Dysbarism (Dysbaric Disorders)

Etiology

Dysbarism is most commonly associated with underwater diving, though it may also result from exposure to other environments involving rapid, extreme, or prolonged changes in ambient pressure. These include high-altitude exposure, aircraft cabin decompression, spaceflight, caisson work, and tunnel-boring operations.[3][1][2] Repeated or prolonged exposure to compressed air or gas may also contribute to delayed skeletal complications such as dysbaric osteonecrosis.[4][5]

Epidemiology

Millions of people in the United States practice scuba diving, although estimates vary depending on whether they include regular, occasional, or recreational divers. The 2026 CDC Yellow Book estimates approximately 0.6 to 3.5 million scuba divers in the United States.[6] Diving-related injuries are relatively uncommon, but emergency departments in the United States have been estimated to evaluate approximately 1394 scuba-related injuries annually.[6] Barotrauma is among the most common diving-related injuries, with middle ear barotrauma representing the most frequent form of barotrauma and the leading cause of morbidity among scuba divers. Pulmonary barotrauma is less common but can result in life-threatening complications, particularly arterial gas embolism. Drowning remains the leading cause of death among divers, with cardiac events and arterial gas embolism also representing important causes of diving-related fatalities.[7]

Pathophysiology

The human body consists predominantly of water, a minimally compressible medium. Therefore, pressure changes produce limited direct effects on most tissues. Air-filled compartments of the body, including the lungs, sinuses, middle ear, gastrointestinal tract, and dental cavities, are primarily affected by barotrauma. These compartments typically communicate with the external environment to permit pressure equilibration. Pressure differentials develop between gas spaces and surrounding tissues when these communication pathways are obstructed. The resulting mechanical stress may exceed tissue tensile strength, leading to injury.

Underwater diving provides a clear physiologic model. Ambient pressure increases by 1 atmosphere for every 10 meters (33 feet) of seawater depth. Boyle's law states that gas volume varies inversely with pressure at constant temperature. This principle may explain pulmonary barotrauma and arterial gas embolism. At a depth of 10 meters, lung volume decreases by approximately 50% as ambient pressure doubles. Breath-holding during ascent or the presence of obstructive airway disease, including asthma and chronic obstructive pulmonary disease, may prevent gas escape during decompression. The resulting alveolar overdistension can lead to rupture, with subsequent pneumothorax, pneumomediastinum, subcutaneous emphysema, or arterial gas embolism.

Arterial Gas Embolism

Arterial gas embolism occurs when pulmonary barotrauma causes gas to enter the pulmonary veins and systemic arterial circulation. Gas bubbles within the arterial circulation can obstruct small vessels, producing distal ischemia and triggering mechanical, inflammatory, and endothelial injury. Bubble-endothelium interactions can activate leukocytes and platelets and promote thromboinflammation, increased vascular permeability, edema, and tissue injury, including infarction and necrosis. Clinical severity depends on the volume and distribution of gas, the rate of embolization, and the vascular territory involved, with cerebral and coronary embolization potentially causing severe or fatal injury.[1][8][9][10]

Sinus or Middle Ear Barotrauma

Sinus or middle ear barotrauma, also known as squeeze injuries, occurs when sinus or nasal congestion or nasal polyp formation obstructs the sinus ostia or eustachian tubes, preventing pressure equalization. A similar pressure-related injury may occur in dental structures, termed barodontalgia, and is observed in both aviation and diving. Barodontalgia occurs more commonly during ascent in aviation, though it can occur during descent as well. In diving, barodontalgia is more common during descent. Multiple etiologic mechanisms have been proposed. Formation of gas pockets during dental procedures, loosening of dental crowns, or bacterial degradation may predispose to barodontalgia.[11][12][13][14]

Impaired pressure equalization in the middle ear may lead to transudation or hemorrhage into the middle ear space, as well as injury to the tympanic membrane. Middle ear barotrauma may rarely lead to inner ear involvement when a sudden pressure differential develops between the middle and inner ear, resulting in rupture of the round or oval window. The resultant pathology may include labyrinthine fistula formation or perilymph leakage. Inner ear barotrauma may result from eustachian tube dysfunction and pressure differentials between the middle and inner ear. Forceful Valsalva maneuvers in the setting of impaired middle ear pressure equalization have been proposed as one mechanism for round or oval window injury. This block-and-lock mechanism produces minimal change in middle ear pressure due to obstruction, while increasing perilymphatic pressure within the cochlea and predisposing to rupture of the round or oval window.[11][12][15][16] See Barotrauma. 

Decompression Sickness

Decompression sickness (DCS), also called the bends, occurs when dissolved inert gas becomes supersaturated during or after a reduction in ambient pressure, resulting in bubble formation within tissues and blood. DCS most commonly occurs after compressed-gas diving but may also occur after other forms of decompression, including caisson work, rapid ascent to altitude, or extravehicular activity. The spine, brain, inner ear, joints, skin, and other tissues may be affected, with clinical manifestations ranging from musculoskeletal pain and skin changes to neurologic and cardiopulmonary complications.[7][2] 

The relationship between dissolved gas and pressure is described by Henry's law, which states that the amount of gas dissolved in a liquid is proportional to its partial pressure at constant temperature. During diving, increased ambient pressure increases the partial pressure of nitrogen in the breathing gas and promotes nitrogen uptake into tissues. During ascent, decreasing ambient pressure can cause tissue inert-gas tension to exceed ambient pressure, producing supersaturation and allowing bubbles to form in tissues and the circulation. These bubbles can produce mechanical, ischemic, inflammatory, and vascular injury.[1] See Decompression Sickness.

Nitrogen Narcosis

Nitrogen narcosis, also known as the rapture of the deep, occurs when nitrogen partial pressure increases during exposure to compressed breathing gas. Elevated nitrogen partial pressure in nervous tissue produces clinical manifestations resembling those of alcohol intoxication, including intellectual and neuromuscular impairment, anesthesia, disorientation, visual disturbance, and alterations in behavior or personality. Increasing depth correlates with symptom severity, with hallucinations and loss of consciousness occurring at greater depths. Hypothermia, fatigue, hypercarbia, and individual susceptibility may increase the severity of narcosis. Symptoms generally resolve rapidly with ascent to shallower depth. Repeated exposure may result in the development of partial tolerance.[17][18]

High-Pressure Neurological Syndrome

High-pressure neurological syndrome, also known as helium tremors, is a dysbaric disorder that occurs during deep dives, typically deeper than 150 meters (approximately 500 feet), particularly in divers breathing helium-oxygen mixtures. Clinical features include neurological and psychological manifestations, including tremor, somnolence, myoclonic jerking, nausea, dizziness, visual disturbance, and impaired cognitive performance, as well as electroencephalographic abnormalities. The exact mechanism is unclear. Proposed mechanisms include pressure-induced alterations in neuronal membrane properties, ion channels, and neurotransmitter systems, particularly γ-aminobutyric acid and N-methyl-D-aspartate receptors. Additional proposed contributors include effects on calcium signaling and other neuronal processes.[19][20] See High-Pressure Neurological Syndrome.

Dysbaric Osteonecrosis

Dysbaric osteonecrosis is a delayed skeletal complication associated with repeated or prolonged exposure to elevated ambient pressure and decompression, most commonly occurring in divers and workers exposed to compressed air or gas. It is considered a long-term manifestation of decompression injury and may be asymptomatic or progress to symptomatic bone and joint disease.[5][21]

• Most commonly affected: proximal femur and humeral head, although other long bones can be involved.[21] 
• Juxta-articular lesions are more clinically important because they can progress to subchondral fracture, articular surface collapse, and secondary osteoarthritis.[21][4]
• Non-articular lesions are often asymptomatic and less likely to cause pathologic fracture.[21]
• Multifocal disease can occur.[4]
• Risk increases with greater cumulative exposure to compressed gas, greater depth, and longer exposure.[22][4]

Decompression-related gas bubbles may also contribute to delayed skeletal injury. Intraosseous gas embolization and vascular injury can impair the microcirculation of bone, resulting in ischemia and osteonecrosis. The proximal femur is particularly susceptible to clinically significant disease because lesions near the articular surface may progress to subchondral fracture and collapse.[21][5]

History and Physical

History and physical examination findings in dysbarism are often ambiguous and may have a delayed and evolving course. Careful attention is needed to diving exposure details and symptom chronology. Diving history should include dive frequency and depth, episodes of rapid ascent and in-dive complications, diver experience level, equipment quality, and prior decompression illness.[1][23]

The timing of symptom onset should also be elicited. The temporal relationship between symptom onset and dive phase helps differentiate barotrauma, gas toxicity, and decompression illness. Barotrauma occurs more commonly during descent, gas toxicities predominate at depth, and decompression illness typically occurs during or after ascent. Arterial gas embolism symptoms generally develop within minutes of surfacing, whereas decompression sickness typically manifests over several hours. The pattern of symptoms further aids diagnosis, with arterial gas embolism more commonly presenting with pulmonary and cerebral manifestations and decompression sickness more frequently affecting joints and the spinal cord. History should likewise include relevant comorbidities and risk factors, such as dehydration, upper respiratory tract infection, allergic disease, high workload, poor physical conditioning, or advanced age.[1][23] 

The physical examination should include evaluation of the ears, pulmonary system, skin, joints, and neurologic function. Many patients with mild decompression sickness demonstrate normal vital signs, mental status, and physical examination findings. More severe cases may present with significant neurologic deficits, including paralysis. The ear and pulmonary examinations should assess for signs of otic or pulmonary barotrauma. A comprehensive neurologic examination is required to avoid missed subtle deficits and should include assessment of the cranial nerves, motor function, sensory function, reflexes, vestibular function, cerebellar function, and mental status using a mini-mental status examination.[1][2]

Dysbaric osteonecrosis may present months to years after repeated or prolonged hyperbaric exposure and may initially be asymptomatic. When lesions involve the hip or shoulder, patients may develop activity-related or weight-bearing pain, reduced range of motion, and functional limitation. Juxta-articular lesions are more likely to become symptomatic and may progress to subchondral fracture or articular collapse. Lesions involving the femoral or humeral shafts are generally less symptomatic but may occasionally predispose to pathologic fracture.[21][5][24] 

Evaluation

Laboratory studies and imaging are generally of limited value in establishing the diagnosis, though they may help exclude alternative diagnoses. Chest radiography may demonstrate findings consistent with barotrauma or near-drowning. Pneumothorax should be excluded before recompression therapy is considered. For acute decompression illness, CT and MRI are often nondiagnostic but may help identify alternative diagnoses or complications. Rarely, CT or MRI of the brain may demonstrate intravascular air within arterial branches. Laboratory studies may show hemoconcentration or elevated creatine phosphokinase in the presence of arterial gas embolism.[1][25][26] 

Dysbaric osteonecrosis should be evaluated initially with plain radiographs of the affected region. MRI is more sensitive for detecting early osteonecrotic lesions and can characterize their location and extent. CT may provide additional information regarding osseous anatomy, structural collapse, and preoperative planning. Bone scintigraphy or single-photon emission computed tomography may be considered in selected patients when clinical suspicion remains high despite nondiagnostic initial imaging.[21][5]

Treatment / Management

The presentation of symptoms in dysbaric disorders is frequently vague and delayed. Consequently, a low threshold for treatment is warranted. Diagnosis is primarily clinical, based on the pressure-exposure history, symptom onset and timing, and physical and neurologic examination. Treatment should not be delayed while awaiting confirmatory testing when decompression illness is suspected.[1][2](B3)

Decompression Illness

Management of decompression illness begins with assessment and stabilization of the airway, breathing, and circulation in the emergency setting. High-flow 100% oxygen should be administered early in management, and the nearest hyperbaric center should be contacted promptly. Recompression should be performed in a hyperbaric chamber. In-water recompression is hazardous and requires advanced planning and specialized equipment. These interventions reduce bubble size, limit ischemic tissue injury, and mitigate ischemia-reperfusion injury.

Tympanic Membrane Rupture

Management of tympanic membrane rupture includes keeping the ear canal dry and allowing adequate drainage. Ear drops are not recommended unless secondary infection develops. Follow-up evaluation with an otolaryngologist is advised. No additional interventions are typically required, as perforations usually heal within approximately 6 weeks. Tympanoplasty is rarely necessary.

Inner Ear Barotrauma

Management of inner ear barotrauma is similar to that of middle ear barotrauma. Additional recommendations include avoiding nose blowing. Rest and anti-vertiginous medications may be beneficial. Hyperbaric oxygen therapy and normobaric oxygen administration are not indicated for either middle or inner ear barotrauma unless decompression sickness or arterial gas embolism is also present.

Middle Ear and Sinus Barotrauma

Management is generally supportive and includes cessation of diving until symptoms resolve and pressure equalization is restored. Analgesics and appropriate treatment of underlying nasal or sinus congestion may be used when indicated. Persistent hearing loss, vertigo, severe pain, tympanic membrane perforation, or suspected inner ear injury warrants otolaryngology evaluation. Diving should be avoided until the underlying condition has resolved and the patient can reliably equalize pressure.

Dysbaric Osteonecrosis

Management depends on lesion location, size, symptoms, structural integrity, and degree of joint involvement. Patients with symptomatic or structurally significant lesions should undergo orthopedic evaluation. Weight-bearing may need to be restricted in patients with large painful lesions at risk for pathologic fracture.[21][27] 

Management of femoral head disease depends on the stage and extent of osteonecrosis and may include observation for small or asymptomatic lesions, joint-preserving procedures for selected early lesions, or total joint arthroplasty for advanced collapse and secondary arthrosis.[21][28][29](A1)

Patients with large lesions involving weight-bearing bone or lesions associated with significant pain require prompt evaluation because of the risk of structural failure and pathologic fracture.[21] When dysbaric osteonecrosis involves the femoral head, conventional osteonecrosis staging systems such as the Ficat classification or the revised ARCO classification may be used to describe disease severity and guide management.[30][31]

Differential Diagnosis

The differential diagnoses to consider for dysbarism include the following:

• Near-drowning with hypoxic encephalopathy
• Middle ear or sinus barotrauma
• Sinusitis or otitis media
• Inner ear barotrauma
• Toxicity from carbon monoxide or other contaminated breathing gases
• Musculoskeletal injury
• Hypoglycemia
• Migraine
• Guillain-Barré syndrome
• Multiple sclerosis
• Transverse myelitis
• Spinal cord compression
• Seizure
• Stroke
• Myocardial infarction
• Subarachnoid hemorrhage
• Seafood toxin exposure
• Envenomation
• Medication effects (eg, mefloquine)
• Osteonecrosis from other causes, including corticosteroid exposure, alcohol use, sickle cell disease, systemic lupus erythematosus, HIV-related factors, irradiation, hematologic disorders, and hypercoagulable states.[32][33]Dysbarism can mimic a wide range of neurologic and systemic disorders. A careful exposure history, detailed symptom chronology, and selective diagnostic testing can help distinguish it from other conditions with overlapping clinical presentations.[1][3]

Prognosis

The prognosis for barotrauma is generally favorable, as most cases are self-limiting. Arterial gas embolism is the most serious complication of pulmonary barotrauma, and injury may be permanent without timely treatment with hyperbaric oxygen therapy. Arterial gas embolism can cause permanent neurologic injury and death, particularly when severe neurologic or cardiopulmonary manifestations occur.[8][34] Inner ear barotrauma typically resolves spontaneously but may result in permanent inner ear damage.[35][36] Nitrogen narcosis also carries a favorable prognosis, as symptoms generally resolve rapidly with ascent. The primary risk arises from impaired judgment, decision-making, and motor coordination, which can lead to underwater accidents and drowning.[17] See Nitrogen Narcosis in Diving. 

The prognosis of dysbaric osteonecrosis depends on lesion size, location, articular surface involvement, and the presence of structural collapse. Small non-articular lesions may remain asymptomatic, whereas large juxta-articular lesions can progress to joint collapse, secondary arthrosis, and substantial functional impairment.[21]