The treatment of an enteral formula with sodium polystyrene sulfonate significantly increases its sodium content, with a modest decrease in potassium content. Clinicians using this method in clinical practice should be aware of the increase in sodium content.
Studies of the metabolic and physiological response to closed-head injury have intimated the presence of persistent hypermetabolism. To more fully define and evaluate the metabolic response to head trauma, a prospective study was conducted in patients with isolated closed-head injuries. Metabolic and cardiopulmonary data were obtained for a 7-day period. Patients with multiple injuries or infections, or those who received steroids, were excluded. The basic treatment regimen utilized hyperventilation, bed rest with head elevation, intracranial pressure monitoring, mild fluid restriction, and mannitol as needed. No exogenous nutritional support was given. Intrastudy trends and comparsion with data from unstressed fasting patients and stressed patients were noted. Mean Glasgow Coma Scale scores were 4.4 +/- 1.5 initially, but rose to a mean of 8.2 +/- 3.7 by Day 7. While the responses of cardiac index, CO2 production, lactate/pyruvate ratio, and arteriovenous O2 content difference (AVO2D) were initially elevated, these parameters declined over the course of 7 days. The AVO2D was equivalent to the fasting level by Day 5. Metabolic data, including most amino acid levels in plasma, showed an initial equivalence to stress control levels and a pattern similar to that in non-stressed control subjects by Day 7. Nitrogen and 3-methyl histidine excretion were persistently elevated for the full 7 days. Patients with isolated closed-head injury seemed to be initially hypermetabolic, but this process appeared to resolve by 1 week; the persistent nitrogen excretion may reflect equilibration of muscle mass to the existing level of activity (bed rest). After the first few days, nitrogen excretion may give an erroneous index of the level of metabolic stress and the type or amount of nutritional support needed.
In order to determine the effects of steroid administration on the metabolic response to isolated closed-head injury, a longitudinal study was performed. Metabolic indices were prospectively evaluated for the first 5 days postinjury in six patients who received steroids and 10 patients who did not. Patients were carefully screened to eliminate those with associated injuries as well as those with abnormalities due to sepsis. Other than steroid administration, a uniform treatment regimen was used in both groups. Metabolic indices measured on postinjury Days 1, 3, and 5 were analyzed. In addition, data were compared to results in large data banks obtained both from overnight-fasted patients (fasted controls) and from polytrauma victims (stressed controls). Both treatment groups were comparable with respect to age, mean Glasgow Coma Scale scores on admission and on Day 5, and initial intracranial pressure. Metabolic data indicated significantly higher levels of nitrogen excretion and somatic protein mobilization in steroid-treated patients than in patients not receiving steroids. In both groups, glucose levels, the lactate/pyruvate ratio, and branched-chain amino acid levels (all metabolic indices that correlate well with level of stress) initially corresponded to values for stressed controls. By Day 5, values for these variables were similar to fasted controls for the group not receiving steroids. In patients receiving steroids, however, the data remained similar to those for stressed controls. It is concluded that steroids prolong the metabolic abnormalities associated with the initial phase of head injury. In view of inconclusive data regarding benefit from steroid administration, serious questions must be raised regarding the use of these catabolic agents in this setting.
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