Electrolyte disorder

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(Trauma)

  1. An initial loss of circulating intravascular volume decreases capillary hydrostatic pressure; Starling forces predict the increased transcapillary influx of extracellular fluid from the interstitial to the intravascular space following subcriticial hemorrhage of less than 10% of blood volume
    1. transfusion of whole blood restores measured deficiencies in red cell mass and plasma volume but deficiencies in extracellular fluid volume persist – infusion of crystalloid replaces the extracellular balance and reduces mortality significantly
      1. 20% of body weight is in the extracellular fluid space but 60% of body weight is free water
  2. depletion of ATP in skeletal muscle in hemorrhagic shock depletes the Na/K ATPase pumps and thus K moves out of the cell and Na moves intracellular (Cl also increases intracellularly as it follows Na) – this hyperkalemia may be worsened with acidosis and increased levels of cortisol seen in trauma; however usually the overall concentration of electrolytes in the extracellular space does not change
    1. in hemorrhagic shock, there is a fall in the normally negative intracellular transmembrane potential reflecting a reduction in the efficiency of the sodium pump induced by tissue hypoxia
  3. Na retention is a hallmark of injury that results in increased secretion of aldosterone and other steroids; the increased delivery of Na to the distal tubule is part of the metabolic alkalosis that commonly accompanies injury (the most common acid-base disturbance in patients who have not deteriorated to severe renal, circulatory, or pulmonary decompensation is either metabolic or respiratory alkalosis); it is important to correct this because of the effect that alkalosis has on the oxygen-hemoglobin dissociation curve; with mild injury typically get hyperkalemia as K is lost from cells or banked blood is given however may also get hypokalmic alkalosis if acid is lost from the stomach (NG suctioning) and significant fluid is lost causing increased absorption of Na in the kidney and more excretion of K in the distal tubule leading to a metabolic alkalosis with hypokalemia (large quantities of Cl lost in gastric juice limits the ability of the kidney to reabsorb Na proximally)
    1. the most common acid-base distubance in severely injured patients or in those who deteriorated to severe renal, circulatory, or pulmonary decompensation is either metabolic acidosis or respiratory alkalosis; foremost among the causes for acidosis following injury is shock – the metabolic acidosis that ensues is the result of tissue hypoperfusion and anaerobic metabolism; metabolic acidosis may also occur inpatients who have a respiratory alkalosis if hypoventialtion occurs suddenly
  4. intial resuscitation of trauma patients should be 2L or lactated Ringer’s and then PRBCs (for children 20 cc/kg of LR then 10 cc/kg of PRBCs)
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