Yanamandra, Uday, Velu Nair, Surinderpal Singh, Amul Gupta, Deepak Mulajkar, Sushma Yanamandra, Konchok Norgais, Ruchira Mukherjee, Vikrant Singh, Srinivasa A. Bhattachar, Sagarika Patyal, and Rajan Grewal. High-altitude pulmonary edema management: Is anything other than oxygen required? Results of a randomized controlled trial. High Alt Med Biol. 17:294-299, 2016.-Treatment strategies for management of high-altitude pulmonary edema (HAPE) are mainly based on the observational studies with only two randomized controlled trials, thus the practice is very heterogeneous and individualized as per the choice of treating physician. To compare the response to different modalities of therapy in patients with HAPE in a randomized controlled manner. We conducted an open-label, randomized noninferiority trial to compare three modalities of therapy (Therapy 1: supplemental O with oral dexamethasone 8 mg q8 hours [n = 42], Therapy 2: supplemental O with sustained release oral nifedipine 20 mg q8 hours [n = 41], and Therapy 3: only supplemental O [n = 50]). Bed rest was mandated in all patients. The study was conducted in a cohort of previously healthy young lowlander males at an altitude of 3500 m. Baseline characteristics of the patients were comparable in the study arms. Complete response was defined as clinical and radiological resolution of features of HAPE, no oxygen dependency, a normal 6-minute walk test (6MWT) on 2 consecutive days, and normal two-dimensional echocardiography. Results were compared by analysis of variance using SPSS version 16.0. There was no statistical difference in duration of therapy to complete response between the three groups (Therapy 1: 8.1 ± 4.0 days, Therapy 2: 6.7 ± 3.9 days, Therapy 3: 6.8 ± 3.2 days; p = 0.15). There were no deaths in any of the groups. We conclude that oxygen and bed rest alone are adequate therapy for HAPE and that adjuvant pharmacotherapy with either dexamethasone or nifedipine does not hasten recovery.

HASH is associated with endothelial dysfunction in form of raised levels of sICAM-1 and VCAM-1.

A bstract Background High-altitude pulmonary edema (HAPE) is a common cause of hospitalization in high altitude areas with significant morbidity. The clinical presentation of HAPE can overlap with a broad spectrum of cardiopulmonary diseases. Also, it is associated with varied radiological manifestations mimicking other conditions and often leading to unnecessary and inappropriate treatment. Patients and methods The primary aim of the study was to study the various radiological manifestations of HAPE through real-world chest radiographs. We present six different chest X-ray patterns of HAPE as a pictorial assay, at initial presentation, and after the resolution of symptoms with supplemental oxygen therapy and bed rest alone. Results HAPE can present as bilateral symmetrical perihilar opacities, bilateral symmetrical diffuse opacities, unilateral diffuse opacities, bilateral asymmetrical focal opacities, and even lobar consolidation with lower zone or less commonly upper zonal predilection. These presentations can mimic many common conditions like heart failure, acute respiratory distress syndrome, pulmonary embolism, aspiration pneumonitis, pneumonia, malignancy, and tuberculosis. Conclusion A holistic clinical–radiological correlation coupled with analysis of the temporal course can help high-altitude physicians in differentiating true HAPE from its mimics. How to cite this article Yanamandra U, Vardhan V, Saxena P, Singh P, Gupta A, Mulajkar D, et al . Radiographical Spectrum of High-altitude Pulmonary Edema: A Pictorial Essay. Indian J Crit Care Med 2021;25(6):668–674.

Systemic hypoxia is associated with conditions like anemia, lung diseases, sleep disorders, breathing, and exposure to high altitude. The physiological responses including blood pressure regulation to acute, chronic, intermittent normobaric, and hypobaric hypoxia have been under intense investigation for the past many years; however, the regulatory mechanisms are incompletely understood. The available literature indicates a differential response to hypoxia in pulmonary versus systemic circulation. Multiple physiological and metabolic changes contribute towards high-altitude acclimatization; yet, in some individuals, exposure to high altitude could be life threatening due to maladaptation. There are a few studies on the prevalence of hypertension in high-altitude natives and sea-level dwellers exposed to high altitude (acute and chronic). Elevated blood pressure is an established risk factor for different cardiovascular disease and the evidence suggests that the blood pressure rises to a modest extent in patients with mild to moderate hypertension upon acute ascent to high altitude (Luks et al., Congenit Heart Dis 5:220-232, 2010), but there is no clear evidence on increased risk of complications due to increased systemic blood pressures. This book chapter reviews available literature on systemic blood pressure responses to high altitude. A. Sarybaev (*)

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