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Diving Emergencies for Dummies, Part II

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altIn last month’s essay we discussed barotrauma, which occurs when gas in the body’s air-filled spaces shrinks with descent and expands with ascent. Perhaps the most common example of this is the diver that has trouble equalizing the pressure between their middle ear and the outside world due to a blocked or inflamed eustachian tube.

Nitrogen narcosis & decompression Sickness Interview with Dr. Jonathan LoPresti

The idea for this essay came from a short review piece that we did on the July edition of EM:RAP. It was our attempt to demystify a core subject in emergency medicine that many of us find confusing.

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In last month’s essay we discussed barotrauma, which occurs when gas in the body’s air-filled spaces shrinks with descent and expands with ascent. Perhaps the most common example of this is the diver that has trouble equalizing the pressure between their middle ear and the outside world due to a blocked or inflamed eustachian tube. This can result in hemorrhage and perforation of the tympanic membrane. In general, barotraumatic injuries are not treated in the hyperbaric chamber because the damage to the tissues is already done and cannot be undone by hyperbaric pressure.

The one complication of barotrauma that does require immediate treatment in a hyperbaric chamber is arterial gas embolism (AGE). This occurs when a diver fails to maintain an open airway or holds his or her breath during ascent, resulting in expansion of gas in the alveoli with subsequent rupture – the so-called pulmonary over-pressure syndrome. Air can then dissect into the pulmonary veins and make its way through the systemic circulation, including the cerebral and coronary arteries. This may manifest as a sudden onset of unconsciousness, myocardial infarction, stroke syndromes or seizures. Because emergency compression in the hyperbaric chamber can effectively shrink these gas bubbles and relieve vascular obstruction, any scuba diver who is in extremis or who falls unconscious within minutes of surfacing should be immediately transported for hyperbaric therapy.
The two other major classes of diving emergencies are related to air’s biggest constituent: nitrogen.

The first, nitrogen narcosis, has several exotic pseudonyms, including “rapture of the deep” and the “Martini effect”. Simply stated, gases at supernormal pressures can have toxic effects. High partial pressures of nitrogen act like a general anesthetic, and have an intoxicating effect. It is estimated that for every increment of 33 feet under seawater, a diver breathing compressed air experiences the equivalent of a standard unit of alcohol. This effect disappears as the diver ascends. Nitrogen narcosis is especially important for commercial divers who perform complex tasks at great depths. In fact, such divers often use a mix of compressed gases that replaces nitrogen with helium, which does not have the same narcotic potential.

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Decompression sickness (DCS) is a consequence of dissolved nitrogen coming out of solution as tiny bubbles during and after the ascent phase of a dive. DCS generally does not occur in short, shallow dives. At greater depths, however, the blood and tissues take up large amounts of nitrogen from the lungs because as the partial pressure of a gas increases, so too does the amount of gas that can be dissolved in liquid. The greater the time spent at depth, the greater is the systemic uptake of nitrogen. When the diver subsequently ascends and the ambient pressure decreases, this dissolved nitrogen can no longer be held in solution and comes out as tiny gas bubbles. These bubbles result in direct cellular damage in the tissues as well as venous and lymphatic congestion, leading to edema and ischemia. This process does not occur to any significant extent with oxygen, which is rapidly metabolized by tissues, but only with inert gases such as nitrogen in the breathing mixture. The reason why 100% oxygen is not used for deep dives is because oxygen at very high partial pressures is also toxic – it causes seizures and pulmonary edema.

In contrast to AGE, symptoms of DCS do not usually begin during ascent or immediately after the diver leaves the water. In most cases, symptoms appear after a short interval, usually within the first hour after the dive is finished. The vast majority occur within 6 hours of diving. Because there may be long-term sequelae of DCS, including osteonecrosis, patients who are only mildly symptomatic or who have a delayed onset of symptoms are nonetheless encouraged to undergo hyperbaric therapy immediately. This may be important for the EP who sees a diver with symptoms suggestive of DCS upon returning from a diving vacation.

The most common symptoms of DCS are musculoskeletal, known commonly as “the bends”. This term originates from the stooped posture of afflicted workers in the pressurized compartments used to build the underwater foundations of bridges in the 1800s. Divers may experience joint pains, swelling and tenderness. More concerning are neurologic symptoms, which can occur in either the peripheral or central nervous system. The most characteristic symptoms involve the lower thoracic and lumbar spinal cord, with paraplegias, bilateral sensory changes, and bowel and bladder dysfunction. The mechanism of spinal cord symptoms appears to be in part due to venous plexus congestion with nitrogen bubbles.

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Patients with suspected DCS should be transported emergently to a chamber for hyperbaric therapy. High flow oxygen via a non-rebreather mask should be administered to provide the greatest possible gradient for offloading nitrogen. Hydration is also essential to optimize perfusion.

To prevent DCS, tables based on both theoretical and experimental data have been developed to determine the maximum allowable time that can be spent at given depths. Depth-sensing dive computers are also carried by many divers; these tell the diver how much time they have left before nitrogen levels become dangerous. In addition, safety stops may be utilized, where the ascending diver remains at a certain depths in stages, giving the excess nitrogen time to offload across a gradient before bubbles are able to form. Although the risk of DCS is greatly reduced by these measures, it is not eliminated – some cases occur in divers who follow all of the accepted standards and guidelines. Conversely, some divers with severe violations of diving tables remain asymptomatic.

As altitude above the surface of the water increases, the further reduction in ambient air pressure may be enough to cause bubbles of nitrogen to come out of solution. Therefore, divers should not fly on commercial airplanes in the 12-24 hours following their last dive to reduce the risk of inducing DCS.

The figure above summarizes the major classes of diving related emergencies.

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Dr. Swadron is currently Vice-Chair for Education and Residency Program Director in the Department of Emergency Medicine at the Los Angeles County/USC Medical Center in Los Angeles. He is an Associate Professor of Clinical Emergency Medicine at the Keck School of Medicine of the University of Southtern California. EM:RAP (Emergency Medicine: Reviews and Perspectives) is a monthly audio program that can be found at www.EMRAP.org
 

 

Editor’s Notes with Christopher Carpenter, MD, MSc

  • The incidence of DCI varies depending upon the training of the diver. Worldwide, indigenous divers with inadequate equipment and poor training may have a 94% DCI incidence including 10% with spin
    al cord symptoms. On the other hand, well-trained first-world recreational divers have had DCI incidence reported at 0.01% (Ladd 2002).
  • Analyses of U.S. Navy dive table effectiveness have revealed that they are 50-95% effective in completely relieving DCI symptoms depending upon the initial symptom severity and time-interval between symptom onset & recompression dive (Thalmann 1996).
  • Evaluating the outcomes of mortality, residual functional disability, and symptom severity scores, a recent Cochrane review identified only two randomized controlled trials (total 268 patients) assessing the effectiveness of recompression therapy for DCI (Bennett 2010). They found no RCT evidence to support (or refute) the use of recompression therapy for non-AGE DCI, but they did find that concomitant administration of a non-steroidal anti-inflammatory agent (tenoxicam, NNT = 10) or heliox mixtures (NNT = 5) may decrease the number of dives required without improving overall recovery rates.
  • Administration of tenoxicam may be cost-effective saving $720 (Australian $) for every 5 patients treated (Gomez-Castillo 2005).
  • The benefits of HBO should be weighed against the risks which, though rare, include pulmonary barotrauma, chamber fires, and cerebral oxygen toxicity.
  • If you believe a patient has DCI or AGE and need Dive Medicine assistance, call 919-684-9111) which is available 24/7. The experts there can provide you access to the nearest HBO chamber, diagnostic & therapeutic advice, and additional resources.

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