Dysbarism

Etiology

Dysbarism is most commonly associated with underwater diving, though it may also result from exposure to other environments involving rapid or extreme pressure changes, including high-altitude exposure, aircraft cabin decompression, blast injuries, spaceflight, caisson work, and tunnel-boring operations.

Epidemiology

The United States is estimated to have more than 9 million recreational scuba divers, with continued population growth. Increasing diver population has been associated with a rising incidence of diving-related dysbarism. The Divers Alert Network reports that more than 1000 diving-related injuries occur annually, although less than 1% of divers experience decompression sickness. Barotrauma is the most common form of diving-related injury, with middle ear barotrauma being the most frequent diving-related complaint. Pulmonary barotrauma is the second leading cause of death in divers, following drowning.[1][2]

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. Pulmonary barotrauma and arterial gas embolism may be explained by this principle. 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 lung tissue tears, and gas enters the systemic circulation. Gas bubbles within the systemic vasculature typically lodge in small vessels, producing ischemia distal to the obstruction and triggering a local inflammatory cascade. Physiologic effects of intravascular gas include protein denaturation, leukocyte activation, and endothelial injury, resulting in microvascular leak, edema, hemorrhage, infarction, and cell death. Even small volumes of air (approximately 0.5 mL) may be fatal, particularly when introduced into cerebral or coronary circulation.[3]

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.

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. The most common mechanism involves eustachian tube obstruction combined with a forceful Valsalva maneuver. 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.[4]

Decompression Sickness

DCS, also called the bends, occurs when divers ascend too quickly without appropriate decompression stops. Dissolved inert nitrogen comes out of solution and forms bubbles within blood and tissues, with the spine, nerves, joints, and skin most commonly affected. The relationship between dissolved gas and pressure is defined by Henry's law, which states that solubility is directly proportional to partial pressure at constant temperature. During diving, increased ambient pressure increases nitrogen dissolution in tissues, whereas sustained undersea pressure maintains gas in solution. Rapid reduction in ambient pressure during ascent allows dissolved nitrogen to come out of solution, analogous to the rapid depressurization of a carbonated beverage, resulting in bubble formation when ascent occurs too quickly.[5]

Nitrogen Narcosis

Nitrogen narcosis, also known as the rapture of the deep, occurs when nitrogen partial pressure exceeds that experienced during breathing compressed air at 100 feet of seawater (fsw). 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 reported at depths exceeding 300 fsw. Hypothermia, fatigue, hypercarbia, and recent alcohol ingestion increase susceptibility to this condition. Symptoms resolve rapidly with ascent to shallower depth. Repeated exposure may result in the development of partial tolerance.[6]

High-Pressure Neurological Syndrome

High-pressure neurological syndrome, also known as helium tremors, is a dysbaric disorder that occurs at depths below 500 fsw 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. The proposed pathophysiology involves compression effects of high ambient pressure on the lipid components of central nervous system cell membranes, with downstream effects on transmembrane proteins, membrane surface receptors, and ion channels. Additional proposed contributors include alterations in neurotransmitter systems, including γ-aminobutyric acid, dopamine, serotonin, acetylcholine, and N-methyl-D-aspartate, as well as effects of inert gases, neuronal calcium ion flux, and genetic susceptibility.[7]

History and Physical

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

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.

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.

Evaluation

Laboratory studies and imaging are generally of limited value in establishing the diagnosis, though they may assist in excluding alternative differential diagnoses. Chest radiography may demonstrate findings consistent with barotrauma or near-drowning. Pneumothorax should be excluded before recompression therapy is considered. Computed tomography (CT) and magnetic resonance imaging (MRI) findings are typically unremarkable but may suggest alternative etiologies for the patient's symptoms. 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.

Treatment / Management

The presentation of symptoms in dysbaric disorders is frequently vague and delayed. Consequently, a low threshold for treatment is warranted. Decompression illness often requires a witnessed response to therapy before a definitive diagnosis can be established.

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 maintaining a dry ear canal 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 both middle and inner ear barotrauma unless decompression sickness or arterial gas embolism is also present.

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)

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.

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. Recent case series report mortality rates ranging from 12% to 30% despite administration of hyperbaric oxygen therapy, with approximately 25% of survivors experiencing permanent neurologic sequelae.[8] Inner ear barotrauma typically resolves spontaneously but may result in permanent inner ear damage.[9] Nitrogen narcosis also carries a favorable prognosis, as symptoms resolve completely with ascent. The risk primarily arises from impaired judgment, which may lead to drowning.