Atmospheric pressure decreases as altitude increases, while the percentage of O2 in air remains constant; thus, the partial pressure of O2 decreases with altitude and at 18,000 ft (5500 m) is about 1/2 that at sea level. About 20% of persons ascending above 8000 ft (2500 m) in < 1 day develop some form of altitude sickness. Persons who have had one attack are slightly more susceptible to another if conditions are similar, but the effects of high altitude vary greatly among and within individuals. Young children are most susceptible, and incidence decreases linearly with increasing age. Abrupt exposure to high altitude (eg, depressurization of aircraft, balloon ascent) causes acute severe hypoxia and loss of consciousness rather than altitude sickness. Most persons acclimatize to altitudes of up to 10,000 ft (3000 m) in a few days. The higher the altitude, the longer full acclimatization takes. Acclimatization is an integrated series of responses that gradually restore tissue oxygenation toward normal in persons exposed to altitude. Features of acclimatization include sustained hyperventilation with persistent partially compensated alkalosis, an initial increase in cardiac output (which is lower than normal maximum cardiac output), increased RBC mass, and increased tolerance for anaerobic work. After many generations at altitude, some ethnic groups have acclimatized in slightly different ways. Pathology
and Pathophysiology
Hypoxia stimulates breathing, increasing tissue oxygenation but also causing respiratory alkalosis, which contributes to symptoms until loss of HCO3 in urine partially compensates. The basic pathophysiology of altitude sickness is disturbance of water and electrolyte balance. Capillary permeability is increased, allowing fluid to accumulate in various locations; the cause is thought to be vascular endothelial damage. In susceptible persons, increased ADH secretion results in tissue fluid retention, and plasma volume is decreased, simulating an increase in Hct. A low hypoxic ventilatory response is not associated with altitude sickness. The roles of atrial natriuretic peptide, aldosterone, renin, and angiotensin are unclear. Hypoxia increases pulmonary vascular resistance and pulmonary artery pressure, but systemic resistance and arterial pressure usually change little. Cerebral blood flow is decreased by hypocapnia, is increased by hypoxia, and consequently varies with the balance between arterial CO2 and O2. The role of this variation in symptomatology is unclear. Symptoms,
Signs, and Diagnosis
Peripheral or facial edema may be due to high altitude or, as at sea level, to strenuous exertion. Thrombophlebitis may occur at extremely high altitude, especially if a person is dehydrated and inactive. Dimmed vision, hemianopsia, scotomata, and even transient blindness have been reported. Persons who have had radial keratotomy may have significant visual disturbances at altitudes > 16,000 ft (> 5000 m) or even as low as 10,000 ft (3000 m). These alarming symptoms disappear rapidly after descent. Retinal hemorrhages may develop at altitudes as low as 9000 ft (2700 m); they are common above 16,000 ft. They are usually asymptomatic unless in the macular region and resolve rapidly without sequelae. Small hemorrhages may also occur under the nails, in the kidneys, and in the brain. The various clinical forms of altitude sickness are not separate entities but parts of a spectrum in which one or more may be present in different degrees. CNS dysfunction is considered a factor in several forms. No test can reliably predict development of altitude sickness. Acute mountain sickness (AMS): This form is the most common and may develop at altitudes as low as 6500 ft (2000 m). It is characterized by headache, fatigue, nausea, dyspnea, and sleep disturbance. Exertion aggravates the symptoms. AMS usually subsides in 24 to 48 h but occasionally evolves into high-altitude pulmonary edema, high-altitude cerebral edema, or both. Laboratory studies are nonspecific and are not helpful in diagnosis. High-altitude pulmonary edema (HAPE): This form is less common but more serious, usually developing 24 to 96 h after rapid ascent above 8000 ft (2500 m). When most persons ascend above 8000 ft, fluid accumulates in lung interstitial tissues and is usually drained away by the lymphatics. When fluid accumulates more rapidly than it is drained, frank alveolar edema develops. Persons who have had one episode of HAPE are likely to have another and should be so warned. Respiratory infections, even minor ones, appear to increase the risk of HAPE. Recently identified persons who have repeated episodes of HAPE are described as HAPE-S (susceptible); the reason for their susceptibility is unknown. Men are 5 times more likely than women to develop HAPE, but AMS and high-altitude cerebral edema affect men and women equally. Children appear to be at a slightly greater risk, as are longtime high-altitude residents when they return after a brief stay at low altitude. The absence of one pulmonary artery is a rare congenital anomaly that greatly increases the risk of HAPE, even at altitudes as low as 5000 ft (1500 m). Persons who develop HAPE repeatedly or at an unusually low altitude should be evaluated for pulmonary artery pathology or old pulmonary embolism. HAPE is a high-pressure edema with increased microvascular permeability. Excessive vasoconstriction in some areas causes overperfusion in others, and the resulting ventilation/perfusion mismatch is considered the precipitating cause. There is new evidence that a decrease in alveolar nitric oxide, perhaps due to absence of nitric oxide synthase, is an important factor in susceptibility to HAPE. HAPE is characterized by increasing dyspnea; irritative cough that produces frothy, often bloody sputum; weakness; ataxia; and, later, coma. Cyanosis, tachycardia, and low-grade fever are common and, with fine or coarse pulmonary rales (often audible without a stethoscope), may lead to a misdiagnosis of pneumonia. Chest x-ray shows Kerley lines and patchy edema unlike that in heart failure. Atrial pressure is normal, but pulmonary artery pressure is greater than that in healthy persons experiencing hypoxia. HAPE may worsen rapidly; coma and death may occur within hours. High-altitude cerebral edema (HACE): Cerebral edema is believed to be present to a mild degree in all forms of altitude sickness. Diffuse or patchy edema of the brain, seen on CT scans, is thought to contribute to HACE and to AMS. Severe edema is manifested as ataxia, headache, mental confusion, and hallucinations. Stiff neck does not occur, and papilledema is not necessary for diagnosis. CSF pressure may be elevated, but the fluid is normal. Gait ataxia is a reliable early warning sign. Coma and death may develop within a few hours of the first symptoms. HACE must be differentiated from other causes of coma (eg, infection, vascular accident, ketoacidosis) by the history, absence of significant fever or paralysis, and normal blood and CSF studies. ProphylaxisAltitude sickness is best prevented by slow ascent, but the safe rate of ascent varies among individuals. Most can ascend to 5000 ft (1500 m) in 1 day without symptoms, but many are affected by ascending to 8000 ft (2500 m). Above this level, a rate of 1500 ft (460 m)/day is advisable. Climbers should learn how fast they can ascend without developing symptoms; a climbing party should be paced for its slowest member. Although physical fitness enables greater exertion with less O2 consumption, it does not protect against any form of altitude sickness. Strenuous effort should be avoided for 24 to 36 h after the ascent is completed, but bed rest is less beneficial than mild exercise. Drinking much more water than usual is important, because overbreathing dry air at altitude greatly increases water loss, and dehydration with some degree of hypovolemia aggravates symptoms. Additional salt should be avoided. Alcohol seems to worsen AMS and diminishes nocturnal ventilation, thus accentuating sleep disturbance. Eating frequent small meals that are high in easily digested carbohydrates improves altitude tolerance and is recommended for the first few days. Acetazolamide 125 mg at bedtime (for most persons) or 125 mg q 8 h is an effective prophylactic for AMS. Sustained-release capsules (500 mg once daily) are also available. Starting acetazolamide before the ascent has no advantage. Acetazolamide inhibits carbonic anhydrase, increasing ventilation and allowing better O2 transport with less alkalosis; it eliminates periodic breathing (almost universal during sleep at high altitude), thus preventing sharp falls in blood O2. Acetazolamide should not be given to patients allergic to sulfa drugs. Low-flow O2 during sleep has the same effect but is inconvenient. Analogs of acetazolamide offer no advantage. Antacids are useless for prevention. Dexamethasone, which minimizes symptoms of AMS, is not recommended for prevention. Retinal hemorrhages require no treatment, generally resolving while the climber remains at high altitude. Acute Mountain Sickness seldom requires treatment other than fluids, analgesics, a light diet, mild activity, and (rarely) descent. Dexamethasone4 mg po q 6 h is effective; Acetazolamide250 mg po q 6 h may alleviate symptoms. Ibuprofen, which decreases platelet aggregation, is more effective than aspirin for altitude headache but may also cause easy bruising. When HAPE is suspected, bed rest and O2 may be tried, but if the condition worsens, immediate descent is essential. If descent is not possible, the person can be placed in a large hyperbaric bag in which the pressure can be increased, simulating descent. This measure helps buy time in an emergency but is not a substitute for descent. Nifedipine 20 mg sublingually followed by a 30-mg slow-release tablet lowers pulmonary artery hypertension and is beneficial. Strong diuretics (eg, furosemide) are contraindicated. Although morphine is effective, the resulting respiratory depression may outweigh the drug's value. Because the heart is normal in HAPE, digitalis is of no value; however, in the subacute form of infantile and adult mountain sickness, the heart fails, and digitalis and descent are necessary to save life. Once the patient is hospitalized, other causes of pulmonary disease are ruled out, and the patient is treated with adequate oxygenation (sometimes by intubation and positive end-expiratory pressure), bed rest, judicious diuresis, postural drainage, and, if superimposed infection is suspected, antibiotics. When promptly treated, patients usually recover from HAPE within 24 to 48 h. Severe HACE requires immediate descent. Supplementary oxygen or pressurization in a hyperbaric bag buys time but does not cure. Dexamethasone 8 mg IV q 4 h helps but not dramatically. Its value in an altitude emergency is dubious. Aviation Decompression Sickness (DCS) may occur at any time within an unpressurized flight, an unexpected aircraft depressurization, altitude chamber operations or high altitude high opening parachute operations. DCS does not generally occur with exposure to altitudes below 18,000 feet. Aviators are generally protected from DCS by maintaining cabin altitudes at lower levels by cabin pressurization, by use of pressure suits, by pre-oxygenation to reduce total body nitrogen or a combination of these measures. Currently, the largest numbers of DCS cases seen in Naval Aviation operations involve low pressure chamber activities at the rate of about 1 case per 1000 chamber exposures. Effects of bubble formation
Because these bubbles may form at different locations, there may be multifocal symptoms that may not necessarily following dermatomal or anatomic distributions. Once bubbles are formed, they expand as dissolved gases continue to come out of solution. Carbon dioxide is highly diffusible and contributes to bubble enlargement, especially if formed in excess by vigorous exercise. For this reason, DCS patients should be kept at rest. Clinical syndromes of DCS Limb pain (musculoskeletal symptoms) : The most common presenting symptom, accounting for 60-70% of altitude
related cases and 80-90% of diving cases. Pain usually begins gradually and is
poorly localized, but increases in intensity and localizes with time as a
throbbing ache. Sometimes the pain is sharp and clearly localized. Pain may be
mild or intermittent at first but may increase steadily and can become very
severe. Often poorly localized, the pain is characteristically hard to describe,
but "deep" and "like something boring into the bone" are
expressions sometimes used. Local inflammation and tenderness are often absent,
and the pain may not be affected by motion. Guarding may be seen. If the painful
area is accessible, inflation of a blood pressure cuff over the site may relieve
the pain and help distinguish it from pain of ischemia or nerve entrapment which
would be made worse by such pressure. Sharp, shooting or encircling pain,
migratory pain and tingling or burning trunk pains arise from CNS involvement
and should be considered Type II DCS and treated accordingly. The skin is often affected during and after the decompression event. There are two distinct manifestations; The most common symptom is a transient, multifocal itching, often associated with a scarlatiniform rash, and is not an indication of development of serious sequelae. Itching or crawling sensations usually occur in hyperbaric chamber dives and do not require recompression as a rule. Cutis Marmorata results from venous obstruction and vasospasm and presents as confluent rings of pallor, surrounded by areas of cyanosis which blanche to the touch. This may be the harbinger of more serious forms of DCS and should be treated by recompression. Rare. Recompression usually provides prompt relief of pain, but swelling of lymphatic tissue may persist after treatment. Type II DCS Early Type II DCS symptoms may seem inconsequential. Fatigue is a very common and early symptom, progressing to weakness, dyscoordination and other difficulties. Many symptoms of Type II DCS are the same as those of arterial gas embolism (AGE), although AGE presents very early, usually within 10 minutes after exposure. Treatment of AGE is also appropriate for DCS. Neurological symptoms may accompany pain or occur independently. They occur in > 50% of patients with decompression sickness. Neurologic symptoms and signs vary from mild paresthesia to major cerebral problems. Seemingly minor early manifestations, such as weakness or numbness in the extremities, may have serious consequences, such as paraplegia, which may be irreversible if treatment is delayed or inappropriate. Spinal cord DCS may present with numbness, weakness and paralysis or urinary dysfunction, and occurs in about 10% of Type II altitude DCS cases. Cerebral DCS is the most common of Type II DCS. Fatigue is a very common symptom. There may be confusion, odd behavior and personality changes. Headache, tremor, hemiplegia, hemisensory losses and scotomata may also occur. These signs and symptoms may range from mild and seemingly inconsequential to fulminant and life threatening. Vestibular involvement may produce severe vertigo by imitating a round or oval window rupture with, tinnitus and hearing loss. The occurrence of any neurological symptom after a dive or flight should be considered a symptom of Type II DCS or AGE. The “Chokes” is the respiratory form of decompression sickness. It results from massive bubble embolization of the pulmonary vascular tree and account for 5-10% of altitude DCS. In some patients, the condition resolves spontaneously, but without prompt recompression, it can rapidly progress to circulatory collapse and death. Substernal discomfort and coughing during deep inspiration or during inhalation of tobacco smoke are often early manifestations. In animal studies, the chokes are strongly associated with exposure to altitude soon after diving. The chokes and other serious manifestations developing at altitude are not necessarily cured by return to ground level and may require prompt chamber recompression. If not treated promptly, the result may be circulatory collapse and death. Special considerations
and Prevention
Significant bubble formation can usually be avoided by restricting the uptake of gas--eg, by limiting the depth and duration of dives to a range that does not require decompression stops during ascent. Decompression sickness seldom develops when dives are kept within appropriate no-stop limits or when decompression tables are followed. Repeated dives may cause decompression sickness. Because excess inert gas remains in the body after every dive, the amount of excess gas increases with each dive. If the interval between dives is < 12 h, repetitive dive tables must be used. OPNAVINST 3710.7
prohibits flight or low pressure chamber exposure within 24 hours of a SCUBA or
compressed air dive or high pressure chamber run. This may be reduced to 12
hours for urgent operational requirements provided there are no symptoms
following the dive and the subject is examined and cleared by a flight surgeon. This refers to
dives at elevations, such as in mountain lakes and may be a factor in increasing
risk for DCS. U.S. Navy dives above 2300 ft. MSL require CNO approval. Triage and referral of altitude DCS cases Type I DCS If symptoms
appear at altitude and resolve on descent, use 100% 02 for two hrs
and observe for recurrence. If none, light duty only and ground for 1 week. Warn
the patient to return promptly if symptoms recur for hyperbaric therapy. If symptoms develop at altitude and persist, or develop after flight, place the patient on 100% 02 while arranging evacuation or recompression. If evacuation is delayed and symptoms resolve, leave on oxygen for 24 hrs. Then, place the patient on limited duty for 1 week, and no physical training for 72 hrs. Recurrence must be treated by hyperbaric therapy. Current U. S. Navy diving medicine protocols are to treat all patients referred for altitude DCS regardless of whether or not symptoms have resolved. Type II DCS All must be
recompressed urgently or evacuated promptly for treatment. Aeromedical evacuation of DCS cases
24 Hour Points of Contact:
Naval
Medical Research Institute (NMRI) Bethesda, MD This section was contributed by CDR Jay S. Dudley, MC, USN (FS).
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