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Near Drowning

Clinical Features
Survival and Prognosis

Drowning accidents account for an estimated 7,000 to 8,000 deaths in the United States annually; most victims are children and young adults. The incidence of near drowning is unknown, but it has been estimated to be as high as 90,000 cases per year. Conventionally, episodes that result in immediate death are called drowning, and those in which the patient survives, even temporarily, are called near drowning. Although the diagnosis is readily apparent from the clinical setting, there is a broad spectrum of clinical severity determined by factors such as length of submersion, water temperature, volume and type of aspirated liquid, and associated complications or injuries.
Immersion accidents are often classified according to whether they occur in freshwater or saltwater. Differences in serum electrolyte concentrations and blood volume changes between these two forms of drowning were stressed in the early literature. Subsequent experimental studies demonstrated that electrolyte and blood volume changes are usually relatively minor or are so transient as to be clinically inapparent by the time the victim has been transported to a medical facility. The clinical problems associated with drowning in saltwater and freshwater are quite similar and include pulmonary injury, cerebral hypoxia, and hypothermia.
Although most drowning victims inhale a significant quantity of water into the lungs, autopsy studies indicate that little or no fluid enters the lungs in about 10% of cases. This phenomenon has been called dry drowning and is presumably caused by reflex laryngospasm, producing airway obstruction and asphyxiation. When this occurs, resuscitation at the scene of the accident usually results in a rapid return of spontaneous ventilation. Recovery is often dramatic and complete if the anoxic episode has not been prolonged.
The differential diagnosis of the cause of the immersion accident includes diving accidents with head or spinal injury, syncope, cardiac arrhythmia, myocardial infarction, seizure disorders, and scuba diving accidents such as decompression injury and systemic air embolism.
In most cases of near drowning, some degree of lung injury occurs because of the aspiration of water and foreign materials such as organic debris, sand, or vomitus. Seawater is markedly hypertonic compared with plasma and other body fluids. Aspirated saltwater causes alveolar edema by exerting an osmotic effect that draws free water into the lungs and by causing irritant damage to alveolar epithelial cells, increasing their permeability. Aspiration of freshwater is thought to cause a loss of surfactant, leading to alveolar instability, but it also causes damage to epithelial and endothelial cells, disrupting the integrity of the gas exchange barrier. In either situation, even in patients who improve rapidly with resuscitative efforts, the lung injury process may progress, leading to acute respiratory distress syndrome with widespread pulmonary edema and microatelectasis.
Tissue hypoxia related to prolonged submersion accounts for most of the other manifestations of near drowning. These include cerebral hypoxia, metabolic acidosis, depressed cardiac function, and dysrhythmias. Hypothermia, often profound, is seen frequently after near drowning and may contribute to the cardiovascular, metabolic, and central nervous system (CNS) changes.
Approximately 90% of patients admitted to the hospital after near drowning have some evidence of pulmonary aspiration. Gas exchange abnormalities and radiographic changes are extremely common and may progress after the patient reaches the emergency department. The mechanism of hypoxemia appears to be intrapulmonary venoarterial shunting due to alveolar edema and collapse. The chest radiograph often shows patchy, ill-defined infiltrates at the time of admission, with resolution or progression to more widespread involvement occurring over the next 12 to 24 hours. Lung compliance is usually reduced. Pulmonary infection is a common complication and may occur as a result of the lung injury process itself, prolonged intubation with acquisition of nosocomial pathogens, or airway obstruction due to aspirated foreign material.
Metabolic acidosis with a widened anion gap is extremely common and may persist for several hours, even when resuscitative efforts have been successful. This may reflect delayed lactic acid clearance or persistent tissue hypoxia with ongoing generation of lactic acid.
Experimental observations suggest that significant changes in blood volume or electrolyte concentrations occur only when the quantity of fluid inhaled has been great enough to severely limit survival. Except for life-threatening cardiac dysrhythmias in the period immediately after rescue, such changes are thought to be relatively unimportant determinants of disordered organ physiology after immersion injury.
Aspiration of freshwater leads acutely to hemodilution, a transient increase in blood volume, and dilution of electrolytes, primarily manifested as hyponatremia. These changes may explain the higher incidence of ventricular fibrillation in freshwater near drowning patients.
The aspiration of saltwater causes hemoconcentration, and a reduction in circulating blood volume as free water is drawn from the vasculature into the alveolar space. In those who survive the initial insult, restoration of normal blood volume and electrolyte concentrations is usually complete within 10 to 30 minutes.
Changes in the hematocrit may occur transiently owing to hemodilution or hemoconcentration. Freshwater aspiration may also be associated with mild degrees of hemolysis.
Injury to the CNS is probably the most serious and least reversible clinical event after immersion injury. Cerebral anoxia occurs within minutes after submersion under water and is compounded by circulatory collapse. The resulting cerebral edema leads to further reduction in cerebral perfusion, seizures, and eventually to irreversible brain damage.
Hypoxemia, acidosis, and hypothermia may contribute to neurologic abnormalities at the time of admission. The clinician should also be alert to associated abnormalities that may have predisposed the patient to a serious immersion accident. These include intoxication with alcohol or other drugs and the possibility of CNS trauma (e.g., subdural hematoma, cervical spine fracture associated with a diving injury).
Changes in cardiovascular function after immersion injury result from hypoxemia, acidosis, and hypothermia. The most life-threatening cardiovascular complication of near drowning is the development of ventricular fibrillation, which occurs most commonly in freshwater drowning and in episodes involving massive fluid aspiration. Ventricular fibrillation in hypothermic patients may be extremely refractory to attempts at cardioversion. In such patients, prolonged and aggressive resuscitation efforts are well justified because of the potential for complete recovery.
Bradycardia, hypotension, and myocardial depression are common in the early hours of hospitalization. In addition to ventricular and supraventricular dysrhythmias, the electrocardiogram may show ST-T-wave changes and the presence of J (or Osborn) waves in patients who are hypothermic. J waves represent prolonged depolarization of the ventricle and manifest as a prominent hump at the junction of the QRS complex and ST segment.
Aspiration of a large amount of seawater may result in hypovolemia because of a shift of intravascular fluid to the intra-alveolar space. If enough freshwater is aspirated, hypervolemia occurs initially. However, with rapid redistribution of fluid, especially as pulmonary edema develops, hypovolemia may exist by the time the patient reaches the hospital.
Hypothermia is a prominent feature of immersion injury and may contribute to many of the physiologic abnormalities seen in near-drowning victims. Hypothermia occurring at the time of the near drowning may also exert a protective effect, particularly in the CNS, by slowing tissue metabolism and minimizing the effects of hypoxia. Ventricular fibrillation is much more common and difficult to treat in patients with a body temperature below 28°C (83°F). When the body temperature is in this range, active core rewarming should be initiated using intravenous solutions warmed to body temperature; warmed electrolyte solutions for gastric, bladder, and peritoneal lavage; and ventilation with warmed, humidified gases. Continuous arteriovenous rewarming or cardiopulmonary bypass should be considered for severe hypothermia. Passive rewarming measures to prevent further heat loss should be undertaken for all hypothermic patients.
The initial treatment should occur at the scene of the immersion accident. The goal of therapy is to restore adequate oxygen delivery as rapidly as possible because tissue hypoxia is the major cause of morbidity and mortality. If the victim cannot be removed from the water quickly, ventilation should be initiated while the victim is still in the water. Attempts to drain water from the lungs are usually ineffective, may delay the initiation of cardiopulmonary resuscitation (CPR), and increase the risk of vomiting and aspiration of gastric contents. An abdominal thrust (Heimlich) maneuver should not be used routinely in submersion victims; it is reserved for cases in which obstruction of the airway with a foreign body is suspected or when the patient does not respond to mouth-to-mouth resuscitation.
Cardiopulmonary resuscitation should be started immediately. After the patient’s vital signs have been established, supplemental oxygen should be administered if available and the trachea should be intubated if the patient is comatose and appropriate equipment and personnel are available. After vital signs have been stabilized, the victim should be transported directly to the hospital.
Immediately upon admission to the hospital, electrolytes and arterial blood gases should be checked to assess metabolic and pulmonary function. There is controversy about whether to correct blood gas values for temperature in hypothermic patients. The clinician should be aware of whether or not the laboratory has corrected blood gas values for hypothermia. Intravenous access should be established and electrolyte solutions administered, with careful attention paid to possible electrolyte abnormalities and intravascular volume state. Measures to correct hypothermia should be initiated if indicated. Management of respiratory failure should follow the guidelines for treating the acute respiratory distress syndrome discussed in Chapter 357.
Although occasionally caused by the aspiration of grossly contaminated material, pulmonary infection is most commonly caused by hospital-acquired pathogens. Careful surveillance and institution of directed antibiotic therapy is most important. The use of prophylactic antibiotics is not recommended. When fever and leukocytosis are prolonged despite antibiotic therapy, the clinician should consider the possibility of bronchial obstruction due to aspirated foreign material, infection of the pleural space, or purulent sinusitis.
A variety of pharmacologic and other interventions directed at controlling cerebral edema have been used in victims of near drowning. Elevating the head of the bed, if the patient is hemodynamically stable, may alleviate cerebral swelling. It is also helpful to minimize the risk of further aspiration of gastric contents. Although controlled hyperventilation may be of some benefit in patients with elevated intracranial pressure, there are no data to support the use of corticosteroids or osmotic agents in this setting. Similarly, controlled hypothermia and barbiturate coma have not improved neurologic recovery or survival of patients who are comatose after immersion injury. Uncontrolled intracranial hypertension is associated with a uniformly poor prognosis.
Survival depends primarily on the success of initial resuscitative efforts and the recovery of neurologic function. Although respiratory failure can often be severe and prolonged, the prognosis for recovery of lung function is excellent in those who survive. The prognosis for neurologic recovery is influenced by age, duration of submersion, water temperature, and delays in the initiation of adequate CPR. The likelihood of survival is enhanced in children younger than 10 years. The importance of water temperature is emphasized by case reports describing submersion for as long as 40 minutes in extremely cold water with subsequent normal psychometric testing. Such cases are almost entirely limited to children. The immediacy and adequacy of initial CPR is more important than therapy, however sophisticated, after the patient has been taken to the hospital.
Prognosis for neurologic recovery can be assessed on the basis of clinical findings in the first hour of therapy. Spontaneous respiration in the period immediately after CPR is a favorable prognostic factor for neurologic recovery. In one retrospective series, all patients who exhibited spontaneous respirations at the conclusion of CPR survived without significant neurologic sequelae, and those who remained apneic died or survived with severe residual neurologic impairment. In another large series, the level of consciousness on admission to the emergency department was an important predictor. Of those who were alert and fully conscious on arrival or obtunded but arousable, 90% survived without neurologic sequelae. Of those who were comatose on arrival in the emergency department, 55% survived with normal function, 10% survived with persistent brain damage, and 34% died.
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