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Children with acute or critical illness may be hypovolemic, euvolemic, or hypervolemic. They may have lost blood (eg, hemorrhagic shock), plasma (eg, severe burns), extracellular fluid (eg, gastroenteritis or diarrhea), or electrolytes. They may have internal compartment fluid redistribution (eg, ascites or capillary leak from sepsis or Dengue shock syndrome) and despite being edematous may still have intravascular volume depletion. Children with acute or critical illness may have renal impairment or high antidiuretic hormone (ADH) levels that results in fluid retention. Decisions about fluid management need to be based on clinical features and understanding of pathophysiology, thus systematic and repeated clinical evaluations are essential to good quality care. In this chapter, several acute clinical syndromes that require careful fluid management will be discussed.
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SHOCK AND FLUID MANAGEMENT
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Cells require oxygen for the production of adenosine triphosphate (ATP), the principal cellular energy source. In pathophysiological terms, shock occurs when cardiac output is insufficient to provide oxygen delivery to tissues for ATP production, leading to cellular dysoxia, with resulting anaerobic metabolism, lactic acidosis, and cellular dysfunction. The assumption behind fluid bolus therapy for shock is that it will improve cardiac output and in turn augment oxygen delivery to tissues. There are several clinical definitions of shock. Hypovolemic, low cardiac output shock manifests as “cold shock” with vasoconstriction, cold limbs, and tachycardia. This type of shock requires urgent fluid resuscitation. Cold shock occurs in severe dehydration (the classic examples being from cholera or gastroenteritis), hemorrhagic shock, and in some (generally late) stages of septic shock.
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Fluid resuscitation for children with fever and signs of shock has been controversial. This is partly because many clinical definitions of shock encompass a continuum from adaptive physiological changes to fever, to states of severe hypotension and dysoxia. Fluid therapy for shock has also been controversial because fluid therapy alone will not deal with shock apart from that which occurs solely from extracellular fluid losses. Therefore, in settings where intensive care support is unavailable, fluid therapy alone in some forms of shock will be insufficient. Many children with fever and 1 or 2 clinical cardiovascular signs of shock do not have hypovolemia or dysoxia. They have high levels of adrenaline and renin-angiotensin, leading to tachycardia and vasoconstriction, and raised levels of ADH, which leads to fluid retention, thus protecting them from hypovolemia and shock. The assumption that fluid boluses will improve cardiac output and in turn augment oxygen delivery to tissues is not certain if the cardiac output is normal or the child is not hypovolemic. In this situation, the benefits of bolus fluid therapy are less and the costs of excess fluid will be tissue edema and perhaps a blunting of the adaptive cardiovascular responses. A transient increase in stroke volume after fluid bolus therapy, because of an increase in venous return and left ventricular end-diastolic (filling) pressure, is often accompanied by a reduction in heart rate. ...