[The comatose child]. / Das bewusstlose Kind.

The child who presents with acute coma runs a high risk of cardiopulmonary insufficiency, direct brain injury or even cerebral herniation. The case-management of such child requires a coma-specific emergent evaluation, immediate treatment of any hypoxicischemic insults and of the underlying cause. The coma-specific examination includes performance of child-adapted Glasgow Coma Score, the evaluation of brain stem functions such as pupillary response to light, cough- and gag reflex, and determination of all vital signs including body temperature. Treatment of hypoxicischemic insults includes control of airways and ventilation in patient with coma defined as GCS <8; liberal treatment of impaired cardiovascular states with isotonic fluids such as 0.9% sodium chloride; and treatment of cerebral herniation with head elevation, mannitol, hypertonic sodium chlorid fluids, steroids and hyperventilation. Immediately treatable causes are hypoglycemia, meningitis/encephalitis, opioid overdose and status epilepticus. Exclusion of rapidly progressive intracranial lesions almost always requires referral to the tertiary centre with head CT-scan facilities. Finally, an extensive etiology search of the stable coma is performed by looking for disease or trauma of the brain, for metabolic causes, for intoxications and for cardiopulmonary problems.

Survivors with bad outcome after hypoxic-ischaemic encephalopathy: full-term neonates compare unfavourably with children.

UNLABELLED: Hypoxic-ischaemic encephalopathy (HIE) is of major importance in neonatal and paediatric intensive care with regard to mortality and long-term morbidity. Our aim was to analyse our data in full-term neonates and children with special regard to withdrawal of life support and bad outcome. PATIENTS: All patients with HIE admitted to our unit from 1992-96 were analysed. Criteria for HIE were presence of a hypoxic insult followed by coma or altered consciousness with or without convulsions. Severity of HIE was assessed in neonates using Sarnat stages, and in children the duration of coma. In the majority of cases staging was completed with electrophysiological studies. Outcome was described using the Glasgow Outcome Scale. Bad outcome was defined as death, permanent vegetative state or severe disability, good outcome as moderate disability or good recovery. RESULTS: In the neonatal group (n = 38) outcome was significantly associated with Sarnat stages, presence of convulsions, severely abnormal EEG, cardiovascular failure, and multiple organ dysfunction (MOD). A bad outcome was observed in 27 cases with 14 deaths and 13 survivors. Supportive treatment was withdrawn in 14 cases with 9 subsequent deaths. In the older age group (n = 45) outcome was related to persistent coma of 24-48 h, severely abnormal EEG, cardiovascular failure, liver dysfunction and MOD. A bad outcome was found in 36 cases with 33 deaths and 3 survivors. Supportive treatment was withdrawn in 15 instances, all followed by death. CONCLUSIONS: Overall, neonates and older patients did not differ with regard to good or bad outcome. However, in the neonatal group there were significantly more survivors with bad outcome, either overall or after withdrawal of support. Possible explanations for this difference include variability of hypoxic insult, maturational and metabolic differences, and the more compliant neonatal skull, which prevents brainstem herniation.

Bronchodilator responsiveness in a ventilator-dependent infant with severe tracheobronchomalacia.

A neonatal case of severe, ventilator-dependent tracheobronchomalacia (TBM) is described. The extent of the malacic segment was determined by endoscopy and tracheobronchography. Additionally, relevant and ever increasing reversible peripheral airway obstruction was documented by measuring the mechanical properties of the respiratory system before and after salbutamol. With the combination of endoscopically guided aortopexy and salbutamol infusion, the infant was eventually weaned from mechanical ventilation at the age of 86 days. We speculate that in ventilator-dependent infants with severe TBM the determination of bronchodilator responsiveness may have clinical consequences.

[Changes in the epidemiology of the acute respiratory distress syndrome (ARDS) in children]. / Cambios en la epidemiología del síndrome de dificultad respiratoria aguda (SDRA) en niños.

OBJECTIVE: Our aim was to analyze, in a retrospective study, changes in acute respiratory distress syndrome (ARDS) within the same pediatric intensive care unit by using the same diagnostic criteria as published in 1982. PATIENTS AND METHODS: Fifteen patients (mean age 5.1 years, range 16 days-15 years) admitted between 1988 and 1994 fulfilling our former criteria for ARDS were included in the study. RESULTS: The incidence of ARDS after the age of 7 days was 0.45% of all admissions between the age of 1 week and 16 years vs 1.79% in the former series of patients (p < 0.001). Thus, the yearly rate of ARDS decreased from 5.7 to 2.1 cases per year. Six patients suffered a chronic underlying disease vs none in 1982 (p < 0.01). Triggering of ARDS by infection/inflammation was present in 14/15 patients vs 7/20 in the first series (p < 0.001). Except for the nadir PaO2/FiO2 ratio (54 mmHg vs 97 mmHg, p < 0.01), and duration of FiO2 > or = 0.5 (204 h vs 39 h, p < 0.01) there was no statistically significant difference with regard to respiratory data. Incidence of multiple organ/system failure and numbers of failing organs/systems remained unchanged. Eight of 15 patients died in the actual series vs 8/20 in 1982 (not significant). CONCLUSIONS: Compared to our former data, the incidence of ARDS has decreased. Although the number of patients with severe chronic disease has increased, mortality remains statistically unchanged. Infection/inflammation is currently the predominant event triggering ARDS. Judging by the PaO2/FiO2 ratio and duration of FiO2 > or = 0.5, pulmonary involvement is more severe. The number of failing organs/systems remains nearly twice as frequent in non-survivors compared to survivors.

NO contributes to neurohypophysial but not other regional cerebral fluorocarbon-induced hyperemia in cats.

The large increase in cerebral blood flow (CBF) after fluorocarbon (FC)-exchange transfusion is thought to be caused by low oxygen content, decreased viscosity, or direct vasodilatory effect of the FC perfusate. The aim of this study was to determine whether nitric oxide (NO)-mediated vasorelaxation is increased in FC-perfused hemoglobin (Hb)-free cats because NO is not scavenged by Hb. We measured regional CBF with radiolabeled microspheres in three groups of anesthetized mechanically ventilated cats. The first group [FC + N(omega)-nitro-L-arginine methyl ester (L-NAME), n = 7] underwent a complete FC-exchange transfusion with FC-43 and subsequent nitric oxide synthase (NOS) inhibition with L-NAME (10 mg/kg i.v.) followed by L-arginine (100 mg/kg i.v.). A second group (FC + saline; n = 6) underwent an identical protocol, but NOS was not antagonized (saline i.v.). In a third group (blood + L-NAME; n = 7), cats were not FC exchanged but NOS was inhibited. In a separate cohort of four FC-perfused cats, NOS activity in brain tissue samples was reduced to 26% of control after NOS inhibition. FC-exchange transfusion nearly doubled hemispheric blood flow in both FC-exchanged groups, whereas it was constant in the blood + L-NAME group. These increases in regional CBF (hemispheres, brain stem, cerebellum, thalamus, and white matter) were not reversed by inhibition of NOS, except in the neurohypophysis, where L-NAME reduced blood flow to levels comparable to values in the blood + L-NAME group. In summary, increases in regional CBF after total FC-exchange transfusion are not caused by a lack of NO scavenging, with the exception of neurohypophysis. These findings suggest an increased vasorelaxation in neurohypophysis of FC-perfused and Hb-free cats caused by unscavenged NO, but this mechanism does not play a major role in FC-related CBF increases in the rest of the cerebral circulation.

Once daily dosing of netilmicin in neonatal and pediatric intensive care.

OBJECTIVE: To examine a once daily dosing regimen of netilmicin in critically ill neonates and children. DESIGN AND SETTING: Open, prospective study on 81 antibiotic courses in 77 critically ill neonates and children, hospitalized in a multidisciplinary pediatric/neonatal intensive care unit. For combined empiric therapy (aminoglycoside and beta-lactam), netilmicin was given intravenously over 5 min once every 24 h. The dose ranged from 3.5-6 mg/kg, mainly depending upon gestational and postnatal age. Peak levels were determined by immunoassay 30 min after the second dose and trough levels 1 h before the third and fifth dose or after adaptation of dosing. RESULTS: All peak levels (n = 28) were clearly above 12 mumol/l (mean 22, range 13-41 mumol/l). Eighty-nine trough levels were within desired limits (< 4 mumol/l) and 11 (11%) above 4 mumol/l, mostly in conjunction with impaired renal function. CONCLUSIONS: Optimal peak and trough levels of netilmicin can be achieved by once daily dosing, adapted to gestational/postnatal age and renal function.

Lung mechanics and gas exchange in ventilated preterm infants during treatment of hyaline membrane disease with multiple doses of artificial surfactant (Exosurf)

Eight premature infants ventilated for hyaline membrane disease and enrolled in the OSIRIS surfactant trial were studied. Lung mechanics, gas exchange [PaCO2, arterial/alveolar PO2 ratio (a/A ratio)], and ventilator settings were determined 20 minutes before and 20 minutes after the end of Exosurf instillation, and subsequently at 12-24 hour intervals. Respiratory system compliance (Crs) and resistance (Rrs) were measured by means of the single breath occlusion method. After surfactant instillation there were no significant immediate changes in PaCO2 (36 vs. 37 mmHg), a/A ratio (0.23 vs. 0.20), Crs (0.32 vs. 0.31 mL/cm H2O/kg), and Rrs (0.11 vs. 0.16 cmH2O/mL/s) (pooled data of 18 measurement pairs). During the clinical course, mean a/A ratio improved significantly each time from 0.17 (time 0) to 0.29 (time 12-13 hours), to 0.39 (time 24-36 hours) and to 0.60 (time 48-61 hours), although mean airway pressure was reduced substantially. Mean Crs increased significantly from 0.28 mL/cmH2O/kg (time 0) to 0.38 (time 12-13 hours), to 0.37 (time 24-38 hours), and to 0.52 (time 48-61 hours), whereas mean Rrs increased from 0.10 cm H2O/mL/s (time 0) to 0.11 (time 12-13 hours), to 0.13 (time 24-36 hours) and to (time 48-61 hours) with no overall significance. A highly significant correlation was found between Crs and a/A ratio (r = 0.698, P less than 0.001). We conclude that Exosurf does not induce immediate changes in oxygenation as does the instillation of (modified) natural surfactant preparations. However, after 12 and 24 hours of treatment oxygenation and Crs improve significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

The paradox of adult respiratory distress syndrome in neonates.

Six full-term newborn infants are described who suffered from severe adult respiratory distress syndrome (ARDS). The triggering event was intrauterine/perinatal asphyxia in five, and group B streptococcal (GBS) septicemia in three. All had severe respiratory distress/failure and were ventilated mechanically with high concentrations of inspired oxygen and positive end-expiratory pressure. Radiography of the chest showed dense bilateral consolidation with air bronchograms and reduced lung volume. Persistent pulmonary hypertension (PPH) was documented in all cases. The coincidence of ARDS and PPH rendered respiratory management extremely difficult. For this reason high-frequency ventilation was instituted in all patients in order to improve CO2 elimination and induce respiratory alkalosis. Acute complications of respiratory therapy were encountered in five patients (pneumothorax, pulmonary interstitial emphysema, pneumopericardium). Three infants died (irreversible septic shock, progressive severe hypoxemia, and sudden cardiac arrest) after 17, 80, and 175 h of life. Histologic examination of the lungs was possible in all fatal cases and revealed typical changes of acute to subacute stages of ARDS. Three infants survived, the mean time of mechanical respiratory support being 703 h. Two patients were still dependent on oxygen after 1 month of life, and all survivors had increased interstitial markings and increased lung volumes on their chest roentgenograms at this time.

Tumor induction in Praomys (Mastomys) natalensis by N,N'-2,7-fluorenylenebisacetamide.

Feeding N,N'-2,7-fluorenylenebisacetamide (CAS:304-28-9) at 0.025% to 15 male and 15 female mastomys considerably shortened their life-span. At death every treated mastomys had several primary tumors; untreated animals at comparable ages had none. Several mastomys with hepatoblastomas and 1 with giant cell hepatitis and a metastasizing pancreatic carcinoma are first reported here. The tumor load per animal averaged 4.0 for treated females, 2.6 for treated males, 1.5 for untreated females, and 0.6 for untreated males. Of 24 hepatic tumors in treated mastomys, 11 metastasized, compared to none of the incipient tumors in 8 of 26 untreated animals. Pancreatic adenomas developed in 27 treated and 1 untreated mastomys, and a metastasizing adenocarcinoma developed in 1 treated animal. All treated females, 3 treated males, and 1 untreated female developed multiple villous adenomas in the small intestine. One untreated female and 8 treated females developed mammary cancers, 4 of which metastasized. Primary tumors of other sites occurred infrequently.