Pathophysiology of Dehydration
The negative fluid balance that causes dehydration results from decreased intake, increased output (renal, GI, or insensible losses), or fluid shift (ascites, effusions, and capillary leak states such as burns and sepsis). The decrease in total body water causes reductions in both the intracellular and extracellular fluid volumes. Clinical manifestations of dehydration are most closely related to intravascular volume depletion. As dehydration progresses, hypovolemic shock ultimately ensues, resulting in end organ failure and death. Young children are more susceptible to dehydration due to larger body water content, renal immaturity, and inability to meet their own needs independently. Older children show signs of dehydration sooner than infants due to lower levels of extracellular fluid (ECF). Dehydration can be categorized according to osmolarity and severity. Serum sodium is a good surrogate marker of osmolarity assuming the patient has a normal serum glucose. Dehydration may be isonatremic (130-150 mEq/L), hyponatremic (< 130 mEq/L), or hypernatremic (>150 mEq/L). Isonatremic dehydration is the most common (80%). Hypernatremic and hyponatremic dehydration each comprise 5-10% of cases. Variations in serum sodium reflect the composition of the fluids lost and have different pathophysiologic effects Isonatremic (isotonic) dehydration occurs when the lost fluid is similar in sodium concentration to the blood. Sodium and water losses are of the same relative magnitude in both the intravascular and extravascular fluid compartments. Hyponatremic (hypotonic) dehydration occurs when the lost fluid contains more sodium than the blood (loss of hypertonic fluid). Relatively more sodium than water is lost. Because the serum sodium is low, intravascular water shifts to the extravascular space, exaggerating intravascular volume depletion for a given amount of total body water loss.[1, 2] Hypernatremic (hypertonic) dehydration occurs when...
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