Decompression Sickness

Decompression sickness follows a reduction in ambient pressure that allows dissolved inert gas (nitrogen, or helium in deep dives) to form bubbles in tissues and blood. It affects scuba divers, compressed-air workers, aviators and astronauts exposed to rapid altitude change, and about 2 to 4 per 10,000 recreational dives. During a dive, inert gas dissolves in tissues in proportion to pressure and time. If the ascent is too fast, supersaturation exceeds the tissue's tolerance, and bubbles form.

Mechanisms of damage: direct mechanical distortion and ischemia of tissue, blockage of small vessels, and bubble-surface activation of endothelium, platelets, complement and neutrophils, so that capillary leak, hemoconcentration and secondary ischemia follow. Venous bubbles can cross a patent foramen ovale (present in about 25% of adults) or pulmonary shunts and cause neurological, cutaneous and inner ear syndromes.

Risk factors: depth over 18 m, long bottom time, rapid ascent, repetitive and multi-day diving, flying within 12 to 24 hours of diving, dehydration, cold, exertion during or after the dive, obesity, older age, previous decompression illness and patent foramen ovale.

Presentations

• Musculoskeletal (about 70%): limb joint pain ("the bends")
• Cutaneous: itch and marbled rash
• Lymphatic: painless swelling
• Neurological (about 25 to 30%): the spinal cord (mainly thoracic and lumbar) is the commonest target, causing girdle pain, ascending paresthesia, weakness, bladder and bowel dysfunction, and cerebral or vestibular signs
• Cardiopulmonary ("the chokes"): substernal pain, cough and dyspnea after a heavy bubble load

Onset is within 1 hour in about 50%, within 6 hours in 90% and rarely beyond 48 hours. Complications: permanent spinal cord deficit, bladder dysfunction, dysbaric osteonecrosis (a long-term consequence of repeated exposure), and cardiopulmonary collapse.

• Deep, dull aching joint pain (shoulder and elbow commonest), relieved by local pressure
• Itching, mottled or marbled skin, and swelling
• Fatigue, headache, malaise, nausea, dizziness, visual disturbance and confusion
• Lower back or girdle pain, paresthesia, numbness, leg weakness and urinary retention
• Inner ear: vertigo, tinnitus, nystagmus and hearing loss, mostly in deep helium-oxygen diving
• Cardiopulmonary: chest tightness, cough and dyspnea, with shock in severe cases
• Red flags: any neurological symptom, urinary retention, dyspnea, collapse and rapid progression

1. Clinical diagnosis from a dive or altitude history and the symptoms. No test confirms the diagnosis, and no test should delay treatment.
2. Dive profile: depth, time, gas, ascent rate, and any missed stops, and the time of symptom onset.
3. Neurological examination (mental state, cranial nerves, motor and sensory function, coordination, gait, bladder), repeated before and after recompression.
4. Radiographs and CT or MRI only to exclude other causes (trauma, disc herniation, stroke), without delaying transfer.
5. Laboratory tests: hematocrit (raised with hemoconcentration), creatine kinase, electrolytes and creatinine.
6. Echocardiography with a bubble study after recovery to search for a patent foramen ovale.

Differentials: arterial gas embolism, musculoskeletal strain, stroke, spinal cord lesion, marine envenomation, carbon monoxide poisoning and oxygen toxicity.

1. First aid: lay the patient flat, give 100% oxygen at 15 L/min by a tight-fitting non-rebreather mask (or demand valve) continuously until recompression, and keep warm.
2. Fluids: oral water if conscious, 1 to 2 L over the first hours, or IV isotonic crystalloid (0.9% saline) 1 L over 1 hour then 100 to 150 mL/h to keep urine output over 1 mL/kg/h. Avoid glucose-containing solutions.
3. Analgesia and adjuncts: paracetamol 1 g orally every 6 hours. Avoid opioids and sedatives that mask neurological assessment. Aspirin and other drugs have limited evidence.
4. Contact a diving medical service early and transfer by the fastest means, with ground transport or a pressurized aircraft at cabin pressure of sea level (or flight altitude under 300 m).
5. Recompression in a hyperbaric chamber is the definitive treatment, for all but the mildest cases:
   • Oxygen table: pressurize to 2.8 atmospheres absolute (18 m of sea water) with three 20-minute oxygen periods separated by 5-minute air breaks, then decompress to 1.9 atmospheres absolute (9 m) for two further oxygen periods, then to the surface. Total time about 4 hours 45 minutes.
   • Extension by two further 20-minute periods at 18 m or more at 9 m when symptoms improve incompletely.
   • Repeat daily treatments at 1.9 to 2.4 atmospheres absolute until there is no further improvement (typically 3 to 5, up to 10).
   • Treatment is effective even after a delay of 24 to 48 hours or more.
6. Neurological decompression sickness with persisting deficit: repeat sessions and early rehabilitation.
7. Cardiopulmonary decompression sickness: high-flow oxygen, IV crystalloid 500 mL boluses, and recompression.
8. Seizures: lorazepam 4 mg IV, and bladder catheter for retention.

Return to diving: not for at least 2 to 4 weeks after pain-only disease with full resolution, and at least 4 to 6 weeks (or permanently) after neurological disease, subject to specialist clearance. A closure of a patent foramen ovale is considered in recurrent neurological cases. No flying for 12 hours after a single no-decompression dive and 18 to 24 hours after repetitive or decompression dives.

Prevention: ascent rate 9 to 10 m a minute or slower, a safety stop of 3 to 5 minutes at 5 m, conservative dive profiles with a computer, adequate hydration, avoidance of strenuous exercise after diving, and enriched oxygen mixtures where trained.