What every physician needs to know:
Underwater diving using self-contained underwater breathing apparatus (SCUBA) has become a common recreational activity. The Professional Association of Diving Instructors has issued >23 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 syndrome and barotrauma.
Decompression Syndrome (aka “the bends”): may be subclassified as Type 1 or Type 2:
Type 1 DCS: characterized by cutaneous and musculoskeletal gas precipitation
Manifestations include joint pain, itching, mottled or raise rash (“cutis marmorata”), or less commonly swelling and pain in lymph nodes.
Type 2 DCS: more serious manifestations that affect the CNS, inner ear, and cardiopulmonary system.
Barotrauma is the second most frequent dive-related injury. Sites of injury include the lungs, middle ear, and the sinuses.
Lungs: Injury arises from pulmonary overinflation due to decreasing surrounding atmospheric pressure during ascent (as described by Boyle’s law). Holding one’s breath or performing a Valsalva maneuver during ascent may result in pulmonary barotrauma.
Middle ear: Injury is commonly seen in inexperienced divers who are not adept at equalizing middle ear pressures during descent. As 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 a 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. Time of onset and the specific symptoms/signs aid in establishing the diagnosis.
The median time to symptom/sign onset is 30 minutes and severe neurologic symptoms tend to present within 10 minutes.
90% of patients will experience onset of some symptoms or signs within 3 hours, and nearly all experience symptoms or signs within 24 hours of emerging from the water.
The onset of symptoms within 10 minutes is more suggestive of gas embolism, whereas DCS tends to present after 10 minutes.
Symptoms of DCS (listed in decreasing order of overall prevalence):
Dizziness, muscle weakness
Skin rash and itching
Decreased coordination or mental status
Pulmonary manifestations, such as wheezing and shortness of breath
Bladder or bowel incontinence (due to spinal cord lesions)
Lymphedema resulting from lymphatic obstruction
Barotrauma to the ears, sinuses, and lungs presents with local pain or shortness of breath during the dive itself. Severe barotrauma can result in pneumothorax or tympanic membrane rupture.
Beware: there are other diseases that can mimic decompression syndrome and barotrauma:
Arterial gas embolism (AGE) may mimic decompression syndrome
Defined as gas bubbles in the arterial system and occurs when change in atmospheric pressure is rapid enough to cause lung injury.
Decreasing surrounding atmospheric pressure during ascent inversely expands lung volumes resulting in barotrauma and subsequent alveolar damage facilitating entry of air bubbles into the pulmonary venous circulation. When air entry is in sufficient quantity to overwhelm the pulmonary capillary network, systemic arterial air embolization ensues.
Classically described in setting of submarine escape training, where participants breathe compressed air at depth and then perform rapid ascents while holding their breath.
Unlike DCS, which requires sufficient time at depth to cause a high nitrogen load, AGE can occur anytime a diver breathes compressed gas, regardless of the depth or duration of the dive. AGE has even been documented following breath holding ascents of as little as one meter (e.g., in swimming pools).
Signs and symptoms:
Shortness of breath, hemoptysis, crepitus
Stroke symptoms such as bilateral or unilateral motor or sensory changes, aphasia vertigo, ataxia, dysmetria, cortical blindness
Stupor/confusion, loss of consciousness
AGE and DCS are often hard to distinguish, and they are managed similarly. Decompression illness is a term that encompasses both AGE and DCS.
AGE can also occur outside the setting of diving, e.g., during central line placement, flushing, or removal.
Re-immersion pulmonary edema can occur, and its mechanism is similar to negative pressure pulmonary edema. In a patient with respiratory distress after ascent from a dive, this diagnosis must be considered.
How and/or why did the patient develop decompression syndrome or barotrauma?
There are two laws of physics that help explain the pathophysiology of DCS and barotrauma:
Henry’s law: amount of gas dissolved in liquid is proportional to the partial pressure of gas. Therefore, as the pressure decreases, the volume of gas dissolved in liquid decreases.
Boyle’s law: P1V1=P2V2. Thus, as pressure decreases, the volume of gas expands assuming a constant temperature.
Under normal conditions, we breathe air at 1 atmospheres absolute (ATA), which is the average atmospheric pressure at sea level. Since water is essentially non-compressible, for every 33 feet of sea water (fsw) a diver descends, an additional 1 ATA is encountered. Gas in a SCUBA tank is also subject to the same increase in ATA during descent, such that the partial pressure of the gas increases. According to Henry’s law, the amount of gas dissolved in liquid is directly proportional to the pressure exerted on the liquid. As such, when the diver descends, the partial pressure of oxygen and more importantly nitrogen increases resulting in a diffusion gradient favouring uptake of nitrogen into the bloodstream and tissues.
Under normal circumstances, the lungs are the vehicle for gas elimination. As the ATA decrease, more nitrogen precipitates from the tissues into the bloodstream and then diffuses into the alveoli for exhalation. If ascent occurs too quickly, gas quickly dissipates from the tissues and serum forming small air bubbles. This process is called “out gassing” or “off gassing”. Slow ascent, on the other hand, allows for equilibrium to gradually be reached and prevents the rapid changes in partial pressure of nitrogen in the bloodstream.
These small 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. Large confluence of gas can lead to air embolism, as described above.
Barotrauma occurs as a direct result of Boyle’s law. If a diver ascends quickly without breathing (during a breath hold or valsalva), the pressure in the lungs decrease and the volume of gas can rapidly expand. This expansion can result in barotrauma to the lungs, middle ear, and sinuses. In severe cases, pneumothorax or tympanic membrane rupture can occur. Barotrauma can be avoided if the diver is able to re-equilibrate with the surrounding environment by breathing to exhale the expanded gas or equalizing the pressure in the middle ear with a valsalva. Therefore, barotrauma is often seen with a rapid ascent and concurrent breath hold.
Which individuals are at greatest risk of developing decompression syndrome or barotrauma?
The incidence of all decompression illness (DCS and AGE) is estimated at 0.324 per 10,000 person-dives among professional divers, but as many as 2-35 per 10,000 person-dives in the community. 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.
Alcohol intake: increases dehydration and inhibits pituitary release of antidiuretic hormone (ADH).
Age: some evidence suggests that people > 42 years of age are at increased risk of DCS.
Obesity: conflicting studies with regards 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, as it promotes increased inert gas uptake. Light exercise during ascent or stop phase can promote gas excretion, but strenuous exercise will promote bubble formation.
Temperature: warm conditions may favor nitrogen uptake, placing a patient at higher risk of “out gassing” when ascending as more nitrogen has been dissolved. 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 of DCS.
Patient foramen ovale (PFO): occurs in ~30% of the normal population and associated with a 2.5-fold increase in the odds of developing serious DCS. The risk of suffering major DCS parallels the PFO size.
Asthma: asthmatics are generally advised not to dive, due to a theoretical risk of bronchospasm triggered by cold or changing environments, inability to quickly respond to an asthma attack while submerged, and supposed increased barotrauma during ascent. There is limited data to support preventing asthmatics from diving, so more studies are warranted. Well-controlled asthmatics with normal PFTs can occasionally be permitted to dive, but this should be assessed on a case-by-case basis.
What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
No laboratory studies make a definitive diagnosis of DCS. However, an elevation in serum CK is associated with severe AGE, 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?
No imaging study can confirm the diagnosis of DCS. However, studies may rule out other causes of the patient’s symptoms. These studies should be performed rapidly as prompt intervention is important in managing DCS successfully.
CXR should always be performed to evaluate for pneumothorax, pneumomediastinum, pulmonary overexpansion injury, or pulmonary edema.
A head CT scan 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 not common to see vascular gas on a head CT under circumstances of suspected DCS or AGE; a “normal” head CT is not useful in excluding either of these conditions. MRI similarly can pick up ischemic lesions of the brain or spinal cord, but can often be falsely reassuring.
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?
Definitive treatment for DCS is hyperbaric oxygen therapy (HBOT) in a recompression chamber. HBOT should be initiated as soon as possible. Delays of > 4 hours from the time of injury to recompression correlate with a marked elevation in the incidence of residual symptoms following therapy.
The US Navy protocol is as follows: HBOT chamber is brought to 2.8 ATA (equivalent of depth of 60 feet) over a few minutes and then 100% FiO2 is initiated. 100% FiO2 is used for 20 minutes at a time, alternating with 5 minute intervals of room air breathing to prevent oxygen toxicity. Upon completion of HBOT therapy, the pressure is increased by no more than 1 foot/minute, with a prolonged period of equilibration at 30 feet. The total therapy time is about 5 hours. The therapy can be continued daily for several days if symptoms warrant it, although there is no data to suggest repeated treatments are necessary.
The mechanism of HBOT is twofold. First, elevated atmospheric pressure in the HBOT chamber allow for increased partial pressure of gasses and dissolution of nitrogen back into liquid (Henry’s law), and the increased pressure also decreases the volume of gas present in the body (Boyle’s law). Second, increased FiO2 results in decreased partial pressure of nitrogen in inspired gas. This enhances the diffusion gradient of nitrogen out of tissues, favoring exhalation and elimination from the body, while also blunting neutrophil responses to injured endothelium.
In lieu of access to HBOT, or in the interim prior to initiation of HBOT, patients suspected of having DCS should receive high-flow oxygen via nonrebreather mask. Outcome data from 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. 100% FiO2 facilitates offloading of nitrogen from plasma and tissues, as noted above.
If helicopter evacuation is necessary, maintaining an altitude below 1000 feet is ideal. Instructions to fly the patient “as low as safely possible” should be given to helicopter transport.
Isotonic IV fluid resuscitation and maintenance IV fluids should be administered to counteract interstitial fluid shifts and decreases in plasma volume arising from endothelial injury.
Aspirin, NSAIDs, and corticosteroids have all been studied and not shown to have benefit in DCS. IV lidocaine has been shown to have benefit in animal models, but there is no robust human data to recommend its use. Barotrauma requires treatment of the underlying organ damage. For example, middle ear barotrauma often only requires supportive care. If severe enough, tympanostomy tubes may be required. If pulmonary barotrauma results in pneumothorax, a chest tube is required. Pneumomediastinum can be managed conservatively.
Middle ear barotrauma: most common adverse effect of HBOT
Pulmonary barotrauma: risk of pneumothorax
Similar mechanism and management as barotrauma caused by diving
Pulmonary toxicity: dysfunction of small airways may be observed when treatment duration and pressure exceed recommended therapeutic protocols
CNS toxicity: generalized tonic-clonic seizures occur with an incidence of approximately 1-4 per 10,000 patient treatments. Risk is higher in patients who are hypercapnic and perhaps in those who are acidemic or septic. An incidence of 7% (23 of 322 patients) was reported in a case series of HBOT for gas gangrene.
Mechanisms of seizures not well-understood
CNS toxicity managed by decreased FiO2 but continuing same elevated atmospheric pressure
Ocular toxicity: myopia can be seen in those who undergo prolonged daily HBOT (which is longer than a typical DCS treatment course).
Confinement anxiety – managed with anxiolytics
Fire (due to elevated FiO2)
What is the prognosis for patients managed in the recommended ways?
Outcome data for SCUBA divers who suffer from DCS is compiled and published by the Diver’s Alert Network. Initiation of HBOT within 4 hours of onset of Type 1 DCS appears successful in > 90% of cases. However, if treatment is delayed beyond 12 hours, > 80% of divers have some residual deficits following treatment. As would be expected with more severe injuries, patients with significant neurologic deficits associated with Type 2 DCS have worse prognoses. Approximately 35% of patients have residual deficits even when they are treated within 4 hours of onset of Type 2 DCS.
What other considerations exist for patients with decompression syndrome or barotrauma?
Clearing a diver after DCS to return to diving is a complex undertaking with potential medical and legal risks. 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 with 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.
The physician must also consider when it is safe for a patient to fly home or drive at altitude. A retrospective review of 126 DCS cases demonstrated that those who flew home on commercial flights < 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 high-altitude areas, as the drop in atmospheric pressure could, at least theoretically, potentiate a recurrence.
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- What every physician needs to know:
- Are you sure your patient has decompression syndrome or barotrauma? What should you expect to find?
- Beware: there are other diseases that can mimic decompression syndrome and barotrauma:
- How and/or why did the patient develop decompression syndrome or barotrauma?
- Which individuals are at greatest risk of developing decompression syndrome or barotrauma?
- What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
- What imaging studies will be helpful in making or excluding the diagnosis of decompression syndrome and barotrauma?
- 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?
- 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?
- What is the prognosis for patients managed in the recommended ways?
- What other considerations exist for patients with decompression syndrome or barotrauma?