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High altitude pulmonary edema (HAPE) in a Himalayan trekker: a case report
INTRODUCTION: High altitude pulmonary edema is a non-cardiogenic form of pulmonary edema that develops in unacclimatized individuals at altitudes over 2500 m. Early recognition of symptoms and immediate descent are important for successful treatment. Despite early signs and symptoms of high altitude...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3984695/ https://www.ncbi.nlm.nih.gov/pubmed/24636661 http://dx.doi.org/10.1186/2046-7648-3-6 |
Sumario: | INTRODUCTION: High altitude pulmonary edema is a non-cardiogenic form of pulmonary edema that develops in unacclimatized individuals at altitudes over 2500 m. Early recognition of symptoms and immediate descent are important for successful treatment. Despite early signs and symptoms of high altitude illness, many trekkers tend to push themselves to the maximum limit. Some of them, such as the case reported here, choose to ascend on horse-back which is extremely dangerous and can be fatal. CASE PRESENTATION: A 55 years of age Indian ethnic South African lady was emergency air-lifted from 4410 m altitude in the Nepal Himalayas to Kathamandu (1300 m) with a suspected case of high altitude pulmonary edema. She had continued ascending despite experiencing mild altitude symptoms at Namche (3440 m), and these symptoms worsened considerably at Tengboche (3860 m). At the very start of her trek, just after Lukla (2800 m), she suffered from sore throat, and had consequently begun a course of antibiotics (azithromycin) for a suspected throat infection. She had planned to continue ascending on horse back to complete the trek, however her condition deteriorated further and she had to be medically evacuated. On admission to the clinic her axillary temperature was 99.4 F, blood pressure 120/60 mmHg, pulse rate 72/min, respiratory rate of 25 breaths/min, and pulse oximeter showed saturation of 90% on room air at rest. Right sided crackles on the axillary and posterior region were heard on chest auscultation. Heel to toe test showed no signs of ataxia. The chest radiograph showed patchy infiltrates on the right side. An echocardiogram was done which revealed a high pulmonary artery pressure of 50 mm of Hg. She was diagnosed as resolving high altitude pulmornay edema. She was treated with bed rest, supplemental oxygen and sustained release nifedipine 20 mg (orally) twice a day. On the third day her crackles had cleared significantly and repeat chest radiograph as shown showed remarkable improvement. She felt much better. A repeat echocardiogram revealed a normal pulmonary artery pressure. CONCLUSION: The case report highlights numerous points: 1) Many high altitude trekkers have invested significant time, money and physical efforts in in their ventures and are determined to ascend despite early warning and illnesses. 2) Despite no history of altitude illnesses in previous altitude exposure,inter-current illness (in this case a nonspecific respiratory tract infection) may contribute to the development of high altitude pulmonary edema. 3) Continuing ascent using other transport means, whilst suffering from symptoms of high altitude illness, worsens the condition and could be life threatening. 4) Acetazolamide does not prevent high altitude pulmonary edema–perhaps more so in the cases that have inter-current illness. 5) Descent is the golden rule in all altitude illnesses. Actually ‘descent’ is advised in any undiagnosed illness at high altitude among sojourners. 6) Finally, an experienced guide who has mountain medicine training is essential. They can be crucial in noticing early signs and symptoms of altitude illnesses to inform the client’s safety as in this case. |
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