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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

Insulin

Insulin is an anabolic hormone, promoting protein synthesis. High-dose intravenous glucose along with insulin has been shown to reduce the donor-site healing time of adolescent patients by 2 days [76]. However, recent data show that high loads of glucose promote de novo lipogenesis in the critically ill [100], questioning the rationale of providing large glucose along with insulin. In combination with data published several years ago, which reported increased liver fat deposits on postmortem evaluation in patients receiving large glucose loads [22], the de novo lipogenesis data indicate that using high glucose loads along with insulin should be restricted until further studies prove its safe use.

By actual knowledge total glucose administration (nutritional and delivered with drugs) should probably not exceed 6g/kg BW/day, i. e. its maximal oxidation capacity.

Electrolyte disorders

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

Sodium

During the first 24 hours, patients receive major amounts of sodium with their fluid resuscitation. Sodium accumulates in the interstitial space with edema. Despite this, hypernatremia occurring during the first 24 hours reflects under-resuscitation, and should be treated with additional fluid. Thereafter, mobilization of this fluid during the first 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 fluidized bed (contraindicated with severe hypernatremia) or in case of fever. Hypernatremia may also herald a septic episode.

Chloride

During the early resuscitation and the surgical debridements of the burn wound, the patients tend to receive significant amounts of NaCl resulting in hyperchloremic acidosis [12]. The excess chloride is difficult to handle for the kidney, but the condition is generally resolves without further intervention.

Calcium, 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 2 mechanisms: large exudative losses [11], 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.

Calcium

Total plasma calcium concentration consists of three fractions [23]: 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 10g/L of albumin, 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 peri-opera- tive blood transfusion and requires intravenous supplementation using any form of available intravenous calcium formulation.

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