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M.Jeschke - Handbook of Burns Volume 1 Acute Burn Care - 2013.pdf
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Critical care of thermally injured patient

also changes. Aldosterone levels increase for several days. ACTH response frequently parallels the cortisol levels, and tends to be elevated for a few weeks. The increase in plasma rennin activity and aldosterone persist for several weeks.

Glucagon concentration is also increased after burn injury, contributing heavily to the hypermetabolic response, while insulin tends to remain within normal values, being paradoxically normal while plasma glucose concentration is elevated.

Low T3 syndrome

The thyroid axis exhibits major abnormalities in the patients with major burns. The most constant finding is a “low T3 syndrome”: TSH is generally normal, with low T3 levels, and T4 levels in the low-normal values, with elevated rT3 levels reflecting an altered de-iodination at the hepatic level. This activation step of thyroxin is under the control of a selenoenzyme, the 5-II de-iodinase: as the selenium status is strongly depressed in critically ill patients with an intense inflammatory response and even worse in those with negative selenium balances such as major burns and trauma patients, substitution of selenium is likely to improve the thyroid function. Indeed in critically ill trauma patients with a Low T3 syndrome, the alterations are improved by selenium supplementation with normalization of T3 levels [13]. The T3 and T4 concentrations are inversely related to the metabolic level.

Gonadal depression

As a general rule, the gonadal axis is depressed in any patient with major burns. In men, post-burn changes in testosterone, 17 -estradiol are greater than in females, even during the first days. Plasma testosterone also decreases steeply in limited burn injury. The alterations last at least 4–5 weeks, but may persist for months in critically ill burned patients. The changes seem proportional to the severity of burns. A decreased pituitary stimulation causes lowered hormonal secretions from the testes. This change contributes to the low anabolic response and opens substitution perspectives. LH is more or less normal, LH-RH is decreased, FSH is low, and Prolactine is low to elevated.

In premenopausal females, amenorrhea is a nearly universal phenomenon, despite a near normal 17 -estradiol plasma concentration. Progesterone levels remains very low for many months after injury. Testosterone response is very different from that of males, with nearly normal concentrations in young females, and normal response to ACTH which elicits an increase in testosterone, while it decreases it men. Prolactine levels are also higher than seen in men.

In children, despite adequate nutritional support, severe thermal injury leads to decreased anabolic hormones over a prolonged period of time [52]. These changes contribute to stunting of growth observed after major burns. Female patients have significantly increased levels of anabolic hormones, which are associated with decreased pro-inflamma- tory mediators and hyper-metabolism, leading to a significantly shorter ICU length of stay compared with male patients

Thermal regulation

Temperature regulation is altered with a “resetting” of the hypothalamic temperature above normal values. The teleological advantage of maintaining an elevated core temperature following burn injury is not fully understood. Major burns destroy the insulating properties of the skin, while the patients strive for a temperature of 38.0 to 38.5°C [106]. Catecholamine production contributes to the changes in association with several cytokines, including interleukin-1 and interleukin-6. Any attempt to lower the basal temperature by external means will result in augmented heat loss, thus increasing metabolic rate.

Ambient temperature should be maintained between 28 and 33 °C to limit heat loss and the subsequent hyper-metabolic response [92]. Metabolic rate is increased as a consequence of several factors such as the catecholamine burst, the thermal effects of pro-inflammatory cytokines and evaporative losses from the wounds, which consumes energy, causing further heat loss. The evaporation causes extensive fluid losses from the wounds, approximating 4 000 ml/m2/%TBSA burns. Every liter of evaporated fluid corresponds to a caloric expenditure of about 600 kcal.

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