Selection of fluids for resuscitation and ongoing use is dictated by clinical circumstances. Crystalloid volume expanders generally are recommended as initial choices because they are effective and inexpensive. Most acutely ill children with signs of shock may safely receive, and usually benefit greatly from, a 20-mL/kg bolus of an isotonic crystalloid over 5 to 15 minutes. This dose may be repeated until a response is noted. Colloids contain larger molecules that may stay in the intravascular space longer than crystalloid solutions and exert oncotic pressure, drawing fluid out of the tissues into the vascular compartment. However, long-term risks of colloids may exceed benefits. Care must be exercised in treating cardiogenic shock with volume expansion because the ventricular filling pressures may rise without improvement of the cardiac performance. Carefully monitoring cardiac output or central venous pressure guides safe volume replacement.
In an effort to improve cardiac output after volume resuscitation or when further volume replacement may be dangerous, a variety of inotropic and vasodilator drugs may be useful (Table 40-2). Therapy is directed first at increasing myocardial contractility, then at decreasing left ventricular afterload. The hemodynamic status of the patient dictates the choice of the agent.
Therapy may be initiated with dopamine at 3 to 15 mcg/kg/min; however, epinephrine or norepinephrine may be preferable in patients with decompensated shock. In addition to improving contractility, certain catecholamines cause an increase in systemic vascular resistance. The addition of a vasodilator drug may improve cardiac performance by decreasing the resistance against which the heart must pump (afterload). Afterload reduction may be achieved with dobutamine, milrinone, amrinone, nitroprusside, nitroglycerin, and angiotensin-converting enzyme inhibitors. The use of these drugs may be particularly important in late shock, when vasoconstriction is prominent.
The lung is a target organ for inflammatory mediators inshock and SIRS. Respiratory failure may develop rapidly andbecome progressive. Intervention requires endotracheal intubation and mechanical ventilation accompanied by the useof supplemental oxygen and PEEP. Care must be taken withthe process of intubation, because a child with compensatedshock may suddenly decompensate on administration of sedative medications that reduce systemic vascular resistance.Severe cardiopulmonary failure may be managed with inhalednitric oxide and, if necessary, extracorporeal membrane oxygenation.
Poor cardiac output accompanied by decreased renal blood flow may cause prerenal azotemia and oliguria/anuria. Severe hypotension may produce acute tubular necrosis and acute renal failure. Prerenal azotemia is corrected when blood volume deficits are replaced or myocardial contractility is improved, but acute tubular necrosis does not improve immediately when shock is corrected. Prerenal azotemia is associated with a serum BUN-to-creatinine ratio of greater than 10:1 and a urine sodium level less than 20 mEq/L; acute tubular necrosis has a BUN-to-creatinine ratio of 10:1 or less and a urine sodium level between 40 and 60 mEq/L (see Chapter 165). Aggressive fluid replacement is often necessary to improve oliguria associated with prerenal azotemia. Because the management of shock requires administering large volumes of fluid, maintaining urine output greatly facilitates patient management.