Gas Embolism and Decompression Sickness

Introduction of gas into the arterial circulation (arterial gas embolism [AGE]) has traditionally been associated with scuba divers and attributed to pulmonary barotrauma during ascent from a dive while breathing compressed gas. However, it may also occur iatrogenically in several clinical circumstances, such as during cardiopulmonary bypass or as a result of inadvertent injection of air during a diagnostic arteriogram or hemodialysis. Additionally, large amounts of gas may enter the venous system (venous gas embolism [VGE]), such as during neurosurgical procedures with the patient in the sitting position, hemodialysis, insertion of a Harrington rod, total-hip replacement, cesarean section, laparoscopy, intrauterine laser surgery, arthroscopy (as a result of air escaping from a faulty air-powered drill), and hydrogen peroxide irrigation or oral ingestion (because of elaboration of gaseous oxygen from tissue and blood catalase). In addition, VGE can occur when a central venous catheter is opened to air. Severe VGE has occurred during orogenital sex after blowing air intravaginally.^[111] VGE has also been reported in patients with adult respiratory distress syndrome (ARDS) who were being ventilated with positive end-expiratory pressure.^[112] VGE in sufficient quantity may overwhelm the ability of the pulmonary vasculature to filter the gas and thereby allow bubbles to pass into the arterial circulation. Even small amounts of venous gas (e.g., VGE caused by decompression from diving) have recently been implicated in neurologic syndromes in scuba divers as a result of transatrial passage through a patent foramen ovale.^{[113] [114] [115] [116] [117] [118]}

The effects of gas embolism are not solely due to obstruction of vessels by bubbles. Bubble-endothelial interaction causes increased capillary permeability and extravsation of fluid.^{[119] [120]} Another effect has been demonstrated in a model of AGE in anesthetized rabbits^{[121] [122]} : small doses of intracarotid air may pass through the cerebral microcirculation and produce impaired vasoregulation, a delayed reduction in cerebral blood flow, and neurophysiologic impairment. Because this reduction in blood flow is abolished in subjects with neutropenia, it has been concluded that leukocytes are required for this effect.^[123] This phenomenon of a delayed reduction in cerebral blood flow may be responsible for the clinical observation of initial neurologic improvement after AGE, followed by delayed deterioration.^[124]

The symptoms of AGE classically consist of impaired consciousness, hemiparesis, or seizures, but they may be of a less severe nature.

A related syndrome that results from the pathologic effects of tissue and blood gas bubbles is the decompression sickness seen in aviators and compressed gas divers. The gas bubbles in these situations occur because of a decrease in ambient pressure at a rate sufficient to induce local inert gas supersaturation and subsequent formation of bubbles in situ from tissue stores. Manifestations commonly consist of paresthesias, joint pain, or in more severe cases, spinal cord injury, vertigo, tinnitus, and hearing loss.^{[125] [126]}

The treatment principles for both forms of gas bubble disease, AGE and decompression sickness, are the same and consist of fluid resuscitation, administration of a high inspired O₂ concentration, and an increase in ambient pressure. Increasing arterial PO₂ by administering supplemental O₂ , even at ambient pressure, as a first aid measure results in an increased rate of resolution of gas bubbles because of the resulting higher partial pressure gradient for diffusion of inert gas from the interior of the bubble into the surrounding tissue or blood.

Fluid resuscitation will replenish intravascular volume, reduce hemoconcentration, and facilitate microcirculatory flow,^[127] principles that have been confirmed by both animal^[128] and human observations.^[119] Excess fluids can worsen pulmonary gas exchange in cardiorespiratory decompression sickness (pulmonary edema secondary to VGE) and are not indicated for isolated AGE.^[127]

Hyperbaric therapy will cause a diminution in gas volume according to Boyle's law and further hasten resolution. The usefulness of hyperbaric treatment of diving-related or aerospace-related gas embolism associated with rapid decompression is well documented.^{[12] [13]} Less recognized but equally documented is the use of HBO for the treatment of iatrogenic embolism. HBO therapy may result in neurologic improvement even after many hours has elapsed between the embolic event and treatment,^{[129] [130] [131]} although severe abnormalities are less likely to resolve if not treated promptly. Treatment of AGE is usually performed at ambient pressures from 2.8 to 6 ATA (see the section "Hyperbaric Treatment Schedules").

The morbidity associated with recompression treatment of gas bubble disease is extremely low and the efficacy high. Therefore, whenever suitable recompression facilities are available, it is usually appropriate for all symptomatic individuals with gas embolism or decompression illness to receive hyperbaric treatment.^{[11] [13] [132] [133]} In addition, most hyperbaric physicians recommend treatment even for asymptomatic patients who have experienced gas embolism to the central nervous system

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The decision to administer recompression treatment should be based on clinical evaluation. The only appropriate role for brain or spinal imaging (e.g., CT, magnetic resonance imaging [MRI]) is to exclude other pathologies such as hemorrhage—and only if there is a high degree of suspicion that bubbles are not the cause of a patient's symptoms. Some authors have suggested that patients with AGE be treated with HBO only if CT of the brain reveals air.^[134] In our experience, brain imaging of patients who respond clinically to HBO shows abnormalities in a minority of cases. Furthermore, HBO-responsive phenomena besides occlusion of vessels by macrobubbles, such as edema or a delayed reduction in cerebral blood flow, may not be detectable with currently available imaging techniques. Unless one has a strong clinical suspicion of a pathologic process other than AGE that requires urgent exclusion (e.g. intracranial hemorrhage), performing CT, MRI, or other imaging before recompression serves only to delay appropriate treatment. Neither single photon emission computed tomography (SPECT) nor positron emission tomography (PET) has yet been demonstrated to provide clinically useful information in the management of patients with gas bubble disease.