Cerebral air embolism in asthmatic scuba divers in a swimming pool.

Significant shallow-water injuries can occur in scuba divers, even in swimming pools. Two asthmatic patients are presented who sustained cerebral air emboli during Scuba classes in a swimming pool. Such injuries may be more common in asthmatics. Asthma is a contraindication to Scuba diving.

(CHEST 1995; 107:1653-54)

AGE=acute gas embolism DAN=divers Alert Network; scuba=self-contained underwater breathing apparatus

Key words: decompression sickness; diving; embolism, air

There are at least 5 million active certified selfcontained underwater breathing apparatus (scuba) divers in the United States, with more than 500,000 new divers trained each year (personal communications, Professional Association of Diving Instructors [PADI], Santa Ana, Calif; Divers Alert Network [DAN], Durham, NC). Diving is now popular throughout the United States, not only in coastal communities. Opportunities exist in almost every state for diving in lakes, caves, abandoned mines and quarries, and behind dams.

Asthma has long been considered a strong contraindication to diving.[1-3] Asthmatics may be more susceptible to barotrauma of ascent. Prospective asthmatic divers will often contact their internist for "medical clearance" to dive. These cases illustrate the risks that asthmatic Scuba divers take, even in shallow water.

CASE REPORTS

CASE 1

A 32-year-old woman presented to the emergency department complaining of persistent bilateral lower extremity paresthesias. Approximately 2 h earlier she had participated in a Scuba diving class in a swimming pool.

When ascending from a depth of 3.6m, she had an episode of near-syncope. She developed transient vertigo, profound weakness, and palpitations when she arrived at the surface. She then experienced persistent lightheadedness and dizziness. There was no depletion of air, contamination of air, or equipment malfunction. About 10 min after surfacing, she developed total body paresthesias and nausea while lying by the side of the pool. Her symptoms partially resolved and she drove herself to the hospital. On arrival, she complained only of persistent paresthesias of the right lower extremity (entire right leg and foot) and left foot.

The patient denied any history of asthma but later admitted that she had a history of episodic shortness of breath since childhood. These episodes were relieved by using an inhaler. Occasionally, she used an inhaler prophylactically before diving. Results of the patient's physical examination (including a detailed neurologic examination) were unremarkable. Her initial diagnostic workup was unremarkable (complete blood cell count, electrolytes, serum urea nitrogen, creatinine, glucose, platelet count, prothrombin time/partial thromboplastin time, sedimentation rate, creatine kinase, ECG, chest radiograph, and arterial blood gas).

In preparation for treatment in a hyperbaric chamber, the patient received high-flow oxygen by mask, intravenous saline solution, dexamethasone, 10 mg intravenously, and aspirin, 650 mg orally. She received hyperbaric oxygen therapy on a US Navy Treatment Table 6A. This involved a "dive" to a simulated depth of 49.5m, of sea water. Her symptoms completely resolved while in the hyperbaric chamber.

Further evaluation included a series of somatosensory evoked responses, brain-stem evoked auditory response, electronystagmogram, audiogram, spectamine and magnetic resonance imaging brain scans, and a transesophageal echocardiogram to look for a patent foramen ovale. She refused pulmonary function testing. The patient required several more hyperbaric oxygen treatments because of recurrent mild and vague complaints during the following week (lethargy, tingling sensation in feet). These symptoms were of questionable significance but resolved. She had no neurologic residue.

CASE 2

A 33-year-old woman developed a severe headache while ascending from a depth of 5.4m in a swimming pool. She was participating in a scuba diving class. After surfacing, she developed a 30-s episode of vertigo that abruptly subsided. Her instructor noted that she had ascended quickly. There was no depletion of air, contamination of air, or equipment malfunction. Several hours later, she had three episodes of vomiting, an episode of near-syncope, and confusion. She presented to our hyperbaric facility about 12 h after the onset of her symptoms.

The patient had a life-long history of asthma. Her pulmonologist had refused to provide her with medical clearance to take scuba diving lessons. She than went to another physician and concealed her history of asthma. She had been using albuterol, beclomethasone, cromolyn, and epinephrine inhalers at the time of her injury.

Her physical examination was positive for bilateral hemorrhagic middle ear effusions (middle ear barotrauma), an air conduction deficit of the right ear, and an abnormal sharpened Romberg test. The patient received bilateral pressure-equalization tubes of her tympanic membranes. She received hyperbaric oxygen therapy on a modified US Navy Treatment Table 6A. She had multiple episodes of bronchospasm during ascent in the chamber. She required eight albuterol breathing treatments in the chamber, and it took more than 8 h to ascend to surface pressure.

Her initial diagnostic evaluation and an in-depth neurologic evaluation (CT, magnetic resonance imaging, EEG, somatosensory evoked potentials, brain-stem evoked auditory response, and audiogram) were normal. The patient did not comply with follow-up examinations, but she did contact us by telephone to relate a persistence of headaches, decreased hearing, and memory loss.

DISCUSSION

Acute gas embolism (AGE) in divers occurs during ascent. According to Boyle's law, there is an inverse relationship between the pressure and volume of an ideal gas (PV=constant). As a diver ascends, the pressure of the gas in the diver's lungs decreases. Therefore, the volume of the gas increases. If divers ascend too quickly or hold their breath while ascending, a gas embolism may occur. The greatest relative changes in pressure occur in shallow water. Consequently, the risk of AGE is theoretically greatest as divers approach the surface. Rapid uncontrolled ascents occasionally occur due to inflation of the buoyancy compensator, inadvertant triggering of a [CO.sub.2] cartridge, gas depletion, or other underwater emergencies.

We have interviewed many asthmatic divers who claimed that their physicians gave them approval to dive in "shallow water only." This is an apparently common recommendation. For reasons stated above, this is an inappropriate recommendation. Asthmatics may have a greater risk of AGE because of possible regional air-trapping on ascent,[3,4] overinflation,[5] and decreased compliance.[6] Asthmatics possibly have an increased risk of acute bronchospasm when diving, as airway resistance and work of breathing increase at depth.[7] Also, contamination of air supply and exposure to cold air may cause bronchospasm. The sudden expansion of gas from pressures of 2,000 psi or greater causes great cooling of the gas according to Charles' law. For cold-induced asthmatics, this constitutes another theoretical hazard.

The history determined the diagnosis of AGE in these two cases. Often, one establishes the diagnosis of AGE (and also decompression sickness) by clinical evaluation. The history and physical examination is still the "gold standard." The paucity of positive findings on diagnostic evaluation in these cases is typical. In the second case, most of the symptoms could be attributed to middle ear, inner ear, or sinus barotrauma. However, confusion and later memory loss warranted a presumptive diagnosis of air embolism and a trial of therapy.

Detailed recommendations are available regarding the medical contraindications of diving.[3,8] These recommendations are rarely based on substantial scientific data. Most of these general guidelines developed from historical consensus among the military, the commercial diving industry, and physicians with expertise in diving medicine (such as the Undersea and Hyperbaric Medical Society).

It is difficult to determine a relative risk of injury for asthmatic divers. The incidence of diving injuries, ie, decompression sickness and AGE, among asthmatics is unknown. Many asthmatic divers attempt to hide the presence of their disease. Several surveys have revealed many asthmatics with active disease who dive on a regular basis.[1,9-11]

DAN attempts to document every significant injury in recreational divers in the United States. DAN recently attempted to detect whether asthmatic divers were at increased risk for diving injuries. The authors show a two fold increase in the risk of AGE in asthmatic divers.1 Yet, because of a small sample size, this difference did not reach statistical significance. Their data came from questionnaires that were completed by divers (70% response rate). The authors could not verify the accuracy of the information.

In summary, based on the limited data available, the known pathophysiology of AGE in divers, and the general standards of practice among diving physicians around the world, asthma is considered a strong contraindication for diving. These cases illustrate the risk of recommending shallow water diving for asthmatic patients.

(*) From the Department of Medicine, Section of Emergency Medicine, Louisiana State University School of Medicine, New Orleans.

REFERENCES

[1] Corson KS, Dovenbarger JA, Moon RE, et al. Risk assessment of asthma for decompression illness[abstract]. Undersea Biomed Res 1991; 18(suppl):16-7 [2] Neuman TS. Pulmonary disorders in diving. In: Bove AA, Davis JC, eds. Diving medicine. Philadelphia: WB Saunders, 1990; 233-38 [3] Davis JC. Medical examination of sport SCUBA divers. San Antonio, Tex: Medical Seminars Inc, 1986; 35-6 [4] Liebow AA, Stark JE, Vogel J, et al. Intra-pulmonary air-trapping in submarine escape training casualties. US Armed Forces Med J 1959; 10:265-89 [5] Schaefer KE, McNulty WP, Carey C, et al. Mechanisms in development of interstitial edema and air embolism on decompression from depth. J Appl Physiol 1958; 13:15-29 [6] Colebatch HJH, Smith MM, Ng CKY. Increased elastic recoil as a determinant of pulmonary barotrauma in divers. Respir Physiol 1976; 26:55-64 [7] US Navy diving manual, vol 1, rev 3. Washington, DC: Naval Sea Systems Command, 1993; 3:16-7 [8] Davis JC. Medical evaluation for diving. In: Bove AA, Davis JC, eds. Diving medicine. Philadelphia: WB Saunders, 1990; 290-301 [9] Bove AA, Neuman T, Kelsen S, et al. Observations on asthma in the recreational diving population [abstract]. Undersea Biomed Res 1992; 19(suppl):18 [10] Corson KS, Moon RE, Nealen ML, et al. A survey of diving asthmatics [abstract]. Undersea Biomed Res 1992; 19(suppl):18-9 [11] Farrell PJS, Glanvill P. Diving practices of SCUBA divers with asthma. BMJ 1990; 300:166

Manuscript received July 15, 1994; revision accepted October 7, 1994.

Source Citation:Weiss, Larry D., and Keith W. Van Meter. "Cerebral air embolism in asthmatic scuba divers in a swimming pool." Chest 107.n6 (June 1995): 1653(2). Academic OneFile. Gale. BROWARD COUNTY LIBRARY. 23 Sept. 2009
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Gale Document Number:A17111810

Disclaimer:This information is not a tool for self-diagnosis or a substitute for professional care.

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