Predisposing Factors for Decompression Sickness

It's not just the dive profile

Two divers can run the identical profile on the same day and walk away with completely different outcomes: one fine, one bent. Decompression sickness (DCS, "the bends") is what happens when dissolved nitrogen comes out of solution as bubbles faster than your body can clear it, the same way a capped bottle of soda fizzes over the moment you crack it open. How likely that is for you, on this dive, is not decided by your computer alone.

Across more than four decades of dive-medicine literature, DCS is treated as a multifactorial condition shaped by external exposure variables (depth, duration, ascent profile, conditions, post-dive behaviour) and intrinsic biological factors (age, body composition, vascular and endothelial function, sex, and how readily you form venous gas emboli, the small bubbles that ride your veins back toward the lungs). This article is about those personal modifiers, the things that shift your risk beyond what the algorithm permits.

For the underlying mechanism, see decompression sickness, what it is and why it happens.

DCS Type I vs Type II

Type I DCS affects musculoskeletal and lymphatic tissues. Symptoms include joint and limb pain (most commonly shoulders, elbows, knees), skin marbling or mottling, and lymphatic swelling. Painful, but not immediately life-threatening.

Type II DCS involves the central nervous system, spinal cord, inner ear, and pulmonary vasculature. Symptoms include paresthesias (pins-and-needles or numbness), weakness or paralysis, bladder or bowel dysfunction, vertigo, hearing loss, and the "chokes" (pulmonary DCS, with chest pain and breathlessness). These are serious presentations that need urgent recompression.

Inner-ear DCS is a Type II presentation. It shows up as true vertigo, nausea, and nystagmus (involuntary jerking eye movement), usually vestibular and coming on after ascent, and is distinct from inner-ear barotrauma (see the article on pulmonary barotrauma and AGE).

When symptoms appear

Most DCS shows up early. Across case series, roughly half of cases are symptomatic within the first hour of surfacing, the large majority within six hours, and almost all within twenty-four. New symptoms appearing several hours after a dive should also prompt thought about other diagnoses. Onset beyond twenty-four hours is uncommon, though genuinely delayed cases do occur, especially after flying.

Physiological risk factors

Age

Age-related decline in cardiovascular efficiency and endothelial function appears to slow gas exchange and raise susceptibility. Several studies link increasing age to higher DCS risk (McKenzie 1984). Reduced vascular compliance and slower nitrogen elimination are the likely reasons. Conservative profiles become more important, not less, as you get older.

Sex

This one has swung back on the evidence. The largest recent analysis, the DAN DSL model of 127,957 dives (Marroni et al. 2026), found female sex carried an adjusted odds ratio of about 4.6, the strongest non-physiological predictor in the whole model, even after accounting for dive profile, workload, gas, and the rest. Animal work points the same way: the physiological traits that make male rats decompression-resistant do not discriminate in females, which implies the resistance mechanism itself differs by sex (Lautridou et al. 2020). The exact human mechanism is not settled (hormonal effects on vascular tone and clotting are the leading candidates, and menstrual-cycle and contraceptive details are not captured in the data), and older single-factor claims really were confounded. But on the best current evidence, sex is a real independent modifier, not a negligible one. You can run it yourself in the calculator above.

Body composition

Nitrogen is roughly five times more soluble in fat than in watery tissues. Divers with more body fat therefore carry a greater nitrogen burden for any given exposure. Weinmann (1991) identifies high body fat as raising DCS risk through both greater solubility and increased tissue mass. Tables and computers do not adjust for body composition.

Patent foramen ovale (PFO)

A patent foramen ovale is a small flap-like opening between the heart's upper chambers, present in roughly one adult in four (about 25 to 30%). It is a normal variant, not a disease. Normally the lungs act as a filter: small bubbles that form in venous blood are trapped and cleared in the pulmonary capillaries before they can reach the arterial side. In a diver with a significant PFO, a right-to-left shunt (blood crossing from the right side of the heart to the left) lets venous bubbles slip straight into the arterial circulation, bypassing that filter. Those arterialised bubbles can then reach the brain, spinal cord, or heart.

Clinical data confirm that divers with right-to-left shunts have markedly higher rates of neurological decompression illness, often on profiles that would not ordinarily cause symptoms (Germonpré et al. 2021; DAN/UHMS 2015 PFO workshop).

Unexplained neurological DCS on a conservative profile, particularly in a diver who followed their computer and was not dehydrated, cold, or fatigued, is a reason to be evaluated for a PFO. The standard test is bubble-contrast echocardiography (a saline "bubble study"), which reveals shunting between the atria. Management ranges from simply diving more conservatively to, in divers with recurrent neurological hits from a large PFO, percutaneous closure, though that remains a specialist decision.

Hydration

Dehydration reduces plasma volume and impairs inert-gas transport: less circulating blood means slower nitrogen delivery to the lungs for elimination. Pre-dive hydration measurably reduces post-dive bubble formation (Gempp et al. 2009), and the dehydration that matters includes alcohol from the night before.

Fitness and endothelial function

Aerobic fitness supports cardiovascular efficiency and faster gas elimination. Endothelial function (how well the lining of your blood vessels regulates blood flow) is poorer in unfit, obese, or older divers, and appears to affect DCS susceptibility on its own, beyond simple cardiac output (Dugrenot 2022). The vessel lining, in other words, is a real variable, not just a bystander.

CO₂ retention

A build-up of carbon dioxide at depth (hypercapnia), from skip-breathing, heavy work of breathing on dense gas, or poor ventilation, widens cerebral blood vessels and may activate existing bubble nuclei. A French military investigation of clustered DCS events implicated CO₂ accumulation as a contributing factor (Daubresse 2024).

Subclinical DCS: bubbles without symptoms

Post-dive Doppler monitoring routinely finds venous gas emboli in divers who feel completely fine. Bubble grades on the Spencer scale (a 0 to 4 Doppler grading of how many bubbles are circulating) turn up in a large share of asymptomatic divers after ordinary, compliant profiles. Alongside the bubbles, laboratory studies find raised endothelial microparticles and platelet-activation markers after recreational dives, even with no reported symptoms.

So there is a spectrum: from fully asymptomatic with subclinical bubbles, through vague fatigue and minor symptoms never blamed on diving, to frank DCS. Those subclinical findings are the physiological reason for conservative gradient-factor settings (the conservatism dial on your computer): even a clean dive involves bubble activity that adds up across a series.

Environmental and operational factors

Cold water exposure

Cold causes peripheral vasoconstriction, reducing perfusion and off-gassing (gas leaving the tissues) in the extremities. Rewarming after a cold dive can then mobilise bubbles as circulation returns, an effect noted across several series (McKenzie 1984; Gorman 1988; Weinmann 1991). A hot shower straight after a dive drives vasodilation and may accelerate bubble growth at exactly the moment tissue nitrogen is still high (Blake 2018).

Exercise at depth and post-dive

Hard physical effort at depth raises cardiac output and nitrogen uptake during the dive. Post-dive exercise (heavy lifting, running) raises circulation just when venous bubbles are being cleared, potentially mobilising them and speeding their growth.

Repetitive dives and short surface intervals

Residual nitrogen from earlier dives adds to the loading of the next one. Computers track residual nitrogen and shorten your no-decompression limits accordingly, but they cannot capture everything: bubble nuclei from one dive may persist and be re-excited on the next. Repetitive diving appears in 55 to 64% of DCS cases in some series (Weinmann 1991; Knight 1988).

Missed or shortened decompression

Profile violations were a factor in 42% of cases in a DAN report (Knight 1988) and 69% of cases in the Adelaide series (Gorman 1988). Skipping or shortening stops is the most direct modifiable risk factor there is.

Previous DCS

A prior DCS episode is associated with a higher chance of recurrence (McIver 1991; Weinmann 1991; Gawthrope 2015). Whether that reflects lasting vascular damage, an ongoing structural factor like a PFO, or simply repeated behaviour patterns is not settled, and is likely a combination.

Flying after diving

Commercial aircraft are pressurised to roughly 0.75 to 0.8 ATA, about the pressure you would feel at 2,000 to 2,500 m of altitude. That drop in ambient pressure can trigger bubble growth if significant nitrogen is still in your tissues. DAN's minimum surface intervals before flying:

• Single no-decompression recreational dive: 12 hours minimum
• Repetitive no-decompression dives: 18 hours minimum
• Dives requiring decompression stops: 24 hours minimum

For technical dives, or any dive that left you with lingering symptoms, treat the 24-hour figure as a floor, not a ceiling.

What you can do

DCS risk comes from gas loading, your ascent, and a stack of personal and environmental modifiers. A profile within limits is necessary but not sufficient: your state on the day matters. The useful split is between what you cannot change (so dive more conservatively) and what you can fix before you splash.

Roughly in order of how much they pay off, biggest and most controllable first:

1. Never skip or shorten your stops, and never rush the ascent. Profile violations show up in a large share of DCS cases (42% in one DAN report, 69% in the Adelaide series). This is the single most controllable factor you have.
2. Ease off on repetitive and multi-day diving. Residual nitrogen and bubble nuclei carry over, so lengthen your surface intervals and dive more conservatively as the days stack up.
3. Arrive hydrated, and skip the alcohol the night before.
4. Manage temperature and exertion. Avoid hard work at depth, and skip the heavy lifting and the hot shower right after a dive.
5. Respect the flying-after-diving intervals above.
6. Know your fixed factors. Age, a significant PFO, prior DCS, and lower fitness have no dial you can turn on the day, so they tell you how much extra conservatism to build in. If you have ever had unexplained neurological DCS, ask a dive physician about a bubble study.

References

• Marroni A, Kot J, Pieri M, Pelliccia R, Balestra C. Identification of DCS risk factors in recreational diving: multifactorial model based on the DAN DSL Database 2024. International Maritime Health 2026;77(1):1–12. doi:10.5603/imh.108038
• Lautridou J, Dugrenot E, Amérand A, et al. Physiological characteristics associated with increased resistance to decompression sickness in male and female rats. J Appl Physiol 2020;129(3):612–625. doi:10.1152/japplphysiol.00324.2020
• Germonpré P, Lafère P, Portier W, et al. Increased risk of decompression sickness when diving with a right-to-left shunt. Front Physiol 2021;12:763408. doi:10.3389/fphys.2021.763408
• Gempp E, Blatteau JE, Pontier JM, et al. Preventive effect of pre-dive hydration on bubble formation in divers. Br J Sports Med 2009;43(3):224–228. doi:10.1136/bjsm.2007.043240
• Daubresse L, Vallée N, Druelle A, et al. Effects of CO₂ on the occurrence of decompression sickness: a review of the literature. Diving and Hyperbaric Medicine 2024;54(2):110–119. doi:10.28920/dhm54.2.110-119
• McKenzie B (1984). Epidemiology of decompression sickness (cited across DAN case-series reviews).
• Gorman DF (1988). Decompression sickness: the Adelaide series.
• Knight R (1988). Decompression sickness in recreational divers (DAN report).
• Weinmann M (1991). Decompression sickness risk factors in recreational diving.
• McIver RG (1991). Recurrent decompression sickness (US Navy series).
• Gawthrope IC (2015). Venous gas emboli and prior decompression sickness.
• Dugrenot E (2022). Endothelial function and decompression susceptibility.
• Blake DF (2018). Temperature, bubble growth, and decompression risk.
• Denoble PJ, Holm JR (eds) (2015). Patent Foramen Ovale and Fitness to Dive: Consensus Workshop Proceedings. DAN/UHMS.
• Denoble PJ, Marroni A (eds) (2019). Differential Diagnosis of Decompression Illness Workshop Proceedings. DAN/UHMS.

Related posts in the series

• Decompression Sickness: What It Is and Why It Happens

• Thermal Stress in Diving

• Immune Suppression and Diving

• Pulmonary Barotrauma and AGE

• Fitness to Dive: Managing Chronic Conditions

• Post-Dive Fatigue

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Predisposing DCS risk factors come up in every technical decompression course I teach: knowing your own risk profile changes how you plan. Enquire about training →