The symptoms of decompression illness (DCI) have been observed in underwater and caisson workers since the early 1800s, when it was coined “caisson disease.” Today, DCI refers to the sequela that result from arterial gas embolism (AGE) and decompression sickness (DCS). Both conditions are the result of rapid changes in ambient pressure that cause dissolved inert gases to emerge in the circulation as bubbles. The rapid growth in popularity of underwater diving with a self-contained underwater breathing apparatus (SCUBA), particularly by travelers, has made DCS a diagnostic possibility even in land-locked areas. Although this chapter focuses on DCI, other dysbaric conditions with neurologic inflictions or complaints are also briefly discussed, which include middle ear barotrauma (MEBT), inner ear barotrauma (IEBT), alternobaric vertigo (ABV), carbon monoxide poisoning, nitrogen narcosis, oxygen toxicity, and swallow water blackouts.

DCS has been observed in those who perform submersion activities (e.g., SCUBA, saturation, or breath-hold diving), high-altitude aviation (e.g., U-2 pilots), and simulated altitude ascents. AGE can occur after resurfacing from depths of only 1 to 1.5 m, whereas DCS is never seen after surfacing from depths of less than 6 m and very rarely occurs after dives less than 10 m in depth. AGE can occur if the diver rapidly ascends to the surface, holds his or her breath during ascent, or has intrinsic lung disease, particularly those with blebs and asthmatics. DCS risk factors include longer submersion times, deeper submersions, high exertion and warm temperatures during the dive, cold temperatures after the dive, older age, obesity, dehydration, and male gender. Divers with a patent foramen ovale (PFO) appear to be at increased risk (odds ratios of 2.6 to 5.6) for neurologic DCI when compared with divers without a PFO. Dive computers and tables are available to advise whether “decompression stops” are required during ascent to mitigate the DCS risk.

DCI is estimated to occur in 3 out of every 10,000 dives, with higher rates in U.S. Navy and commercial divers and the lower rates in recreational divers. The Divers Alert Network produces an annual report, which profiles diving-related complications. Data from the most recent report are outlined in Table 131.1.

DCS is less commonly seen in high-altitude flying, when compared with submersion activities, and when observed, the symptoms are typically less severe and rarely include neurologic manifestations. A notable recent exception are Air Force U-2 pilots who fly at altitudes of up to 70,000 ft in suits that are pressurized to approximately 30,000 feet above sea level.

DCI is believed to result from bubbles of inert gas, particularly nitrogen, being formed in the circulation during decompression. In the case of submersion, at increasing pressures, inert gases, mostly nitrogen, become intensely dissolved in the blood and tissues of the body. The amount dissolved will increase if the temperature rises. Upon ascent (whether that is resurfacing from a dive or ascending in elevation, as in aviation), these inert gases come out of solution. Ideally, the gas is delivered to the alveoli, where it is expired. In reality, gas bubbles can be observed in the blood of all divers via ultrasound upon emergence from a dive. Typically, the pulmonary circulation filters the bubbles and the diver does not experience any symptoms. However, if the quantity of bubbles is too great, they will buildup and occlude small veins and lymphatic vessels. At high bubble loads, the pulmonary vasculature also develops occlusions, increasing right heart pressures and raising the possibility of opening an otherwise closed PFO through which bubbles can pass into the arterial circulation.

In addition to vessel occlusion, intravascular bubbles are known to irritate the endothelium, causing capillary leakage, and platelet, complement, and cytokine activation, leading to third spacing, hemoconcentration, small-vessel thrombosis, and eventually hypotension. The occlusive action in the venules combined with small-vessel thrombosis is hypothesized to be the cause of the cerebral, vestibular, and spinal cord injuries and dysfunction in neurologic DCS. Inert gases preferentially dissolve in tissue with a high lipid content, such as the central nervous system (CNS), where the emergence of nitrogenous bubbles are suspected to contribute to neurologic dysfunction and injury.

AGE has a slightly different pathophysiology. Alveolar gas that abruptly expands on decompression (Boyle law) and is not ventilated appropriately will force itself through the alveolar-capillary membrane and directly enter the arterial circulation, where it produces mechanical obstructions. The most notable clinical sequela occur when the cerebral or coronary vessels are occluded, producing ischemic strokes and myocardial infarctions.