The main organs that are affected are the pulmonary, neurologic, cardiac, and renal systems.
After the patient is submerged, he or she aspirates a small amount of water causing reflex laryngospasm. Apnea leads to hypoxia and loss of consciousness. Once unconscious, most patients will aspirate a moderate amount of water. Approximately 10% of patients will maintain laryngospasm, causing what was previously described as “dry drowning.”15
Aspirated fresh water and salt water cause different path physiologic effects on the pulmonary system but ultimately lead to the same result. Aspirated fresh water causes surfactant to washout, thus altering the surface tension properties of the alveolus. The alveoli collapse, preventing ventilation and causing an intrapulmonary shunt. Some of the fluid diffuses into the cell walls of the alveoli, leading to cell rupture and edema. Most water, however, is absorbed into the plasma volume. The ultimate effects of fresh water aspiration are ventilation–perfusion (V/Q) mismatch from alveolar collapse and shunt (Fig. 136-1).15,16
Pathophysiology of drowning.
Salt water causes V/Q mismatch via a different mechanism. The aspirated hypertonic saltwater pulls fluid from the plasma into the alveolar spaces causing pulmonary edema. The fluid-filled alveoli thus are not ventilated, creating an intrapulmonary shunt (Fig. 136-1).14
Regardless of whether the event occurred in fresh water or sea water, the end result is pulmonary edema with a decrease in pulmonary compliance. This leads to an increased V/Q mismatch resulting from intrapulmonary shunting.
Most neurologic sequelae are because of hypoxia and ischemia. Decreased ventilation causes hypoxemia. Cardiopulmonary arrest leads to decreased cerebral blood flow. The combination of hypoxemia and decreased cerebral perfusion rapidly leads to ischemia. The neuronal cell destruction that occurs with ischemia subsequently causes cerebral edema and increased intracranial pressure (ICP). Despite a number of trials in previous decades, monitoring of ICP following drowning has not proven to influence management and thus is not recommended.17–19 The presence of pupillary reactivity and motor activity on initial examination in ER may help to predict which patients survive. However, these findings have not been shown to assist in the differentiation of neurologically intact versus vegetative state survivors.20 An EEG can be helpful in these patients.21 Predictors of poor outcome are burst suppression, generalized suppression, status epilepticus, and nonreactivity.22,23 The data on the long-term neurological outcome in drowning patients is scarce.24 MRI is better than CT scan in ascertaining the degree of brain swelling and edema.22 With cases of brain injury, tight glycemic control should be maintained, after CPR for 12–24 hours for children who remain comatose hypothermia has been recommended, but there is no strong scientific evidence for it.24 Approximately 10% of drowning survivors will suffer severe neurologic sequelae.24
Cardiac arrhythmias normally occur as a consequence of hypoxia, acidosis, and hypothermia. Decreased oxygen tension sensed by the carotid bodies leads to activation of the autonomic nervous system and frequently results in bradycardia and peripheral vasoconstriction. Sinus bradycardia and atrial fibrillation are the most commonly observed rhythms.25 Catecholamine release that accompanies the stress response also contributes to increased systemic vascular resistance. The cardiovascular picture often resembles cardiogenic shock. Decrease in cardiac output is usually related to the degree of hypoxemia and can be reversible with treatment of the underlying cause.
The possibility of long QT syndrome should be kept in the differential when someone dies suddenly in water. It is difficult to confirm in the absence of family history, a previously abnormal ECG, and if an autopsy is not performed.26,27
Clinically, significant electrolyte derangements are uncommonly observed. Most patients who survive drowning aspirate less than 10 mL/kgwater. Dog studies have shown that more than 11 mL/kg water need to be aspirated for fluid shifts and more than 22 mL/kg for significant electrolyte imbalances.1,6 Acidosis that is commonly seen is initially because of apnea-related hypercarbia causing respiratory acidosis, profound hypercalcemia, and hypermagnesemia.28
Renal failure can occur because of hypothermia and shock-induced acute tubular necrosis. The cause is multifactorial including lactic acidosis, myoglobinuria because of muscle injury, hypoxemia, and hypo perfusion.29
Disseminated intravascular coagulation (DIC) is uncommonly seen in the drowning victim and is a late finding when present.30 Anemia can occasionally be seen in drowning victims. As the volume of aspirated water is rarely sufficient to cause hemodilution, any decrease in hemoglobin should be assumed to be because of blood loss.
Hypothermia (core body temperature <35ºC) is often seen in drowning victims.31 It may contribute to bradycardia, ventricular fibrillation, acute respiratory distress syndrome (ARDS), and shock. Older literature has emphasized the importance of the “diving reflex.”32 This occurs in mammals when the face contacts cold water. The body responds with breath holding, vasoconstriction, bradycardia, and decreased cardiac output. The outcome is increased blood flow to cardiac and cerebral tissues. While there are a number of animals that exhibit this, it is not believed to play a significant role in humans. There is recent data to suggest that induced hypothermia may exert neuroprotective properties on victims of cardiac arrest.19,33 While this is a promising avenue, further research needs to be performed in this area. Therapeutic hypothermia in the pediatric drowning victim cannot be universally recommended at this time.34,35