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Emergency And Acute Medicine – Decompression Sickness
Core Description
Decompression sickness is a multisystem disease caused by the formation of inert gas bubbles, primarily nitrogen, that escape from solution into body tissues and fluids during or after a reduction in ambient pressure.
Etiology And Pathophysiology
Decompression sickness occurs when nitrogen that has dissolved in body tissues under increased ambient pressure comes out of solution too rapidly during ascent. As ambient pressure increases, the partial pressure of inspired nitrogen rises, leading to progressive nitrogen absorption into tissues, particularly with longer exposure times. When ascent occurs too quickly, the pressure gradient overwhelms the body’s ability to eliminate nitrogen gradually. Tissues become supersaturated, and gas bubbles form.
According to Henry’s law, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas. Increased partial pressure results in greater gas dissolution, while decreased partial pressure causes gas to come out of solution. Nitrogen bubbles act as foreign bodies, triggering inflammatory and coagulation pathways, increasing vascular permeability, reducing intravascular volume, and causing hemoconcentration.
Clinical manifestations depend on bubble location. Bubbles may obstruct blood flow or lymphatics, leading to ischemia, infarction, or lymphedema, or they may cause mechanical tissue distention resulting in pain.
Risk Factors
Dive-related factors include greater depth, longer bottom time, multiple dives within a day, rapid ascent, and cold water exposure. Human factors include obesity, dehydration, pulmonary disease, and intercurrent illness. Proper use of dive tables or computers reduces but does not eliminate risk. Predive vigorous exercise may reduce risk. Approximately 50% of patients develop symptoms within 1 hour and 90% within 6 hours. Air travel after diving can precipitate decompression sickness because of reduced cabin pressure.
Clinical Presentation
Cutaneous Manifestations
Skin findings include scarlatiniform, erysipeloid, or mottled rashes. Cutis marmorata, a mottled appearance, often indicates more severe disease. A peau d’orange appearance may occur due to lymphatic obstruction.
Musculoskeletal Manifestations (The Bends)
Patients experience dull, deep muscular or joint pain, most commonly affecting the elbows and shoulders. Pain is typically not worsened by movement and is not reproducible with palpation.
Gastrointestinal Manifestations
Symptoms include nausea, vomiting, and abdominal pain.
Pulmonary Manifestations (The Chokes)
Pulmonary symptoms result from obstruction of pulmonary vasculature by gas bubbles and include acute respiratory distress, substernal chest pain or pressure, cough, dyspnea, and hypoxia.
Central Nervous System Manifestations
Neurologic symptoms include weakness, fatigue, numbness, paresthesias, agitation, headache, dizziness, vertigo, seizures, bladder or bowel incontinence, lethargy, and visual disturbances. The spinal cord, particularly the lower thoracic and lumbar regions, is most commonly affected.
Inner Ear Manifestations (The Staggers)
Vestibular involvement causes dizziness, vertigo, tinnitus, and nausea. These symptoms resemble inner ear barotrauma but carry a worse prognosis.
History And Physical Examination
A detailed dive history is essential, including depth, duration, ascent profile, surface intervals, and timing of symptom onset. Physical examination should be comprehensive, with particular attention to a detailed neurologic assessment to identify subtle or evolving deficits.
Essential Evaluation
Diagnosis is primarily clinical and based on recognition of risk factors and characteristic presentations. Neurologic findings should be carefully documented, including improvement or progression. Definitive diagnosis may be supported by a trial of pressure, as rapid symptom relief during recompression in a hyperbaric chamber is often diagnostic.
Diagnostic Testing And Interpretation
Laboratory studies may show elevated hematocrit due to hemoconcentration. Electrolytes, renal function, glucose, and urinalysis should be obtained, with increased urine specific gravity suggesting volume depletion. Arterial blood gas analysis and pulse oximetry are used to monitor oxygenation.
Imaging may include chest radiography to assess for pulmonary barotrauma or noncardiogenic pulmonary edema. Extremity radiographs may help exclude traumatic causes of pain. Head CT is indicated for altered mental status or focal neurologic deficits.
Differential Diagnosis
Consider musculoskeletal injury unrelated to bubble formation, inner or middle ear barotrauma, arterial gas embolism, cerebrovascular accident, and trauma.
Prehospital Management
Early recognition is critical, as postdive extremity pain may be misattributed to muscle strain and neurologic symptoms may be minimized by patients. If air evacuation is required, altitude should be limited to less than 1,000 feet or a pressurized aircraft should be used. In-water recompression is controversial, technically difficult, and requires extensive support.
Initial Stabilization
Airway, breathing, and circulation should be managed promptly. Administer 100% normobaric oxygen via mask or endotracheal tube to enhance nitrogen elimination, reduce bubble size, and improve tissue oxygenation. Maintain the patient in a supine position to minimize cerebral involvement. Early recompression in a hyperbaric chamber is essential.
Emergency Department Management
Administer intravenous 0.9% normal saline to correct dehydration and maintain urine output of 1–2 mL/kg/hour. Dehydration is common due to pressure-induced diuresis, exertion, dry compressed air breathing, and capillary leak. Adequate hydration promotes nitrogen elimination.
Arrange urgent hyperbaric oxygen recompression therapy and transfer to the nearest facility. Insert a prophylactic chest tube for known pneumothorax to prevent tension pneumothorax during recompression. Inflate endotracheal and Foley catheter balloons with saline or water to prevent compression-related damage.
Provide analgesics and antiemetics as needed. Diazepam may be used for severe vertigo. Adjunctive NSAIDs or heliox may reduce the number of recompression treatments required. Consultation with Divers Alert Network is recommended for expert guidance and referral.
Disposition And Follow-Up
All patients with suspected or confirmed decompression sickness should be referred for hyperbaric therapy. Stable patients with mild symptoms may be discharged after treatment. Patients should avoid air travel after treatment, as reduced ambient pressure may worsen symptoms.
Follow-Up Recommendations
Ensure hyperbaric medicine follow-up and reinforce diving safety counseling.
Key Clinical Lessons And Common Errors
Musculoskeletal decompression sickness can be difficult to distinguish from benign musculoskeletal pain. Significant fatigue alone may represent decompression sickness. Even mild or resolving symptoms warrant hyperbaric recompression therapy. Do not delay recompression for laboratory testing or imaging when decompression sickness is the likely diagnosis. In-water recompression should be avoided.
Core Description
Decompression sickness is a multisystem disease caused by the formation of inert gas bubbles, primarily nitrogen, that escape from solution into body tissues and fluids during or after a reduction in ambient pressure.
Etiology And Pathophysiology
Decompression sickness occurs when nitrogen that has dissolved in body tissues under increased ambient pressure comes out of solution too rapidly during ascent. As ambient pressure increases, the partial pressure of inspired nitrogen rises, leading to progressive nitrogen absorption into tissues, particularly with longer exposure times. When ascent occurs too quickly, the pressure gradient overwhelms the body’s ability to eliminate nitrogen gradually. Tissues become supersaturated, and gas bubbles form.
According to Henry’s law, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas. Increased partial pressure results in greater gas dissolution, while decreased partial pressure causes gas to come out of solution. Nitrogen bubbles act as foreign bodies, triggering inflammatory and coagulation pathways, increasing vascular permeability, reducing intravascular volume, and causing hemoconcentration.
Clinical manifestations depend on bubble location. Bubbles may obstruct blood flow or lymphatics, leading to ischemia, infarction, or lymphedema, or they may cause mechanical tissue distention resulting in pain.
Risk Factors
Dive-related factors include greater depth, longer bottom time, multiple dives within a day, rapid ascent, and cold water exposure. Human factors include obesity, dehydration, pulmonary disease, and intercurrent illness. Proper use of dive tables or computers reduces but does not eliminate risk. Predive vigorous exercise may reduce risk. Approximately 50% of patients develop symptoms within 1 hour and 90% within 6 hours. Air travel after diving can precipitate decompression sickness because of reduced cabin pressure.
Clinical Presentation
Cutaneous Manifestations
Skin findings include scarlatiniform, erysipeloid, or mottled rashes. Cutis marmorata, a mottled appearance, often indicates more severe disease. A peau d’orange appearance may occur due to lymphatic obstruction.
Musculoskeletal Manifestations (The Bends)
Patients experience dull, deep muscular or joint pain, most commonly affecting the elbows and shoulders. Pain is typically not worsened by movement and is not reproducible with palpation.
Gastrointestinal Manifestations
Symptoms include nausea, vomiting, and abdominal pain.
Pulmonary Manifestations (The Chokes)
Pulmonary symptoms result from obstruction of pulmonary vasculature by gas bubbles and include acute respiratory distress, substernal chest pain or pressure, cough, dyspnea, and hypoxia.
Central Nervous System Manifestations
Neurologic symptoms include weakness, fatigue, numbness, paresthesias, agitation, headache, dizziness, vertigo, seizures, bladder or bowel incontinence, lethargy, and visual disturbances. The spinal cord, particularly the lower thoracic and lumbar regions, is most commonly affected.
Inner Ear Manifestations (The Staggers)
Vestibular involvement causes dizziness, vertigo, tinnitus, and nausea. These symptoms resemble inner ear barotrauma but carry a worse prognosis.
History And Physical Examination
A detailed dive history is essential, including depth, duration, ascent profile, surface intervals, and timing of symptom onset. Physical examination should be comprehensive, with particular attention to a detailed neurologic assessment to identify subtle or evolving deficits.
Essential Evaluation
Diagnosis is primarily clinical and based on recognition of risk factors and characteristic presentations. Neurologic findings should be carefully documented, including improvement or progression. Definitive diagnosis may be supported by a trial of pressure, as rapid symptom relief during recompression in a hyperbaric chamber is often diagnostic.
Diagnostic Testing And Interpretation
Laboratory studies may show elevated hematocrit due to hemoconcentration. Electrolytes, renal function, glucose, and urinalysis should be obtained, with increased urine specific gravity suggesting volume depletion. Arterial blood gas analysis and pulse oximetry are used to monitor oxygenation.
Imaging may include chest radiography to assess for pulmonary barotrauma or noncardiogenic pulmonary edema. Extremity radiographs may help exclude traumatic causes of pain. Head CT is indicated for altered mental status or focal neurologic deficits.
Differential Diagnosis
Consider musculoskeletal injury unrelated to bubble formation, inner or middle ear barotrauma, arterial gas embolism, cerebrovascular accident, and trauma.
Prehospital Management
Early recognition is critical, as postdive extremity pain may be misattributed to muscle strain and neurologic symptoms may be minimized by patients. If air evacuation is required, altitude should be limited to less than 1,000 feet or a pressurized aircraft should be used. In-water recompression is controversial, technically difficult, and requires extensive support.
Initial Stabilization
Airway, breathing, and circulation should be managed promptly. Administer 100% normobaric oxygen via mask or endotracheal tube to enhance nitrogen elimination, reduce bubble size, and improve tissue oxygenation. Maintain the patient in a supine position to minimize cerebral involvement. Early recompression in a hyperbaric chamber is essential.
Emergency Department Management
Administer intravenous 0.9% normal saline to correct dehydration and maintain urine output of 1–2 mL/kg/hour. Dehydration is common due to pressure-induced diuresis, exertion, dry compressed air breathing, and capillary leak. Adequate hydration promotes nitrogen elimination.
Arrange urgent hyperbaric oxygen recompression therapy and transfer to the nearest facility. Insert a prophylactic chest tube for known pneumothorax to prevent tension pneumothorax during recompression. Inflate endotracheal and Foley catheter balloons with saline or water to prevent compression-related damage.
Provide analgesics and antiemetics as needed. Diazepam may be used for severe vertigo. Adjunctive NSAIDs or heliox may reduce the number of recompression treatments required. Consultation with Divers Alert Network is recommended for expert guidance and referral.
Disposition And Follow-Up
All patients with suspected or confirmed decompression sickness should be referred for hyperbaric therapy. Stable patients with mild symptoms may be discharged after treatment. Patients should avoid air travel after treatment, as reduced ambient pressure may worsen symptoms.
Follow-Up Recommendations
Ensure hyperbaric medicine follow-up and reinforce diving safety counseling.
Key Clinical Lessons And Common Errors
Musculoskeletal decompression sickness can be difficult to distinguish from benign musculoskeletal pain. Significant fatigue alone may represent decompression sickness. Even mild or resolving symptoms warrant hyperbaric recompression therapy. Do not delay recompression for laboratory testing or imaging when decompression sickness is the likely diagnosis. In-water recompression should be avoided.
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