Variable Radiomorphologic Data of High Altitude Pulmonary Edema: Features from 60 Patients

doi:10.1378/chest.100.5.1306

Chest

Volume 100, Issue 5, November 1991, Pages 1306-1311

https://doi.org/10.1378/chest.100.5.1306 Get rights and content

The purpose of the study was to collect radiomorphologic data of a large population of subjects with high altitude pulmonary edema. A blinded retrospective analysis of 60 patients severe enough to warrant hospital admission is reported. Immediately after rescue to low altitude, the severity of HAPE was graded using a quadrant-based scoring system (0-4 each quadrant). Its distribution and the morphologic features were noted. HAPE was more severe in the base, and specifically, the right lower quadrant, as compared to the other quadrants. It was often located both centrally and peripherally (60 percent) and in 92 percent was characterized by air space disease of homogeneous (n = 40) rather than patchy distribution (n = 15). In recurrent HAPE (n = 13), radiomorphologic data were as variable as among different HAPE patients. We conclude that HAPE does not have one common radiomorphologic condition. Based on the literature, earlier experience, and follow-up observations, we hypothesize that it may start patchy and peripheral, supporting the concept of uneven vasoconstriction with overperfusion and/or permeability leak. Later on, such as in the severe cases studied, it becomes homogeneous. Recurrent episodes generally do not show an identical distribution of HAPE, suggesting that structural abnormalities are not involved in the pathogenesis of HAPE.

Section snippets

Battent Population

Our inclusion criteria were an acute exposure to an altitude between 2,500 and 4,600 meters with clinical and roentgenographic signs of pulmonary edema, recovering without any specific treatment. Two patients were excluded because of pneumonia coexisting with possible HAPE. Sixty patients, 2 women and 58 men, were evaluated. They were 20 to 71 years old (median 35.0 years). Nineteen had a positive history for HAPE; in the case of multiple roentgenographic proof, only the more severe episode was

Results

At the moment of hospital entry, the sum score of HAPE averaged 13.1 (extreme values 3 to 16) and was significantly higher for severe (mean 14.2) as compared to mild cases (mean 11.9, p less than 0.02, Table 1); however, it did not differ depending on the presence or absence of cerebral edema. The mean score of the right lower quadrant was 3.7 and higher than the scores of the other three quadrants (p less than 0.01, (Fig 1). Similarly, the right side dominated more often (n = 27, 45 percent,

Discussion

Early roentgenographic descriptions of HAPE, mostly illustrations in clinical papers without quantitative evaluation of chest roentgenographic data^1,^3,^4,^5,^7,^9,^10,^12,²¹ mention lung infiltrates, as well as an enlarged main pulmonary artery, and several reports have since shown the characteristic patchy aspect including involvement of the lung periphery.^9,^12,^13,¹⁵ Classification of edema types from roentgenograms would be desirable, and some authors have pointed out and debated the irregular,

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Ascent to high altitude triggers a wide range of physiological changes. However, ascent is also associated with three acute pathologies: acute mountain sickness, high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE). Awareness and understanding of these conditions allows measures to be taken to reduce the risk of them developing through careful planning and, where appropriate, pharmacological prophylaxis. Both HACE and HAPE are life threatening, necessitating prompt diagnosis and management. Acute mountain sickness, although usually benign, may progress, to HACE or HAPE, if not managed appropriately. This review examines each pathology providing options for risk reduction, diagnosis and management, as well as considering comorbidity at altitude, drawing upon recent advances and consensus guidelines in the field.
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The rats were kept in supine anteroposterior position during roentgenographical assessment of HAPE. As per Vock's criteria for roentgenographically assessing HAPE in humans [26], the lungs were divided into 4 quadrants where normal parenchyma was given a score of zero. Areas of the lung with questionable pathologic areas were scored as 1; clearly visible interstitial disease <50% of any lung quadrant was scored as 2.
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In this study, we detail the process of rapidly inducing HAPE in male SD rats within 18 h of simulated high-altitude exposure without causing high rates of mortality. Thereafter, we confirmed HAPE using roentgenography. We assessed Sulfotransferase 1A1 (SULT1A1), IL-1 beta, TNF- alpha and IFN-gamma using ELISA. Finally, H&E staining of lung tissues was also performed.
A roentgenographically confirmed HAPE model was demonstrated. SULT 1A1 levels are found to be highest in rats suffering HAPE, as previously confirmed in human patients. Inflammation was also assessed based on levels of inflammatory proteins like IL-1b, TNF-a, and IFN-g in addition to H&E staining of lung tissues. Inflammation and HAPE were observed to be synergistic events and not cause and effect of each other.
This rat model of HAPE will help researchers and clinicians in evaluating performance of therapies, potential biomarker and also further elucidate underlying molecular processes causing HAPE.
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The Lake Louise criteria have been derived to assist in the clinical diagnosis of HAPE: the presence of any 2 symptoms in combination with any 2 physical findings among those listed in Box 2 satisfy a presumptive diagnosis in unacclimatized individuals who have recently ascended to high altitudes.126 When available, chest radiography (Fig. 1) initially shows patchy, heterogeneous peripheral alveolar infiltrates progressing eventually to widespread, confluent airspace involvement.127,128 Portable lung ultrasonography provides a more feasible imaging option in remote locations and shows progressively larger numbers of extravascular fluid comet tails in patients ascending to altitude and suffering from HAPE.129,130
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We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high-altitude pulmonary edema (HAPE). Individual susceptibility is the most important determinant for the occurrence of HAPE. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressure 36-51 mm Hg), caused by an inhomogeneous hypoxic pulmonary vasoconstriction which leads to an elevated pulmonary capillary pressure and protein content as well as red blood cell-rich edema fluid. Furthermore, decreased fluid clearance from the alveoli may contribute to this noncardiogenic pulmonary edema. Immediate descent or supplemental oxygen and nifedipine or sildenafil are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent, average gain of altitude not exceeding 300 m/d above an altitude of 2500 m. If progressive high altitude acclimatization would not be possible, prophylaxis with nifedipine or tadalafil for long sojourns at high altitude or dexamethasone for a short stay of less then 5 days should be recommended.
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The susceptible number of sojourners is often difficult to determine, but figures of 0.2% in individuals ascending to the Campana Margherita Hut on Monta Rosa (4,559 m) to 2.5% at 4,400 m on Denali or on the way to Everest Basecamp,15 to 15% in Indian troops flown rapidly to 3,500 m87 have been reported. Imaging of the thorax reveals patchy opacities with inconsistent predominance of location, but often infiltrates are seen initially in the region of the right middle lobe87–90 (Fig 2). A recent study91 using chest ultrasonography at 4,240 m in Nepal demonstrated that the “comet-tail sign” (echogenic patterns in the peripheral lung arising with increased lymphatic flow in the lobular septae), which has been used to track the course of cardiogenic pulmonary edema, was useful in diagnosing HAPE and following up patients with HAPE.
High-altitude illnesses have profound consequences on the health of many unsuspecting and otherwise healthy individuals who sojourn to high altitude for recreation and work. The clinical manifestations of high-altitude illnesses are secondary to the extravasation of fluid from the intravascular to extravascular space, especially in the brain and lungs. The most common of these illnesses, which can present as low as 2,000 m, is acute mountain sickness, which is usually self-limited but can progress to the more severe and potentially fatal entities of high-altitude cerebral edema and high-altitude pulmonary edema. This article will briefly review normal adaptation to high altitude and then more extensive reviews of the clinical presentations, prevention, and treatments of these potentially fatal conditions. Research on the mechanisms of these conditions will also be reviewed. A better understanding of these disorders by practitioners will lead to improved prevention and rational treatment for the increasing number of people visiting high-altitude areas around the globe. There will not be space for writing about high-altitude residents, medical conditions in low-altitude residents going to high altitude, or training for athletes at high altitude. These topics deserve another article.

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Reprint requests: Dr. Vock, Department of Radiology, University Hospital, Bern, Switzerland CH-3010

Manuscript received October 1; revision accepted March 26.

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Chest

Clinical InvestigationsVariable Radiomorphologic Data of High Altitude Pulmonary Edema: Features from 60 Patients

Section snippets

Battent Population

Results

Discussion

Lancet

Chest

Clin Chest Med

Am J Cardiol

Chest

Acute pulmonary edema of high altitude.

N Engl J Med

High altitude pulmonary edema.

Medicine

Acute pulmonary edema of altitude: clinical and physiologic observations.

Circulation

Physiologic studies of pulmonary edema at high altitude.

Circulation

High altitude pulmonary edema: a rare disease?

JAMA

High-altitude pulmonary edema in persons without the right pulmonary artery.

N Engl J Med

High altitude pulmonary edema.

Radiol Clin North Am

Radiologic distinction of cardiogenic and noncardiogenic edema.

Am J Roentgenol

High-altitude pulmonary edema: findings at high-altitude chest radiography and physical examination.

Radiology

Pulmonary edema fluid protein in high-altitude pulmonary edema.

JAMA

The lung at high altitude: bronchoalveolar lavage in acute mountain sickness and pulmonary edema.

J Appl Physiol

Effect of high blood flow, ventilation, breathing pattern and alveolar hypoxia on lung fluid flux.

Clinical Investigations
Variable Radiomorphologic Data of High Altitude Pulmonary Edema: Features from 60 Patients