Aerospace Decompression Illness

Etiology

During exposure to high altitudes, ADI may occur through various mechanisms, including the use of high-altitude chambers by the military or improper pressurization of aircraft or flight suits. No specific altitude threshold guarantees the absence of decompression sickness. Commercial aircraft typically have a pressurized cabin; however, failure of that system or noncommercial air travel can lead to decompression sickness. The majority of cases of ADI occur with exposures above 25,000 feet. 

Patients engaging in scuba diving before flying are at increased risk of ADI during the flight. Although no standardized guidelines exist, recommendations suggest a waiting period of 12 hours before flying for individuals who have conducted only 1 dive per day. Individuals engaged in multiple dives or requiring decompression stops are advised to wait up to 48 hours before flying.[5][6] However, decompression illness may still occur in some individuals who follow standard procedures before flying.[7][8]

Epidemiology

Exposure to high altitudes may give rise to ADI through diverse mechanisms, including the use of high-altitude chambers by the military or improper pressurization of aircraft or flight suits. No specific altitude threshold can guarantee that decompression sickness will not occur. Although commercial aircraft usually feature pressurized cabins, system failure or noncommercial air travel can still result in decompression sickness. The majority of ADI cases manifest with exposures exceeding 25,000 feet. 

Patients who SCUBA dive before flying are at increased risk of ADI in flight. No consistent guidelines exist, but recommendations suggest waiting 12 hours before flying if they have been making only 1 dive daily. Those participating in multiple dives or those requiring decompression stops should consider waiting up to 48 hours before flying.[5][6] Decompression illness may still occur in individuals who follow standard procedures before flying.[7][8]

Pathophysiology

The pathophysiology of decompression illness is elucidated by combining Henry's and Boyle's laws. Henry's law states that when the pressure over a liquid decreases, the gas dissolved in the liquid also decreases. An illustrative example is when a soda bottle is opened, gas escapes and forms bubbles in the soda. These bubbles consist of carbon dioxide gas escaping from the liquid due to a decrease in barometric pressure. This phenomenon aligns with Boyle's law, which states that the volume of gas is inversely related to the pressure it undergoes at a constant temperature.

Nitrogen is usually dissolved in the human body as a gas and forms bubbles as barometric pressure decreases, thereby affecting various areas. These nitrogen bubbles contribute to dysfunction by inducing nerve compression, vascular stenosis, and distal ischemia. They activate inflammatory pathways and promote platelet aggregation, leading to the release of vasoactive substances that cause vasoconstriction. In addition, these bubbles contribute to axonal degeneration and demyelination.

Tissues exhibit varying rates of gas dissolution, with fat dissolving 5 times more nitrogen than the blood. Fat stores over 50% of the body's nitrogen. When humans engage in diving activities, more nitrogen dissolves in the blood as the depth increases. Excess nitrogen remains dissolved in the body for at least 12 hours after each dive. Flying within 12 to 24 hours after diving increases the risk of decompression illness.

History and Physical

Individuals with decompression illness typically present a history involving recent diving, flying, noncommercial air travel, altitude chamber use, or employment as an altitude chamber technician. Some individuals might not readily recognize the significance of this information and may not volunteer it. Essential components of the patient's history include a rapid ascent during flying or recent diving, closely followed by altitude exposure. Specific symptoms vary based on the affected organ system.

Musculoskeletal

The musculoskeletal system is commonly affected by decompression illness, where nitrogen bubbles involve the joints, particularly the elbows, shoulders, hips, wrists, knees, and ankles. This condition manifests as localized deep pain of varying severity and ranges from mild to severe. The pain is usually experienced during altitude changes, descent, or several hours later. Both active and passive joint movements exacerbate the pain in individuals with decompression illness.

Neurological

Neurological decompression illness manifests with a spectrum of symptoms arising from nitrogen bubbles affecting various parts of the nervous system, including the brain and spinal cord, presenting challenges such as cognitive impairment, sensory disturbances, and motor dysfunction.

Nitrogen bubbles in the brain: These bubbles can cause neurological symptoms such as confusion, memory loss, dysphasia, headache, scotoma, diplopia, blurred vision, extreme fatigue, behavioral changes, seizures, dizziness, vertigo, nausea, and vomiting.

Nitrogen bubbles located in the spinal cord: These bubbles in the spinal cord can result in paresthesias, ascending weakness, paralysis, band-like pain around the chest or abdomen, urinary and fecal incontinence, and muscle weakness.

Nitrogen bubbles in other areas of the nervous system: Nitrogen bubbles affecting other areas of the nervous system may cause paresthesias, tinnitus, and hearing loss.

Respiratory

Nitrogen bubbles in the lungs contribute to symptoms such as burning and deep chest pain, which are intensified by breathing. Individuals may experience shortness of breath and a persistent dry cough.

Integumentary

The integumentary system may also be affected by decompression illness and can include symptoms such as edema or pruritis. In addition, individuals may exhibit mottled skin or livedo reticularis.

Dysbaric osteonecrosis is a rare and late complication that destroys bone tissue, especially in the shoulder and hip. This condition may manifest independently of decompression illness, and in many cases, it remains asymptomatic. When occurring near a joint, the associated changes may progressively worsen over time, potentially leading to debilitating arthritis.

Evaluation

The diagnosis of ADI relies on clinical assessment, necessitating a thorough physical examination that includes vital signs and oxygen saturation. Depending on symptoms, an electrocardiogram may be considered. Currently, no specific diagnostic tests exist to establish the diagnosis definitively.[9][10] Improvement with hyperbaric oxygen therapy serves as a supportive diagnostic indicator.

For patients with an altered level of consciousness, it is essential to assess their blood glucose level, complete blood count, electrolytes, oxygen saturation, ethanol level and drug screen, carboxyhemoglobin level, blood urea nitrogen, and creatinine.

If the patient's mental status does not improve with hyperbaric oxygen therapy, healthcare providers should consider performing a computed tomography of the head. Magnetic resonance imaging (MRI) proves valuable for patients with CNS involvement who show no improvement with hyperbaric oxygen therapy. Notably, obtaining imaging should not delay the prompt transfer for treatment. In cases of persistent symptoms, MRI can help direct further treatment in patients and exclude other potential causes. 

Treatment / Management

In aviation, decompression illness predominantly arises from nonpressurized aircraft flights, cabin pressure fluctuations, and flying shortly after diving. Instances also occur after the use of altitude chambers. If ADI occurs while flying, patients should receive 100% oxygen through a face mask, with unconscious individuals positioned horizontally. Notably, the Trendelenburg position is no longer recommended.[11]

The descent should be initiated immediately with the intention to land, regardless of symptom resolution during the descent. In cases of joint pain, it is recommended to keep the affected extremity still. Oral rehydration with an isotonic crystalloid solution that does not contain glucose is beneficial, whereas intravenous rehydration is recommended in severe cases. Oral rehydration fluids should be non-carbonated, non-caffeinated, and non-alcoholic, preferably isotonic, with drinking water deemed acceptable. Upon landing, individuals should seek care from a healthcare professional knowledgeable in aviation or hyperbaric medicine, even if symptoms have resolved. 

The manifestations are treated similarly to scuba diving decompression illness, primarily with oxygen at ground level or hyperbaric oxygen. Oxygen washes inert gas from the lungs by forming a gradient from the tissues to the lungs, allowing for the removal of inert gas via perfusion and diffusion. ADI is a relatively rare clinical event, necessitating consideration by clinicians within the appropriate historical context. Clinicians are advised to identify local hyperbaric chambers and seek consultation with a physician experienced in hyperbaric medicine. The Divers' Alert Network (DAN) is an excellent source of information. Treatment and management may vary depending on the grade or form of decompression illness and the resources available.[12]

The United States Air Force utilizes 100% oxygen at ground level for 2 hours after the type I decompression sickness at altitude if it resolves upon descent. In more severe cases, clinicians utilize hyperbaric chambers. During 100% oxygen therapy, recompression treatment aims to increase oxygen concentration, reduce nitrogen concentration, diminish carbon monoxide concentration, minimize gas bubble size, and alleviate inflammation.

The United States Navy developed tables that function as standard models for recompression protocols. Treatments are usually given once or twice daily for up to 300 minutes. Healthcare providers typically administer 100% oxygen at pressures between 2.5 and 3 atmospheres absolute.

Pretreatment with 100% oxygen for 30 minutes aids in a nitrogen "washout" from body tissues and helps prevent ADI when flying to altitudes between 18,000 and 43,000 feet for 10 to 30 minutes. Continued oxygen administration during the flight is essential for its beneficial effects. However, using 100% oxygen during flight does not prove effective in preventing ADI. 

Differential Diagnosis

Discriminating decompression illness in aviation-related events can be challenging. A review of 18 cases treated as ADI reveals that over 50% are likely misdiagnoses.[13] 

The potential differential diagnoses include dehydration, electrolyte imbalance, viral syndrome, psychosis, hypoxia, ophthalmic migraines, CNS lesions, tympanic membrane rupture, otitis media, external auditory canal occlusion, round window rupture, bronchospasm, pneumopericardium, supraventricular tachycardia, enteritis, motion sickness, food poisoning, urinary tract infection, prostatitis, anticholinergic effect, radiculopathy, neurapraxia, hypoxia, sprain, fracture, acute arthritis, disk herniation, dermatitis, arterial occlusion, carbon monoxide poisoning, substance abuse, medication adverse effects, myocardial infarction, and pneumothorax.

Diagnostic testing may be necessary to exclude alternative causes for a patient’s presentation, as decompression sickness can mimic many possible disease processes. The lack of a definitive diagnosis should not delay treatment, and if decompression sickness is suspected, oxygen therapy should be promptly administered.

Prognosis

The protocol developed by the United States Air Force, involving 2 hours of 100% oxygen at ground level for type I ADI, results in 94% of subjects requiring no hyperbaric therapy. Notably, these results stem from studies conducted in altitude chambers, where the onset of decompression illness is rapid.

For type II ADI, the prognosis declines as the time to treatment increases. Approximately 75% of patients achieve complete symptom resolution, while an additional 16% experience residual symptoms resolving within the subsequent 3 months. The likelihood of complete resolution varies from 57% to 75%, particularly with treatment delays exceeding 12 hours.[14]

Complications

Potential complications of ADI include paralysis, dysbaric osteonecrosis and arthritis, permanent residual neurological symptoms, and, in severe cases, death.