Diving Medicine: Questions Physicians Often Ask, Part 2

July 1, 2004

Most sport-diving problems are mild and self-limited; however, serious or life-threatening situations can arise. In a previous article (CONSULTANT, June 2004, page 961), we addressed fitness and safety issues. In this article, we review the principal medical problems associated with sport diving.

Most sport-diving problems are mild and self-limited; however, serious or life-threatening situations can arise. In a previous article (CONSULTANT, June 2004, page 961), we addressed fitness and safety issues. In this article, we review the principal medical problems associated with sport diving.

1How often do medical problems associated with diving occur?

The problems that occur most frequently-perhaps as often as on every dive-are generally mild and self-limited and can be managed by the diver. These include barotrauma to the middle ear during descents and ascents, and problems that occur at the surface. About once in every 1000 dives, symptoms persist and the diver seeks medical attention, usually from a primary care clinician. Tips for safer diving are listed in Box I.

Serious medical problems are infrequent. Decompression sickness occurs 2 or 3 times in every 10,000 scuba dives.1 About 100 deaths occur among scuba divers in the United States each year.2 In about 20% of the cases, the cause was arterial gas embolism; in 50%, the diagnosis is not obvious, but panic and drowning are often listed as the causes of death.3,4 Although alcohol use is associated with about 50% of nondiving drowning deaths, the latest Diver Alert Network statistics show that it is associated with only about 5% of scuba diving accidents and deaths.2

Middle ear barotrauma serious enough to cause signs and symptoms (eg, hearing loss, fluid sensation, pain, fluid distention, infection, or perforation of the eardrum) occurs in about 10% to 20% of diving activities. Except for perforation of the eardrum, these symptoms can be managed with vasoconstrictors. The diver can resume diving as soon as he or she can achieve pressure equilibration in the middle ear.

Divers with any postdive residual symptoms-such as dizziness, nystagmus, or equilibrium problems-or a history of loss of consciousness require careful evaluation. Divers who present with a history of near-drowning, but who are unlikely to have decompression sickness or arterial gas embolism, need to be observed for delayed onset of pulmonary edema. This condition usually manifests within 24 hours of the accident.

Less serious symptoms, such as subcutaneous emphysema, pruritus, rash, and exceptional fatigue, should be noted during the examination and the patient instructed to return immediately for reevaluation if there are signs of progression or if new symptoms emerge.

2How are the more serious or life-threatening conditions associated with diving best managed?

Although diving is a relatively safe activity, unforeseen events or violations of rules may sometimes result in serious or life-threatening situations. The chief of these is decompression illness, which includes 2 serious conditions associated with breathing compressed gas underwater: arterial gas embolism and decompression sickness. (Resources to contact about serious diving problems are listed in Box II.)

Arterial gas embolism. This condition, which can occur with a single ascent from depths less than 10 ft, results from overinflation of the lungs by expanding pulmonary gas during reduction of surrounding pressure (pulmonary barotrauma). It is usually associated with breath-holding during ascent from a scuba dive. Other causes include running out of air at depth and conditions that retain air in the lungs, such as asthma, emphysema, emphysematous blebs, pleural adhesions, and bronchiolitis. The onset is sudden, either during or shortly after the causative event.

As predicted by Boyle's law ("the volume of a mass of gas in an enclosed space changes inversely with absolute pressure"), retained gas in the lungs expands during ascent. If the gas is not allowed to escape freely, it overinflates the lungs and elevates alveolar pressure. When the pressure exceeds the elastic limit of the alveoli, explosive rupture of the alveoli and adjacent capillaries occurs. This can result in the escape of gas into pulmonary veins and thence to the heart. If the gas reaches the carotid arteries, embolization of cerebral vessels is virtually inevitable.

Once embolic occlusion of the brain's circulation has occurred, arterial gas embolism can present with any of the symptoms of a cerebrovascular accident. Embolization of the coronary arteries may lead to myocardial ischemia and infarction. Immediate bubble reduction is essential to restore circulation to the embolized areas and prevent permanent brain and/or heart damage. Animal models demonstrate that bubbles largely disappear from the arterial circulation within minutes of entry. Residual symptoms are attributed to the effects of the bubble-endothelium interaction (ie, an inflammatory reperfusion-type insult to the endothelium).

Signs and symptoms. Signs of arterial gas embolism, which usually emerge when the diver surfaces or almost immediately thereafter, include loss of consciousness and/or other CNS manifestations, such as headache, blindness, seizures, paralysis, nausea, vomiting, dizziness, nystagmus, and loss of equilibrium. The first-response treatment is the immediate administration of 100% oxygen by face mask (Box III). This intervention is so effective that symptoms completely resolve in 50% of divers.5 If the diver becomes asymptomatic, we recommend one washout hyperbaric oxygen recompression treatment. The vasculature sensitized by the gas emboli may interact with inert gas being released from the diver's tissues and cause a pernicious type of decompression sickness, even though diving tables or computer limits were not violated.

Treatment. If signs or symptoms of brain injury persist after first- response interventions in the emergency department and/or recompression chamber, ancillary interventions are required. These include corticosteroids, intravenous lidocaine at dosages similar to those used in managing arrhythmias, intravenous fluids, and management of intercurrent problems such as seizures, pneumothorax, and hypoxemia/ apnea.6,7

Decompression sickness. This condition most often occurs after prolonged or repetitive dives. It results from nitrogen bubble formation in tissues when ascents occur faster than the rate at which the body can effectively eliminate the inert gas load (eg, nitrogen, if air is used in the scuba tanks) incurred during the dive. It may present with a variety of signs and symptoms that are not always clearly related to causes such as exceeding diving table or computer limits. Decompression sickness may also result from such conditions as predisposition to joint pain (the bends) because of atrial ventricular shunts, or disordered decompression (such as from flying after diving or compression vasoneuropathy from interference with blood flow in an extremity).

When the vestibular system, spinal cord, or brain is affected, the consequences may be significant. Neurologic problems occur in more than 50% of patients with decompression sickness. Onset may be sudden or gradual during decompression or up to 24 hours after diving. A particularly difficult condition to manage is decompression sickness symptoms that occur along with, or following treatment of, arterial gas embolism. In these cases, the depth of dive may be much less than expected for decompression sickness.

Signs and symptoms. Mild manifestations include rashes, pruritus, joint pain (the bends), fatigue, headache, flu-like syndromes, and edema. Serious manifestations include nystagmus, vertigo, chokes (respiratory distress followed by circulatory collapse), altered mental status, paralysis, aphasia, paresis, paresthesias or neuropathies, shock, and death. The earlier the symptoms appear, the more serious decompression sickness is likely to be. Even minor early manifestations, such as weakness or numbness in the extremities, may eventuate in catastrophic consequences, such as paraplegia, that may be irreversible without timely treatment.

Treatment. The first-response treatment of decompression sickness is administration of 100% oxygen by face mask. Supplemental interventions include rehydration and, possibly, administration of aspirin to prevent sludging. Hyperbaric oxygen recompression is the definitive treatment. More than 1 recompression treatment may be required if symptoms do not resolve. The earlier recompression treatment is started, the more likely the complete resolution of symptoms.8

We recommend hyperbaric oxygen treatment for any diver who manifests symptoms of decompression sickness following a dive with compressed gas, regardless of the depth or duration of the dive. This treatment is recommended even if the diver presents 3 or 4 days after the diving activity, because it may prevent occult, delayed nervous system and bone problems, such as plaques and osteonecrosis.

Loss of consciousness. Any loss of consciousness and/or disorientation in the water may result in drowning. Besides arterial gas embolism and decompression sickness, other causes of loss of consciousness include panic, breath-holding after hyperventilation, nitrogen narcosis, arrhythmias, myocardial infarction, carbon monoxide poisoning, drug overdoses (effects of drugs are likely to be magnified under pressure), and middle or inner ear injury.

In the case of loss of consciousness or altered mental status, try to determine whether a significant inert gas load was involved. In any case, a diver who loses consciousness immediately after ascent should be assumed to have arterial gas embolism and be treated immediately with hyperbaric oxygen recompression. If an inert gas load has not occurred-for example, if a diver experiences an arrhythmia when entering the water-recompression is not needed.

3Does an episode of decompression sickness or arterial gas embolism have long-term consequences?

If the diver's problem resulted from a diving table or computer limit violation and if he was treated with hyperbaric oxygen recompression and recovered completely, no residual long-term consequences are anticipated. We allow the diver to return to diving in a couple of weeks.

If diving table or computer limits were not violated and nothing can be identified that interfered with off-gassing (that is, the release by tissues, transport by the bloodstream, and exchange of the inert gas in the lungs with the ambient environment) during the ascent or after the diver left the water (ie, disordered decompression), the diver may be "bends-prone." In this case, we discourage future diving. We also discourage future diving if residual neurologic impairment or a clinically significant patent foramen ovale is present after appropriate treatment with hyperbaric oxygen recompression.

4Does sport diving have any other long-term health risks?

Otolaryngologic problems are a possible adverse consequence. Middle-ear barotrauma occurs in most diving activities. Recurrent ear squeezes may cause scarring of tympanic membranes and hearing loss. Scarring of tympanic membranes and "surfers' nodules" in ear canals are frequently observed in divers who dive frequently for many years. Chronic sinusitis and pharyngitis have been observed in the women breath-hold divers of Japan who daily perform multiple dives to collect foodstuffs (although in all other parameters that were studied, these women were healthier than their nondiving counterparts).

Osteonecrosis is another possible long-term consequence of diving, although it is rare in sport divers. Juxta-articular osteonecrosis, which can lead to collapse of the joint, is most often observed in commercial divers who make long, deep dives, often violate diving table limits, and have recurrent episodes of decompression sickness. Plaque lesions similar to those seen in multiple sclerosis were noted coincidentally in divers' brains and spinal cords in cases in which autopsies were done for non-diving-related causes of death. Most had diving histories similar to those of divers in whom osteonecrosis develops. Although the plaques were identified, no neurologic consequences could be ascribed to them. Consequently, the long-term effects of these lesions are not known. n

References:

REFERENCES:

1. Bove AA. Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med. 1998; 25:175-178.

2. Vann R, Denoble P, Uguccioni D, et al, eds. Report on Decompression Illness, Diving Fatalities and Project Dive Exploration. Durham, NC: Divers Alert Network; 2002.

3. Strauss M. The panic syndrome. Physician Sportsmedicine. 1973;1:39-42.

4. Strauss MB, Shane SL. The no-panic syndromes in underwater diving. Physician Sportsmedicine. 1982; 10:89-99.

5. Dick AP, Massey EW. Neurologic presentation of

decompression sickness and air embolism in sport

divers. Neurology. 1985;35:667-671.

6. Moon RE, Sheffield PJ. Guidelines for treatment of decompression illness. Aviat Space Environ Med. 1997;68:234-243.

7. Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000;342:476-482.

8. Bayne CG. Acute decompression sickness: 50 cases. JACEP. 1978;7:351-354.

FOR MORE INFORMATION:

m Bennett PB, Elliot DH, eds. The Physiology and Medicine of Diving. 4th ed. Philadelphia: WB Saunders Company; 1993.

m Dierker RC, Strauss MB. Treating swimmer's ear. US Pharmacist. 1990;15:72-74.

m Joiner JT, ed. NOAA Diving Manual: Diving for Science and Technology. 4th ed. Washington, DC: US Dept of Commerce, National Oceanic and Atmospheric Administration; 2001.

m Moon RE, Camporesi EM, Kisslo JA. Patent foramen ovale and decompression sickness in divers. Lancet. 1989;1:513-514.

m Strauss MB, Aksenov IV. Diving Science: Essential Physiology and Medicine for Divers. Champaign, Ill: Human Kinetics; 2004.

m Strauss MB, Borer RC Jr. Diving medicine: contemporary topics and their controversies. Am J Emerg Med. 2001;19:232-238.

m Strauss MB, Orris WL. Injuries to divers by marine animals: a simplified approach to recognition and management. Mil Med. 1974;139:129-130.

m US Navy Diving Manual. NAVSEA 09994-LP-001-9110. Flagstaff, Ariz: Best Publishing; 1993.