Decompression Sickness

01Pathophysiology

Decompression sickness is fundamentally a disease of dissolved gas physics, governed by Henry's Law: the amount of gas that dissolves in a liquid is directly proportional to the partial pressure of that gas above the liquid. During a dive, as ambient pressure increases with depth, nitrogen from breathing gas dissolves progressively into blood and tissues (particularly fat, cartilage, and myelin, which have high nitrogen solubility). The deeper and longer the dive, the greater the nitrogen tissue load.

During a controlled, slow ascent, this dissolved nitrogen is gradually offloaded through the lungs without forming clinically relevant bubbles. However, when a diver ascends too rapidly, the ambient pressure drops faster than the body can eliminate the dissolved gas. Nitrogen then supersaturates and comes out of solution, forming gas bubbles within tissues and the vasculature. This is conceptually identical to opening a carbonated bottle quickly: the rapid pressure drop causes dissolved $C{O}_{2}CO\_2$ to form visible bubbles.

These nitrogen bubbles cause injury through several mechanisms. Mechanical obstruction of small vessels leads to local ischemia. Endothelial damage from bubble-vessel wall interaction activates the coagulation cascade and triggers platelet aggregation, creating a prothrombotic and proinflammatory state. Complement activation and leukocyte adhesion amplify tissue injury beyond what the physical bubble alone would cause. The spinal cord is disproportionately vulnerable because of its watershed blood supply and high lipid content in myelin, which accumulates nitrogen readily. This explains why lower thoracic and lumbar cord involvement with paraparesis and bladder dysfunction is the hallmark neurological presentation.

In the presence of a patent foramen ovale (PFO), venous gas bubbles that would normally be filtered by the pulmonary capillary bed can shunt directly into the arterial circulation, causing paradoxical embolization to the brain and other organs. This converts a venous gas burden into an arterial event and explains why PFO is a recognized risk factor for severe or recurrent decompression sickness, even after relatively conservative dive profiles.

02Classification and Clinical Manifestation

Decompression sickness is classified into two types based on the organ systems involved and clinical severity.

A few points that test-writers rely on: Type I joint pain is the single most common presentation overall. Type II neurological (spinal cord) involvement is the most common serious manifestation. The symptom timeline matters: approximately 50% of patients develop symptoms within 1 hour of surfacing, and roughly 90% within 6 hours. Symptoms appearing beyond 24 to 48 hours should prompt reconsideration of the diagnosis.

03Diagnostic Workup

Decompression sickness is a clinical diagnosis. There is no single blood test or imaging study that confirms it. The diagnosis rests on three pillars: a compatible dive exposure (or equivalent pressure reduction such as altitude), symptom onset within an appropriate time window, and clinical findings consistent with bubble-mediated injury.

The best initial step when evaluating a patient with suspected DCS is a thorough history focusing on the dive profile (depth, bottom time, ascent rate, number of dives, surface interval) combined with a complete neurological examination. Many vignettes will describe a patient who "felt fine during the dive" but develops joint pain, numbness, or weakness within hours of surfacing. The dive history is the anchor of the diagnosis.

Laboratory studies such as CBC and metabolic panel are ordered as baseline assessments but do not confirm or exclude DCS. Hemoconcentration (elevated hematocrit) is commonly seen due to plasma extravasation from endothelial injury. Coagulation studies may show consumptive changes in severe cases.

Precordial Doppler ultrasound can detect venous gas emboli and is used in research settings, but it has poor diagnostic specificity: asymptomatic bubbles are common after routine dives, and their presence alone does not establish the diagnosis. Conversely, absence of detectable bubbles does not rule out DCS, since tissue-phase bubbles may not be visible on Doppler.

MRI of the spine is indicated when spinal cord DCS is suspected. It may demonstrate T2-weighted signal abnormalities in the affected cord segments. However, MRI may be normal in the acute phase, and imaging should never delay transfer to a hyperbaric facility. CT of the head is primarily useful to exclude alternative diagnoses such as hemorrhagic stroke in patients with altered mental status.

A bubble contrast echocardiogram is not part of the acute workup but is valuable in the post-recovery evaluation of patients with recurrent or unexplained severe DCS, to identify a PFO that may warrant closure.

The pragmatic reality tested on exams: if the clinical picture fits, initiate treatment. Waiting for confirmatory imaging or labs is an incorrect answer.

04Management and Treatment

Immediate management begins at the dive site. The single most important first step is administration of 100% oxygen by non-rebreather mask. High-concentration oxygen establishes a large diffusion gradient that accelerates nitrogen washout from tissues and shrinks existing bubbles. This should be initiated even before transport. Concurrent IV fluid resuscitation with isotonic crystalloids is essential because endothelial injury and capillary leak cause significant intravascular volume depletion and hemoconcentration. The patient should be placed in the supine position. Trendelenburg or head-down positioning is no longer recommended, as it does not improve outcomes and may worsen cerebral edema.

Hyperbaric oxygen therapy is the definitive treatment and should be initiated as soon as possible. The US Navy Treatment Table 6 is the standard protocol for most cases: the patient breathes 100% $O_{2}O\_2$ at a pressure of 2.8 atmospheres absolute (ATA) for approximately 4 hours and 45 minutes, with periodic air breaks to reduce the risk of oxygen toxicity. At 2.8 ATA, bubble volume is physically compressed (per Boyle's Law: $P_1{V}_1=P_2{V}_{2}P\_1V\_1\; =\; P\_2V\_2$), the nitrogen partial pressure gradient favoring bubble reabsorption is dramatically enhanced, and tissue oxygenation is restored to ischemic areas. Mild Type I cases may be treated with the shorter Treatment Table 5 (approximately 2 hours 15 minutes at 2.8 ATA), but Table 6 is the default when neurological involvement is present or suspected.

If symptoms do not fully resolve after the initial session, repeat HBOT sessions (typically daily or twice daily at 2.0 to 2.4 ATA for 90 to 120 minutes) are administered until no further improvement is observed. Most treatment courses involve 5 to 10 sessions for Type II disease.

Contraindications and cautions: the only absolute contraindication to HBOT is an untreated pneumothorax (risk of tension pneumothorax under pressure). Patients with seizure history require monitoring, as hyperbaric oxygen can lower the seizure threshold. Claustrophobia may complicate chamber treatment but is not a contraindication.

For patients with identified PFO and recurrent DCS, referral for percutaneous PFO closure should be considered, though this remains an individualized decision.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students get questions on decompression sickness wrong is by confusing DCS with arterial gas embolism. Both occur after diving and both are treated with hyperbaric oxygen, but the mechanism and timeline are different. AGE results from pulmonary overexpansion injury (a diver holding their breath during ascent or having air trapping from bullae), and symptoms are immediate and dramatic, often with loss of consciousness within seconds to minutes of surfacing. DCS results from dissolved nitrogen coming out of solution during a too-rapid ascent, with symptom onset over minutes to hours. Exam vignettes will use the timeline and mechanism of ascent to distinguish them.

Another common trap is not recognizing spinal cord DCS. A vignette describing a diver who develops progressive lower extremity weakness, a thoracic sensory level, and urinary retention after a deep dive is testing your ability to recognize Type II neurological DCS rather than defaulting to a standard stroke or cord compression workup. The dive history is the giveaway. Ordering MRI before initiating transfer to a hyperbaric facility is a tested incorrect answer choice.

Students also fall for the distractor of treating DCS with return to depth (in-water recompression). This sounds physiologically logical but is dangerous due to drowning risk, hypothermia, and inability to administer 100% oxygen at depth with standard equipment. The correct field management is surface-level 100% oxygen and urgent transport.

Finally, remember the flying-after-diving rule: patients who fly too soon after diving (generally within 12 to 24 hours, depending on the dive profile) can develop DCS at altitude because the reduced cabin pressure triggers bubble formation from residual tissue nitrogen loads. Any vignette describing symptom onset during or after a flight following recent diving is pointing you directly toward this diagnosis.

The core competency being tested is the ability to link a pressure-exposure history to a compatible clinical syndrome, initiate the correct first step (high-flow oxygen, IV fluids, and transfer), and identify hyperbaric oxygen therapy as the definitive treatment without delaying for unnecessary diagnostic studies.