Pulmonary Medicine

Diving Medicine and Medical Complications of Diving (DCS and Barotrauma)

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What every physician needs to know:

Underwater diving using self-contained underwater breathing apparatus (SCUBA) has become a very common recreational activity. The Professional Association of Diving Instructors (PADI), one of the largest, world-wide scuba certifying agencies, has issued over 17 million entry-level certifications since 1967. SCUBA diving is inherently risky, as participants are submerged in a hostile environment where they are at risk for potential life-threatening problems.

Decompression syndrome (DCS), hypothermia, drowning, barotrauma, immersion pulmonary edema, and gas embolism are important medical complications of diving. This discussion focuses on decompression illness and barotrauma.


Decompression Syndrome may be subclassified as Type 1 or Type 2:

  • Type 1 DCS manifests as joint pain, cutaneous symptoms, or swelling and pain in lymph nodes.

  • Type 2 DCS comprises neurologic, inner ear, and cardiopulmonary symptoms.

Barotrauma is the second most frequent dive-related injury (2008 Diver's Alert Network Annual Dive Report). Sites of injury include the lungs, the middle ear, and the sinuses.

  • Lungs: Lung injury arises from pulmonary over-inflation that is due to decreasing surrounding atmospheric pressure during ascent (as described by Boyle's law ). Holding the breath or performing the Valsalva maneuver during ascent may result in pulmonary barotrauma.

  • Middle ear: Middle ear injury is commonly seen in inexperienced divers who are not adept at equalizing middle ear pressures during descent. As the surrounding water pressure increases, a diver must be able to equalize the pressure in the middle ear by auto-insufflation. Auto-insufflation involves forcing air up the Eustachian tube, typically by swallowing or by performing the Valsalva maneuver. Otherwise, pain followed by hemorrhage, development of serous middle ear effusion, or tympanic membrane rupture may develop. Symptoms of vertigo may be related to rupture of the round window or, in the acute setting, may reflect neurologic involvement of DCS.

  • Sinuses: Sinus pressure and pain may be observed in divers who dive with sinus congestion or when the effect of decongestants wears off during diving.

Are you sure your patient has decompression syndrome or barotrauma? What should you expect to find?

Decompression syndrome is a clinical diagnosis

  • Patient complaints are extremely variable, but the time of onset of symptoms and signs may aid in diagnosis.

  • The median time to onset of symptoms and signs post-diving is approximately thirty minutes. More than 70 percent of patients experience the onset of some symptoms or signs within one hour, and more than 97 percent experience symptoms or signs within 24 hours of diving.

  • Barotrauma to the ears and sinuses presents with local pain during the dive itself. Air embolism that may occur during ascent because of pulmonary over-pressurization is discussed below.

Symptoms of decompression syndrome

Symptoms of DCS, listed in decreasing order of overall prevalence:

  • Paraesthesia

  • Pain

  • Dizziness

  • Muscle weakness

  • Fatigue

  • Nausea

  • Headache

  • Decreased coordination

  • Skin rash and itching

  • Pulmonary manifestations, such as wheezing and shortness of breath

  • Muscle aches

  • Disorientation

  • Alterations in consciousness

  • Barotrauma events leading to pneumothorax or pneumomediastinum

  • Lymphedema resulting from lymphatic obstruction

  • Bladder or bowel incontinence

  • Nystagmus

  • Hearing impairment

Beware: there are other diseases that can mimic decompression syndrome and barotrauma:

Arterial gas embolism may mimic decompression syndrome

  • Arterial gas embolism (AGE) is classically described in the setting of submarine escape training, where participants breathe compressed air at depth and then perform rapid ascents while holding the breath. The subsequent pulmonary over-inflation caused during breath holding ascent by decreasing surrounding atmospheric pressure and inversely expanding lung volumes (as described by Boyle's law ) results in pulmonary over-inflation and barotrauma. The resulting alveolar damage facilitates entry of air bubbles into the pulmonary venous circulation in sufficient quantity to overwhelm the pulmonary capillary network and cause systemic arterial embolization of those bubbles.

  • Unlike DCS, which requires sufficient time at depth to cause a high nitrogen load, AGE can occur any time a diver breathes compressed gas, regardless of the depth or duration of the dive. DCS has even been documented to occur following breath holding ascents of as little as one meter (e.g., in swimming pools). Common presenting symptoms and signs are listed below.

Signs and symptoms of patients presenting with arterial gas embolism

  • Loss of consciousness

  • Stupor/confusion

  • Unilateral motor or sensory changes

  • Bilateral motor or sensory changes

  • Monoplegia

  • Asymmetric multiplegia

  • Focal paralysis

  • Convulsions

  • Aphasia

  • Vertigo

  • Ataxis

  • Dizziness

  • Headache

  • Dysmetria

  • Decreased coordination

  • Calculation errors

  • Construction difficulty

  • Cortical blindness

  • Gaze preference

  • Homonymous hemianopsia

  • Nystagmus

  • Chest pain

  • Shortness of breath

  • Hemoptysis

  • Crepitus

  • Cardiac arrest

  • Nausea

  • Vomiting

How and/or why did the patient develop decompression syndrome or barotrauma?

Development of decompression syndrome

Under normal conditions, we breathe air at one atmosphere absolute pressure (ATA). Since water is essentially non-compressible, for every 33 feet of sea water (fsw) a diver descends, an additional one ATA is encountered. When a SCUBA diver breathes compressed gas from a SCUBA tank, the gas is also further compressed in direct relation to the ATA that the diver experiences (as demonstrated by Boyle's Law ). According to Dalton's law, the increase in ambient pressure increases proportionately the partial pressures of the constituent gases contained in the breathed mixture. Understanding these physical relationships is key to comprehending the physiology of diving medicine.

Under one ATA (or 760 mmHg) condition, the air we breathe is made up of 21 percent oxygen and 78 percent nitrogen, along with 1 percent inert gases. (A value of 79 percent nitrogen is used for simplicity.) The partial pressure of oxygen in such a gas mixture is 1 ATA x (0.21) = 0.21; for nitrogen, the calculation is 1 ATA x (0.79) = 0.79. At 66 FSW (1 ATA starting + 2 ATA due to depth = 3 ATA pressure), the partial pressure of oxygen is 3 (0.21) = 0.63; for nitrogen, the partial pressure is 3 (0.79) = 2.37.

As the patient breathes the compressed gas, nitrogen and oxygen are absorbed into the blood stream over time until equilibrium (saturation) is reached at that depth. DCS is essentially a problem of ascent. If the patient ascends too rapidly, he or she is at risk for forming nitrogen bubbles that then migrate into the blood stream because of the supersaturation of nitrogen at the new (decreased) pressure closer to the water surface.

Traditionally, gas bubbles were thought to be the only cause of DCS. However, current research has demonstrated that the gas bubbles cause a shearing force on endovascular surfaces, potentiating an inflammatory response and impairing vascular integrity. Thus, although bubbles are the proximate cause of injury, progression of injury appears to be mediated via several pro-inflammatory pathways.

Which individuals are at greatest risk of developing decompression syndrome or barotrauma?

A variety of factors may predispose a person to development of DCS:

Dehydration: Strong evidence exists that hydration status affects the incidence and time to onset of DCS. Logically, then, excessive intake of alcohol should be avoided prior to diving, as alcohol inhibits pituitary release of antidiuretic hormone (ADH).

Age: Some evidence suggests that people over the age of 42 years are at increased risk of DCS.

Obesity: There are conflicting studies with regard to whether obesity plays a role in DCS.

Work and exercise: Work or exercise at depth or shortly after diving is strongly associated with DCS.

Temperature: It has been theorized that warm conditions favor nitrogen uptake or off-gassing, with the notion that better perfusion may aid in mobilizing dissolved nitrogen in peripheral tissues for elimination in the lungs. Similarly, a popular belief is that cold conditions slow the process, but no definitive studies have demonstrated a causal relationship between thermal conditions and development or magnitude of DCS. Although discussions on issues like the role of hot showers in development of DCS following diving have been done, no studies have specifically examined the question concerning the relationship between thermal conditions and DCS.

Patient formane ovale (PFO): A PFO, which occurs in about 30 percent of the normal population, is associated with a 2.5-fold increase in the odds for developing serious DCS. The risk of suffering major DCS parallels the PFO size.

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

No laboratory studies provide for a definitive diagnosis of DCS. However, an elevation in serum CPK is associated with severe arterial gas embolism, and hemoconcentration is associated with DCS. The hemoconcentration is thought to be secondary to endothelial damage, which causes extravasation of fluid into interstitial spaces and resultant decrease in plasma volume of up to 35%.

What imaging studies will be helpful in making or excluding the diagnosis of decompression syndrome and barotrauma?

Prompt intervention is important in managing DCS successfully, so very few imaging studies will have an impact on management decisions. A chest X-ray should be done to evaluate for pneumothorax, pneumomediastinum, pulmonary overexpansion injury, or pulmonary edema.

A head CT scan is also appropriate and should be strongly considered in any patient who has altered mental status in order to evaluate alternative diagnoses, such as subdural or epidural hematoma. It is important to recognize is that it is not common to see "bubbles" on a head CT scan under circumstances of suspected DCS or AGE, so a "normal" CT scan of the head is not useful in excluding either of these conditions.

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of decompression syndrome and barotrauma?


What diagnostic procedures will be helpful in making or excluding the diagnosis of decompression syndrome and barotrauma?

No specific procedures are useful in excluding the diagnosis of DCS and barotrauma. At times, prompt resolution of symptoms and signs during recompression treatment may be the only means by which to establish a diagnosis of DCS.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis decompression syndrome and barotrauma?


If you decide the patient has decompression syndrome or barotrauma, how should the patient be managed?

Decompression syndrome

Definitive treatment for DCS is hyperbaric oxygen therapy (HBOT) in a recompression chamber. In some instances, provision of HBOT requires patient evacuation via helicopter; generally, maintaining an altitude below one thousand feet is considered acceptable. Instructions to fly the patient "as low as safely possible" should be given to the helicopter transport medical staff. All patients suspected of having DCS should receive high-flow oxygen via nonrebreather mask.

Outcome data from the Diver's Alert Network demonstrate that patients with DCS who have received oxygen at ambient pressure have improved outcomes compared with those who do not. Patients should be placed on maintenance intravenous fluids to counteract interstitial fluid shifts and decreases in plasma volume arising from endothelial injury.

HBOT constitutes the "gold standard" for treatment of DCS. Outcome data demonstrate that delays of as little as four hours from the time of injury to recompression correlate with a marked elevation in the incidence of residual symptoms following therapy. When logistics preclude advanced interventions like recompression therapy, the patient should be placed on 100 percent oxygen via a nonrebreather mask in order to maximize nitrogen off-loading, and intravenous fluids should be administered if the patient is unable to take fluids orally.

The benefits of HBOT in DCS are attributable to the effects of both high pressure and high-dose oxygen. The beneficial effects of high pressure include reduction in volume of any residual inert gas bubbles (typically, nitrogen) in accordance with Boyle’s Law. As a consequence, blood flow may be restored through vessels previously occluded by larger bubbles.

In addition, increased pressure increases the solubility of inert gases in accordance with Henry’s Law, allowing any residual nitrogen in the gas phase to dissolve more readily into solution and decreasing the overall nitrogen gas bubble load.

Breathing 100 percent oxygen under hyperbaric conditions enhances the diffusion gradient of nitrogen out of tissues and blunts neutrophil responses to injured endothelium. Animal studies have documented neutrophil activation and adherence to endothelium via beta-2 integrins. This adherence pathway can be temporarily inhibited with use of hyperbaric oxygen.


Middle ear barotrauma is the most common adverse effect of HBOT. As ambient pressure within the hyperbaric chamber increases, the patient must be able to equalize the pressure in the middle ear by auto-insufflation; if the patient is unable to do so, pain followed by hemorrhage, serous effusion, or tympanic membrane rupture will develop. Standard treatment protocols include instructing patients about auto-insufflation techniques and using oral or topical decongestants when needed.

When these interventions fail, tympanostomy tubes must be placed. The incidence of tube placement has been reported to be approximately 4 percent. Studies describe an overall incidence of aural barotrauma or 1.2 - 7 percent.

Pulmonary barotrauma during HBOT is extremely rare, but it should be suspected when any significant chest or hemodynamic symptoms occur during or shortly after decompression. Because the offending gas in virtually all cases is pure oxygen, gas absorption in the body may occur. However, if symptoms develop, decompression should be stopped and the patient evaluated. If pneumothorax is suspected, placement of a chest tube is appropriate. Preexisting pneumothorax should be treated with chest tube drainage prior to initiating HBOT.

Oxygen Toxicity

Biochemical oxygen toxicity may be manifested as injuries to the lungs, the central nervous system, or the eyes. Pulmonary injury may impair lung mechanics (through increased elasticity), vital capacity, and gas exchange. Changes are typically observed only when treatment duration and pressure exceed recommended therapeutic protocols. One report described reversible changes in the function of small airways but no evidence of pathology) in 4 of 21 patients treated daily for ninety minutes at 2.4 ATA for 21 days. Most studies have failed to identify any adverse pulmonary effects from using standard treatment protocols.

CNS oxygen toxicity is manifested as grand mal seizures. Seizures occur with an incidence of approximately 1 to 4 of 10,000 patient treatments. The risk for seizures is higher in patients who are hypercapnic and perhaps in those who are acidemic or septic. An incidence of 7 percent (23 of 322 patients) was reported in a case series of HBOT used for gas gangrene.

Seizures are managed by reducing the inspired oxygen tension while leaving the patient at the same ambient pressure (in order to avoid pulmonary overexpansion injury when the patient is experiencing tonic convulsions). Pathologic changes occurring in association with isolated, oxygen-mediated seizures have not been found in studies of guinea pigs, rabbits, or humans.

Progressive myopia has been reported in patients who undergo prolonged daily HBOT. This is not an issue with HBOT administered for DCS or air embolism, where patients typically receive one to a few treatments. Pregnant women are generally advised to avoid SCUBA diving; however, experimental and clinical evidence does not indicate detrimental effects of HBOT on neonates or the unborn fetus when typical HBOT protocols are used. The apparent lack of adverse effect is likely due to the relatively short duration of hyperoxia.


Confinement anxiety, which may occur with HBOT, is managed with sedating agents.

Any environment with an elevated concentration of oxygen presents a risk for fire. Scrupulous attention to avoiding an ignition source is standard in HBOT programs.

What is the prognosis for patients managed in the recommended ways?

Outcome data for sport SCUBA divers who suffer from DCS is compiled and intermittently published by the Diver’s Alert Network. This information is somewhat dated, but trends are likely to be valid. HBOT within four hours of onset of Type 1 DCS (see above) appears to be successful in more than 90 percent of cases. However, if treatment is delayed beyond twelve hours, more than 80 percent of divers have some residual deficits following treatment. As would be expected with more sever primary injuries, patients with significant neurological deficits associated with Type 2 DCS have worse prognoses. Approximately 35 percent of patients have residual deficits even when they are treated within four hours of onset of DCS.

What other considerations exist for patients with decompression syndrome or barotrauma?

Evaluation of a diver after DCS for a return to diving (i.e., clearing a diver to return to diving) is a complex, potentially medical and legally risky undertaking. A careful risk/benefit assessment must be conducted by both the diver and the physician. In cases in which the risks clearly outweigh the benefits, divers should be instructed to refrain from diving for the remainder of their lives.

At a minimum, prior to clearing a diver to return to diving, the physician should ensure that the diver is completely asymptomatic and back to his or her pre-dive baseline function. Divers who have ongoing symptoms should not be cleared. Given the potential life-threatening implications of improperly clearing a diver to return to diving, referral of the patient to a diving medicine specialist is appropriate.

Other important considerations in managing patients with DCS concern when and how the patient may return home. A retrospective review of 126 cases of DCS demonstrated that those who flew home on commercial flights fewer than 72 hours after recompression had a higher likelihood of recurrence of symptoms and signs of DCS. Similarly, physicians should be wary if patients must drive through mountainous regions or other high-altitude areas, as the drop in atmospheric pressure could, at least theoretically, potentiate a recurrence.

What’s the evidence?

Benson, J, Adkinson, C, Collier, R. "Hyperbaric oxygen therapy of iatrogenic cerebral arterial gas embolism". Undersea Hyperb Med. vol. 30. 2003. pp. 117-126.

This retrospective review of nineteen patients treated for iatrogenic cerebral AGE reports that five (26%) resolved all signs and symptoms immediately after HBOT, and eleven (58%) exhibited some improvement. Within two months post-treatment, three additional patients completely resolved and six had further improvement. The authors conclude that diagnosis of cerebral AGE should be made on clinical suspicion without reliance on imaging studies and patients promptly referred for HBOT.

Neuman, TS, Thom, SR. "Physiology and medicine of hyperbaric oxygen therapy". Elsevier. 2008.

The most recent text in the HBOT field, this book offers a comprehensive review of diving medicine disorders and use of HBOT.

Smith, RM, Neuman, TS. "Elevation of serum creatinine kinase in divers with arterial gas embolization". N Engl J Med. vol. 330. 1994. pp. 19-24.

This report evaluated 142 patients with diving-associated injuries. All with gas embolism (22 were included in the analysis) had elevated serum creatine kinase activity. Changes in serum creatine kinase of similar magnitude were not present in 22 subjects who had uncomplicated dives or in a comparative group of 11 patients with blunt trauma. Logistic-regression analysis revealed a significant correlation between peak serum creatine kinase values and clinical outcome from gas embolism.

This is the latest revision of the standard reference used by divers worldwide.
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