The definition of dysbarism is any adverse medical condition that results from changes in ambient pressure. These changes in pressure must occur either at a rate or duration exceeding the capacity of the body to adapt safely. The term dysbarism covers decompression sickness (DCS), nitrogen narcosis, high-pressure neurological syndrome (HPNS), barotrauma, and arterial gas emboli (AGE).
Although the most common cause of dysbarism is underwater diving, dysbaric injury can occur following exposure to any environments with extreme pressure changes. Other examples include high altitude, aircraft cabin decompression, explosions or blasts, outer space, caissons, and tunnel-boring operations.
There are over 9 million recreational scuba divers in the United States alone, and that 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).
The human body is mostly comprised of water, which is minimally compressible, thus pressure changes do not typically directly affect these portions of the body. 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 usually connected to the outside world to allow for free air exchange, but if they are blocked the high-pressure air will push on tissues surrounding the low-pressure area and this 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 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 happens when lung tissue tears and gas bubbles enter into 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 which lead 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.
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 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 ear and the 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.
DCS (also called “the bends”) happens when divers ascend too quickly and do not take proper “decompression stops.” Dissolved inert gas (nitrogen) comes out of 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.
Nitrogen narcosis (also known as the “rapture of the deep”) occurs when the partial pressure of nitrogen exceeds that experienced breathing compressed air at 100 feet of sea water (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/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 that 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 by repeated exposure.
Lastly, HPNS (also known as helium tremors) is a dysbarism that occurs below 500 fsw when a diver is breathing a helium-oxygen mixture. It’s characterized by neurological, psychological, and EEG abnormalities 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 CNS and its influences on transmembrane proteins, membrane surface receptors, and ion channels. There also appears to be a role of neurotransmitters (such as GABA, dopamine, serotonin, acetylcholine, and NMDA), anesthetic gases, neuronal calcium ions, and genetics in HPNS pathophysiology.
History and Physical
It is important to keep in mind 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 frequency of dives, depth of dives, a history of rapid ascent or other problems during the dive, the experience of the diver, the quality of equipment used, and history or prior decompression illnesses.
Ask the patient about their symptom 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 will be 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 are 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, URI, 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 will have a normal exam, vitals, and mental status. More serious cases may involve significant neurological abnormalities such as paralysis. During the ear and pulmonary exam, look for signs of otic or pulmonary barotrauma. A thorough neurologic exam is mandated so as not to miss subtle findings of injury including cranial nerves, motor, sensory, reflexes, vestibular, cerebellar function, and a mini-mental status exam.
In general, diagnostic workup 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 of barotrauma or near-drowning. It is very important to rule out pneumothorax when considering recompression therapy. CT and MRI are usually normal but may be helpful in finding other causes of the patient’s symptoms. Rarely CT or MRI of the brain may show air densities in arterial branches. Laboratory studies may reveal hemoconcentration or elevated CPK (in the presence of AGE).
The differential diagnoses to consider are the following:
- Near drowning with hypoxic encephalopathy
- Middle ear/sinus barotrauma
- Inner ear barotrauma
- Carbon monoxide toxicity (or other contaminated breathing gases)
- Musculoskeletal injury
- Guillain-Barre syndrome
- Multiple sclerosis
- Transverse myelitis
- Spinal cord compression
- Myocardial Infarction
- Subarachnoid hemorrhage
- Seafood toxin
- Medications (e.g., mefloquine)
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 likely is fatal if not properly treated with HBO2. Recent case series suggest the mortality rates range from 12% to 30% with HBO therapy and around 25% of survivors experience permanent neurologic sequelae. 
Inner ear barotrauma usually resolves spontaneously but may result in permanent inner ear damage.
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.
Deterrence and Patient Education
Absolute contraindications to diving include spontaneous pneumothorax, acute asthma with abnormal PFTs, cystic or cavitary lung disease, obstructive or restrictive lung disease, seizures, atrial septal defect (ASD), symptomatic coronary artery disease (CAD), chronic perforated TM, inability to equalize sinus or middle ear pressure, or intra-orbital gas.
Middle ear barotrauma can be prevented by avoiding diving with significant nasal congestion, descending feet first, descending at a slow rate with the use of an anchor line, and avoiding forceful Valsalva at depth or upon ascent. When someone fails to equalize pressures passively, they may perform one of many equalizing techniques to open the Eustachian tube and allow free gas exchange. These include Valsalva, yawning, swallowing, wiggling jaw, Toynbee, Edmonds, among others. Prophylaxis with pseudoephedrine or nasal steroids before dives has been shown to decrease the incidence of middle ear barotrauma.
Including other gases (such as hydrogen or nitrogen) into the helium-oxygen mixture suppresses the neurological effects of HPNS. Also, because faster compression rate and higher maximum pressure experienced by a diver lead to more severe presentations of HPNS, divers should not dive to depths greater than 500 feet and should descend slowly or incorporate stops during compression to avoid HPNS.
Enhancing Healthcare Team Outcomes
Dysbarism includes medical conditions resulting from changes in ambient pressure; they include barotrauma, nitrogen narcosis, high-pressure neurological syndrome, and decompression illness. Because of the varied presentation, these disorders are best managed by an interprofessional team. However, it is important to consult with a diving expert or the individual in charge of the hyperbaric chamber when it comes to management. The presentation of symptoms for DCI often is vague and delayed; therefore, it is important to have a low threshold for treatment.