Decompression Illness 2015-11-15T15:57:04+00:00

Pathophysiology and Hyperbaric Effects

Decompression illness (DCI) is an affliction of gas separation causing bubbles (foreign bodies) in the tissues and blood resulting from a decrease in ambient pressure. The gas separation results in a number of responses ranging from an immune “foreign body” response, ischemia, and finally a reperfusion injury. The separation of gas, to form bubbles in the blood or tissue, impedes blood and lymphatic flow by direct mechanical obstruction, as well as directly disrupts or distorts tissues when intratissue bubble formation occurs. Intravascular gas perturbs the vessel’s endothelial surface and the cell surfaces of the platelets and white blood cells. Should recompression relieve the bubble(s), a reperfusion injury in the affected area will likely occur.

Often, intravascular gas embolism (IGE) complicates DCI and may result from either a variant of DCI or a complication arising from separate, concurrent pulmonary barotrauma with gas embolization. Intravascular gas embolic occlusion potentially blocks off-gassing tissue areas during decompression and may potentiate the local DCI injury in the involved area.

All tissues, including bone, are susceptible to DCI. When the involvement includes the nervous system or heart, a potential life threatening condition exists. The spectrum of DCI symptomatology extends from simple malaise to full cardiovascular collapse. Central nervous system (CNS) injury may be subtle or blatant and peripheral nerves may be involved. DCI may also present as a variant of the systemic inflammatory response syndrome.

DCI has classically been categorized into Type I and Type II (and recently Type III when the injury occurs concurrent with and is complicated by intravascular gas embolism. Type I involves joints and their ligaments, lymphatics, and skin. Type II involves the central nervous system (brain and spinal cord, autonomic nervous system, and peripheral nervous system), the lungs (chokes), and the cardiovascular system.

A more recent proposal would classify DCI into a descriptive format that imparts more historical information about the injury. The evolution, manifestation, time of onset, gas burden and any evidence of barotrauma are fused into one diagnostic run-on sentence. This classification at first appears cumbersome, but the approach is useful in packaging vital, pertinent patient information at the time of admission to a treatment facility.

Recompression treatment in acute DCI has three main effects: bubble compression, aerobic support for ischemic tissues, and an anti-inflammatory effect. Recompression causes reduction of the size of bubbles in tissues and in vessels in accordance with the ideal gas law. Besides shrinking the bubbles mechanically to improve liquid flow, their resulting smaller size forces them back into solution. Recompression provides aerobic support by filling the plasma fraction of blood with an increased content of dissolved oxygen to support the oxygen needs of downstream tissues. This also promotes the diffusion of the inert gas out of the separated gas phase bubble, and facilitates the blockade of potential inflammatory mediators. Hyperbaric oxygen therapy blunts leukocyte adhesion and blocks lipid peroxidation. Thus, hyperbaric oxygen therapy recompression allows dissolution of the separated gas and attenuates the inflammatory response which occurs during reperfusion of acutely injured ischemic tissue.

DCI may involve the spinal cord or the brain. DCI can produce a spectrum of injury ranging from a transient ischemic attack-like event (TIA), a small stroke, or a major stroke. CNS ischemia produces two zones of injury. The umbra, is a region of ischemically destroyed or infarcted tissue and is surrounded by the penumbra, a region of viable, yet functionally impaired tissue. Penumbral regions of a CNS injury have been found to fill with polymorphonuclear leukocytes (PMN’s) and macrophages. In the early post DCI period, extravasated leukocytes in an ischemic CNS tissue function as an oxygen sink. The goal of hyperbaric oxygen therapy is to minimize conversion of penumbral to umbral tissue in regions of marginal oxygenation in the brain or spinal cord.

The DCI injury involves acute, subacute, and chronic phases. Further understanding of the immune/ inflammatory processes may lead to modifications of current treatments or new treatment modalities. Thus far, the use of pharmacologic agents has been disappointing in DCI patients. Drugs have failed to ameliorate acute, subacute, and chronic neurologic DCI injury. Recompression is the only effective treatment of this devastating disease.

Lymphocytes can be immunomodulated by different oxygen tensions. Subacutely and chronically they may roam the penumbra much as they would in a healing wound. If perfusion of the penumbra is not re-established, then dysfunctional regions of poorly perfused neuronal tissue may never again become functional. Successful reperfusion modulated by lymphocytes, macrophages and fibroblasts may account for the accelerated recovery in neurologically injured DCI patients undergoing a “tailing” series of hyperbaric oxygen treatments. New capillary growth in the ground substance matrix can be accelerated in ischemically injured CNS tissue undergoing hyperbaric oxygen therapy. However, the gradual recovery in a few patients with untreated severe neurological injuries from DCI was observed at the turn of the century.


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