Prevention of acute tubular necrosis and the subsequent complications associated with acute renal failure (hyperkalemia, acidosis, hypocalcemia, fluid overload) is important. The use of pharmacologic agents to augment urine output is indicated when the intravascular volume has been replaced. The use of loop diuretics, such as furosemide, or combinations of a loop diuretic and a thiazide agent may enhance urine output. Infusion of low-dose dopamine, which produces renal artery vasodilation, also may improve urine output. Nevertheless, if hyperkalemia, refractory acidosis, hypervolemia, or altered mental status associated with uremia occurs, dialysis or hemofiltration should be initiated.
Shock results in impairment of tissue perfusion and oxygenation and activation of inflammation and cytokine pathways. The major complication of shock is multiple organ system failure, defined as the dysfunction of more than one organ, including respiratory failure, renal failure, liver dysfunction, coagulation abnormalities, or cerebral dysfunction. Patients with shock and multiple organ failure have a higher mortality rate and, for survivors, a longer hospital stay.
Early recognition and goal-directed intervention in patients with shock improve survival. However, delays in treatment of hypotension increase the incidence of multiple organ failure and mortality. Goal-directed therapy focused on maintaining mixed venous oxygen saturation may improve survival.
*Primarily splanchnic and renal in low doses (3–5 mcg/kg/min).
†Low dose (<0.3 mcg/kg/min).
Prevention strategies for shock are focused, for the most part, on shock associated with sepsis and hypovolemia. Some forms of septic shock can be prevented through use of immunizations (Haemophilus influenzae type b, meningococcal, pneumococcal vaccines). Decreasing the risk of sepsis in a critically ill patient requires adherence to strict hand washing, isolation practices, and minimizing the duration of indwelling catheters. Measures to decrease pediatric trauma do much to minimize hemorrhage-induced shock.
Unintentional injury is the leading cause of death in children 1 to 18 years of age. In 2010, approximately 52% of these deaths were caused by motor vehicle crashes. Most remaining unintentional injury-related deaths were the result of drowning (15%), poisoning (9%), burns (5%), and suffocation (4%). Geography, climate, population density (access to care), and population traits vary by region and affect the frequency, etiology, and severity of injuries.
Injury occurs through interaction of the host (child) with the agent (e.g., car and driver) through a vector and an environment (e.g., roadways, weather) that is conducive to exposure. The age of the child may determine the exposure to various agents and environments. For example, most injuries in infants and toddlers occur in the home as the result of exposure to agents found there (water heaters, bathtubs, softbedding). Gender affects exposure to injury, with boys having a fatal injury rate greater than that of girls.
The recognition that much of the morbidity and mortality are determined at the scene of an injury has stimulated the development of prevention measures. The Haddon matrix combines the epidemiologic components (host, agent, physical and social environments) with time factors (before, during, and after the event) to identify effective interventions focused on different aspects of the injury event. Primary strategies (preventing the event), secondary strategies (minimizing the severity of injury), and tertiary strategies (minimizing longterm impact) can be targeted for each epidemiologic component. Such strategies typically fall into one of three areas: education, enforcement, and environment (including engineering).
Education is often the first strategy considered but requires behavioral change and actions on the part of people. Most educational strategies are not well evaluated.