84	M.G. Jeschke

low T3 levels and T4 levels in the low-normal values, with elevated rT3 levels reßecting an altered deiodination at the hepatic level. If a low T3 is present, there are two options: to administer selenium because selenium deÞciency is associated with low T3 levels, and/or thyroid hormone should be replaced.

Postburn the gonadal axis is depressed in any patient with major burns. In men, postburn changes in testosterone and 17beta-estradiol are greater than in females, even during the Þrst days. Plasma testosterone also decreases steeply in limited burn injury. The alterations last at least 4Ð5 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 prolactin is low to elevated.

In premenopausal females, amenorrhea is a nearly universal phenomenon, despite a near normal 17beta-estradiol plasma concentration. Progesterone levels remain 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 elicits an increase in testosterone, while it decreases it men. Prolactin 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 [37]. These changes contribute to stunting of growth observed after major burns. Female patients have signiÞcantly increased levels of anabolic hormones, which are associated with decreased proinßammatory mediators and hypermetabolism, leading to a signiÞcantly shorter ICU length of stay compared with male patients

6.3.7Electrolyte Disorders

Burns is a condition where nearly any electrolyte abnormality can be observed. The causes for these disturbances are many and include ßuid resuscitation with crystalloids, exudative and evaporative losses, impaired renal regulation, and responses to counter regulatory hormones.

6.3.7.1 Sodium

During the Þrst 24 h, patients receive major amounts of sodium with their ßuid resuscitation. Sodium accumulates in the interstitial space with edema. Despite this, hypernatremia occurring during the Þrst 24 h reßects under-resuscitation and should be treated with additional ßuid. Thereafter, mobilization of this ßuid during the Þrst weeks frequently results in hypernatremia, and its resolution requires free water. Hypernatremia may also result from persistent evaporative losses from the wounds, particularly in case of treatment on a ßuidized bed (contraindicated with severe hypernatremia) or in case of fever. Hypernatremia may also herald a septic episode.

6 Critical Care of Burn Victims Including Inhalation Injury	85

6.3.7.2 Chloride

During the early resuscitation and the surgical debridements of the burn wound, the patients tend to receive signiÞcant amounts of NaCl resulting in hyperchloremic acidosis. The excess chloride is difÞcult to handle for the kidney, but the condition is generally resolved without further intervention.

6.3.7.3 Phosphate and Magnesium

Burns have high requirements for phosphate and magnesium in absence of renal failure. Those requirements start early and are largely explained by two mechanisms: large exudative losses and increased urinary excretion associated with acute protein catabolism and stress response. Stimulation of sodium excretion is usually required and can usually be achieved by the simultaneous administration of free water (D5W IV or enteral water) along with furosemide with or without thiazide diuretics.

6.3.7.4 Calcium

Total plasma calcium concentration consists of three fractions: 15 % is bound to multiple anions (sulfate, phosphate, lactate, citrate), about 40 % is bound to albumin in a ratio of 0.2 mmol/l of calcium per 10 g/l of albumin, and the remaining 45 % circulating as physiologically active ionized calcium. Calcium metabolism is tightly regulated. As albumin levels vary widely in burns and only ionized calcium is biologically active, only ionized calcium is a true indicator of status, as total plasma calcium determination is not a reliable indicator of calcium status: the use of conversion formula is unreliable:

[Ca] calculated = total [Ca] measured + (0.2× (45 − [albumin]))

Hypocalcemia may occur during the early resuscitation phase or in the context of massive perioperative blood transfusion and requires intravenous supplementation using any form of available intravenous calcium formulation. Hypercalcemia remains a poorly recognized cause of acute renal failure in patients with major burns that occurs as early as 3 weeks after injury. The triad of hypercalcemia, arterial hypertension, and acute renal failure is well known in other critical illnesses, while the association of hypercalcemia and renal failure in patients with major burns is much less reported in the literature. In a recent retrospective study, hypercalcemia was shown to occur in 19 % of the burned patients with hospital lengths of stay of more than 28 days and was noted to be associated with an increased mortality. Hypercalcemia may also occur in patients with smaller burns requiring a stay of more than 20 days in the ICU. Ionized calcium determination enabled earlier detection, while using total calcium determination Òwith albumin correctionÓ was only slightly sensitive, as shown by normal corrected values in 15 cases with ionized hypercalcemia. Treatment of hypercalcemia includes hydration, volume expansion, and early mobilization. As most causes of severe hypercalcemia depend on increased osteoclast activation, drugs that decrease bone turnover are effective. The treatment of choice in cases that do not resolve with the simple measures relies on the bisphosphonates, pamidronate