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SUMMARY Little is known about the effects of hyperoxia on the cerebral circulation of human infants. Using duplex Doppler we measured the changes in cerebral blood flow velocity in a group of full term (n=15) and premature infants (n=17, median gestational age 31 weeks) in response to a transient threefold increase in oxygen tension. Measurements of blood gas tensions as well as blood pressure and cerebral blood flow velocity were made over a period of 20 minutes on three occasions for each infant; during normal oxygenation, hyperoxia, and normal oxygenation. There was a fall in cerebral blood flow velocity in 15 of the 17 premature infants with hyperoxia and the median reduction was 0-06 cm/second for every 1 kPa increase in oxygen tension. There was no significant change in either PCO2 or blood pressure during the period of hyperoxia. The cerebral blood flow velocity fell in all 15 infants born at full term during hyperoxia, but there was a simultaneous and significant reduction in PCO2 at the same time as the hyperoxia. Analysis of variance suggested that in the infants born at full term the change in carbon dioxide had most effect in the reduction of cerebral blood flow velocity, rather than the hyperoxia itself. We conclude that in premature infants, cerebral vascular resistance may be altered by a fall in cerebral blood flow velocity in the presence of hyperoxia.Hyperoxia has a consistent and predictable effect on cerebral blood flow in healthy adult brains. Little is known, however, about the effect of hyperoxia on cerebral blood flow in newborn infants, although oxygen is commonly used to treat lung disease in this population. Periods of prolonged hyperoxia cause vasoconstriction of the neonatal retinal circulation (which arises from the internal carotid artery) and so would also be expected to have a similar effect on the cerebral circulation. Whether the central nervous system of the extremely premature newborn infant is also sensitive to the effects of hyperoxia is unknown.We report the use of duplex Doppler ultrasound to study the physiological effect of extremely short periods of hyperoxia on the cerebral circulation in healthy and ill infants born prematurely and at full term. Methods

ABSTRACT. Little is known about the vasoactivity of cerebral arterioles in extremely premature infants. We have assessed the effects of a small rise in PaCOz of 1 kPa (7.5 rnm Hg) on cerebral blood flow velocity measured by duplex Doppler ultrasound. Nineteen mechanically ventilated infants of 33 wk gestational age or less in whom direct arterial blood pressure monitoring was available, were studied on 45 occasions. There was a close relationship between increasing PaC02 and increasing cerebral blood flow velocity ( p < 0.005) but on seven of 45 occasions

SUMMARY The case notes of 20 infants with hyperkalaemia (defined as two successive serum potassium measurements of >7-5 mmol/l) were reviewed. The incidence of hyperkalaemia was also looked at in an unselected population of 200 low birthweight infants. The mean gestational age of the 20 affected infants was 29 weeks and the mean birth weight 1235 g. The incidence of hyperkalaemia in the cohort of 200 infants weighing less than 1500 g at birth was 3-5%. Hyperkalaemia was associated with a high incidence of cardiac arrhythmia (60%), impaired renal function (50%), and changes on cerebral ultrasonography (88%). Hyperkalaemia responds slowly to conventional treatment with dextrose, insulin, and exchange resins. There is a close temporal relation in some infants between hyperkalaemia and cardiac arrhythmias and periventricular leukomalacia, suggesting a causal association.There are little published data on the incidence and consequences of neonatal hyperkalaemia. It is known to cause cardiac arrythmias, -4 and recent evidence suggests that increased potassium concentrations in cerebrospinal fluid or brain parenchyma may cause spasm of the intracerebral arteries.5 Both these factors could impair the neonatal cerebral circulation.We looked at the incidence of hyperkalaemia in an unselected population of very low birthweight infants (n=200), and reviewed the case notes of 20 infants known to have had hyperkalaemia to estimate the incidence of cardiac arrhythmia, renal impairment, and cerebral abnormality.

SUMMARY Thirty‐four fullterm infants with postasphyxial encephalopathy (PAE) were studied with ultrasound to assess cerebral blood‐flow velocity (CBFV). A control group of 126 healthy infants also had CBFV recordings during the first week of life. Measurements for the majority of the asphyxiated group fell into two abnormal patterns in relation to the control group: four had low CBFV (<2 SD below the mean) and 17 had high CBFV (≥2 SD above the mean); all had severe PAE. Median age at the first high measurement was 26 hours. There were no statistically significant differences between infants with normal and abnormal CBFV in measurements of PaCO2 or mean arterial blood‐pressure. A Pourcelot Resistance Index (PRI) < 0·55 was common in the presence of high CBFV, but never seen with low measurements. 21 of the 34 infants died of their asphyxial insult and four of the survivors have severe cerebral palsy at a median age of two years. Three of the four with low CBFV died, and no infant with CBFV >3 SD survived without severe impairment. The positive predictive value of CBFV measurements < 2 SD or > 3 SD for death or severe impairment is 94 per cent, compared with 83 per cent for low PRI alone. The authors believe that high CBFV is the result of vasoparalysis of cerebral arterioles and that it represents a form of irreversible cerebral injury. RÉSUMÉ Asphyxie sévère à la naissance et Vitesse anormale du flux sanguin cérébral Trente quatre nourrissons nés à terme, avec encéphalopathie post‐asphyxique (PAE) ont béfnéié d'une mesure d'ultrason pour apprécier la vitesse du flux sanguin cérébral (CBFV). Un groupe contrôle de 126 nourrissons en bonne santé ont également bénéficié d'enregistrements CBFV durant la première semaine de vie. Par comparaison avec le groupe contrôle, les mesures de la majorité du groupe des asphyxies se présentaient sous deux aspects: quatre présentaient des CBFV bas (plus de deux écarts types au dessous de la moyenne); tous avaient eu une PAE grave. L'âge médian pour la première mesure élevée de 26 heures. II n'y avait pas de différence significative entre les enfants avec CBFV normales ou anormales dans la mesure de la PaCO2 et la pression artérielle moyenne. Un index de résistance de Pourcelot (PRI) inférieur à 0,55 était habituel dans les cas de CBFV élevées, mais jamais avec les CBFV basses. 21 des 34 nourrissons moururent des suites des lésions asphyxiques et quatre des survivants présentaient une IMC grave à l'âge moyen de deux ans. Trois des quatre nourrissons avec CBFV bassesf moururent et il n'y eut aucun survivant sans infirmité sévère pour les CBFV supérieures à trois écarts‐types. La valeur prédictive de mesures CBFV < 2 SD ou >3 SD pour la mort ou l'infirmité grave fut de 94 pour cent, comparée aux 83 pour cent d'un PRI bas isolé. Les auteurs pensent qu'une CBFV élevée est le résultat d'une paralysie vasomotrice des artérioles cérébrales et qu'elle traduit une forme de dommage cérébral irréversible. ZUSAMMENFASSUNG Schwere Asphyxie bei der Geburt und abnorme cerebrale Durchblutungsges...