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M.Jeschke - Handbook of Burns Volume 1 Acute Burn Care - 2013.pdf
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M. M. Berger et al.

Glucose control

There is no prospective adult trial addressing glucose management in major burns, but the retrospective studies suggest that toxic levels of hyperglycemia ( > 10 mmol/l) should be avoided and treated to prevent graft failure and infections (both increased with hyperglycemia) [41]. By contrast data are available in children: tight glucose control (90 to 120 mg/dl) has been shown to reduce infections and mortality [75]. Despite a demonstrated benefit of insulin administration on the maintenance of skeletal muscle mass, it is unknown if this effect translates to improved clinical outcomes in the thermally injured patient [8]. Optimal glycemic level remains uncertain: indeed feeding interruptions due to the procedures expose the patients to the risk of hypoglycemia. A good compromise is probably to opt for a glucose target 5–8 mmol/l (70–120 mg/dl) as in the majority of critically ill patients.

Endocrine changes

Stress response (Fig. 2)

In the post-burn state, pronounced hormonal and metabolic changes take place starting immediately after injury [7]. There is a tremendous increase in stress hormones after major burns, the increase being particularly marked during the first 2–3 weeks, but the alterations will persist for weeks and even months.

In response to the afferent stimuli from the burn wound, an intense sympatho-adrenal response is elicited. Catecholamine secretion contributes to arterial pressure maintenance, but also to a massive increase in cardiac after-load. The concentration of epinephrine and norepinephrine remains elevated for several days after injury and contributes to the integrated neuro-endrocrine stress response.

Cortisol increases markedly, and the intensity of the response is modulated by optimization of pain control with good analgesia. However, the plasma value remains far above normal for at least 2 weeks. As with many other hormones, the circadian rhythm

Fig. 2. Extensive organ involvement during the acute stress response

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