Pulmonary Decompression Sickness (Chokes)

Etiology

Pulmonary DCS occurs when inert gas bubbles vigorously form in the venous circulation or lung parenchyma, typically after a rapid decrease in ambient pressure, such as from ascent from a dive. The gas bubbles mechanically obstruct the pulmonary vessels, compromising pulmonary gas exchange. Irritation of the vascular endothelium triggers the inflammatory cascade, resulting in pulmonary edema. Without timely recognition and treatment, these events can lead to acute cardiopulmonary decompensation and death.

Risk factors for developing pulmonary DCS include rapid ascent or omitted decompression, deep or prolonged dives, repetitive dives, heavy work at depth, cold while decompressing, and individual physiological variables affecting gas absorption and elimination.

Epidemiology

The incidence of DCS among divers ranges from 0.01% to 0.095%, depending on the environment and type of diving performed. According to Vann et al, pulmonary DCS comprises up to 5.6% of DCS cases and is the initial presenting condition in 0.9% of those cases.[1] More recent data from Divers Alert Network (DAN) show that pulmonary DCS comprised 1.4% of DCS cases reported from 2014 through 2017.[2] In 2018, 4 out of 624 DCS cases reported to DAN involved pulmonary DCS.[3]

Pathophysiology

Seawater weighs approximately 64 pounds per cubic foot (1,024 kilograms per cubic meter). Freshwater weighs slightly less, but the two are considered equivalent when determining the diving depth and calculating decompression schedules at or near sea level. When a diver descends underwater, the ambient pressure increases as a function of the surrounding water's weight. For the diver to inflate the lungs, breathing gas must be supplied at a pressure equivalent to the ambient water pressure via self-contained underwater breathing apparatus (scuba) or surface-supplied diving equipment.

By convention, divers typically refer to nitrogen as an inert gas even though it is not chemically or biologically inert, as is helium, another breathing gas divers use for deep dives. Most divers breathe compressed air, which is roughly 78% nitrogen. However, nitrogen narcosis can ensue at depths of 66 feet (20 meters) or greater.[4][5] Divers use helium-oxygen mixtures for deeper dives to avoid nitrogen narcosis, as helium is virtually nonnarcotic. Some advanced recreational divers may use helium-nitrogen-oxygen mixtures (trimix) to balance nitrogen's narcotic effects and the cost of diluting the breathing gas with helium.

At atmospheric pressure, the partial pressure of inert gas in the body tissues is in equilibrium with that of the surroundings. As a diver's breathing gas pressure increases with increasing depth, the partial pressure of inert gas in the breathing mix also rises in alignment with Dalton's Law, which asserts that the total pressure of a gas mixture is the sum of the partial pressures of the gases in the mixture at constant temperature and volume.[6] This effect results in a positive pressure gradient between the inert gas in the lungs and the inert gas dissolved in the body tissues. Gas molecules in the lungs move along the pressure gradient and pass through the alveolar-capillary interface, dissolving in the blood and body tissues as a function of partial pressure, time, tissue perfusion, and the physical characteristics of the gas.

Ascent in the water column reduces the partial pressure of the inert gas in the lungs. The pressure gradient reverses at a certain point in the ascent, with the inert gas pressure in the tissues exceeding that in the lungs, and a state of tissue supersaturation exists. The inert gas molecules in the body then exit the tissues, enter the blood, and pass through the alveolar-capillary membrane into the lungs, where they are exhaled. Diving decompression algorithms are engineered to control tissue supersaturation, which minimizes gas bubble formation in situ and allows divers to ascend safely.

Asymptomatic venous gas emboli (VGE) composed mostly of inert gas are well-documented in divers even after appropriate decompression.[7][8][9] These VGE travel through the right heart chambers and the pulmonary arteries and lodge in the pulmonary capillaries, where they are eventually eliminated. Larger quantities of VGE form if the pressure gradient becomes too high. These bubbles can obstruct pulmonary circulation, disrupt the vascular endothelium, activate the inflammatory cascade, and cause pulmonary edema, pulmonary hypertension, and decreased cardiac output.[10][11][12][13] These complications can result in rapid-onset hypoxemia, hypercarbia, and death.[14] Patients can rapidly decompensate despite an initially stable presentation and appropriate recompression treatment.[15]

History and Physical

Divers with pulmonary DCS may have a history of omitted decompression or rapid ascent from a deep dive, though this condition can occur after seemingly normal decompression. Symptoms develop within minutes to several hours after ascent and include substernal pain, cough, and dyspnea, mimicking thrombotic pulmonary embolism. Pulmonary DCS can, and often does, occur alongside other DCS symptoms, including neurologic deficits, joint pain, swelling, torso pain, tinnitus, hearing loss, vertigo, and blotchy or marbled skin rash. If the diver experiences panic or uncontrolled ascent, pulmonary barotrauma signs and symptoms may also be present.[16]

Pulmonary DCS can occur in aviators who fly high-performance aircraft. Pilots, especially in the military, presenting with pulmonary DCS symptoms after altitude exposure should be carefully evaluated and treated with hyperbaric oxygen therapy (HBOT) if indicated.[17]

Initial vital signs may be within normal limits, but tachypnea, tachycardia, and hypoxemia may develop rapidly. Crackles may be appreciated on auscultation, though wheezing may also be heard if the patient has a preexisting pulmonary condition. Individuals with pulmonary DCS can deteriorate quickly due to pulmonary edema, respiratory failure, right ventricular dysfunction, and cardiovascular collapse even after receiving the appropriate treatment.

Evaluation

Pulmonary DCS is a clinical diagnosis that may accompany other symptoms of decompression sickness. The condition must be suspected in a patient presenting with sudden dyspnea, chest pain, and coughing after a precipitating event, particularly one that involves rapid decompression. Imaging studies are not diagnostic for pulmonary DCS, though chest imaging may show diffuse infiltrates bilaterally. In cases of significant decompression stress, radiologic imaging of the abdomen may show gas in the portal and mesenteric vessels, which supports a diagnosis of DCS. In rare cases in neurological DCS, magnetic resonance imaging of the brain and spine may reveal initial edema, followed by ischemic changes or infarcts.[18][19]

The arterial blood gas analysis results may suggest impaired gas exchange in the form of hypoxemia, hypercarbia, or respiratory acidosis but are not diagnostic. If accompanying frank gas in the abdominal veins impedes blood flow through the mesentery or abdominal organs, laboratory findings such as elevated aspartate transaminase, alanine transaminase, blood urea nitrogen, creatinine, amylase, lipase, and lactic acid may suggest end-organ ischemia.

Treatment / Management

Prehospital management of suspected pulmonary DCS must focus on patient assessment and supportive care, including maintaining oxygenation and ventilation using high-flow O2 via face mask, cardiac monitoring, and pulse oximetry. Waveform capnography, if available, may help recognize early pulmonary decompensation. The traditional left Trendelenburg position is no longer recommended as it may cause harm; instead, the patient should be maintained in a horizontal position. Intravenous access should be obtained in the field if possible.[20](B3)

Since pulmonary DCS can mimic many other conditions, differential diagnosis in the emergency department is critical. Divers Alert Network (DAN) maintains a 24-hour emergency hotline at +1-919-684-9111 and can connect emergency medicine providers with their on-call diving physicians. DAN can also help locate the nearest recompression facility. This organization has a global reach; DAN medics in the US can connect international callers with the appropriate resources in their area.

If pulmonary DCS is suspected, the patient must be given high-flow oxygen at the maximum possible concentration, which addresses hypoxemia and accelerates the reabsorption of extra-alveolar gas. Intravenous access should be obtained if not already completed in the field. The medical team should be alert for patient deterioration. Once stable enough for transfer from the emergency department, the patient must be promptly evacuated to a hyperbaric chamber and placed in the care of the hyperbaric team. Patients initially taken to hospitals without hyperbaric chambers must be transferred to a facility equipped to treat pulmonary DCS, with staff trained to manage such cases.

The definitive treatment for pulmonary DCS is prompt recompression in a hyperbaric chamber using an established HBOT protocol, such as the U.S. Navy's DCS treatment algorithm found in the U.S. Navy Diving Manual. Systemic complications warrant referrals to other specialists.[21]

Differential Diagnosis

Obtaining a detailed dive history is necessary to facilitate an accurate diagnosis. Ideally, the history should be obtained directly from the diver or a dive buddy who followed the same dive profile. Timing of symptom presentation is also critical information; for example, if the symptoms began before the diver ascended from the dive, DCS becomes much lower on the differential.

Conditions presenting with acute shortness of breath, chest pain, and coughing comprise the differential diagnosis of pulmonary DCS. These conditions include the following:

• Pulmonary barotrauma
• Pulmonary oxygen toxicity (unlikely in most dive settings)
• Water aspiration
• Breathing gas contamination
• Alkaline aspiration secondary to water intrusion in the breathing loop if the diver was using a closed-circuit or semi-closed-circuit rebreather
• Myocardial infarction
• Pulmonary embolus
• Acute pulmonary edema

Other diagnoses that can be considered in extreme environments are anaphylaxis, drowning, and asthma exacerbation.

Prognosis

The prognosis of pulmonary DCS varies depending on several factors. Chief among these is the volume of gas in the pulmonary vasculature and, thus, the degree of impediment created within the pulmonary circulation. The prognosis also depends on the promptness of treatment and the extent of inflammatory damage to the pulmonary vasculature. Mild-to-moderate pulmonary DCS has a generally favorable prognosis, especially if treated promptly. Severe cases may lead to death or long-term pulmonary complications, especially if treatment is delayed.

Complications

Pulmonary DCS can lead directly to hypoxemia, hypercarbia, acidosis, global ischemia, and death if not treated rapidly. Accompanying neurologic DCS symptoms may resolve with hyperbaric treatment or over time, but the patient may be left with permanent neurologic deficits in severe cases. Accompanying end-organ ischemia, as described above, may result in temporary or permanent organ failure.[22][23][24]