In recent years, approximately 30 percent of DCS cases reported to the Divers Alert Network (DAN), have been Type I, and about 70 percent have been Type II.
Cutaneous manifestations of DCS include pruritus, subcutaneous emphysema, and scarlatiniform, erysipeloid, or mottled rashes. Localized swelling or peau d'orange may result from lymphatic obstruction.
Periarticular joint pain is typically described as a deep, dull ache, although it may be throbbing or sharp. There may be a vague area of numbness or dysesthesia around the affected joint. Movement of the affected extremity usually aggravates the pain, but inflation of a blood pressure cuff around the involved joint may relieve the pain for as long as the cuff is inflated. The shoulders and elbows are the joints most often affected in scuba divers, although essentially any joint may be involved.
Neurologic DCS may be manifested by a vast array of symptoms and signs. In fact, essentially any symptom is compatible with neurologic DCS. Classically, however, neurologic DCS involves the lower thoracic, lumbar, and sacral portions of the spinal cord and produces paraplegia or paraparesis, lower extremity paresthesias, and bladder dysfunction. Historically, urinary retention was such a frequent manifestation of spinal cord DCS that a urethral catheter used to be part of the diver's standard equipment. Hallenbeck and colleagues have convincingly demonstrated that at least some cases of spinal cord DCS result from venous infarction of the cord due to obstruction of venous drainage in the epidural vertebral venous plexus.
Pulmonary DCS results from massive venous air embolization and usually does not become symptomatic until at least 10 percent of the pulmonary vascular bed is obstructed. Signs and symptoms include chest pain, cough, dyspnea, shock, and pulmonary edema. The clinical course is often fulminantly downhill.
Many divers develop intravascular bubbles but no apparent illness; these have been called "silent bubbles" and their clinical significance is unclear.
A variety of laboratory abnormalities may be demonstrated in DCS, but most of them have little clinical relevance to acute care. Two tests that may be useful, though, are the urine specific gravity and hematocrit, because intravascular volume depletion and hemoconcentration are common in serious DCS. (This hemoconcentration may exacerbate the increased erythrocyte aggregation that has been demonstrated to occur at mild increased ambient pressure.) These two tests can help guide fluid replacement, which is an integral part of therapy.
Dysbaric casualties should be rapidly referred for hyperbaric treatment. However, the patient should also be evaluated for life-threatening nondysbaric injuries and, if present, resuscitation commenced.
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