Interpretation of the metabolic effects of trauma and sepsis.

Abstract

By interpreting the data acquired during the examination and investigation of a patient the pathologist can make an important contribution to treatment. This interpretative role is not confined to diagnosis from surgical biopsy specimens or routine blood and urine samples. It can include the interpretation of the metabolic changes which follow trauma and accompany sepsis. These metabolic effects have been studied increasingly during the past 50 years, and there is now a considerable amount of information about the state of patients in these conditions. We should go beyond the mere description of these responses and attempt to say what they mean. Even to use the word 'responses" carries interpretative overtones, and one soon begins to seek the object of these metabolic events. To do so inevitably introduces a teleological approach to the problem but we need not be ashamed of this. Teleology was first introduced into this subject by Hunter,1 and Krebs2 has adequately defended its use for this purpose. Indeed, the furtherance of pathology would often be difficult without it.Up till now the interpretation of the metabolic response to trauma has depended on two ideas. The first, proposed by Hunter,' was that all these changes were defensive, and the second, proposed later by Cuthbertson,3 was that the response could be divided into two linked parts, an early and a late, which he called the "ebb" and "flow" phases. There is little difficulty in accepting the division of the metabolic effects of trauma into two parts, an early group of changes precipitated by the injury and lasting about a day, and a second, later group of quite different changes which reach their peak during the second week after the injury. Can these two groups of effects really be linked together; can they always be described as defensive; and while "flow" may be a useful description for the hypermetabolism and catabolism of the second phase, is "ebb", which implies depression of metabolism, such a good word for the early changes in all species? During the past few years similarities between the metabolic responses to trauma and sepsis have become apparent.4 Sepsis leads to a state that combines many of the changes of the ebb and flow phases of trauma. What light can this throw on our understanding of these events, where similar changes are produced by apparently dissimilar stimuli?Trauma and sepsis affect all tissues and metabolic pathways to some extent. Our knowledge of these changes is insufficient to be able to interpret them all; but enough is now known to attempt the interpretation of the overall changes in energy metabolism 1108 copyright.

GROWTH AND DEVELOPMENT SYMPOSIUM: Impacts of inflammation on cattle growth and carcass merit1,2

“…Increased lipid metabolism is a common characteristic in pyogenic bacterial infections, particularly those that induce sepsis. These infections increase fatty acid oxidation, particularly by peripheral tissues, and decrease glucose usage (Stoner, 1987). In lactating cows, LPS administration lead to an increase in NEFA within 2 h of administration with retum to basal concentrations 1 h later (Waldron et al, 2003).…”

Nutritional support of hospitalised dogs and cats

“…Even relatively simple surgical procedures increase energy expenditure, often 5 or 10% above normal. Calorie needs increase with the seriousness of the injuries (Cerra 1987;Stoner 1987;Brandi et a1 1988). Thus two broken bones result in higher energy needs than one broken bone.…”

“…Fat and protein are the primary fuel sources. Significant amounts of carbohydrate are contraindicated during stress, especially when hyperglycemia indicates insulin resistance, as demonstrated in humans (Abbott et a[ 1983;Cerra 1987;Stoner 1987;Brandi et al 1988;Hensle and Askanazi 1988) and dogs (Shaw and Wolfe 1985; Johnson ef a1 1986).…”

A Review of metabolic staging in severely injured patients

“…The metabolic response to injury in this immune phase of the inflammatory response is characterized by hypercatabolism and hypermetabolism [ 8 , 19 , 24 , 56 ]. This phase corresponds to the post-shock catabolic response or hypermetabolic flow phase of Cuthbertson [ 6 , 18 , 23 ].…”

“…The hypermetabolic response after a severe injury has been described as a hyperdynamic response with increased body temperature, oxygen and glucose consumption, CO 2 production, glycogenolysis, lipolysis, proteolysis and futile substrate cycling [ 18 , 23 , 24 , 56 - 58 ]. The consequences of hypermetabolism are a great loss of body weight associated with a tremendous loss in essential body structures [ 58 ].…”