eMedicine Specialties > Emergency Medicine > Environmental

Decompression Sickness

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

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

The increasing popularity of scuba diving and the growth of commercial diving have increased the frequency of deep-pressure injuries. Even in regions far from coasts, individuals are diving in quarries, lakes, rivers, and caves. In addition, the ability to travel rapidly between areas of disparate altitudes in a matter of hours (including the exacerbation caused by decreased pressures in flight) increases the chance of experiencing decompression injuries. Emergency physicians worldwide should know the physiologic effects and management of decompression sickness.

Pathophysiology

Changes in pressure affect only compressible substances in the body. The human body is made primarily of water, which is noncompressible; however, the gases of hollow spaces and viscous organs and those dissolved in the blood are subject to pressure changes. Physical characteristics of gases are described by the following 4 gas laws, which quantify the physics and problems involved in descending under water.

Boyle law

For an in-depth discussion on the Boyle law, please see the article on Dysbarism.

Dalton law

Pt = PO₂ + PN₂ + Px

(Pt = total pressure, PO₂ = partial pressure of oxygen, PN₂ = partial pressure of nitrogen, Px = partial pressure of remaining gases)

In a mixture of gases, the pressure exerted by any given gas is the same as the pressure the gas would exert if it alone occupied the same volume. Thus, the ratio of gases does not change, even though the overall pressure does. The individual partial pressures, however, change proportionally.

Dalton's problem (see Media file 1): As an individual descends, the total pressure of breathing air increases; therefore, the partial pressures of the individual components of breathing air have to increase proportionally. As the individual descends under water, an increasing amount of nitrogen dissolves in the blood. Nitrogen at higher partial pressures alters the electrical properties of cerebral cellular membranes, causing an anesthetic effect termed nitrogen narcosis. Every 50 ft of depth is equivalent in its effects to one alcoholic drink. Thus, at 150 ft, divers may experience alterations in reasoning, memory, response time, and other problems such as idea fixation, overconfidence, and calculation errors. Even when no signs of nitrogen narcosis are noted, divers may significantly overestimate diving time during deep dives.

Illustration of Dalton gas law. As an individual descends, the total pressure of breathing air increases and the partial pressures of the individual components have to increase proportionally. Nitrogen at higher partial pressures alters the electrical properties of cerebral cellular membranes, causing an anesthetic effect. Oxygen at higher partial pressures can cause CNS oxygen toxicity.

Henry law

%X = (PX / Pt) X 100

(%X = amount of gas dissolved in a liquid, PX = pressure of gas X, Pt = total atmospheric pressure)

At a constant temperature, the amount of gas that dissolves in a liquid with which it is in contact is proportional to the partial pressure of that gas (ie, a gas diffuses across a gas-fluid interface until the partial pressure is the same on both sides).

Henry's problem (see Media file 2): With increasing depth, nitrogen in compressed air equilibrates through the alveoli into the blood. Over time, increasing amounts of nitrogen dissolve and accumulate in the lipid component of tissues. As an individual ascends, a lag occurs before saturated tissues start to release nitrogen back into the blood. This delay creates problems.

Illustration of Henry gas law. If nitrogen is added to a bottle, it diffuses into and equilibrates with the fluid. If pressure is suddenly released (decreased), such as when an individual ascends rapidly, a lag occurs before nitrogen can diffuse back to the nonfluid space. This delay causes nitrogen to bubble while still in the fluid.

Charles law

For an in-depth discussion on the Charles law, please see the article on Dysbarism.

Organ involvement associated with decompression sickness

As discussed in the section describing the Henry law, a reduction in pressure while ascending at the end of a dive can release dissolved gas (principally nitrogen) from solution in the tissues and blood, consequently forming bubbles in the body.

DCS results from the effects of these bubbles on organ systems. The bubbles may disrupt cells and cause a loss of function. They may act as emboli and block circulation, as well as cause mechanical compression and stretching of the blood vessels and nerves. The blood-bubble interface may act as a foreign surface, activating the early phases of blood coagulation and the release of vasoactive substances from the cells lining the blood vessels.¹ DCS may be divided into 3 categories: (1) type I (mild), (2) type II (serious), and (3) arterial gas embolization (AGE).

Type I decompression sickness

Type I DCS is characterized by one or a combination of the following: (1) mild pains that begin to resolve within 10 minutes of onset (niggles); (2) pruritus, or "skin bends," that causes itching or burning sensations of the skin; and (3) skin rash, which generally is a mottling or marbling of the skin or a papular or plaquelike violaceous rash. On rare occasions, skin has an orange-peel appearance.

Lymphatic involvement is uncommon and is usually signaled by painless pitting edema. The mildest cases involve only the skin or the lymphatics. Some authorities consider anorexia and excessive fatigue after a dive as manifestations of type I DCS.

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

Muscle splinting causes decreased function. Upper limbs are affected about 3 times as often as lower limbs. The pain caused by type I DCS may mask neurologic signs that are hallmarks of the more serious type II DCS. Dysbaric osteonecrosis is a phenomenon that occurs in divers with high numbers of dives. This is a persistent problem, suggesting that the mechanisms involved in the disorder are not yet understood.

Type II decompression sickness

Type II DCS is characterized by the following: (1) pulmonary symptoms, (2) hypovolemic shock, or (3) nervous system involvement. Pain is reported in only about 30% of cases. Because of the anatomic complexity of the central and peripheral nervous systems, signs and symptoms are variable and diverse. Symptom onset is usually immediate but may be delayed as long as 36 hours.

• Nervous system
  • The spinal cord is the most common site affected by type II DCS; symptoms mimic spinal cord trauma. Low back pain may start within a few minutes to hours after the dive and may progress to paresis, paralysis, paresthesia, loss of sphincter control, and girdle pain of the lower trunk. Vertebral back pain after a dive is a poor prognostic sign and can be a hall mark of spinal DCS with anticipated poor long-term outcome.²
  • Dysbaric myelitis occurs in half of the cases of neurological DCS. Venous ischemia is the most likely cause. Bladder problems, such as neurogenic bladder, may be common in the acute phase of DCS, may be the primary presentation, and may be prolonged.
  • DCS can be dynamic and does not follow typical peripheral nerve distribution patterns. This strange shifting of symptoms confuses the diagnosis, differentiating DCS from traumatic nerve injuries.
  • Pulmonary filtration protects the nervous system by stopping bubbles at the lungs, unless a bypass such as a patent foramen ovale or atrial septal defect is present. This filtration is size dependent. Tiny bubbles, or microemboli, that escape entrapment and continue to the brain do not cause infarction. Normal cerebral circulation starts with the highly oxygenated arterial blood flowing through the gray matter where much of the oxygen is extracted. This less oxygenated blood then flows to the long draining veins that supply the white matter of both the cerebral medulla and the spinal cord. At this level, even small additional decreases of oxygen content by embolization can be enough to damage the blood-brain barrier and initiate a cascade that ends with axonal damage. The result can be perivenous syndrome.³
  • Neurological deficits after a spinal cord injury can be multifocal. Sensory and motor disturbances can present independently, often resulting in a situation of "dissociation." This dissociation is found in most cases of spinal cord DCS.
• Eyes
  • When DCS affects the brain, many symptoms can result. Negative scotomata, devoid of any lights or shapes, are the earliest symptom. Negative scotomata become positive after a few minutes.
  • Other common symptoms include headaches or visual disturbances, dizziness, tunnel vision, and changes in mental status. However, 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.⁴
• Ears
  • Labyrinthine DCS (the staggers) causes a combination of nausea, vomiting, vertigo, and nystagmus, in addition to tinnitus and partial deafness. This alternobaric vertigo can be difficult to differentiate from dysbaric eustachian tube dysfunction.⁵ A history of eustachian tube problems depicted by past otitis media, past eustachian tube dysfunction, and problems equalizing pressure in the ears during the dive is associated with an increased prevalence of alternobaric vertigo.^6,7 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. Instead, those patients complained of tinnitus and hearing loss. For more on dysbarism in the ear, please see the article on Dysbarism.
  • A study of offshore professional divers found higher incidence of dizziness, vertigo, and ataxia than nondiver controls. With an incidence range from 14-28%, 61% of the divers had prior DCS, mostly type I, which was found to correlate more than the total number of dives.⁸
  • The pathophysiology for inner ear DCS is believed related to a left to right shunt in the labyrinthine artery.⁶ However, such a shunt should also cause cerebral symptoms that do not happen. The reason may lay with a difference in nitrogen washout in the inner ear compared to the brain. Experimental models suggest that the washout time for the inner ear is about 8 times as long compared to the brain (half-times of 8.8 and 1.2 minutes, respectively).⁹
• Lungs
  • Pulmonary DCS (the chokes) is characterized by the following: (1) burning substernal discomfort on inspiration, (2) nonproductive coughing that can become paroxysmal, and (3) severe respiratory distress.
  • This occurs in about 2% of all DCS cases and can cause death. Symptoms can start up to 12 hours after a dive and persist for 12-48 hours.
• Circulatory system
  • Hydration status appears to be affected by scuba diving. A number of influences play a role. First, many scuba divers engage in their sport in hot tropical environments. This naturally increases fluid requirements as the body works harder to keep itself cool. The same effect can even be found in colder climates where the diver uses a heated dry suit. Scuba diving is a physically demanding activity and thus utilizes more fluids. The breathing gases, whether they are compressed air or technical gas mixtures, are also dry, thus robbing the body of moisture in the exhaled gases. Most people underestimate their fluid requirements in these situations. Add to this, the drying effect of commercial airliner altitude pressures and the vacationer's preferred beverages being alcoholic. The average diver is thus set up for the possibility of significant dehydration.
  • A study of simple hematocrits after a single tropical dive found increases that were statistically significant and greater with the depth of the dive.¹⁰ While the changes were overall small, they do highlight the drying effect of diving. Another study found significant increases in hematocrit with a median of 43 (the range was up to 60). They attempted to correlate more significant increases (to above 48) with neurological DCS. They did find this association in women but not in men.¹¹ In addition, a swine study found that dehydration significantly increased the risk of severe cardiopulmonary and CNS DCS and of overall death.¹² A human study also found a significant decrease in venous bubble formation with predive hydration.¹³
  • Hypovolemic shock is commonly associated with other symptoms. For reasons not yet fully understood, fluid shifts from the intravascular spaces to the extravascular spaces. The signs of tachycardia and postural hypotension are treated via oral rehydration if the patient is conscious or intravenously if the patient is unconscious. The treatment of DCS is less effective if dehydration is not corrected.
  • Thrombi may form because of the activation of the early phases of blood coagulation and the release of vasoactive substances from cells lining the blood vessels.¹ The blood-bubble interface may act as a foreign surface, causing this effect. Bubble formation in DCS has been believed not only to cause mechanical stretch or damage and blockage of blood flow by embolization but also to act as a foreign body and to activate the complement and coagulation pathways creating a thrombus.^14,15,16 Recent studies appear to leave this concept unresolved. Some of the studies' authors indicate that they have supported this hypothesis, while others could not find a correlation with degree of injury.
  • To assist with studying of DCS, it has been classified as type A for the more serious neurologic DCS (stroke-like). Type B is for the mild, or doubtful, neurologic symptoms. Studies suggest that the etiology is different for the two types and not explained by patent foramen ovale with left to right shunting.^17,18
  • Patent foramen ovale (PFO) or congenital atrial septal defect (ASD) also comes into play in DCS.^19,20 These defects allow bubbles to pass from right to left circulation, bypassing the screening effects of the pulmonary circulation. This has been found to correlate with a higher prevalence of high spinal cord and head (brain)/neck DCS injury, which was more profound when a procedural violation during the dive led to DCS. Patients with only a large patent foramen ovale had an increased risk of DCS when decompression rules were not violated.
  • Although the overall prevalence of patent foramen ovale in the general population is significant (about 15-30%),^21,22,23 the prevalence of serious type II DCS is very low. Therefore, routine screening of divers for patent foramen ovale is not recommended. However, in the face of a serious DCS episode, it could be considered in evaluation of the patient for future diving. Serious active divers and professionals might consider routine screening for either atrial defect.²⁴ There are two reported cases of women with breast pain after diving that were found to have PFO.²⁵
  • In a small sample of divers of which about one half experienced DCS on ascent, a PFO was found in 53% of those with DCS. In all of these symptomatic divers, they had the neurological form of DCS due to paradoxical embolization. In the other half, which did not experience DCS, only 1 (statistically 8%) was found to have a PFO. In addition, the complaint of breast pain in women who were found to have PFOs has been reported. All divers who experience neurological DCS or expect to push the limits of the diving tables should consider screening echocardiographic evaluations for PFO or ASD. In addition, serious active divers and professionals might consider routine screening for either atrial defect.
  • In a two samples of divers of which about one-half suffered significant DCS on ascent, a PFO was found in 50-53% of those with DCS. In all of these symptomatic divers they had the neurological form of DCS from paradoxical embolization. In the other half, which did not suffer DCS, only 1 (statistically 8%) was found to have a PFO. Of note is that only 1 out of 4 divers with serious DCS received any PFO screening. All divers who suffer neurological DCS, and frequent divers in general, should be considered for screening for PFO. This should be done with agitated saline contrast echocardiogram testing.^26,23
  • Another interesting feature of PFO is the relationship with migraines, in particular those with aura. In limited studies, approximately 48% of migraine patients with aura were found to have PFO. Interestingly, for many years, HBO physicians had noted that many patients with neurologic DCS had a prior history of recurrent migraines. When a group of divers was specifically studied for this condition, results showed that 47.5% of divers with a large right to left shunt at rest from PFO who had been victims of DCS had a history or migraines with aura.^27,28
  • The diagnosis of the shunt from an atrial defect is made through transcranial Doppler after an injection of agitated NSS through the antecubital vein to create minute bubbles and scanning at rest and with Valsalva. This was found more sensitive than transesophageal echocardiography using similar provocative maneuvers.²⁹ Therefore, a reasonable conclusion is that individuals with a history of migraine, especially those with aura, should consider specific screening for a PFA or ASD.

Arterial gas embolization

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

Differentiating cerebral AGE from type II neurologic DCS is usually based on the suddenness of symptoms. AGE symptoms typically occur within 10-20 minutes after surfacing. Multiple systems may be involved. Clinical features may occur suddenly or gradually, beginning with dizziness, headache, and profound anxiousness. More severe symptoms, such as unresponsiveness, shock, and seizures, can quickly occur. Neurologic symptoms vary, and death can result. DCS of the CNS is clinically similar to AGE. Since the treatment of either requires recompression, differentiating between them is not of great importance. During the numerous dives involved in the recovery of wreckage from TWA Flight 800, rapid ascents resulting in AGE were uncommon even under stressful conditions.³⁰

Acclimatization

Research is showing that experiencing DCS initiates a stress response in the body. The bubble formation causes the release of a stress protein (HSP70). The presence and preconditioning of HSP70 decreases the likelihood of developing DCS during a subsequent dive. This mechanism may be the cause for observed acclimatization with continued diving.^31,32

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 Experience yields a safer diver, though at the other extreme, over confidence can lead to pushing too close to limits.

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.^37,38
• In 1995, 590 cases of DCS were analyzed (of a total 1132) by DAN.³⁶
• Of these, 27.3% were type I (pain-only DCS) and 64.9% were type II (neurologic DCS).
• The remaining 7.8% were AGE cases.
• A study from the US military in Okinawa reported 94 cases of DCS over 7 years.³⁹
• The annual incidence of DCS was 13.4 per 100,000 dives or 1 per 7400 dives.
• Another study from Britain 1992-1996 found that the annual incidence of diving accidents increased from 4 per 100,000 dives to 15.4 per 100,000 dives during that time.
• In another study, the lifetime incidence of DCS was 1 per 5463 dives. For severe DCS, it was 1 in 20,291 dives. It was also found that the more experienced divers were less likely to get DCS, presumably through more meticulous adherence to safety concerns and safer diving profiles.⁴⁰
• The DAN PDE study has followed about 8,000 divers for around 100,000 dives since 1995.⁴¹
• The incidence of DCS in this population is 3.6 per 10,000 dives (or about 36,000 cases since the study began). 
• Through the PGE study, two groups were specifically observed. One is for divers in the colder North Sea and the other for divers in temperate regions, primarily the Caribbean.
• The colder water group has seen a dramatic decrease in DCS from 400 to 100 cases per 10,000 dives over the most recent 3-year data period.
• For the warmer water group, the yearly incidence is 50 per 10,000 or less. 
• DAN also participates in a diver's insurance program for injuries while traveling in general (though most of the travel is diving related).⁴²
• The incidence of diving-related injuries, though not just DCS, is around 55 claims per 10,000 insured.
• DAN Project PGE data for 2004 based upon almost 24,000 dives.⁴¹
• In this group, about 1300 reported an incident during the dive that could have been equipment, procedural, or equalization issues.
• Twelve non-DCS injuries (of which some were dysbarism related) were reported.
• Two cases of type I DCS, 3 cases of type II, none of AGE (see article on Dysbarism), and 2 cases that were undetermined.
• DAN has analyzed their data in a very detailed manner.
• 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 at 0.0013% (1.3 per 100,000 dives).³⁹
• A New Zealand report states that the most common cause of death was drowning, but pathologists were frequently imprecise.³⁸
• 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 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.
• Divers Alert Network (DAN) studied mortalities over an 11-year period (1992-2003) to try and identify causes. Not surprisingly, asphyxia was a common cause for death, with entrapment and insufficient gases as the two most common in this category. Arterial gas embolism (AGE), also a common cause of death, was caused overwhelmingly by emergency ascent with insufficient gases as a key contributing factor. For those older than 40 years, there was an association with cardiovascular disease.⁴⁴ In AGE, mortality and morbidity is directly related to time to hyperbaric oxygen (HBO) treatment. If recompression with HBO occurs within 5 minutes, the death rate is only 5% with little residual morbidity in the survivors. If delayed 5 hours, mortality increases to 10% with residual symptoms in half of the survivors.⁴⁵

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. Many conditions would be considered to disqualify these divers from future participation in scuba diving.⁴⁶

DAN data also notes a steadily aging trend in their data.^41,42

Clinical

History

When taking the history, remember that symptoms or signs that appear during or following a dive are pressure-related until proven otherwise based on a diagnostic or therapeutic recompression. Therefore, having the forethought to ask about pressure exposure aids in the diagnosis. The following specifics about the dive should be elicited:

• Location of the dive (eg, ocean, lake, river, quarry, or cave)
• Timing of events during the dive and over the prior 72 hours (eg, time dives occurred, length of dives, surface intervals, safety stops, flying, and method of timing used [eg, watch with tables, dive computer])
• Maximum dive depth and the rate of ascent
• Approximate times spent at specific depths
• Work of the patient during the dive (Consider currents, distance swam, water temperature, and primary activity [eg, wreck diving, artifact recovery].)
• Gases and equipment used (compressed air, rebreathing equipment, mixed gases)
• Problems encountered (violation of no–decompression-limit dive tables, equipment, entanglement, dizziness, marine bites or stings)
• Patient's physical condition before, during, and after the dive (eg, fatigue, drug or alcohol intake, fever, vertigo, nausea, overexertion, pulled muscles)
• First aid delivered (eg, oxygen, positioning, medications, fluids)
• Ask the patient about the following symptoms:
  • General symptoms of profound fatigue or heaviness, weakness, sweating, malaise, or anorexia
  • Musculoskeletal symptoms of joint pain, tendonitis, crepitus, back pain, or heaviness of extremities
  • Mental-status symptoms of confusion, unconsciousness, changes in personality
  • Eye and ear symptoms of scotomata (negative then positive), diplopia, tunnel vision, blurring, extraocular motor paresis, tinnitus, or partial hearing loss
  • Skin symptoms of pruritus or mottling
  • Pulmonary symptoms of dyspnea, nonproductive cough, or hemoptysis
  • Cardiac symptoms of inspiratory, substernal, or sharp or burning chest pain
  • Gastrointestinal symptoms of girdle abdominal pain, fecal incontinence, nausea, or vomiting
  • Genitourinary symptoms of urinary incontinence or urinary retention
  • Neurologic symptoms of paresthesia (general or over a joint), paresis, paralysis, migrainous headache, vertigo, dysarthria, or ataxia
  • Lymphatic symptoms of edema

Physical

Physical examination findings may include the following:

• General - Fatigue, shock
• Mental status - Disorientation, mental dullness
• Eyes - Visual field deficit, pupillary changes, air bubbles in the retinal vessels, or nystagmus
• Mouth - Liebermeister sign (a sharply defined area of pallor in the tongue)
• Pulmonary - Tachypnea, respiratory failure, respiratory distress, or hemoptysis
• Cardiac - Tachycardia, hypotension, dysrhythmia, or Hamman sign (crackling sound heard over the heart during systole)
• Gastrointestinal - Vomiting
• Genitourinary - Urinary bladder distention, decreased urinary output
• Neurologic - Hyperesthesia, hypoesthesia, paresis, anal sphincter weakness, loss of bulbocavernosus reflex, spotty motor or sensory deficits, focal seizure, generalized seizure, or ataxia
• Musculoskeletal - Subjective joint pain without objective findings, or decreased range of motion because of muscle splinting of involved joint or tendon
• Lymphatic - Lymphedema
• Skin - Pruritus, mottling/marbling, hyperemia, violaceous color, cyanosis, or pallor
• Diagnostic maneuvers - Pain, frequently musculoskeletal, occurs in 50-60% of DCS cases. Two specific maneuvers can aid the practitioner in diagnosing DCS.
  • Place a large blood pressure (BP) cuff over the area of pain and inflate it to 150-250 mm Hg. In patients with nitrogen bubbling in the joint or tendons, this increase can force some of the nitrogen back into solution, resulting in a temporary decrease in pain.
  • Milking the muscle toward the affected joint may increase pain by pushing more nitrogen bubbles toward the joint.
• Differentiating between AGE and DCS
  • AGE - (1) Any type of dive can cause AGE, (2) the onset is immediate (<10-120 min), and (3) neurologic deficits manifest in only the brain.
  • DCS - (1) The dive must be of sufficient duration to saturate tissues, (2) the onset is latent (0-36 h), and (3) neurologic deficits manifest in spinal cord and brain.

Causes

• Predisposing causes of DCS
  • Inadequate decompression or surpassing no-decompression limits (This includes increased depth and duration of the dives and repeated dives.)
  • Inadequate surface intervals (ie, failure to decrease accumulated nitrogen)
  • Failure to take recommended safety stops
  • Flying or going to higher altitude soon (12-24 h) after diving (This increases the pressure gradient.)
  • Smoking⁴⁷
• A principal cause of DCS is rapid ascent. A major cause of rapid ascent may be panic. Anxiety traits can be identified during instruction.⁴⁸
• Individual predisposing physiologic characteristics
  • Obesity (nitrogen is lipid soluble)
  • Fatigue
  • Age
  • Poor physical condition
  • Dehydration
  • Illness affecting lung or circulatory efficiency
  • Prior musculoskeletal injury (scar tissue decreases diffusion)
• Predisposing environmental factors
  • Cold water (vasoconstriction decreases nitrogen offloading)
  • Heavy work (vacuum effect in which tendon use causes gas pockets)
  • Rough sea conditions
  • Heated diving suits (leads to dehydration)³⁰
• Divers who have been chilled on decompression dives (or dives near the no-decompression limit) and take very hot baths or showers may stimulate bubble formation.
• Improper use of decompression tables may increase the diver's risk.
  • DCS may occur even if the decompression tables and no-decompression limits are strictly observed.
  • The decompression tables and no-decompression limits list the maximum time allowed for a dive based on the maximum depth achieved.
  • The limits take into consideration nitrogen saturation of lipid tissues.
  • According to the Henry law, once nitrogen has saturated tissues, a standard ascent to the surface with decreasing ambient pressure can allow nitrogen to bubble out of solution.
  • Once the no-decompression limit has been passed, 1 or more decompression stops are required during ascent to allow delayed diffusion of nitrogen out of the lipid tissues back into the blood. Nitrogen is then exhaled through the lungs.
  • These tables also include calculations based on the surface interval between dives and residual nitrogen offloading during the time between dives. The original tables have the following 3 problems:
    • The tables are based on young, healthy, and fit US Navy volunteers. Since many civilian divers do not fit this profile, the tables have limitations.
    • The rapidly expanding use of dive computers takes into account the actual time spent at each depth. This allows for more time under water and removes a built-in factor that helps keep divers in the conservative range.
    • The number of casual divers is increasing.
• See the discussion under Deterrence/Prevention for more information.

Differential Diagnoses

Other Problems to Be Considered

General - Dehydration, electrolyte imbalance, viral syndrome, exhaustion
Mental status - Psychosis, hypoxia
Eyes - Ophthalmic migraine, CNS lesion
Ears - Tympanic membrane rupture, otitis media, external canal occlusion, round window rupture
Pulmonary - Bronchospasm
Cardiac - Pneumopericardium, supraventricular tachycardia
Gastrointestinal - Enteritis, motion sickness, viral food poisoning
Genitourinary - Urinary tract infection, prostatism, anticholinergic effect
Neurologic - Radiculopathy, neurapraxia, hypoxia, round window rupture, alternobaric vertigo
Musculoskeletal - Sprain, strain, fracture, fatigue, acute arthritis, herniated disk
Skin - Dermatitis, allergic reaction, envenomation, contusion, arterial occlusion

As emphasized above, symptoms that occur following scuba diving need to be considered as possible DCS. Many times, the only way to assist with this determination is a trial hyperbaric oxygen (HBO) recompression. However, some have temporally linked symptoms to diving that ultimately are determined to be non–diving-related issues. The take-home point is to consider DCS as a possibility but not to exclude other possibilities, especially if symptoms are atypical and the dive profile would not normally have been expected to cause a problem.

Workup

Laboratory Studies

• No specific tests exist for decompression sickness (DCS). When diving is involved, consider determining whether the patient has any pressure-related injuries. Obtain baseline laboratory studies, but these will have no bearing on initial management. They may be useful in the differential diagnosis while HBO therapy is administered.
• Do not delay HBO therapy (and transfer, if necessary). In individuals with change in mental status, prudence dictates obtaining studies to help further evaluation. If the individual is in extremis (eg, shock), obtain appropriate resuscitation studies.
• Change in mental status
  • Blood glucose level, CBC
  • Sodium, magnesium, calcium, and phosphorous levels
  • Oxygen saturation
  • Ethanol level and drug screen
  • Carboxyhemoglobin level
• Shock
  • Blood glucose level, CBC
  • Electrolytes and BUN level
  • Creatinine levels
  • Type and screen/cross
  • Prothrombin time, activated partial thromboplastin time
  • Carboxyhemoglobin level

Imaging Studies

• Chest radiography
• Because dysbaric injuries involving the lungs and chest can occur concomitantly with DCS, obtain a chest radiograph to screen for overpressurization injuries.
• Chest radiography reveals evidence of pneumothorax, pneumomediastinum, subcutaneous emphysema, pneumopericardium, alveolar hemorrhage, and decreased pulmonary blood flow caused by nitrogen pulmonary emboli.
• Head CT scan: If mental status does not initially improve in response to hyperbaric repressurization, consider other etiologies.
• MRI has been found useful in the management of neurologic DCS.^49,50,51,52
• The diagnosis is still clinical, and the patient's transfer to an HBO facility should not be delayed.
• MRI has revealed focal spinal lesions that correlated with the patient's symptoms and examination. MRI readily detects cerebral damage in AGE⁵³ but yields low sensitivity in DCS.
• MRI may prove useful in patients who do not show initial improvement to HBO therapy. In these individuals, the MRI may localize the area of DCS injury or exclude other etiologies for the patient's symptoms.
• Spinal MRI found lesions more commonly in divers with severe spinal DCS and none at all in those that ultimately had a favorable outcome. Therefore, in an HBO center, it may be a useful diagnostic adjunct to help guide management.²
• MRI is also useful for monitoring injured divers through successive HBO treatments.
• Cerebral MRI has even identified abnormalities in the brain that correlated with hours of diving in the air-breathing range even when no clinical or historical signs of neurologic DCS were present.⁵⁴
• Note that negative MRI findings cannot be used to exclude AGE or DCS. Also, improvement in MRI findings does not necessarily correlate with clinical improvement.⁵⁵ It has also been correlated with neuropsychological deficits in older divers.⁵⁶
• The decision to pursue HBO referral is based on clinical presentation and should not be guided by MRI findings.

Other Tests

• ECG
• Oxygen saturation

Procedures

• Diagnostic repressurization: If diagnosis of DCS versus dysbarism or some other entity is unclear, order repressurization in a hyperbaric chamber (transfer if necessary) for diagnostic and therapeutic reasons.
• Intubation: Intubation delivers 100% oxygen when less-invasive delivery methods do not work or are inappropriate.
• Needle decompression and thoracostomy: These procedures help in the treatment of tension pneumothorax, simple pneumothorax, and subcutaneous emphysema.

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. Problems with air supply, hypothermia, potential oxygen toxicity, dehydration, and the uncontrolled environment make it less than ideal and increase the risks of drowning.⁵⁷ However, in remote areas without reasonable-distance HBO chamber support, this may be the only option.
  • In Thailand, home to the diving Urak Lawoi fishermen, 72.1% exceed the no-decompression limits, yet medical treatment and HBO facilities are distant (10 h and 16 h, respectively). In this population, one third reported having experienced DCS, and in-water recompression has been shown to be an appropriate first-aid measure. Much more research needs to be performed on the concept of in-water decompression, since over half of the Urak Lawoi (not just one third) were classified as experiencing recurring nondisabling DCS and about one quarter as having disabling DCS.^58,59,60
  • A shorter in-water recompression protocol was also developed for use in the remote Northern Pacific Clipperton Atoll in an attempt to address the above concerns.⁵⁷
• 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.⁶¹
• 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.⁶²
• 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 the patient into the 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.⁶³ 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 to wash nitrogen out of the lungs and set up an increased diffusion gradient to increase nitrogen offloading from the body.
• Do not put the patient into the 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.⁶³ It also wastes time and complicates movement of the patient.
• Perform intubation, aggressive resuscitation, and chest tube thoracostomy, if indicated.
• Administer intravenous fluids for rehydration until urinary output is 1-2 mL/h. Rehydration improves circulation and perfusion.
• 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.⁶²
• Treat the patient for nausea, vomiting, pain, and headache.
• Contact the closest hyperbaric facility (or DAN for referral) to arrange transfer and try to keep all diving gear with the diver. The diving gear may provide clues as to why the diver had trouble (eg, faulty air regulator, hose leak, carbon monoxide contamination of the compressed air).
• Patients with type I or mild type II DCS can dramatically improve and have complete symptom resolution. This improvement should not dissuade the practitioner from HBO referral or transfer, as relapses have occurred with worse outcomes.

Consultations

• Diving medicine and HBO specialists: Symptoms temporally related to diving should necessitate a consultation with a diving medicine specialist or HBO specialist to determine if symptoms are related to diving and if HBO therapy is appropriate.
• DAN: DAN is an excellent resource, especially if local support is not available. Visit their Web site at Divers Alert Network. Use of this service is similar to use of a poison control center. DAN maintains a database of diving-related injuries and provides consultation services, including extent-of-injury assessment, recommendations for management, and referral to HBO therapy or local diving medicine specialists. Emergency contact 24 hours per 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)
• HBO treatment
• Patients with mild type I DCS probably do not require treatment other than breathing pure oxygen at sea level for a short time. Divers with type I DCS symptoms do, however, require close observation, as symptoms may portend the onset of more serious problems requiring hyperbaric recompression. Consult a diving medicine or HBO specialist for all diving-related injuries. The only effective treatment for gas embolism is recompression; other treatments are merely for symptoms.
• Several types of hyperbaric chambers exist, ranging from small monoplace (single person) chambers to complex multiple place, multiple lockout chambers large enough for multiple patients and attendants. All chambers have the ability to maintain critical care monitoring and mechanical ventilation. A major difference with the size of chambers clinically is that some patients experience claustrophobia with the small monoplace chambers. Increased oxygen toxicity issues have been reported with the monoplace chambers because the entire environment is oxygenated, whereas, with the larger chambers, patients breath the oxygen via mask, but the ambient environment is not supplementally oxygenated.
• The basic theory behind HBO therapy is, first, to repressurize the patient to simulate a depth where the bubbles from nitrogen or air are redissolved into the body tissues and fluids. Then, by breathing intermittently higher concentrations of oxygen, a larger diffusion gradient is established. The patient is taken slowly back to surface atmospheric pressure. This allows gases to diffuse gradually out of the lungs and body. The addition of helium to oxygen has been shown to yield an advantage over oxygen alone even in severe neurologic DCS or treatment-refractory DCS.^64,65
• Treatment tables govern the exact combination of timing and depths. These were developed primarily by the US Navy with some minor modifications by the US Air Force. Table 6 is most commonly used; however, specific details concerning the tables are beyond the scope of this article. While most will improve with a single HBO treatment, 38.5% will have relapses, half of those within 24 hours. Observation for 24 hours is strongly recommended after HBO treatment.⁶⁶ Another study reported complete resolution of symptoms in 49% with the first treatment and an additional 26.5% with additional treatments. However, 24.5% had long-term residual symptoms.⁶⁷ In Israel, 48% had complete recovery with HBO, while another 48% had partial recovery. Unfortunately, 4% did not respond to the therapy.⁶⁸
• Traditionally, the treatment protocols were staged, meaning that time would be spent at certain depths as the individual was "brought back to the surface." Recent studies suggest that a linear approach is more effective than the staged approach. Other variations on the tables are being researched to try to find shorter-term approaches. In addition, use of combination gases such as Trimix are being looked at in the same regard.
• Other mentioned adjuncts to HBO include negative-pressure breathing and intravenous perfluorocarbon emulsion.
• With early recognition and treatment, more than 75% of patients improve. Even with significant delays in recognition and treatment, positive results are obtained.^69,70 Studies of the Miskito Indians of Central America highlight this. They are diving seafood harvesters who dive repeatedly without consideration for diving tables or profiles. They have a high prevalence of the bends and neurologic DCS that affects the thoracolumbar spine in particular. Despite very high rates of DCS, and sometimes days' delays in HBO treatment (if sought at all), HBO treatment yields positive results, with 30% regaining strength and many more ambulating. However, HBO treatment is usually only sought for significant neurologic symptoms, while painful DCS, such as the bends, is usually treated with only analgesia.^71,72
• Differentiating inner ear barotrauma or dysbarism from inner ear labyrinthine or alternobaric vertigo is difficult. The difference is that dysbarism responds well to treatment, and inner ear DCS is less responsive and is associated with a higher frequency of permanent damage. Patients with inner ear DCS may be asymptomatic after treatment yet still have vestibular problems at detailed testing. Therefore, both conditions must be considered in the differential diagnosis, and the patient must be treated for both conditions. A recent recommendation is to perform immediate tympanocentesis and then to follow with HBO therapy.
• Inner ear DCS is less responsive to HBO treatment than is DCS affecting other sites. HBO typically results in significant improvement in severe neurologic DCS if it is identified early and the patient is rapidly transported to an HBO facility.
• Rapid treatment is also crucial in the face of AGE. Those with AGE who reach recompression within 5 minutes have a death rate of only 5%. This rapid treatment also results in little morbidity. However, when AGE recompression is delayed 5 hours, the mortality rate approaches 10%. More than 50% of the survivors experience residual signs.
• 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. 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).⁷³ This can be difficult when there are mountains to traverse in flight. An effort should also be made to minimize the transport time. 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).

Medication

Three main drugs have been mentioned in relation to DCS. No definitive studies support their use. Thus, no consensus exists about dosages. Case reports suggest that they may be helpful.

Antiplatelet agents

With the potential for activation of coagulation factors, as discussed above, therapy aimed at mitigating this effect is helpful. Obtain guidance from a specialist in diving medicine or HBO.

Aspirin (Anacin, Ascriptin, Bayer aspirin)

Blocks prostaglandin synthetase action, inhibiting prostaglandin synthesis and preventing formation of platelet-aggregating thromboxane A2. Mechanism of action in treatment of DCS unclear.

Dosing

Adult

No consensus; doses used in treating cardiac disease appear to be best choice

Pediatric

Administer as in adults

Interactions

Effects may decrease with antacids and urinary alkalinizers; corticosteroids decrease serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and 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 with Reye syndrome, do not use in children (<16 y) with flu

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

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 in patients with severe anemia, history of blood coagulation defects, or who are taking anticoagulants

Corticosteroids

These agents have anti-inflammatory properties and cause profound, varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli. Which mechanism provides the potential for benefit is unclear.

Methylprednisolone (Solu-Medrol, Depo-Medrol)

Useful in treating inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation. Mechanism of action in treatment of DCS unclear.

Dosing

Adult

No consensus; doses used in treating spinal cord injury may be used as guide

Pediatric

Administer as in adults

Interactions

Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust methylprednisolone dose); monitor patients for hypokalemia when taking concurrently with diuretics

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Anesthetics

These agents stabilize the neuronal membrane and prevent initiation and transmission of nerve impulses, thereby producing local anesthetic activity. Their effect in DCS is unclear.

Lidocaine (Dilocaine)

Decreases permeability to sodium ions in neuronal membranes, inhibiting depolarization and blocking transmission of nerve impulses. Mechanism of action in DCS is unknown.

Dosing

Adult

No consensus; standard cardiac doses may be used as guide; low therapeutic levels were maintained in one study

Pediatric

Administer as in adults

Interactions

Concurrent cimetidine or beta-blocker increases toxicity; coadministration with procainamide or tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Contraindications

Documented hypersensitivity; Adams-Stokes syndrome; Wolff-Parkinson-White syndrome; severe sinoatrial, atrioventricular, or intraventricular block if artificial pacemaker not in place

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use a solution without preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory depression, and bradycardia; may increase risk of adverse CNS and cardiac effects in elderly persons; high plasma concentrations can cause seizures, heart block, and atrioventricular conduction abnormalities

Follow-up

Further Inpatient Care

• Admission is indicated at an institution only with HBO capability.

Further Outpatient Care

• A patient with DCS is most likely not discharged from the ED to outpatient care. Patients can dramatically improve or have complete resolution in type I or mild type II DCS with just oxygen and rehydration. However, this improvement should not dissuade the practitioner from referral or transfer for HBO, as relapses have occurred with worse outcomes. Therefore, referral to a hyperbaric facility is strongly advised.

Inpatient & Outpatient Medications

• Nonsteroidal anti-inflammatory drugs provide some benefit for musculoskeletal complaints. This decision is best left to the specialists.

Transfer

• Transfer to a hyperbaric facility is strongly advised.
  • An important issue is timely 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).⁷³ 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

• The key to preventing DCS is exercising conservatism in the diving profile and always putting safety first. Even with those, DCS can still occur. The total amount of saturated nitrogen was thought at one time to be the primary determinant of an individual's risk of developing DCS. Thus, the diving tables reflected close attention to the time spent at depths and surface intervals for repetitive dives. Recent research and thought suggests that the rate of ascent from depths may be a more critical factor.
  • 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- to 5-minute safety stop at 15-20 ft (4.6-6 m).^74,75 Therefore, the time of ascent was increased for a 60-ft dive from 1 minute to a maximum of 7 minutes.
  • Doppler bubble research has revealed that the release of bubbles from tissues is a critical factor in the development of DCS. The tissues that appear to saturate the fastest are in the spinal cord, with maximum saturation occurring in as few as 12 minutes. Desaturation, or offgassing, is much slower. Thus, even a no-decompression dive at 60 ft (20 m) for 20 minutes maximally saturates spinal tissues. As mentioned above, these are the tissues most commonly affected in type II DCS.
  • Even the slower 7-minute ascent to reach the surface from a 60-ft (20 m) dive still leaves a sizable amount of dissolved nitrogen in the faster-saturating spinal tissues. The remaining nitrogen can then bubble even on this slower ascent.
  • According to DAN, recent data from a European study revealed that increasing this ascent time to 18 minutes eliminated the dangerous bubbles. Therefore, one or more additional stops at deeper level(s) are likely needed to lengthen ascent time adequately and thus protect against 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.⁷⁵ 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.
• Being active during the decompression stops may also decrease the likelihood of bubble formation.^76,77,78
• Close attention to adequate hydration before and immediately after a dive may also have protective effects. In an individual with normally functioning kidneys, the frequency of urination and the concentration color of the urine are easy indicators of whether sufficient fluids are being taken in. A long time between urinating and a deep color are signs of inadequate intake. Note that these fluids should not be heavily caffeinated and should be alcohol free.
• 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.⁷⁹ 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.
• Everyone loves to play with bubbles. Children, pets, even scuba divers live to watch and even play with bubbles whether they be soap bubbles in the air, or air bubbles floating up in water. However, when bubbles are inside, such as a trapped gas bubble in the intestine or stomach, everyone gets uncomfortable. This is even truer for divers. The effects of trapped gas in various body cavities are discussed in Dysbarism. Microscopic bubbles, in particular those made of nitrogen that cause DCS, are discussed.
  • It is believed that the nitrogen bubbles start as minute gas nuclei, present before the dive, rather than supersaturation of the blood and tissues, that act as the seed for large bubble formation.⁸⁰ Once the bubbles form, they create a foreign body interface which platelets then adhere to.⁸¹ In severe DCS, significant decreases in platelet count have been documented. These decreases may some day be used as a marker for severity of injury.^82,83
  • To this point, the major way to avoid this bubbling has been through conservative diving using tables or computers that are based on the experiences of fit military divers. By staying "within" the tables, it was hoped that excessive tissue nitrogen saturation could be avoided so that it would not come out of solution as bubbles on ascent. Computer models are being validated that may lead to more accurate determination of these tables.⁸⁴
  • The next step in the efforts to avoid DCS was to ascend slowly. Over recent years, the recommended ascent rate has decreased steadily, as mentioned above, to the point where it is recommended to stop ascent at decompression stops to allow the exhalation of nitrogen gas, rather than its bubbling in the blood.
• Research has continued to look for the "holy grail" "ahah" starting point for the nitrogen bubbling in a hope that it can be influenced. The researchers may be almost there.
  • The gas nuclei and nitrogen interface appear to hold the key to better prevention strategies regarding DCS. In particular, the protection appears to be related to nitric oxide and nitric oxide synthase. A progression of studies from rats to trained, fit, military divers and now in experienced recreational divers is showing that inhibiting nitric oxide synthase increases the number and sizes of bubbles and that administering a nitric oxide donor decreases the number and size of bubbles.⁸⁵ This effect occurred with a long-acting agent at 20 hours and 30 minutes before the dive. More recently, a short-acting nitric oxide donor, the common sublingual medication nitroglycerin (0.4 mg), administered 30 minutes prior to the dive, also provides this same level of "protection" by decreasing the bubble formation.⁸⁶
  • There has also been work looking at the toxic effects of oxygen under pressure. It is possible that oxidation and free radicals may also be an important instigating factor. It causes vasoconstriction, which causes ischemia, activation of the inflammation cascade, and subsequent damage of the vascular endothelium. Antioxidants, maintaining normal hemostasis, and prevention of inflammatory responses may help stop the DCS process from starting.⁸⁷
  • Another significant event has been the discovery of the positive benefit of a period of aerobic exercise at around 80% of maximal oxygen uptake in humans and 85-90% in rats.⁸⁸
    • The timing of this exercise appears to be the key. A period of exercise of 90 minutes in rats and 40 minutes in humans timed at 20 hours and 24 hours, respectively, before the dive, was found to have significant long-lasting effects on the number and size of nitrogen bubble formation.^89,90,91,88 When the same exercise is completed at 2 hours and 30 minutes prior to the dive, the results are less clear. In some groups, a benefit was noted; in others, no benefit was noted.^92,93
    • In one study, it was demonstrated that the positive effect of the exercise the day before was wiped out by a second period of exercise prior to the dive. It has also been demonstrated that, it is not the overall level of fitness, but rather the timing of the exercise that provided the protection. This level of protection appears to be similar to that offered by the nitric oxide donor.^94,95
    • It has also been demonstrated that regular exercise, physical conditioning, and diving also appear to have a protective effect against bubble formation and DCS.⁹⁶
  • The next step is to see exactly what biochemical effects the exercise causes. It appears that nitric oxide is the protective agent in the predive exercise.{Ref46}
  • A controversy has long existed about post dive activity and exercise. It was believed that intense activity after a dive would promote bubble formation. In small studies on trained, fit, military divers, a positive benefit has been found to mild exercise, at 30% of maximal oxygen uptake, during the 3-minute decompression stop on ascent. Other recent studies incorporating similar aerobic exercise, at 80% of maximal oxygen uptake, starting at 30 and 40 minutes post dive, have failed to demonstrate any adverse effects on trained, fit, military divers.⁷⁸
• So, the question is, what should the average diver do, or not do, based upon the research?
  • As with anything in medicine, broad recommendations can only be reached after a sufficient number of large studies show benefit. This level of weight has not yet been reached in the diving literature.
  • Clearly, the benefit of aerobic exercise the day prior to a dive is evident. For the many recreational divers that are relatively sedentary as they fly long distances to remote areas and then start diving soon after arrival, this may have important consequences.
  • As with any physical activity, including scuba diving, the person must be physically fit before engaging in a stressful activity. This should be completed in consultation with a physician, in particular one with experience with the recreational activity.
  • All medications should only be taken on the recommendation of a physician who is familiar with the patient and the patient’s health history and only after consideration of the risks and benefits of the medication. In this specialized, off-label use, a specialist in diving medicine should be the consultant. Nitroglycerin is mentioned above. Nitroglycerin has many adverse effects such as dilation of blood vessels, lowering of blood pressure, and headaches.
  • A period of pre-breathing normobaric (regular oxygen bottle) oxygen for 30 minutes was found to decrease venous bubble formation for the subsequent dive and repetitive dives afterwards with no further prebreathing.⁹⁷ In swine models, pre-breathing oxygen at depth for as little as 5 minutes before rapid decompression helped prevent type II DCS and when breathed for 15 or 45 minutes, it decreased type I DCS symptoms.⁹⁸ It also was found in swine models to decrease venous ischemia and osteonecrosis from DCS.⁹⁹ As with the statement about nitroglycerin above, oxygen is a medical gas and its use needs to prescribed by a physician.
  • In addition, a 30-minute predive sauna session at 65 º C (149 º F) was shown to decrease venous bubble formation, though the mechanism is not known.¹⁰⁰
  • What to do after the dive is less clear and needs more investigation in less fit populations. While the research appears promising that there is at least no adverse effect to exercise after diving, and that some benefit may exist, there is insufficient weight to the research to recommend any changes.
• A puzzling situation is when an individual experiences DCS when all facets of the dive appeared normal and highly conservative. This lead to a search for other possible influencing etiologies. The identification of the injured diver’s thrombotic state was found to be a possible explanation.
  • A high percentage of the unexplained DCS injured divers were found to have moderate increases in total plasma homocysteine, a substance found to be implicated in the formation of atherosclerosis (hardening of the arteries), and deficiencies in folate and vitamin B-12, common nutritional substances.^101,102 These 3 chemicals are easily screened for with common laboratory testing.
  • Correction of folate and B-12 deficiencies are easily treated with vitamin supplementation. Studies suggest that the homocysteine level increase can be treated favorably with folate and vitamin B-6 supplements. Again, this should also be completed under the advice of a physician.
• Current research is aiming at fine-tuning the prevention of DCS. Transcranial, precordial, and subclavian vein Doppler examination; echocardiography; and regular ultrasonographic imaging have been used to detect the presence of bubbles in the vascular system of the volunteers being studied.^71,103,104 At the same time, various HBO decompression models are being evaluated using the same studies.^105,106 As the database expands across the full spectrum of divers (not just young, healthy divers), the tables and recommended dive profiles will continue to improve. However, since people respond differently to DCS, a universal profile is unlikely to be established. For this reason, all divers should fully understand their dive profiles (especially if generated by computer) and should always be conservative and allow plenty of room for individual variation and error.
• Future trends are promising. Efforts are underway to identify specific biomarkers for DCS.¹⁰⁷ Promising animal research on changes that occur within 30 minutes of surfacing has been underway. Likewise, promising research related to the use of intravenous perfluorocarbons is underway as well.^108,109 They appear to decrease DCS symptoms through a combination of decreasing bubble formation, hemodynamic protection against gas embolism, enhanced oxygen delivery to tissues, and increased pulmonary nitrogen washout though this last effect is hypothesized but not shown.^110,111 The effects are further enhanced by oxygen prebreathing (before HBO treatment) with increased oxygen delivery.¹¹²

Complications

• Residual paralysis, myocardial necrosis, and other ischemic injuries may occur without immediate recompression. These may occur even in adequately treated patients.

Prognosis

• Early symptom recognition, prompt diagnosis, and appropriate treatment are keys to a positive outcome with DCS. With these, a success rate of greater than 75-85% can be achieved.

Patient Education

• Diver education is paramount. The symptoms, signs, and management of DCS and AGE must be learned to facilitate early recognition and treatment.
  • Of 590 patients with DCS whose characteristics were studied (results discussed in Epidemiology), 9 continued to dive after developing neurologic symptoms, including 1 patient with paralysis in both legs.
  • Approximately 7% of patients who reported to DAN reported a delay in seeking treatment until more than 96 hours after symptom onset, and 35% of all cases were reported to DAN more than 4 hours after symptom onset.
• For excellent patient education resources, visit eMedicine's Environmental Exposures and Injuries Center. Also, see eMedicine's patient education articles Barotrauma/Decompression Sickness and The Bends - Decompression Syndromes.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose DCS can be disastrous because DCS can cause long-term neurologic disability even with treatment.
• 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. If DCS symptoms are serious and AGE is present, the specialist will most likely attempt to dissuade the patient from future participation in diving.

Special Concerns

• Diving while pregnant is not recommended because of unknown effects of nitrogen diffusion across the maternal-placental membrane. The fetus is not believed to be protected from decompression problems and is at risk of malformation and gas embolism. However, normal pregnancies have been reported even after repetitive dives.¹¹³
• 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,¹¹⁴ 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 increased medical problems. As with any physical activity, the advice and recommendations of a physician familiar with diving medicine should be sought.
• Most divers use a compressed air source. Dive shops usually refill dive tanks. The equipment is typically a gasoline-powered air compressor that uses filtered ambient air. An improper setup or malfunctioning equipment may compress carbon monoxide from exhaust fumes (or other gases nearby) along with the air. This is a recognized danger in the diving industry. Filling stations should have safeguards in place; however, the potential for injury still exists. According to the Dalton law, even small amounts of carbon monoxide in the tanks have higher partial pressures at depth that may exacerbate clinical effects.
• Because the symptoms of carbon monoxide poisoning (eg, dyspnea, headache, fatigue, dizziness, visual changes, unconsciousness) can mimic DCS or AGE, differentiate these conditions by looking for carbon monoxide specifically with co-oximetry. Failure to recognize carbon monoxide poisoning is not a serious omission as long as the patient is recognized as having a diving injury. The hyperbaric treatment of DCS and AGE is also the treatment of choice for carbon monoxide poisoning. For more information on this topic, please see the article on Toxicity, Carbon Monoxide.
• Two other situations deserve mention. The first is related to the use of special "technical diving" gases such as Trimix (a combination of oxygen, nitrogen, and helium).
  • There is a practical limit to the use of compressed air in scuba diving of around 132 ft (40 m, 4 atm) where the bottom times are so short (or actually nonexistent using standard tables) and the risk of nitrogen narcosis is high. Since many interesting sites, such as wrecks, are deeper than that, many divers have started using a Trimix that lowers the nitrogen load to avoid narcosis, decreases the oxygen content to avoid toxicity, and replaces the two with helium that also is a lighter gas.
  • Depending on the goal depth, multiple tanks with different mixes for different depth ranges may need to be carried. This is a highly technical and riskier activity.
  • Even with the Trimix, the limit is still fuzzy as the overall gas density increases. This increases the work of breathing and thus respiratory fatigue. If this is added to the additional load of general physical exertion, a situation of hypercapnia (increasing carbon dioxide in the bloodstream) can ensue that causes worsening of the overall fatigue. If not corrected by ascending, death can, and has, occurred.¹¹⁵
  • Trimix has been used in HBO treatment to shorten treatment courses with success.
• The other situation relates to breath-hold diving (without scuba tanks). In the past, a breath-hold dive was simply a free dive from the surface without supplemental air.
  • The average person was limited by his or her physical prowess for how deep he or she could go, or the length of time he or she could stay under. Neither was a major concern except in the circumstance of forced hyperventilation thinking this would help just before the dive. The result here could be hypoxia with loss of consciousness before the hypercapnic, carbon dioxide, need to take a breath.
  • The addition of fins increased the depth and distance but again not to a concerning level. In recent years, oversized fins have appeared on the market, as have motorized underwater scooters. Both of these have allowed much greater depths in the free dives and can allow more rapid ascent and then immediate dive again. Professional and recreation spear fisherman, especially in tournaments, are now achieving depth and underwater times where they can start accumulating nitrogen loads and with the rapid ascents, DCS has been reported.¹¹⁶
  • Another group of note are the extreme-depth unlimited free divers. They use a weighted sled to achieve record depths measured in the several hundreds. The combination of extreme depth and 5- to 7-minute times involved allow sufficient nitrogen loads that again can result in DCS.
    • The risk is even greater in those that are preparing for a competition where in the course of a day they can have repeated weighted free dives to increasing depths with limited surface intervals.
    • Frequent Valsalva on descent to equalize pressure also can unmask a previously unknown PFO or ASD and allow neurological DCS.¹¹⁷
    • Morbidity and mortality is increasing in these extreme free divers who keep pushing physiologic limits to dangerous extremes due to reasons elucidated above plus various barotraumas causing disabling symptoms.¹¹⁸

Multimedia

Media file 1: Illustration of Dalton gas law. As an individual descends, the total pressure of breathing air increases and the partial pressures of the individual components have to increase proportionally. Nitrogen at higher partial pressures alters the electrical properties of cerebral cellular membranes, causing an anesthetic effect. Oxygen at higher partial pressures can cause CNS oxygen toxicity.

Media file 2: Illustration of Henry gas law. If nitrogen is added to a bottle, it diffuses into and equilibrates with the fluid. If pressure is suddenly released (decreased), such as when an individual ascends rapidly, a lag occurs before nitrogen can diffuse back to the nonfluid space. This delay causes nitrogen to bubble while still in the fluid.

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Keywords

decompression sickness, DCS, diving emergency, diving injury, the bends, the staggers, the chokes, niggles, underwater ascent, free dive, assisted dive, self-contained breathing apparatus, SCUBA, scuba diving, deep-pressure injury, decompression injury, altitude sickness, arterial gas embolization, type I decompression sickness, type I DCS, skin bends, type II decompression sickness, type II DCS, negative scotomata, labyrinthine decompression sickness, labyrinthine DCS, hypovolemic shock, pulmonary decompression sickness, pulmonary DCS, acclimatization, Divers Alert Network, DAN, pressure-related injury, no-decompression limits, decompression tables, hyperbaric oxygen recompression, HBO therapy, dysbaric injury, hyperbaric repressurization, neurologic decompression sickness, neurologic DCS, decompression illness, DCI

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

Eric M Kardon, MD, FACEP, Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center
Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

James Steven Walker, DO, MS, Clinical Professor of Surgery, Department of Surgery, University of Oklahoma Health Sciences Center
James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association
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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