The metabolic response to injury

The metabolic effects of exogenous cortisone are similar to the sequence of events following injury. A close correlation was found between urinary cortisol excretion and nitrogen losses in surreal patients (MIO). For these reasons it was considered that the adrenocortical hormones initiated and controlled the metabolic response to injury. There are serious objections, however, to this hypothesis, as the complete interdependence of the responses has been demonstrated in man and animals. 

All these studies indicate that the metabolic response to injury cannot be explained completely in terms of increased adrenocortical activity and confirm the hypothesis of Ingle (II) that the secretions of the adrenal cortex play a permissive rather than a causative role in postoperative metabolic changes. In other words, the presence of the adrenocortical secretions is necessary for the metabolic response to occur, but the secretions do not themselves initiate the response. 

M13. Munro, H. N., Nutritional factors influencing the metabolic response to injury. Wound Healing, Lister Centenary Symp. pp. 171-179. Livingstone, Edinburgh, 1966. 

Lowry SF. Modulating the metabolic response to injury and infection. Proc Nutr Soc 1992 51 267-77. 

Miksche and Caldwell (Mil) have recently reported that after thyroidectomy rats with such injuries show no significant changes in heat production or average body temperature. Caldwell et al. (C4) had earlier reported that thyroidectomy did not prevent the metabolic response to injury in burned rats and an earlier review by Moore (M13) of the literature found the metabolic data on the thyroid in relation to trauma difficult to interpret. He concluded that, on the whole, it would seem that the thyroid partakes in the general alteration in endocrine and metabolic activity but without the early, massive, and systematic nature characteristic of adrenocorticol and antidiuretic alterations. 

As described above, it is now fairly certain that the source of most of the additional nitrogen lost in the urine in the flow phase of the metabolic response to injury is labile body protein, and not liver or gut... 

Although a considerable amount of work has been reported on the effect of environmental conditions on bodily function, particularly with reference to thermoregulation (G5) and although there is a considerable literature on the body s response to injury (e.g., see bibliography of this review), little work has been done on the interaction of environmental conditions and injury. However, studies on the effects of environmental stress are of relevance to the problem of the metabolic response to injury. 

The various transmitters and mediators in this scheme—and the metabolic response to injury involves a multiplicity of effectors and homeostatic regulators—are neural or hormonal the latter including "local hormones such as bradykinin. Hormones may also be involved as effectors. One of the salient features of stress, whether or not accompanied by physical injury, is an increased secretion of the hormones of the adrenal cortex. Much work has been done on this field since the early studies of Browne (B18) on the excretion of cortin in the urine after trauma. 

One of the posterior pituitary hormones—antidiuretic hormone (ADH, vasopressin)—may play a part in the metabolic response to injury. The reduced blood volume and increased plasma electrolyte concentration found after trauma may be expected to stimulate ADH secretion and the oliguria or anuria often found to follow injury would surest this is so (J2). 

It is very difficult to plan experiments to study pathways involved in control of the metabolic response to injury since some surgical or at least stressful preparation of the experimental animal before administration of the injury is almost always necessary. 

Uloodglucose eoiicenlration. This will be maintained even in the face of prolonged starvation. Ketosis develops during starvation and carbohydrate deficiency. Hyperglycacmia is frequently encountered as part of the metabolic response to injury. 

The problems faced by the traumatized individual are listed in Table I.The metabolic response to injury can be thought of as a protective physiological response designed to keep the individual alive until healing processes repairthe damage that has been done. It is mediated by a complex series of neuroendocrine and cellular prexesses, all of which contribute to the overall goal—surx ival. 

The metabolic response to injury has two pha.scs, the ehh and the flow (Fig. 2). The ebb phase is short and corresponds nrughly to clinical shock. The physiological changes which (Kcur here restore adequate vascular volume and maintain essential tissue perfusion. The ebb phase may progress cither to death or to the fiow phase, which may last from days to weeks depending on the extent of the injury. In this phase, metabolism is altered to etisure that energy is available for dependent tissues at the expense of muscle and fat. stores. 

Table 2 Biochemical changes In the metabolic response to injury...

The metabolic responses to injury and to starvation arc quite different. After injury the body is at war. defences are mobilized, metabolic activity increases and resources are directed to the site of action. In starvation, the body is in a stale of famine, resources are rationed and mctabi>lic activity is limited to the minimum for survival. The two situations are quite distinct, but in the clinical situation both can occur together. The severely injured patient is often not fed as a priority. Where starvation and the metabolic response to injury occur together, a good clinical outcome becomes less likely. If a seriously traumatized patient is also nutritionally depleted he or she may be exposed to ... 

The metabolic response to injury is a protective physiological response. 

Increa.sed energy rei/uireinent of the cancer patient. The host reaction to the tumour is similar to the metabolic response to injury, with increased metabolic rate and altered tissue metabolism. 

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