High Altitude Illness

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Slide 1 : High altitude illness Lt Col Rajesh Deshwal, MD
Slide 2 : Ascent to a high altitude subjects the body to a decrease in barometric pressure that results in adecreased partial pressure of oxygen in the inspired gas in the lungs
Slide 3 : This change leads in turn to lesspressure driving oxygen diffusion from the alveoli and throughout the oxygen cascade
Slide 4 : A normal initial"struggle response" to such an ascent includes increased ventilation, which is the cornerstone ofacclimatization (West, 2000). Hyperventilation may cause respiratory alkalosis and dehydration
Slide 5 : Alkalosis may depress the ventilatory drive during sleep, with consequent periodic breathing andhypoxemia
Slide 6 : Normal Symptoms at AltitudeHyperventilation/dyspnea on exertion (NO dyspnea at rest)Increased urinationAwaken many times at night (sometimes to urinate)Periodic breathing at night
Slide 7 : During EARLY acclimatization, renal suppression of carbonic anhydrase and excretion ofdilute alkaline urine combat alkalosis and tend to bring the pH of the blood to normal
Slide 8 : Otherphysiologic changes during normal acclimatization include increased sympathetic tone
Slide 9 : Increasederythropoietin levels, leading to increased hemoglobin levels and red blood cell massIncreased tissuecapillary density and mitochondriaHigher levels of 2,3-diphosphoglyceride, enhancing oxygenutilization
Slide 10 : Even with normal acclimatization, however, ascent to a high altitude decreases maximalexercise tolerance and increases susceptibility to cold injury due to peripheral vasoconstriction
Slide 11 : Finally, if the ascent is made faster than the body can adapt to the stress of hypobaric hypoxemia,altitude-related disease states can result
Slide 12 : Edema of AltitudePeripheral edema and facial edema are relatively common It is likely to worsen with ascent, and is more common in women than menIt resolves rapidly with descent
Slide 13 : AMS AND HACE
Slide 14 : At altitudes over 2400m / 8000 ft, the diagnosis of AMS is based on a headache plus at least one of the following symptoms: GI upset (loss of appetite, nausea, vomiting)Fatigue/weakness Dizziness/light-headedness Insomnia (more than just the usual frequent waking)
Slide 15 : Develops 6–12 h after ascent to a high altitude
Slide 16 : AMS must be distinguished from exhaustion, dehydration, hypothermia, and alcoholic hangover (Hackett and Roach, 2001)
Slide 17 : AMS and HACE are thought to represent opposite ends of a continuum ofaltitude-related neurologic disorders. HACE (but not AMS) is an encephalopathy whose hallmarks areataxia and altered consciousness with diffuse cerebral involvement but generally without focalneurologic deficits
Slide 18 : Retinal hemorrhages occur frequently at 5000 m even in individuals without clinical symptoms of AMS or HACE
Slide 19 : It is unclear whether retinalhemorrhage and cerebral hemorrhage at high altitude are caused by the same mechanism.However, one report revealed a correlation between HACE and retinopathy (Weidman and Tabin, 1999)
Slide 20 : The most important risk factors for the development of altitude illness are the rate of ascent and ahistory of high-altitude illnessExertion is a risk factor, but lack of physical fitness is not
Slide 21 : An attractivebut still speculative hypothesis proposes that AMS develops in people who have inadequate cerebrospinal capacity to buffer the brain swelling that occurs at high altitude (Ross, 1985)
Slide 22 : Oneprotective factor in AMS is high-altitude exposure during the preceding 2 months (Schneider et al,2002)
Slide 23 : Children andadults seem to be equally affected, but people >50 years of age may be less likely to develop AMSthan younger people
Slide 24 : Most studies reveal no gender difference in AMS incidence (Hackett and Roach,2001)
Slide 25 : Burgess et al (2004) showed that sleep desaturation—a common phenomenon at high altitude—is associated with AMS
Slide 26 : Pathophysiology
Slide 27 : The exact mechanisms causing these syndromes are unknownEvidence points to a central nervoussystem process
Slide 28 : Magnetic resonance imaging (MRI) studies have suggested that vasogenic(interstitial) cerebral edema is a component of the pathophysiology of HACE (Hackett et al, 1998)
Slide 29 : Inthe setting of high-altitude illness, the MRI findings are confirmatory of HACE,with increased signal in the white matter and particularly in the splenium of the corpus callosum
Slide 30 : Onthe basis of quantitative (as opposed to visual) analysis with lower-resolution imaging (Fischer et al,2004), a 3-tesla MRI study by Schoonman et al (2008) revealed that, in AMS and other conditions,hypoxia is associated with mild vasogenic cerebral edema
Slide 31 : This finding is in keeping with case reports of suddenly symptomatic brain tumors and of cranial nerve palsies at high altitude without AMS(Basnyat et al, 2000)Vasogenic edema may become cytotoxic (intracellular) in severe HACE
Slide 32 :
Slide 33 : Impaired cerebral autoregulation in the presence of hypoxic cerebral vasodilatation and alteredpermeability of the blood-brain barrier due to hypoxia-induced chemical mediators like histamine,arachidonic acid, and vascular endothelial growth factor (VEGF) may all contribute to vasogenicedema (Schilling and Wahl, 1999; Levine et al, 1999)
Slide 34 : In 1995, Severinghaus first proposed VEGF as a potent promoter of capillary leakage in the brain at high altitude, and studies in mice (Schoch et al,2002) have borne out this role
Slide 35 : Although preliminary studies of VEGF in climbers have yieldedinconsistent results (Maloney et al, 2000; Walter et al, 2001) and have revealed no association with altitude illness.
Slide 36 : Indirect evidence for a role for this cytokine in AMS and HACE comes from the observation that dexamethasone, when used in the prevention and treatment of AMS and HACE, blocks hypoxic upregulation of VEGF (Klekamp et al, 1997)
Slide 37 : Increased sympathetic activity triggered by hypoxia may also contribute to blood-brain barrier leakage(Reeves, 1993)
Slide 38 : Moreover, enhanced optic-nerve sheath diameter with increasing severity of AMS hasbeen noted and suggests an important role for increased intracranial pressures in the pathophysiology of AMS (Sutherland et al, 2008)
Slide 39 : Finally, the effect of hypoxia on reactive oxidant species and the roleof these species in clinical AMS are unclear
Slide 40 : The pathophysiology of the most common and prominent symptom of AMS—headache—remainsunclear because the brain itself is an insensate organ; only the meninges contain trigeminal sensorynerve fibers
Slide 41 : In 1999, Sanchez del Rio and Moskowitz proposed that the cause of high-altitude headache is multifactorial and that various chemicals and mechanical factors activate a final common pathway, the trigeminovascular system
Slide 42 : In the genesis of high-altitude headache, the response tononsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids provides indirect evidence for involvement of the arachidonic acid pathway and inflammation (Ferrazzini et al, 1987; Broome et al,1994; Burtscher et al, 1998)
Slide 43 : Although the International Headache Society acknowledges that highaltitude may be a trigger for migraine (Baumgartner et al, 2007), It is unclear whether high-altitudeheadache and migraine share the same pathophysiology
Slide 44 : Prevention and Treatment
Slide 45 : Gradual ascent, with adequate time for acclimatization, is the best method for the prevention ofaltitude illness
Slide 46 : Above 3000 m, a graded ascent of 300 m from the previous day’s sleeping altitude isgenerally recommended, and taking every third day of gain in sleeping altitude as an extra day foracclimatization is helpful
Slide 47 : Spending one night at an intermediate altitude before proceeding toa higher altitude may enhance acclimatization and attenuate the risk of AMS
Slide 48 : Management of Altitude IllnessAcute mountain sickness (AMS),mildDiscontinuation of ascentTreatment with acetazolamide (250 mg q12h)
Slide 49 : AMS, moderateImmediate descent for worsening symptomsUse of low-flow oxygen if availableTreatment with acetazolamide (250 mg q12h) and/ordexamethasone (4 mg q6h)Hyperbaric therapy
Slide 50 : High-altitude cerebral edema(HACE)Immediate descent or evacuationAdministration of oxygen (2–4 L/min)Treatment with dexamethasone (8 mg PO/IM/IV; then 4 mg q6h)Hyperbaric therapy if descent is not possible
Slide 51 : Pharmacologic prophylaxis at the time of travel to high altitudes is warranted for people with a historyof AMS or when a graded ascent and acclimatization are not possible—e.g., when rapid ascent isnecessary for rescue purposes or when flight into a high-altitude location is required
Slide 52 : Acetazolamide(125–250 mg twice a day), administered for 1 day before ascent and continued for 2 or 3 days, iseffective (Hackett and Roach, 2001)
Slide 53 : Higher doses generally are not required (Basnyat et al, 2003)
Slide 54 : Paresthesia and a tingling sensation are common side effects of acetazolamideDexamethasone (8mg/d in divided doses) is also effective (Hackett et al, 1988)
Slide 55 : A randomized, double-blind, placebo controlled trial by Gertsch et al (2004) clearly showed that ginko biloba is not effective in the prevention of AMS To date, no trials of NSAIDs in the prevention of AMS have been reported
Slide 56 : For the treatment of mild AMS, rest alone with analgesic use may be adequate (Basnyat and Murdoch, 2003)
Slide 57 : Descent and the use of acetazolamide and (if available) oxygen are sufficient to treat most cases of moderate AMSEven a minor descent (400–500 m) may be adequate for symptom reliefFor moderate AMS or early HACE, dexamethasone (8 mg orally or parenterally) is highly effective
Slide 58 : ForHACE, immediate descent is mandatory. When descent is not possible because of poor weatherconditions or darkness, a simulation of descent in a portable hyperbaric chamber is effective and, likedexamethasone administration, “buys time.”
Slide 59 : Like nifedipine, phosphodiesterase inhibitors have no role in the treatment of AMS or HACE
Slide 60 :
Slide 61 : HAPE
Slide 62 : Unlike HACE (a neurologic disorder), HAPE is primarily a pulmonary problem and therefore is notnecessarily preceded by AMS (Basnyat and Murdoch, 2003)
Slide 63 : HAPE develops within 2–4 days afterarrival at high altitude; it rarely occurs after more than 4 or 5 days at the same altitude, probably because of remodeling and adaptation that renders the pulmonary vasculature less susceptible to the effects of hypoxia (West and Mathieu-Costello, 1999)
Slide 64 : A rapid rate of ascent, a history ofHAPE, respiratory tract infections, and cold environmental temperatures are risk factors
Slide 65 : Men are more susceptible than women
Slide 66 : People with abnormalities of the cardiopulmonary circulation leading topulmonary hypertension—e.g., patent foramen ovale (PFO), mitral stenosis, primary pulmonaryhypertension, and unilateral absence of the pulmonary artery—are at increased risk of HAPE, even atmoderate altitudes
Slide 67 : Echocardiography is recommended when HAPE develops at relatively low altitudes (<3000 m) and whenever cardiopulmonary abnormalitiespredisposing to HAPE are suspected
Slide 68 : The initial manifestation of HAPE may be a reduction in exercise tolerance greater than that expectedat the given altitude. Although a dry, persistent cough may presage HAPE and may be followed by theproduction of blood-tinged sputum, cough in the mountains is almost universal and the mechanism ispoorly understood (Mason and Barry, 2007)
Slide 69 : Symptoms - At least two of the following: Dyspnea at rest  Cough  Weakness or decreased exercise performance Chest tightness or congestion
Slide 70 : Signs - At least two of the following: Crackles or wheezing in at least one lung field Central cyanosisTachypneaTachycardia
Slide 71 : Tachypnea and tachycardia, even at rest, are importantmarkers as illness progressesCrackles may be heard on auscultation but are not diagnostic
Slide 72 : HAPEmay be accompanied by signs of HACE
Slide 73 : Patchy or localized opacities or streaky interstitialedema may be noted on chest radiography
Slide 74 :
Slide 75 :
Slide 76 :
Slide 77 : In the past, HAPE was mistaken for pneumonia due to thecold or for heart failure due to hypoxia and exertion Kerley B lines or a bat-wing appearance are notseen on the radiograph
Slide 78 : Electrocardiography may reveal right ventricular strain or even hypertrophy.
Slide 79 : Hypoxemia and respiratory alkalosis are consistently present unless the patient is takingacetazolamide, in which case metabolic acidosis may superveneAssessment of arterial blood gases isnot necessary in the evaluation of HAPE; an oxygen saturation reading with a pulse oximeter isgenerally adequate
Slide 80 : A subclinical form of HAPE probably exists, but hard evidence correlating it with the development of clinically relevant HAPE is lacking (Cremona et al, 2002)
Slide 81 : Pathophysiology
Slide 82 : HAPE is a noncardiogenic pulmonary edema characterized by patchy pulmonary vasoconstriction thatleads to overperfusion in some areas (Hackett and Roach, 2001)
Slide 83 : This abnormality leads in turn toincreased pulmonary capillary pressure (>18 mmHg) and capillary “stress” failure (Maggiorini et al, 2001)
Slide 84 : The exact mechanism for the vasoconstriction is unknownEndothelial dysfunction due tohypoxia may play a role by impairing the release of nitric oxide, an endothelium-derived vasodilator (Duplain et al, 2000)
Slide 85 : At high altitude, HAPE-prone persons have reduced levels of exhaled nitric oxide (Busch et al, 2001)
Slide 86 : The effectiveness of phosphodiesterase-5 inhibitors in alleviating altitude-inducedpulmonary hypertension, decreased exercise tolerance, and hypoxemia supports the role of nitricoxide in the pathogenesis of HAPE (Ghofrani et al, 2004; Richalet et al, 2005)
Slide 87 : Maggiorini andcolleagues (2006) demonstrated that prophylactic use of tadalafil, a phosphodiesterase-5 inhibitor,decreases the risk of HAPE by 65%
Slide 88 : The endothelium synthesizes endothelin-1, apotent vasoconstrictor whose concentrations are higher than average in HAPE-prone mountaineers(Yanagisawa et al, 1988; Sartori et al, 1999)
Slide 89 : Bosentan, an endothelin receptor antagonist, has been shown to attenuate hypoxia-induced pulmonary hypertension (Modesti et al, 2006), but further field studies with this drug are necessary
Slide 90 : Exercise and cold lead to increased pulmonary intravascular pressure and may predispose to HAPE
Slide 91 : Inaddition, hypoxia-triggered increases in sympathetic drive may lead to pulmonary venoconstriction and extravasation into the alveoli from the pulmonary capillariesConsistent with this concept, alphaadrenergic blockade by phentolamine improves hemodynamics and oxygenation in HAPE more than do other vasodilators (Hackett et al, 1992)
Slide 92 : In the study of tadalafil Maggiorini and colleagues (2006) also investigated dexamethasone in the prevention of HAPE Surprisingly, dexamethasone reduced the incidence of HAPE by 78%—a greater decrease than with tadalafil
Slide 93 : Besides possibly increasing the availability of endothelial nitric oxide, dexamethasone may have altered the excessive sympathetic activity associated with HAPE: the heart rate of subjects in the dexamethasone arm of the study was significantly loweredFinally, people susceptible to HAPE alsodemonstrate enhanced sympathetic activity during short-term hypoxic breathing at low altitudes(Duplain, 1999).
Slide 94 : Because many patients with HAPE have fever, peripheral leukocytosis, and an increased erythrocytesedimentation rate, inflammation has been considered an etiologic factor in HAPE
Slide 95 : However, Swensonand colleagues (2002) provided evidence that inflammation in HAPE is an epiphenomenon rather thanthe primary problem
Slide 96 : Although inflammation may not be the main trigger for HAPE, inflammatoryprocesses like viral respiratory tract infections do predispose to HAPE, even in people constitutionallyresistant to its development (Durmowicz et al, 1997)
Slide 97 : Another proposed mechanism for HAPE is impaired transepithelial clearance of sodium and water fromthe alveoliAdrenergic agonists upregulate the clearance of alveolar fluid in animal models
Slide 98 : In adouble-blind, randomized, placebo-controlled study of HAPE-susceptible mountaineers, prophylacticinhalation of the -adrenergic agonist salmeterol reduced the incidence of HAPE by 50% (Sartori et al,2002)
Slide 99 : GeneticsAlthough gene polymorphism may influence susceptibility to HAPE, the data on this point are unclear.
Slide 100 : Although angiotensin-convertingenzyme gene polymorphism appears to confer a performance advantage at high altitude, an association with susceptibility to HAPE is lacking (Dehnert et al, 2002).
Slide 101 : Endothelial nitric oxide synthase gene polymorphism has been associated with susceptibility to HAPEin Japan (Droma et al, 2002) but not in Europe (Weiss et al, 2003).
Slide 102 : Prevention and Treatment
Slide 103 : Allowing sufficient time for acclimatization by ascending gradually is the best way to prevent HAPE
Slide 104 : High-altitude pulmonary edema(HAPE)Immediate descent or evacuationMinimization of exertion while patient is kept warmAdministration of oxygen (4–6 L/min) to bring O2 saturation to>90%Adjunctive therapy with nifedipinee (30 mg extended release q12h)Hyperbaric therapy if descent is not possible
Slide 105 : Sustained-release nifedipine (30 mg), given once or twice daily, prevents HAPE in people who must ascend rapidly or who have a history of HAPE (Bartsch et al,1991)
Slide 106 :
Slide 107 : Acetazolamide has been shown to blunt hypoxic pulmonary vasoconstriction (Teppema et al, 2007)and this observation warrants further study in HAPE prevention; however, one recent field study failedto show a decrease in pulmonary vasoconstriction in partially acclimatized individuals givenacetazolamide (Basnyat et al, in press)
Slide 108 : Descent and the use of supplementary oxygen (aimed at bringing oxygen saturationto >90%) are the most effective therapeutic interventions
Slide 109 : Exertion should be kept to a minimum,and the patient should be kept warm. Hyperbaric therapy in a portable altitude chamber may be usedif descent is not possible and oxygen is not available
Slide 110 : Oral sustained-release nifedipine (30 mg once or twice daily) can be used as adjunctive therapy (Oelz et al, 1991)
Slide 111 : Inhaled agonists, which are safeand convenient to carry, are useful in the prevention of HAPE and, by extension, may be effective inits treatment, although no trials have yet been carried out
Slide 112 : Inhaled nitric oxide (Anand et al, 1998)and expiratory positive airway pressure (Larson, 1985) may also be useful therapeutic measures but may not be available in high-altitude settings
Slide 113 : No studies have investigated phosphodiesterase inhibitors in the treatment of HAPE, but reports have described their use in clinical practice (Fagenholz et al, 2007). The mainstays of treatment remain descent and (if available) oxygen.
Slide 114 : REASCENTIn AMS, if symptoms abate (with or without acetazolamide), the patient may reascend gradually and with caution to a higher altitude.
Slide 115 : Unlike that in acute respiratory distress syndrome (another noncardiogenic pulmonary edema), the architecture of the lung in HAPE is usually well preserved, withrapid reversibility of abnormalities .
Slide 116 : This fact has allowed some people with HAPE to reascend slowly after a few days of descent and rest (Litch and Bishop, 2001) In HACE, reascent after a few days is not advisable.
Slide 117 : Thank You

 


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