Biomedical subjects
Publications and source records attributed to G Spielman.
Diffuse axonal injury (DAI), the severest form of diffuse brain injury, causes extensive damage throughout the cerebrum, diencephalon and brainstem. The effects of this injury, however, are not isolated to the brain. This paper discusses diffuse axonal injury, the metabolic complications to be anticipated from the systems' response to cerebral trauma in general, and the nursing implications.
The increased energy expenditure associated with severe trauma to the head appears genuine but exhibits wide variation in its magnitude. Patients with severe acute trauma to the head without barbiturate treatment are hypermetabolic with an average energy expenditure 26 per cent over predicted. Barbiturate therapy abolishes this hypermetabolism and decreases energy expenditure to 14 per cent below predicted. In the individual patient, there appears to be a close relationship between the degree of suppression of energy expenditure and the serum barbiturate level. However, this relationship would appear to be different in each patient, and therefore, for this group, a significant correlation between energy expenditure and serum barbiturate level does not exist. The wide variability of energy expenditure in individual patients makes the estimation of energy expenditure by population predictive formulas imprecise. This may lead to incorrect estimates of caloric requirements and inappropriate provision of exogenous energy substrates. Although for those patients receiving energy expenditure and serum barbiturate levels in the individual may further aid in estimating the caloric expenditure for each individual, in order to provide appropriate amounts of calories to the patient with trauma to the head, energy expenditure should be measured in each instance.
Heterotopic ossification (HO) occurs in up to 75% of patients who survive severe head injury and is a major factor in prolonging their rehabilitation. Prevention of HO has not been emphasized in acute care management of patients with head injury. But with spinal cord injuries and total hip arthroplasty, HO has been prevented by use of disodium etidronate (EHDP). This study compares the incidence and severity of HO in 10 patients with severe head injury who were treated with EHDP and 10 matched controls without drug treatment. Patients selected for EHDP treatment were consecutive admissions who had Glasgow Coma Scores (GCS) less than nine. Treatment was begun within two to seven days of injury with 20mg/kg/day via nasogastric tube and was discontinued if the patient awakened within two weeks (low risk of HO). After three months EHDP was given orally at 10mg/kg/day for an additional three months. Ten patients completed the treatment regime and were compared to 10 patients with similar injuries. Of the 10 patients treated with EHDP, two developed HO, while clinically significant HO was found in seven of the 10 nontreated patients (chi square = p less than 0.025). This finding could not be explained on the basis of differences in the two groups; the groups were alike in age, sex, length of coma, extracranial fracture, spasticity, type of head injury, and injury severity (GCS). These data suggest that HO may be prevented by early use of EHDP, and the results warrant further clinical trials.