Decompression Sickness and Dysbarism

The human body has the ability to adjust to increases in ambient pressure, up to a point. However, the increased pressure increases the partial pressures of the gases that are inspired. A number of effects can occur. Toxicity to oxygen or nitrogen or to contaminants has deleterious effects. A scuba (self-contained underwater breathing apparatus) diver can mitigate these effects by staying within established time parameters. Those with advanced technical training use specialized mixtures to avoid these toxicities.

Even when a diver stays within the parameters or uses the specialized gases, issues can still occur and cause injury. In addition, the sudden or too rapid decrease in pressure (ie, decompression) can have a number of ill effects. Some of these effects relate to the gross expansion of gas in the usual gas-containing cavities and organs in the body. The result can be dysbarism. Other effects are due to the expansion of microscopic gas particles within the tissues of the body. This is decompression sickness (DCS).

DCS, a complex resulting from changed barometric pressure, includes events related to high altitude and aerospace events as well ^[1] ; however, the discussion of DCS in this article focuses on decompression associated with sudden decrease in pressures during underwater ascent, usually occurring during free or assisted dives. People involved with tunneling projects, in submarines during emergencies, and in breath-hold free diving may also experience the physiologic effects of decreased pressure brought on by such ascents.

The increasing popularity of scuba diving and the growth of commercial diving have increased the frequency of deep-pressure injuries. In addition, the ability to travel rapidly between areas of disparate altitudes in a matter of hours (including the exacerbation caused by decreased pressures in flight) increases the chance of experiencing DCS and dysbaric events and makes it more likely that physicians far from water bodies will encounter them. Accordingly, all physicians, especially emergency physicians, should be familiar with the physiologic effects and management of these deep-pressure injuries.

Special concerns in diving

Pregnancy

Diving while pregnant is not recommended, because of unknown effects of nitrogen diffusion across the maternal-placental membrane. The fetus is not believed to be protected from decompression problems and is at risk of malformation and gas embolism. However, normal pregnancies have been reported even after repetitive dives.

Age

There is no absolute lower age limit, but as a rule, children younger than 12 years should not dive. Diving is a potentially dangerous activity that calls for respect, common sense, and absolute adherence to safety rules. The inherent tendency of children to be distracted and to lack a sense of mortality or time makes it difficult for them to dive safely without close supervision. At the other end of the age spectrum, advanced age brings increased medical problems.

Carbon monoxide toxicity

Most divers use a compressed air source, and their tanks are usually refilled at dive shops. The equipment is typically a gasoline-powered air compressor that uses filtered ambient air. Improper setup or equipment malfunction may compress carbon monoxide from exhaust fumes (or other gases nearby) along with the air, leading to carbon monoxide toxicity. Although filling stations should have safeguards in place, the potential for injury remains.

The symptoms of carbon monoxide poisoning can mimic those of DCS or arterial gas embolization (AGE), necessitating differentiation by means of co-oximetry. Failure to recognize carbon monoxide poisoning is not a serious omission, as long as the patient is recognized as having a diving injury. The hyperbaric therapy used for DCS and AGE is also the treatment of choice for carbon monoxide poisoning.

Use of technical diving gases

There is a practical limit to the depth scuba divers can reach using compressed air, about 40 m (132 ft, 4 atm). At this depth, bottom times are extremely short (or, actually, nonexistent according to standard tables), and the risk of nitrogen narcosis is high. Because many interesting sites (eg, wrecks) are deeper than this, many divers have started using "technical diving" gases such as Trimix, which lowers the nitrogen load to avoid narcosis, decreases the oxygen content to avoid toxicity, and adds helium (also a lighter gas). Depending on the target depth, multiple tanks with different mixes for different depth ranges may be carried. This is a highly technical and risky activity.

Even with Trimix, the depth limit remains fuzzy, because the overall gas density increases, increasing the work of breathing and thus leading to respiratory fatigue. With the additional load imposed by general physical exertion, hypercapnia can ensue that exacerbates overall fatigue. If this is not corrected by ascending, death can occur.

Breath-hold diving

The depth an average diver can reach is limited by his or her physical prowess and capacity for breath holding. Neither was a major concern except in the case of forced hyperventilation just before a dive (on the assumption that this would help), which could result in hypoxia with loss of consciousness before elevated carbon dioxide triggers the need to take a breath. Fins increased the depth and distance, but again, not to a concerning level.

The availability of oversized fins and motorized underwater scooters has allowed much deeper free dives, as well as more rapid ascent immediately followed by another dive. Professional and recreational spear fishers are now achieving depths and underwater times at which they may start accumulating nitrogen loads and, with rapid ascents, develop DCS.

In addition, extreme-depth unlimited free divers, who use a weighted sled to achieve record depths measured in the several hundreds, may develop DCS as a consequence of the nitrogen loads induced by the combination of extreme depth and 5- to 7-minute underwater times. The risk is especially high in individuals preparing for a competition, who may undertake multiple weighted free dives to increasing depths with limited surface intervals in the course of a day. Frequent Valsalva maneuvers on descent to equalize pressure can also unmask a previously unknown cardiac issue (eg, patent foramen ovale [PFO] or atrial septal defect [ASD]) and allow neurologic DCS.

Gas laws

Changes in pressure affect only compressible substances in the body. The human body is made primarily of water, which is noncompressible; however, the gases on hollow spaces and viscera, as well as those dissolved in the blood, are subject to pressure changes. Physical characteristics of gases are described by the following four gas laws, which quantify the physics and problems involved in descending under water.

Boyle's law

Boyle's law may be expressed as follows:

• PV = K

where P = pressure, V = volume, and K is a constant. At a constant temperature, the volume of a perfect gas varies inversely with the pressure. Similarly, the pressure varies inversely with the volume. Simply stated, this means that if pressure is doubled, volume is halved, and if volume is doubles, pressure is halved.

For every 10 m (33 ft) of descent, pressure increases by 1 atm. Thus, at 10 m, lung volume during a breath-hold dive is one half that at the surface; at 20 m (66 ft), one third; at 30 m (99 ft), one quarter; and at 40 m (132 ft), one fifth. (See the first image below.) It follows that ascending from 30 m to the surface without venting (exhaling) would cause the lungs, with minimal ability to expand further, to increase pressure to three times normal, with the greatest change occurring in the last 10 m, where it would double. (See the second image below.) Boyle's law is the key law explaining the pressurization issues and injuries described in this article. ^[2]

Dalton's law

Dalton's law may be expressed as follows:

• Pt = PO₂ + PN₂ + Px

where Pt = total pressure, PO₂ = partial pressure of oxygen, PN₂ = partial pressure of nitrogen, and Px = partial pressure of remaining gases. In a mixture of gases, the pressure exerted by any given gas is the same as the pressure the gas would exert if it alone occupied the same volume. Thus, the ratio of gases does not change, even though the overall pressure does. The individual partial pressures, however, change proportionally.

During descent, Pt of breathing air increases; thus, partial pressures of the individual gaseous components must increase proportionally (see the image below). An increasing amount of nitrogen dissolves in the blood, and the higher PN₂ alters the electrical properties of cerebral cellular membranes, causing an anesthetic effect (nitrogen narcosis). Every 15 m of depth has the same effect as one alcoholic drink. By 45 m, divers may experience alterations in reasoning, memory, and response time, as well as other problems (eg, idea fixation, overconfidence, and calculation errors). Even when no signs of nitrogen narcosis are noted, divers may significantly overestimate diving time during deep dives.

Descent also increases the amount of dissolved oxygen. Breathing 100% oxygen at 2 atm (10 m) may cause central nervous system (CNS) oxygen toxicity in as little as 30-60 minutes. At 90 m, the normal 21% oxygen in compressed air can become toxic because PO₂ is approximately equal to 100% at 10 m. This is why many deep divers use specialized mixtures that replace nitrogen with helium and use varying percentages of oxygen, depending on depth.

Henry's law

Henry's law may be expressed as follows:

• %X = (PX/Pt) × 100

where %X = amount of gas dissolved in a liquid, PX = pressure of gas X, and Pt = total atmospheric pressure. At a constant temperature, the amount of gas that dissolves in a liquid with which it is in contact is proportional to the partial pressure of that gas. That is, a gas diffuses across a gas-fluid interface until the partial pressure is the same on both sides.

With increasing depth, nitrogen in compressed air equilibrates through the alveoli into the blood. Over time, increasing amounts of nitrogen dissolve and accumulate in the lipid component of tissues. As an individual ascends, a lag occurs before saturated tissues start to release nitrogen back into the blood. When a critical amount of nitrogen has been dissolved in the tissues, ascending too quickly causes the dissolved nitrogen to return to its gas form while still in the blood or tissues, causing bubbles to form. (See the image below.)

Further reductions in pressure while flying or ascending to a higher altitude also contribute to bubble formation. The average commercial airline, in an effort to reduce costs, pressurizes cabins to only about 2438 m (8000 ft). If a person flies too soon after diving, this additional decrease in pressure may be enough to precipitate bubbling. If the bubbles are still in the tissue, they can cause local problems; if they are in the blood, embolization may result.

Charles' law

Charles' law may be expressed as follows:

• V1/V2 = T1/T2 (for a gas at constant pressure)
• P1/P2 = T1/T2 (for a gas at constant volume)

where V = volume of gas, P = pressure, T = temperature, 1 = initial, and 2 = final. At a constant pressure, the volume of a given mass of a perfect gas varies directly with the absolute temperature. This means that decreasing temperature decreases pressure. A closed diving bell descending will have decreased pressure due to decreased temperature. An open diving bell descending will have a decrease in volume due to pressure and decreased temperature.

Gas bubbles

Gas bubbles inside the body (eg, in the intestine or stomach) can cause significant discomfort. This is even truer for divers. Gas that is trapped in various body cavities can give rise to a range of manifestations in different organ systems. The following discussion focuses on microscopic bubbles, in particular the nitrogen bubbles that cause DCS.

Not only does the quantity and size of the bubbles matter, but so too do their location and the reactions they cause. If bubbles end up in the lungs and are not too large, they are simply filtered and exhaled. If, however, a right-to-left shunt is present (eg, from PFO), they bypass the natural pulmonary filtration and continue to the brain or other organs. Nitrogen bubbles are believed to start as minute gas nuclei present before the dive, rather than from the supersaturation of the blood and tissues that seeds large bubble formation. ^[3]

All divers have bubbles ^[4] ; however, few develop DCS. Thus, other factors besides bubbles must be involved. The presence of bubbles alone does not increase the risk of DCS. ^[5]

Microbubbles precede larger venous gas emboli. ^[6] These emboli can occlude blood flow in smaller vessels and cause direct ischemia and damage. Bubbles have also been found to alter vascular endothelium through adhesion molecule–mediated endothelial activation, in addition to activating platelets. In neurologic tissue, this leads to focal ischemia.

Microparticles, 0.1- to 1-μm diameter vesicular structures derived from vascular walls, possibly as a result of oxidative stress, ^[7] have been found to increase 3.4 times with dives and decompression stress. ^[8] They appear to activate neutrophils and interact with platelet membranes. ^{[4, 9]} Endothelial cells, blood platelets, or leukocytes shed microparticles upon activation and cell apoptosis. In particular, release of platelet microparticles could reflect bubble-induced platelet aggregation. Once the bubbles form they create a foreign-body interface to which platelets then adhere. In severe DCS, significant decreases in platelet count have been documented. ^{[10, 11]}

Endothelial nitric oxide (NO) synthase (NOS) produces NO through the combination of arginine and oxygen. Through relaxation of smooth muscles, NO inhibits platelet aggregation and inhibits inflammation, contributing to blood-vessel homeostasis. Its presence may reduce bubble formation. ^{[12, 13]} However, the increasing PO₂ at depth drives the reaction towards NO. Once the body’s natural processes for dealing with oxidizers are overwhelmed, an excess of oxidative excitatory neurotransmitters results. ^[13]

Nitrogen dioxide, a nascent gas nucleation site synthesized in some microparticles, initiates decompression inflammatory injury. ^[9] It is also an oxidizer that exists in equilibrium with dinitrogen tetroxide. ^[13]  Another contributor to vascular inflammation that lies within the microparticles is interleukin (IL)-1β; concentrations increase in response to high-pressure environments and continue to increase for 13 hours afterward. ^[14] Additional inflammatory factors adhere to the exterior of the microparticles.

There appears to be a relationship among bubbles, microparticles, platelet-neutrophil interactions, and neutrophil activation, but the nature of this relationship remains to be fully defined. ^{[4, 15]}

Manifestations of decompression sickness

DCS results from the effects of gas (mainly nitrogen) bubbles on organ systems. The bubbles may disrupt cells and cause a loss of function. They may act as emboli and block circulation, as well as cause mechanical compression and stretching of the blood vessels and nerves. The blood-bubble interface may act as a foreign-body interface, activating the early phases of blood coagulation and the release of vasoactive substances from the cells lining the blood vessels. ^[16] DCS may be divided into the following three categories:

• Type I (mild)
• Type II (serious)
• AGE

Type I decompression sickness

Type I DCS is characterized by one or more of the following:

• Mild pain that begins to resolve within 10 minutes of onset (niggles)
• Pruritus ("skin bends"), causing itching or burning sensations of the skin
• Cutis marmorata (cutaneous DCS)

Pain (the bends) is the most common symptom of type I DCS (70-85% of patients). It is often described as a dull, deep, throbbing, toothache-type pain, usually in a joint or tendon area but also in tissue. The shoulder is the most commonly affected joint. The pain is initially mild and slowly becomes more intense. Because of this, many divers attribute early DCS symptoms to overexertion or a pulled muscle. The pain caused by type I DCS may mask neurologic signs indicative of the more serious type II DCS. 

Cutis marmorata is a rash that generally consists of widespread mottling or marbling of the skin or a papular or plaquelike violaceous (blue-red) rash. It typically starts as an intense multifocal itching, and then hyperemia develops, followed by the rash. ^[17]  The similarities of this rash to livedo reticularis or livedo racemosa, along with a small number of divers with cutis marmorata who also have vague neurologic symptoms, has led to theories of the rash being centrally mediated in DCS. ^{[18, 19]} One theory is that gas embolization of the brainstem affects autonomic control of vasodilation and vasoconstriction. ^[19]

Lymphatic involvement is uncommon and typically causes painless pitting edema. The mildest cases involve only the skin or the lymphatic vessels.

Some authorities consider anorexia and excessive fatigue after a dive as manifestations of type I DCS.

Delineation of mild type I DCS symptoms and signs can be useful when treatment is being considered. It is important that there are no concomitant spinal or central neurologic symptoms or signs. ^[20]

Type II decompression sickness

Type II DCS is characterized by one or more of the following:

• Pulmonary symptoms
• Hypovolemic shock
• Nervous system involvement (variable and diverse)

Pain occurs in only about 30% of cases. Symptom onset is usually immediate but may occur up to 36 hours later.

Pulmonary DCS (the chokes) occurs in about 2% of all DCS cases and can cause death. It is characterized by the following:

• Burning substernal discomfort on inspiration
• Nonproductive coughing that can become paroxysmal
• Severe respiratory distress.

Symptoms can start up to 12 hours after a dive and persist for 12-48 hours.

Hydration status is affected by scuba diving. Most divers underestimate their fluid requirements when diving. Add to this the drying effect of commercial airliner altitude pressures and the vacationer's preferred beverages being alcoholic. The average diver is thus set up for the possibility of significant dehydration. In small arteries, the effects of decompression stress are amplified in a dehydrated state. ^[21]

A study of simple hematocrits after a single tropical dive found increases that were statistically significant and greater with the depth of the dive. ^[22]  This increase in hematocrit is also associated with capillary leakage (capilalry leak syndrome). The bubbles can alter the blood-vessel walls, allowing protein and fluid leakage. This can becomes so severe as to cause hypovolemic shock. ^[23]

Hypovolemic shock is commonly associated with other symptoms. For reasons not yet fully understood, fluid shifts from the intravascular spaces to the extravascular spaces. Thrombi may form because of the activation of the early phases of blood coagulation and the release of vasoactive substances from cells lining the blood vessels. ^[16]  

PFO and congenital ASD can also play a role in DCS. ^{[24, 25]} These defects allow bubbles to pass from the right circulation to the left , bypassing the screening effects of the pulmonary circulation. This correlates with a higher prevalence of high spinal cord and head (brain)/neck DCS injury.

Although the overall prevalence of PFO in the general population is significant (~15-30%), ^{[26, 27, 28, 29]} the prevalence of serious type II DCS is low. There is no recommendation for routine screening of general divers (who never had DCS) for PFO or ASD. ^[30] However, in the face of a serious DCS episode, evaluation for such defects should be considered to guide recommendations for future diving. Serious active divers and professionals, and any with neurologic DCS, might consider routine screening for either atrial defect. ^[31]

PFO is known to have a relationship with migraines, particularly those with aura. One study found that that 47.5% of divers with a large right-to-left shunt at rest from PFO who had been affected by DCS had a history or migraines with aura. ^{[32, 33]}  It is reasonable to suggest that divers with a history of migraine, especially those with aura, should consider specific screening for PFO or ASD. Closure of PFOs, once found, in continuing divers appears to prevent symptomatic and asymptomatic neurologic events during long-term follow-up. ^[34]

It may be useful to classify DCS as either type A (the more serious neurologic DCS [strokelike] form) or type B (mild or doubtful neurologic symptoms). Studies suggest that the etiology is different for the two types and is not explained by PFO with shunting. ^{[35, 36]}

DCS can be dynamic and does not follow typical peripheral nerve distribution patterns. This strange shifting of symptoms can make it difficult to differentiate DCS from traumatic nerve injuries.

The spinal cord is the site most commonly affected by type II DCS. Neurologic deficits after a spinal cord injury can be multifocal. Sensory and motor disturbances can present independently, often resulting in a situation of "dissociation." This dissociation is found in most cases of spinal cord DCS. Magnetic resonance imaging (MRI) studies have seemingly revealed arterial patterns of infarction in spinal DCS. ^[37]

Manifestations of DCS related to the nervous system include the following:

• Back pain - Low back pain may start within a few minutes to hours after the dive and may progress to paresis, paralysis, paresthesia, loss of sphincter control, and girdle pain of the lower trunk; outcomes are worse in patients who have onset of symptoms within 30 minutes of surfacing ^[37] ; vertebral back pain after a dive can be a hallmark of spinal DCS with anticipated poor long-term outcome ^{[38, 39]}
• Dysbaric myelitis - This occurs in half of the cases of neurologic DCS; venous ischemia is the most likely cause
• Bladder problems - Such problems (eg, neurogenic bladder) may be common in the acute phase of DCS, may be the primary presentation, and may be prolonged
• Decreases in blood pressure and/or increases in intraspinal cerebrospinal fluid (CSF) pressure - These can compromise circulation, thus increasing ischemic injury
• Impaired pulmonary filtration of bubbles - If this filtration is bypassed (eg, by PFO or ASD) or if hypoxia is present, bubbles may be allowed to pass into arterial circulation ^[40] ; even small additional decreases of oxygen content through embolization can be enough to damage the blood-brain barrier and initiate a cascade ending with axonal damage, possibly resulting in perivenous syndrome ^[41]

When DCS affects the brain, ocular symptoms can result. Negative scotomata, devoid of any lights or shapes, are the earliest symptom. these scotomata become positive after a few minutes. Other common symptoms include the following:

• Headaches or visual disturbances
• Dizziness
• Tunnel vision
• Changes in mental status

Isolated diplopia, without other neurologic or ocular symptoms, is not consistent with DCS.

Head and neck issues account for 80% of diving illnesses, and 65% of these issues involve the ears. ^[42]  Labyrinthine DCS (the staggers) causes a combination of nausea, vomiting, vertigo, and nystagmus, in addition to tinnitus and partial deafness. This alternobaric vertigo can be difficult to differentiate from dysbaric eustachian tube dysfunction. ^[43] In inner-ear DCS (IEDCS), vertigo is the most common major presenting complaint (77-100%). ^{[44, 45]}

The pathophysiology of IEDCS is believed to be related to a left-to-right shunt in the labyrinthine artery. ^[46]  Such a shunt should also cause cerebral symptoms, but these do not occur, possibly because of a difference in nitrogen washout time in the inner ear as compared with the brain. ^[47] Some research has noted a correlation between IEDCS and the presence of a PFO. ^{[42, 44, 45, 48, 49]} The vestibular tissue is more vulnerable than the cochlea; the cochlea has greater blood flow, smaller volume, and faster gas washout than the vestibular tissue and thus is vulnerable to arterial bubbles for a shorter time. ^[50]

A potential cause of postdive dizziness is superior semicircular canal dehiscence. This is difficult to differentiate from other causes. A key feature is sound- or pressure-induced vertical torsional nystagmus. If present, it may be identified on high-resolution computed tomography (CT) of the temporal bones. ^[51]

Arterial gas embolization

A too-rapid ascent, especially if emptying of the lungs is incomplete, causes the lung volume to expand rapidly. Because this expansion is limitied by the musculoskeletal cage, overpressurization of the lungs (pulmonary overinflation syndrome) results. A limit is reached beyond which damage will occur. ^{[52, 53]}  Resulting injuries include the following:

• Pneumothorax
• Pneumomediastinum
• Subcutaneous emphysema
• Rupture into the pulmonary vein causing a large AGE

Large gas emboli can develop when a rupture into the pulmonary vein allows alveolar gas to enter the systemic circulation. These emboli can lodge in coronary, cerebral, and other systemic arterioles. They continue to expand as ascending pressure decreases, thus increasing the severity of clinical signs. Symptoms and signs depend on where the emboli travel. Coronary artery embolization can lead to myocardial infarction or dysrhythmia. Cerebral artery emboli can cause stroke or seizures.

Manifestations of dysbarism

Lungs

During descent, the lungs decrease in size, but only if the diver is holding his or her breath. Hemoptysis can occur when lung volume decreases below the residual volume. Because a scuba diver breathes from a compressed air source, the loss of volume from depth is negated. During training, the incidence of pulmonary barotrauma is higher than in normal nontraining dives. This risk is even further exacerbated by practice of an emergency free ascent, a maneuver only used if there is a sudden interruption in air supply. ^[54]

Ears

Ear barotrauma is the most common barotrauma complaint of scuba divers. ^{[55, 56]}  Too-rapid ascent or descent and preexisting infection or inflammation are the most common causes of internal ear injuries.

Middle-ear barotitis occurs from failure to equalize pressures adequately and results in pain. Large pressure differences can stretch the tympanic membrane excessively and cause hemorrhage or rupture; they can also damage the ossicles and round window. Excessive nasopharyngeal air pressure (from equalizing) may also cause damage to not only the middle ear and adjacent structures but also the eustachian tube.

On ascent, if air is not allowed to pass from the middle ear through the eustachian tube, a pressure imbalance occurs. At extremes, a hemorrhagic tympanum, or even rupture, can result.

If the tympanic membrane develops extreme bulging, without rupture, facial nerve baroparesis can occur. This rare condition occurs from prolonged overpressurization of the middle ear due to eustachian tube dysfunction and a deficient facial nerve canal. ^[57]  It results in unilateral palsy (paralysis) of the facial muscles. Symptoms that can accompany the facial paralysis include same-side pressure, otalgia, loss of hearing, tinnitus, altered sensation of the tongue, or alternobaric vertigo from asymmetric middle-ear pressures. ^[58]  

Middle-ear barotitis usually is self-limited in that when the middle ear pressure is relieved, the pressure on the nerve resolves and the symptoms reverse. Pressure may be relieved with myringotomy. ^[59]

External-ear issues (eg, external ear squeeze) also can occur if cerumen or other obstruction (eg, tight-fitting hood) occludes the canal. External otitis is the most common ear-nose-throat complaint in divers, resulting from prolonged water contact or contaminants in the water. Exostosis of the external auditory canal has also been described from prolonged dives in cold water. ^[55]

Frequent scuba dives (eg, four dives daily on 5 consecutive days) have been found to cause damage to ear structures; however, these cumulative effects were not seen when surface intervals exceeded 11 hours, suggesting that extending surface intervals may offer protection against middle-ear barotrauma. ^[60]

Evidence of tympanic membrane injury from barotrauma has also been found in patients receiving repeated hyperbaric oxygen (HBO) treatments. Examination of the tympanic membrane via otoscopy appears reasonable after scuba diving.

Inner-ear barotrauma results from rupture of the round window membrane. It is frequently associated with middle-ear overpressurization on ascent but has also been documented on descent. ^[61]  Injuries can include perilymph fistula formation, intralabyrinthine membrane tear, and hemorrhage. ^[62]  The leading symptom is sudden loss of hearing; tinnitus and vertigo are less common. Inner-ear barotrauma can be difficult to distinguish from inner-ear DCS. If there is any thought that it might be DCS, HBO treatment should be rapidly initiated. Limited study data suggest that HBO treatment will not worsen inner-ear barotrauma if the diagnosis is wrong. ^[62]  

Progressive hearing loss in the 4000- to 8000-Hz range has also been described in active divers. This hearing loss is believed to result from inner ear barotrauma, DCS, or noise-induced deafness.

Sinuses

Sinus squeeze can be painful and disabling. The pressure may cause blood-vessel rupture with resultant epistaxis or, more seriously, violation of the thin bone surrounding the sinuses. Results have included severe sinusitis extending into the bony structures, ^[63]  orbital-wall fracture, ^[64]  pneumocephalus, ^{[65, 66]}  and periorbital emphysema without radiographic etiology. ^[67]  Another reported issue has been optic neuropathy from sphenoidal sinusitis due to barotrauma. ^[68]  Trigeminal nerve baroesthesia has also been reported.

Teeth

Barodontalgia (tooth squeeze) may be thought of as either direct or indirect. Direct barodontalgia involves the dental structures directly and results from the pressure exposure, not pain present before, but worsened by, diving. Indirect barodontalgia involves referred pain from disease in air spaces such as the sinuses or ears, which leads the affected individual to believe that the pain is dental in origin.

Direct barodontalgia can be classified as follows on the basis of to the type of pain experienced (though this does not have bearing on underlying pathology):

• Class I - Irreversible pulpitis; sharp momentary pain on ascent
• Class II - Reversible pulpitis; dull throbbing pain on ascent
• Class III - Necrotic pulp; dull throbbing pain on descent
• Class IV - Periradicular (in the associated nerve); persistent severe pain on both descent and ascent

Dental barotrauma can be also be categorized by frequency, as follows ^[69] :

• Faulty restorations and dental caries without pulp involvement (29.2%)
• Necrotic pulp or periradicular inflammation (27.8%)
• Vital pulp pathology (13.9%)
• Recent postoperative dental treatment (11.1%) 

In one study, barotrauma disrupted diving in more than one third of instances. ^[70]

Temporomandibular joint

Stress or anxiety about keeping the mouthpiece in the mouth during a dive can lead to excessive teeth clenching. With poor-fitting mouthpieces, possibly in conjunction with poor bite occlusion, the resulting abnormal forces can cause or exacerbate temporomandibular joint (TMJ) dysfunction.. ^[69]  The prevalence of TMJ dysfunction in the diving population has been reported to be in the range of 24-68% (somewhat higher in women). It is more prevalent in cold-water dives, because it is more difficult for the lips to seal the regulator in the mouth. ^[69] TMJ symptoms can be localized to the joint or can radiate to the ears, teeth, or temples. 

Headache

Many causes of headache are known to be associated with scuba diving, including ear, sinus, and tooth squeeze. ^[71]  Other causes associated with the diving environment include the following:

• Inadequate ventilation (retention of carbon dioxide)
• Contamination of the pressurized air from exhaust fumes (carbon monoxide toxicity)
• Pressure on the face from the mask or hood (irritation of facial or scalp nerves)
• Prolonged extension at the neck (impingement on the occipital nerve)
• Rapid cold temperature change
• Excessive exertion coupled with resultant dehydration or hypoglycemia
• TMJ symptoms that may be interpreted as headache
• AGE
• DCS

Face and mask

The space between the mask and the face is compressible and requires equalization of pressure on descent. Failure to equalize pressure creates a vacuum effect that can cause discomfort, a ring around the face that can persist for hours, frank petechiae of the face or hemorrhage into the sclerae from capillary rupture, or all of the above. Diplopia has also resulted from orbital hematoma due to mask barotrauma. ^[72]

Eyes

The use of hard contact lenses has been found to cause the development of small bubbles in the precorneal tear film when divers ascend from 149 ft (45 m) to 70 ft (21 m), presumably because of the impermeability of the overlying hard lenses; the bubbles increase in number and size as decompression progresses. When soft membrane lenses are worn in the same decompression conditions, the bubbles do not form. Accordingly, divers who elect to wear contact lenses while diving are advised to use soft membrane lenses.

Orbital hematoma from mask barotrauma has been reported, ^[72] as has subcutaneous orbital emphysema. ^[73]

Gastrointestinal tract

Diving does not usually pose a major problem in the gastrointestinal (GI) tract, because gas present at the surface is compressed and then reexpanded to the same volume as before the dive. Occasionally, however, gas is added to the GI system during a dive. For example, small amounts of air may be swallowed during a dive as a result of the unnatural breathing from a regulator and the use of pressure-equalization techniques.

Usually, changes in bowel-gas volume changes cause only discomfort. However, preventing gas from decompressing or diffusing can lead to an overdistended pocket and the potential for rupture. Excessive amounts of gastric air or intestinal air trapped by constipated stool or external issues, (eg, adhesions or a too tight weight belt) can yield rupture. Cases of pneumoperitoneum and of gastric rupture specifically associated with scuba diving have been reported. ^{[74, 75]}

Acclimatization

DCS initiates a stress response in the body. Bubble formation causes the release of the stress protein HSP70. The presence and preconditioning of HSP70 decreases the likelihood of developing DCS during a subsequent dive. This mechanism may be the reason for the acclimatization observed with continued diving. ^{[76, 77]}

Training is essential to avoid injuries caused by overpressurization. In one study, more than 41,000 simulated submarine escape ascents were performed from 30 ft (9 m) and 60 ft (18 m). ^[78] No pulmonary barotrauma occurred, middle-ear barotrauma was infrequent (4% incidence), and only 2.1% of those with middle-ear barotrauma experienced tympanic membrane rupture.

Decompression sickness

Predisposing factors for DCS include the following:

• Inadequate decompression or surpassing no-decompression limits - This includes increased depth and duration of the dives and repeated dives
• Doing a dive requiring decompression stops indicating longer or deeper dives ^[79]
• Inadequate surface intervals (ie, failure to decrease accumulated nitrogen)
• Failure to take recommended safety stops
• Flying or going to higher altitude soon (12-24 h) after diving (increases the pressure gradient) ^[80]
• Smoking ^[81]
• Drinking alcohol the night before diving
• Cold exposure after the dive
• Prior history of DCS ^[79]

A principal cause of DCS is rapid ascent. A major cause of rapid ascent may be panic. Anxiety traits can be identified during instruction. ^[82]

Individual predisposing physiologic characteristics include the following:

• Male sex ^[83]
• Obesity - Some studies have found that neither body fat or body mass index (BMI) correlates with venous gas embolism and resultant DCS ^{[84, 85]} ; however, one study found that the frequency and severity of DCS increased as BMI rose to obese levels, ^{[86, 87]}  and another correlated body mass with risk of DCS ^[88]
• Fatigue
• Age and poor aerobic conditioning ^{[84, 85]}
• Dehydration
• High-fat meal ^[89] or diet ^{[87, 90]}
• Illness affecting lung or circulatory efficiency
• Prior musculoskeletal injury (scar tissue decreases diffusion)

Predisposing environmental factors include the following:

• Cold water
• Heavy work
• Rough sea conditions, strong current ^[83]
• Heated diving suits ^{[91, 92]}

In divers who have been chilled on decompression dives (or dives near the no-decompression limit), very hot baths or showers may stimulate bubble formation.

Improper use of decompression tables may increase the diver's risk. Even if the decompression tables and no-decompression limits are strictly observed, DCS may still occur. The original decompression tables have the following three limitations:

• They are based on young, healthy, and fit US Navy volunteers, but many civilian divers do not fit this profile
• They list the maximum time allowed for a dive, based on the maximum depth achieved; however, the rapidly expanding use of dive computers takes into account the actual time spent at each depth, rather than just the maximum depth, thus allowing for more time under water and removing a built-in factor (shorter maximum depth time) that helps keep divers in the conservative range
• The number of casual divers is increasing, and this can lead to mistakes from lack of practice of the stringent safety routines required

Dysbarism

Dysbarism can result from any factor that prevents free flow of air out of air-filled spaces and allows overpressurization on ascent, including the following:

• Asthma - Bronchospasm from breathing dry compressed air, aspirating salt water or cold water, exertion, and anxiety, anything that permits local air trapping
• Emphysema - Air trapping disease, air blebs, abnormal gas exchange
• Infections - Mucus plugging (localized air trapping), coughing on ascent
• Environmental allergies - Mucosal inflammations (impeded air flow), sneezing on ascent
• Structural lesions, pathology, obstruction, or inflammation (eg, polyps, tumors) - Nasal or sinus, external auditory canal, lungs
• Poor training or experience and panic or anxiety - Diving when conditions listed above are present, too-rapid an ascent or inadequate pressure-equalization techniques

The principal cause of dysbarism is too-rapid ascent, and the most common cause of too-rapid ascent is panic and subsequent loss of control. Beginners are more likely to panic and have less experience in dealing with urgencies that can occur during a dive, but even experienced divers may have anxiety or panic disorders. Poor control of such disorders may disqualify an individual from continued participation in diving.

In 2023, according to data from the Business of Diving Institute and the Sports and Fitness Industry Association (SFIA), approximately 3,063,000 people aged 6 years or older engaged in scuba diving in the United States. ^[93] Of these, approximately 2,374,000 were casual divers (those who went diving one to seven times during the year), and 689,000 were core divers (those who went diving eight or more times during the year). Worldwide, it has been estimated that there are about 6 million active divers. ^[94]

The Divers Alert Network (DAN) receives reports of and tracks injuries and fatalities from the dive community. According to the 2022 annual report (available through the DAN Publication Library), there were 146 reported fatalities from diving-related activities in 2020, 59 from the United States and Canada and 87 from elsewhere. The report noted 754 diving injuries during 2020, including 198 cases of DCS, 360 cases of barotrauma, and 32 cases of AGE.

A study from the US military in Okinawa reported 94 cases of DCS over 7 years. ^[95] The annual incidence of DCS was 13.4 cases per 100,000 dives or 1 per 7,400 dives.

Another study from Britain for the period 1992-1996 found that the annual incidence of diving accidents increased from 4 cases per 100,000 dives to 15.4 cases per 100,000 dives during that time.

In another study, the lifetime incidence of DCS was 1 case per 5463 dives. For severe DCS, it was 1 case in 20,291 dives. It was also found that the more experienced divers were less likely to get DCS, presumably through more meticulous adherence to safety concerns and safer diving profiles. ^[96]

Internationally, minor incidents related to diving have been reported occur in 1.3% of dives. Decompression injuries (not distinguished with respect to dysbarism vs DCS) have been reported to occur at a rate of 2 cases per 10,000 dives. ^[97]

Early symptom recognition, prompt diagnosis, and appropriate treatment are key to a positive outcome with DCS. With these, a success rate of greater than 75-85% is achievable.

It is believed by many that no efficacious treatment options exist for inner-ear barotrauma; however, this belief is mistaken. Treatment options can range from conservative measures to acute high-dose steroid administration (started ≤ 3 wk after injury) to surgery for perilymphatic fistula repair. ^[98]  

The decision as to when a diver can return to scuba diving is not an easy one. It requires a specialist with the appropriate experience in treating diving injuries to determine the risk for recurrent inner-ear injury and to communicate that adequately to the scuba diver. The presence of an ear-node-throat disorder, even inner-ear barotrauma, does not automatically contraindicate future diving if proper education is provided and recommendations followed.

Separating mortality data for DCS from those for barotrauma is impossible. As noted, the 2022 annual report from DAN, which has been tracking diving injuries since the 1980s, cited 146 reported fatalities from diving-related activities in 2020.

Mortality figures that have been reported include the following:

• In South Africa, mortality was found to be as low as 0.016% ^[99]
• The US military in Okinawa reported fatalities at 0.0013% (1.3 deaths per 100,000 dives) ^[95]
• A New Zealand report stated that the most common cause of death was drowning, but pathologists were frequently imprecise ^[100]
• In the United States, 3-9 deaths per 100,000 dives occur annually; the most common cause of dive-related death is drowning (60%), followed by pulmonary-related illnesses
• Diving fatalities in the United States and Canada have fluctuated year to year but have averaged around 83 over the past two decades.
• Mortality is around 10-20 diving fatalities per 100,000 DAN members and increases by about one case per year.
• In the breath-hold free-diving group, fatalities have been increasing worldwide; there were 22 in 2004
• An increase in diving deaths in those older than 50 years in the United Kingdom has been noted since 2009 ^[101]