Chokes, or pulmonary decompression sickness, is a rare but severe manifestation of decompression sickness (DCS) that can be rapidly fatal even with appropriate treatment.
Seawater weighs approximately 64 pounds per cubic foot/1024 kilograms per cubic meter. Freshwater weighs slightly less, but the two are considered equivalent when determining diving depth and calculating decompression schedules. When a diver descends in the water, the pressure around him or her increases as a function of the weight of the surrounding water. For example, at 33 feet of seawater (FSW)/10 meters of seawater (MSW), the pressure is twice atmospheric pressure (2 atmospheres absolute, or ATA, 1 ATA = 1.01325 bar = 760 mmHg); at 66 fsw/20 MSW, three times atmospheric pressure (3 ATA); at 99 fsw/30 MSW, four times (4 ATA), and so on. In order for the diver to inflate his or her lungs, breathing gas must be supplied at a pressure equivalent to the ambient water pressure. This is the function of diving equipment, whether it is self-contained underwater breathing apparatus (SCUBA) or surface-supplied.
Most divers breathe compressed air, which is roughly 78% nitrogen. However, nitrogen produces measurable decrements in cognitive performance, beginning at a depth of about 3 ATA/3 bar/66 fsw/20 MSW. This effect, known as nitrogen narcosis, becomes debilitating beyond approximately 200 fsw/60 msw . Dives deeper than that are typically made using a mixture of helium and oxygen since helium has almost no narcotic properties. Many technical divers use a combination of helium, nitrogen, and oxygen (“trimix”) at shallower depths to help offset the effects of nitrogen narcosis (and the considerable cost of using only helium as a diluent). Of note, though nitrogen is not chemically inert, it is often referred to by divers as an “inert” gas.
At atmospheric pressure, the dissolved inert gas in the body is in equilibrium with that of the atmosphere. As the pressure of the diver's breathing gas increases with increasing depth, the partial pressure of inert gas in the breathing mix rises as well. This creates a positive pressure gradient between the inert gas in the lungs and the gas dissolved in the blood and body tissues. Inert gas molecules in the lungs then pass through the alveolar-capillary interface and become dissolved in the body as a function of partial pressure and time. In other words, the farther a diver descends and the longer he or she stays at depth, the more inert gas becomes dissolved in the blood and body tissues.
As a diver ascends toward the surface, the inert gas pressure in the lungs decreases and the pressure gradient between the lungs and the body equilibrates and then reverses. When the partial pressure of dissolved inert gas in the body is higher than the partial pressure of inert gas in the lungs, the tissues become supersaturated. The gas molecules in the body then pass through the alveolar/capillary membrane into the lungs and are exhaled. This is a simplified description of the process known as decompression. There are detailed algorithms designed to control this process and allow the diver to return safely to the surface.
Body tissues will tolerate some supersaturation; however, "silent," or asymptomatic; bubbles may form in the venous blood even after normal, uneventful decompression. The physical process by which these bubbles form is the same as that which occurs in a carbonated beverage after the lid is removed. These bubbles pass through the right heart and become lodged in the arterial side of the pulmonary capillaries, where they are gradually reduced in size and eliminated by the process described above. However, if the pressure gradient becomes too great or if the decompression process goes awry, these venous bubbles may become large and/or numerous enough to obstruct the flow of blood through the pulmonary vasculature  which can result in rapid onset hypoxemia, hypercarbia, and death.
Rates of decompression sickness in divers range from 0.01% to 0.095% depending on the environment and type of diving performed . Figures reported to the Divers Alert Network and cited by Vann et al. show that pulmonary DCS comprises 5.6% of DCS cases and is the initial presenting symptom in 0.9% of those cases .
In addition to mechanically obstructing blood flow through the pulmonary vasculature, bubbles may directly contact and damage the vascular endothelium and activate the inflammatory cascade , all of which can result in or contribute to pulmonary edema, pulmonary hypertension , and decreased cardiac output . These complications can result in rapid decompensation and death despite a relatively stable initial presentation and appropriate recompression treatment .
Pulmonary DCS is highly unlikely in the setting of normal, uneventful decompression. More frequently, a diver suffering from pulmonary DCS will present with a history of omitted or improper decompression. Symptoms are similar to those of a thrombotic pulmonary embolus; specifically, substernal pain, cough, and dyspnea, which may progress quickly to pulmonary edema, respiratory failure, right ventricular dysfunction, and cardiovascular collapse. The diver may also have other signs and symptoms of decompression sickness such as neurological deficits; inner ear symptoms such as vertigo, hearing loss and tinnitus; trunk or pelvic pain; a marbled skin rash, or cutis marmorata; pain in the joints of the extremities; and/or extremity swelling. Divers with pulmonary DCS who initially appear relatively stable may decompensate rapidly, even after appropriate treatment is initiated.
Rarely, pulmonary decompression sickness can occur in aviators who fly high-performance aircraft. Pilots, especially military pilots, who present with symptoms of pulmonary DCS after altitude exposure, should be carefully evaluated and treated with hyperbaric oxygen therapy if necessary. 
Since decompression sickness is a clinical diagnosis and there are no radiological or laboratory studies that are diagnostic, it is important that a practitioner obtains as thorough a dive history as possible. This should include all dives in the dive series leading up to the event. The diver's computer, if available and the data can be accessed, is a valuable source of information. A health history, medical examination, and neurological examination should be completed. As noted previously, the provider should be alert for other symptoms of DCS.
Pre-hospital treatment of suspected pulmonary DCS consists of administration of high-flow oxygen at the maximum possible percentage, support of respiration and circulation, and immediate evacuation to a facility with a hyperbaric chamber and staff that are capable of treating critically ill divers. In the pre-hospital setting, depending on the location of the nearest appropriate hyperbaric facility, it may be more prudent to transport the diver to the nearest facility capable of caring for a critically ill patient.
The definitive treatment for pulmonary DCS is immediate recompression in a hyperbaric chamber and administration of an established hyperbaric oxygen treatment protocol, such as the U.S. Navy's treatment algorithm found in the U.S. Navy Diving Manual. A diver who presents with pulmonary DCS may also have other DCS symptoms and should be examined as thoroughly as his/her condition allows, mindful of the potential for rapid decompensation. Treating practitioners should be prepared to perform intubation and mechanical ventilation, invasive hemodynamic monitoring, and pharmacological support of blood pressure.
Differential diagnosis includes pulmonary edema (immersion or other etiology), myocardial infarction or other acute heart failure, water aspiration, breathing gas contamination, pulmonary oxygen toxicity (unlikely in most dive settings), and alkaline aspiration secondary to water intrusion in the breathing loop of a closed or semiclosed-circuit rebreather.
Pulmonary decompression sickness is a grave illness that may be accompanied by other life-threatening complications. Death may result despite appropriate and aggressive treatment.
Pulmonary DCS is best prevented by strictly adhering to established decompression protocols. Post-treatment, if the diver wants to return to diving, he or she should be evaluated by a practitioner trained and experienced in assessing fitness to dive. The practitioner should collaborate with the diver to isolate the events that led up to the DCS incident and provide counseling regarding future diving based on those events and the outcome of the diver's treatment.
EMS may initially transport a diver with pulmonary decompression sickness to a hospital that does not have a hyperbaric unit capable of treating a critically ill diver. Emergency department physicians in these facilities should immediately contact a physician trained and experienced in managing diving injuries . The Divers Alert Network (DAN) maintains a 24-hour emergency number at (US) +1 919-684-9111 and has a diving physician on call at all times. Outside the US, please refer to the DAN website at https://www.diversalertnetwork.org/contact/international.asp for the nearest DAN organization. DAN can also help locate the nearest recompression facility. Once a diagnosis of pulmonary DCS is established, the diver should be transferred to a recompression facility without delay, preferably via critical care conveyance since the diver may decompensate on transport. If the diver is transported via aircraft, altitude should be maintained as close to 1000 feet / 300 meters MSL (mean sea level) as safely possible per the U.S. Navy Diving Manual, Revision 7. Some authors suggest maintaining an altitude of 150 meters / 500 feet above the level at which the diver is retrieved .
Care of a critically ill diver in the receiving facility requires close collaboration between the emergency medicine team, hyperbaric team, critical care team, inpatient/hospitalist team, respiratory care practitioners, and nursing staff. The diver should be recompressed as soon as possible after arrival. Post-treatment, the diver should be placed in a care unit appropriate to his or her condition and expected progression. Pharmacists review drug treatments and check for drug-drug interactions. Hyperbaric nurses monitor patients, provide treatment, educate patients and their families, and provide real-time updates to the team. Aggressive resuscitative and life support measures may be necessary. Hyperbaric treatment may be repeated based on the diver's response to the initial treatment and the care team's assessment of the diver's ability to tolerate additional hyperbaric oxygen therapy (V).
|||Kirkland PJ,Cooper JS, Nitrogen Narcosis In Diving 2018 Jan; [PubMed PMID: 29261931]|
|||Assessment of the interaction of hyperbaric N2, CO2, and O2 on psychomotor performance in divers., Freiberger JJ,Derrick BJ,Natoli MJ,Akushevich I,Schinazi EA,Parker C,Stolp BW,Bennett PB,Vann RD,Dunworth SA,Moon RE,, Journal of applied physiology (Bethesda, Md. : 1985), 2016 Oct 1 [PubMed PMID: 27633739]|
|||Butler BD,Katz J, Vascular pressures and passage of gas emboli through the pulmonary circulation. Undersea biomedical research. 1988 May; [PubMed PMID: 3388630]|
|||Decompression illness., Vann RD,Butler FK,Mitchell SJ,Moon RE,, Lancet (London, England), 2011 Jan 8 [PubMed PMID: 21215883]|
|||Nossum V,Hjelde A,Brubakk AO, Small amounts of venous gas embolism cause delayed impairment of endothelial function and increase polymorphonuclear neutrophil infiltration. European journal of applied physiology. 2002 Jan [PubMed PMID: 11990728]|
|||Wang HT,Fang YQ,Bao XC,Yuan HR,Ma J,Wang FF,Zhang S,Li KC, Expression changes of TNF-α, IL-1β and IL-6 in the rat lung of decompression sickness induced by fast buoyancy ascent escape. Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc. 2015 Jan-Feb [PubMed PMID: 26094301]|
|||Zwirewich CV,Müller NL,Abboud RT,Lepawsky M, Noncardiogenic pulmonary edema caused by decompression sickness: rapid resolution following hyperbaric therapy. Radiology. 1987 Apr; [PubMed PMID: 3823462]|
|||Neuman TS,Spragg RG,Wagner PD,Moser KM, Cardiopulmonary consequences of decompression stress. Respiration physiology. 1980 Aug [PubMed PMID: 6776599]|
|||Neubauer JC,Dixon JP,Herndon CM, Fatal pulmonary decompression sickness: a case report. Aviation, space, and environmental medicine. 1988 Dec; [PubMed PMID: 3240220]|
|||Balldin UI,Pilmanis AA,Webb JT, Pulmonary decompression sickness at altitude: early symptoms and circulating gas emboli. Aviation, space, and environmental medicine. 2002 Oct [PubMed PMID: 12398262]|
|||Gertler SL,Stein J,Simon T,Miyai K, Mesenteric venous thrombosis as sole complication of decompression sickness. Digestive diseases and sciences. 1984 Jan [PubMed PMID: 6692739]|
|||Hibi A,Kamiya K,Kasugai T,Kamiya K,Kominato S,Ito C,Miura T,Koyama K, Acute kidney injury caused by decompression illness successfully treated with hyperbaric oxygen therapy and temporary dialysis. CEN case reports. 2017 Nov [PubMed PMID: 28900861]|
|||L'Abbate A,Kusmic C,Matteucci M,Pelosi G,Navari A,Pagliazzo A,Longobardi P,Bedini R, Gas embolization of the liver in a rat model of rapid decompression. American journal of physiology. Regulatory, integrative and comparative physiology. 2010 Aug [PubMed PMID: 20463181]|
|||Mitchell SJ,Bennett MH,Bryson P,Butler FK,Doolette DJ,Holm JR,Kot J,Lafère P, Consensus guideline: Pre-hospital management of decompression illness: expert review of key principles and controversies. Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc. 2018 May-Jun [PubMed PMID: 30028914]|