Biomedical subjects
Publications and source records attributed to A G Whitelaw.
Four neonates who developed an intracranial haemorrhage antenatally are described. In two, there was a congenital deficiency of one of the clotting factors (factor V and factor X respectively) and two had neonatal isoimmune thrombocytopenia.
Mean arterial pressure (MAP) and heart rate (HR) were studied in 12 hypotensive preterm neonates given dopamine. A significant, although temporary, elevation in MAP (8 +/- 3 mm Hg; p less than .01) occurred in five neonates in response to 5 micrograms/kg.min, but an increase in MAP was found in all infants (11 +/- 6 mm Hg; p less than .01) when the infusion rate was doubled. This elevation was sustained only in five who previously showed some response to the slower infusion. HR was unaffected except for an increase of 22 +/- 12 beat/min (p less than .01) in the five showing sustained MAP elevation with 10 micrograms/kg.min. Dobutamine failed to raise MAP in the seven who relapsed, and refractory shock resulted. We conclude that time should not be wasted when starting dopamine at less than 10 micrograms/kg.min in hypotensive preterm infants, as lower rates are unlikely to produce a response and delay may cause further compromise.
A total of 22 infants of less than 31 weeks' gestation who were mechanically ventilated for a minimum of 12 hours for respiratory distress syndrome were studied. The coefficient of variation of direct systolic pressure was measured each minute from six to 36 hours of age and averaged per hour after birth with a microcomputer-based system of data collection. At the start of recording, the ultrasound scan appeared normal in each infant, but intraventricular hemorrhage developed in ten infants less than 36 hours of age. Twelve infants remained free of intraventricular hemorrhages. BP fluctuation was greater for a longer proportion of measured time in infants in whom intraventricular hemorrhage did not develop compared with those in whom it did develop P less than .05). These findings do not support a causal relationship between BP fluctuation and intraventricular hemorrhage within the range of coefficient of variation studied.
Between April 1980 and March 1986, 19 infants underwent cerebrospinal fluid (CSF) shunting procedures for post-haemorrhagic ventricular dilatation at the Hammersmith Hospital, London. A total of 58 shunt-related procedures have been performed on these children. The major perioperative complication was seizure activity (eight children). Postoperative complications included infection (12 shunts) and blockage (29 shunts). Prophylactic antibiotics failed to prevent shunt infection. The likelihood of the first shunt failing was significantly reduced by greater weight of the infant and lower CSF protein at surgery. Long-term outcome was poor: three have died and another four are quadriplegic with severe mental retardation. Only four children are developmentally normal. These outcomes cannot be related to the shunt surgery or its complications, but correlate best with pre-operative parenchymal brain-lesions, as shown on ultrasound scans.
Mean arterial pressure and intracranial pressure were measured serially in six infants with intracranial hypertension (intracranial pressure greater than 20 mm Hg), and cerebral perfusion pressure was calculated from their difference. Overall, mean arterial pressure increased with rising intracranial pressure at a mean rate of 0.20 mm Hg/mm Hg. This caused a fall in cerebral perfusion pressure with increasing intracranial pressure at a mean rate of 0.80 mm Hg/mm Hg overall, although cerebral perfusion pressure was well maintained in one infant. Thus the rise in blood pressure was usually insufficient to compensate for the increase in intracranial pressure. In infants with acute encephalopathy vigorous blood pressure support is as important as lowering intracranial pressure.
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A comparison has been made between 39 infants with a birthweight of 1500 g or less and a bilirubinlevel of 240 mumol/l or above, born between January 1980 and December 1983 and 19 infants with the same criteria, born between January 1984 and December 1985. Eight of the 22 high risk and two of the 17 low risk infants were diagnosed to have sensorineural deafness (SND) during the first period and this was strongly associated with the duration of the hyperbilirubinaemia. During the second period, more active intervention for hyperbilirubinaemia led to an increased number of exchange transfusions and a marked drop in the mean duration of hyperbilirubinaemia (less than 240 mumol/l). None of the very low birth weight (VLBW) infants born in the second period have developed SND. To investigate the independent effect of hyperbilirubinaemia on hearing, six low risk infants with bilirubin levels less than 320 mumol/l were studied by serial auditory brainstem responses (ABR). Impairment of the ABRs was found in four infants, with further deterioration with the persistence of high bilirubin levels in two. Although recovery of hearing thresholds was noted in all infants with impaired ABRs, an absence of wave I was noted in three infants at 6 months of age, which could indicate damage to the auditory nerve-cochlear complex. These findings suggest that hyperbilirubinaemia in itself can have an adverse effect on hearing and that careful management of hyperbilirubinaemia may reduce the incidence of sensorineural deafness.
Ladd and Wright fontanelle pressure meters were applied to the heads of 18 babies, and simultaneously the intracranial pressure was monitored directly. Increasing the force with which the meters were applied caused a linear increase in registered fontanelle pressure. No universally optimal application force could be determined. To obviate this, application force was increased until the fontanelle pressure was calibrated with directly measured intracranial pressure. Subsequent variations in intracranial pressure were significantly correlated to fontanelle pressure, but not closely enough for clinical reliability. The correlation was similar if the meter was affixed instead directly to the scalp with collodion gel, and the clinical reliability improved. Applanation fontanometers are strongly affected by variations in the method by which they are applied and may not be a reliable reflection of intracranial pressure. If directly affixed to the scalp, however, they may yield clinically useful data.
Over a six-year period seventeen infants of birthweight less than 1,200 grams (including nine of birthweight less than 1,000 grams) underwent major gastrointestinal surgery. Fourteen of the seventeen (82%) survived, a higher rate than previously reported. Nine infants had necrotising enterocolitis, three had oesophageal atresia and five had other types of intestinal obstruction. Six infants who were unfit to be transferred to the operating theatre underwent surgery on the neonatal unit: of these, four survived. We feel the outlook is optimised by conservative surgical intervention and by maximal medical support with intensive care monitoring, post-operative mechanical ventilation and intravenous alimentation. Survival after surgery is now very much the rule in the extremely low birthweight infant, even in those who are too sick to be transferred to the operating theatre.
Computerised continuous measurement of mean arterial blood pressure (MAP) and serial cranial ultrasonography in 33 infants of less than 31 weeks' gestation showed that a MAP of less than 30 mm Hg for over an hour was significantly associated with severe haemorrhage, ischaemic cerebral lesions, or death within 48 hours. No severe lesions developed with a MAP greater than or equal to mm Hg.
To investigate cardiovascular effects in 32 ventilated neonates, given either pancuronium or pethidine, computer based data were analysed for five minutes preceding and for 20 minutes after administration of the drugs. Heart rate and direct mean arterial pressure remained unchanged but arterial pressure variability decreased with each drug.
Simultaneous assessment of intracranial pressure by anterior fontanelle palpation and direct measurement from a cerebrospinal fluid cannula showed that mean pressure was significantly different between 'soft' (5.4 mm Hg) and 'tense' (14.0 mm Hg) fontanelles, but with considerable overlap. Normal fontanelle tone was often confirmed, whereas clinical assessment of raised intracranial pressure was unreliable.
One hundred and twenty five measurements of arterial oxygen saturation (Stcao2) obtained with a transcutaneous pulse oximeter were compared with direct arterial oxygen tension (Pao2) in 13 preterm infants with predominantly fetal haemoglobin. Stcao2 of 86-92% corresponded to Pao2 of 5-13 kPa. Stcao2 above 92%, however, was sometimes associated with Pao2 above 13 kPa.
Lumbar CSF pressure (CSFP) was measured on 61 occasions, in 49 babies undergoing lumbar puncture as part of a septic screen, by means of Gaeltec pressure transducers. In normal circumstances, intracranial pressure (ICP) has the same value. Measurements were made when the baby was horizontal and quiet, with the head deflexed. For acceptance of the measurement, it was essential for the CSF to be clear and to show pressure pulses with respiration, heartbeat and jugular occlusion. The mean CSFP and standard deviation were 2.8 +/- 1.4 mm Hg (3.8 +/- 1.9 cm water), with a normal range of 0 to 5.7 mm Hg (0 to 7.6 cm water). This value is similar to previous reports of CSFP measured invasively in infants, but is much lower than the "ICP" established noninvasively. No relationship was found between birthweight, gestational age, current weight, postmenstrual age, or postnatal age and CSFP.
Post haemorrhagic ventricular dilatation occurs in a minority of newborn infants, but is associated with a high risk of cerebral palsy and developmental delay. Neither the relation of ventricular size to cerebrospinal fluid (CSF) pressure, nor the effect of CSF removal on prognosis, have been established. Normal CSF pressure measured at subarachnoid cannulation was mean (SD) 2.8 (1.4) mm Hg. Values were significantly higher in post haemorrhagic ventricular dilatation--9.1 (3.7) mm Hg when the ventricles were expanding, and 4.5 (2.4) mm Hg when they were static or contracting. No significant relation between head circumference and CSF pressure was found in this series. Raised CSF pressure is associated with progressive ventricular dilatation, and may contribute to the increased risk of neurological abnormality.
The transportation of seriously ill, extremely low birthweight (less than 1 000 g) infants with conditions requiring surgery can be hazardous. In two such infants, considered to be too ill to be transferred to the operating theatre, surgery was carried out on the neonatal unit. The outcome was good in both cases. Peri-operative management is described in detail.
A series of 29 newborn infants had been studied after intrapartum hypoxia defined as meconium aspiration, an Apgar score of less than or equal to 6 at 5 min or a peripheral blood pH of 7.2 or less after resuscitation. Two independent sets of techniques were used; one concerned with the critical system in hypoxic damage, the central nervous system, the other assessing the central biochemical events in hypoxia. Both sets of data were assembled, then graded separately and only then combined. In this way detailed neurological assessment has been combined with measurement of urinary excretion of the ATP metabolites, hypoxanthine and xanthine. The essential metabolic consequence of hypoxia is a reduction in the synthesis of the energy currency of cells, ATP. This is associated with an outflow of ATP metabolites from cells. The extent of neurological damage was related to the magnitude of the hypoxanthine and xanthine excretion; neither were closely related to the initial blood pH. Infants who were normal neurologically had normal oxypurine excretion. Infants with neurological abnormalities for less than 48 h had lower excretion than those who were abnormal for more than 48 h. The duration of abnormal oxypurine excretion after an acute episode of hypoxia was studied in two infants with respiratory distress and in two other infants with apnoeic attacks. Severe hypoxia was followed by abnormal oxypurine excretion for at least 40 h after an acute episode. It is justifiable to suggest that abnormalities of oxypurine excretion should indicate intrapartum hypoxia in newborn infants. This excretion should also quantify the metabolic damage.
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