Civil aviation can result in some unique medical problems that are unfamiliar to most physicians. One such problem, decompression sickness, is not mentioned in most medical texts, and is not included in most medical school instruction. If not promptly recognized and treated, decompression sickness can result in permanent disability or death. I report a case of altitude-induced decompression sickness after a flight in an unpressurised aircraft. 

DECOMPRESSION SICKNESS (DCS) is an illness caused by a reduction in ambient pressure, resulting in the formation of bubbles of inert gas (usually nitrogen) within body tissues. DCS can occur as a result of high altitude exposure.

 The risk of DCS is increased when a compressed air dive is immediately followed by exposure to reduced atmospheric pressure, such as a flight in an aircraft. The risk is further increased when a flight is accomplished after several deep dives in succession without adequate time for re-equilibration. The incidence of DCS among private pilots is unknown. Many cases of DCS probably go unrecognized, with spontaneous recovery. Even when the illness is recognized and treated, there is no requirement for reporting DCS by either the pilot or treating physician.

Case Report

A healthy, experienced, 59-year-old private pilot planned a cross-country flight from Missouri to California. He had an uneventful ascent to an altitude of 28,000 feet above mean sea level (MSL) in the unpressurized airplane, and began using supplemental oxygen after passing 12,000 feet MSL, as required by federal aviation regulations. After 1 hour at his cruising altitude, the pilot noticed the onset of weakness and paresthesias of the right arm. A few minutes later, he felt extreme fatigue and chest tightness associated with a dry cough. These symptoms progressively worsened, and were soon accompanied by left arm weakness and paresthesias. He had no dyspnea, diaphoresis, visual or auditory symptoms, or alteration in consciousness. There was no previous history of similar symptoms or of pulmonary, cardiac, or neurologic problems. The pilot remained on oxygen by mask, and began to slowly descend, landing his aircraft in New Mexico. He remained ill, and was immediately transported to a local hospital.

Upon arrival at the emergency department, he was diaphoretic and ashen. He continued to complain of weakness and paresthesias of both arms, but more severe on the right. Supine blood pressure was 115/88 mm Hg, supine pulse rate 98/min, and respiratory rate 20/min. When the patient was standing, blood pressure dropped to 75/41 mm Hg, with pulse unchanged. There was no skin rash, mottling, or oedema. Head and neck examination was unremarkable. Cardiac rate and rhythm were regular, with normal heart sounds. Mild crackles were heard at both lung bases. Abdominal examination was unremarkable. On neurologic examination, the patient was alert and fully oriented. All cranial nerves were normal. Examination of the right upper extremity revealed severe flexor weakness at the elbow and wrist, severe weakness of grip strength, numbness of the forearm, and severely impaired fine motor control. The left upper extremity also showed flexor weakness and decreased grip strength, but not as severe as on the right. Sensation was normal. Strength and sensation in the lower extremities was normal. Gait was not tested because of orthostasis.

Chest x-ray films showed mild increase in interstitial markings. Electrocardiogram showed a 1 mm elevation in ST segments in leads V2 and V5. Perfusion scans of the lungs were normal. Arterial blood gas values, with the patient breathing room air, were pH 7.40, P02 111 mm Hg, Pco2 33.4 mm Hg, and oxygen saturation 96%. Serum potassium level was 3.3 mg/dL; remaining electrolyte values were normal.

A diagnosis of altitude-induced decompression sickness was made. The patient was maintained on 100% oxygen by mask, and transported by pressurized aircraft to the Hyperbaric Medicine Division at Brooks Air Force Base in Texas, arriving approximately 12 hours after landing his aircraft. Upon arrival, findings on physical examination were unchanged. The patient was immediately placed in the hyperbaric chamber for compression therapy. Following a standard hyperbaric treatment, some neurologic improvement was noted, although the deficits of the right upper extremity persisted. Over the next 4 days, the patient received an additional seven treatments. The first 5 of these treatments produced improvement. The decision to terminate treatments was made when there was no further improvement after the final two treatments. At the conclusion of hyperbaric therapy, there was persistent weakness of the right shoulder and weakness of the intrinsic muscles of the right hand. At follow-up 1 year later, the patient had complete recovery in the muscles of the right hand, but continued to have mild weakness in the right shoulder.

discussion

One of the most serious physiologic problems associated with aviation is decompression sickness (DCS). As early as 1917, Henderson predicted the possibility of DCS in aviators flying at more than 20,000 feet. DCS occurs when a person is subjected to a reduction in ambient pressure. During decompression, body tissues become supersaturated with inert gas (nitrogen). Excess nitrogen in the tissues diffuses into the blood, is carried to the lungs, and eliminated in expired air. The amount of nitrogen remaining in body tissues is directly proportional to the nitrogen partial pressure around the person. If the amount of dissolved nitrogen exceeds some threshold, the critical supersaturation point, some of the nitrogen comes out of solution in the form of bubbles. These bubbles are the basis for the development of symptoms of DCS. The etiology, pathophysiology, epidemiology, and clinical manifestations of altitude decompression sickness were described by Fryer in his 1969 monograph.

Decompression sickness is rare for unpressurised flights that do not exceed an altitude of 29,000 feet. There has been a recent proliferation of unpressurised private aircraft that can exceed altitudes of 24,000 feet; Beech, Piper, Cessna, and Mooney all currently manufacture such aircraft.

The clinical manifestations of DCS are variable, with many of the symptoms being protean. The varied nature of DCS has led Behnke to compare it with the spirochete as the "great imitator." The many signs and symptoms of DCS can occur in any combination, which can make the diagnosis difficult. Wirjosemito, et al. noted that the clinical manifestations of serious altitude DCS include, in descending order of frequency, joint and limb pain, headache, visual disturbances, extremity paresthesia, mental confusion, extremity weakness, fatigue, cerebella signs, pulmonary manifestations (chokes), and extremity numbness.

Several factors may predispose a pilot to the development of DCS. Risk of DCS increases as the altitude of exposure increases, as the rate of ascent increases, and as the duration of exposure lengthens. Personal factors that increase risk of DCS include age (susceptibility increases with age), body build (obese individuals are at greater risk), and recent joint injury.

Initial management of decompression sickness consists of hydration, delivery of 100% oxygen, and transfer to a compression chamber for the compression therapy. Serious cases of DCS may require other supportive measures (e.g., intubation and pressor agents).

Compression (hyperbaric) therapy is the definitive treatment of DCS. The longer the delay in treatment, the poorer the outcome. Rudge and Shafer, in a study of altitude-induced DCS cases treated by the United States Air Force, noted that patients treated rapidly with compression therapy recovered faster than patients whose treatment was delayed.

The Divers Alert Network, located at Duke University, provides 24-hour information regarding the diagnosis and management of DCS, and can supply up-to-date information on compression chamber locations. The number for this service is (919) 684-8111.