Drowning and Submersion Injury

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Chapter 67 Drowning and Submersion Injury

Drowning is a leading cause of childhood morbidity and mortality in the world. Although the factors that put children at risk of drowning are increasingly well defined, the treatment of drowning has not advanced. Prevention is the most important step to reducing the impact of drowning injury, followed by early initiation of cardiopulmonary resuscitation (CPR) at the scene.

Epidemiology

In 2006, 4,248 people died from unintentional drowning in the USA. Compared with other types of injuries, drowning has one of the highest case fatality rates. Highest drowning death rates were seen in children aged 1-4 yr and 15-19 yr (2.81 and 1.47/100,000, respectively). In children, drowning is second only to motor vehicle injury as a leading cause of death from unintentional injury. Morbidity in nonfatal cases of drowning is much harder to determine. The ratio of hospitalized survival rate to death rate for drowning varies from 1 : 1 to 1 : 4 by age group and by state. Some estimates indicate that for each child who dies from drowning, 6 more are seen in an emergency department (ED). The Centers for Disease Control and Prevention (CDC) reported that in 2001, 3,372 people suffered fatal drowning and 4,174 were treated in the ED for nonfatal drowning. Estimates of drowning survivors with permanent, severe neurologic damage are not available.

The risk of drowning and the circumstances leading to it vary by age. Drowning risk also relates to male gender, exposure to water, and supervision. These factors are embedded in the context of geography, climate, socioeconomic status, and culture.

Global Impact of Drowning

The World Health Organization (WHO) estimates that 388,000 people died from drowning in 2004. Of these, 175,000 were younger than 20 yr. Deaths in low-income and middle-income countries accounted for the vast majority of these cases (98%). In these countries, drowning surpasses motor vehicle injury as the major cause of injury death. Given the relative size of the pediatric population in many of these countries, drowning is one of the leading causes of death globally. These data exclude any cases of drowning due to intentional harm or assault, accidents of watercraft or water transport, and drowning related to forces of nature/cataclysmic storms, which usually claim large numbers of lives per incident.

Some patterns of pediatric drowning are similar in all countries. By most accounts, the highest rates are seen in males and in children 1-4 yr old.

Whereas bathtubs and places of recreation (i.e., pools, spas) are significant locations for drowning in U.S. children, these are virtually unreported locations for drownings in developing countries. Instead, the predominant locations are near or around the home, involving bodies of water used for activities of daily living. These include water-collecting systems, ponds, ditches, creeks, and watering holes. In tropical areas, death rates increase during monsoon season, when ditches and holes rapidly fill with rain, and are highest during daylight hours, when caregivers are busy with daily chores.

Drowning during natural disasters such as storms and floods is important in all areas of the world. The largest numbers of flood-related deaths occur in developing nations, and most of these are due to drowning during the storm surge. In the USA and much of Europe, advances in weather monitoring and warning systems have reduced such deaths. Analyses of the largest and most recent flooding incidents, including Hurricane Katrina, showed that drowning caused the most deaths, particularly when people became trapped in their vehicles or attempted to rescue others.

Pathophysiology

Drowning victims drown silently and do not signal distress or call for help. Vocalization is precluded by efforts to achieve maximal lung volume or keep the head above the water, or by aspiration leading to laryngospasm. Young children can struggle for only 10-20 sec before being finally submerged. A swimmer in distress is vertical in the water, pumping the arms up and down. This splashing or efforts to breathe are often misconstrued by nearby persons as merely “playing” in the water until the victim sinks.

Once submersion occurs, all organs and tissues are at risk for hypoxia. In minutes, hypoxia leads to coma and then cardiac arrest, adding ischemia to the succession of events. Global hypoxia is the injury of drowning, with the severity of injury dependent primarily on its duration.

Anoxic-Ischemic Injury

After experimental submersion, a conscious animal initially panics, trying to surface. During this stage, small amounts of water enter the hypopharynx, triggering laryngospasm. There is a progressive decrease in arterial blood oxygen saturation (SaO2), and the animal soon loses consciousness from hypoxia. Profound hypoxia and medullary depression lead to terminal apnea. At the same time, the cardiovascular response leads to progressively decreasing cardiac output and oxygen delivery. By 3-4 min, the circulation abruptly fails because of myocardial hypoxia. Ineffective cardiac contractions with electrical activity may occur briefly, but there is no effective perfusion (pulseless electrical activity). Some drowning victims have a primary cardiac arrest secondary to a variant of an inherited prolonged QT syndrome. With early initiation of CPR, spontaneous circulation may initially be successfully restored. The extent of the global hypoxic-ischemic injury becomes more evident over subsequent hours.

With modern intensive care, the cardiorespiratory effects of resuscitated drowning victims are usually manageable and are less often the cause of death than irreversible hypoxic-ischemic central nervous system (CNS) injury (Chapter 63). CNS injury is the most common cause of mortality and long-term morbidity. Although the duration of anoxia before irreversible CNS injury begins is uncertain, it is probably on the order of 3-5 min. Victims with reported submersions of less than 5 min survive and appear normal at hospital discharge.

Several hours after cardiopulmonary arrest, cerebral edema may occur, although the mechanism is not entirely clear. Severe cerebral edema can elevate intracranial pressure (ICP), contributing to further ischemia; intracranial hypertension is an ominous sign of profound CNS damage.

All other organs and tissues may exhibit signs of hypoxic-ischemic injury. In the lung, damage to the pulmonary vascular endothelium can lead to acute respiratory distress syndrome (ARDS; Chapter 65). Aspiration may also compound pulmonary injury. Myocardial dysfunction (so-called stunning), arterial hypotension, decreased cardiac output, arrhythmias, and cardiac infarction may also occur. Acute tubular necrosis, cortical necrosis, and renal failure are common complications of major hypoxic-ischemic events (Chapter 529). Vascular endothelial injury may initiate disseminated intravascular coagulation (DIC), hemolysis, and thrombocytopenia. Many factors contribute to gastrointestinal damage; bloody diarrhea with mucosal sloughing may be seen and often portends a fatal injury. Serum levels of hepatic transaminases and pancreatic enzymes are often acutely increased. Violation of normal mucosal protective barriers predisposes the victim to bacteremia and sepsis.

Pulmonary Injury

Pulmonary aspiration (Chapter 65) occurs in a majority of drowning victims, but the amount aspirated is usually small. Aspirated water does not obstruct airways and is readily moved into the pulmonary circulation with positive pressure ventilation. It can wash out surfactant and cause alveolar instability, ventilation-perfusion mismatch, and intrapulmonary shunting. In humans, aspiration of small amounts (1-3 mL/kg) can lead to marked hypoxemia and a 10-40% reduction in lung compliance. The composition of aspirated material can affect the patient’s clinical course: Gastric contents, pathogenic organisms, toxic chemicals, and other foreign matter can injure the lung or cause airway obstruction. Clinical management is not significantly different in saltwater and freshwater aspirations, because most victims do not aspirate enough fluid volume to make a clinical difference. A few children may have massive aspiration, increasing the likelihood of severe pulmonary dysfunction.

Hypothermia

Hypothermia (Chapter 69) is common after submersion. It is often categorized, according to core body temperature measurement, as mild (34-36°C), moderate (30-34°C), or severe (<30°C). Drowning should be differentiated from cold water immersion injury, in which the victim remains afloat, keeping the head above water without respiratory impairment. The definition of cold water varies from 60 to 70°F.

Heat loss through conduction and convection is more efficient in water than in air and, if the water is cool, cannot be matched by the body’s thermogenic mechanisms (shivering and nonshivering thermogenesis, vasoconstriction, active movements). Children are at increased risk for hypothermia because they have a relatively high ratio of body surface area to mass, decreased subcutaneous fat, and limited thermogenic capacity. Hypothermia can develop as a result of prolonged surface contact with cold water while the head is above water (immersion) or after submersion, which involves the potential additional impact of swallowing or aspirating large quantities of very cold fluid. Hypothermia may develop more quickly with immersion in fast-flowing water as a result of increased convection.

Depending on water and air temperature, insulation, body surface area, thermogenic capacity, and physical condition, heat loss can lead to significant core temperature decreases. As core temperature drops to <35°C, cognition, coordination, and muscle strength become progressively impaired. The likelihood of self-rescue decreases at this point. With progressive hypothermia, there may be loss of consciousness, water aspiration, decreases in heart rate and cardiac output, ineffective breathing, and cardiac arrest.

Immediate effects of cold water immersion are respiratory and cardiovascular. Victims who drown in water <60-70°F also experience cold water shock, a dynamic series of cardiorespiratory physiologic responses. In human adults, immersion in icy water results in intense involuntary reflex hyperventilation and to a decrease in breath-holding ability to <10 seconds, which leads to fluid aspiration, contributing to more rapid and deep hypothermia. Severe bradycardia occurs in adults but is transient and rapidly followed by supraventricular and ectopic tachycardias and hypertension. There is no evidence that the diving reflex, or bradycardia that may occur in children after submersion, has any protective effect.

It may theoretically be possible for the brain to rapidly cool to a neuroprotective level, if the water is cold enough, the cooling process is quick, and cardiac output lasts long enough for sufficient heat exchange to occur. Once submersion-associated hypoxia, apnea, and cardiovascular compromise decrease blood circulation, the effect of hypothermia’s neuroprotection is mitigated.

After the child is removed from the water, body temperature may continue to fall as a result of cold air, wet clothes, hypoxia, and hospital transport. Hypothermia in pediatric drowning victims is observed even after drowning in relatively warm water and in warm climates. Unrecognized progressive hypothermia can lead to further decompensation. In hypothermic victims, compensatory mechanisms usually attempt to restore normothermia at body temperatures >32°C; at lower temperatures, thermoregulation may fail and spontaneous rewarming will not occur.

With moderate to severe hypothermia, progressive bradycardia, impaired myocardial contractility, and loss of vasomotor tone contribute to inadequate perfusion, hypotension, and possible shock. At body temperature <28°C, extreme bradycardia is usually present, and the propensity for spontaneous ventricular fibrillation (VF) or asystole is high. Central respiratory center depression with moderate to severe hypothermia results in hypoventilation and eventual apnea. A deep coma, with fixed and dilated pupils and absence of reflexes at very low body temperatures (<25-29°C), may give the false appearance of death.

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