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High Altitude Edema

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461. Severe facial edema at high altitude. Full Text available with Trip Pro

Severe facial edema at high altitude. We present a complication associated with high altitude of unusual severity. Pronounced facial edema developed in a 27-year-old woman during a trek to Kilimanjaro, Tanzania. The development of facial edema has previously been documented in visitors unaccustomed to high altitude. The possible pathophysiological mechanisms are discussed, and the importance of adhering to recommended ascent rates is emphasized for all high-altitude treks.

2008 Journal of Travel Medicine

462. Association of polymorphisms in pulmonary surfactant protein A1 and A2 genes with high-altitude pulmonary edema. (Abstract)

Association of polymorphisms in pulmonary surfactant protein A1 and A2 genes with high-altitude pulmonary edema. A potential pathogenetic cofactor for the development of high-altitude pulmonary edema (HAPE) is an increase in capillary permeability, which could occur as a result of an inflammatory reaction and/or free-radical-mediated injury to the lung. Pulmonary surfactant protein A (SP-A), the most abundant surfactant protein, has potent antioxidant properties and protects unsaturated (...) case-control study.Blood samples were collected at an altitude (> or = 3,500 m).Twelve low-altitude native (LAN) subjects with a history of HAPE, 15 healthy LAN sojourners without a history of HAPE (LAN control subjects), and 19 healthy high-altitude natives (HANs) without a history of HAPE (HAN control subjects).The SNPs in four exons and intermediate introns of the SP-A1 and SP-A2 were screened by polymerase chain reaction and sequencing. Biochemical parameters related to oxidative stress

2005 Chest

463. Polymorphisms of renin-angiotensin system genes with high-altitude pulmonary edema in Japanese subjects. (Abstract)

Polymorphisms of renin-angiotensin system genes with high-altitude pulmonary edema in Japanese subjects. The renin-angiotensin system (RAS), including angiotensin-converting enzyme (ACE) and angiotensin II type 1 receptor (AT(1)R), plays an important role in the pathogenesis of pulmonary hypertension, which is suggested to be critical in the development of high-altitude pulmonary edema (HAPE). Investigating the associations of the polymorphisms in the genes of RAS with HAPE is to elucidate

2004 Chest

464. Pulmonary blood flow heterogeneity during hypoxia and high-altitude pulmonary edema. (Abstract)

Pulmonary blood flow heterogeneity during hypoxia and high-altitude pulmonary edema. Uneven hypoxic pulmonary vasoconstriction has been proposed to expose parts of the pulmonary capillary bed to high pressure and vascular injury in high-altitude pulmonary edema (HAPE). We hypothesized that subjects with a history of HAPE would demonstrate increased heterogeneity of pulmonary blood flow during hypoxia. A functional magnetic resonance imaging technique (arterial spin labeling) was used (...) to quantify spatial pulmonary blood flow heterogeneity in three subject groups: (1) HAPE-susceptible (n = 5), individuals with a history of physician-documented HAPE; (2) HAPE-resistant (n = 6), individuals with repeated high-altitude exposure without illness; and (3) unselected (n = 6), individuals with a minimal history of altitude exposure. Data were collected in normoxia and after 5, 10, 20, and 30 minutes of normobaric hypoxia FI(O(2)) = 0.125. Relative dispersion (SD/mean) of the signal intensity

2005 American Journal of Respiratory and Critical Care Medicine

465. Heterozygotes of NOS3 polymorphisms contribute to reduced nitrogen oxides in high-altitude pulmonary edema. (Abstract)

Heterozygotes of NOS3 polymorphisms contribute to reduced nitrogen oxides in high-altitude pulmonary edema. High-altitude pulmonary edema (HAPE), which develops on exertion under hypoxic conditions, aggravates due to endothelial dysfunction. Repeat events of the disorder suggests of genetic susceptibility. Endothelial nitric oxide synthase gene (NOS3), a regulator of vasodilation, has emerged as a strong candidate marker. In the present study, we investigated G894T, 27-base-pair 4b/4a (variable (...) number of tandem repeat), -922A/G, and -786T/C polymorphisms of NOS3, individually or in combination, for an association with HAPE.A cross-sectional case control study.Blood samples of HAPE-resistant lowlanders (HAPE-r) were obtained at sea level, and blood samples of patients with HAPE (HAPE-p) were obtained at Sonam Norboo Memorial Hospital, Leh, at 3,500 m.The study groups consisted of 60 HAPE-r inducted two to three times to altitudes > 3,600 m; and 72 HAPE-p, who had HAPE on their first visit

2006 Chest

466. Chest ultrasonography for the diagnosis and monitoring of high-altitude pulmonary edema. (Abstract)

Chest ultrasonography for the diagnosis and monitoring of high-altitude pulmonary edema. The comet-tail technique of chest ultrasonography has been described for the diagnosis of cardiogenic pulmonary edema. This is the first report describing its use for the diagnosis and monitoring of high-altitude pulmonary edema (HAPE), the leading cause of death from altitude illness.Eleven consecutive patients presenting to the Himalayan Rescue Association clinic in Pheriche, Nepal (4,240 m (...) ) with a clinical diagnosis of HAPE underwent one to three chest ultrasound examinations using the comet-tail technique to determine the presence of extravascular lung water (EVLW). Seven patients with no evidence of HAPE or other altitude illness served as control subjects. All examinations were read by a blinded observer.HAPE patients had higher comet-tail score (CTS) [mean +/- SD, 31 +/- 11 vs 0.86 +/- 0.83] and lower oxygen saturation (O(2)Sat) [61 +/- 9.2% vs 87 +/- 2.8%] than control subjects (p < 0.001

2007 Chest

467. Pregabalin-withdrawal encephalopathy and splenial edema: a link to high-altitude illness? (Abstract)

Pregabalin-withdrawal encephalopathy and splenial edema: a link to high-altitude illness? A postherpetic-neuralgia patient abruptly discontinued pregabalin. Thirty hours later, unexplained nausea, headache, and ataxia developed, progressing to delirium 8 days later. Magnetic resonance imaging indicated T2-hyperintense lesions of her splenium. Similar magnetic resonance imaging abnormalities, interpreted as focal vasogenic edema, develop in some epileptic patients after rapid anticonvulsant (...) withdrawal. Patients with high-altitude cerebral edema have similar splenial-predominant magnetic resonance imaging abnormalities that accompany these same neurological symptoms. This case is the first to associate anticonvulsant-withdrawal splenial abnormalities with neurological symptoms, with gabapentin-type anticonvulsants, and is among the first in nonepileptic patients, suggesting that sudden anticonvulsant withdrawal alone, unaccompanied by seizures, can initiate symptomatic focal brain edema

2005 Annals of Neurology

468. Salmeterol for the prevention of high-altitude pulmonary edema. Full Text available with Trip Pro

Salmeterol for the prevention of high-altitude pulmonary edema. Pulmonary edema results from a persistent imbalance between forces that drive water into the air space and the physiologic mechanisms that remove it. Among the latter, the absorption of liquid driven by active alveolar transepithelial sodium transport has an important role; a defect of this mechanism may predispose patients to pulmonary edema. Beta-adrenergic agonists up-regulate the clearance of alveolar fluid and attenuate (...) pulmonary edema in animal models.In a double-blind, randomized, placebo-controlled study, we assessed the effects of prophylactic inhalation of the beta-adrenergic agonist salmeterol on the incidence of pulmonary edema during exposure to high altitudes (4559 m, reached in less than 22 hours) in 37 subjects who were susceptible to high-altitude pulmonary edema. We also measured the nasal transepithelial potential difference, a marker of the transepithelial sodium and water transport in the distal airways

2002 NEJM Controlled trial quality: uncertain

469. Prevention of high-altitude pulmonary edema by nifedipine. (Abstract)

Prevention of high-altitude pulmonary edema by nifedipine. Exaggerated pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in high-altitude pulmonary edema. We previously found that nifedipine lowered pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with high-altitude pulmonary edema. We therefore hypothesized that the prophylactic administration (...) of nifedipine would prevent its recurrence.Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented high-altitude pulmonary edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment

1991 NEJM Controlled trial quality: uncertain

470. Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor. (Abstract)

Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor. The pathogenesis of high-altitude pulmonary edema (HAPE) is considered an altered permeability of the alveolar-capillary barrier secondary to intense pulmonary vasoconstriction and high capillary pressure, but previous bronchoalveolar lavage (BAL) findings in well-established HAPE are also consistent with inflammatory etiologic characteristics.To determine whether inflammation is a primary event in HAPE (...) at 4559 m compared with HAPE-resistant subjects (66 vs 37 mm Hg; P =.004). Despite development of HAPE in the majority of HAPE-susceptible subjects, there were no differences in BAL fluid total leukocyte counts between resistant and susceptible subjects or between counts taken at low and high altitudes. Subjects who developed HAPE had BAL fluid with high concentrations of plasma-derived proteins and erythrocytes, but there was no increase in plasma concentrations of surfactant protein A and Clara cell

2002 JAMA

471. Effects of altitude and exercise on pulmonary capillary integrity: evidence for subclinical high-altitude pulmonary edema. Full Text available with Trip Pro

Effects of altitude and exercise on pulmonary capillary integrity: evidence for subclinical high-altitude pulmonary edema. Strenuous exercise may be a significant contributing factor for development of high-altitude pulmonary edema, particularly at low or moderate altitudes. Thus we investigated the effects of heavy cycle ergometer exercise (90% maximal effort) under hypoxic conditions in which the combined effects of a marked increase in pulmonary blood flow and nonuniform hypoxic pulmonary (...) developed a permeability edema with high BALF RBC and protein concentrations in the absence of inflammation. We found that exercise at altitude (3,810 m) caused significantly greater leakage of RBCs [9.2 (SD 3.1)x10(4) cells/ml] into the alveolar space than that seen with normoxic exercise [5.4 (SD 1.2)x10(4) cells/ml]. At altitude, the 26-h postexercise BALF revealed significantly higher RBC and protein concentrations, suggesting an ongoing capillary leak. Interestingly, the BALF profiles following

2006 Journal of applied physiology (Bethesda, Md. : 1985) Controlled trial quality: uncertain

472. High-altitude pulmonary edema in children with underlying cardiopulmonary disorders and pulmonary hypertension living at altitude. Full Text available with Trip Pro

High-altitude pulmonary edema in children with underlying cardiopulmonary disorders and pulmonary hypertension living at altitude. Pulmonary hypertension has not been described as a predisposing risk factor for high-altitude pulmonary edema (HAPE) in children. Previous studies have shown an association of HAPE with abnormally increased pulmonary vasoreactivity to hypoxia but generally normal pulmonary artery pressure (PAP) after recovery.To describe HAPE of relatively rapid onset and its (...) management in a series of children residing at moderate to high altitudes, all of whom had underlying pulmonary hypertension.From 1997 to 2003, 30 children came to our center with high-altitude illness. Of these, 10 children (aged 4-18 years; male-female ratio, 8:2) living at moderate to high altitudes (1610-3050 m) underwent cardiac catheterization after recovery from HAPE, and all were found to have chronic pulmonary hypertension (mean PAP, 38 +/- 9 mm Hg; pulmonary vascular resistance, 8.6 +/- 2.8 U x

2004 Archives of Pediatrics & Adolescent Medicine

473. Adult respiratory distress syndrome secondary to high altitude pulmonary edema. Full Text available with Trip Pro

Adult respiratory distress syndrome secondary to high altitude pulmonary edema. 7347049 1982 10 21 2018 11 13 0093-0415 133 4 1980 Oct The Western journal of medicine West. J. Med. Adult respiratory distress syndrome secondary to high altitude pulmonary edema. 335-7 Zimmerman G A GA Crapo R O RO eng Case Reports Journal Article United States West J Med 0410504 0093-0415 IM Adult Altitude Sickness complications Humans Hypoxia complications Male Pulmonary Edema complications Respiratory Distress

1980 Western Journal of Medicine

474. High-Altitude Pulmonary Edema in Vail, Colorado, 1975-1982 Full Text available with Trip Pro

High-Altitude Pulmonary Edema in Vail, Colorado, 1975-1982 Between 1975 and 1982 a total of 47 cases of high-altitude pulmonary edema occurred in Vail, Colorado, elevation 2,500 m (8,200 ft). All occurred in visitors from lower altitudes. The mean age of the patients was 35.6 years, and 93% were men. Most patients had tachycardia, tachypnea and fever. The mean time of onset of cough and shortness of breath was 2.5 days after arrival. The average total ascent of the patients was 2,330 m (7,644

1986 Western Journal of Medicine

475. [Changes of plasma fibrinolysis system and the effect of captopril in high altitude pulmonary edema]. (Abstract)

[Changes of plasma fibrinolysis system and the effect of captopril in high altitude pulmonary edema]. To investigate the changes of plasma fibrinolysis system and the effect of captopril in patients with high altitude pulmonary edema.The plasma levels of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) were measured before and after treatment in the captopril-group (group A, 35 cases) and the routine-group (group B, 37 cases) of patients with HAPE, while 20

2003 Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases Controlled trial quality: uncertain

476. [Low-concentration nitrous oxide inhalation in the treatment of high-altitude pulmonary edema]. (Abstract)

[Low-concentration nitrous oxide inhalation in the treatment of high-altitude pulmonary edema]. To investigate the therapeutic effect of low-concentration of nitroic oxide (NO) inhalation in high-altitude pulmonary edema.Sixty-five male patients with high-altitude pulmonary edema were randomized into three groups. Patients in the conventional therapy group received oxygen, intravenous furosemide, aminophylline and dexamethasone; patients in the nifedipine group received oral nifedipine (10 mg (...) of the nifedipine group (2.4 +/- 1.4 d, 4.1 +/- 1.7 d, 6.8 +/- 1.8 d, respectively) and the conventional therapy group (3.7 +/- 1.2 d, 5.5 +/- 1.8 d, 9.6 +/- 3.1 d, respectively).Low-concentration NO inhalation on the basis of conventional and nifedipine therapies was very effective in the treatment of high-altitude pulmonary edema, which deserves further and larger scale investigation.

1998 Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases Controlled trial quality: uncertain

477. Effects of inhaled nitric oxide and oxygen in high-altitude pulmonary edema. (Abstract)

Effects of inhaled nitric oxide and oxygen in high-altitude pulmonary edema. High-altitude pulmonary edema (HAPE) is characterized by pulmonary hypertension, increased pulmonary capillary permeability, and hypoxemia. Treatment is limited to descent to lower altitude and administration of oxygen.We studied the acute effects of inhaled nitric oxide (NO), 50% oxygen, and a mixture of NO plus 50% oxygen on hemodynamics and gas exchange in 14 patients with HAPE. Each gas mixture was given in random

1998 Circulation Controlled trial quality: uncertain

478. High-altitude pulmonary edema at a ski resort. Full Text available with Trip Pro

High-altitude pulmonary edema at a ski resort. Medical records of 150 patients with high-altitude pulmonary edema seen over a 39-month period in a Colorado Rocky Mountain ski area at 2,928 m (9,600 ft) (mean age 34.4 years; 84% male) were reviewed. The mean time to the onset of symptoms was 3 +/- 1.3 days after arrival. Common symptoms were dyspnea, cough, headache, chest congestion, nausea, fever, and weakness. Orthopnea, hemoptysis, and vomiting were rare, occurring in 7%, 6%, and 16 (...) %, respectively. Symptoms of cerebral edema occurred in 14%. A temperature exceeding 100 degrees F occurred in 20%, and 17% had a systolic blood pressure of 150 mm of mercury or higher. Blood pressures were higher in patients older than 50 years (142 mm of mercury). Rales were present in 85%, and a pulmonary infiltrate was present in 88%; both were most commonly bilateral or on the right side. The amount of infiltrate was mild. Men appeared to be more susceptible than women to high-altitude pulmonary edema

1996 Western Journal of Medicine

479. Endotracheal intubation and mechanical ventilation following respiratory arrest from high altitude pulmonary edema. Full Text available with Trip Pro

Endotracheal intubation and mechanical ventilation following respiratory arrest from high altitude pulmonary edema. 10214107 1999 05 06 2018 11 13 0093-0415 170 3 1999 Mar The Western journal of medicine West. J. Med. Endotracheal intubation and mechanical ventilation following respiratory arrest from high altitude pulmonary edema. 174-6 Litch J A JA Himalayan Rescue Association, Kathmandu, Nepal. jlitch@yahoo.com eng Case Reports Journal Article United States West J Med 0410504 0093-0415 AIM (...) IM Adult Altitude Sickness Fatal Outcome Humans Intubation, Intratracheal Male Pulmonary Edema complications Respiration, Artificial Respiratory Insufficiency etiology therapy 1999 4 24 1999 4 24 0 1 1999 4 24 0 0 ppublish 10214107 PMC1305538 Clin Chest Med. 1985 Sep;6(3):491-507 3907949 West J Med. 1997 Sep;167(3):180-1 9308415 N Engl J Med. 1994 Apr 14;330(15):1056-61 8080509 West J Med. 1980 Oct;133(4):335-7 7347049 Wilderness Environ Med. 1996 Aug;7(3):259-60 11990122

1999 Western Journal of Medicine

480. Polymorphisms of the tyrosine hydroxylase gene in subjects susceptible to high-altitude pulmonary edema. (Abstract)

Polymorphisms of the tyrosine hydroxylase gene in subjects susceptible to high-altitude pulmonary edema. A blunted hypoxic ventilatory response (HVR) has been observed in some sufferers of high-altitude pulmonary edema (HAPE), and was proposed as a potential mechanism in its pathogenesis. Tyrosine hydroxylase (TH) is a rate-limiting enzyme in the carotid body responding to hypoxia to synthesize dopamine neurotransmitter to heighten ventilation. The association of constitutional susceptibility

2003 Chest

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