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Nifedipine for the treatment of high altitude pulmonary edema.
Wilderness & Environmental Medicine 2012 March
OBJECTIVE: The purpose of this study was to assess the risk factors, patient profile, clinical features, and oral nifedipine as a treatment option for a series of 110 patients with high altitude pulmonary edema (HAPE) in a military hospital in India.
METHODS: This was a prospective cross-sectional study in a military hospital. In all, 110 patients with HAPE admitted and treated over a period of 3 years are reported. The following measurements were noted: dyspnea, cough, chest pain, cyanosis, pulse rate, blood pressure, respiratory rate, crepitations, radiographic abnormalities, electrocardiogram, peripheral pulse oximetry (Spo(2)) at admission, Spo(2) normalization time, total leukocyte count, and length of hospital stay.
RESULTS: The risk factors identified for development of HAPE in our patients were improper acclimatization/faster rates of ascent, higher defined height (10 500 feet [3200 m]) for first stage acclimatization due to logistic reasons (usually 9000 feet [2743 m]), cold exposure, severe exercise, and respiratory infection. All patients were treated with reduction of altitude, supplemental oxygen therapy with nasal prongs, and bed rest. Oral nifedipine or placebo was administered to alternating patients. None of the patients deteriorated during their hospital stay, and all recovered fully to be discharged an average of 4.01 days (range 2-6 days) after admission. Patients were monitored for time taken for normalization of oxygen saturation, duration of hospital stay, time needed for resolution of lung crepitations, and radiographic infiltrates. Nifedipine administration was not found to be better than placebo for any of these variables (P > .05).
CONCLUSIONS: Improper acclimatization remains the foremost risk factor for HAPE. In addition to descent and supplemental oxygen, nifedipine appears to provide no additional benefit in the resolution of HAPE.
METHODS: This was a prospective cross-sectional study in a military hospital. In all, 110 patients with HAPE admitted and treated over a period of 3 years are reported. The following measurements were noted: dyspnea, cough, chest pain, cyanosis, pulse rate, blood pressure, respiratory rate, crepitations, radiographic abnormalities, electrocardiogram, peripheral pulse oximetry (Spo(2)) at admission, Spo(2) normalization time, total leukocyte count, and length of hospital stay.
RESULTS: The risk factors identified for development of HAPE in our patients were improper acclimatization/faster rates of ascent, higher defined height (10 500 feet [3200 m]) for first stage acclimatization due to logistic reasons (usually 9000 feet [2743 m]), cold exposure, severe exercise, and respiratory infection. All patients were treated with reduction of altitude, supplemental oxygen therapy with nasal prongs, and bed rest. Oral nifedipine or placebo was administered to alternating patients. None of the patients deteriorated during their hospital stay, and all recovered fully to be discharged an average of 4.01 days (range 2-6 days) after admission. Patients were monitored for time taken for normalization of oxygen saturation, duration of hospital stay, time needed for resolution of lung crepitations, and radiographic infiltrates. Nifedipine administration was not found to be better than placebo for any of these variables (P > .05).
CONCLUSIONS: Improper acclimatization remains the foremost risk factor for HAPE. In addition to descent and supplemental oxygen, nifedipine appears to provide no additional benefit in the resolution of HAPE.
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