Spectrum of outcome in infants with extreme neonatal jaundice.

UNLABELLED: The increasing number of case reports on neurologic sequelae related to hyperbilirubinaemia may represent a re-emergence of kernicterus in the industrialized world. However, not much has been written about infants who survived extreme levels of serum bilirubin without neurologic damage. We present three cases of extreme neonatal hyperbilirubinaemia, all with peak serum bilirubin levels >600 micromol/L. Two of the infants developed neurologic sequelae, but the third infant did not. In contrast to the two with sequelae, the infant without sequelae was female, had a positive Coombs' test, less clinical signs compatible with bilirubin encephalopathy, and a shorter exposure to serum bilirubin values >400 micromol/L. CONCLUSION: The basic mechanism of bilirubin neurotoxicity remains unknown, and it is not clear why some infants do not develop neurologic injury at serum bilirubin levels at which others do. We speculate that a comparison between patients with sequelae and those without may yield important information.

Reduced autonomic activity during stepwise exposure to high altitude.

Several studies have shown increased sympathetic activity during acute exposure to hypobaric hypoxia. In a recent field study we found reduced plasma catecholamines during the first days after a stepwise ascent to high altitude. In the present study 14 subjects were exposed to a simulated ascent in a hypobaric chamber to test the hypothesis of a temporary reduction in autonomic activity. The altitude was increased stepwise to 4500 m over 3 days. Heart rate variability (HRV) was assessed continuously in seven subjects. Baroreceptor reflex sensitivity (BRS) was determined in eight subjects with the 'Transfer Function' method at baseline, at 4500 m and after returning to baseline. Resting plasma catecholamines and cardiovascular- and plasma catecholamine- responses to cold pressor- (CPT) and mental stress-test (MST) were assessed daily in all and 12 subjects, respectively. Data are mean +/- SEM. Compared with baseline at 4500 m there were lower total power (TP) (35 457 +/- 26 302 vs. 15 001 +/- 11 176 ms2), low frequency (LF) power (3112 +/- 809 vs. 1741 +/- 604 ms2), high frequency (HF) power (1466 +/- 520 vs. 459 +/- 189 ms2) and HF normalized units (46 +/- 0.007 vs. 44 +/- 0.006%), P < or = 0.001. Baroreceptor reflex sensitivity decreased (15.6 +/- 2.1 vs. 9.5 +/- 2.6 ms mmHg(-1), P = 0.015). Resting noradrenaline (NA) decreased (522 +/- 98 vs. 357 +/- 60 pmol L(-1), P = 0.027). The increase in systolic blood pressure (SBP) and NA during mental stress was less pronounced (21 +/- 4 vs. 10 +/- 2% and 25 +/- 9 vs. -2 +/- 8%, respectively, P < 0.05). The increase in SBP during cold pressor test decreased (16 +/- 3 vs. 1 +/- 6%, P = 0.03). Diastolic blood pressure, HR and adrenaline displayed similar tendencies. We conclude that a transient reduction in parasympathetic and sympathetic activity was demonstrated during stepwise exposure to high altitude.

[Primary pulmonary hypertension in children]. / Primaer pulmonal hypertensjon hos barn.

Primary pulmonary hypertension is a clinical syndrome with severe pulmonary hypertension where other causal diseases are excluded. The condition is progressive, fatal and disappointingly resistant to therapy. In this article we present three children with the disease. Two of the patients died shortly after diagnosis, one of them during heart catheterization. The third patient showed good response to treatment with calcium channel blockers, diuretics and nightly supplementary oxygen. Quality of life and hemodynamics improved during the first six months of treatment, and remained virtually unchanged for another two years. Her condition then deteriorated rapidly, and she died three years after diagnosis. According to the literature and our experience, investigations with non-invasive methods such as oxygen saturation measurement, echocardiography, and a simple exercise test provide sufficient information to start therapy and monitor therapeutic response. Some patients show vasodilatory response to treatment with drugs, and might benefit from therapy with calcium channel blockers.

A piglet survival model of posthypoxic encephalopathy.

The aim of this study was to produce a neonatal piglet model which, avoiding vessel ligation, exposed the whole animal to hypoxia and produced dose-dependent clinical encephalopathy and neuropathologic damage similar to that seen after birth asphyxia. Twenty-three piglets were halothane-anesthetized. Hypoxia was induced in 19 piglets by reducing the fractional concentration of inspired oxygen (FiO2) to the maximum concentration at which the EEG amplitude was below 7 microV (low amplitude) for 17-55 min. There were transient increases in Fio2 to correct bradycardia and hypotension. Posthypoxia, the piglets were extubated when breathing was stable. Four were sham-treated controls. We aimed at 72-h survival; seven died prematurely due to posthypoxic complications. EEG and a videotaped itemized neurologic assessment were recorded regularly. We found that 95% of the animals showed neuropathologic damage. The duration of low amplitude EEG during the insult and the arterial pH at the end of the insult correlated with cortical/white matter damage; r = 0.75 and 0.81, respectively. Early postinsult EEG background amplitude (r = 0.86 at 3 h) and neurologic score (r = 0.79 at 8 h) correlated with neuropathology. Epileptic seizures in seven animals were always associated with severe neuropathologic damage. We conclude that EEG-controlled hypoxia and subsequent intensive care enabled the animals to survive with an encephalopathy which correlated with the cerebral hypoxic insult. The encephalopathy was clinically, electrophysiologically, and neuropathologically similar to that in the asphyxiated term infant. This model is suitable for examining mechanisms of damage and evaluation of potential protective therapies after birth asphyxia.

Calcium antagonist treatment and cardiovascular responses to a cold pressor test at high altitude.

OBJECTIVE: We assessed the effects of the calcium antagonist felodipine on blood pressure, heart rate, oxygen saturation and cardiovascular responses to a cold pressor test at an altitude of 5200 m. Sixteen healthy climbers participated. A double-blind, placebo-controlled, randomized, crossover design was used. Placebo or felodipine were taken for 2 days and the treatment was changed after 3 days washout. RESULTS: During felodipine treatment there were no significant changes in blood pressure (125/89 vs 127/86 mmHg), heart rate (82 vs 81 beats.min-1) or oxygen saturation (86% vs 86%). Moreover, there were no changes in the cardiovascular responses to the cold pressor test. CONCLUSION: Felodipine is well tolerated at high altitude. It does not induce hypotension in normotensive men and does not affect cardiovascular reactivity to cold stress.

Acute effects of two different doses of magnesium sulphate in infants with birth asphyxia.

The effects of two different doses of magnesium sulphate (MgSO4) were evaluated in a group of 15 full term infants with Apgar scores of < 6 at 10 minutes, studied within 12 hours of delivery. Seven infants received 400 mg/kg MgSO4 and eight received 250 mg/kg. After the larger dose, mean arterial pressure (MAP) fell by a mean of 6 mm Hg (13%) at one hour but was not significantly reduced thereafter. Respiratory depression lasted three to six hours. EEG readings and heart rate were not significantly different. Mean serum Mg2+ increased from 0.79 to 3.6 mmol/l at one hour. After 250 mg/kg MgSO4, MAP, EEG, tone and heart rate were unchanged. One infant developed transient respiratory depression. Mean serum Mg2+ rose from 0.71 to 2.42 mmol/l at one hour. MgSO4 (400 mg/kg) has an unacceptable risk of hypotension; 250 mg/kg MgSO4 was not associated with hypotension although respiratory depression can occur.