Pathophysiology of Drowning and Near-Drowning

Drowning, as a cause of death, involves impairment of the respiratory system via either immersion (upper airway above water) or submersion (upper airway under water). The pathophysiology of drowning is complex and involves both the salinity and temperature of the submersing liquid.

With accidental or planned submersion, breath holding is the first conscious response. After the initiation of breath holding several events occur in parallel.

1. The body continues aerobic metabolism and CO₂ continues to rise. The rate of rise varies in sources, but seems to fall somewhere about 12-13 mmHg/mL for the first 60s then 3.4-6 mmHg/mL per minute afterwards. Most adult humans will have a very pronounced hypercapnic respiratory drive and will attempt to breathe at PaCO₂ values of 43-53 mmHg, equating to 60-90 seconds of breath hold.
2. The elevation in PaCO₂ stimulate the neural respiratory centers via changes in CSF pH and at carotid body chemoreceptors. This leads to a struggle phase with involuntary movements of internal intercostal muscles and diaphragmatic movement. Shortly after this initiation, individuals may attempt to breathe. Swallowing (either the motion alone or swallowing water) may be able to prolong the breath hold by allowing some movement of the respiratory musculature. Inhalation during a submersion leads to intake of water into the pharynx and, in some people, laryngospasm. Involuntary attempts at ventilation during a breath hold or laryngospasm can also lead to negative pressure pulmonary edema.
3. Depending on water temperature and inter-individual variations, the diving response may take place. The diving response seems to be an innate reflex in children, seen in 90% of 12 month old infants, and decreases in frequency with age, as seen in 66% adults. This reflex is triggered by some combination of apnea and facial immersion and leads to stimulation of both sympathetic and parasympathetic centers. This allows for reduction in perfusion to non-essential organs and tissues via profound peripheral vasoconstriction and hypertension, reduction in heart rate through vagal parasympathetics and suppression of central respiratory generation leading to apnea. This allows for reduction in metabolism and oxygen utilization in the periphery while preferentially perfusing the CNS.

Continued apnea, either from breath holding, laryngospasm or some combination of both will lead to desaturation and loss of consciousness. Desaturation can lead to laryngeal loss of muscular tone and frank aspiration of fluid. At this point, the aspirated fluids will directly fill alveoli, dilute pulmonary surfactant leading to atelectasis and increase the transcapillary hydrostatic gradients to disrupt capillary barriers. This leads to an acute lung injury much like ARDS and increased transpulmonary shunting, up to 75% in some studies of seawater drowning.

Finally, if continued, apnea and aspiration of fluids in drowning can lead to respiratory acidosis, ventricular fibrillation and cardiac arrest.