Decompression Sickness 

Updated: Mar 05, 2019
Author: Stephen A Pulley, DO, MS, FACOEP; Chief Editor: Joe Alcock, MD, MS 

Overview

Practice Essentials

The human body has the ability to adjust to increases in ambient pressure, to a limit. However, the increased pressure increases the partial pressures of the gases that are inspired. A number of effects can occur. Toxicity to oxygen or nitrogen, or contaminants, have deleterious effects. A scuba (self-contained underwater breathing apparatus) diver can mitigate these effects by staying within established time parameters to avoid these toxicities. Those with advanced technical training use specialized mixtures to avoid these toxicities. Even when staying within the parameters, or perhaps using the specialized gases, issues can still occur and cause injury. In addition, the sudden or too rapid decrease in pressure (ie, decompression) can have a number of ill effects. Some relate to the gross expansion of gas in the usual gas-containing cavities and organs in the body. The result can be dysbarism. Other effects are due to the expansion of microscopic gas particles within the tissues of the body. This is decompression sickness (DCS). Also see Dysbarism.

Healthcare professionals worldwide, regardless of specialty, need to be aware of the ill effects of exposure to increased pressure. The ability to travel great distances relatively quickly, the increasingly unusual areas being dived, along with the delay in onset of symptoms can find a person suffering from DCS showing up in a medical setting seemingly quite far from bodies of water. DCS symptoms can be of rapid onset, straightforward, or insidiously mild and delayed. Healthcare practitioners need to consider activity in the days prior to any medical visit, and be aware of the issues and nuances of diving injuries, every time they encounter a patient so that they do not miss the opportunity to properly treat these patients. The encounters may not even be an official medical visit. It could be while traveling or on vacation.

If a patient has DCS, immediate 100% fraction of inspired oxygen (FIO2) along with hydration, either oral or intravenous isotonic crystalloids, is an important first step in mitigating the effects. The patient needs referral to a hyperbaric oxygen (HBO) facility experienced in treating DCS. When in doubt, consult a diving medicine specialist, or the Divers Alert Network worldwide emergency number (+1-919-684-9111) for advice and referral. Proper timely management of these injuries yields high rates of success. Missing them can be catastrophic.

Background

Although decompression sickness (DCS), a complex resulting from changed barometric pressure, includes high-altitude–related and aerospace-related events,[1] 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 4,500 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.[2] However, as a testament to physical limitations, in 2012, when he tried to break his own record by diving to 819 ft (250 m), he suffered a narcosis blackout on ascent, causing a violation of his safety and decompression plan. As a result, he suffered a severe type II neurologic DCS that ended his record-breaking career.[3] Humans began experimenting with crude diving bells as early as 330 BCE. These bells 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, and of physicians far from water bodies encountering them. Emergency physicians, all physicians, and other advanced healthcare providers worldwide should know the physiologic effects and management of DCS.

In summary, acute DCS is a purely clinical diagnosis that requires a fair amount of clinical suspicion to avoid missing cases. Most of the time the diagnostic yield is improvement with hyperbaric oxygen (HBO) therapy. No specific tests exist for DCS. When diving is involved, consider determining whether the patient has any pressure-related injuries. Obtain baseline diagnostic studies, but these have no bearing on initial management. They may be useful in the differential diagnosis while undergoing HBO therapy, especially if there is no improvement with HBO. They may also be useful in expanding the knowledge base about this disorder.

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.[4]

While there is no absolute lower age limit, children younger than 12 years should not dive. Although one limited study found no venous bubble formation after a routine, single, shallow dive,[5] another, in persons aged 12-14 years, documented bubbling after 25-minute dives to 10 m (32 ft).[6] 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, one should seek the advice and recommendations of a physician familiar with diving medicine.

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, and unconsciousness) can mimic DCS or arterial gas embolization (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 Carbon Monoxide Toxicity.

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). 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.

Technical diving gases

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 are 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. 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 occur.

Trimix has been used in HBO treatment to shorten treatment courses with success.

Breath-hold diving

The average person is 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, elevated 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.

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 patent foramen ovale (PFO) or atrial septal defect (ASD) and allow neurological DCS. 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.

Pathophysiology

Gas laws

Changes in pressure affect only compressible substances in the body. The human body is made primarily of water, which is noncompressible; however, the gases 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 four 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

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 (15 m) of depth is equivalent in its effects to one alcoholic drink. Thus, by 150 ft (46 m), 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. See the image below.

Illustration of Dalton gas law. As an individual d 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.

Descending also increases the amount of dissolved oxygen. Breathing 100% oxygen at 2 atm (33 ft, 10 m) may cause CNS oxygen toxicity in as few as 30-60 minutes. At 300 ft (91 m), the normal 21% oxygen in compressed air can become toxic because the partial pressure of oxygen is approximately equal to 100% at 33 ft (10 m). For these reasons, deep divers (usually professional or military but increasingly sport divers as well) use specialized mixtures that replace nitrogen with helium and allow for varying percentages of oxygen depending on depth.

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

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. (See the image below.)

Illustration of Henry gas law. If nitrogen is adde Illustration of Henry gas law. If nitrogen is added to a bottle, it diffuses into and equilibrates with the fluid. With a sudden release of pressure (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.

When a critical amount of nitrogen dissolves in the tissues, ascending too quickly causes the dissolved nitrogen to return to its gas form while still in the blood or tissues, causing bubbles to form. Further reductions in pressure while flying or ascending to a higher altitude also contribute to bubble formation. The average commercial airline cabin pressurizes to only 8,000 ft (2,438 m) to save fuel costs. If a person flies too soon after diving, this additional decrease in pressure may be enough to precipitate bubbling. If the bubbles are still in the tissue, they can cause local problems; if they are in the blood, embolization may result. (See the discussion under Prevention for more information.)

Charles law

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

Bubbles

When bubbles are inside the body, such as a trapped gas bubble in the intestine or stomach, the results are 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 decompression sickness (DCS), are discussed here.

Not only does the quantity and size of the bubbles matter, but the type of reactions these bubbles cause is important as well. Location is also important. If bubbles end up in the lung and are not too large, they simple get filtered and exhaled. However, if a right to left shunt is present, such as from a PFO, they bypass the natural filtering effect of the lungs and continue on to the brain or other organs. Nitrogen bubbles are believed to start as minute gas nuclei present before the dive, rather than from supersaturation of the blood and tissues that acts as the seed for large bubble formation.[7] All divers have bubbles.[8] However, few divers develop DCS. Thus, more than bubbles have to be involved. The presence of bubbles alone does not increase the risk of DCS.[9]

Microbubbles precede larger venous gas emboli.[10] These emboli can occlude blood flow in smaller vessels and cause direct ischemia and damage. Bubbles have also been found to alter vascular endothelium through adhesion-molecule-mediated endothelial activation, in addition to activating platelets. In neurological tissue this leads to focal ischemia. The TREK-1 potassium channel mediates this effect in a neuroprotective manner.[11, 12] It was not clear whether the contact of the bubbles with the vascular epithelium (causing damage and platelet response) or if there was a direct mechanism for platelet activation. A glycoprotein (GP)–IIb/IIIa inhibitor inhibited platelet aggregation, suggesting that there is a direct effect.[13]

Microparticles, 0.1- to 1-μm diameter vesicular structures[14] derived from vascular walls, have been found to increase 3.4 times with dives and decompression stress. The microparticles may result from oxidative stress (see the next paragraph).[15] They appear to activate neutrophils and interact with platelet membranes.[8, 16] Endothelial cells, blood platelets, or leukocytes shed microparticles upon activation and cell apoptosis (normal programmed cell death). In particular, the release of platelet microparticles could reflect bubble-induced platelet aggregation. This could be the cause of coagulation and thrombosis, thus interfering with blood flow.[17] Once the bubbles form they create a foreign body interface to which platelets then adhere.[18] In severe DCS significant decreases in platelet count have been documented. These decreases may someday be used as a marker for severity of injury.[19, 20] Microparticles bearing proteins CD66b, CD41, CD31, CD142, CD235, and von Willebrand factor were found 2.4- to 11.7-fold higher in the blood from divers with DCS compared with non-DCS divers.[14]

Endothelial nitric oxide synthase produces nitric oxide through the combination of arginine and oxygen. It is a powerful vasodilator that, through relaxation of smooth muscles, inhibits platelet aggregation and inhibits inflammation. The combination contributes to blood vessel homeostasis. The presence of nitric oxide may reduce bubble formation.[21, 22] However, the increasing partial pressure of oxygen at depth drives the reaction towards nitric oxide. Once the body’s natural processes for dealing with oxidizers, which this is, are overwhelmed, it yields an excess of oxidative excitatory neurotransmitters.[22] Nitrogen dioxide, a nascent gas nucleation site synthesized in some microparticles, initiates decompression inflammatory injury.[16] It is also an oxidizer that exists in equilibrium with dinitrogen tetroxide.[22]

Another contributor to inflammatory vascular reaction lies within the microparticles. Interleukin-1beta concentrations increase in response to high-pressure environments and continue to increase for 13 hours afterwards. This corresponds to vascular damage. Other inflammatory factors adhere to the exterior of the microparticles. The combination of inflammatory agents contributes to the vascular damage.[23]

There appears to be a relationship among bubbles, microparticles, platelet-neutrophil interactions, and neutrophil activation. However, exactly what that relationship is still remains obscure.[8, 24]

Simulated diving conditions with air and oxygen adversely affect cellular respiration through mitochondrial function in fibroblasts.[25]

Organ involvement associated with decompression sickness

As discussed in the section describing the Henry law above, 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 body interface, activating the early phases of blood coagulation and the release of vasoactive substances from the cells lining the blood vessels.[26] DCS is divided into three categories: (1) type I (mild), (2) type II (serious), and (3) 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) cutis marmorata.

Cutis marmorata, cutaneous DCS, is a rash that generally is widespread mottling and/or marbling of the skin or a papular or plaquelike violaceous (blue-red) rash. On rare occasions, skin has an orange-peel appearance. Cutis marmorata typically starts as an intense multifocal itching, then hyperemia develops, followed by the already-described purplish rash.[27] In the past, it was thought to be a benign disorder from bubble formation, with theories for its presence of vascular occlusion ranging from right-to-left shunt (eg, from a PFO), to supersaturation of subcutaneous fat tissues.[28] A newer theory is gas emboli amplification in cutaneous capillaries.[29, 30] One study reports a near 100% presence of PFO on contrast echocardiography.[31] However, similarities of this rash with livedo reticularis or livedo racemose (due to sympathetic overloads), along with a small number of divers with cutis marmorata who also have vague neurologic symptoms, has led to more recent theories of the rash being centrally mediated in DCS.[29, 31] Specifically, a newer hypothesized theory is for gas embolization of the brainstem affecting autonomic control of vasodilation and vasoconstriction.[31]

Lymphatic involvement is uncommon and typically causes 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 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.

Cutaneous abnormalities, joint and muscular pain, and neurologic manifestations (covered in the next section) were the three most common symptoms. The initial symptoms started within 6 hours of surfacing in 99% of cases with an overall mean delay to onset of 62 minutes. The shorter the time to onset, the more serious the symptoms.[32]

Delineation of mild type I DCS symptoms and signs can be useful when considering treatment (refer to the later section on HBO therapy). General fatigue, nondermatomal distribution skin sensory aberrations, rash, pruritus, isolated limb pain (not symmetric), and subcutaneous edema that are not progressive out to 24 hours are all examples. It is important that there are no concomitant spinal or central neurologic symptoms or signs (see the next section on type II DCS for details).[33]

Type II decompression sickness

The following characterizes type II DCS: (1) pulmonary symptoms, (2) hypovolemic shock, or (3) nervous system involvement. Pain occurs 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 occur up to 36 hours later.

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. Patients with the worst outcomes (still having multiple neurological sequelae with less than 50% resolution after hyperbaric oxygen therapy) were those who had onset of symptoms within 30 minutes of surfacing.[34]

Vertebral back pain after a dive is a poor prognostic sign and can be a hallmark of spinal DCS with anticipated poor long-term outcome.[35, 36]

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. Intraspinal pressure and perfusion appear to play important roles in the injury. Just as the cerebrum is contained in a confined, nonexpandable, space, so is the spinal cord. Decreases in blood pressure and/or increases in CSF intraspinal pressure can compromise circulation, thus increasing ischemic injury. Despite improvement in examination findings with treatment, it has been found that there can be significant cord damage as a result. Similar to intracerebral pressure monitoring and drainage, consideration should be given for similar intraspinal pressure monitoring and drainage.[37]

Pulmonary filtration protects the nervous system by stopping bubbles at the lungs. A shortcut, such as a PFO or ASD, can bypass this filtration. Additionally, hypoxia may open intrapulmonary anastomoses, thus also allowing venous bubbles to pass into arterial circulation.[38] 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.[39]

DCS can be dynamic and does not follow typical peripheral nerve distribution patterns. This strange shifting of symptoms confuses the diagnosis of differentiating DCS from traumatic nerve injuries. 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.

MRI studies have seemingly revealed arterial patterns of infarction in spinal DCS.[34]

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 DCS. Mask barotrauma caused a periorbital hematoma in one diver. Physical examination and CT scan of the orbits confirmed the diagnosis.[40]

Ears

Head and neck issues account for 80% of diving illnesses. Of these 65% involve the ears.[41] (Also, see Dysbarism.) 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.[42] 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.[43, 44] In inner-ear DCS (IEDCS), vertigo was the major presenting complaint in 77-100%. Hearing loss occurred in 6-40% and a combination of both in 18%. Additional skin and neurologic symptoms were present in 15%. Symptoms occurred within 120 minutes of surfacing with a median delay of 20 minutes.[45, 46]

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 in 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.[47]

The pathophysiology for IEDCS is believed related to a left to right shunt in the labyrinthine artery.[43] 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 eight times as long compared with the brain (half-times of 8.8 and 1.2 min, respectively).[48] However, more recent research has found a correlation between IEDCS and the presence of a patent foramen ovale; 74-82% of those who sought screening were found to have a right-to-left shunt from PFO (compared with up to 25-30% incidence of PFO in the general population).[41, 45, 46, 49, 50] The vestibular tissue is more vulnerable than the cochlea because the cochlea has greater blood flow, smaller volume, and faster gas washout. This decreases the time that it is vulnerable to arterial bubbles compared with the vestibular tissue.[51]

IEDCS was found to respond slowly to hyperbaric oxygen therapy and incomplete recovery was noted in most (90%).[41] Time/delay to hyperbaric recompression did not change the clinical outcome. Paradoxical AGE is also hypothesized.[46, 49]

Another condition to consider in the differential diagnosis of postdive dizziness is superior semicircular canal dehiscence. It is difficult to differentiate. A key feature is sound- or pressure-induced (Valsalva) vertical torsional nystagmus. A high resolution CT scan of the temporal bones identifies it if it is present.[52]

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 is affected by scuba diving. Mild dehydration has been found to occur in both the intra and extracellular compartments during deep dives.[53] Numerous 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 occur 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. In small arteries, the effects of decompression stress are amplified in a dehydrated state.[54]

A study of simple hematocrits after a single tropical dive found increases that were statistically significant and greater with the depth of the dive.[55] 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.[56] In addition, a swine study found that dehydration significantly increased the risk of severe cardiopulmonary and CNS DCS and of overall death.[57] A human study also found a significant decrease in venous bubble formation with predive hydration.[58] The increase in hematocrit is also associated with capillary leakage. The bubbles can alter the blood vessel walls, allowing protein and fluid leakage. It can becomes so severe as to cause hypovolemic shock.[59]

Hypovolemic shock is commonly associated with other symptoms. For reasons not yet fully understood, fluid shifts from the intravascular spaces to the extravascular spaces. Treat the signs of tachycardia and postural hypotension with oral rehydration if the patient is conscious, or intravenously if the patient is unconscious. The treatment of DCS is less effective if dehydrated.

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.[26] 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.[60, 61, 62] 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, classify type A for the more serious neurologic DCS (strokelike). 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.[63, 64]

Right-to-left shunt

PFO or congenital ASD also come into play in DCS.[65, 66] These defects allow bubbles to pass from right to left circulation, bypassing the screening effects of the pulmonary circulation. This correlates with a higher prevalence of high spinal cord and head (brain)/neck DCS injury. This was more profound when a procedural violation during the dive led to DCS. As mentioned earlier, a significant incidence of IEDCS is associated with right-to-left shunt.[45, 46, 48, 49, 50] ASDs of greater than 10 mm were associated with shunt-mediated decompression injury/DCS. This accounts for only 1.3% of the general population.[67] Patients with only a large PFO had an increased risk of DCS when decompression rules were not violated. Smaller defects usually required a diving violation creating the environment where there are a large number of venous gas bubbles, delayed tissue nitrogen desaturation, and increased right atrial pressure from Valsalva-type straining.[68]

Although the overall prevalence of PFO in the general population is significant (about 15-30%),[69, 70, 71, 72] the prevalence of serious type II DCS is low. In a group treated for DCS, 63% had a right-to-left shunt through agitated saline contrast transcranial Doppler ultrasound examination. In the control group, only 32% had the anomaly. Patients with cerebral, spinal, inner ear, or cutaneous DCS had a higher incidence of the shunt. There is no recommendation for routine screening of general (never had DCS) divers for PFO or ASD.[73] However, in the face of a serious DCS episode, consider the evaluation, for a right-to-left shunt, to guide recommendations for future diving. Serious active divers and professionals might consider routine screening for either atrial defect (see Prevention).[74] Two women with breast pain after diving were found to have PFO.[75]

In two samples of divers, of which about half suffered significant DCS on ascent, a patent foramen ovale was found in 50-53% of those with DCS. All symptomatic divers 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, only 1 out of 4 divers with serious DCS received any PFO screening. All divers who suffer neurological DCS; frequent divers in general, whether amateur or professional; and especially extreme divers; should be considered for screening for PFO or ASD. This should be done with agitated saline contrast echocardiogram testing (see later section on Diagnostic Studies).[71, 76, 77] Another survey of health issues in divers had a cohort of 268 respondents. Of the 27 who reported DCS, 25 had a not-known PFO.[78]

Another interesting feature of patent foramen ovale is the relationship with migraines, in particular those with aura. In limited studies, approximately 48% of migraine patients with aura had a 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.[79, 80]

The diagnosis of the shunt from an atrial defect is through transcranial Doppler scanning, after an injection of agitated sterile saline 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. Transcranial Doppler screening was found to have a negative predictive value of 100% and a positive predictive value of 92%.[81, 82] Therefore, a reasonable conclusion is that divers with a history of migraine, especially those with aura, should consider specific screening for PFO or ASD (see later section on Prevention).

Once found, patent foramen ovale closure in continuing divers appears to prevent symptomatic (major DCI) and asymptomatic (ischemic brain lesions) neurological event during long-term follow-up (see later section on Prevention).[83]

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 (July 17, 1996 off the coast of East Moriches, Long Island, NY), rapid ascents resulting in AGE were uncommon even under stressful conditions (115-130 ft, 35-40 m; 3,167 dives; 1,689 h).[84, 85]

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.[86, 87] Repeated compression-decompression stress acclimated (ie, developed reduced susceptibility) to rapid decompression.[88]

Etiology

Predisposing causes of decompression sickness (DCS) include the following:

  • Inadequate decompression or surpassing no-decompression limits: This includes increased depth and duration of the dives and repeated dives.
  • Doing a dive requiring decompression stops indicating longer and/or deeper dives [89]
  • Inadequate surface intervals (ie, failure to decrease accumulated nitrogen)
  • Failure to take recommended safety stops
  • Flying or going to higher altitude soon (12-24 h) after diving (increases the pressure gradient) [90]
  • Smoking [91]
  • Drinking alcohol the night before diving
  • Cold exposure after the dive
  • Prior history of DCS [89]

A principal cause of DCS is rapid ascent. A major cause of rapid ascent may be panic. Anxiety traits can be identified during instruction.[92]

Individual predisposing physiologic characteristics include the following:

  • Being male [93]
  • Obesity: Obesity had been thought to be a risk factor because nitrogen is lipid soluble. However, studies have shown that neither body fat or body mass index (BMI) correlates with venous gas embolism and resultant DCS. [94, 95] However, one study found a direct correlation between frequency and severity of DCS as BMI increased to obese levels. [96, 97] Another also correlated body mass with risk of DCS. [98]
  • Fatigue
  • Age and poor aerobic conditioning: These do appear to influence risk of venous gas embolism and DCS. [94, 95]
  • Dehydration
  • High-fat meal [99] or diet [97, 100]
  • Illness affecting lung or circulatory efficiency
  • Prior musculoskeletal injury (scar tissue decreases diffusion)

Predisposing environmental factors are as follows:

  • Cold water (vasoconstriction decreases nitrogen offloading)
  • Heavy work (vacuum effect in which tendon use causes gas pockets)
  • Rough sea conditions, strong current [93]
  • Heated diving suits (leads to dehydration and increases nitrogen upload) [84, 101, 102]

Divers who have been chilled on decompression dives (or dives near the no-decompression limit) and then 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 (see the comment below about the US Navy tables). 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, one or more decompression stops are required during ascent to allow delayed diffusion of nitrogen out of the lipid tissues back into the blood. Nitrogen then exhales through the lungs. Current recommendations are for routine decompression stops, even if within the times of the tables. 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 three problems. First, 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. Second, the rapidly expanding use of dive computers takes into account the actual time spent at each depth, rather than just the maximum depth. This allows for more time under water and removes a built-in factor (the shorter maximum depth time) that helps keep divers in the conservative range. Third, the number of casual divers is increasing. This can lead to mistakes from lack of practice of the stringent routine/adherence to safety principles needed

See the discussion under Prevention for more information.

Epidemiology

Frequency

United States

Between 1987 and 2003 the Sports & Fitness Industry Association (formerly 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 6 years of 2000-2006, a decrease of 23% to 3.2 million had occurred. Moreover, by 2012 there were 2.87 million divers. 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.[103, 104, 105, 106] “As of 2015, more than 23 million scuba diver certifications have been issued across the globe.”[107] Worldwide, there are an estimated 7 million active divers.[108] Experience yields a safer diver, though at the other extreme, over confidence can lead to pushing too close to limits.[109, 110]

Due to variability in reporting and collection of information, mainstream medical journal publication of diving-related injury statistics is inconsistent. To improve statistical collection of information, the Divers Alert Network (DAN), based in North Carolina in the United States, acts as a medical information and referral service for diving-related injuries. In addition to this role, it provides education, acts as a clearinghouse for reports of diving-related injuries from around the world, and participates in studies related to diving injuries and illnesses.

Their efforts to be the clearinghouse and repository of injury reports have been hampered in recent years (from 2003 forward) in the United States because of a change in federal law that makes medical confidentiality more stringent and thus their abilities to obtain reports and follow-up that much more difficult.[111] They also have sponsored an ongoing long-term research study entitled Project Dive Exploration (PDE). According to DAN, fewer than 1% of divers experience DCS.[112]

International

See Morbidity and Mortality below.

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.[113] In 2001 in the United Kingdom, they did away with a requirement for mandatory diving physicals. They instead opted for a self-reporting format. An apparent consequence is that an increase in diving deaths in those older than 50 years in the United Kingdom has been noted since 2009.[114]

DAN data also notes a steadily aging trend in their data.[115, 116]

Mortality and Morbidity

Separating mortality data for decompression sickness (DCS) from those for barotrauma is impossible. Pathologists demonstrated little knowledge of diving accidents while performing autopsies and missed the more subtle diving injuries.[117, 118]

Divers Alert Network (DAN) has been tracking diving injuries since the 1980s. They started publishing that information in 1988. The information comes from a variety of sources. When they become aware of an incident, they do their best to investigate and obtain the details of the events and injuries. In 2015, DAN identified 127 recreational diving fatalities worldwide. Another 13 were found that were not recreational. Of those, 67 were either Americans or Canadians who died in those countries and related territories, or overseas. Florida had the most, double that of California, at number two. Males represented 80% of the fatalities, and 90% were older than 40 years. A top cause for fatality, in cases that had an enough information to draw conclusion, is health problems. Over the 28 years that DAN has collected fatality data, they have received reports of 3341 fatalities. During that time, the average number of annual deaths of Americans or Canadians, at home or abroad, has decreased from 90 to 80. In about half (1549) the cases, over 24 years since 1992, a cause of death was able to be determined. Drowning accounted for 66% (1,001), 16% (250) were cardiac related, AGE occurred in 13% (201), other varied issues at 3% (46), DCS at 1% (15), and immersion pulmonary edema was cited in 1% (15). During the approximately 23-28 years of data, the age of fatalities has steadily increased in the older-than-50-years segment. In addition, the body mass index for overweight and obese divers who died has also steadily increased. Between 2004 and 2015, DAN received reports of approximately 610 additional fatalities in the breath-hold (free-diving) community.[119]

In 1995, 590 cases of DCS were analyzed (of a total 1,132) by DAN.[112] 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. In 2015, DAN received 3,589 emergency calls of which 2,124 were determined to be a diving-related medical issue. Of those, 599 were classified. Type I DCS cases breakdown to be cutaneous at 173, pain only at 138 (23%), inner ear at 31, and pulmonary at 9. Type II DCS cases represent 279 (47%). Barotrauma cases accounted for 1,211 cases (see Dysbarism), of which 41 were due to AGE.[119]

A study from the US military in Okinawa reported 94 cases of DCS over 7 years.[120] The annual incidence of DCS was 13.4 cases per 100,000 dives or 1 per 7,400 dives.

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

In another study, the lifetime incidence of DCS was 1 case per 5,463 dives. For severe DCS, it was 1 case in 20,291 dives. It was also found that the more experienced divers were less likely to get DCS, presumably through more meticulous adherence to safety concerns and safer diving profiles.[121]

Internationally, minor incidents related to diving occur in 1.3% of dives. Decompression injuries (not separated as to dysbarism or DCS) occurred at a rate of 2 cases per 10,000 dives.[122]

The DAN PDE (Project Dive Exploration) study has followed about 8,000 divers for around 100,000 dives since 1995.[115] The incidence of DCS in this population is 3.6 cases per 10,000 dives (or about 36 cases since the study began). Through the PDE 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. A more recent summary of the PDE data reports 10,248 divers, of which 71% are male with a mean age of 41 years. They completed 122,129 dives of which over 17,000 involved Nitrox gas. There have been 38 episodes of DCS, for a rate of 3.1 cases per 10,000 dives.[119]

DAN also participates in a diver's insurance program for injuries while traveling in general (though most of the travel is diving related).[116] The incidence of diving-related injuries, although not just DCS, is around 20.5 claims per 10,000 insured over a 7-year period.[123] The annual death rate from the same data was between 12 and 23 deaths per 100,000 insured.[124]

DAN PDE data for 2004 is based upon almost 24,000 dives.[115] In this group, about 1,300 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.

A large New Zealand charter dive operation also keeps detailed records. During a 6-year period, they had 97,144 dives. Of these, there were 55 injuries from scuba diving. The majority, 35, were soft-tissue mechanical injuries. There was one cardiac-related death. Only four divers were diagnosed with DCS and received HBO therapy. The prevalence was 0.41 cases per 10,000 dives.[125]

Available mortality rates are as follows:

  • In South Africa, the mortality rate was found to be as low as 0.016%. [126]
  • The US military in Okinawa reported fatalities at 0.0013% (1.3 deaths per 100,000 dives). [120]
  • A New Zealand report states that the most common cause of death was drowning, but pathologists were frequently imprecise. [118]
  • 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 a 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 to 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, resulted 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. [127] 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. [128]
  • An increase in diving deaths in those older than 50 years in the United Kingdom has been noted since 2009. [114]

Prognosis

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

Patient Education

Diver education is paramount. They must learn the symptoms, signs, and management of decompression sickness (DCS) and AGE to facilitate early recognition and treatment. Of 590 patients with DCS whose characteristics were studied (results discussed in Epidemiology), nine continued to dive after developing neurologic symptoms, including one 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. In addition, 35% of all cases were reported to DAN more than 4 hours after symptom onset.

For patient education resources, visit the First Aid and Injuries Center. Also, see the patient education articles Barotrauma/Decompression Sickness and The Bends - Decompression Syndromes.

 

Presentation

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 via hyperbaric oxygen (HBO). Therefore, having the forethought to ask about pressure exposure aids in the diagnosis. Having a familiarity with diving aids the healthcare provider in raising concern for pressure-related injuries. However, some patients have symptoms temporally linked to diving that ultimately are determined to be nondiving-related issues. The take-home point is to consider decompression sickness (DCS) as a possibility but not to exclude others, especially if symptoms are atypical and the dive profile would not normally be expected to cause a problem.

The examiner needs to elicit the following specifics about the dive(s):

  • 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 (ie, consider currents, distance swam, water temperature, and primary activity [eg, wreck diving, artifact recovery, or commercial work])
  • Gases and equipment used (ie, compressed air, rebreathing equipment, mixed gases, or none as in a free dive)
  • Problems encountered (eg, violation of no–decompression-limit dive tables, equipment, entanglement, dizziness, or marine bites or stings)
  • Patient's physical condition before, during, and after the dive (eg, fatigue, hydration, drug or alcohol intake, fever, vertigo, nausea, overexertion, or pulled muscles)
  • First aid delivered (ie, oxygen, positioning, medications, and 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 Examination

Physical signs and examination findings in decompression sickness (DCS) 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 arterial gas embolization (AGE) and DCS

For 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.

For 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.

Differentiating carbon monoxide poisoning

The symptoms of carbon monoxide poisoning (eg, dyspnea, headache, fatigue, dizziness, visual changes, and unconsciousness) can mimic DCS or AGE. Sources for this carbon monoxide can include improper filling of tanks or boat engine exhausts, among others. 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. Also see Carbon Monoxide Toxicity and Carbon Monoxide Screening.

Complications

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

 

DDx

Diagnostic Considerations

Diagnostic considerations include the following:

  • 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
  • Toxicology - Carbon monoxide poisoning, marine life envenomation, substance abuse, medication adverse effects

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

Differential Diagnoses

 

Workup

Laboratory Studies

Acute decompression sickness (DCS) is a purely clinical diagnosis that requires a fair amount of clinical suspicion to avoid missing cases.[34] Most of the time, the "test" is improvement with hyperbaric oxygen (HBO) therapy. No specific tests exist for 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 undergoing HBO therapy. They may also be useful in expanding the knowledge base about this disorder.

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 (ie, shock), obtain appropriate resuscitation studies.

For changes in mental status, evaluate the following:

  • Blood glucose level, CBC count
  • Sodium, magnesium, calcium, and phosphorous levels
  • Oxygen saturation
  • Ethanol level and drug screen
  • Carboxyhemoglobin level

For shock, evaluate the following:

  • Blood glucose level, CBC count
  • Electrolytes and BUN level
  • Creatinine levels, lactic acid
  • Type and screen/cross
  • Prothrombin time/international normalized ratio, activated partial thromboplastin time
  • Carboxyhemoglobin level

Imaging Studies

Chest radiography

Because dysbaric injuries involving the lungs and chest can occur concomitantly with decompression sickness (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 scanning

If mental status does not initially improve in response to hyperbaric repressurization, consider other etiologies. Pursuing a noncontrast CT scan of the head to evaluate for structural issues is part of that consideration.

Chest or abdominal/pelvis CT scanning

In a patient with persistent symptoms of dyspnea or discomfort in the thorax that have normal conventional chest radiographs, CT scanning can identify subtle or early findings for pneumothorax or pneumomediastinum. If available, noncontrasted CT does not take long to accomplish. Identification of these barotraumas before doing HBO therapy is useful as the pressure changes can exacerbate these conditions.

Differentiating pneumoperitoneum from DCS as the cause for abdominal pain can be of similar importance. A unique gas pattern has been documented in the venous systems related to DCS.[129] Gas appeared in the portal venous system, omental veins, and peripheral veins in the pelvis.

See Dysbarism for more information.

MRI

MRI has been found useful in the management of neurologic DCS.[130, 131, 132, 133] 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 arterial gas embolization (AGE),[134] but iy 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 after the first, or subsequent, treatment.[35] A normal MRI correlates with better outcome.[135] Do not delay HBO treatment to obtain an MRI.

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.[136]

Note that negative MRI findings do not exclude the possibility of AGE or DCS. Also, improvement in MRI findings does not necessarily correlate with clinical improvement.[137] It has also been correlated with neuropsychological deficits in older divers.[138]

Diffusion Tensor MRI (DTI) has been demonstrated to be useful for investigating DCS.[139]

MRI in a guinea pig model was able to identify small bubbles and blood in the inner ear. It may have future utility in management of inner-ear DCS.[140]

The decision to pursue HBO referral should be based on the purely clinical presentation and not be guided, or delayed, by obtaining MRI or other diagnostic findings.

Other Tests

Other tests may include ECG and/or oxygen saturation evaluation.

Procedures

Diagnostic repressurization

If diagnosis of decompression sickness (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, tension pneumoperitoneum, and subcutaneous emphysema.

See Dysbarism for more information.

 

Treatment

Prehospital Care

Extricate the patient from the water. Immobilize if trauma is suspected.

Generally, in-water recompression (IWR) is not believed to be a safe option. Problems with air supply, hypothermia, potential oxygen toxicity with seizure, dehydration, and the uncontrolled environment make it less than ideal and increase the risks of drowning.[141] However, in remote areas without reasonable-distance hyperbaric oxygen (HBO) chamber support, this may be the only option.

Studies exist of indigenous native fishermen divers. 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 decompression sickness (DCS).[142, 143, 144] In Yucatan, Mexico, an alarming incidence of DCS is present.[145] There is a similar population in Vietnam.[146] The economic drive for valuable ocean species, coupled with the nature of their remote location, along with general education, conspire to create high rates of DCS. Education (see Prevention) and IWR have been shown to be appropriate first-aid measures. Much more research needs to be performed on the concept of IWR, as 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.[142, 143, 144] A shorter IWR protocol is also in use in the remote Northern Pacific Clipperton Atoll in an attempt to address the above concerns.[141] IWR has been used successfully in the fishing population in Vietnam. Better outcomes were obtained when the recompression was done with oxygen instead of air.[146] IWR is probably not for the extremes in DCS. Mild type I DCS will probably improve with 100% oxygen and rehydration. Type II DCS with disabling signs would make IWR too risky.[147]

A consensus statement from Divers Alert Network (DAN) and the Undersea and Hyperbaric Medical Society (UHMS) addresses the concept of IWR. They recognize that many diving activities occur in remote areas that lack the resources for an HBO therapy and are distant from appropriate facilities. In the case of significant or progressive symptoms, IWR may be a reasonable emergent alternative to avoid delays, sometimes many hours, but with the need for specific training, equipment, and protocols.[33] The requirements are as follows:

  • Enough properly trained personnel that understand the protocol [141, 146, 147, 148] and principles, in addition to the risks: In addition to the patient, this would include a continuous dive buddy and a surface supervisor at a minimum.
  • Certification in the use of 100% oxygen for diving emergencies
  • Adequate thermal protection, enough 100% oxygen, a writing board for communication, and a means for maintaining a constant depth (no deeper than 30 ft [9 m]).
  • Either a full-facemask or a mouthpiece-retaining device: The concept here is that if the DCS diver were to have a seizure, due to oxygen toxicity or the DCS, or lose consciousness for another reason, he or she would still receive the oxygen without risk of aspiration while the dive buddy starts the ascent to the surface. Two available products are the Dräger or rEvo, safety mouthpieces with retaining head straps. [149] The former may not be in production anymore.
  • Restriction on the use of technical specialty gases: Only use 100% oxygen. [148]
  • Diving medicine specialist consultation: Seek out a diving medicine specialist as soon as is possible for consultation.

Administer 100% oxygen, intubate if necessary, and intravenously administer isotonic crystalloid (saline or lactated Ringer solution).

The use of first aid oxygen has proven so beneficial that the 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 occurred 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.[150] The consensus statement from DAN/UHMS highlights the importance of 100% normobaric (not HBO) treatment by trained individuals as an important first aid measure. They also mention that if there is a limitation in supply (due to a prolonged transport), less than 100% can be used with the intent being to continue some oxygen therapy throughout the transport until reaching definitive medical care.[33]

Many divers dehydrate for a number of reasons delineated earlier in this article. Oral rehydration can be appropriate if not contraindicated. These fluids are ideally isotonic but can be regular drinking water. Carbonation, caffeine, and alcohol are to be avoided. If oral fluids are contraindicated, administer isotonic crystalloid intravenous fluids for rehydration until urinary output is 1-2 mL/kg/h. Avoid intravenous dextrose solutions. Rehydration improves circulation and perfusion. It also decreases postdive venous gas emboli formation.[33]

Aspirin is commonly considered and given in diving accidents for its antiplatelet activity if the patient is not bleeding or allergic. However, there are no current data to support this practice.[151] The nitrogen bubbles interact with platelets, leading to adhesion and activation, which is thought to contribute to microvenous obstruction and resultant ischemia in DCS; however, no studies or trials of the effect or benefit of aspirin on this process have been conducted. Giving aspirin could increase bleeding, especially in severe DCS.[152, 153, 154] Other drugs that have been used in DCS have insufficient clinical evidence. These include nitroglycerine, corticosteroids, lidocaine, and pentoxifylline.[33]

Thus far, there is no substantive data showing a benefit for other adjunctive treatments, such as recompression with helium/oxygen, and in the past, NSAIDs.[155] However, a benefit has been found for NSAID use in conjunction with HBO therapy.[33]

Perform cardiopulmonary resuscitation and advanced cardiac life support, if required, as well as needle decompression of the chest, or abdomen, if indicated.

Do not put the patient into the Trendelenburg position. Placing the patient in a head-down posture used to be a standard treatment of diving injuries to prevent cerebral gas embolization. Avoid this practice.[33] The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier.[156] It also wastes time and complicates movement of the patient.

Transport to the nearest emergency department 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 a standard treatment of diving injuries to prevent cerebral gas embolization. Avoid this practice.[33] The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier.[156] It also wastes time and complicates movement of the patient.

Perform intubation and aggressive resuscitation including advanced cardiac and trauma life support. Be alert for the potential of tension pneumothorax and perform needle decompression followed by chest tube thoracostomy, if indicated. Also be aware of the potential for pneumoperitoneum from ruptured viscus. The air collection can be so great as to interfere with hemodynamics. Emergent needle decompression of the peritoneum is the corrective procedure.

Many divers dehydrate for a number of reasons delineated earlier in this article. Oral rehydration can be appropriate if not contraindicated. These fluids are ideally isotonic but can be regular drinking water. Carbonation, caffeine, and alcohol are to be avoided. If oral fluids are contraindicated, administer isotonic crystalloid intravenous fluids for rehydration until urinary output is 1-2 mL/kg/h. Avoid intravenous dextrose solutions. Rehydration improves circulation and perfusion. It also decreases postdive venous gas emboli formation.[33]

Aspirin is commonly considered and given in diving accidents for its antiplatelet activity if the patient is not bleeding, or allergic However, there are no current data to support this practice.[151] The nitrogen bubbles interact with platelets, leading to adhesion and activation, which is thought to contribute to microvenous obstruction and resultant ischemia in DCS; however, no studies or trials of the effect or benefit of aspirin on this process have been conducted. Giving aspirin could increase bleeding, especially in severe DCS.[152, 153, 154] Other drugs that have been used in DCS have insufficient clinical evidence. These include nitroglycerine, corticosteroids, lidocaine, and pentoxifylline.[33]

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 or HBO specialist to determine if symptoms are related to diving and if HBO therapy is appropriate. Before contacting the specialist, ideally, complete a detailed neurological examination. However, this is not always possible if the patient is not with a physician. Also, detailed information about the dive and symptoms should be readily at hand for discussion. Those engaged in scuba diving should have the means (communication equipment) and the contact information for the regional diving medicine specialists and HBO centers, in addition to the DAN contact numbers. They should also know how to access the local emergency medical systems and should know their capabilities. Early involvement of a specialist in diving medicine can confirm, allay, or heighten concerns related to symptoms post diving. They can also direct emergency therapy and decrease time to definitive treatment.[33]

An increasing number of divers have significant medical issues. Many acquired them as they have aged. Surveys of health issues in divers found a group with significant health problems. Forty-nine percent had consulted a diving medicine specialist. Twenty-three percent modified their diving to decrease risk.[78, 157]

Divers Alert Network

Divers Alert Network is an excellent resource, especially if local support is not available. While their emergency contact numbers are below, visit their Web site at International DAN or IDAN for the full contact information. 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 World[wide] Emergency Number: +1-919-684-9111 (accepts collect calls)
  • DAN America Emergencies: +1-919-684-9111 (accepts collect calls); nonemergency: +1-919-684-2948
  • DAN Brasil Emergencies: +1-919-684-9111 (accepts collect calls); in Brasil:  0800 684 9111
  • DAN Europe Emergencies: +39-06-4211-8685; nonemergency: +39-085-893-0333
  • DAN Southern Africa Emergencies: 0800-020-111 (within South Africa); +27-828-10-60-10 (outside South Africa, accepts collect calls); nonemergency: 0860-242-242 (within South Africa), +27-11-266-4900 (outside South Africa)
  • DAN Japan Emergencies: +81-3-3812-4999; nonemergency: +81-45-228-3066
  • DES Australia: 1-800-088-200 (toll free within Australia—English only); +61-8-8212-9242 (from outside Australia—English only)
  • DES New Zealand: 0800-4DES-111 (within New Zealand—English only)
  • Korean Hotline: 055-549-0912 (Korean and English)
  • China: +852-3611-7326

Note: Numbers do change from time to time. See https://www.diversalertnetwork.org/contact/international.asp for the latest list.

HBO treatment

Again, acute DCS is a purely clinical diagnosis that requires a fair amount of clinical suspicion. When the slightest suspicion or possibility is noted, timely transfer with 100% FIO 2 oxygen for HBO should be pursued.[34] Accessing consultation as discussed above is advised if any confusion or concerns are noted.

Patients with mild type I decompression sickness (DCS) probably do not require treatment other than breathing pure 100% FIO2 oxygen and hydration. However, as discussed with regard to inner-ear DCS (IEDCS) and cutis marmorata, there are newer theories that they are more serious and they should be considered for HBO therapy. Divers with type I DCS symptoms do, however, require observation for 24 hours, 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.[33]

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 breathe the oxygen via mask, but the ambient environment is not supplementally oxygenated. In addition, the ability of attendants to be in with the patient allows for resuscitation or other intensive treatment in the sickest of patients. The number of hyperbaric chambers across the United States has increased rapidly as HBO therapy has extended to treat is many clinical entities ranging from wound care to multiple sclerosis. However, of 361 chambers contacted and interviewed nationwide, only 43 were judged to have the equipment and staff to treat high-acuity patients. This was thought to be an inadequate number for the United States.[158]

The basic theory behind HBO therapy is 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.[159, 160]

Treatment tables govern the exact combination of timing and depths. Developed primarily by the US Navy, there were some minor modifications by the US Air Force. Treatment Table 6 is most commonly used for initial treatment. Follow-up treatments followed Treatment Table 5. The US Navy introduced Treatment Table 9 in 1999 for follow-up treatment in incomplete resolution of DCS. Both Tables 6 and 5 start at a depth of 60 ft (18 m). In contrast, Table 9 starts at 45 ft (13.5 m). The advantage of Table 9 is that there is less risk of oxygen toxicity as the patients are breathing 100% oxygen. This decreases the risk to not only the patient, but the chamber attendant, if there is one.[161] However, more detail concerning the tables are beyond the scope of this article. While most improve with a single HBO treatment, 38.5% have relapses, half of those within 24 hours. Observation for 24 hours is strongly recommended after HBO treatment.[162] 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.[163] In Israel, 48% had complete recovery with HBO, while another 48% had partial recovery. Unfortunately, 4% did not respond to the therapy.[164] Yet, HBO effectiveness rates as high as 99% have been reported.[32] Of 103 patients (75% male), 53 (51%) had complete relief (with 28 only requiring one treatment), 45 (44%) had partial relief, and 5 (5%) had no relief of symptoms.[165]

Delay to treatment has long been felt to yield worse outcomes. Studies that are more recent conflict with that traditional thinking. In one study, a longer delay to treatment was related to incomplete recovery but the increased risk appeared negligible.[166] In another, delays in treatment of longer than 17 hours could not be correlated with increased number of HBO treatments or worse outcome in DCS.[167] Instead, the severity of the neurologic dysfunction and rapid onset of symptoms after surfacing were the main factors in predicting the severity of DCS and the resistance to treatment with worse outcomes.[32, 34, 166] In Israel, they specifically looked at delayed recompression defined as greater than 48 hours. They found no significant difference in outcome between early and delayed treatment groups. Complete recovery occurred in 78% versus 76%, respectively; partial recovery occurred in 15.6% versus 17.1%, respectively; and no improvement occurred in 6.2% versus 6.6%, respectively.[168]

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. Another mentioned adjunct to HBO includes negative-pressure breathing.

An interesting area of research relates to the use of intravenous perfluorocarbon (PFC) emulsions.[169, 170] PFCs are synthetic liquids made up of carbon and fluorine that has the ability to dissolve significant amounts of gases especially oxygen. As they are hydrophobic, they have to be emulsified in order to use them intravenously in water based organism such as humans. This is being studied as a temporary blood substitute in numerous clinical settings.[171] It is being studied in the setting of the treatment of DCS in conjunction with HBO therapy.

One such PFC, trade name Oxycyte, provides protection and improves outcomes in spinal DCS at 5 mL/kg IV. Improved oxygenation is the presumed mechanism.[172, 173, 174] PFCs 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 (this last effect is hypothesized but not shown).[175, 176] There was concern for decreased platelet counts as both decompression and PFCs appeared to cause that decrease. Oxycyte PFC was not found to affect platelets or clotting or bleeding.[177] The positive effects of PFCs are further enhanced by oxygen prebreathing (before HBO treatment) with increased oxygen delivery.[178] A swine study found no benefit, but also no harm, in using HBO treatment.[179]

With early recognition and treatment, more than 75% of patients improve. Even with significant delays in recognition and treatment, positive results are obtained.[180, 181] 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.[182, 183]

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, consider both conditions in the differential diagnosis, and treat the patient for both. One recommendation is to perform immediate tympanocentesis and then to follow with HBO therapy. IEDCS is less responsive to HBO treatment than is DCS affecting other sites. Incomplete recovery has been reported in 68% of those receiving HBO therapy.[46] 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 arterial gas embolization (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 delays 5 hours, the mortality rate approaches 10%. More than 50% of the survivors experience residual signs.

Transfer to a hyperbaric facility is strongly advised. An important issue is timely transport of the patient to the closest hyperbaric facility. Frequently, this is accomplished by land transport, although air transportation is occasionally required. The effort is 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 [152 m] above sea level depending on the dive location).[33, 184] This can be difficult when there are mountains to traverse in flight. In this situation, explore options other than rotary-wing transportation to the closest chamber. Another potential issue is bubble creation due to the vibration of the helicopter.[185] 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, and military C-130 Hercules).

Those involved in diving activities, especially in remote areas, should arrive with a plan, including contact information, for evacuation if it were to become necessary. These types of evacuations, if there are no local HBO facilities, can be excessively expensive. Thus, part of the planning could be a consideration of commercial insurance.

Prevention

Key to preventing decompression sickness (DCS) is exercising conservatism in the diving profile and always putting safety first. Education is key in this regard. In Vietnam, severe DCS in fishermen divers was decreased by 75%, and mortality also dropped, after a concerted educational effort.[146] This is important as there are real human and economic costs regarding DCS in fishermen divers. During a 3-year period in Yucatan, Mexico, 282 divers received treatment for DCS. The total societal economic impact was $1.6 million (US).[186] Even with education and a conservative approach, DCS can still occur. The total amount of saturated nitrogen at one time was thought 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. Further research and thought suggests that the rate of ascent from depths may be a more critical factor.[109, 110]

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).[187, 188] 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 off gassing, is much slower. Thus, even a no-decompression dive at 60 ft (20 m) for 20 minutes maximally saturates spinal tissues. As mentioned earlier, spinal cord is tissue 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, data from a European study revealed that increasing this ascent time to 18 minutes eliminated the dangerous bubbles. Therefore, one would need one or more additional stops at deeper level(s) to lengthen ascent time adequately and thus protect against DCS. Research has shown that a safety stop of 2.5-5 minutes at 50 ft (15 m) in addition to another stop at 20 ft (6 m) for 3-5 minutes decreases 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.[188] 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. Adding scuba tanks at each safety level is prudent in case diver air supplies reach a critical level.

Breathing 100% fraction of inspired oxygen (FIO2) oxygen during the decompression stops may help prevent DCS.[189] One should consider the partial pressure of oxygen at the decompression stop depth to prevent toxicity. Being active during the decompression stops may also decrease the likelihood of bubble formation.[190, 191, 192]

Close attention to adequate hydration before and immediately after a dive may also have protective effects. See Pathophysiology for discussion of the mechanism. 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 caffeinated and should be alcohol free.

The culture of diving, at least in military naval diving, may have some impact on prevention of diving accidents. The two most common causes of naval 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.[193] 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 dive master, and the generally isolated situation of a number of divers not knowing each other, could lead to the same overall environment.

When an air bubble expands within a normally air-containing structure such as ears, sinuses, lungs, and GI system, a problem emerges. Another issue is when nitrogen that is saturated in tissues and blood expands with decreasing pressure. Normally, it returns to the lungs and is exhaled. It does not have any other ready exit to the outside. When the bubbles occur, they cannot be exhaled from the lungs.  They can interfere with blood flow directly causing ischemia, or their expansion in tissues causes dysfunction of those tissues. If in a sensory nerve‒containing area, such as the synovium of the joints, they can cause pain. This causes DCS. However, another mechanism is also at work. That is the interaction between the bubbles and the normal blood clotting system. The interface causes clot formation and inflammation, which further increases ischemia and dysfunction.

To this point, the major way to avoid this bubbling has been through conservative diving using tables or computers based on the experiences of fit military divers. By staying within the table parameters, 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.[194] The next step in the process to avoid DCS was to ascend slowly. The recommended ascent rate has decreased steadily, as mentioned above, to the point where the recommendation is to stop ascent at decompression stops to allow the exhalation of nitrogen gas, rather than it bubbling in the blood.

Despite these measures, individuals with similar body types and diving the same profiles resulted in some getting DCS and others not. The hope is that further research will decrease the risk and incidence of DCS.

Predive

The gas nuclei and nitrogen interface appear to be key in better prevention strategies regarding DCS. In particular, the protection appears to relate to the interplay of 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. Administration of a nitric oxide donor decreases the number and size of bubbles.[195] 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 a dive, was found to provide this same level of protection by decreasing bubble formation.[196] Because it is arginine and oxygen that are converted by nitric oxide synthetase to nitric oxide, one might surmise that taking the common L-arginine amino acid would help drive the equation to nitric oxide. Caution is advised as this has not been studied in this realm. In relation to erectile dysfunction, nitric oxide plays a role in erection. Apparently, significant improvement has not been found and it is hypothesized that some other mechanism prevents it.[171]

Toxic effects of oxygen under pressure have also been studied. Oxidation and free radicals may also be important instigating factors. It causes vasoconstriction, which causes ischemia, activation of the inflammation cascade, and subsequent damage to the vascular endothelium. Antioxidants, maintaining normal hemostasis, and preventing inflammatory responses may help stop the DCS process from starting.[197] After a DCS neurologic injury, many (about 30%) have incomplete recovery despite appropriate management. Inflammatory changes are believed to be at least part of the reason. There has been study of several substances in this realm, and preliminary data suggest that they may be useful. Fluoxetine, a common antidepressant medication in the serotonin-specific reuptake inhibitor (SSRI) class, has been found to decrease the incidence of DCS and improve motor function recovery by the limiting the inflammatory process.[198] It is thought to be safe in diving, as well as protective against DCS.[199] Based on rat models, it decreases inflammation through cytokine interleukin 10 suppression.[200] Ascorbic acid 2 g daily for 6 days before a dive decreased neutrophil activation and microparticle generation.[15] Simvastatin has been found to decrease the incidence of DCS in a rat population through its anti-inflammatory properties.[201] Again, the reader is cautioned about taking any substance with the end goal of decreasing DCS until more advanced studies are completed and the individual has discussed their use with a physician well versed in diving medicine.

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.[202] The timing of this exercise appears to be key. A period of exercise of 90 minutes in rats and 40 minutes in humans timed at 20 hours and 24 hours before the dive, was found to have significant long-lasting effects on the number and size of nitrogen bubble formation.[202, 203, 204, 205] 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.[206, 207] The exercise at 24 or 2 hours predive appears to affect bubble formation as it has no effect on enhancing nitrogen washout.[208] It also did not decrease the median number of circulating venous gas emboli.[209]

In one study, there was demonstration that the positive effect of the exercise the day before was eliminated by a second period of exercise prior to the dive. 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.[210, 211] The next step is to see exactly what biochemical effects the exercise causes. Nitric oxide appears to be the protective agent in the predive exercise.[64]

Regular exercise, physical conditioning, and diving also appear to have a protective effect against bubble formation and DCS.[212] In addition, a single HBO treatment 18 hours before a dive protected swine from DCS, possibly through induction of heat shock proteins.[213]

So, the question is what should the average diver do, or not do, based on 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 evidence has not yet been reached in the diving literature. Specific medical recommendations cannot be made because the knowledge has to be applied with consideration of the individual. Consultation with a physician experienced and knowledgeable in diving medicine is strongly advised.

Clearly, the benefit of aerobic exercise the day prior to a dive is evident. For the many recreational divers who 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 means being aerobically and strength conditioned. This should be completed in consultation with a physician, in particular one with experience with the recreational activity.

Only take medications 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. Others also mentioned are L-arginine, fluoxetine, ascorbic acid, and simvastatin, with the same caution advised for all.

A period of prebreathing normobaric (regular oxygen bottle) 100% FIO2 oxygen for 30 minutes was found to decrease venous bubble formation for the subsequent dive and repetitive dives afterwards with no further prebreathing.[152, 214] In swine models, prebreathing oxygen at depth for as little as 5 minutes before rapid decompression helped prevent type II DCS. When breathed for 15 or 45 minutes, it decreased type I DCS symptoms.[215] It also was found in swine models to decrease venous ischemia and osteonecrosis from DCS.[216] In a rat model, oxygen prebreathing was not found to decrease DCS, but was found to decrease inflammatory reactions, and protein infiltration, in lung tissue.[217] As with the statement about nitroglycerin above, oxygen is a medical gas and its use needs to prescribed by a physician. In addition, if oxygen were to be used at depth, the toxic effects of partial pressures of oxygen must be considered.

A study conducted on Sprague-Dawley rats using 79% helium/21% oxygen predive (helium preconditioning) also showed a benefit. There was a decrease in DCS incidence, delay in onset of DCS, decreased decompression-related neurological issues, and decreased depression of platelet counts. Administration of the helium-oxygen mixture was for 5 minutes, followed by 5 minutes on room air, then repeated for a total of 3 cycles over 30 minutes.[218]

In addition, a 30-minute predive sauna session at 65ºC (149ºF) was shown to decrease venous bubble formation, although the mechanism was not known.[219] Nowadays, the mechanism is being demystified. A heat stress of 45ºC/113ºF for 1 hour decreased nitric oxide synthetase activity. It potentiates heat stress protein (HSP)70 and decreased HSP90. Glutathione (GSH) activity was found inversely related to the nitric oxide synthetase activity.[220] The protective effects of HSP70 are believed to be related to the antioxidation and antiapoptosis.[221] It showed an effect on decreasing vascular gas emboli, along with decreasing vascular dysfunction as measured through “flow-mediated dilation.” Vibration decreased the emboli,[222] and dark chocolate only decreased the “flow-mediated dilation.”[223]

In contrast to this, being warm during the bottom portion of a dive actually increases nitrogen uptake, whereas being cool during that phase of the dive decreases uptake. On ascent, the reverse is true. Being warm on ascent increases off gassing of nitrogen, while being cool delays this process. In this modern age of dry suits and suit warmers, one might be tempted to manipulate the temperature to be cool on descent and at the bottom and warm on the ascent. One is cautioned against doing this, as being too cool at the bottom can inhibit overall functioning and being too warm on ascent can promote localized gas bubbling.[101, 102]

What to do after the dive is less clear and needs more investigation in less-fit populations. Although the research appears promising that exercise after diving does not have an adverse effect and that some benefit may exist, the research is insufficient to recommend any changes.

Postdive activity and exercise are controversial. Intense activity after a dive was believed to promote bubble formation. In small studies on trained, fit, military divers, a positive benefit has been found for mild exercise, at 30% of maximal oxygen uptake, during the 3-minute decompression stop on ascent. Other studies incorporating similar aerobic exercise, at 80% of maximal oxygen uptake, starting at 30 minutes and 40 minutes post dive, have failed to demonstrate any adverse effects on trained, fit, military divers.[192] Postdive exercise is believed to dilate intrapulmonary arteriovenous anastomoses. This allows for a mechanism of right-to-left shunt and thus arterialization of the venous gas emboli (bubbles). As a result, the incidence of DCS increases.[224]

A puzzling situation is when an individual experiences DCS when all facets of the dive appeared normal and highly conservative. This prompted a search for other possible influencing etiologies. The identification of the injured diver’s thrombotic state is 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.[225, 226] These three 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 be under the advice of a physician.

Current research is aiming at fine-tuning the prevention of DCS. Transcranial, precordial, and subclavian vein Doppler examination, along with echocardiography and regular ultrasonographic imaging, have been used to detect the presence of bubbles in the vascular system of the volunteers being studied.[182, 227, 228, 229] At the same time, various HBO decompression models are being evaluated using the same studies.[230, 231] As the database expands across the full spectrum of divers (not just young, healthy divers), the tables and recommended dive profiles 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.[232] S-100B is a sensitive biomarker being studied in brain injury in general and neurologic DCS specifically.[233] Serum procalcitonin has been suggested as a potential decompression stress biomarker. Endothelial damage is theorized to increase permeability and inflammatory cytokines, leading to the elevated levels.[234] D-dimer is a biomarker for activation of coagulation. In combination with a severity score, it improved judging of the severity in neurological DCS.[235] Lactate dehydrogenase (LDH) is a marker of cell injury that has been used in decompression research.[236]

Increased hematocrit correlates with hydration status after diving. The importance of adequate hydration has already been discussed as a risk factor in DCS. Platelet count decreases can correlate with increased platelet aggregation. This is one of the contributing causes of DCS.

Studies have identified a medication class with an adverse effect. Sildenafil, a phosphodiesterase-5 blocker, was found to promote the onset and severity of neurological DCS.[21] It is a potent smooth muscle relaxation vasodilator that is used in erectile dysfunction. Several medications are available in this class. Of note is that there are pulmonary hypertension medications also in this same class. Many divers engage in diving while on vacation, when sexual activity may increase. Many of these medications are available without a prescription in other countries. Thus, divers must be aware of the potential for this class to worsen DCS and avoid their use before diving. The half-lives of these medications range from 4 hours for sildenafil and vardenafil to 17.5 hours for tadalafil.[237] Clearance of a medication from the body requires 4-5 half-lives. Thus, the time to clear sildenafil and vardenafil would be 16-20 hours and for tadalafil it would be 70-87.5 hours, about half of a one-week vacation. Numerous common medications can prolong the effects of these medications. A diver prescribed one of these medications should discuss their use with the prescribing physician and consider consultation with a diving medicine specialist.

One study found a patent foramen ovale (PFO) or atrial septal defect (ASD) in 56% of those with DCS.[238] Closure of documented right-to-left shunt appears to prevent both symptomatic DCS and asymptomatic brain ischemia.[83, 239, 238] However, routine screening of all divers is not recommended. Also controversial is prophylactic transcatheter closure of a PFO without documented DCS. As mentioned earlier, only large PFOs appear to greatly increase the risk in diving. The complication rate for this procedure is about 1%, which is much greater than the incidence of developing serious neurologic DCS. A proper medical approach to everything is to balance risk versus benefit. In this case, the weight appears to angle more towards risk. A better approach is to screen those divers who have developed DCS of the cerebral, spinal, inner ear, and cutaneous types. Also for consideration would be divers with a history of migraine with aura and ischemic strokes (especially if younger). The screening study is agitated saline echocardiography under strict protocol, with meticulous technique and provocative maneuvers.[240, 241, 242] Those individuals found to have a PFO should then consult closely with a diving medicine specialist. It may be that using the strategies mentioned in this article in a very conservative manner is a better approach to mitigate risk than would be a recommendation for a surgical procedure. If the later procedure is chosen, the patient must be rescreened to ensure that the closure was complete.[68, 243, 244]

Delaying significant changes in altitude and resultant decreases in barometric pressure for 24 hours after the last dive had been a recommended strategy. This could include flying or ascending a mountain. Consensus guidelines from DAN in 2002 apply to jetliner cabin altitudes of 2,000-8,000 ft (610-2,438 m). Below 2,000 ft (610 m), the pressure change was thought to be inconsequential. Most commercial airlines pressurize to 8,000 ft (2,438 m). One should avoid flying within 12 hours of a single no-decompression dive. This extends to 18 hours for multiple dives either per day or over several days. There is no consensus if a dive involves decompressions stops. Obviously, it should be much more than 18 hours. If the individual develops DCS, except for travel to receive treatment (see earlier), measure the delay to flying in multiples of days.[245] However, in one study using inflight transthoracic echocardiography, 8 (14%) of 56 study participants who followed the 24-hour recommendation still had bubbles during the return flight. Therefore, a longer interval between the last dive and flying (eg, 36 h) may be more appropriate.[90]

Finally, to add to the mix of influencing factors, diet can have an adverse effect on the risk of developing DCS. Previously mentioned were specific nutritional deficiencies, including folate and vitamin B-12. Hydration status is also important. Additionally, meals high in cholesterol and triglycerides have been identified as increasing the risk for DCS.[99]

A summary of protective strategies is as follows:

  • Good aerobic conditioning through regular cardiovascular exercise
  • Exercise 24 or 2 hours prior to diving
  • Hot environmental exposure prior to diving
  • Ensure good hydration before and after the dive
  • Prebreathing 100% FIO 2 oxygen predive
  • Prebreathing sessions of 79% helium-21% oxygen
  • Using Nitrox (higher percentage of oxygen, lower nitrogen) with a maximum depth limit depending upon the exact mixture [89, 246]
  • Regular diving has a protective acclimatization effect
  • A slow ascent with more than one safety/decompression stop, with (1) breathing oxygen during decompression stops and (2) being active (but not excessive exercise) during decompression stops
  • Allow for a period of 24-36 hours after the last dive prior to flying or high-altitude ascent
  • Avoid high-fat meals prior to diving
  • Avoid alcohol the evening before, or day of, diving
  • Normal body temperature (not chilled or hyperthermic) post-diving [89]

Consider the following recommendations when there is a history of DCS:

  • The decision to continue diving must be made in consultation with a diving medicine specialist
  • If prior DCS is noted, with or without a right-to-left shunt, adopting a highly conservative dive profile greatly decreases the risk or DCS recurrence [239, 247]
  • To prevent recurrent DCS, the use of oxygen-enriched breathing mixtures may help [239] ; caution is advised related to oxygen partial pressures at depth and the potential for oxygen toxicity
  • Consider the protocols in the commercial and military disciplines related to return to diving after suffering from DCS; there are no similar recommendations for the recreational population, [248] so it is very important that those effected consult with a diving medicine specialist; especially important is full understanding of the risks and strategies to avoid recurrence.

Although there is mention of specific medications, individual recommendations cannot be made. Any medication taken related to diving should be done in consultation with a diving medicine specialist.

Long-Term Monitoring

Do not discharge a patient with decompression sickness (DCS) from the emergency department 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 diving medicine or HBO specialist consultation, and referral or transfer for HBO therapy. Observe these patients for 24 hours as relapses have occurred with worse outcomes. Therefore, referral to a hyperbaric facility is strongly advised.

 

Medication

Medication Summary

There have been several medications and nutritionals mentioned in the study of the management of decompression sickness (DCS). The medications/nutritionals can have adverse effects and interactions that could affect a diver in a negative manner. The reader is cautioned about taking any substance with the end goal of decreasing DCS until more advanced studies are completed and the individual has discussed their use with a physician well versed in diving medicine.

While many of the mechanisms of action are unclear and need further study before general recommendations can be made, the following medications/nutritionals may be helpful in DCS:

  • Aspirin: Aspirin blocks prostaglandin synthetase action, inhibiting prostaglandin synthesis and preventing the formation of platelet-aggregating thromboxane A2. Its mechanism of action in the treatment of DCS unclear. It has been suggested that aspirin could do harm; therefore, it is no longer recommended for routine use in DCS. [151, 152, 153, 154]
  • NSAIDs: There is a benefit for NSAID use in conjunction with HBO therapy. [33]
  • NASIDs can help control pain.
  • Opiates are also available for pain control as needed.
  • Methylprednisolone: Methylprednisolone is useful in treating inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, it may decrease inflammation. Its mechanism of action in the treatment of DCS is unclear.
  • Lidocaine: Lidocaine decreases the permeability to sodium ions in neuronal membranes, inhibiting depolarization and blocking transmission of nerve impulses. Its mechanism of action in DCS is unknown.
  • Ascorbic acid: Ascorbic acid 2 g daily for 6 days before a dive decreased neutrophil activation and microparticle generation. [15]
  • Folic acid and/or cyanocobalamin: A high percentage of the unexplained DCS-injured divers had moderate increases in total plasma homocysteine and deficiencies in folate and vitamin B-12. [225, 226] Simple blood testing can identify issues.
  • Pyridoxine: Increases in total plasma homocysteine may be treated favorably with folate and vitamin B-6 supplements. [225, 226]
  • Fluoxetine: This agent, a common antidepressant medication in the serotonin-specific reuptake inhibitor (SSRI) class, decreases the incidence of DCS and improve motor function recovery by limiting the inflammatory process. [198] Based on rat models, it is believed to decrease inflammation through cytokine interleukin 10 suppression. [200]
  • Simvastatin: Simvastatin decreased the incidence of DCS in a rat population through its anti-inflammatory properties. [201]
  • Nitroglycerin sublingual: The common sublingual medication nitroglycerin (0.4 mg), administered 30 minutes prior to a dive, provided some level of protection by decreasing bubble formation. [196] It is a short-acting nitric oxide donor. Inhibiting nitric oxide synthase increases the number and size of bubbles, and administering a nitric oxide donor decreases the number and size of bubbles. [195] This effect also occurred with a long-acting agent at 20 hours before the dive. Nitroglycerin has many adverse effects. These include dilation of blood vessels, lowering of blood pressure, and headaches. These symptoms could be disabling should they occur during a dive.
  • Arginine: Nitric oxide synthetase converts arginine and oxygen to nitric oxide. One might surmise that taking the common L-arginine amino acid would help drive the equation to nitric oxide. This has not been studied.