Traumatic head injury in infants and toddlers.

AIM: To describe the presenting characteristics, type of injury and hospital course in young children with traumatic head injury, and to identify characteristics indicating that the trauma was inflicted. METHODS: A retrospective medical record review of 91 children less than 3 years of age who were admitted to a tertiary teaching hospital in Norway from 1995 through 2005 with a traumatic head injury. Patients were identified by diagnostic codes, and categorized by type of injury as skull fractures (n = 39), epidural haemorrhage (EDH) (n = 12), subdural haemorrhage (n = 27) and parenchymal brain injury (n = 13). Further the cases were classified as inflicted injury (n = 17), accident (n = 35) or indeterminate (n = 39). RESULTS: The mechanism of injury was similar for EDHs and isolated skull fractures, and none were classified as inflicted. Sixty-three percent of the cases with subdural haematoma were classified as inflicted. When compared to the accident group, children in the inflicted group more frequently had subdural haemorrhage without a skull fracture (OR = 6.9, CI = 1.7-28.2), and seizures (OR = 9.5, CI = 2.1-43.3). CONCLUSIONS: Inflicted and accidental head injuries differed in presenting characteristics and injury type. Nearly two-third of the subdural haemorrhages were classified as inflicted, but none of the epidural EDHs or skull fractures. Inflicted injuries tended to present with seizures.

Prolonged hypoxemia enhances and acute hypoxemia attenuates laryngeal reflex apnea in young lambs.

To determine the influence of an altered carotid body function on the laryngeal chemoreflex (LCR) response, reflex apnea was induced by laryngeal water stimulation during normoxia or acute hypoxia in unanesthetized awake lambs in which the ventilatory response to acute hypoxia was attenuated by prolonged postnatal hypoxemia. Prolonged hypoxemia (H) was induced in seven lambs for 12 d after birth through exposure to 0.10 fraction of inspired oxygen. Five control lambs were kept in 0.21 fraction of inspired oxygen. Studies were performed repeatedly during the first 7 wk after birth. The ventilatory response to LCR stimulation, expressed as a percent decrease in minute ventilation, was tested in 0.21, 0.14, and 0.10 fraction of inspired oxygen. H after birth resulted in a markedly increased inhibition of ventilation in response to LCR stimulation and postponed the age-related decrease in LCR response. A potential failure to recover from apnea occurred only in the H lambs, and in these lambs there was a significantly greater requirement for mechanical ventilation after LCR stimulation. Acute hypoxemia preceding LCR stimulation significantly attenuated the ventilatory response in both control and H lambs, with a stronger effect in the H lambs. There was no difference between the two groups in heart rate response to LCR stimulation. Acute hypoxemia significantly augmented reflex bradycardia in the H lambs. These results show that there is a relationship between H immediately after birth--which is known to delay resetting of carotid chemoreceptors--and augmented ventilatory inhibition in response to LCR stimulation. They do not confirm the theory that acute hypoxia reinforces reflex apnea.

Long-lasting effect of prolonged hypoxemia after birth on the immediate ventilatory response to changes in arterial partial pressure of oxygen in young lambs.

The effect of prolonged hypoxemia (H) after birth on the evolution of the ventilatory response to changes in arterial partial pressure of O2 was determined in unanesthetized, awake lambs. H was induced for 12 d after birth in seven lambs through exposure to 0.10 fraction of inspired O2 (FiO2). Five control (C) lambs were kept in 0.21 FiO2. The ventilatory response (percent increase from baseline) to acute hypoxia was tested with 0.14 FiO2 and 0.10 FiO2. The tonic activity of the peripheral chemoreceptors was assessed by the transient pure oxygen inhalation test (Dejours' test). The occlusion technique was used to measure the baseline neuromuscular drive of breathing. A markedly decreased early ventilatory response to acute hypoxia persisted in the H lambs for at least 5 wk after termination of H compared with the C group. The second phase of the response was significantly lower only at 12 d (the end of H) and was thereafter comparable to that in the C lambs. The ventilatory response to hyperoxia was significantly lower in the H lambs only at the end of hypoxemia at 12 d and rapidly normalized after return to normoxia. H did not significantly affect resting neuromuscular drive. These results show that postnatal maturation of the ventilatory response to changes in arterial partial pressure of O2 can be delayed by prolonged postnatal hypoxemia. The effect on the response to hyperoxia is transient, whereas the response to acute hypoxia is affected for an extended time. This study illustrates the importance of an adequate postnatal arterial partial pressure of O2 for the development of the ventilatory response to acute hypoxia.

Increased survival rate in very low birth weight infants (1500 grams or less): no association with increased incidence of handicaps.

The incidence of major handicaps was studied in a selected high-risk population of 1919 very low birth weight (less than or equal to 1500 gm) infants born between 1976 and 1985. Seventy-four percent of these infants were discharged alive. We have handicap information on 632 infants who have been followed for up to 7 years of age; 462 were evaluated at 18 months or later. Patients lost to follow-up represent 55% of the eligible population, but inpatient morbidity factors were available for the entire population and were used to calculate synthetic estimates of handicap rates. The overall incidence of severe major handicaps at 18 months was 18.0% (83/462). Cerebral palsy was found in 7.6%, and 6.5% were mentally retarded (IQ less than or equal to 70). Severe retinopathy of prematurity was present in 5.5%, and 5.4% of the infants had neurosensory hearing loss. Thirty-one infants (6.7%) had more than one handicap, the most common combination being cerebral palsy and mental retardation. Outcome of infants grouped by 250 gm birth weight intervals was compared for two periods (1976 to 1980, and 1981 to 1985); the numbers of survivors in each birth weight group increased during the second period, especially in the 500 to 750 gm and the 751 to 1000 gm groups. The observed incidence of major handicaps decreased from the first 5-year period to the second 5-year period (p less than 0.001). The largest decreases in the observed proportion handicapped occurred in the two lowest birth weight groups. The incidence of multiple handicaps also dropped; again, the two lowest birth weight groups showed the largest decrease. We conclude that an increased survival rate of very low birth weight infants need not be associated with an increased incidence of major handicaps.

Detection of intraventricular hemorrhage (IVH) by transcephalic impedance (TCZ) in premature infants.

Transcephalic impedance was measured serially in 45 preterm infants less than 1500 g birth weight in order to test the method for the early detection of intraventricular hemorrhage. TCZ increased in all seventeen (38%) infants who developed IVH diagnosed by CT-scan or autopsy. Five of 8 infants monitored 4-8 weeks following confirmed IVH developed hydrocephalus documented by repeat CT-scans; all 5 were discovered early by the TCZ-method 2-3 weeks before physical findings or an increasing head circumference indicated the possibility of hydrocephalus. TCZ appears to be a useful non-invasive clinical guide to the occurrence and course of IVH in the newborn.