The importance of trace elements such as zinc is well recognized in the context of metabolic response to injury and wound healing. There is post-injury lowering of zinc as part of the so-called 'triggered' biochemical response to trauma even if the trauma is of relatively modest severity (Stoner, 1984). In the catabolic phase of metabolic response to trauma, which starts 24-48h post-injury, the predominant feature is protein or muscle catabolism resulting in the release of amino acids for synthesis of glucose (gluconeogenesis) and production and excretion of urea nitrogen in the urine. Albumin concentration may fall for up to a week and then takes weeks to recover. The extent of zinc loss, which is linked to proteins, mainly ablumin, correlates very closely with the amount of nitrogen loss in the urine (Cuthbertson et al., 1972). As wound healing is known to be impaired in zinc deficient patients and animals (Hallmans, 1979), a combination of possible existing zinc deficiency and post injury reduction of zinc would be expected to delay wound healing. Hypozincaemia is known to occur in cirrhosis of liver, malabsorption syndrome,
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Maitra et al. (1992) studied this question.
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