Decompression illness and diving emergencies

Overview

Pathophysiology — the unifying mechanism is bubbles on ascent

Both syndromes under the DCI umbrella share a single root cause: gas bubbles form when ambient pressure falls faster than dissolved inert gas can be cleared. The physics is governed by two gas laws — Henry's law (the amount of gas dissolved in a liquid is proportional to its partial pressure above the liquid; this explains nitrogen uptake at depth) and Boyle's law (P1V1 = P2V2; pressure inversely controls gas volume; this explains both alveolar expansion on ascent and bubble shrinkage during recompression). Understanding these two laws and the two distinct routes to bubble injury is the key to the entire topic.[1][5]

Henry's law and nitrogen absorption at depth

At sea level, breathing air at 1 atmosphere absolute (ATA), tissues are equilibrated with dissolved nitrogen at the partial pressure of nitrogen (~0.79 ATA). Every 10 m of seawater depth adds 1 ATA of pressure. At 30 m (4 ATA), the alveolar partial pressure of nitrogen is ~3.2 ATA — four times the surface value. By Henry's law, the amount of nitrogen dissolved in tissues is proportional to this partial pressure, so the body's nitrogen load rises progressively with depth and bottom time. Different tissues absorb and release nitrogen at different rates depending on their solubility and perfusion: fat dissolves approximately five times more nitrogen than water, so adipose tissue and the lipid-rich myelin sheaths of spinal cord white matter are large, slow-loading, slow-offloading nitrogen reservoirs. This is the physiological basis of dive tables and dive computers, which calculate a decompression schedule that allows staged nitrogen washout on ascent to avoid supersaturation.[1][2]

The supersaturation threshold and bubble nucleation

On ascent, if ambient pressure falls faster than nitrogen can diffuse out of tissue into blood and be exhaled, the tissue becomes supersaturated — the dissolved nitrogen partial pressure exceeds the ambient pressure, and nitrogen comes out of solution as bubbles. Bubbles are thought to nucleate on pre-existing gas micronuclei on hydrophobic surfaces (vascular endothelium, joint cartilage, fat globules). Risk factors for supersaturation and bubble formation include: greater depth and bottom time (higher nitrogen load), repetitive dives (residual nitrogen), rapid ascent or missed decompression stops (insufficient time for washout), cold water (peripheral vasoconstriction slows nitrogen washout from tissues), exertion (increased perfusion and micronuclei generation), and dehydration (increased blood viscosity, reduced washout efficiency).[1][5]

Four mechanisms of bubble injury

Once formed, bubbles damage tissue by four distinct but interacting mechanisms:[2][5]

1. Mechanical obstruction and disruption — Bubbles physically occlude vessels (venous, capillary, and arterial) causing distal ischaemia, and mechanically disrupt tissue architecture — especially the delicate white-matter tracts of the spinal cord. The valveless epidural venous plexus of the cord is particularly prone to bubble trapping and venous infarction. [1]

2. Endothelial damage and capillary leak — The bubble-blood interface denudes endothelial cells, exposing subendothelial collagen and triggering complement activation, leukocyte adhesion, and cytokine release. This produces a secondary inflammatory cascade — capillary leak, tissue oedema, microvascular sludging — that persists and progresses even after the bubbles themselves have shrunk. This inflammatory component explains why symptoms can continue to evolve after the patient has left the water, and why treatment must be aggressive and early. [1]

3. Platelet activation and coagulopathy — The bubble surface activates platelets and the coagulation cascade, producing microthrombi, consuming platelets and fibrinogen, and creating a localised prothrombotic state that compounds the ischaemic injury. A mild disseminated intravascular coagulation (DIC)-like picture can occur in severe cases. [1]

4. Autochthonous bubble formation in enclosed spaces — In tissues that cannot expand (spinal cord within the bony canal, inner ear within the temporal bone), bubble growth directly compresses and destroys tissue. In the spinal cord, bubble-induced oedema in the confined canal compounds the ischaemia — a vicious cycle of swelling and reduced perfusion that makes spinal cord DCS the most serious and least reversible form. [1]

AGE — alveolar rupture from pulmonary barotrauma

The mechanism of AGE is purely mechanical and governed by Boyle's law: during ascent, the gas in the lungs expands as ambient pressure falls. At 30 m (4 ATA), a full lung of gas will quadruple in volume on ascent to the surface if not exhaled. If a diver holds their breath (panic, unconsciousness), ascends too fast, or has trapped gas (obstructed airway, mucus plug, ruptured bleb, pre-existing lung disease), the expanding gas over-distends and ruptures alveoli. Gas then tracks into the pulmonary venous circulation → left heart → systemic arterial tree. The brain is the most common final destination, producing a focal cerebral deficit; coronary embolisation can cause arrhythmia or ischaemia. Gas can also track into the pleural space (pneumothorax) or mediastinum (pneumomediastinum). AGE occurs during or within minutes of surfacing — this timing is the cardinal clue that distinguishes it from DCS. It can occur after ascent from surprisingly shallow depths — even a few metres in a breath-hold diver — and is the leading cause of death in recreational diving fatalities involving pulmonary barotrauma.[1][5]

The crossover: paradoxical embolism via PFO

Venous bubbles from DCS are normally filtered by the pulmonary capillary bed (where they are gradually reabsorbed). But in a diver with a patent foramen ovale (PFO) — present in approximately 25-30% of the population — or a pulmonary arteriovenous malformation, venous bubbles can cross directly into the arterial system and embolise the brain or inner ear. This paradoxical embolisation explains why some divers develop cerebral or inner-ear DCS disproportionate to the dive profile, and why PFO is over-represented in recurrent neurological DCS. Investigation for PFO with bubble-contrast echocardiography is warranted after recurrent or disproportionate neurological/inner-ear DCS.[1][7][8]

Classification of DCS — Type 1 and Type 2

The traditional classification divides DCS by severity and organ system. Modern diving medicine increasingly describes DCS by symptom/organ system (because the type boundary is blurred and prognosis tracks the organ involved), but the Type 1/Type 2 framework remains the exam staple and is useful for triage.[1][5]

Why the spinal cord is so vulnerable

The spinal cord is the classic and most feared target of serious DCS for three converging reasons: it is rich in lipid (myelin), which dissolves large amounts of nitrogen (Henry's law: fat dissolves ~5× more nitrogen than water, and myelin is essentially lipid); its venous anatomy — a long, valveless epidural venous plexus — allows bubbles to accumulate and obstruct venous outflow, producing venous infarction of white-matter tracts; and the resulting oedema in the confined bony spinal canal compounds the ischaemia in a vicious cycle of swelling and reduced perfusion. The clinical result is a mixed picture: motor weakness (often ascending), sensory disturbance with a level, and autonomic failure (bladder retention is an early and important sign — catheterise and scan). Spinal cord DCS is the scenario most likely to leave permanent deficit even after appropriate treatment, which is why any diver with limb weakness, gait disturbance, or urinary symptoms after a dive is treated as a hyperbaric emergency.[2][6]

AGE — the stroke of ascent

Arterial gas embolism must be suspected in any diver who loses consciousness, seizes, or develops a focal neurological deficit during ascent or within minutes of reaching the surface. The mechanism is mechanical: the expanding alveolar gas (Boyle's law) ruptures into the pulmonary vasculature. The embolic load travels to the brain (producing a cortical/stroke-like syndrome) or the coronary arteries (producing arrhythmia or ischaemia). It can occur after ascent from surprisingly shallow depths — even a few metres — in a breath-hold diver. Importantly, AGE and DCS can coexist in the same diver from the same precipitating event, and the treatment is identical — so the bedside distinction is academic once oxygen and retrieval are underway.[1][5]

Diagnosis — clinical, with adjuncts

DCI is a clinical diagnosis made on the basis of a diving/altitude exposure and compatible symptoms within the time window. There is no blood test that confirms DCS, and waiting for investigations must never delay 100% oxygen and contact with a hyperbaric service.[1][2]

[1] [1]

The mimics — what else to consider

Several conditions overlap with DCI and must not be missed: inner-ear barotrauma (alternative cause of vertigo/hearing loss during descent — NO recompression; distinguished by onset during descent and no systemic features); pneumothorax (dyspnoea and chest pain from the same barotrauma event — drain before chamber); acute stroke in a cerebral presentation (the diving history and time course usually point to AGE/DCS, but thrombolysis may be appropriate in genuine stroke — discuss with neurology and hyperbarics); carbon monoxide poisoning from contaminated breathing gas (check COHb); and immersion pulmonary oedema (dyspnoea, cough, frothy sputten during or after a dive — treated with oxygen and diuretics, not recompression). The history almost always resolves the diagnosis.[1]

Management — oxygen, fluids, recompression, retrieval

The management ladder is the same for DCS and AGE, and every step should be initiated in parallel, not sequentially. The single most important phone call is to the nearest hyperbaric service or the Divers Alert Network (DAN) — retrieval logistics dominate outcome.[1][2]

[1]

The three mechanisms of recompression — know them by name

[1]

Flying after diving

After recompression or after a dive without incident, a diver must observe a surface interval before flying to allow residual nitrogen washout, because aircraft cabin pressure is typically equivalent to 1500-2400 m altitude (lower ambient pressure → residual bubbles expand). Guidelines: wait at least 12 hours after a single no-decompression dive, 18 hours after multiple dives or multiple days of diving, and more than 24 hours after dives requiring decompression stops. After recompression treatment for DCS, the hyperbaric physician advises the no-fly interval (often several days). Premature flying risks recurrence or worsening of DCI.[5]

Evidence on recompression and adjuncts — what the trials show

Recompression is the universally accepted standard of care for DCI, yet the evidence base for which table and which adjuncts is surprisingly thin. A fellowship candidate should know what is established and what is genuinely uncertain.[2][3]

Recompression itself is standard but unproven by RCT. No randomised trial has ever compared recompression against no recompression — and none ever will, because withholding it would be unethical. The US Navy Treatment Table 6 (2.8 ATA, 100% oxygen, ~4-5 h) is the global default on the basis of decades of observational experience; Moon 2014 confirms it as the recommended schedule for most cases of DCS, with additional treatments for residual manifestations.[2]

Adjunctive therapy — the Cochrane / Bennett view. Bennett 2010 (a systematic review of all RCTs) found only two trials that could be pooled in no useful way. One showed that adding the NSAID tenoxicam to standard recompression did not improve the odds of recovery but did reduce the number of repeat recompressions required (a likely economic and symptom-duration benefit). The other showed a heliox table reduced the odds of multiple recompressions versus an oxygen table. Neither improved the odds of recovery. The bottom line: recompression is standard; adjuncts (NSAID, heliox) may reduce the treatment burden but are not proven to improve outcome, and the overall RCT evidence is sparse.[3]

Does delay matter? — the timing evidence. General teaching and clinical practice insist on recompressing as soon as feasible, and most series show that earlier treatment trends toward better outcome. Hadanny 2015 showed that even delayed recompression (started 48 h or more after surfacing) still achieved complete recovery in 76% of divers, with a (non-significant) trend favouring the US Navy Table 6 protocol over shorter schedules — so a delayed presentation is never a reason to withhold recompression. Blatteau 2011, in a large spinal-cord DCS cohort, found that after statistical adjustment the time-to-recompression did not independently predict recovery, whereas clinical severity (motor deficit, bladder dysfunction, a high severity score) and symptom progression before treatment did. The synthesis: recompress as soon as you can, but never refuse a delayed case — late is still better than never.[2][4][6]

PFO and DCI — the 2025 position. A patent foramen ovale (present in ~25-30% of the population) is over-represented in divers with cerebral and inner-ear DCS because it permits paradoxical embolisation of venous bubbles. Wilmshurst 2015 and 2019 review the role of PFO and risk mitigation strategies (conservative diving profiles, gas switching to reduce bubble load). The 2025 joint SPUMS/UKDMC position statement (Smart, Wilmshurst et al.) provides the current framework for PFO assessment and closure decisions in divers — closure is considered on a case-by-case basis for recurrent, disproportionate neurological DCS, but is not universally recommended for all divers with PFO.[7][8][9]

[1] [1]

Clinical pearls

Red flags

Prognosis

[1]

Most divers treated promptly recover completely. The chief predictor of incomplete recovery is clinical severity at presentation — particularly spinal cord involvement with motor deficit and bladder dysfunction, and progression of symptoms before treatment reaches the chamber. Time-to-recompression matters at the population level (recompress as soon as feasible) but, after adjustment, severity dominates: Blatteau 2011 found that age, depth, bladder dysfunction, symptom progression, and a high severity score independently predicted bad recovery in spinal cord DCS, while the absolute time to recompression and the choice of initial table did not. The practical message is to treat aggressively and early, but never abandon a delayed or severe case — late recompression and repeat treatments still achieve meaningful recovery, and residual neurological deficit warrants ongoing rehabilitation and formal fitness-to-dive assessment.[1][2][4][6]

Key trials and evidence

[1] [1] [1] [1] [1] [1] [1] [1]

References

1. [1]Vann RD, Butler FK, Mitchell SJ, Moon RE. Decompression illness Lancet, 2011.PMID 21215883
2. [2]Moon RE. Hyperbaric oxygen treatment for decompression sickness Undersea Hyperb Med, 2014.PMID 24851553
3. [3]Bennett MH, Lehm JP, Mitchell SJ, Wasiak J. Recompression and adjunctive therapy for decompression illness: a systematic review of randomized controlled trials Anesth Analg, 2010.PMID 20332190
4. [4]Hadanny A, Fishlev G, Bechor Y, et al. Delayed recompression for decompression sickness: retrospective analysis PLoS One, 2015.PMID 25906396
5. [5]Bove AA. Diving medicine Am J Respir Crit Care Med, 2014.PMID 24869752
6. [6]Blatteau JE, Gempp E, Simon O, et al. Prognostic factors of spinal cord decompression sickness in recreational diving: retrospective and multicentric analysis of 279 cases Neurocrit Care, 2011.PMID 20734244
7. [7]Wilmshurst PT. The role of persistent foramen ovale and other shunts in decompression illness Diving Hyperb Med, 2015.PMID 26165532
8. [8]Wilmshurst P. Risk mitigation in divers with persistent (patent) foramen ovale Diving Hyperb Med, 2019.PMID 31177512
9. [9]Smart D, Wilmshurst P, Banham N, Turner M, Mitchell SJ. Joint position statement on atrial shunts (persistent [patent] foramen ovale and atrial septal defects) and diving: 2025 update. South Pacific Underwater Medicine Society (SPUMS) and the United Kingdom Diving Medical Committee (UKDMC) Diving Hyperb Med, 2025.PMID 40090026