Dysbarism

Etiology

Although underwater diving is the most common cause of dysbarism, dysbaric injury can occur following exposure to any environment with extreme pressure changes. Other examples include high altitude, aircraft cabin decompression, explosions or blasts, outer space, caissons, and tunnel-boring operations.

Epidemiology

There are over 9 million recreational scuba divers in the United States alone, and the number continues to rise. Because of this increasing population, the incidence of diving-related dysbarism has also increased. According to the Divers Alert Network (DAN), more than 1000 diving-related injuries occur annually, but less than 1% of divers experience DCS. Barotrauma is the most common form of diving-related injury, with middle ear barotrauma being the most common diving-related complaint. Pulmonary barotrauma is the second leading cause of death in divers (behind drowning).[1][2][3]

Pathophysiology

The human body is mostly comprised of water, which is minimally compressible. Thus, pressure changes do not typically directly affect these body portions. However, the areas of the body that are air-filled (lungs, sinuses, middle ear, gas in bowels, and cavities in teeth) are the structures affected by barotrauma. Usually, these structures are connected to the outside world to allow for free air exchange. Still, if they are blocked, the high-pressure air pushes on tissues surrounding the low-pressure area, which can cause tissue damage when the pressure gradient exceeds the tensile strength of the tissues involved. 

In the example of an undersea diver, the ambient pressure increases by 1 atmosphere (atm) for every 10 meters (33 feet) of depth. According to Boyle’s Law, if the temperature is constant, the volume of a gas varies inversely with pressure. Boyle’s law can explain pulmonary barotrauma and AGE. The lung volume is cut in half while the pressure doubles when a diver reaches a depth of 10 meters. Divers who hold their breath as they ascend (or those with obstructive airway diseases such as asthma or chronic obstructive pulmonary disease [COPD]) can suffer an overexpansion injury and alveolar rupture. This can cause pneumothorax, pneumomediastinum, subcutaneous emphysema, or AGE.

AGE

AGE happens when lung tissue tears and gas bubbles enter the systemic circulation. Gas bubbles in the systemic vasculature usually lodge in small vessels, producing ischemia distal to the blockage and local activation of the inflammatory cascade. Some physiological effects of gas bubbles include protein denaturation, leukocyte activation, and endothelial damage, leading to microvascular leak and edema, hemorrhage, infarct, and cell death. Even a small amount of air (0.5 mL) can be fatal, especially if it reaches the cerebral or coronary vasculature.[4]

Sinus or Middle Ear Barotrauma

Sinus or middle ear barotrauma (also known as "squeeze" injuries) can occur when a diver has sinus or nasal congestion or a nasal polyp that blocks the openings to the sinuses or the Eustachian tubes. This leads to a failure to equalize pressure. This phenomenon can also occur in teeth. It is then called barodentalgia. It is seen in aviation and diving. It occurs more commonly during ascent when flying but can occur during descent. There are several theories on etiology. If there are gas pockets from dental surgery, a loose crown, or bacterial degradation. In the ear, this can lead to transudate or bleeding into the middle ear and trauma to the tympanic membrane. Middle ear barotrauma may rarely be associated with inner ear barotrauma when there is a sudden pressure differential between the inner and middle ear, leading to round or oval window rupture. This may result in a labyrinthine fistula or perilymph leakage. The most common scenario is when the Eustachian tube is blocked, and a person performs an "explosive" Valsalva maneuver. This "block and lock" scenario leads to no change in middle ear pressure because of the blockage but increases the perilymph pressure in the cochlea and leads to rupture of the round or oval window.[1]

DCS

DCS (also called "the bends") happens when divers ascend too quickly and do not take proper "decompression stops." Dissolved inert gas (nitrogen) comes from the solution and forms bubbles in the blood and tissues (most commonly in the spine, nerves, joints, and skin). According to Henry’s Law, if the temperature is constant, the amount of gas that dissolves into liquid is directly proportional to the partial pressure of that gas. When diving, the higher partial pressure causes more nitrogen to be dissolved in tissue over time, and the increased undersea pressure keeps the gas in solution. Similar to when you open a soda bottle quickly, and the rapid reduction in pressure leads to bubble formation, a similar phenomenon occurs when a diver’s nitrogen comes out of solution and forms bubbles if the diver surfaces too quickly.[5]

Nitrogen Narcosis

Nitrogen narcosis (also known as the "rapture of the deep") occurs when the partial pressure of nitrogen exceeds that experienced when breathing compressed air at 100 feet of seawater (fsw). The increased nitrogen partial pressure in nervous tissue causes signs and symptoms similar to drunkenness, including intellectual and neuromuscular impairment, anesthesia, disorientation, impaired vision, changes in behavior or personality, etc. The greater the depth, the worse the symptoms become, often leading to hallucinations and loss of consciousness when divers go deeper than 300 fsw. Divers who are hypothermic, fatigued, hypercarbic, or who recently ingested alcohol are more susceptible. Symptoms resolve rapidly on ascent to a shallower depth. Divers can build tolerance through repeated exposure.[6]

HPNS

HPNS (helium tremors) is a dysbarism that occurs below 500 fsw when a diver breathes a helium-oxygen mixture. Neurological, psychological, and electroencephalogram abnormalities characterize it, including tremors, somnolence, myoclonic jerking, nausea, dizziness, visual disturbances, and decreased mental performance. The exact mechanism is unclear, but it appears to be related to the compression effect of pressure on the lipid component of cell membranes of the central nervous system and its influences on transmembrane proteins, membrane surface receptors, and ion channels. There also appears to be a role of neurotransmitters (such as γ-aminobutyric acid [GABA], dopamine, serotonin, acetylcholine, and N-methyl-d-aspartate [NMDA]), anesthetic gases, neuronal calcium ions, and genetics in HPNS pathophysiology.[7]

Toxicokinetics

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History and Physical

It is important to remember that the presentation of history and physical exam findings is often ambiguous and may evolve. When taking a history, focus the interview on diving and symptom history. Diving history includes asking about the frequency and depth of dives, a history of rapid ascent or other problems during the dive, the diver's experience, the quality of equipment used, and history or prior decompression illnesses.

Patients should be asked about their history, specifically when the first symptoms started. The stage of the dive, when symptoms occur, can help differentiate barotrauma from gas toxicity and decompression illness. Barotrauma is more likely to occur on descent, gas toxicities are most prominent at depth, and decompression illness (DCI) usually occurs on or after ascent. AGE symptoms occur within a few minutes of surfacing, while DCS symptoms usually take hours to present. Another helpful distinguishing factor between AGE and DCS is the type of symptoms. AGE usually presents with pulmonary and cerebral problems. DCS presents more often with joint and spinal cord involvement. Other items to address are past medical history and risk factors for dysbarism, such as dehydration, upper respiratory infections, allergies, high workload, poor fitness, and increasing age. A physical examination should include an ear, pulmonary, skin, joint, and neurological evaluation. Many minor DCS patients have normal exams, vitals, and mental status. More serious cases may involve significant neurological abnormalities, such as paralysis. During the ear and pulmonary exam, otic or pulmonary barotrauma signs should be examined. A thorough neurologic exam is mandated so as not to miss subtle findings of injury, including cranial nerves, motor, sensory, reflexes, vestibular, and cerebellar function, and a mini-mental status exam.

Evaluation

In general, diagnostic workups with labs and imaging are not significantly helpful in establishing the diagnosis but may help rule out other differential diagnoses. A chest X-ray may show changes in barotrauma or near-drowning. It is very important to rule out pneumothorax when considering recompression therapy. CT and MRI are usually normal but may help find other causes of the patient’s symptoms. Rarely does a CT or MRI of the brain show air densities in arterial branches. Laboratory studies may reveal hemoconcentration or elevated creatine phosphokinase (in the presence of AGE).

Treatment / Management

The presentation of symptoms for these dysbarisms is frequently vague and delayed. Because of this, it is important to have a low threshold for treatment. In cases of DCI, the definitive diagnosis is often not made until there is a witnessed response to treatment.

DCI

For DCI, treatment starts with assessing and stabilizing the airway, breathing, and circulation in the emergency setting. Begin administration of high-flow 100% oxygen early and contact the closest hyperbaric center. Recompression should always be done in a hyperbaric chamber; in-water recompression is dangerous and requires significant advanced planning and equipment. These interventions shrink bubbles, prevent ischemic tissue damage, and reduce ischemia-reperfusion injury.

Tympanic Membrane Rupture

In tympanic membrane rupture, management includes keeping the ear canal dry and allowing drainage. Ear drops are not recommended unless an infection develops. The patient should follow up with an otolaryngologist. Usually, no other interventions are necessary since the perforations typically heal within 6 weeks. Membrane grafting is rarely needed.

Inner Ear Barotrauma

The treatment of inner ear barotrauma is similar to that of middle ear barotrauma. The patient needs to avoid blowing their nose. Rest and anti-vertiginous medications are helpful. For both middle ear barotrauma and inner ear barotrauma, hyperbaric oxygen (HBO₂) recompression and oxygen are unnecessary unless the patient also has signs of DCS or AGE.

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
• Inner ear barotrauma
• Carbon monoxide toxicity (or other contaminated breathing gases)
• Musculoskeletal injury
• Hypoglycemia
• Migraine
• Guillain-Barre syndrome
• Multiple sclerosis
• Transverse myelitis
• Spinal cord compression
• Seizure
• Stroke
• Myocardial infarction
• Subarachnoid hemorrhage
• Seafood toxin
• Envenomation
• Medications (eg, mefloquine)

Prognosis

The prognosis for barotrauma is good as most of these conditions are self-limiting. AGE, however, is the most serious potential complication of pulmonary barotrauma and is likely fatal if not properly treated with HBO₂. Recent case series suggest the mortality rates range from 12% to 30% with HBO₂ therapy, and around 25% of survivors experience permanent neurologic sequelae.[8] Inner ear barotrauma usually resolves spontaneously but may result in permanent inner ear damage.[1][9] Nitrogen narcosis also carries a good prognosis as it resolves completely with ascent. The main danger stems from poor judgment, which can lead to drowning.[7]