Decompression Sickness in Divers

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This course explores the physiology, risk factors, and management of two critical diving-related conditions: Decompression Sickness (DCS) and Pulmonary Overinflation Syndrome (POIS). Learners will explore the mechanisms behind nitrogen bubble formation, the physiological effects of rapid pressure changes, and the clinical presentations associated with these conditions.

Key topics include the etiology and pathophysiology of DCS, the role of nitrogen narcosis, and factors influencing susceptibility, such as patent foramen ovale (PFO), fatigue, and dehydration. The course emphasizes early symptom recognition, appropriate interventions—high-flow oxygen therapy and hyperbaric oxygen therapy (HBOT)—and strategies for preventing these life-threatening complications.

Introduction

Decompression sickness (DCS), often referred to as “the bends,” results from rapid reductions in ambient pressure that cause dissolved gases (nitrogen) to form bubbles in the blood or tissues (1). If a diver’s ascent is too rapid, nitrogen in the bloodstream and tissues does not have time to dissipate, leading to bubble formation that can obstruct vessels, trigger inflammation, and damage tissues, leading to various symptoms such as joint pain, fatigue, dizziness, and even life-threatening conditions (2)(28).

A slow, controlled ascent combined with proper buoyancy management reduces the risk of pulmonary barotrauma and its dangerous consequences (3). Two critical physiological conditions, decompression sickness (DCS) and pulmonary overinflation syndrome (POIS), can transform a routine dive into a life-threatening emergency (1)(4).

Pulmonary Overinflation Syndrome arises with the rapid expansion of a diver’s lungs during ascent, causing alveolar rupture and allowing air bubbles to leak into tissue planes or the circulation (4)(5). Both DCS and POIS fall under the broader category of Decompression Illness (DCI), which also includes Arterial Gas Embolism (AGE) [6]. Although these conditions have distinct mechanisms, their initial treatments—high-flow oxygen and, in many cases, hyperbaric oxygen therapy (HBOT)—are the same (4)(6).

Even divers who follow standard decompression tables and safe diving protocols may still experience DCI. Prevention hinges on appropriate training, conservative dive planning, scheduled stops, and controlled ascents (2). Recognizing symptoms early and ensuring prompt, coordinated care can improve outcomes.

An apt analogy for bubble formation in DCS is the release of dissolved gas when opening a carbonated beverage: once the pressure decreases, the gas emerges, forming bubbles. Proper buoyancy control and gradual decompression help minimize such bubble formation, allowing divers to enjoy the underwater environment (7) safely.

Etiology

Decompression sickness (DCS) occurs when a sudden drop in ambient pressure causes dissolved gases—most often nitrogen—to leave the solution and form bubbles in the bloodstream (2)(8). While nitrogen is inert, excessive vasculature can trigger vascular blockage and inflammatory responses (9)(10). Breathing compressed air at pressures more significant than 1 ATM increases the partial pressures of nitrogen and oxygen in the bloodstream (11). The physical effects on the central nervous system (CNS) contribute to nitrogen narcosis (11).

This phenomenon suggests that nitrogen’s impact arises from physical interactions rather than chemical changes, influencing cognitive and motor functions during deep dives.

Nitrogen’s partial pressure increases with depth and decreases with altitude, explaining why deep-sea divers are at heightened risk (2)(4). Prolonged dives at great depths drive higher nitrogen levels into bodily tissues (9)(10).

A slow ascent releases nitrogen from the body, while a rapid ascent causes sudden decompression, leading to gas bubble formation in tissues and circulation (2)(7).. Aviators in unpressurized aircraft and astronauts working in reduced-pressure environments face a similar danger (12).

Epidemiology

DCS is uncommon due to technological advancements and established safety protocols, with an estimated rate of 3 cases per 10,000 dives in sport diving and 1.5 to 10 per 10,000 dives among commercial divers (1)(13). Longer and deeper dives increase this risk, 2.5 times higher in males than females [1]. A retrospective analysis of case reports from 3,322 air and N₂-O₂ dives identified 190 DCS events and categorized outcomes into six groups:

1. severe neurological
2. cardiopulmonary
3. mild neurological
4. pain-related
5. lymphatic or skin-related
6. constitutional or nonspecific symptoms

(14)

Pathophysiology

Decompression sickness (DCS) occurs when gas bubbles form within tissues and circulation, causing vascular obstruction and inflammation (1) The resulting ischemia and inflammation can affect most organs, producing pruritic, netlike, red skin lesions (cutis marmorata), bone and joint necrosis (manifested as localized pain), and painful, swollen lymph nodes (15)(16).

Mild DCS may induce transient edema in the nervous system, while severe cases can leave permanent lesions in the brain’s white and gray matter (2)(17). DCS can also affect the inner ear if inert gas elimination there is slower than in the brain, allowing bubbles to form—in divers switching from helium-oxygen mixtures to nitrogen-rich gases, or in those with a patent foramen ovale, even without gas changes (2)(18). In rare instances, vigorous gas decompression in the abdomen can lead to gut necrosis, pancreatic edema, and liver damage due to bubble formation in abdominal tissues and the portal and mesenteric vessels (2)(19)(20).

Symptoms

Symptoms of decompression sickness may include joint pain, dizziness, headache, difficulty with clear thinking, extreme fatigue, tingling or numbness, weakness in the arms or legs, and skin rashes (1)(2).

Case Study

A 29-year-old woman was training for advanced scuba certification at a Florida dive school. Her weekend schedule included multiple dives, such as wrecks and night dives.

Diving Profile

• Day 1, Dive 1: 70 feet for 25 minutes
• Day 1, Dive 2 (Night Dive): 50 feet for 40 minutes

She reported feeling well after these two dives.

• Day 2, Dive 3 (Morning): 55 feet for 40 minutes

Onset of Symptoms

She planned a fourth dive to 60 feet two hours after completing the third dive. Just before entering the water, she felt fatigued and noticed pain in her left elbow.

Dive 4 and Post-Dive Experience

Despite her symptoms, she proceeded with the fourth dive, and her elbow pain subsided at depth. However, the pain returned upon surfacing. She did not report these symptoms and went home later that day.

Further Observations

That evening, her husband noticed she appeared more fatigued than usual and confused. She also complained of worsening elbow pain. Concerned about her condition, she sought medical evaluation the following day.

Medical Evaluation

Although her dive computer did not indicate any “omitted decompressions,” the physician suspected decompression sickness (DCS) based on her symptoms and recent dive profile.

Treatment and Outcome

She underwent hyperbaric treatment for two days. Throughout therapy, her symptoms resolved.

Patent Foramen Ovale (PFO) Consideration

Subsequent testing, including an agitated saline echocardiogram, revealed a Patent Foramen Ovale (PFO). It remains unclear whether the PFO played a role in her episode of DCS, as she had followed standard dive profiles without any recorded decompression violations.

Summary

This 29-year-old advanced scuba trainee presented with symptoms consistent with DCS—fatigue, localized joint pain, and cognitive changes—despite following standard dive profiles and having no recorded decompression violations. Hyperbaric oxygen therapy resolved her symptoms. Subsequent testing uncovered a Patent Foramen Ovale (PFO), which may increase susceptibility to DCS, although its specific influence in this case remains uncertain.

Clinical Suspicion and Management

Scuba divers who surface unconscious or lose consciousness within 10 minutes of surfacing may show signs of arterial gas embolism (AGE) (6)(21). Immediate treatment includes essential life support and administration of the highest possible concentration of oxygen (22). Because relapses can still occur even if the diver appears to recover, rapid evacuation to a hyperbaric treatment facility is essential in all suspected cases.

Understanding and Managing Decompression Sickness and Pulmonary Over-Inflation Syndrome

When a diver breathes pressurized air underwater, excess inert gas (nitrogen) accumulates in body tissues (2)(9)(10). The amount of dissolved nitrogen is related to the dive depth and how long the diver remains submerged (23). As the diver ascends, respiration removes excess nitrogen from the body. However, if it is too rapid, gas has dissolved, or the ascent is too fast, nitrogen can come out of the solution and form bubbles within tissues (2)(4). These bubbles obstruct blood flow and disrupt oxygen delivery, leading to decompression sickness.

POIS is an umbrella term for four specific disorders: Arterial Gas Embolism (AGE), pneumothorax, mediastinal emphysema, and subcutaneous emphysema (5). All these arise when the lungs are overdistended and rupture due to expanding gases during ascent. As pressure decreases, the volume of inhaled gas increases according to Boyle’s law (P1V1 = P2V2) (24).

Symptoms develop rapidly when excess gas cannot escape the lungs. AGE is the most severe manifestation, occurring when gas enters the pulmonary veins and then systemic circulation, causing vascular obstruction, tissue hypoxia, and an inflammatory cascade (5)(6)921). Patients may present with loss of consciousness or stroke-like symptoms within ten minutes of surfacing (6)(21).

Management requires urgent recompression in a hyperbaric chamber. The other three disorders—pneumothorax, mediastinal emphysema, and subcutaneous emphysema—present with milder symptoms such as hoarseness, throat fullness, shortness of breath, difficulty swallowing, and chest pain. In these cases, observation and supplemental oxygen can often suffice, although more severe presentations may call for shallow recompression or chest tube placement in the event of a significant pneumothorax (22).

Arterial gas embolism occurs when gas enters the arterial circulation—often through ruptured pulmonary vessels—and then travels to tissues throughout the body, including the heart and brain. These gas bubbles can disrupt blood flow or damage vessel walls, causing neurological symptoms that range from mild to life-threatening and demand urgent intervention (2)(4).

By contrast, DCS is more common (2). Modern divers rely on dive tables first developed by the U.S. Navy or advanced dive computers that calculate safe ascent rates and decompression times.

Divers can still develop DCS when they make errors, disregard decompression guidelines, or, in rare cases, follow all protocols yet still experience symptoms. DCS emerges when dissolved gases- a sizable portion as nitrogen—exit the solution and form bubbles in tissues or the bloodstream. These bubbles may resolve without adverse effects or cause lethal complications if they distort tissues, block vessels, or initiate an inflammatory process via endothelial injury and neutrophil activation.

Longer or deeper dives increase the partial pressures of gases and thus the number of bubbles that are “on-gas” in the body (30. Proper decompression stops enable “off-gassing.” Omitting or shortening these stops increases the risk of decompression sickness (DCS).

Several factors increase the risk of DCS, such as poor physical fitness, older age, obesity, dehydration, alcohol consumption, bodily injury, repetitive dives, or traveling to altitude soon after diving (2)(3). Fit, well-hydrated divers who follow dive computer or table limits reduce their risk of decompression sickness. DCS often presents as either Type I (“pain-only”) or Type II (“serious”).

Type I involves limb or joint pain, often in the shoulders, and is unchanged by range of motion (25). Type II is more severe and may affect neurological structures, including the brain, spinal cord, or inner ear. If not addressed, it can lead to fatal or long-term complications (25).

Whether a diver suffers from POIS or DCS, hyperbaric recompression with high-flow oxygen is the cornerstone of treatment. Recompression decreases bubble size and accelerates the expulsion of inert gases, mitigating ischemia, hypoxia, and further tissue damage (26). When administered by trained professionals with appropriate safety measures, hyperbaric oxygen therapy reduces mortality and morbidity in divers experiencing these conditions (4)(26).

Risk Factors

Several factors increase the risk of decompression sickness (DCS), including dehydration, patent foramen ovale (PFO), preexisting injuries, exposure to cold environments, high body fat percentage, and recent alcohol consumption (2)(27).

In broader terms, decompression sickness is determined by dive depth, dive duration, and the rate of ascent. Additional risk factors include altitude exposure after a dive, demanding conditions such as chilly water and strong currents, dives below 60 feet (18 meters), multiple or consecutive dives over several days, strenuous exercise, and specific physiological considerations like fatigue and dehydration (22).

Specific medical and physiological aspects can further elevate the risk of DCS. Individuals with certain congenital heart defects—including PFO, atrial septal defect, and ventricular septal defect—face a heightened risk because venous bubbles can bypass the lungs via these openings, allowing gas to enter the arterial system with the potential to cause stroke or other serious complications (28)(29)

Additional factors, such as being over age 30, being female, having low cardiovascular fitness, high body fat, or a history of alcohol or tobacco use, can compromise the body’s ability to off-gas after a dive safely. Fatigue, seasickness, or preexisting injuries also increase vulnerability (30).

Preexisting lung diseases, like asthma or emphysema, may lead to thin-walled air pockets (bullae) that do not collapse during exhalation (30). As a diver ascends, these trapped air pockets can expand, rupturing and allowing air to escape into the arterial system, resulting in a collapsed lung or air embolism (31).

Maintaining good health and fitness, staying hydrated, avoiding alcohol or tobacco before diving, and diving within safe limits are all critical steps in mitigating these risks (25). Individuals with known heart or lung conditions should seek evaluation from a dive medicine specialist before participating in scuba diving.

Clinical Presentation, Evaluation, and Diagnosis of Decompression Sickness (DCS)

A majority of individuals (75%) with decompression sickness (DCS) develop symptoms within the first hour following the triggering event (2)(4). Early recognition and immediate stabilization are critical. Administer high-flow oxygen when suspecting DCS, regardless of normal oxygen saturation levels. This approach clears nitrogen gas pockets from tissues and reduces bubble-related damage.

The clinical presentation of DCS varies depending on the affected systems, but symptoms can emerge within minutes to several hours after rapid decompression. The severity of symptoms often corresponds with the degree of nitrogen bubble formation and tissue involvement.

• Type I DCS involves skin, muscles, bones, and joints. The shoulder is the most affected joint, although any joint may be involved (25). Skin findings include cutis marmorata, a mottled, netlike rash, either localized or widespread (15)(16). Lymph nodes can swell and cause pain.
• Type II DCS presents with more severe symptoms, including headache, visual and hearing disturbances, nausea, tinnitus, poor coordination, and altered mental status (2). Neurological symptoms may include sensorimotor weakness, abnormal reflexes, and varying levels of consciousness (2).
• Pulmonary DCS (Chokes) is a rare but life-threatening manifestation that may mimic conditions such as pulmonary embolism, asthma exacerbation, or myocardial infarction (1)(2). Symptoms include chest pain, shortness of breath, and crackles or rales on lung auscultation. Patients with preexisting lung conditions, such as asthma, may exhibit wheezing (1)(2). Absent breath sounds often indicate a pneumothorax, a potential complication of pulmonary DCS.
• Abdominal DCS may present with abdominal pain, nausea, or chest discomfort and can signify gas bubble formation in the abdomen, mediastinum, or other visceral organs (1).

Diagnosis of Decompression Sickness

DCS is a clinical diagnosis based on history, symptom presentation, and physical findings. Immediate recompression therapy not only serves as the gold standard for treatment but can also provide diagnostic confirmation if symptoms improve. A focused history should include details about the dive profile, depth, duration, rate of ascent, and any omitted decompression stops. Physical examination should screen for additional injuries, including wounds or fractures.

While a full diagnostic workup often remains unnecessary for decompression sickness (DCS), certain imaging studies can provide valuable information in specific cases. A chest X-ray plays a crucial role in evaluating patients with dyspnea, as it helps rule out pneumothorax, a condition that contraindicates hyperbaric oxygen therapy (HBOT) (32). Bone X-rays may reveal acute gas bubbles in joints or chronic necrosis in individuals with prolonged diving exposure (1). CT or MRI scans of the abdomen and thorax can detect gas inclusions in abdominal and thoracic organs, offering insights into potential complications.

Brain and spinal CT or MRI scans may identify edema, infarcts, hemorrhages, or gas pockets in cerebrospinal fluid spaces, often correlating with neurological symptoms (1)(2). An echocardiogram may uncover a patent foramen ovale (PFO), a structural heart defect that can increase susceptibility to DCS (28)(29). These imaging tools support accurate diagnosis and guide treatment decisions.

Laboratory results are nonspecific but may show elevated inflammatory markers (C-reactive protein, white blood cell count) or evidence of organ damage in renal, hepatic, or pancreatic function tests (33).

Early recognition, rapid administration of high-flow oxygen, and prompt hyperbaric oxygen therapy (HBOT) initiation remain the cornerstone of effective DCS management (32). Imaging and laboratory tests may provide supportive evidence but should not delay treatment in suspected cases.

Treatment

Immediate management for decompression sickness includes stabilizing blood pressure, administering high-flow oxygen, and, if necessary, providing intravenous fluids. Positioning the individual on their left side with the head of the bed lowered can also be beneficial. The definitive treatment is hyperbaric oxygen therapy, in which the patient breathes 100% oxygen inside a high-pressure chamber (32).

This environment prevents conditions that enable gas bubbles to form in the bloodstream. It forces nitrogen back into the solution, allowing the body to clear it over several hours. Divers with suspected decompression sickness should not attempt to treat themselves by returning to deeper depths.

Conclusion

Decompression sickness (DCS) and pulmonary overinflation syndrome (POIS) represent significant risks for divers, arising from rapid pressure changes during ascent (2)(4)(26). Despite advances in dive technology, adherence to decompression protocols, and widespread diver education, these conditions remain relevant concerns. Early recognition of symptoms, such as joint pain, neurological deficits, or cognitive changes, coupled with immediate intervention through high-flow oxygen and hyperbaric oxygen therapy, remains critical for favorable outcomes.

Divers must prioritize proper training, conservative dive planning, and adherence to safe ascent practices to mitigate these risks.

Understanding the pathophysiology, risk factors, and clinical manifestations of DCS and POIS empowers divers and healthcare providers to respond to these emergencies. Factors such as patent foramen ovale (PFO), dehydration, fatigue, and physical fitness significantly influence susceptibility to these conditions.

Preventative strategies, including adequate hydration, avoiding alcohol, and maintaining physical fitness, are vital in reducing risk. As diving continues to grow in popularity, ongoing education, improved safety practices, and access to hyperbaric facilities remain essential for minimizing the incidence and severity of decompression-related illnesses.

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