ventilated for three days. Twelve days later he collapsed and had a hypoglycaemic convulsion. For the next three months he was fed intravenously and became hypoglycaemic when attempts were made to restart oral feeds. At the age of 4 months the diagnosis of hypopituitarism was suggested because of his micropenis. During a hypoglycaemic episode (blood glucose concentration 10 mmol/l; 18 mg/100 ml) the plasma cortisol value was noted to be low at 100 nmoll1 (3-6 Ag/lOO ml) and concentrations of both plasma

SUMMARY Neurological symptoms in hypertensive subjects may be a reflection of intracranial vascular disease and not just a consequence of hypertension. Two hypertensive children with renovascular disease, neurological symptoms, and severe cerebral arterial disease were treated by extracranial-intracranial arterial bypass surgery with improvement of symptoms and easier control of blood pressure. Where revascularisation surgery is appropriate, this should be undertaken before neurological complications arise.Renal arterial disease may reflect more widespread arterial disease including that in intracranial vessels.' This association is not widely recognised, but is important as neurological symptoms may otherwise be attributed erroneously to the effect of the hypertension alone.Identification of cerebral abnormalities in these patients has implications, not only because of the possibility of specific treatment for stenosed areas, as in the two children we report, but also because lowering their blood pressure may lead to cerebral ischaemia, and hence permanent neurological damage. We report two children with severe hypertension secondary to renal arterial disease, both of whom had symptoms or signs suggestive of intracranial involvement. The difficulties experienced in management and the importance of timing of surgical intervention in the treatment of the cerebral arterial abnormalities is stressed. After three years both grafts are pulsatile, he has had no further neurological problems, and his rate of growth has been normal. His blood pressure is maintained at a level appropriate to his age (110/70 1177