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Complications of SCUBA diving

Complications of SCUBA diving
Literature review current through: May 2024.
This topic last updated: May 20, 2024.

INTRODUCTION — Although estimates are difficult, the number of active self-contained underwater breathing apparatus (SCUBA) divers in the United States alone is likely between 2.5 and 3.5 million people [1]. The number of international divers is even more difficult to estimate, but SCUBA remains popular worldwide and is a significant aspect of the tourism industry in many countries. Based on data from training and certification agencies, there are approximately 200,000 diving instructors globally [2].

Diving is generally considered a safe activity. In 2020, the Divers Alert Network (DAN) reported 189 fatalities worldwide for the year 2018 [3]. Although fatality rates are low, a variety of diving-related injuries and illnesses may occur, including:

Barotrauma, including arterial gas embolism (AGE)

Decompression sickness (DCS)

Nitrogen narcosis

Immersion pulmonary edema

The pathophysiology, evaluation, diagnosis, and treatment of complications of compressed gas diving are reviewed here. The imaging and management of pneumothorax, ear barotrauma, and air embolism are discussed separately. (See "Treatment of secondary spontaneous pneumothorax in adults" and "Ear barotrauma" and "Air embolism".)

TERMINOLOGY — The terms decompression sickness (DCS) and decompression illness (DCI) are often used interchangeably, but this is not correct [4]. DCS refers to the pathophysiologic condition that occurs when bubbles form in the tissues due to supersaturation with an inert gas. This process is distinct from arterial gas embolism (AGE), which stems from pulmonary overinflation and barotrauma. DCI is often used to encompass both conditions.

In this topic, we refer to DCS and AGE separately when discussing the distinct pathophysiology and presentation of each disease. We use the collective term DCI only when it is relevant clinically, such as when discussing treatment, which is the same for both conditions. (See 'Management of arterial gas embolism and decompression sickness' below.)

GAS LAWS — The majority of diving-related medical conditions are related to the behavior of gases under varying pressures, which is governed by two basic gas laws:

Boyle's law states that at a constant temperature, the volume of a gas varies inversely with the ambient pressure. In other words, the volume of a gas decreases as pressure increases and increases as pressure decreases. This law helps to explain the principles behind diving-related barotrauma and air embolism.

Henry's law states that at a constant temperature, the amount of a gas that is dissolved in a liquid is directly proportional to the partial pressure of that gas. This law helps to explain decompression sickness (DCS).

BAROTRAUMA — Barotrauma is the most common form of diving-related injury and develops when an air-filled body space fails to equilibrate its pressure with the environment following changes in ambient pressure. Barotrauma can occur due to under-pressurization (during descent) or over-pressurization (during ascent), with the latter generally causing more severe sequelae. During descent, decreasing air volume in a space that also contains tissue leads to mucosal edema, vascular engorgement, and hemorrhage. During ascent, increasing gas volume in a confined space can produce tissue disruption and rupture. Gas-filled spaces potentially affected by barotrauma include sinuses, middle ear, lungs, and any artificial spaces created by equipment, such as a tight wetsuit seal or drysuit.

Pulmonary barotrauma

Arterial gas embolism — Arterial gas embolism (AGE) is the most serious potential complication of pulmonary barotrauma. It occurs when air bubbles enter the pulmonary vasculature. This can occur when numerous venous bubbles overwhelm pulmonary capillary filtration or when gas that has ruptured from alveoli dissects into the vessels [5-7]. (See "Air embolism".)

After reaching the systemic arterial circulation, gas emboli typically break up as they reach vascular branch points and ultimately lodge in vessels with diameters ranging from 30 to 60 micrometers. At such locations, they produce distal ischemia and local activation of inflammatory cascades [8]. The symptoms and signs produced depend upon the final location of gas emboli. Life-threatening consequences can occur with embolization to the cerebral and coronary arteries. Cerebral manifestations are most common. The treatment of AGE, including hyperbaric oxygen therapy, is reviewed below. (See 'Management of arterial gas embolism and decompression sickness' below.)

The presentation of AGE varies widely, with signs ranging from subtle neurologic changes to cardiac arrest. Manifestations of cerebral emboli range from focal motor, sensory, or visual deficits to seizures, loss of consciousness, apnea, and death. Findings can be extremely subtle, such as discrete alterations in a mini mental status examination, "feeling off," or mild cognitive impairment [9].

Rarely, divers may present in cardiac arrest. Initially, this was thought to be due to coronary artery gas embolism. However, although coronary AGE may cause electrocardiographic (ECG) changes or arrhythmia, it is an unlikely cause of sudden cardiac arrest. Cardiac arrest is more likely to be caused by obstruction of the central circulation by air emboli [10,11].

AGE can affect other organ systems. Embolization to the hepatobiliary system has been reported, as have elevations in liver function tests and creatine kinase [12]. Embolization to the kidneys can produce hematuria, proteinuria, and renal failure.

Barotrauma of descent — As a diver descends, the air in the lungs becomes compressed. Although pulmonary edema and hemorrhage may occur when lung volume decreases below residual volume, such injury (sometimes referred to as "lung squeeze") is uncommon because the lungs are continually re-inflated during normal inhalation. It occurs more often in breath-hold divers [13]. When pulmonary edema does occur in divers, it is more often caused by immersion pulmonary edema. (See 'Breath-hold or free diving' below and 'Immersion pulmonary edema' below.)

Barotrauma of ascent — As a diver ascends and transalveolar pressure exceeds 20 to 80 mmHg, alveolar rupture can occur [14-16]. This can happen in depths as shallow as 1 to 1.5 meters [5,8]. Divers who hold their breath as they ascend (because they run out of air or panic) are at increased risk. Such injuries may occur in divers without underlying pulmonary pathology or a history of rapid ascent.

Although some had hypothesized that obstructive lung disease (eg, asthma) increases the risk of such episodes, the risk has not been quantified and may not be as significant as previously suggested [17]. Nevertheless, divers with a history of lung disease should be evaluated by a physician prior to diving. (See "Evaluation of adults wishing to SCUBA dive".)

Pneumomediastinum — Following alveolar rupture, gas can dissect along the perivascular sheath into the mediastinum to produce pneumomediastinum. Symptoms of pneumomediastinum include a sensation of fullness in the chest, pleuritic chest pain that may radiate to the shoulders, dyspnea, coughing, hoarseness, and dysphagia. Crepitation in the neck due to associated subcutaneous emphysema may be present, and a crunching sound heard over the heart during systole (Hamman's sign/Hamman's crunch) may be appreciated upon auscultation (movie 1 and figure 1).

The diagnosis can be confirmed on the basis of chest and neck radiographs, though computed tomography (CT) is more sensitive. Typically, a radiolucent band is seen along the cardiac border on the posteroanterior film and retrosternally on the lateral view (image 1). No specific treatment is required, but we suggest having patients breathe 100% oxygen to hasten resorption of extra-alveolar gas. There are rare (and severe) cases where hyperbaric oxygen has been used, but this is not routinely necessary [18].

A careful history and neurologic examination should be performed to rule out concomitant AGE that would require hyperbaric oxygen treatment.

Pneumothorax — Pneumothorax is relatively uncommon, developing in about 10 percent of episodes of pulmonary barotrauma. Patients with a history of spontaneous pneumothorax, bullae, or cystic lung disease may be at increased risk of pneumothorax or other pulmonary barotrauma [19]. A history of spontaneous pneumothorax is a contraindication to SCUBA diving.

Pneumothorax develops when gas ruptures from the lung parenchyma into the pleural space. If this occurs at depth, the pleural gas expands as the diver ascends (as described by Boyle's law) and can result in a tension pneumothorax. Manifestations can include dyspnea, chest pain, tachycardia, hypotension, cyanosis, distended neck veins, tracheal deviation, hyperresonance to percussion, unilateral decrease in breath sounds, and accompanying subcutaneous emphysema (approximately 25 percent of cases).

If a pneumothorax results in severe hypoxemia or hemodynamic compromise (tension pneumothorax), immediate pleural decompression is required. This is usually accomplished by inserting a large-bore needle into the second intercostal space just over the third rib in the mid-clavicular line of the affected hemithorax, followed by tube thoracostomy. (See "Treatment of secondary spontaneous pneumothorax in adults" and "Thoracostomy tubes and catheters: Indications and tube selection in adults and children".)

As with pneumomediastinum, a careful history and neurologic examination should be done to rule out concomitant AGE that would require hyperbaric oxygen treatment.

Ear barotrauma — Barotrauma of the middle ear during descent ("ear squeeze") is the most common disorder among divers [20-23]. Pressure in the middle ear normally equilibrates with ambient pressure via the eustachian tube with a variety of maneuvers the diver can perform, such as Valsalva.

Pain and discomfort begin when a pressure differential of 60 mm Hg develops between the middle ear and ambient environment [24]. However, if upon descent this equilibration is prevented by mucosal edema secondary to an upper respiratory infection or anatomic variation, the negative pressure in the middle ear can lead to its filling with serous fluid or blood or to inward rupture of the tympanic membrane [25,26]. If the pressure differential exceeds 90 mm Hg, a Valsalva maneuver will not be sufficient to equilibrate pressures [24]. Equilibration may also be impeded when an artificial closed air space is created by external material, such as cerumen, ear plugs, or a tight-fitting hood. (See "Ear barotrauma".)

Symptoms vary from a sensation of pressure to hearing loss and pain, which may suddenly be relieved when the tympanic membrane ruptures. Acute, unilateral tympanic membrane rupture can produce vertigo, nausea, and disorientation as cold water leaks into the middle ear, creating temperature differences and uneven caloric stimulation of the vestibular system. (See "Evaluation of the patient with vertigo", section on 'Other vestibular signs'.)

Over-pressurization of the middle ear can occur during ascent (often termed "reverse squeeze"), but tympanic membrane rupture is rare. Another rare complication is temporary paralysis of the tympanic branch of the facial nerve caused by ischemic neuropraxia secondary to inflammation and swelling around the middle ear [24].

Divers should attempt to prevent ear barotrauma by the use of maneuvers that open the eustachian tubes and equalize pressure between the middle ear and the ambient environment (table 1). Treatment of middle ear barotrauma consists of topical and systemic decongestants, analgesics, and antihistamines. Antibiotics should be used if purulent otorrhea is observed [27] or if there is perforation of the tympanic membrane. Most tympanic membrane ruptures heal spontaneously if normal eustachian tube function is restored and infection is controlled. Patients should follow up with an otolaryngologist specialist. (See "Acute otitis media in adults", section on 'Treatment of acute otitis media'.)

Inner ear barotrauma is a fairly uncommon injury but should be excluded in all cases of middle ear barotrauma [22,28]. Inner ear injury can occur following the development of a sudden pressure differential between the inner and middle ear, leading to rupture of the round or oval window [29,30]. The main symptoms are tinnitus, vertigo, and hearing loss, which in turn can cause disorientation and panic. The resulting labyrinthine fistula and leakage of perilymph can result in permanent inner ear damage. It can be difficult to distinguish from inner ear symptoms of decompression sickness (DCS).

Long-term follow-up of a small cohort of divers who experienced inner ear barotrauma and inner ear DCS treated with hyperbaric recompression noted that persistent vestibular deficits were common (though often asymptomatic) in this population [31]. The primary treatment of this complication is complete bed rest for 7 to 10 days with the head elevated to avoid increases in cerebrospinal fluid pressure, which can increase the leakage of perilymph [30,32,33]. Deteriorating inner ear function generally requires tympanotomy and patching of the round or oval window [30]. If an inner ear injury is suspected, we recommend urgent referral to a head and neck surgeon for evaluation and definitive treatment.

Sinus barotrauma — Sinus barotrauma is the second most common disorder among divers following ear barotrauma. During descent, increases in ambient environmental pressure can lead to mucosal engorgement, edema, and inflammation producing blockage of the sinus ostia; the frontal sinus is most commonly affected due to the relatively long and tortuous course of its duct [34,35]. Common symptoms include headache, epistaxis, and localized sinus pain. Treatment includes the use of topical and systemic decongestants and antibiotics if purulent nasal discharge is seen.

If a one-way valve blockage occurs at a sinus ostium, a sudden decrease in ambient pressure during ascent may lead to a pressure difference sufficient to rupture the sinus and produce pneumocephalus. The treatment in such cases is admission for careful observation, including frequent neurologic examinations, and prophylactic antibiotics against meningitis [36,37]. Normobaric oxygen (typically via nasal cannula) may hasten reabsorption of the air [37]. Antibiotic coverage should be directed at nasopharyngeal flora and traditionally has included agents in the penicillin or cephalosporin classes.

Dental barotrauma — During ascent or descent, the volume of air in spaces at the roots of infected teeth or adjacent to fillings can change rapidly, leading to toothache or breakdown of the tooth [38]. Dental barotrauma is a common complication, reported in 66 of 709 (9 percent) experienced divers in one series [20]. Over-the-counter pain medication (eg, acetaminophen) is generally sufficient for initial treatment, but follow-up with a dentist is recommended, and diving should be avoided until the underlying problem has been addressed.

DECOMPRESSION SICKNESS — The pathophysiology, symptoms, and signs of decompression sickness (DCS) are summarized in the table (table 2) and discussed below; treatment, including hyperbaric oxygen therapy, is reviewed below. (See 'Management of arterial gas embolism and decompression sickness' below.)

Pathophysiology — As a diver descends and breathes gas (often air) under increased pressure, the tissues become saturated with dissolved nitrogen as predicted by Henry's law. As the diver returns to the surface, the sum of the gas tensions in the tissue may exceed the ambient pressure and lead to the liberation of free gas from the tissues in the form of bubbles; the location of bubble formation depends somewhat upon tissue characteristics. The liberated gas bubbles can alter organ function by blocking blood vessels, rupturing or compressing tissue, or causing endothelial damage and subsequently activating clotting and inflammatory cascades [7,39]. The volume and location of these bubbles determine whether and what symptoms occur [40]. Gas bubbles are generally present in the venous circulation due to low pressure and high gas tension [5]. The presence of bubbles alone does not necessarily mean that DCS will develop.

Risk factors — Several factors can increase the risk of developing DCS.

Right-to-left shunt — Right-to-left shunts (eg, pulmonary arteriovenous malformations) or congenital or acquired defects through which there may be transient right-to-left shunting (eg, patent foramen ovale [PFO], atrial septal defect, ventricular septal defect, patent ductus arteriosus, and partially corrected Tetralogy of Fallot) increase the risk of paradoxical air emboli [19,41,42]. As an example, the presence of a PFO is associated with a two- to fivefold increase in the risk for developing severe DCS, although the overall incidence of this complication is low (4 to 6 per 10,000 dives) [43-47]. Among patients with a PFO, the risk is increased with larger PFO and increased atrial septal mobility [45,46,48].

Air travel and altitude — Patients who travel by air soon after SCUBA diving are at increased risk for developing DCS due to the decrease in ambient pressure [49,50]. Therefore, many experts suggest a waiting period before flying after diving, although research is limited and the optimal waiting period is not known. We concur and believe that a passenger should be advised to wait 12 hours before flying if they have been making only one dive per day. Individuals who have participated in multiple dives, or those requiring decompression stops, should consider waiting up to 48 hours before flying [51,52]. (See "Assessment of adult patients for air travel".)

Travel to altitude (such as mountains, volcanoes, etc) by car or other vehicle after diving may also increase the risk of DCS, and comparable waiting periods should be observed.

Additional factors — Multiple risk factors for DCS have been proposed, including obesity, age, and sex, but there is no consensus about their significance. The most significant risk factor is the diving profile.

Symptoms and signs — Approximately 90 percent of patients with DCS develop symptoms within three hours of surfacing; only a small percentage become symptomatic more than 24 hours after diving [53]. DCS can manifest as a wide range of symptoms and signs (table 2), and it may affect multiple organ systems simultaneously. Symptoms may be static, wax and wane, or steadily worsen. Listed below are common symptoms and signs organized by organ system.

Although DCS has been categorized using several classification schemes, these are typically used for research purposes [54]. When evaluating a patient, it is more useful to describe the specific symptoms and organ systems involved.

Musculoskeletal – Localized joint pain is the most common manifestation of DCS and is described as type I DCS [8,53,55,56]. Joints appear particularly vulnerable to the development of gas bubbles because local regions of negative pressure are created during the movement of lubricated articular surfaces. Symptoms are believed to result from bubbles in periarticular tissues, which impair blood flow and stretch noncompliant tissues. Pain is described as deep and throbbing and is generally not aggravated or alleviated by palpation or movement. The elbow and shoulder are affected three times more often than the knee and hip.

Neurologic – Approximately 60 percent of divers with DCS have signs and symptoms of nervous system involvement. The great majority of cases involve damage to the spinal cord, usually the upper lumbar or lower thoracic regions. Paresthesias and weakness may progress to paraplegia, and loss of sphincter control (particularly of the bladder) may occur [57]. "Girdle" or back pain and urinary retention may be early signs of neurologic DCS. Paresthesias or numbness often occur in a non-dermatomal distribution and may not localize to a spinal cord "level."

Cerebral manifestations can occur and may include memory loss, ataxia ("the staggers"), visual disturbances, and changes in personality, speech, or affect [58]. Most of these manifestations are believed to be caused by formation and coalescence of gas bubbles within low-pressure venous plexi and consequent venous obstruction. However, microvascular arterial embolization or bubble formation within nervous tissue may also play a role [5,8,59,60].

Cutaneous – The spectrum of possible cutaneous findings includes pruritus without skin changes, a scarlatiniform rash with pruritus often over the trunk and thighs, and a mottled, livedoid dermatitis commonly referred to as "cutis marmorata" (picture 1) [61]. This term continues to be used, although the rash is more correctly called livedo racemosa, which describes an irregular, broken rash caused by thrombotic and embolic phenomena [61].

Livedo racemosa (cutis marmorata) is often centrally distributed and commonly associated with more severe cases of DCS. A case series of divers with livedo racemosa reported bubbles in the underlying arterioles and venules of the skin detectable with ultrasound [24].

A few observational studies have reported right-to-left shunts (eg, PFO) in patients with cutaneous DCS [39].

Lymphatic – Lymphatic obstruction by bubbles, although rare, can lead to pain, lymphadenopathy, and localized edema, usually with follicular depressions and a peau d'orange effect [62]. These lesions are mainly seen on the chest and torso. Isolated lymphatic DCS is generally considered mild and self-limited, although it may not respond immediately to hyperbaric oxygen therapy, and swelling may persist after initial treatment [63].

Cardiopulmonary – Rarely, DCS presents with cardiopulmonary symptoms and signs, usually in the context of significant decompression stress from extreme depth, prolonged diving time, or a combination. Gas bubbles may occlude portions of the cardiopulmonary circulation and produce dry cough, chest pain, wheezing, dyspnea, and pharyngeal irritation ("the chokes"). Obstruction of right ventricular outflow can cause acute right-sided cardiac failure ("air lock") and circulatory collapse, and death may ensue. Gas bubbles may traverse the pulmonary capillary bed or a PFO to produce arterial gas embolism (AGE) [10]. (See "Air embolism".)

Inner ear – Inner ear DCS may manifest with vertigo, nausea, vomiting, ataxia, deafness, or tinnitus. It can occur in isolation or in combination with other symptoms. Although commonly associated with deep or mixed-gas diving, it can occur after recreational dives.

The presentation of inner ear DCS may be similar and difficult to distinguish from inner ear barotrauma, such as a perilymph fistula [64]. (See 'Ear barotrauma' above.)

Constitutional symptoms – In isolation (ie, when not associated with any focal symptoms or signs), constitutional symptoms such as malaise, fatigue, and headache are due to general decompression stress and not of clinical significance [8].

OTHER COMPLICATIONS

Nitrogen narcosis — Nitrogen narcosis is caused by the raised partial pressure of nitrogen in nervous system tissue and usually occurs at depths greater than 30 meters (100 feet) [65]. It has been called "rapture of the depths" because it induces symptoms and signs similar to alcohol or benzodiazepine intoxication, such as impairment of intellectual and neuromuscular performance and changes in behavior and personality. Hallucinations and loss of consciousness can occur at depths greater than 90 meters (300 feet).

A diver's susceptibility to nitrogen narcosis is increased by other factors that have intoxicating effects on the central nervous system, such as hypercarbia, fatigue, alcohol use, and hypothermia (core temperature below 35°C) induced by cold water. Divers recover rapidly upon ascent to a shallower depth. The main danger stems from impaired judgment, which can lead to other serious accidents (drowning, omission of decompression, rapid ascents, etc). If a diver remains persistently altered or confused after returning to the surface, alternative diagnoses should be sought [65].

Immersion pulmonary edema — Immersion pulmonary edema is a form of noncardiogenic pulmonary edema. The mechanism is not well understood but presumably stems from failure of pulmonary capillaries under stress caused by central redistribution of blood and the resulting increased pulmonary vascular pressures. The condition commonly occurs in young, healthy athletes (often swimmers or triathletes) in whom there is likely a genetic predisposition, as recurrence is common. The condition may also occur in older divers with underlying cardiopulmonary risk factors, such as hypertension, ischemic coronary disease, or cardiomyopathy.

The presentation of immersion pulmonary edema is similar to other forms of pulmonary edema and includes dyspnea, hypoxia, crackles, and possibly hemoptysis [66-68]. Symptoms generally start at depth (while diver is immersed) or at least while swimming (as it occurs in triathletes). Immersion pulmonary edema is not a form of decompression sickness (DCS) or gas embolism, but it can cause a diver to ascend rapidly or to omit decompression stops, and thus, it may contribute to DCS or acute gas embolism. Therapies used to treat other forms of noncardiogenic pulmonary edema should be used for the immersion form [66]. (See "Noncardiogenic pulmonary edema", section on 'Treatment'.)

EVALUATION OF THE SICK DIVER — Evaluation of the sick diver should include a careful history, including a diving profile, assessment of symptoms associated with arterial gas embolism (AGE) and decompression sickness (DCS), and a focused examination including signs associated with AGE and DCS (table 2 and table 3). Such signs can range from the subtle (eg, errors in mini-mental status assessment) to the severe and life threatening (eg, seizure).

The risk of developing DCS depends upon exposure to high partial pressures of nitrogen. Thus, the likelihood of DCS increases with the time and depth of the dive. DCS is exceedingly unlikely among those diving to 10 meters or less. Although dive tables and computer models are available to minimize risk, following these tables does not eliminate such risk, and DCS can still occur.

AGE develops independently of the time of gas exposure and can occur during dives limited to shallow water [8,69]. While often associated with breath holding or rapid ascent, AGE can occur in the absence of such factors.

Diving profile — A diving profile should be obtained from the diver whenever possible or from their diving partner or others in their diving group. Details should include:

Time (duration) of dive – This includes bottom time, time at various depths, and safety or decompression stops.

Depth – Maximum depth of dive and time spent at various depths.

Breathing gas Most often, divers breath compressed air. However, they may use other gas mixtures such as "Nitrox," which has a higher percentage of oxygen than air, to decrease the risk of DCS. Technical divers may use multiple breathing gases that they change during the dive depending on depth to mitigate other risks, such as oxygen toxicity.

Symptoms – Did the patient experience any symptoms during the dive (eg, any discomfort, breathing problems, difficulty clearing ears), and when exactly during the dive did they occur (eg, during descent, at depth, during ascent, post dive)?

Events – During the dive, did any unusual events occur, such as running out of air or an equipment malfunction? Ask whether ascent was too rapid, decompression stops were missed, or warning alarms sounded.

Decompression stops, dive tables, and computer profiles – Ask about the dive plan. Ask if any decompression stops were planned during the dive and whether they were done. Was the diver following dive tables or using a computer? Were the tables or computer algorithms violated? Did any computer alarms sound indicating a violation or missed decompression stop? Such violations suggest the diver has had significant decompression stress and is at higher risk for DCS.

If a computer profile is available (from the diver or their partner), record the information, which will assist hyperbaric medicine consultants. Such records may reveal significant events like rapid ascents.

Altitude exposure after diving (eg, did the patient travel by flight from a dive location?)

Number of recent dives – Ask about the number of dives today and on previous days (eg, was this the third dive of the day on the fourth consecutive day of diving?). Repetitive dives over multiple days increase the risk of DCS due to cumulative exposure.

Past diving history — Ask if the sick diver has ever experienced DCS or AGE before, or if the diver has ever experienced similar symptoms before while diving. Repeated episodes could indicate an underlying physiologic problem, such as a patent foramen ovale (PFO), or may reflect significant risk-taking behavior.

Symptom timing and course — The timing of symptom onset is critical to the differential diagnosis. Symptoms that begin during descent or while at depth are generally not due to DCS or AGE. They may be caused by barotrauma of descent, immersion pulmonary edema, or unrelated medical problems (eg, cardiac disease).

Symptoms of DCS can present upon surfacing, or onset may be delayed. However, the great majority manifest within 24 hours of a dive. Symptoms of AGE generally present within 10 minutes (and usually almost immediately) after surfacing. Loss of consciousness immediately after surfacing is highly suggestive of AGE. Symptoms of AGE and DCS can be static, waxing, or waning (table 2 and table 3). Each symptom should be described in relation to the time of onset, severity, and progression.

DCS can manifest a wide range of symptoms and signs, and it may affect multiple organ systems simultaneously, including the nervous system (eg, spinal cord injury is common) and musculoskeletal system (eg, joint pain is most common finding). (See 'Symptoms and signs' above.)

The presentation of AGE varies widely, with signs ranging from subtle neurologic changes to cardiac arrest. Manifestations of cerebral emboli range from focal motor, sensory, or visual deficits to seizures, loss of consciousness, apnea, and death. (See 'Arterial gas embolism' above.)

Some symptoms, such as joint or other musculoskeletal pain, may have been present prior to diving and are exacerbated by the activity of diving. Such a history suggests that the symptoms are not related to DCS.

Physical examination — While performing a careful general examination of the sick diver, clinicians should pay close attention to the following:

Pulmonary and cardiac – Look, listen, and palpate for signs of pneumomediastinum, such as crepitus and subcutaneous air. Patients may manifest wheezing, crackles, cough, or hemoptysis.

Neurologic – A careful, focused neurologic examination is crucial in the sick diver. Examination should include assessment of the cranial nerves, strength, sensation, reflexes, a Romberg test, and mental status (eg, mini mental status test).

In some cases, the only findings from AGE are deficiencies in executive function [9]. The only manifestations in such cases may be difficulty with tasks such as drawing a clock or performing serial 7's. Neurologic findings may be patchy and may not localize to a single lesion or spinal cord level. (See "The detailed neurologic examination in adults".)

Musculoskeletal – A joint affected by DCS may become swollen, or a faint rash may develop over the area. Joint pain is generally described as a deep, boring pain at rest and is not particularly exacerbated by movement or manipulation. Back or "girdle" pain may be an early sign of DCS affecting the spinal cord.

Skin – DCS may manifest as a scarlatiniform rash or livedo racemosa ("cutis marmorata"). Lymphedema may produce swelling.

Ears, nose, and throat – Inspect for signs of barotrauma. This may include hemotympanum or perforation of the tympanic membrane.

Urinary retention – Urinary retention may be an early sign of worsening neurologic function due to DCS.

Laboratory studies — No laboratory test results are specific to the diagnosis of AGE or DCS, but some abnormalities are common. In DCS, particularly in severe cases, endothelial leak may cause significant hemoconcentration, raising the hematocrit [8,63], and there are reports of decreased serum albumin concentrations [70]. AGE is associated with an elevation in the serum creatine kinase (CK) concentration, the degree of elevation correlating with the severity of injury. This is thought to be due to widespread injury to skeletal muscle [71]. Elevations of transaminases and lactate dehydrogenase (LDH) have been observed in patients with severe AGE [12].

Diagnostic imaging — No available imaging test can diagnose AGE or DCS, but suggestive findings may be seen. Imaging is used primarily to rule out co-existing conditions.

Chest radiograph – A plain chest radiograph should be obtained in any diver complaining of chest pain or shortness of breath, or who is otherwise critically ill, and studied closely for signs of pneumothorax (image 2), pneumomediastinum (image 1), subcutaneous emphysema (image 3), pulmonary edema, and aspiration pneumonia. In severe cases of AGE, air may be seen in the aorta (image 4), cardiac chambers, axillary vessels (image 5), and hepatic vasculature (image 6) [10].

Head computed tomography (CT) – A CT of the head may be obtained if needed to rule out other causes of neurologic findings, such as intracranial hemorrhage. Occasionally, arterial gas may be seen, but such cases are the exception, and a normal head CT does not rule out AGE.

Magnetic resonance imaging (MRI) – MRI is not sensitive for the diagnosis of AGE or DCS, particularly early in the course of disease. However, well-described patterns of abnormalities may be seen on brain and spine MRI. Areas of cerebral ischemia may be seen in patients with AGE. Gray and white matter lesions in the brain, spinal cord lesions, spinal cord edema, and micro-hemorrhages may be seen in patients with DCS. Imaging findings often lag behind the clinical course. They may not be present at initial presentation and then may appear to worsen as patient improves clinically. Definitive hyperbaric oxygen therapy should not be delayed to obtain MRI imaging [72].

Diagnosis and differential diagnosis — The diagnoses of AGE and DCS are made clinically based primarily on the history and physical examination; laboratory and imaging studies may not manifest associated abnormalities (table 2 and table 3). In mild, uncomplicated cases of DCS (eg, isolated joint pain), additional testing is often unnecessary. In more severe cases or when the diagnosis is unclear, adjunctive testing can be useful primarily to exclude other life-threatening causes (eg, intracranial hemorrhage, myocardial infarction, pulmonary edema).

Many medical conditions can mimic diving injuries, and it is important to keep a broad differential diagnosis and to avoid cognitive bias. Important alternative diagnoses to consider include acute coronary syndrome (ACS), pulmonary embolism, stroke, vertebral artery dissection, herniated disc with nerve impingement, and infection (eg, meningitis).

A sick diver who is unable to provide a useful history poses a diagnostic challenge. In such cases, we strongly recommend obtaining consultation with a specialist in hyperbaric and diving medicine or calling the Divers Alert Network early in the workup. This can help avoid delays implementing hyperbaric oxygen treatment when needed. (See 'Additional resources' below and 'Hyperbaric oxygen therapy' below.)

While not exhaustive, the presentations below are relatively common among divers and may stem from diving illness or diseases that can mimic diving illness:

Chest pain or shortness of breath – All divers who complain of shortness of breath or chest discomfort need a thorough evaluation, including a chest radiograph and electrocardiogram (ECG). The history is important when evaluating such complaints. Key components of the history include the timing of symptoms and dive profile, particularly any history of rapid ascent. Symptoms that begin at depth (ie, during the dive) are unlikely to be due to DCS or AGE and suggest an alternative diagnosis such as ACS, pulmonary embolism, or immersion pulmonary edema. Symptoms that begin just after surfacing suggest barotrauma or DCS; however, they may be caused by pulmonary embolism or ACS.

Severe cases of decompression illness (particularly gas embolism) can cause ECG abnormalities and elevations in cardiac biomarkers. These changes are not specific to DCS and appear similar to ischemic changes from other causes. ST segment depressions and elevations, and arrhythmias (eg, atrial fibrillation), have all been described in the setting of DCS.

There are reported cases of Takotsubo cardiomyopathy related to diving [73,74]. It is unclear if this is due to stress from cold water, exertion, or co-existing conditions such as AGE, DCS, or immersion pulmonary edema. We have a low threshold to perform further testing in patients with any signs of compromised cardiac function (cardiac biomarkers, serial ECGs, and an echocardiogram), particularly in divers with cardiac risk factors.

Neurologic symptoms – Differentiating neurologic symptoms and signs due to diving illness from those caused by ischemic stroke, a herniated disc, or vertebral artery dissection can be extremely difficult. Symptoms that begin at depth suggest a cause other than DCS or AGE. Diffuse or patchy symptoms or signs that are difficult to localize to a single brain or spinal cord lesion suggest DCI. Advanced neuroimaging often helps to rule out alternative diagnoses (eg, stroke), but every effort should be made not to delay hyperbaric oxygen therapy if there is high suspicion for DCI.

MANAGEMENT OF ARTERIAL GAS EMBOLISM AND DECOMPRESSION SICKNESS — The prehospital and emergency department treatment of arterial gas embolism (AGE) and significant decompression sickness (DCS) are the same [7]. Initial treatment includes administration of 100% oxygen and hydration with intravenous (IV) isotonic fluid. Definitive treatment is hyperbaric oxygen therapy.

Prehospital care — We concur with the basic prehospital interventions proposed in a 2017 expert guideline, which include the following [75]:

Provide normobaric oxygen (ie, surface oxygen, or 1 atmosphere) administered at as close to 100% as possible, usually given by nonrebreather mask.

Place the patient in a horizontal position.

Keep the patient warm but avoid hyperthermia. (See "Accidental hypothermia in adults".)

Hydrate the patient. Oral rehydration may be used if possible (eg, mild case without hemodynamic instability or laboratory abnormalities), but IV hydration with isotonic crystalloid should be administered if necessary. This may be done initially with IV fluid boluses (500 to 1000 mL) and then an infusion, depending on the severity of illness.

Rapid transfer to a higher level of care should be arranged immediately. Ideally, the injured diver should be transported directly to a facility with a hyperbaric oxygen chamber where they can be treated with recompression therapy if necessary. If no such facility is nearby, the diver should be taken to the closest medical facility where an evaluation can be performed and transfer to a hyperbaric chamber arranged. In remote locations, there may be instances where the risk of transport outweighs the potential benefit. However, we recommend that the decision not to transfer be made in collaboration with a physician experienced in diving medicine. Resources to reach such assistance are provided. (See 'Additional resources' below.)

Emergency department care — The injured diver with suspected AGE or severe DCS is assessed in the emergency department (ED) to determine the extent of injury and whether hyperbaric oxygen therapy is needed. Evaluation and treatment occur concurrently. As soon as the need for hyperbaric oxygen therapy is recognized, immediate transport should be arranged as rapidly as possible. Transport should not be delayed for any study or therapy except life-saving interventions.

Treatment in the ED includes the following interventions:

Assess and stabilize the airway, breathing, and circulation as necessary.

Continue administering normobaric oxygen at as close to 100% as possible.

Decompress any pneumothorax. An appropriate thoracostomy device must be in place prior to any recompression treatment to avoid further barotrauma. A pigtail catheter or comparably small device is often sufficient.

Continue rehydration. Oral rehydration may be used for mild cases; IV hydration with isotonic crystalloid is administered for moderately or severely injured divers.

Place a bladder (Foley) catheter if there is evidence of urinary retention.

Obtain imaging and laboratory studies as indicated by workup. (See 'Evaluation of the sick diver' above.)

Severely ill patients should be kept horizontal (Trendelenburg or reverse Trendelenburg positioning is no longer recommended); patients with mild illness may sit or otherwise assume any position of comfort.

For severely injured divers, early administration of prophylaxis against deep vein thrombosis (DVT) may be needed. No high-quality evidence is available to inform the timing, patient selection, or method of DVT prevention in divers. In the author's opinion, prophylaxis is appropriate for any diver who requires hospital admission, provided there are no contraindications. (See "Prevention of venous thromboembolic disease in acutely ill hospitalized medical adults".)

Adjunctive treatments — Several treatments for AGE and DCS, including non-steroidal antiinflammatory drugs (NSAIDs), aspirin, glucocorticoids, and lidocaine, have been proposed, but none has sufficient evidence to support routine use [8,76].

An NSAID may be given if there are no contraindications (eg, gastric ulcers, kidney injury). This is done primarily for pain relief, although there is limited evidence that it may reduce the number of recompression treatments, a result possibly due to antiinflammatory effects. In a randomized trial of 180 divers with decompression illness (DCI), treatment with tenoxicam 20 mg for seven days reduced the median number of recompression treatments needed from three to two but had no effect on functional outcomes [77].

Hyperbaric oxygen therapy

Methods, benefits, and risks — Recompression in a hyperbaric oxygen chamber is the gold standard for treatment of both DCS and AGE. Recompression therapy should begin as soon as possible once the need is recognized, but delays do not preclude treatment. There are many documented cases of marked improvement with delayed therapy [78-80], and there is no universally accepted period of delayed presentation for which treatment is considered futile [81]. Resources are available to help identify the closest hyperbaric treatment facility. (See 'Additional resources' below.)

The exact protocol, duration, and number of hyperbaric oxygen treatments is determined by the hyperbaric physician and can be modified based on the patient's response to therapy. Minor cases may resolve with a single treatment, while severe cases may require a series of treatments [81].

Hyperbaric oxygen therapy is generally considered safe and low risk. The most common side effect is middle ear barotrauma, which occurs in approximately 2 percent of patients. The injury generally resolves with rest and time, and symptoms may be treated with decongestants. For emergency hyperbaric treatments when patients are unable to equilibrate pressures in their eustachian tubes, emergency myringotomies or tympanostomy tubes may be required.

Oxygen toxicity affecting the central nervous system may occur, with seizures being the most serious manifestation. The estimated incidence is between 1 in 5000 and 1 in 10,000 treatments. Seizures resolve after oxygen is removed and are not a permanent condition. Other, more rare side effects include transient worsening of myopia, pulmonary oxygen toxicity, and pulmonary barotrauma. Although it has not been extensively studied, no significant long-term side effects from hyperbaric oxygen treatment have been reported.

Mechanism — The administration of pure oxygen displaces inert gases (primarily nitrogen) from the lungs and increases the oxygen and nitrogen gradients between the lungs and other tissues. This increased gradient enhances the removal of nitrogen from the tissues. A gradient is created by the administration of surface oxygen (ie, at 1 atmosphere) but is increased substantially in the hyperbaric chamber under higher pressures [8].

An additional rationale for hyperbaric oxygen therapy includes the reduction of bubble size caused by higher pressures, oxygenation of ischemic tissue, reduced cerebral edema, and decreased inflammatory response (due to reduction in neutrophil adhesion to vasculature endothelium [81]).

Prognosis — The prognosis for DCS is generally good. Some studies report that 80 percent of patients had complete resolution of their symptoms [8]. At least one study of spinal cord decompression reported that divers presenting with more severe initial signs had higher likelihood of residual disease [60]. Patients with inner ear DCS have higher rates of residual symptoms [82]. The timing of recompression treatment and its effect on prognosis have not been clearly established, but it is generally accepted that early treatment is better, and recompression should be performed as soon as possible [78].

COMPLICATIONS OF OTHER TYPES OF DIVING

Closed-circuit rebreathers — Rebreather diving is a form of technical diving involving a closed-loop system that recycles breathing gas, removes carbon dioxide, and periodically injects oxygen as needed [83]. This system enables longer, deeper dives while breathing gases with less nitrogen. While rebreather divers are theoretically at lower risk for decompression sickness (DCS) and barotrauma, they are at increased risk of other conditions described here that are rare in open-circuit (SCUBA) diving.

Hypoxia – Due to the complex closed breathing circuit, divers may become hypoxic during a dive. Symptoms can range from nausea, euphoria, tunnel vision, paresthesias, and dizziness to loss of consciousness. They may begin insidiously but progress rapidly to incapacitation or unconsciousness before the diver can take corrective action.

Hyperoxia (oxygen toxicity) – As it is common to breathe higher partial pressures of oxygen while on a rebreather (to minimize the risk of DCS), oxygen toxicity can ensue. Risk increases with depth, and toxicity is rare at depths less than six meters. The range of possible symptoms is broad. These may include nausea, limb twitching, auditory and visual disturbances, dizziness, and seizures. Less severe symptoms may progress rapidly to incapacitation and seizures.

Hypercarbia – With a closed-circuit system, carbon dioxide must be removed from the exhaled breath before it is re-inhaled. This is done using a "scrubber," similar to those in anesthesia circuits, that depends upon an exothermic reaction between the scrubber and the exhaled breath. Scrubbers can fail for several reasons, causing the diver to become hypercarbic. Symptoms of hypercarbia can include dyspnea, air hunger, dizziness, and headache. Symptoms similar to nitrogen narcosis may also develop, including impaired judgment and poor-decision making, loss of consciousness, and death.

"Caustic cocktail" – While the scrubber requires some moisture to work effectively (present in exhaled breath), excessive liquid (eg, saltwater) can create a toxic slurry. If this happens, and the diver inadvertently inhales this mixture, it can be catastrophic. Potential injuries range from oropharyngeal burns to full-thickness liquefactive necrosis resulting in perforation of the trachea-bronchial system or the esophagus. Symptoms may include severe pain, laryngospasm, stridor, and dysphagia. Emergency airway management may be required.

Breath-hold or free diving — The pathophysiology of breath-hold or free diving is beyond the scope of this topic. However, clinicians should know that breath-hold divers can develop DCS (generally with repeated deep dives) and arterial gas embolism (AGE). In addition, they may suffer from a condition commonly referred to as "shallow water blackout," more correctly termed hypoxia of ascent, which involves losing consciousness just before reaching or at the water surface. Breath-hold divers are also more likely to suffer barotrauma of descent (lung squeeze) than scuba divers [13].

DIVING WITH COEXISTING CONDITIONS — The physiologic changes engendered by diving are generally well tolerated, but a number of medical conditions can increase the potential for complications [84]. Diving has been successfully undertaken in the presence of a variety of medical conditions, but decisions about the safety of diving must be individualized in the context of the individual's overall health. The rate of mishaps during SCUBA dives among participants both with and without chronic medical conditions appears to decrease when pre-dive safety checklists are used [85]. Screening of patients with medical conditions who wish to dive is discussed separately. (See "Evaluation of adults wishing to SCUBA dive".)

Lung disease — The presence of chronic obstructive lung disease, lung bullae or cysts, cystic fibrosis, sarcoidosis, pulmonary fibrosis, or a history of spontaneous pneumothorax or pneumomediastinum should be considered absolute contraindications to diving. (See "Evaluation of adults wishing to SCUBA dive", section on 'Pulmonary'.)

Cardiovascular disease — Cardiovascular conditions that may cause a loss of consciousness or incapacitation of any kind are broadly considered contraindications to diving. They include arrhythmia, ischemic heart disease, decompensated heart failure, and septal defects. (See "Evaluation of adults wishing to SCUBA dive", section on 'Cardiovascular'.)

ADDITIONAL RESOURCES — When managing a patient with severe diving-related illness, we recommend obtaining consultation with a clinician with expertise in diving medicine and hyperbaric treatment. If such consultation is not readily available, we recommend calling the Divers Alert Network, an international organization, for telephone consultation and information regarding the nearest hyperbaric chambers (Divers Alert Network emergency hotline: +1 United States country code (919) 684-9111).

SUMMARY AND RECOMMENDATIONS

Sickness while SCUBA diving – Decompression sickness (DCS) and barotrauma (including arterial gas embolism [AGE]) are specific to diving, but injuries such as immersion pulmonary edema, hypothermia, trauma, and submersion-related injuries can occur while diving.

Barotrauma – Barotrauma is the most common form of diving-related injury and develops when an air-filled body space fails to equilibrate its pressure with the environment. Barotrauma can cause lung injury (including pneumothorax), ear or sinus injury, or AGE. AGE can manifest a wide range of symptoms and signs depending on its extent and the arteries affected. AGE develops independently of the time of gas exposure and can occur during dives limited to shallow water. AGE that compromises cerebral, coronary, or pulmonary vasculature can be life threatening. (See 'Barotrauma' above.)

DCS – DCS occurs when a diver returns to the surface and gas tensions in the tissue exceed the ambient pressure, causing free gas to leave tissues in the form of bubbles. These gas bubbles can impair organ function by blocking blood vessels, compressing or rupturing tissue, or activating clotting and inflammatory cascades. DCS is highly unlikely with dives ≤10 meters. Symptoms usually manifest upon surfacing and can affect a wide range of organ systems (table 2). Possible findings are myriad and can include joint pain (elbow and shoulder are common), signs of spinal cord injury, signs of brain injury, characteristic rashes, localized edema, vertigo, ataxia, tinnitus, and (less frequently) compromised cardiac function. (See 'Decompression sickness' above.)

Evaluation of the sick diver – Essential aspects of evaluation are the history, including the diving profile, and the physical examination, including assessment of symptoms and signs associated with AGE and DCS (table 2 and table 3). The timing of symptom onset is critical to diagnosis. Symptoms caused by AGE typically manifest within 10 minutes of surfacing (and often immediately). Symptoms that begin during descent or at depth are generally not due to AGE or DCS. They may be caused by barotrauma of descent, immersion pulmonary edema, or unrelated medical problems (eg, myocardial ischemia, stroke). (See 'Evaluation of the sick diver' above.)

Management – Basic initial treatment of AGE or DCS includes:

Stabilization of airway, breathing, and circulation as needed

Administration of oxygen as close to 100% as possible

Keeping the patient warm while avoiding hyperthermia

Hydration; sick patients can receive intravenous (IV) boluses (500 to 1000 mL) of isotonic crystalloid followed by an infusion

Horizontal positioning

Definitive treatment for DCS and AGE is hyperbaric oxygen therapy, which should be implemented as rapidly as possible once the need is determined. (See 'Hyperbaric oxygen therapy' above.)

Resources to help clinicians with diagnosis and management are available. (See 'Additional resources' above.)

Diving with medical conditions – Screening of patients with medical conditions who wish to dive is discussed separately. (See "Evaluation of adults wishing to SCUBA dive".)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Dipak Chandy, MD and Gerald Weinhouse, MD, who contributed to an earlier version of this topic review.

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