Decompression illness

Summary

Decompression illness is caused by intravascular or extravascular bubbles that are formed as a result of reduction in environmental pressure (decompression). The term covers both arterial gas embolism, in which alveolar gas or venous gas emboli (via cardiac shunts or via pulmonary vessels) are introduced into the arterial circulation, and decompression sickness, which is caused by in-situ bubble formation from dissolved inert gas. Both syndromes can occur in divers, compressed air workers, aviators, and astronauts, but arterial gas embolism also arises from iatrogenic causes unrelated to decompression. Risk of decompression illness is affected by immersion, exercise, and heat or cold. Manifestations range from itching and minor pain to neurological symptoms, cardiac collapse, and death. First-aid treatment is 100% oxygen and definitive treatment is recompression to increased pressure, breathing 100% oxygen. Adjunctive treatment, including fluid administration and prophylaxis against venous thromboembolism in paralysed patients, is also recommended. Treatment is, in most cases, effective although residual deficits can remain in serious cases, even after several recompressions.

Introduction

Decompression illness is caused by bubbles in blood or tissue during or after a reduction in environmental pressure (decompression). It includes two pathophysiological syndromes: arterial gas embolism and the more common decompression sickness. Arterial gas embolism occurs mainly during hyperbaric exposure (eg, diving) and rarely during hypobaric exposure (eg, altitude).

Arterial gas embolism occurs when expanding gas stretches and ruptures alveolar capillaries—pulmonary barotrauma—allowing alveolar gas to enter the arterial circulation (figure 1). This syndrome can occur after ascent from a depth as shallow as 1·0–1·5 m if the starting lung volume is close to total lung capacity.¹ It can be caused by gas becoming trapped as a result of airways obstruction in disorders such as asthma² or by the presence of pulmonary blebs, cysts, or bullae.³ Arterial gas embolism can also arise in the absence of decompression through iatrogenic accidents involving vascular catheters and mechanical ventilation.

Decompression sickness starts with the formation and increase in size of extravascular and intravascular bubbles when the sum of the dissolved gas tensions (oxygen, carbon dioxide, nitrogen, helium) and water vapour exceeds the local absolute pressure. In diving and during compressed-air tunnel and caisson work, this state of supersaturation is made possible by the increase in tissue inert gas partial pressure that occurs when the gas (usually nitrogen, but occasionally helium) is respired at high pressure. Supersaturation arises during decompression if the rate of ambient pressure reduction exceeds the rate of inert gas washout from tissue. Ascent to altitude in aviation and extravehicular activity during spaceflight involves exposure to decreased barometric pressure. In these settings, supersaturation arises as a result of pre-existing dissolved nitrogen at sea level (partial pressure of nitrogen of about 570 mm Hg), which can also cause bubble formation.

Venous gas emboli formed from dissolved gas are easily detected by ultrasonography. In divers, 3·6 m is the minimum dive depth after which venous gas emboli can be seen⁴ whereas the decompression sickness threshold, after saturation dives lasting 1–3 days, is about 6 m.⁵ During direct decompression from sea level to altitude, the threshold for formation of venous gas emboli is around 3600 m whereas the decompression sickness threshold is about 5500 m.6, 7

Bubbles can have mechanical, embolic, and biochemical effects with manifestations ranging from trivial to fatal. Clinical manifestations can be caused by direct effects from extravascular (autochthonous) bubbles such as mechanical distortion of tissues causing pain, or vascular obstruction causing stroke-like signs and symptoms. Secondary effects can cause delayed symptom onset up to 24 h after surfacing. Endothelial damage by intravascular bubbles can cause capillary leak, extravasation of plasma, and haemoconcentration.⁸ Impaired endothelial function, as measured by decreased effects of vasoactive compounds, has been reported in animals⁹ and might occur in man. Hypotension can occur in severe cases.¹⁰ Other effects include platelet activation and deposition,¹¹ leucocyte-endothelial adhesion,¹² and possibly consequences of vascular occlusion believed to occur in thromboembolic stroke such as ischaemia-reperfusion injury, and apoptosis.¹³

Arterial gas embolism most often affects the brain but can occasionally affect the heart and other organs. Decompression sickness produces symptoms related to the effects of bubbles on periarticular tissues, spinal cord, brain, lungs, skin, and the audiovestibular system. Concurrent arterial bubbles from arterial gas embolism exacerbate decompression sickness,¹⁴ possibly by reducing tissue perfusion and impairing inert gas washout or by increasing bubble size. Decompression sickness symptoms after recreational diving (figure 2) typically consist of pain or mild neurological manifestations such as numbness or paraesthesias. Most patients with altitude-related decompression sickness have similar manifestations,15, 16, 17, 18 although cerebral symptoms have been reported in U-2 pilots.19, 20

Small quantities of venous gas emboli are common in diving²¹ although they are usually asymptomatic because most of the time they are effectively filtered by the pulmonary circulation. However, large numbers of venous gas emboli can cause cough, dyspnoea, and pulmonary oedema (cardiorespiratory decompression sickness, or chokes)²² and can overcome the pulmonary capillary filter.²³ Moreover, a patent foramen ovale or other right-to-left cardiac shunt is present in about 27% of the normal population,²⁴ and theoretically some venous gas emboli could enter the arterial circulation and reach the CNS, where they could grow from the inward diffusion of supersaturated inert gas.²⁵ Patent foramen ovale has been statistically associated with cerebral, spinal, and vestibulocochlear manifestations,26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36 and with cutaneous manifestations.³⁰