Richard E. Moon, M.D.
Decompression sickness (“bends,” DCS) arises from the generation of bubbles of inert gas in the tissue and/or blood in volumes sufficient to interfere with organ function, caused by rapid decompression during ascent from diving, flying, or a hyperbaric/hypobaric chamber. Bubble formation occurs when the speed of decompression exceeds the rate at which diffusion and perfusion reduce the tissue inert gas partial pressure. The resulting clinical manifestations include joint pains (limb bends), cutaneous eruptions or rashes (skin bends), neurological dysfunction (peripheral or central nervous system bends), cardiorespiratory symptoms and pulmonary edema (chokes), shock and death. Several mechanisms have been hypothesized by which bubbles may exert their deleterious effects. These include direct mechanical disruption of tissue, occlusion of blood flow, platelet deposition and activation of the coagulation cascade, endothelial dysfunction, and capillary leakage, complement activation, and leukocyte-endothelial interaction.
The diagnosis of DCS is made on the basis of signs and/or symptoms after a dive or altitude exposure. Manifestations most commonly include paresthesias, hypesthesia, joint pain, skin rash, and malaise. More serious signs and symptoms include motor weakness, ataxia, dyspnea, urethral and anal sphincter dysfunction, shock and death.
Chest radiography prior to HBO2 treatment in selected cases may be useful to exclude pneumothorax (which may require tube thoracostomy placement before recompression) and to exclude causes unrelated to diving for which treatment other than HBO2 would be appropriate (e.g. herniated disc). However, imagining studies are generally not helpful, and should not be relied upon to confirm the diagnosis of DCS or be used in deciding whether a patient with suspected DCS needs HBO2.
In addition to general supportive measures, included fluid resuscitation, airway protection, and blood pressure maintenance, the definitive treatment of decompression sickness is compression to suitable pressures greater than sea level. Improvement of decompression sickness symptoms as a result of compression was first noted in the Nineteenth Century. Recompression was first reported as a specific treatment for that purpose in 1896. Oxygen breathing was observed to improve the signs of decompression sickness in animals. The use of oxygen with pressure to accelerate gas diffusion and bubble resolution in humans was first suggested in 1897 and eventually tested in human DCS and recommended for the treatment of divers. The rationale for treatment with hyperbaric oxygen (HBO2) includes immediate reduction in bubble volume, increasing the diffusion gradient for inert gas from the bubble into the surrounding tissue, oxygenation of ischemic tissue and reduction of CNS edema. It is also likely that HBO2 has other beneficial pharmacological effects, such as a reduction in neutrophil adhesion to the capillary endothelium. The efficacy of administration of oxygen at increased ambient pressure (hyperbaric oxygen, HBO2) is widely accepted, and HBO2 is the mainstay of treatment for this disease.1
1 Hyperbaric Oxygen 2003: Indications and Results, The Hyperbaric Oxygen Therapy Committee Report by John J. Feldmeier, D.O., Chairman and Editor. Copyright 2003, Undersea and Hyperbaric Medical Society, Inc., Kensington, MD.