Diving, Chokes

Article Author:
Eric Hexdall
Article Editor:
Jeffrey Cooper
Updated:
11/16/2017 1:39:20 AM
PubMed Link:
Diving, Chokes

Introduction

Chokes, or pulmonary decompression sickness, is a rare but severe manifestation of decompression sickness (DCS) that can be rapidly fatal if not treated.

Etiology

Seawater weighs approximately 64 pounds per cubic foot/1024 kilograms per cubic meter. Fresh water 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.  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.

Epidemiology

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 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. 

Pathophysiology

In addition to mechanically obstructing blood flow through the pulmonary vasculature, bubbles may directly contact the vascular endothelium and activate the inflammatory cascade, which can result in or contribute to pulmonary edema and acute respiratory distress syndrome (ARDS). Radiographic examination may show pulmonary edema, but this is not diagnostic. Pulmonary artery hypertension may occur and can lead to acute right heart failure and subsequent cardiovascular collapse.

History and Physical

Pulmonary DCS following normal, uneventful decompression is extremely rare. 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 symptoms of decompression sickness. 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.

Evaluation

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.

Differential diagnosis includes pulmonary edema (immersion or other etiology), 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.

Treatment / Management

Pre-hospital treatment of 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.

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. Practitioners, who are mindful that a diver with even mild pulmonary symptoms could decompensate quickly, may elect to conduct the examination in the chamber once the diver is at treatment pressure. Treating practitioners should be prepared to perform intubation and mechanical ventilation, invasive hemodynamic monitoring, and pharmacological support of blood pressure.