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The person may effectively drown without any sort of liquid. In cases of dry drowning in which the victim was immersed, very little fluid is aspirated into the lungs. The laryngospasm reflex essentially causes asphyxiation and neurogenic pulmonary edema (œdema).
In normal breathing, the diaphragm contracts, causing the lungs to expand (lungs are above the diaphragm). This expansion draws air into the lungs by generating a negative pressure or vacuum. Air first travels through the rigid larynx and upper airways before filling the inflatable alveoli in the lungs.
When water or other foreign bodies are inhaled, laryngospasm occurs and the person's larynx spasms shut. As a result, the vacuum created by the diaphragm cannot be filled by the inrush of air into the lungs, and the vacuum persists. In an attempt to force air in through the spasmed larynx, the person may breathe deeper and with more effort, but this only increases the vacuum's force inside the chest. The obstruction to the inflow of oxygen causes hypoxia, and the obstruction to the outflow of carbon dioxide causes acidosis, both resulting in death.
In addition, a multifactorial form of pulmonary edema is produced. The heart continues to beat normally during this time, and blood continues to circulate, though pulmonary oxygen and carbon dioxide gas exchange is markedly reduced. The volume of blood in the pulmonary circulation increases, by pulling in more blood from the abdomen, head, arms and legs; abnormally large volumes of this blood enter the pulmonary circulation via the superior and inferior vena cavae (great veins) in response to the persistent partial vacuum. From the vena cavae, the increased blood volume flows through the right atrium and into the right ventricle. The blood volume is great enough to stretch out the ventricle, similar to water entering a balloon.
The ventricle typically responds to this increased volume of blood by contracting and pumping with increased strength—a phenomenon known as the Frank–Starling mechanism. On being ejected from the right ventricle, the blood is forced into the pulmonary artery and then to the pulmonary circulation.
In the lungs, the nature of the vasculature changes. The vessels that carry deoxygenated blood (the pulmonary arteries) to the lungs become extremely narrow—narrow enough that red blood cells have to pass through in single file. The walls of the vasculature also become extremely thin to allow oxygen to enter the red blood cells and carbon dioxide to leave. In the case of dry drowning, however, there is no oxygen available in the lungs; there is only a partial vacuum. This partial vacuum draws some of the fluid from the vasculature and into the airspaces of the lungs, creating pulmonary edema, and the patient is now drowning in their own fluids.
At the same time, the sympathetic nervous system responds to the emergency of the closed larynx. Among other things, it constricts much of the body's vasculature. This vasoconstriction increases the blood pressure against which the left ventricle must pump, and may cause enough backpressure to ripple back through the left ventricle, into the left atrium, and into the pulmonary vasculature. This additional pressure on the blood in the lungs' blood vessels exacerbates the edema described above.
Additionally, the actions of the sympathetic nervous system can damage the lungs' vasculature, allowing even more fluid to escape into the lungs' airspaces.
Dry drowning was cast into the media spotlight in June 2008 after the death of a 10-year-old boy in South Carolina several hours after swimming. In this case, "dry drowning" may have been a misnomer, however. The incident described by the boy's mother did relate an episode of forceful apnea that would have indicated laryngospasm and therefore dry drowning. What is clear is that this boy's death involved the delayed effects of an injury suffered by his lungs while in the swimming pool. Typically, dry drowning involves laryngospasm and immediate hypoxia and death, not delayed pulmonary edema. Theoretically, it is possible that the negative inspiratory forces of the diaphragm against the closed upper airway in laryngospasm could cause enough barotrauma to trigger alveolar injury and pulmonary edema. In this case of barotrauma, the dry-drowning survivor could suffer laryngospasm too brief to cause death, but long enough to cause delayed pulmonary edema and death several hours later. This phenomenon would be similar to the delayed pulmonary edema of a "wet drowning" victim, however, and therefore fairly impossible to distinguish. It is unclear as to why the media labeled the 10-year-old's death a case of "dry drowning" rather than a "secondary drowning" or "delayed-submersion injury."[original research?]