eMedicine Specialties > Emergency Medicine > Environmental

Dysbarism

Stephen A Pulley, MS, DO, FACOEP,, Assistant Professor, Department of Emergency Medicine, Philadelphia College of Osteopathic Medicine; Attending Faculty, Emergency Medicine Residency, Albert Einstein Medical Center; Attending Physician, Montgomery Hospital Medical Center

Updated: Sep 17, 2009

Introduction

Background

Although dysbarism includes problems associated with high altitude and aerospace endeavors, dysbarism also relates to the increasing pressures of descending under water that are usually experienced in free or assisted dives. Exposure to the physiologic effects of pressure during descent also can be experienced in submarines during emergencies and in tunneling projects.

Since 4500 BCE, humans have engaged in free (breath-hold) diving to obtain food and substances from shallow ocean floors at depths of 100 ft or more. The 2007 record-setting breath-hold unlimited dive of Herbert Nitsch to 702 ft (214 m) attests to this human feat.¹ Humans began experimenting with crude diving bells as early as 330 BCE. These bells were submerged containing only air. In 1690, the first diving bell with a replenishing air supply was tested. The first crude underwater suit dates back to 1837, and helium was first used in place of nitrogen in 1939.

All of these early diving methods required a physical connection to a support platform or boat. The Aqua-Lung, developed by Cousteau and Gagnan in 1943, and the submarine escape appliances, developed by Momsen and Davis in the 1930s, were the forerunners of today's self-contained underwater breathing apparatus (SCUBA) that frees divers from the limitations of tethering.

The increasing popularity of scuba diving and growth of commercial diving is increasing the incidence of exposures to deep pressures. Moreover, even far from the coasts, more individuals are diving in quarries, lakes, rivers, and caves. Add to this the ability to travel rapidly from anywhere in the world in a matter of hours (and the exacerbation of dysbarism caused by decreased pressures in flight), and the potential for dysbaric events can be appreciated. For these reasons, emergency physicians worldwide should maintain an expectation and knowledge of the physiologic effects and management of dysbaric injuries.

Pathophysiology

The effects of increasing pressure occur only on compressible substances in the body. The human body is made primarily of water, which is noncompressible. The gases of hollow spaces and viscous organs and those dissolved in the blood, however, are at the mercy of pressure changes. The physical characteristics of gases are described by the 4 gas laws. It is these laws that quantify the physics and problems involved in descending under water.

The Boyle law

PV = K

(P = pressure, V = volume, K = 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 the pressure is doubled, the volume is halved and vice versa.

Boyle's problem (see Media files 1-2): Every 33 ft of descent increases the pressure by 1 atm. Therefore, lung volume during a breath-hold dive at 33 ft is one half that at the surface. At 66 ft, it is one third that at the surface; at 99 ft, it is one quarter; and, at 132 ft, it is one fifth. Similarly, going from 99 ft to the surface without venting (exhaling) would cause the lungs, with minimal ability to expand further, to increase pressure to 3 times normal, with the greatest change occurring in the last 33 ft, where it would double. This is the key law explaining the pressurization issues and injuries described in this article.

The Boyle gas law. Every 33 ft of descent increases the pressure by 1 atm. Therefore, lung volume during a breath-hold dive at 33 ft is one half that at the surface. At 66 ft, it is one third that at the surface; at 99 ft, it is one quarter; and at 132 ft, it is one fifth.

The Boyle gas law. Descending to 33 ft decreases lung volume by one half. If an individual takes a breath from a SCUBA tank, then surfaces without venting (exhaling), pressure in the lungs, with minimal ability to further expand, increases to twice normal, which probably causes rupture. The greatest change occurs in the top 33 ft when surfacing.

For an in-depth discussion on the Dalton law, please see the article on Decompression Sickness (DCS).

The Henry law

For an in-depth discussion on the Henry law, please see the article on Decompression Sickness.

The Charles law

V1/V2 = T1/T2 (for a gas at constant pressure)

P1/P2 = T1/T2 (for a gas at constant volume)

(V = volume of gas, P = pressure, T = temperature, 1 = initial, 2 = final)

At a constant pressure, the volume of a given mass of a perfect gas varies directly with the absolute temperature. Simply stated, this means that decreasing temperature decreases pressure.

Charles's problem: A closed diving bell descending will have a decrease in pressure due to a decrease in temperature. An open diving bell will have a decrease in volume as it descends due to pressure and decreased temperature.

Organ involvement

The areas affected by the Boyle law can be divided into compressible and noncompressible spaces. Compressible spaces include the lungs, the hollow viscera of the gastrointestinal system, and the space behind the facemask. Examples of noncompressible spaces include the sinuses, air spaces in tooth fillings, middle ear canals, and occluded external ear canals.

• Concomitant decompression sickness (DCS)
  • The same situations that may cause overpressurization injury also may result in DCS. Therefore, any diver who experiences ringing or roaring in the ears, loss of hearing, vertigo, dizziness, nausea, or vomiting during or shortly after a decompression dive or a dive near the no-decompression limits should be presumed to have inner-ear DCS.
  • Any symptom that occurs after diving (from minutes to days) should be presumed to be related to diving. Other symptoms of DCS include paresis, paralysis, paresthesia, joint pain, dyspnea, and rash. For more information on this topic, please see the article on Decompression Sickness.
• Pulmonary
  • As an individual descends, the lungs decrease in size according to the Boyle law. This is true only if the diver is holding his or her breath. When former breath-hold record-holder Ferreras-Rodriguez went to 417 ft, his 50-inch chest decreased to 20 inches.² In the process, hemoptysis can occur when the lung volume decreases below the residual volume. Since a scuba diver breathes from a compressed air source, the loss of volume from depth is negated.
  • Early diving instruction recommended a rate of ascent no faster than 60 ft (18 m) per minute. The more recent recommendation was to ascend no faster than 30 ft (10 m) per minute and to make a 3-5 minute safety stop at 15-20 ft.³ Normally, divers are taught to ascend no faster than a rate of 1 ft per second, with newer recommendations being even slower (one half ft/s or slower). They also are instructed to breathe normally during ascent. This slow rate of ascent allows for a gradual offloading of nitrogen and emptying of air-filled spaces (eg, the lungs).
  • One or more additional stops at deeper level(s) are likely needed to lengthen ascent time adequately and thus protect against decompression sickness (DCS). Research has shown that a safety stop at 50 ft (15 m) of 2.5-5 minutes in addition to another stop at 20 ft (6 m) for 3-5 minutes will decrease venous bubble formation at least for a no-decompression dive of 82 ft (25 m). The supposition here is that this can decrease the risk of DCS.³ Obviously, this requires that more of the air reserve is allotted for the ascent. In addition, premeasured weighted ropes attached to the diving platform for the set safety stops can help maintain the desired depth and prevent drifting away from the surface vessel. Additional scuba tanks could be added at each safety level in case diver air supplies reach a critical level. 
  • A too-rapid ascent, especially if emptying of the lungs is incomplete, causes the lung volume to expand rapidly. The musculoskeletal cage limits expansion, which then causes overpressurization of the lungs, pulmonary overinflation syndrome. A limit is reached beyond which damage will occur. Resulting injuries include pneumothorax, pneumomediastinum, subcutaneous emphysema, and rupture into the pulmonary vein causing a large arterial gas embolism (AGE).^4,5 A pulmonary arteriovenous malformation allows a dysbaric injury to cause a cerebral air embolism. Air embolism and the effects of nitrogen bubble embolization are discussed in the article on Decompression Sickness.
  • It has been found that during training, there is a higher incidence of pulmonary barotrauma when compared to 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 (eg, run out of air).⁶
  • 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 and 60 ft. No pulmonary barotrauma occurred, and a low (4%) incidence of middle ear barotrauma occurred. Of the 4% who experienced middle ear barotrauma, only 2.1% experienced tympanic membrane rupture. The authors of the study note that medical screening and quality training are essential for the program's success.⁷
  • Pulmonary edema is an uncommon complication associated with cold water diving, especially in combination with heavy exertion.⁸ Pulmonary edema has also recently been described in warm water scuba diving.⁹
  • People who have asthma are susceptible to pulmonary complications from extremes in atmospheric pressure because of the lung's ability or inability to release the air it contains.¹⁰ In one survey, 10% of participants in scuba diving reported a history of asthma. Forced vital capacity and forced expiratory volume have both been shown to be adversely affected in people with asthma. Decreased forced vital capacity and forced expiratory volume can lead to air-trapping and increases the risk of barotrauma and arterial gas embolism (see Decompression Sickness).¹¹
  • Sports may cause long-term exacerbation of asthma. Still, the percentage of divers with asthma is comparable to the general population, and the frequency of complications from asthma remains low. Although the risk of pulmonary barotrauma is increased, this risk appears to be small.¹² People with well-controlled asthma and normal airway function and reactivity are not likely to be at an increased risk.¹³ Under the right circumstances, patients with asthma can safely participate in recreational diving without any apparent increased risk of an asthma-related event.¹² Because of the risks involved with scuba diving, everyone with a history of pulmonary conditions should have an evaluation by a health care provider specializing in diving medicine, and they should heed the specialist's recommendations.
• Ear squeeze
  • Dysbarism most commonly affects the ears. The eustachian tube functions to equalize middle ear and ambient environment pressures. Rapid descent increases external pressure on the tympanic membrane and requires the diver to add air pressure in the pharynx to equalize. 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. Large variances can also damage the ossicles and round window.¹⁴ On ascent, if air is not allowed to pass from the middle ear through the eustachian tube, a pressure imbalance occurs, which, at extremes, causes similar damage. Too-rapid ascent and descent, or preexisting infection or inflammation, are the most common causes of internal ear injuries. External ear squeeze also can occur if cerumen or other obstruction occludes the canal.
  • Frequent scuba dives (4 dives per day on 5 consecutive days) have been shown to cause damage to ear structures when evaluated with tympanometry and otoscopic examination. These cumulative effects were not seen when surface intervals exceeded 11 hours. Therefore, extending surface intervals may offer protection against middle ear barotrauma in recreational scuba diving.¹⁵ Similar evidence of tympanic membrane injury (mild to severe hemorrhage or rupture) from barotrauma has also been found in patients receiving repeated hyperbaric oxygen (HBO) treatments. Examination of the tympanic membrane via otoscopy immediately following an HBO "dive" is recommended to determine the need for prophylaxis (see later in this article) or discontinuation of the activity.¹⁶ A similar recommendation appears reasonable after scuba diving.
  • If the round window membrane is ruptured, inner ear barotrauma is the result. The leading symptom is the sudden loss of hearing. Tinnitus and vertigo are less common. However, hearing loss or vertigo may not be present. Tinnitus may be the only symptom and can occur hours or even days after a dive.¹⁷ In the past, inner ear barotrauma was believed to disqualify an individual from future diving. However, individuals who completely recover from ear barotrauma may return to diving with extreme caution.^18,19 As opposed to sudden hearing loss, a progressive hearing loss in the 4000- to 8000-Hz range has been described in active divers. This hearing loss is believed to result from inner ear barotrauma, DCS, or noise-induced deafness.
  • In one survey, approximately one fourth of responding divers reported problems with hearing or tinnitus.²⁰ However, a more recent investigation of hearing acuity in active recreational divers failed to identify any statistically significant hearing loss with the exception of a change in air conduction at 6000 Hz. Whether this was related to diving was not clear.²¹ Hearing loss associated with professional diving is believed to be related to noise or inner ear damage and not related to middle ear barotrauma. No statistical hearing changes were found in a group of sport divers.
  • Vertigo can result for several reasons. On descent, an obstruction of one ear canal (eg, by cerumen or a tight-fitting hood) can allow cold water to enter unilaterally, causing caloric stimulation. The inability to properly equalize middle ear pressures can cause the round window to implode and rupture. This vertigo persists even after ascending and usually is accompanied by sensorineural hearing loss and tinnitus. On ascent and, occasionally, on descent, when the differences in middle ear pressures on each side are greater, the unbalanced stimulation may cause alternobaric vertigo. This vertigo can persist for several days. Finally, vertigo may be caused by inner ear DCS. In inner ear DCS, vertigo was the major presenting complaint. In contrast to this, in dysbaric barotrauma, vertigo was not found to be the presenting complaint or a significant problem.²² Instead, those patients complained of tinnitus and hearing loss. For more on inner ear DCS, please see the article onDecompression Sickness.
  • Divers who experience inner ear DCS or barotrauma require detailed ear, nose, and throat (ENT) diagnostic evaluation at follow-up. Many divers with inner ear DCS are asymptomatic but still have significant cochleovestibular deficits. Inner ear barotrauma has a better short- and long-term outcome than inner ear DCS.²³ Alternobaric vertigo occurs more frequently in divers who have a history of otitis media or eustachian tube dysfunction at the time of diving.²⁴
  • Divers with a history of otitis media or eustachian tube dysfunction may experience difficulty clearing their ears during diving. Otitis media dysfunction, eustachian tube dysfunction, or both can be considered risk factors for developing alternobaric vertigo. Differentiating inner ear barotrauma from inner ear DCS is difficult. Consequently, all divers who experience vertigo or tinnitus postdive should be considered for HBO therapy. Failure to treat inner ear DCS can lead to permanent disability. One study recommended bilateral tympanic paracentesis (needle through the tympanic membrane) before HBO therapy. For more on inner ear DCS, please see Decompression Sickness.
• Sinus squeeze
  • The sinuses, being air-filled spaces, also have the need to equalize. Preexisting illness, such as polyps or infection, can interfere with the free exchange of gas.
  • Sinus squeeze can be painful and disabling. The pressure may cause blood vessel rupture with resultant epistaxis.
• Headache
  • In a larger context, many causes of headache can be associated with scuba diving. Ear, sinus, and tooth squeeze are potential etiologies of headache caused by scuba diving.²⁵ However, the diving environment can lead to other causes of headache. For example, inadequate ventilation can cause retention of carbon dioxide. Contamination of the pressurized air from exhaust fumes can produce carbon monoxide toxicity. Pressure on the face from the mask or hood can irritate the facial or scalp nerves. Prolonged extension at the neck can cause impingement on the occipital nerve and result in a muscle tension headache. Rapid cold temperature change can also cause a headache.
  • Excessive exertion coupled with resultant dehydration, hypoglycemia, or both may cause a headache. The pressure environment can also trigger a migraine in patients with a prior history of migraines. Finally, the constant clenching of the regulator mouthpiece can stress the temporomandibular joint (TMJ) and cause pain that may be interpreted as earache or headache.
  • Etiologies covered in the article on DCS include arterial gas embolism and DCS (see Decompression Sickness). Because of the wide variety of etiologies of headache and the difficulty in differentiating them clinically, all divers with postdive headache should complete a thorough examination by a health care provider and be considered for HBO. Consideration for HBO is particularly appropriate in the presence of any focal neurologic issues.
• Tooth squeeze
  • Barodontalgia is caused by air trapped under a filling. Barodontalgia is more likely to occur in older or temporary fillings or in fillings with surrounding caries. Caries allow air under pressure to be forced under the filling. On ascent, the same defect does not allow airflow out, and the expanded air puts pressure on the sensitive dentine causing pain. There are methods to decrease the likelihood of these issues during dental work that are beyond the purpose of this article. Interested readers are referred to the References.^26,27
  • Dental procedures may not relieve the pain. Hyperbaric therapy may then be needed.
• Mask squeeze
  • The space between the mask and face is compressible and requires equalizing 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.
• Eye problems
  • The use of hard contact lenses by divers has been found to cause the development of small bubbles in the precorneal tear film under the contact lens when going from 149 ft to 70 ft. The bubbles increase in number and size as decompression progresses.²⁸
  • Symptoms include soreness, decreased visual acuity, and seeing halos around lights. These symptoms start at the time of bubble formation and persist for about 2 hours after returning to sea level. No bubbles were noted under the same decompression conditions when soft membrane lenses were worn. The lack of permeability of the hard lens was presumed to be the reason for bubble formation. Divers who elect to wear contact lenses while diving are advised to use soft membrane lenses.
  • Isolated diplopia, without other neurologic or ocular symptoms, is not consistent with decompression sickness. Mask barotrauma has been reported to cause an orbital hematoma in one diver. Physical examination and CT scan of the orbits confirmed the diagnosis.²⁹ In a breath-hold free diver, subcutaneous orbital emphysema has been reported with trauma or preexistent facial injuries/surgery.³⁰
• Gastrointestinal problems
  • Diving does not usually pose a major problem in the 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. Small amounts of air may be swallowed during a dive due to the unnatural breathing from a regulator and ear and sinus pressure-equalization techniques. Certain dietary practices can add gas to the GI system. However, the amount of pressure added from dietary conditions should not be significant during an average length dive.
  • Bowel gas volume changes usually only cause discomfort. 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, such as adhesions, can yield rupture. Cases of pneumoperitoneum and of gastric rupture specifically associated with scuba diving have been reported.³¹ Pneumoperitoneum is usually the result of a ruptured hollow viscus in the abdomen.³²
  • Failure to treat in a timely manner can result in serious illness. In the pressurized environment, air can enter the abdomen from other routes such as the lung or female genital systems. Therefore, the finding of pneumoperitoneum postdiving does not always indicate a ruptured hollow viscus. A detailed workup should be performed to identify an area of rupture to avoid unnecessary surgery. Strong consideration should be given to HBO therapy during workup or needed surgery.

Frequency

United States

Between 1987 and 2003, the Sporting Goods Manufacturers Association estimated the number of scuba divers who dive at least once a year in the United States to have risen 32.1% from 2.4 to 3.2 million participants. However, over the past 6 years (2000-2006), a decrease of 23% to 3.2 million has occurred. The peak year was 1998 at 3.5 million. Of equal importance is the breakdown of those divers. Only about one third of divers were active or regular participants. Approximately two thirds of divers were casual divers, with many as little as a single dive in a year.^{33,34,35,36,37,38} Experience yields a safer diver, though at the other extreme, over confidence can lead to pushing to close to limits.

Due to variability in reporting and collection of information, there is inconsistency in the mainstream medical journal publication of diving-related injury statistics. To improve statistical collection of information, the Divers Alert Network (DAN), based in North Carolina in the United States, acts as a medical information and referral service for diving-related injuries. In addition to this role, it provides education, acts as a clearinghouse for reports of diving-related injuries from around the world, and participates in studies related to diving injuries and illnesses. Their efforts to be the clearinghouse and repository of injury reports has been hampered in recent years, from 2003 and on, in the United States due to a change in federal law that makes medical confidentiality more stringent and thus their abilities to obtain reports and follow-up that much more difficult. They also have sponsored ongoing long-term research including a study entitled Project Dive Exploration (PDE).

International

See Morbidity and Mortality below.

Mortality/Morbidity

• Separating mortality data for DCS from those for barotrauma is impossible. Pathologists demonstrated little knowledge of diving accidents while performing autopsies and missed the more subtle diving injuries.^39,40
• No known data are available on the incidence of dysbaric injuries. However, the distribution of ear, nose, and sinus disorders indicates that, of 1001 disorders found in 650 divers, 64.6% were ear problems. Approximately 23.9% were related problems of the lower jaw, teeth, temporomandibular joint (TMJ), and related muscles. Finally, 3.1% of these complaints were related to the nose, 6.6% to sinuses, and 1.8% to miscellaneous problems.⁴¹
• Dysbarism can produce some long-term morbidity, primarily in the form of hearing loss. This may be the result of tympanic membrane rupture, ear ossicle dislocation, or round window rupture. The incidence of these complications is unknown.
• In a study of 709 experienced US and Australian divers, mild barotrauma was common. Findings include ear squeeze, 52.1%; sinus squeeze, 34.6%; tooth squeeze, 9.2%; tympanic membrane rupture, 5.4%; round/oval window rupture, 1.1%; subcutaneous emphysema, 0.7%; pneumothorax, 0%; arterial gas embolism, 0%; decompression sickness, 4.4%; and permanent disabilities (hearing loss, tinnitus, balance disorder), 2.3%.⁴²
• Mortality rates are as follows:
• In South Africa, the mortality rate was found to be as low as 0.016%.⁴³
• The US military in Okinawa reported fatalities in 0.0013% (1.3 per 100,000) dives.⁴⁴
• A New Zealand report states that the most common cause of death was drowning, but pathologists were frequently imprecise.⁴⁰
• In the United States, 3-9 deaths per 100,000 dives annually occur. 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 deaths over the past two decades.
• The mortality rate 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 steadily increased worldwide over the past decade to 22 in 2004. Note that only 5 or less were related to free-diving competitive activities, either training or competition. Most fatalities were during snorkeling, spear fishing, or collecting of marine specimens.

Age

Many scuba divers start out in the sport young and relatively healthy. With time, they develop medical conditions. Likewise, other divers have significant medical issues upon entering the sport. An Australian study identified that a significant prevalence of medical conditions existed in experienced divers.⁴⁵ Many conditions would be considered to disqualify these divers from future participation in scuba diving.

DAN data also notes a steadily aging trend in their data.

Clinical

History

• Any symptom or sign that appears during or following a dive is pressure-related until proven otherwise based on diagnostic or therapeutic recompression. Specifics about the dive should be elicited as follows:
  • Location - Ocean, lake, river, quarry, or cave
  • Timing - Time dives occurred, length of dives, surface intervals, safety stops, and type of timing used (eg, watch with tables, dive computer) (The diver's logbook or dive computer, along with all of his or her dive equipment, should accompany the diver each step of the way.)
  • Activities - Over the 72 hours prior to the dive (especially flying) and after the dive (including how transported)
  • Depth - Deepest point, approximate time spent at that depth, and rate of ascent
  • Work - Currents, distance swam, water temperature, and primary activity (eg, wreck diving, artifact recovery)
  • Gases and equipment - Compressed air, rebreathing equipment, and mixed gases
  • Problems - Violation of no-decompression limit dive tables, equipment, entanglement, dizziness, and marine bites or stings
  • Condition - Physical condition before, during, and after the dive (eg, fatigue, alcohol ingestion, fever, vertigo, nausea, overexertion, pulled muscles)
  • First aid received - Oxygen, positioning, medications, and fluids
  • Eyes or face - Hemorrhage and numbness
  • Ears - Pain, hearing loss, tinnitus, bloody discharge, and vertigo
  • Nose or sinuses - Pressure or pain associated with sinus locations, bloody nasal discharge, and numbness in infraorbital nerve distribution
  • Mouth - Dental pain
  • Neck - Edema, crackling, and hoarseness
  • Pulmonary - Dyspnea, hemoptysis, and chest pain
  • Gastrointestinal - Bloating, cramps, and pain
  • Musculoskeletal - Symptoms probably related to DCS
  • Skin - Rash or marks
  • Neurologic - Seizure, unconsciousness, confusion, headache, visual disturbance, paresis, and paresthesia (more likely related to DCS)

Physical

• Physical examination findings may include any of the following:
  • Distress secondary to pain
  • Eyes or face - Subconjunctival or scleral hemorrhage or edema, periorbital edema, nystagmus, facial petechiae, and red ring
  • Ears - Tympanic hemorrhage or perforation, hemotympanum, external canal blood, cerumen, mass, lack of mobility on pneumatoscopy, and evidence of sensorineural hearing loss
  • Nose or sinuses - Pain over sinuses with percussion or epistaxis
  • Mouth - Tooth tenderness to percussion
  • Neck - Subcutaneous emphysema, vocal changes, and neck vein distention
  • Pulmonary - Respiratory distress, decreased breath sounds, hyperresonance, and tracheal shift
  • Gastrointestinal - Distention
  • Skin - Subcutaneous emphysema
  • Neurologic - Unconsciousness, changes in mental status, blindness, hemiplegia, paresis, and paresthesia

Causes

• Anything that prevents free flow of air out of air-filled spaces and allows overpressurization on ascent
• 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 principle cause of dysbarism or DCS injuries is from too-rapid an ascent. The most common cause of too-rapid ascent is panic and subsequent loss of control. With scuba diving being an unfamiliar environment, beginners are more likely to panic and less experienced to deal with urgencies that occur during a dive. A diver's tendency toward stress or panic should be of concern to instructors and dive masters.⁴⁶ During instruction, major efforts should be directed toward making the students feel comfortable in the unfamiliar environment. Anxiety or panic disorders can develop in experienced divers. Poor control of anxiety or panic disorders may disqualify the individual from continued participation in diving.

Differential Diagnoses

Workup

Laboratory Studies

• No specific tests are required for the diagnosis of dysbarism. When diving is involved, the primary consideration should be a pressure-related injury. Baseline laboratory studies usually have no bearing on initial management. They could be useful in excluding other entities on the differential diagnosis list while HBO therapy is pursued. Transfer should not be delayed. For a patient with a mental status change, routine evaluation of reversible causes is mandated. If the individual is in extremis (eg, shock), appropriate resuscitation studies should be obtained.
• Change in mental status or medically unstable
  • Serum glucose level, CBC
  • Electrolytes, magnesium, calcium, phosphorous, BUN, and creatinine levels
  • Oxygen saturation
  • Ethanol level, drug screen
  • Carboxyhemoglobin level
  • Type and screen, cross-match
  • Prothrombin time (PT), activated partial thromboplastin time (aPTT)

Imaging Studies

• Chest radiography
  • Chest radiography is the primary diagnostic imaging study for overpressurization injuries.
  • Chest radiography can identify evidence of pneumothorax, pneumomediastinum, subcutaneous emphysema, pneumopericardium, and alveolar hemorrhage.
• Sinus radiography
  • Opacification of the sinuses confirms the presence of pathology in that area.
  • It does not confirm that the pathology is related to diving.
• CT scanning
  • CT differentiates pathology in areas of concern better than radiography.
  • Chest CT, especially spiral CT, is recommended for evaluation of the lungs after a pulmonary barotrauma event. It can show preexisting pathology, such as small lung cysts.⁴⁷
  • Although this information is not helpful for treatment of a dysbaric injury, it can help determine future fitness for diving. CT scanning has also been advocated for detection of arterial gas embolism in postmortem examinations (see Decompression Sickness).⁴⁸

Other Tests

• Diagnostic repressurization: When a question exists as to whether the patient's problem is dysbarism or DCS, repressurization in a hyperbaric chamber can be pursued for diagnostic and therapeutic reasons. (This may require patient transfer.)
• Electrocardiography

Treatment

Prehospital Care

• Extricate the patient from water and immobilize if trauma is suspected. Generally, in-water recompression is not believed to be a safe option. More is discussed about this in Decompression Sickness.
• Administer 100% oxygen, intubate if necessary, and intravenously administer saline or lactated Ringer solution.
• The use of first aid oxygen has proven so beneficial that the Divers Alert Network (DAN) has made a major effort to place oxygen at dive locations, in particular those that are remote with lengthy transport times to the nearest hyperbaric chambers, and to ensure that people are trained in its use. A study of the use of first aid oxygen found that the median time to its use after surfacing was 4 hours and 2.2 hours after the onset of DCS symptoms. Forty-seven percent of victims received the oxygen. Complete relief of symptoms was found in 14% of victims. Even more striking was that 51% of victims showed improvement. This was with the oxygen before HBO treatment. Even after a single HBO treatment, those that had received oxygen before the HBO dive, even if many hours earlier, had better outcomes.⁴⁹
• Aspirin is commonly considered and given in diving accidents for antiplatelet activity if the patient is not bleeding. However, there are no current data to support this practice.⁵⁰
• Perform cardiopulmonary resuscitation and advanced cardiac life support, if required, as well as needle decompression of the chest if tension pneumothorax is suspected.
• Do not put patient into Trendelenburg position. Placing the patient in a head-down posture used to be considered a standard treatment of diving injuries to prevent cerebral gas embolization. This practice should be abandoned. The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier.⁵¹ It also wastes time and complicates movement of the patient.
• Transport to the nearest ED and hyperbaric facility, if feasible, and try to keep all diving gear with the diver. Diving gear may provide clues as to why the diver had trouble (eg, faulty air regulator, hose leak, carbon monoxide contamination of compressed air).

Emergency Department Care

• Administer 100% oxygen. Intubate if indicated.
• Do not put the patient into the Trendelenburg position.
  • Placing the patient into a head-down, Trendelenburg position previously was considered standard in the ED management of diving injuries to prevent cerebral gas embolization.
  • Do not put patient into Trendelenburg position. Placing the patient in a head-down posture used to be considered a standard treatment of diving injuries to prevent cerebral gas embolization. This practice should be abandoned. The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier.⁵¹ It also wastes time and complicates movement of the patient.
• Intravenous fluids should be administered for rehydration until urinary output is 1-2 mL/kg/h.
• Provide aggressive resuscitation, if required.
• Aspirin is commonly considered and given in diving accidents for antiplatelet activity if the patient is not bleeding. However, there are no current data to support this practice.⁵⁰
• The patient should be treated for nausea, vomiting, pain, and headache.
• Needle chest decompression and chest tube thoracostomy may be indicated to treat simple or tension pneumothorax.
• Try to keep all diving gear with the diver.

Consultations

• Diving medicine or HBO specialists
• Symptoms temporally related to diving indicate that consultation with a diving medicine or HBO specialist is needed.
• The goal of this discussion is to determine the likelihood that symptoms are diving-related and the appropriateness of treatment with HBO therapy.
• Otorhinolaryngologist
• Urgent consultation with an ENT specialist may be useful.
• The barotraumas of the middle and inner ears are caused by failure of the eustachian tube to release pressure. Early investigation into the use of natural or artificial eustachian tube surfactant shows promise as a potentially effective way to aid this process.⁵²
• Divers who experience inner ear DCS or barotrauma require detailed ENT diagnostic evaluation at follow-up. Most are asymptomatic but still have significant cochleovestibular deficits.²² Inner ear barotrauma has a better short- and long-term outcome than inner ear DCS.
• The specialist may often request sending the patient to the office. In such cases, consider inquiring about the ENT specialist's comfort with diving-related issues.
• Divers Alert Network: Divers Alert Network (DAN) is an excellent resource, especially if local support is not available. Using this service should be considered similar to the use of a poison control center. It maintains a database of diving-related injuries and provides 24-hour-a-day consultative services including extent of injury assessment, recommendations for management, and referral to HBO therapy or local diving medicine specialists. Emergency contact 24 hours a day can be reached at the following numbers:
• DAN America: 1-919-684-8111 or 1-919-684-4DAN (4326) (accepts collect calls)
• DAN Latin America: 1-919-684-9111 (accepts collect calls)
• DAN Europe: 39-06-4211-8685
• DAN Southern Africa: 0800-020111 (within South Africa); 27-11-254-1112 (outside South Africa)
• DAN Japan: 81-3-3812-4999
• DAN SEAP DES New Zealand: 0800-4DES 111
• DAN SEAP Singapore Naval: 6758-1733
• DAN SEAP Malaysia: 05-930 4114
• DAN SEAP Philippines: 02-815-9911
• DAN SEAP DES Australia: 1-800-088-200 (within Australia); 61-8-8212-9242 (outside Australia)

Medication

Oxygen is the main therapy used in the treatment of diving injuries. Predive treatment with nonsedating decongestants (specifically pseudoephedrine-see below) can decrease the incidence of ear discomfort and clinical trauma to the tympanic membrane by 75%. No data are available concerning the efficacy of this medication in postdive treatment.

Decongestants

By promoting nasal or sinus drainage, these agents may prevent ear discomfort. However, their exact mechanism of action is not yet understood.

Pseudoephedrine (Actifed, Sudafed)

Stimulates vasoconstriction by directly activating alpha-adrenergic receptors of respiratory mucosa, which may improve sinus drainage.

Dosing

Adult

60 mg PO q4-6h; do not exceed 4 doses in 24 h or 120 mg of long-acting q12h

Pediatric

<6 years: Not established
6-12 years: 30 mg PO q4-6h; not to exceed 4 doses in 24 h
>12 years: Administer as in adults

Interactions

Propranolol, MAOIs, and sympathomimetic agents may increase toxicity; methyldopa and reserpine may reduce effects

Contraindications

Documented hypersensitivity; severe anemia; postural hypertension or hypotension; closed-angle glaucoma; head trauma; cerebral hemorrhage

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease, diabetes mellitus, prostatic hypertrophy, and increased intraocular pressure

Oxymetazoline hydrochloride 0.05% nasal spray (Afrin, Sinarest, Allerest)

Stimulates alpha-adrenergic receptors and causes vasoconstriction when applied directly to mucous membranes. Decongestion occurs without drastic changes in blood pressure (BP), vascular redistribution, or cardiac stimulation.

Dosing

Adult

2-3 sprays in each nostril q12h

Pediatric

<6 years: Not recommended
>6 years: Administer as in adults

Interactions

May reverse hypotensive action of guanethidine; methyldopa may result in increased vasopressor response; concurrent MAOI and ephedrine may result in hypertensive crisis; pressor sensitivity to mixed-acting agents such as ephedrine may be increased; guanethidine potentiates effects of epinephrine and inhibits effects of ephedrine; phenothiazines may reverse action; TCAs potentiate vasopressor response and may result in dysrhythmias

Contraindications

Documented hypersensitivity; concomitant MAOI therapy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, coronary artery and ischemic heart disease, diabetes mellitus, increased intraocular pressure, or prostatic hypertrophy; because of increase in vasoconstriction, hypertensive patients may experience change in BP; do not use topical decongestants for longer than 3-5 d

Bronchodilators

These agents act to decrease muscle tone in both the small and large airways in the lungs, thereby increasing ventilation.

Ipratropium bromide nasal spray (Atrovent)

Chemically related to atropine. Has antisecretory properties, and when applied locally, inhibits secretions from serous and seromucous glands lining nasal mucosa.

Dosing

Adult

Metered dose inhaler:
2 sprays in each nostril q4h; do not exceed 12 inhalations in 24 h

Pediatric

Metered dose inhaler:
<3 years: Not established
3-12 years: 1-2 inhalations tid; not to exceed 6 inhalations in 24 h
>12 years: Administer as in adults

Interactions

Drugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol increases effects

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use for more than 5 d; not indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Beclomethasone dipropionate 0.042% nasal spray (Vancenase)

Inhibits bronchoconstriction mechanisms, produces direct smooth muscle relaxation, may decrease number and activity of inflammatory cells, and may decrease airway hyperresponsiveness.

Dosing

Adult

2 sprays in each nostril q12h

Pediatric

<6 years: Not established
>6 years: Administer as in adults

Interactions

Ketoconazole may increase plasma levels, but this does not appear to be clinically significant

Contraindications

Documented hypersensitivity; bronchospasm; status asthmaticus; other types of acute episodes of asthma

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Weight gain, increased bruising, cushingoid features, acneiform lesions, mental disturbances, and cataracts may occur (taper medication slowly if these changes occur)

Antiplatelet agents

Because dysbaric illness has the potential for activation of coagulation factors, as discussed in the article on DCS, therapy aimed at mitigating this effect may be helpful. Guidance should be obtained from either a diving medicine or HBO specialist.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Blocks prostaglandin synthetase action, which, in turn, inhibits prostaglandin synthesis and prevents formation of platelet-aggregating thromboxane A₂. Acts on hypothalamus heat-regulating center to reduce fever.

Dosing

Adult

Not established; doses used in treating cardiac disease would appear the best choice

Pediatric

Generally avoided in children because of potential for Reye syndrome in viral illness

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease salicylate serum levels; anticoagulants may have additive hypoprothrombinemic effects and increase bleeding time; may antagonize uricosuric effects of probenecid; may increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs

Contraindications

Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K deficiency; bleeding disorders; asthma; because of association of aspirin with Reye syndrome, do not use in children (<16 y) with flu

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, history of blood coagulation defects, or taking anticoagulants

Follow-up

Further Inpatient Care

• Admission is rarely required. Pneumothorax, pneumomediastinum, or air embolism requires admission.
• Patients with signs of other dysbaric or decompression injuries should be transferred to a facility with HBO capability.

Further Outpatient Care

• Consider reevaluation by an ENT specialist.

Inpatient & Outpatient Medications

• Topical and systemic decongestants (eg, pseudoephedrine)
• Analgesics (eg, acetaminophen, ibuprofen, narcotics) if needed
• If bleeding or evidence of effusion is present, an appropriate antibiotic should be prescribed (eg, amoxicillin, erythromycin, trimethoprim/sulfamethoxazole [TMP/SMX], or topical cortisporin otic if tympanic membrane is intact).

Transfer

• For individuals with symptoms that are more than minimal, consult a diving medicine specialist or HBO specialist to determine appropriateness of treatment with HBO. Many times, dysbaric or other injuries can mimic decompression sickness and a diagnostic HBO treatment may be warranted to help determine this.
• DAN is an excellent resource if local support is not available.
• If HBO treatment is advised, an important issue is transport of the patient to the closest hyperbaric facility.
  • This is frequently accomplished by land transport; however, air transportation is occasionally required. An effort should also be made to minimize the transport time.
  • Helicopter transport requires the pilot to maintain an altitude of less than 500 ft (152 m) above the departure point (which could be more than 500 ft above sea level depending on the dive location).⁵³ Flight paths through mountainous regions may make this difficult. In this situation, explore options other than rotary-wing transportation to the closest chamber. Fixed-wing transport should be limited to aircraft that can maintain cabin pressure at normal surface pressure of 1 atm (eg, Lear Jet, Cessna Citation, military C-130 Hercules).

Deterrence/Prevention

• All patients treated for diving-related injuries should be instructed to not return to diving until they have consulted with a diving medicine specialist. The specialist will make a determination on the appropriateness of returning to the activity.
• Future prophylaxis with decongestants along with improved instruction may decrease recurrences. As mentioned above related to middle ear barotrauma, evidence of trauma to the tympanic membrane via otoscopy after a dive may guide prophylactic treatment to help prevent future middle ear barotrauma.¹⁶ Many HBO centers use a topical vasoconstrictor nasal spray for this purpose (oxymetazoline).⁵⁴ However, studies have shown that there is minimal benefit to this approach, whereas predive treatment with oral pseudoephedrine (60 or 120 mg) at least 30 minutes prior to a dive decreased pain and evidence of tympanic membrane injury.^55,56,57
• The culture of diving, at least in military naval diving, may have some impact upon prevention of diving accidents. The two most common causes of diving accidents, or near misses, were leadership failures and decreased situational awareness. These came into play when the overall risk was underestimated and the time was not closely monitored. In addition, the need for junior divers to ask questions was rebuffed by the posture of the senior divers not being interested in providing answers.⁵⁸ While this was found in the US Navy, correlations could be considered in the average dive situation, namely daily dive charters. A lack of leadership, in the form of a divemaster, and the generally isolated situation of a number of divers not knowing each other, could lead to the same overall environment.

Prognosis

• With early recognition of diving-related injuries, most individuals have good outcomes and minimal residual problems.
• ENT disorders, even inner ear barotrauma, do not automatically contraindicate future diving when proper education is given and followed.
  • A common misconception exists that there are no efficacious treatment options for inner ear barotrauma. The first step is a full neurotological evaluation, including high-resolution CT of the temporal bones, by an ENT specialist with experience with diving-related cochleovestibular (middle and inner ear) dysbaric injuries.⁵⁹ Treatment options can range from conservative, to acute high-dose steroid administration (started within 3 wk of the injury), to surgery for perilymphatic fistula repair.⁶⁰
  • The diver commonly asks when he or she can return to scuba diving. The decision is partly dictated by the presence of a significant residual sensorineural hearing loss, evidence for noncompensated vestibular damage, and CT findings of possible enhanced cerebrospinal fluid–perilymph connection. The decision is not an easy one and 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. In addition, animal studies suggest that the use of a free radical scavenger greatly decreases symptoms.

Patient Education

• Improved instruction in equalization and control of ascent minimizes future problems.
• For excellent patient education resources, visit eMedicine's Environmental Exposures and Injuries Center. Also, see eMedicine's patient education articles Barotrauma/Decompression Sickness; Ear Pain, Scuba Diving; and The Bends - Decompression Syndromes.

Miscellaneous

Medicolegal Pitfalls

• The same situations that can cause overpressurization injury also can result in DCS. Any diver who experiences ringing or roaring in the ears, loss of hearing, vertigo, dizziness, nausea, or vomiting during or shortly after a decompression dive or a dive near the no-decompression limits should be presumed to have inner ear DCS.
• Any symptom that occurs after diving (from minutes to days) should be presumed to be related to diving.
• Other examples of DCS include paresis, paralysis, paresthesia, joint pain, dyspnea, and rash.
• Failure to consider the diagnosis, even in a patient with less impressive symptoms, is a potential area of liability.
• All patients treated for diving-related injuries should be instructed not to return to diving until they have consulted with a diving medicine specialist. The specialist can determine when a return to diving is appropriate.

Special Concerns

• Diving while pregnant is not recommended because of the unknown effects of nitrogen diffusion across the maternal-placental membrane. The fetus is believed to not be protected from decompression problems and is at risk of malformation and gas embolism. However, normal pregnancies have been reported even after repetitive dives.⁶¹
• While no absolute lower age limit has been established, children younger than 12 years should not dive. Though one limited study found no venous bubble formation after a routine single shallow dive,⁶² diving can be a dangerous activity that requires respect, common sense, and absolute adherence to safety rules. The inherent nature of children to be distracted and have no sense of mortality or time makes it difficult for them to dive safely without close supervision.
• Advanced age brings with it increasing medical problems. As with any physical activity, the advice and recommendations of a physician familiar with diving medicine should be sought for older individuals.

Multimedia

Media file 1: The Boyle gas law. Every 33 ft of descent increases the pressure by 1 atm. Therefore, lung volume during a breath-hold dive at 33 ft is one half that at the surface. At 66 ft, it is one third that at the surface; at 99 ft, it is one quarter; and at 132 ft, it is one fifth.

Media file 2: The Boyle gas law. Descending to 33 ft decreases lung volume by one half. If an individual takes a breath from a SCUBA tank, then surfaces without venting (exhaling), pressure in the lungs, with minimal ability to further expand, increases to twice normal, which probably causes rupture. The greatest change occurs in the top 33 ft when surfacing.

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Keywords

decompression sickness, DCS, the bends, ear squeeze, sinus squeeze, tooth squeeze, mask squeeze, barotrauma, Boyle law, Dalton law, Henry law, Charles law, scuba diving, diving, self-contained underwater breathing apparatus, SCUBA, air embolism, hyperbaric chamber, pressure during descent, high altitude, dysbaric injury

Contributor Information and Disclosures

Author

Stephen A Pulley, MS, DO, FACOEP,, Assistant Professor, Department of Emergency Medicine, Philadelphia College of Osteopathic Medicine; Attending Faculty, Emergency Medicine Residency, Albert Einstein Medical Center; Attending Physician, Montgomery Hospital Medical Center
Stephen A Pulley, MS, DO, FACOEP, is a member of the following medical societies: American College of Osteopathic Emergency Physicians and American Osteopathic Association
Disclosure: Nothing to disclose.

Medical Editor

Steven A Conrad, MD, PhD, Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center
Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eddy Lang, MDCM, CCFP (EM), CSPQ, Assistant Professor, Department of Family Medicine, McGill University; Consulting Staff, Department of Emergency Medicine, The Sir Mortimer B Davis-Jewish General Hospital
Eddy Lang, MDCM, CCFP (EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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