Decompression sickness (DCS) - overview
Decompression sickness (DCS) is caused by inert gas (usually nitrogen) coming out of solution as bubbles in tissues and blood during or after ascent from increased ambient pressure.
Bubbles produce direct mechanical and vascular injury and trigger an inflammatory response; clinical effects range from local joint pain and skin changes to life‑threatening spinal cord, brain or cardiopulmonary injury. DCS and arterial gas embolism (AGE) are often grouped together as decompression illness (DCI).
Pathophysiology
- Gas uptake and bubble formation: during exposure to increased ambient pressure inert gas dissolves in tissues; with ascent pressure falls and gas may form bubbles if ascent, gas load or tissue saturation are unfavourable.
- Two principal mechanisms of injury:
- Direct (primary): bubble embolisation and mechanical/vascular injury causing arterial occlusion, venous outflow obstruction and endothelial damage with disturbed microvascular flow and blood-brain barrier disruption.
- Secondary (inflammatory): bubbles activate platelets, coagulation, complement and leukocytes producing an inflammatory cascade that can cause delayed or progressive tissue injury.
- Paradoxical arterialisation: venous bubbles may pass to the arterial circulation through intracardiac or intrapulmonary shunts (most commonly a patent foramen ovale, PFO) and cause focal cerebral or spinal ischaemia (see NICE IPG371).
- Timing: symptoms from direct bubble effects commonly occur immediately or within minutes-hours of surfacing; inflammatory‑mediated presentations may be delayed and evolve over hours to days. DCI...
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