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more intense in the supine position&#44; and cough with bubbly pinkish expectoration&#46; On arrival in the medical center&#44; the patient was normotensive&#44; with signs of hypoperfusion and cyanosis&#44; tachycardiac at 120<span class="elsevierStyleHsp" style=""></span>bpm&#44; tachypneic &#40;&#62;30 breaths&#47;min&#41;&#44; with SatO<span class="elsevierStyleInf">2</span> of around 90&#37; and FiO<span class="elsevierStyleInf">2</span> of 0&#46;6 with work of breathing and low-grade fever of 37<span class="elsevierStyleHsp" style=""></span>&#176;<span class="elsevierStyleSmallCaps">C</span>&#46; Auscultation revealed moist rales&#44; mainly in both lung bases&#46; ECG showed sinus tachycardia at 110<span class="elsevierStyleHsp" style=""></span>bpm with normal axis along with the ST depression in the inferior and anteroseptal aspects&#46; After administration of empirical treatment &#40;oxygen therapy by reservoir cannula with FiO<span class="elsevierStyleInf">2</span> of 1&#46;0&#44; furosemide&#44; acetylsalicylic acid and antibiotic coverage&#41;&#44; the patient was transferred to the tertiary hospital&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">On arrival at the hospital&#44; arterial blood gases &#40;FiO<span class="elsevierStyleInf">2</span> 0&#46;6&#41; were determined&#44; showing normal pH&#44; oxygen partial pressure of 69&#46;9<span class="elsevierStyleHsp" style=""></span>mmHg&#44; and normal carbon dioxide and lactic acid&#46; Clinical laboratory tests were significant for slightly raised CRP and leukocytosis with neutrophilia&#44; with normal D-dimer and cardiac markers&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Chest X-ray showed a normal cardiothoracic index with a bilateral reticular cotton&#8211;wool pattern with no central predominance &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; The CT-angiogram ruled out pulmonary thromboembolism and concluded findings indicative of acute pulmonary edema&#46; Alveolar opacities and ground glass opacities were also observed&#44; with a symmetrical&#44; generalized distribution in the parenchyma of both lungs&#44; slightly more predominantly in the lower lobes&#44; which showed thickening of the interlobular septa and a significant increase in pulmonary arterial trunk diameter &#40;35<span class="elsevierStyleHsp" style=""></span>mm&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">Transthoracic echocardiogram showed signs of pulmonary hypertension with slight tricuspid insufficiency and an estimated 70<span class="elsevierStyleHsp" style=""></span>mmHg systolic pressure in the pulmonary artery&#44; without pericardial effusion&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The patient was admitted to the ward&#44; and his oxygen requirements decreased progressively in the first 24<span class="elsevierStyleHsp" style=""></span>h&#46; Treatment continued with the patient placed in a sitting position&#44; receiving low-flow oxygen therapy &#40;nasal prongs at 2<span class="elsevierStyleHsp" style=""></span>l&#47;min&#41;&#44; and minimum-dose furosemide&#46; After 3 days of hospitalization&#44; he was completely asymptomatic at discharge&#46; Follow-up echocardiography and cardiopulmonary exertion test one year later were both normal&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">HAPE generally occurs within 2&#8211;5 days after arrival at high altitudes&#44; and around 50&#37; of cases are associated with acute mountain sickness&#46; High altitude is considered to be between 1500 and 3700<span class="elsevierStyleHsp" style=""></span>m&#44; 3700&#8211;5500<span class="elsevierStyleHsp" style=""></span>m very high &#40;the incidence of HAPE at this altitude is 0&#46;6&#8211;6&#37;&#41;&#44; and &#62;5500<span class="elsevierStyleHsp" style=""></span>m extreme &#40;2&#8211;15&#37;&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Onset of clinical symptoms is insidious&#44; with decreased exercise tolerance&#44; progressive dyspnea&#44; orthopnea&#44; wet cough&#44; hemoptysis&#44; chest pain&#44; headache&#44; and confusion&#46;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">3&#44;4</span></a> Saturation is estimated to be 10&#37; lower than expected according to the altitude&#44; and the patient&#39;s general status is usually better than expected from their level of hypoxemia&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The main risk factor is individual susceptibility due to a low hypoxic ventilatory response&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a>The risk factor most susceptible to modification is the rate of ascent&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> and altitude gained during sleep is more significant than that gained during the day&#46; Other factors include the intensity of the exercise &#40;more than the exercise itself&#41;&#44; male sex&#44; anxiolytic medication&#44; and low temperatures&#46; A previous episode of HAPE carries a risk of recurrence of 60&#37;&#44; so it is very important that the patient is warned&#46; A gradual ascent of about 500<span class="elsevierStyleHsp" style=""></span>m per day to levels above 2500<span class="elsevierStyleHsp" style=""></span>m allows the physiological processes in the body to compensate adequately for the reduced partial pressure of oxygen at the new altitude&#46; Avoiding exercise and alcohol during the first 48<span class="elsevierStyleHsp" style=""></span>h until acclimatization also minimizes the risk&#46; Pre-existing conditions that lead to increased pulmonary blood flow&#44; such as pulmonary hypertension&#44; increased pulmonary vascular reactivity&#44; or a patent foramen ovale&#44; are predisposing factors for the appearance of the HAPE&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">The key factor in the pathophysiology of the disease is the initial adaptation to altitude&#44; in which the individual will typically increase ventilation&#46; Activation of the pulmonary and cerebral hypoxic vasoconstriction reflex results in an exaggerated vasoconstriction response&#44; raising pulmonary artery systolic pressure&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> The subsequent transudative capillary leak and the increase in perfusion increase blood pressure and hydrostatic pressure&#44; causing damage to the alveolar&#8211;capillary barrier&#44; and ultimately&#44; increased vascular permeability leading to acute&#44; non-uniform pulmonary edema&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Treatment consists of oxygen therapy and descending around 1000<span class="elsevierStyleHsp" style=""></span>m or to a level where symptoms resolve&#44; minimizing exertion during the descent&#46; Pharmacological treatment mentioned in the literature includes vasodilators&#44; such as nifedipine &#40;dihydropyridinic calcium channel blocker antagonists&#41;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> or sildenafil&#44;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> phosphodiesterase inhibitors&#44;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> and dexamethasone&#46; 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Scientific Letter
High-Altitude Acute Pulmonary Edema after 48 Hours in a Ski Station
Edema agudo de pulmón por altura tras 48 horas de estancia en una estación de esquí
Paula Isabel García Flores
Corresponding author
paulaflores89@gmail.com

Corresponding author.
, Alberto Caballero Vázquez, Ángela Herrera Chilla, Ana Dolores Romero Ortiz
Servicio de Neumología, Hospital Universitario Virgen de las Nieves, Granada, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Acute non-cardiogenic pulmonary edema consists of the rapid appearance of alveolar edema for causes other than increased pulmonary capillary pressure&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">1</span></a> One of the etiologies of this entity is acute high-altitude pulmonary edema &#40;HAPE&#41;&#44; an uncommon but potentially fatal presentation &#40;50&#37; mortality in untreated patients&#41;&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">It is one of the so-called &#8220;altitude sicknesses&#8221;&#44; the benign form of which occurs in 75&#37; of the population exposed to an altitude of between 2500 and 3000<span class="elsevierStyleHsp" style=""></span>m&#44; manifesting as symptoms such as nausea&#44; vomiting&#44; asthenia&#44; anorexia&#44; headache&#44; dizziness&#44; sleep disturbances or even dyspnea&#46; The malignant form is less frequent&#44; and develops with acute pulmonary edema and&#47;or cerebral edema syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">2</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">We report the case of a 40-year-old white man with no significant clinical history&#44; regular athlete&#44; former smoker&#44; normally resident at about 11<span class="elsevierStyleHsp" style=""></span>m above sea level&#44; who had ascended to Sierra Nevada &#40;maximum height 3300<span class="elsevierStyleHsp" style=""></span>m&#41; in less than 3<span class="elsevierStyleHsp" style=""></span>h&#46; He skied intensively for a 48<span class="elsevierStyleHsp" style=""></span>h period before experiencing a feeling of tiredness that forced him to interrupt his activity&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">He notified the emergency department of the ski resort of symptoms of sudden dyspnea&#44; more intense in the supine position&#44; and cough with bubbly pinkish expectoration&#46; On arrival in the medical center&#44; the patient was normotensive&#44; with signs of hypoperfusion and cyanosis&#44; tachycardiac at 120<span class="elsevierStyleHsp" style=""></span>bpm&#44; tachypneic &#40;&#62;30 breaths&#47;min&#41;&#44; with SatO<span class="elsevierStyleInf">2</span> of around 90&#37; and FiO<span class="elsevierStyleInf">2</span> of 0&#46;6 with work of breathing and low-grade fever of 37<span class="elsevierStyleHsp" style=""></span>&#176;<span class="elsevierStyleSmallCaps">C</span>&#46; Auscultation revealed moist rales&#44; mainly in both lung bases&#46; ECG showed sinus tachycardia at 110<span class="elsevierStyleHsp" style=""></span>bpm with normal axis along with the ST depression in the inferior and anteroseptal aspects&#46; After administration of empirical treatment &#40;oxygen therapy by reservoir cannula with FiO<span class="elsevierStyleInf">2</span> of 1&#46;0&#44; furosemide&#44; acetylsalicylic acid and antibiotic coverage&#41;&#44; the patient was transferred to the tertiary hospital&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">On arrival at the hospital&#44; arterial blood gases &#40;FiO<span class="elsevierStyleInf">2</span> 0&#46;6&#41; were determined&#44; showing normal pH&#44; oxygen partial pressure of 69&#46;9<span class="elsevierStyleHsp" style=""></span>mmHg&#44; and normal carbon dioxide and lactic acid&#46; Clinical laboratory tests were significant for slightly raised CRP and leukocytosis with neutrophilia&#44; with normal D-dimer and cardiac markers&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Chest X-ray showed a normal cardiothoracic index with a bilateral reticular cotton&#8211;wool pattern with no central predominance &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; The CT-angiogram ruled out pulmonary thromboembolism and concluded findings indicative of acute pulmonary edema&#46; Alveolar opacities and ground glass opacities were also observed&#44; with a symmetrical&#44; generalized distribution in the parenchyma of both lungs&#44; slightly more predominantly in the lower lobes&#44; which showed thickening of the interlobular septa and a significant increase in pulmonary arterial trunk diameter &#40;35<span class="elsevierStyleHsp" style=""></span>mm&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">Transthoracic echocardiogram showed signs of pulmonary hypertension with slight tricuspid insufficiency and an estimated 70<span class="elsevierStyleHsp" style=""></span>mmHg systolic pressure in the pulmonary artery&#44; without pericardial effusion&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">The patient was admitted to the ward&#44; and his oxygen requirements decreased progressively in the first 24<span class="elsevierStyleHsp" style=""></span>h&#46; Treatment continued with the patient placed in a sitting position&#44; receiving low-flow oxygen therapy &#40;nasal prongs at 2<span class="elsevierStyleHsp" style=""></span>l&#47;min&#41;&#44; and minimum-dose furosemide&#46; After 3 days of hospitalization&#44; he was completely asymptomatic at discharge&#46; Follow-up echocardiography and cardiopulmonary exertion test one year later were both normal&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">HAPE generally occurs within 2&#8211;5 days after arrival at high altitudes&#44; and around 50&#37; of cases are associated with acute mountain sickness&#46; High altitude is considered to be between 1500 and 3700<span class="elsevierStyleHsp" style=""></span>m&#44; 3700&#8211;5500<span class="elsevierStyleHsp" style=""></span>m very high &#40;the incidence of HAPE at this altitude is 0&#46;6&#8211;6&#37;&#41;&#44; and &#62;5500<span class="elsevierStyleHsp" style=""></span>m extreme &#40;2&#8211;15&#37;&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Onset of clinical symptoms is insidious&#44; with decreased exercise tolerance&#44; progressive dyspnea&#44; orthopnea&#44; wet cough&#44; hemoptysis&#44; chest pain&#44; headache&#44; and confusion&#46;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">3&#44;4</span></a> Saturation is estimated to be 10&#37; lower than expected according to the altitude&#44; and the patient&#39;s general status is usually better than expected from their level of hypoxemia&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">The main risk factor is individual susceptibility due to a low hypoxic ventilatory response&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">5</span></a>The risk factor most susceptible to modification is the rate of ascent&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">6</span></a> and altitude gained during sleep is more significant than that gained during the day&#46; Other factors include the intensity of the exercise &#40;more than the exercise itself&#41;&#44; male sex&#44; anxiolytic medication&#44; and low temperatures&#46; A previous episode of HAPE carries a risk of recurrence of 60&#37;&#44; so it is very important that the patient is warned&#46; A gradual ascent of about 500<span class="elsevierStyleHsp" style=""></span>m per day to levels above 2500<span class="elsevierStyleHsp" style=""></span>m allows the physiological processes in the body to compensate adequately for the reduced partial pressure of oxygen at the new altitude&#46; Avoiding exercise and alcohol during the first 48<span class="elsevierStyleHsp" style=""></span>h until acclimatization also minimizes the risk&#46; Pre-existing conditions that lead to increased pulmonary blood flow&#44; such as pulmonary hypertension&#44; increased pulmonary vascular reactivity&#44; or a patent foramen ovale&#44; are predisposing factors for the appearance of the HAPE&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">The key factor in the pathophysiology of the disease is the initial adaptation to altitude&#44; in which the individual will typically increase ventilation&#46; Activation of the pulmonary and cerebral hypoxic vasoconstriction reflex results in an exaggerated vasoconstriction response&#44; raising pulmonary artery systolic pressure&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> The subsequent transudative capillary leak and the increase in perfusion increase blood pressure and hydrostatic pressure&#44; causing damage to the alveolar&#8211;capillary barrier&#44; and ultimately&#44; increased vascular permeability leading to acute&#44; non-uniform pulmonary edema&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Treatment consists of oxygen therapy and descending around 1000<span class="elsevierStyleHsp" style=""></span>m or to a level where symptoms resolve&#44; minimizing exertion during the descent&#46; Pharmacological treatment mentioned in the literature includes vasodilators&#44; such as nifedipine &#40;dihydropyridinic calcium channel blocker antagonists&#41;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> or sildenafil&#44;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">3</span></a> phosphodiesterase inhibitors&#44;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">4</span></a> and dexamethasone&#46; 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Article information
ISSN: 15792129
Original language: English
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