|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
An asphyxiated patient, whether an older child or an infant with aborted SIDS or birth asphyxia, poses an important challenge for the intensive care pediatrician. Asphyxia produces injury to a number of target end organs.
Asphyxia produces hypoxia with mixed metabolic and respiratory acidosis. The resultant hypoxia produces a fall in cardiac output by depression of the medullary cardiac regulation center, along with bradycardia and decreased myocardial contractility.[25] As compensation for this decreased cardiac output, blood flows preferentially to the cerebral and coronary circulations at the expense of shunting blood away from the kidneys and GI tract. Clinically asphyxiated children are cold and mottled, with evidence of a low-output shock state. Specific therapy for cardiovascular dysfunction secondary to asphyxia consists of correction of the respiratory abnormality, correction of the acidosis, and chronotropic and inotropic pharmacologic support. (Appropriate monitoring and general treatment of circulatory failure are discussed in the section on acute circulatory failure in children.)
Respiratory decompensation after asphyxiation is commonly characterized by pulmonary edema, which may be secondary to increased microvascular pressure from hypoxic myocardial failure or may reflect capillary endothelial damage with a resultant capillary leak.[364] Treatment of both conditions includes cardiovascular support and the use of CPAP or PEEP with positive-pressure ventilation. Respiratory support is effected by the establishment of a patent airway, supplementation of inspired oxygen, CPAP, and mechanical ventilation.
CNS complications of asphyxia include intraventricular hemorrhage, cortical infarction, and cerebral edema. Intraventricular hemorrhage is a problem in premature infants and is thought to occur as a consequence of hypoxic-ischemic necrosis of the paraventricular germinal matrix. This area undergoes liquefaction and ruptures into the ventricular system several hours to days after the initial asphyctic injury.[365]
Cortical infarction occurs in children of all ages. This condition usually develops in a "watershed pattern" and affects the motor cortex controlling the upper extremities and the visual cortex.[366]
Cerebral edema is a relatively late consequence of asphyxia that occurs 8 to 72 hours after injury. Because the ultimate neurologic outcome depends principally on the degree of cortical injury occurring at the time of asphyxia, aggressive management of cerebral edema can be expected to only prevent or reduce the amount of additional damage resulting as a late complication. Measures that ensure adequate oxygenation and hemodynamic stability should be instituted. Patients who demonstrate purposeful movements and normal brainstem examination 24 hours after their hypoxic insult have a good neurologic recovery. Children without these findings at 24 hours are more likely to suffer severe neurologic deficits or death.[367] (Treatment of cerebral edema is discussed in the CNS section.)
Asphyxia may cause renal ischemia and subsequent tubular or glomerular necrosis, as well as thrombosis of the renal vein or glomerular capillary bed. Metabolic complications in an asphyxiated infant or child may include hypoglycemia, hypocalcemia, hypomagnesemia, and metabolic acidosis, all of which produce profound myocardial depression and systemic hypotension.[368] Hypervolemia and hypo-osmolality are common problems associated with fluid resuscitation and the syndrome of inappropriate ADH secretion. Every attempt should be made to minimize free water overload.
The major hematologic complication of asphyxia is the development of DIC. In the newborn, as well as in older children, levels of vitamin K-dependent factors (II, VII, IX, X) may be low as a result of asphyctic hepatic dysfunction; these conditions may respond to vitamin K supplementation.
Splanchnic ischemia may produce necrosis of the intestinal mucosa with ulceration or perforation anywhere within the GI tract.[369] Monitoring is difficult and consists mainly of testing all nasogastric secretions and stool for blood, monitoring bowel sounds and abdominal girth, and
|
|
|
|
|
|
|
|
|
|
|
|
|
