5.11.1 Zinc Supplementation
What evidence is there for zinc supplementation in ABI?
- Based on a single RCT there is Level 1 evidence that zinc supplementation in ABI patients has a positive effect on neurological recovery as measured by the Glasgow Coma Scale. However, no significant improvement in mortality rates could be attributed to zinc supplementation.
“Zinc is an essential element for humans that constitutes less than 0.1% of body weight, yet is vitally important for normal nucleic acid and protein metabolism” 86. Serum hypozincemia and increased urinary zinc excretion are common following head injury and are thought to be an adaptive responsive to inhibit the proliferation of infective organisms. Levels of serum albumin, the major transport carrier for zinc, are also markedly depressed following brain injury and likely help to explain a portion of the reductions in serum zinc levels. Urinary excretion of zinc appears to be proportional to the severity of head injury 87. Zinc is an important trace mineral in protein synthesis. Moderate zinc deficiency has been associated with cell death.
Two RCTs were identified which examined the effect of parenteral zinc supplementation following ABI 86;88. Young et al.88reported on improvements in protein synthesis and neurological recovery in patients who received supplementation. Surprisingly, there were no differences in either the serum or cereobrospinal fluid zinc concentrations between the groups.
5.11.2 Increased Nitrogen Feeds
What evidence is there of a benefit of enhanced enteral nutrition post ABI?
- Based on a single RCT, there is Level 2 evidence that high nitrogen feedings of approximately 2 g protein/kg are necessary to restore the substantial nitrogen loses that occur post-ABI.
Following brain injury, the incidence of metabolic changes will influence cell turnover, use of substrate and body composition 89. Twyman 89noted that urinary urea nitrogen levels increase by a factor of three compared with normal levels within 10 days after severe head injury. On average, about 5 to 10 g of urea nitrogen are excreted daily from a normal individual; however, ABI patients’ lose a mean of 21 g urinary urea in a single day 89. Following brain injury, nitrogen losses result from the conversion of endogenous protein to energy with the extra stress demand 90. Hadley et al. 91 also reported that attainment of a positive nitrogen balance is complicated because increasing the amount of nitrogen feeding will not be retained, rather it will cause an increased amount of nitrogen excretion.“Positive nitrogen balance in brain injured patients usually does not occur until the catabolic stimulus begins to subside” 91.