If You Had Altitude Sickness When Young Will You Have It Again
Sports Health. 2010 Jul; 2(four): 291–300.
Return to Action at Altitude After Loftier-Altitude Disease
Kevin DeWeber
*Uniformed Services Academy of the Health Sciences, Bethesda, Maryland
Keith Scorza
‡Army Community Hospital, Fort Belvoir, Virginia
Abstract
Context:
Sports and other activities at high altitude are popular, all the same they pose the unique risk for high-altitude disease (HAI). Once those who have suffered from a HAI recover, they commonly desire or demand to perform the same activity at altitude in the firsthand or distant futurity.
Evidence Acquisition:
As based on key text references and peer-reviewed journal manufactures from a Medline search, this article reviews the pathophysiology and general treatment principles of HAI.
Results:
In addition to the blazon of HAI experienced and the electric current level of recovery, factors needing consideration in the render-to-play programme include concrete activity requirements, flexibility of the activity schedule, and available medical equipment and facilities. Most important, adherence to prudent acclimatization protocols and gradual ascent recommendations (when in a higher place 3000 yard, no more than 600-thou net meridian gain per mean solar day, and 1 rest day every 1 to 2 rising days) is powerful in its preventive value and thus strongly recommended. When these are not practical, prophylactic medications (acetazolamide, dexamethasone, salmeterol, nifedipine, or phosphodiesterase inhibitors, depending on the type of prior HAI) may exist prescribed and can reduce the run a risk of disease. Athletes with HAI should be counseled that physical and mental performance may be adversely afflicted if action at altitude continues before recovery is complete and that there is a gamble of progression to a more than serious HAI.
Conclusion:
With a thoughtful programme, most recurrent HAI in athletes can be prevented.
Keywords: altitude illness, athlete, activity
Mountaineering, trekking, downhill skiing, and other sports at high distance are popular throughout the globe. Participants often travel to remote parts of the world to reach new heights, to relish nature, and to challenge the limits of endurance. Although these activities can exist extremely gratifying, there are risks that must be considered. In add-on to the typical able-bodied injuries, these sports are unique in their gamble of causing high-altitude illness (HAI).
Although a dandy deal is known virtually the diagnosis and treatment of HAI, there is a dearth of literature on how to prudently send an athlete back to altitude sports one time he or she has been treated. This article examines the medical literature regarding the pathophysiology, treatment, and prevention of HAI, and it presents reasonable guidelines for returning loftier-altitude athletes back to activity and competition.
Physiology of Acclimatization to Altitude
HAI results from the effects of hypobaric hypoxia on the body. Equally one ascends, atmospheric pressure gradually decreases; therefore, the partial pressure of oxygen declines, which results in decreased arterial force per unit area of oxygen and arterial oxygen saturation. Although the human body has mechanisms to adapt to hypoxia, disease results if ascent occurs too speedily. Such illness manifests itself in 3 syndromes: acute mountain sickness (AMS), loftier-distance cerebral edema (HACE), and high-altitude pulmonary edema (HAPE).
Acclimatization is the process of adapting to hypobaric hypoxia, to minimize its furnishings on the body. This procedure is nearly effective if washed incrementally every bit a person gains elevation; however, the rate of acclimatization varies among individuals. Most persons can acclimatize upward to approximately 5500 m if given sufficient time (weeks to a few months for full effect), and they deacclimatize in the same time frame upon returning to low altitude. Higher up this altitude, the torso is unable to fully recoup, and some affliction occurs.
Increased ventilation is the torso'southward first adjustment, every bit driven past the hypoxic ventilatory response. The resulting tachypnea somewhat increases arterial pressure of oxygen simply as well results in respiratory alkalosis because of the concomitant driblet in arterial carbon dioxide. Individuals vary in the force of their hypoxic ventilatory response; those with a lower response are at higher risk of HAI. Hypoxia also causes generalized pulmonary arteriolar vasoconstriction, presumably to evenly distribute claret throughout the lungs and maximize oxygen absorption. This vasoconstriction leads to pulmonary avenue hypertension, which plays a larger role in the pathophysiology of HAPE than it does in acclimatization.13 Pulmonary arterioles that are exposed to high pressures begin to remodel past increasing intimal smooth muscle. This process, which occurs over several days, protects the downstream pulmonary capillaries from overperfusion, thereby preventing capillary wall damage and alveolar flooding. This structural change likely explains why HAPE rarely occurs after iii to v days at a particular altitude.25
The respiratory alkalosis induced past increased ventilation necessitates bicarbonate excretion by the kidneys to maintain a reasonable blood pH. This excretion causes a fluid diuresis, leading to a small increase in hemoglobin concentration inside 2 days afterwards ascent. Hypoxia as well stimulates the kidneys to produce erythropoietin, leading to new red blood cell product inside 5 days. Over weeks to months, ruby-red blood cell mass stabilizes in proportion to the level of hypoxemia, and plasma volume increases, resulting in a 5% to 6% lasting increase in hematocrit and significantly increased total blood volume; it reverses in nigh the same time frame after descent.
Because of the sigmoidal shape of the oxyhemoglobin dissociation curve (Figure 1), oxygen saturation of arterial blood is maintained upwards to 3000 m despite the significant subtract in atmospheric partial pressure level of oxygen. The respiratory alkalosis described to a higher place shifts the curve to the left. Although this may facilitate increased oxygen binding in the lungs, it inhibits release of oxygen to the tissues. This change is beginning by increased production of 2,three-diphosphoglycerate in the red blood cells, which shifts the curve back to the right.17 Only at farthermost altitude (>5500 m) has an alkalosis-driven left shift of the curve been shown to predominate.28
Oxyhemoglobin dissociation curve showing the change in oxygen saturation of hemoglobin (SAO2) with changes in fractional force per unit area of oxygen (POtwo). 2,3-DPG, two,3-diphosphoglycerate.
The cardiovascular response to high altitude begins inside hours, with a moderate increase in heart rate, blood pressure, and cardiac output owing to increased sympathetic tone. After nearly 24 hours, cardiac output decreases because of bicarbonate diuresis (see below), and heart rate gradually decreases to sea-level baseline with acclimatization (except at very high altitude). Cerebral claret catamenia significantly increases on precipitous ascent to altitude and returns to normal over three to five days. Overall, cerebral oxygen commitment and free energy metabolism are fairly well maintained.xiii
Distance can have a significant result on the athletic performance of endurance athletes. When exposed to moderate altitudes, the numerous physiologic responses that occur can compromise performance, lowering maximum aerobic power by equally much every bit xv% to 20%.31 The optimal training regimen for events at distance varies, depending on the athlete'due south altitude of residence and the altitude of the planned upshot. For aerobic competitions at greater than 2000 m, ten to 20 days of acclimatization may be necessary. Highly anaerobic activities at intermediate altitudes (1500 to 3500 g) practise not crave acclimatization; nonetheless, symptoms of AMS may become a trouble.17
For decades, using altitude in training regimens for elite athletes has been of great involvement. Although a detailed discussion of this topic is beyond the scope of this commodity, a few points are worth noting. Approaches to distance grooming include three bones models: preparation and living at distance (live loftier, train loftier), living at distance and training at sea level (live high, train low), and living at sea level and training at distance (live low, railroad train high). In locations where these models are not geographically viable, techniques of simulated altitude have been employed, such as hypobaric living environments. "Live loftier, train high" methods are widely used because of a general consensus amidst athletes that information technology improves endurance operation. Nonetheless, although preparation for iii to viii weeks at distance does allow acclimatization, empiric performance information are equivocal. The positive results seen in some uncontrolled studies tin exist explained by a placebo effect.31 "Live loftier, train low" methods (usually training in oxygen-enhanced environments to simulate bounding main-level normoxia) have clear benefit not only in acclimatization but also in enhancing exercise performance at distance and sea level.37 "Live low, train high" methods (involving intermittent hypoxic exposures with or without exercise preparation) accept been shown to be effective in preacclimatization in athletes before ascending to high altitude, only the effect on performance has shown mixed results.37
Types of HAI
HAI presents as 3 syndromes: AMS, HACE, and HAPE. AMS and HACE are generally considered different manifestations along a spectrum of progressive cerebral pathology. HAPE, however, has a unique pathophysiology that tin occur in isolation or in conjunction with AMS or HACE.
Astute Mount Sickness
The Lake Louise Consensus on the Definition and Quantification of Distance Affliction defined AMS equally a high-altitude-related headache plus one or more of the post-obit symptoms: anorexia, nausea, or vomiting; fatigue or weakness; dizziness or lightheadedness; or difficulty sleeping.15 AMS is by far the most common form of HAI. It tin can occur at any altitude above 1500 m, but information technology most typically occurs with rapid rise higher up 2500 thou.17 Symptoms tin can manifest every bit early every bit one hour after ascent, but they more than commonly begin after 6 to 10 hours.13 AMS severity is classified as mild or moderate to severe (based on severity of the above symptoms), although severe AMS is generally regarded as HACE.
The effect of AMS on the body ranges from an badgerer to a temporarily incapacitating condition, and recovery tin can range from a few days to many weeks, depending on severity and treatment. A written report of 840 Indian soldiers with incapacitating but untreated AMS at 5486 m described that 37% recovered within 3 days, 21% in 4 to 7 days, and 13% by 14 days. The remaining 37% took 15 to 150 days to recover.34 Although most persons with mild AMS are able to participate in their high-altitude activity, they may not function at their highest levels. Talbot et al documented a lower rate of race completion amongst those treated for HAI in a 238-mile race at high altitude.35
AMS is considered a cognitive class of HAI, given that neurological dysfunction is ofttimes a part of this syndrome. Neuropsychological tests in patients with AMS take detected subtle to overt deficits in memory storage and recollect, speech, concentration, and finger-borer speed.19 Deficits in retention, reaction fourth dimension, and concentration can final upward to 75 days after unmarried exposures to 5000 yard.five Many victims of AMS, despite having normal neurological exams, develop reversible brain lesions on magnetic resonance imaging (MRI), including edema of the globus pallidus,twenty cortical atrophy, and periventricular hyperintensity.14
High-Distance Cerebral Edema
The main risk of untreated AMS is its potential to progress to HACE. The suspected pathophysiology of HACE is cerebral edema due to hypoxia-induced cerebral overperfusion and increased expression of vascular leakage mediators. Whether AMS is also due to cerebral edema or vasodilatation lone is not known.13 All brains nifty to some caste at distance, but at that place is no definitive correlation of this swelling to AMS or HACE.26 MRI is usually abnormal in patients with HACE, demonstrating increased indicate in the white affair, particularly in the splenium of the corpus callosum.eighteen
When HACE occurs, it progresses in severity over 24 to 36 hours. HACE can occur at altitudes above 2000 m, but it most commonly occurs with precipitous ascent beyond 3000 chiliad. In addition to AMS symptoms, contradistinct level of consciousness and ataxia are the distinguishing features of this syndrome. Papilledema and urinary retention or incontinence occur in half of HACE victims, whereas a 3rd take aberrant plantar reflexes. Less ordinarily noted findings include abducens nerve palsy, pupil differences, visual field loss, spoken communication difficulty, hearing loss, and flapping tremor. If untreated, HACE can progress to coma and expiry from brain herniation secondary to cerebral edema.16
Loftier-Altitude Pulmonary Edema
HAPE is an uncommon course of HAI, simply it accounts for nearly deaths attributable to these illnesses. In surveillance of Himalayan expeditions, the fatality charge per unit is reported to be about 50% in untreated cases.22 The pathophysiology of HAPE begins with hypobaric hypoxia, which causes elevated pulmonary avenue pressure, leading to regional overperfusion and hydrostatic damage to small-scale pulmonary arterioles. These changes somewhen cause alveolar edema and hemorrhage.21
HAPE tin occur as low as 1400 thousand but is well-nigh common above 2500 thousand.12 It is defined by at least 2 symptoms (dyspnea at rest, coughing, weakness or decreased exertional performance, breast tightness or congestion) and at least 2 signs (crackles or wheezing, primal cyanosis, tachypnea, or tachycardia).15 Chest radiographs usually reveal findings consistent with noncardiogenic pulmonary edema: unilateral or bilateral fluffy infiltrates with normal center size.17 Signs and symptoms of AMS commonly precede the onset of HAPE. The incidence of HACE increases in patients with HAPE; therefore, rather than just attribute such changes to severe hypoxia, HACE must be considered in all HAPE patients with mental status changes.16 Owing to acclimatization changes within the lungs, HACE rarely occurs after 3 to five days at a detail altitude.sixteen
Risk Factors for HAI
The chief take chances factors for all types of HAI include increased distance and rapid ascension rate. As the altitude and rising rate increase, hypoxic stress may overpower the body'due south ability to adjust. AMS occurs in nearly twenty% to 25% of tourists who visit 2500 m and in virtually twoscore% to l% of trekkers near 4000 thousand. More than ninety% of trekkers feel AMS if they ascend to 4000 m over several hours, every bit opposed to days. The incidence of HACE in tourists is virtually 0.01% at 2500 m and i% to two% in mountaineers at 4000 k. The incidence of HAPE in climbers is between ii% and vi% at 4000 m only more than 15% at 5500 m.xiii
Prior history of HAI is a stiff predictor of futurity HAI. If a person is exposed to the aforementioned acclimatization regimen (or lack thereof), the same distance, and the aforementioned ascent rate at which HAI previously occurred, HAI will likely recur.34 The approximate charge per unit of recurrence for HAPE has been documented at 60% in the absenteeism of preventive measures.one
AMS and HACE seem to affect men and women equally, although men appear to be more susceptible to HAPE.17 HAI is less common in persons older than 50 years, whereas HAPE is more than common and more severe in children and young adults.thirteen Physical fitness is not protective against HAI. Furthermore, physical exertion at altitude tin can increase the incidence and/or severity of HAI, presumably because information technology worsens tissue hypoxia.13 Medications and drugs that reduce ventilatory drive or modify sleep patterns, such as alcohol, benzodiazepines, and other sedatives/hypnotics, may exacerbate progression to HAI and should thus be used with circumspection.xiii
Cold air creates additional physiologic stress and elevates pulmonary arterial pressures; therefore, it is a take chances factor for HAPE.13 Genetic factors are believed to provide a predisposition to HAPE.17 Such factors include increased sympathetic activeness, decreased endogenous nitric oxide production, and defects in the transepithelial fluid transport mechanism in alveolar cells.17
Factors that appear to be protective of HAI include residence at more 900 m and slow ascent.17 Boring ascent, generally regarded as 600 m per twenty-four hour period, is thought to allow sufficient time for acclimatization to occur, but information technology is non absolutely protective. Extremes in altitude combined with individual susceptibility may all the same pb to HAI.17
Treating HAI
Treatment for HAI depends on the item syndrome that occurs, the severity, and the availability of handling modalities (see Tables 1 and 2). In full general, minimum handling should include rest and halt of rise. Balance prevents increases in hypoxia and permits more than time for acclimatization. It may be the only handling needed for balmy AMS. Descent to a lower altitude increases tissue oxygenation and should be washed for moderate to severe AMS, HAPE, or HACE. Keeping patients with HAPE warm is too important to minimize the pulmonary artery hypertension associated with hypothermia.
Table 1.
Medical therapies for high-altitude affliction. a
| Indication | Medications b | Route | Preventive Dose | Treatment Dose |
|---|---|---|---|---|
| AMS | Acetazolamide | Orally | 125-250 mg twice a day | 250 mg twice a day |
| Dexamethasone | Orally, intramuscularly, intravenously | ii mg every 6 60 minutes or four mg every 12 hr c | 4 mg every half dozen hr | |
| HACE | Dexamethasone | Orally, intramuscularly, intravenously | 2 mg every half-dozen 60 minutes or 4 mg every 12 hour c | 8 mg immediately, then 4 mg every 6 60 minutes |
| HAPE | Nifedipine | Orally | xx-30 mg sustained release every 12 hr | 10 mg quick release, and so twenty-30 mg sustained release every 12 hr |
| Salmeterol | Inhalation | 125 mg every 8 hr | Unknown | |
| Sildenafil | Orally | 50 mg every 8 hr | Unknown | |
| Tadalafil | Orally | ten mg twice a solar day | Unknown | |
| Adjunctive Therapies d | ||||
| Whatsoever HAI | Oxygen | Cannula or mask | — | Initially 2-4 L/min, titrate arterial oxygen saturation >90% |
| Portable hyperbaric bedroom | Full-body immersion | — | Varies by model, 2-4 psi for at to the lowest degree two hr | |
| Descent | — | — | Minimum 500 m for moderate AMS, 500-1000 m for HAPE, k m for HACE |
Tabular array 2.
Mechanisms of action, side furnishings, and contraindications to common medical therapies for high-altitude affliction.eight,thirteen,23
| Medication | Mechanism of Activeness | Common Side Effects | Contraindications |
|---|---|---|---|
| Acetazolamide | Carbonic anhydrase inhibitor. Causes bicarbonate diuresis, stimulates respiration (increased arterial pressure of oxygen), decreases cerebral spinal fluid formation, and may increase ion send through the blood-encephalon barrier. | Weight loss, diarrhea, anorexia, nausea, vomiting, altered taste, confusion, paresthesias, somnolence, depression, polyuria | Severe hepatic or renal insufficiency, hyponatremia, hypokalemia, adrenal gland failure, noncongestive angle-closure glaucoma, metabolic acidosis. Avoid use: concomitant long-term high-dose aspirin therapy, sulfonamide allergies, pulmonary obstacle, emphysema, concurrent use of topiramate, potassium-wasting diuretics, ophthalmic carbonic anhydrase inhibitors |
| Dexamethasone | Unknown. May decrease brain blood volume or reduce blood-brain barrier leaks. | Mood changes, hyperglycemia, hypertension, dyspepsia, rebound symptoms upon withdrawal | Known systemic fungal infections. Avoid use: peptic ulcer affliction or history of upper gastrointestinal haemorrhage. Reduce adverse events by minimizing duration of apply. |
| Nifedipine | Calcium-channel blocker. Decreases pulmonary artery pressures by decreasing smooth muscle tone. | Hypotension, palpitations, peripheral edema, flushing, constipation, reflux, nausea, dizziness, headache | Apply circumspection in conjunction with other antihypertensive medications and in individuals with recent myocardial infarction, aortic stenosis, congestive heart failure, hepatic or renal insufficiency, hypotension, or unstable angina. |
| Salmeterol | Beta-agonist. Increases clearance of alveolar fluid by upregulating transepithelial sodium transport. | Tachyarrhythmia, dizziness, headache, tremor, throat irritation | Caution in those with cardiovascular disorders (arrhythmias, hypertension, coronary insufficiency), laryngeal spasms, or milk allergies |
| Sildenafil | Phosphodiesterase inhibitor. Causes pulmonary vasodilatation by relaxation of pulmonary vascular smooth musculature | Flushing, rash, headache, dizziness, congestion | Contraindicated with employ of nitrates. Caution with utilize of alpha-blockers, hepatic or renal insufficiency, cardiovascular disease, bleeding disorders, and retinal abnormalities. |
| Tadalafil | Phosphodiesterase inhibitor. Causes pulmonary vasodilatation past relaxation of pulmonary vascular smoothen musculature | Reflux, nausea, flushing, myalgias, backache, headache, upper respiratory infection | Contraindicated with utilise of nitrates. Caution with use of alpha-blockers, recent stroke, sickle prison cell anemia, multiple myeloma, leukemia, or severe renal impairment. Dose adjustments with renal or hepatic insufficiency and concurrent use of CYP3A4-inhibiting medications. |
In mild to moderate AMS, oxygen can be used as a substitute for or in addition to descent. A few hours of oxygen therapy may be sufficient to alleviate symptoms. Oxygen should exist used with descent in all patients with HAPE or HACE. Unfortunately, oxygen equipment is cumbersome and may be available only at base camps or medical facilities.
If available, commercially made, portable hyperbaric treatment bags provide an alternative to descent. AMS may respond rapidly to hyperbaric therapy, simply HAPE and HACE will require prolonged handling.
Medications can exist useful in the prevention and treatment of AMS. Care should be taken, however—these may be banned substances. For instance, acetazolamide and oral glucorticosteroids are both on the banned substance listing for the World Anti-Doping Agency and the U.s. Anti-Doping Agency. Equally of January 1, 2010, salmeterol requires a proclamation of utilize. Consultation with the World Anti-Doping Agency (world wide web.wada-ama.org) and/or the US Anti-Doping Agency (www.usada.org) is recommended before prescribing medication to athletes. In addition, there are piffling data on the effects of these medications on performance in full general or at altitude. Studies have shown varying effects—positive, negative, and neutral—depending on the medications and conditions under which the testing occurred.6,7,xi
Acetazolamide, a carbonic anhydrase inhibitor, tin can greatly assist acclimatization. It centrally acts to stimulate the hypoxic ventilatory response, reducing pulmonary avenue hypertension and maintaining oxygenation during sleep. Information technology stimulates the kidneys to excrete bicarbonate, assuasive farther respiratory acclimatization. It also decreases cerebral spinal fluid production and thereby mitigates increases in cerebral spinal fluid force per unit area. Although the optimal dose is continually debated, numerous studies have shown acetazolamide to be effective in preventing AMS in persons who are speedily taken to altitudes of 3000 to 4500 m.13,17 In addition to its condom value, acetazolamide is useful for treatment of AMS. It may exist used to care for HACE merely only in conjunction with corticosteroids. Recent studies have suggested that acetazolamide attenuates pulmonary vascular responses to hypoxemia and decreases pulmonary vascular resistance. These findings suggest that acetazolamide may be effective in the prevention and treatment of HAPE, simply further studies are necessary before considering it a substitute for known therapies.33
Dexamethasone is the almost usually used and well-nigh widely studied steroid for treating HAI. Its mechanism of action is unknown, but information technology may deed in the brain by decreasing blood volume or blocking capillary leakage. Although it has no effect on acclimatization, it is benign for the prevention and handling of AMS and HACE.23 Because dexamethasone does non enhance acclimatization, rebound symptoms of AMS or HACE are possible after discontinuation, and so circumspection is advised when withdrawing treatment. There is limited prove that dexamethasone may play a role in the prevention of HAPE, only further studies are necessary before recommending its use.24
Nifedipine, the almost studied pharmacologic handling for HAPE, is proven to exist beneficial in the prevention and treatment of HAPE.4,27 Nifedipine acts on the pulmonary smoothen muscles, reducing pulmonary artery pressure. It is not necessary in almost cases, however, because descent and oxygen are highly effective.
Salmeterol, a long-acting inhaled b-agonist, appears to be effective for the prevention of HAPE. It acts by increasing clearance of alveolar fluid via stimulation of the alveolar transepithelial sodium transport mechanism.30 In a study of 37 patients with a prior history of HAPE, assistants of salmeterol reduced its incidence from 74% to 33%.29 These results have non been validated in follow-upward studies. Salmeterol is typically used as an adjunct to nifedipine as prophylaxis; nevertheless, in that location are reports that information technology has been used every bit handling. This has not yet been formally investigated in clinical trials.23 Albuterol has anecdotal evidence of effectiveness in treating HAPE only has not yet been studied.thirteen
Because of their pulmonary vasodilatory furnishings, the phosphodiesterase inhibitors tadalafil and sildenafil may be useful in the prevention of HAPE. Maggiorini et al24 compared dexamethasone, tadalafil, and placebo in 29 adults with previous HAPE during ascension to 4559 m. HAPE developed in seven of 9 participants receiving placebo, one of the eight receiving tadalafil, and none of the 10 receiving dexamethasone. Sildenafil has been shown to improve do performance at altitude,33 and tadalafil failed to better practice operation in ane study,x simply neither amanuensis has been formally evaluated in the treatment of HAPE.
Return-to-Distance Planning for Athletes After HAI
There are 2 categories of render-to-altitude planning for a person with a history of HAI: The first involves the athlete with a remote history of HAI; the second involves the athlete who is currently experiencing or has only recovered from a HAI but wants to or must resume his or her loftier-distance activity. In either case, the physician and the athlete must formulate a plan. Consideration should be given to the severity of the athlete's HAI, the future ascension and activity requirements, the flexibility of the itinerary, and the availability of medical treatment.3
Athletes With Remote History of HAI
In the athlete with a remote history of HAI and a full recovery, attention must be given to proper acclimatization protocols and graded ascension, if possible. Such precautions are effective in the prevention of HAI17,32 (see Table 3).
Table 3.
Graded ascension and acclimatization recommendations.
| Avert precipitous ascents beyond 3000 k. |
| Spend 2 to three nights at 2500-3000 m before ascending further. |
| Above 3000 m, permit ane boosted night of acclimatization every 600-900 m at each new altitude. |
| Limit increases in sleeping altitudes to 600 g each twenty-four hour period once higher up 2500 m. |
| Preexposure to 5 or more days to a higher place 3000 1000 in the 2 months before rising may enhance acclimatization rate. |
Schneider et al32 performed a prospective report on the influence of prior HAI history, altitude preexposure, and ascent rate on the incidence of AMS during ascent to 4559 m. Participants were non allowed to use condom medications. The researchers plant that in persons with a prior history of AMS, preexposure to 5 or more days (not necessarily consecutive) above 3000 m during the prior ii months reduced the incidence of AMS from 58% to 29%. Recurrence of AMS was only 33% in those who limited ascent to less than 640 m per day once in a higher place 2000 m. In those who had a history of preexposure to altitude and slow rising, the incidence was only vii%. Bärtschtwo reported 2 climbers with prior histories of 2 to 4 episodes of HAPE who successfully undertook a collective 3 ascents to 6000 to 7000 m past ascending but 330 to 350 grand per twenty-four hours net sleeping altitude. None of them developed HAPE. These studies illustrate the preventive ability of acclimatization and slow ascent even afterwards a severe class of HAI.
If an athlete has no recent exposure to loftier altitude or is unable to comply with graded ascent recommendations, employ of rubber medication may be prudent. Once more, caution should be used in athletes who fall nether World Anti-Doping Agency or U.s.a. Anti-Doping Agency jurisdiction. For those with a history of AMS, acetazolamide should be adequate. For those who cannot tolerate acetazolamide, dexamethasone may exist used in its place. Although there are no bear witness-based recommendations regarding the combination of these medications, dexamethasone can be used every bit treatment for AMS symptoms that occur despite acetazolamide prophylaxis.17
Those with prior HACE or HAPE should strongly consider adherence to acclimatization and graded ascent recommendations, given the seriousness of the illness and the high hazard of recurrence. If medical care will not be readily available, if descent will not be applied, or if rise will be faster than recommended, strong consideration should be given to pharmacologic prophylaxis. For those with prior HACE, the prophylaxis regimen is identical to that of AMS.thirteen Prophylaxis for HAPE could include nifedipine, salmeterol, or tadalafil. Nifedipine is the most studied of these agents; still, no studies have shown articulate superiority of 1 agent over the other. Dexamethasone and acetazolamide may have benefit in the prevention of HAPE; however, further studies are necessary before their use is recommended over that of established agents. The usefulness and safety of combination treatments is unknown.
Firsthand Return to Activity Subsequently a Contempo HAI
When because return to activity at distance for those with a current or recent HAI, one must make several considerations in addition to those described above. The first is the safety of continued action at altitude and what activity should be allowed. The second is how long the athlete'due south symptoms take to resolve and how before long physical and mental functions normalize. Theoretically, a person could experience a worse episode of HAI on altitude reexposure before complete recovery.
Mild AMS is ordinarily a self-limiting illness. Anecdotal evidence supports the acceptability of treating the athlete in place without descent. However, physical and/or mental functioning may exist impaired, thereby leading to performance decrements and perchance placing the athlete at a greater hazard for injury. These risks need to be weighed confronting the disadvantages of treatment (mainly, time lost). Talbot et al35 documented the incidence of AMS in a 10-day 238-mile race at high altitude in which no prophylaxis was allowed. Those who sought handling were allowed oxygen, analgesics, or descent. Eleven cases of balmy AMS were identified by questionnaire before the race began, but none of the participants sought treatment. Of those 11, merely 64% completed the race, compared to the overall race completion rate of 74%. Thirty-iii other cases of AMS were treated during the race. Although 88% returned to the competition, just 58% finished.
Ideally, the athlete with mild AMS should residuum at altitude until asymptomatic and avert excessive exertion. Pharmacologic treatment can be considered. Options include symptom-based treatments, such as acetaminophen or nonsteroidal anti-inflammatory drugs for headache and antiemetics for nausea. Initiation of HAI medications may also be considered. Acetazolamide may expedite acclimatization, whereas acetazolamide and dexamethasone can both help to control symptoms and prevent progression of illness. If bachelor, oxygen therapy and portable hyperbaric chambers tin can effectively eliminate symptoms—and quickly, ofttimes in a matter of hours. Most athletes are able to go on with their activities.
If an athlete is unable to remain at a stock-still altitude for acclimatization, prophylaxis should be instituted before further rise. In situations where prophylaxis and rest are not possible, athletes should be counseled about the risk of prolonged or worsening AMS symptoms. They should be further counseled on the risk of progression to HACE and/or the development of HAPE.
Moderate AMS presents every bit protracted or worsening headache, nausea, vomiting, dizziness, anorexia, and/or fatigue, and it can exist quite disabling. Treatment options are identical to those of mild AMS; yet, the athlete will likely require a longer duration (1 to 2 days) of resting at distance. If such interventions are non effective or available, descent greater than 500 thousand should be considered. Strong consideration should be given to the employ of dexamethasone and/or acetazolamide.13 Affected athletes should not be allowed to keep untreated. One time the symptoms of moderate AMS are gone, there all the same may be subtle neuropsychological deficits that will persist until weeks after return to low distance. The athlete should understand the possible furnishings of these deficits not only on the electric current activity but on functioning when back at home.
The information from Schneider et al32 can exist extrapolated for those who have been treated for recent AMS. Provided that the athlete is at an altitude of to the lowest degree 3000 grand and has been at that altitude for at least 5 days before resuming ascent, the take chances of recurrent AMS may exist low if he or she follows ascension rate recommendations. If this is not possible, condom medication may be prudent.
Higher altitude, greater severity of disease, connected ascent, and a history of astringent HAI imply a greater take a chance of experiencing HACE and/or HAPE. These factors should further prompt strong consideration of the utilise of prophylaxis medications. Further ascent should exist limited to a 600-m cyberspace gain per day, and a rest day should be immune every 600 to 1200 m to allow continued acclimatization. Mountaineers should be cautioned that even these measures cannot preclude all cases of HAI. Further illness should exist recognized quickly and treated aggressively.
HACE is generally regarded as severe AMS, oft presenting with classic findings of ataxia and/or mental status changes. When HACE occurs, activity should cease, and immediate aggressive therapy should be commenced. Treatment involves immediate descent, oxygen supplementation, and dexamethasone. Hyperbaric handling can be used if descent is not possible.
One time the patient is in a hospital, a breast radiograph should be performed to rule out HAPE, which often occurs concurrently. Encephalon MRI should exist considered if alternate causes of mental condition changes are possible. If coma ensues, treatment involves airway management and bladder drainage. Attempts to subtract intracranial pressure with diuretics and/or controlled hyperventilation should just be done cautiously, if at all, because maintenance of adequate intravascular volume and perfusion pressures are critical.16 Hospital discharge criteria for athletes with HACE include normal level of consciousness and oxygen saturation on room air, grossly normal neurological examination (or at least stable if persistent deficits are present) and control of seizures if present. The time for recovery from HACE varies considerably. At that place is non a potent correlation between recovery time and the severity of illness at presentation. One case series documented a range of 1 solar day to 12 weeks for symptoms and neuropsychological role to normalize and 1 day to 5 weeks for MRI findings to resolve.38 Nineteen cases in another series took up to 3 days for symptoms to resolve, but resolution of papilledema required 3 to four weeks.34
Given the variability of recovery times and the known hazard for recurrence of severe HAI, render to altitude should be done charily. Full recovery before reascent is prudent. Attention to conscientious acclimatization, dull ascent, rest days, and pharmacologic prophylaxis should be considered. Preexposure to distance in the months before activity may provide boosted protection. Some climbers are even using dexamethasone on summit day for HACE prevention, although this has no proof of efficacy.
HAPE is a medical emergency. As with HACE, activity should be suspended, and ambitious treatment should brainstorm immediately. Treatment should begin with immediate descent because this provides the quickest recovery. The athlete should be provided warmth, residual, and oxygen supplementation—maintaining an arterial oxygen saturation of at least 90%. Portable hyperbaric therapy may be lifesaving if descent and oxygen are not immediately available. Nifedipine and salmeterol may be useful adjuncts to handling; however, nifedipine should be avoided in patients with concomitant HACE, given that it can excessively lower blood pressure. If arterial oxygen saturation remains at least 90% on 2 to 4 Fifty per infinitesimal of oxygen, athletes tin be observed for several hours and discharged with outpatient low-flow oxygen. Arterial oxygen saturation should be checked at to the lowest degree every day, and oxygen can be discontinued once saturation is maintained above 90% on room air. In athletes with concomitant HACE, with oxygen requirements greater than 4 Fifty per minute, with comorbid cardiopulmonary conditions, or at extremes of age, admission to a hospital should be considered. Dexamethasone should be used but in patients with concomitant HACE because it does not take proven efficacy for HAPE.13
The physician should counsel the athlete to resume normal activities gradually and just afterwards oxygen saturation is normal on room air. Athletes may crave up to two weeks to regain complete strength and stamina.17 Those who are treated at some degree of altitude probably benefit from the remodeling of pulmonary arterioles, which is part of acclimatization. They may be able to charily resume activeness at altitude earlier than others.
There is some limited evidence that patients with recent HAPE may cautiously render to altitude immediately later on treatment. One small example serial described 3 mountaineers who adult HAPE and were treated at moderate altitude for 2 to iv days earlier returning to their expeditions. With no medical prophylaxis only with a boring ascension (less than 600 m per mean solar day) and several rest days, they all reached their summits without any symptoms of HAI. One even reached the summit of Mountain Everest at 8850 yard.21 In these instances, however, prophylaxis with nifedipine or salmeterol may have been advisable.9
Conclusion
HAI is a relatively common occurrence for those who participate in activities at distance. HAI has an fantabulous prognosis if treated promptly; notwithstanding, prevention with graded ascent and time for acclimatization is ideal. Athletes with remote histories of HAI can return to distance charily, with stiff consideration for prudent ascent protocols and/or condom medications. Those with a recent HAI may also return to altitude, although full recovery from HACE and HAPE are strongly advised, and prophylaxis may exist prudent.
Footnotes
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