Emergency Medicine · Environmental Emergencies
The facts most likely to be tested
Decompression sickness results from the formation of nitrogen gas bubbles in tissues and blood following a rapid decrease in ambient pressure.
Henry's Law dictates that the amount of dissolved gas in a liquid is proportional to the partial pressure of that gas above the liquid.
Type I decompression sickness presents with joint pain (the bends) and skin manifestations such as cutis marmorata or pruritus.
Type II decompression sickness involves the central nervous system, cardiopulmonary system, or inner ear (the staggers).
Neurologic deficits including paresthesias, paralysis, or altered mental status are hallmark signs of severe, systemic involvement.
Hyperbaric oxygen therapy is the definitive treatment as it reduces bubble size and promotes the clearance of inert nitrogen gas.
Air travel should be avoided for at least 24 hours after diving to prevent the recurrence of symptoms due to further pressure changes.
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A 32-year-old male presents to the emergency department complaining of severe, aching pain in his right shoulder and left knee shortly after surfacing from a deep-sea scuba dive. He admits to a rapid ascent due to a malfunctioning buoyancy control device. On physical examination, he has a mottled, violaceous skin rash on his chest and abdomen. He is currently alert and oriented, but reports numbness and tingling in his lower extremities. His vital signs are stable.
What is the most appropriate next step in management?
Hyperbaric oxygen therapy
The patient exhibits signs of both Type I (joint pain, skin rash) and Type II (neurologic symptoms) decompression sickness, requiring immediate recompression via hyperbaric oxygen therapy.
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Etiology / Epidemiology
Occurs when dissolved nitrogen forms bubbles in tissues/blood during rapid ascent. High risk in scuba divers and aviators.
Clinical Manifestations
Type I: bends (joint pain), skin bends (mottled rash). Type II: neurologic deficits, staggers (vestibular), chokes (pulmonary).
Diagnosis
Primarily a clinical diagnosis. Hyperbaric oxygen therapy is both diagnostic and therapeutic.
Treatment
100% oxygen is the immediate first-line intervention. Do not delay transfer to hyperbaric chamber.
Prognosis
Early treatment prevents permanent neurologic sequelae. 100% recovery is common if treated within hours.
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Epidemiology & Etiology
Caused by rapid reduction in ambient pressure, leading to the formation of inert gas bubbles (Henry's Law). Primarily affects scuba divers who ascend too quickly or skip decompression stops. Also seen in high-altitude aviators following rapid cabin depressurization.
Pertinent Anatomy
Bubbles can form in the venous circulation, arterial system, or extravascular tissues. Involvement of the spinal cord and inner ear accounts for the most severe clinical presentations.
Pathophysiology
Rapid ascent prevents nitrogen from being exhaled, causing it to precipitate into bubbles. These bubbles cause mechanical obstruction, endothelial damage, and an inflammatory response similar to systemic inflammatory response syndrome. Secondary platelet activation and thrombosis exacerbate tissue ischemia.
Clinical Manifestations
Type I presents with dull, aching joint pain (the bends) and cutaneous manifestations like cutis marmorata. Type II is more severe, featuring paralysis, bladder dysfunction, and chokes (substernal chest pain/dyspnea). Red flags include altered mental status, seizures, and cardiopulmonary collapse.
Diagnosis
Diagnosis is clinical based on history of pressure change and symptom onset. Hyperbaric oxygen therapy is the gold standard for both confirmation and treatment. Imaging like MRI may show spinal cord lesions but should never delay definitive treatment.
Treatment
Administer 100% oxygen via non-rebreather mask immediately to promote nitrogen washout. Provide IV fluids for volume resuscitation. The definitive treatment is hyperbaric oxygen therapy (HBOT) in a recompression chamber. Contraindications to air travel include flying within 24 hours of a dive.
Prognosis
Prognosis is excellent with prompt recompression. Delayed treatment increases the risk of permanent spinal cord injury and dysbaric osteonecrosis. Patients require neurologic monitoring until symptoms resolve.
Differential Diagnosis
Arterial Gas Embolism: occurs within 10 minutes of surfacing
Nitrogen Narcosis: occurs at depth, not during ascent
Pulmonary Barotrauma: associated with pneumothorax
Myocardial Infarction: presents with chest pain without diving history
Stroke: focal deficits without preceding pressure change