[Respiratory changes during ascension to 8,000 meters mountain]. / Cambios respiratorios durante la ascensión a una montaña de más de 8.000 metros.

BACKGROUND: Our goal was to determine whether spirometric alterations occur during expeditions to 8,000-metre peaks, and whether these are modified by acclimatization or are related to acute mountain sickness, to arterial oxygen saturation (SaO2) or to muscular deterioration due to chronic hypoxic exposure. SUBJECTS AND METHOD: Forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), inspiratory (MIP) and expiratory (MEP) maximal static pressures, grip strength in both hands, and SaO2 at rest and exercise were measured in eight subjects during an expedition to Gasherbrum II (8,035 m). RESULTS: Upon arrival at the base camp (5,200 m), both FVC and FEV1 decreased, with no changes in the FEV1/FVC ratio. FVC did not improve after a brief pressurisation in a portable hyperbaric chamber. A month later, FVC in the base camp returned to normal values. FVC fall correlated with both the severity of acute mountain sickness and weight loss. Resting SaO2 improved with acclimatisation and correlated with the previous hypoxic ventilatory response, both before and after acclimatisation. Acclimatisation led to a decrease in the exercise-induced SaO2 fall. Stay at a high altitude lowered body weight and grip strength, although MIP and MEP remained unchanged. CONCLUSIONS: We observed a restrictive alteration was corrected by with acclimatisation. This phenomenon seems to be related to a subclinical high-altitude pulmonary oedema rather than to an increase in the pulmonary vascular volume. Despite the high-altitude muscular deterioration, respiratory muscle weakness was not

Cambios respiratorios durante la ascensión a una montaña de más de 8.000 metros / Respiratory changes during ascension to 8,000 meters mountain

FUNDAMENTO: Conocer si durante las expediciones a montañas de más de 8.000 m ocurren alteraciones espirométricas y si éstas se modifican por la aclimatación, se relacionan con el mal agudo de montaña, con la saturación arterial de oxígeno (SaO2) o con el deterioro muscular por la hipoxia crónica. SUJETOS Y MÉTODO: En 8 sujetos participantes en una expedición al Gasherbrum II (8.035 m) estudiamos la capacidad vital forzada (CVF), el volumen espiratorio máximo por segundo (VEMS), las presiones máximas inspiratoria (PIM) y espiratoria (PEM), la fuerza prensil en ambas manos y la SaO2 en reposo y durante el ejercicio. RESULTADOS: Al llegar al campamento base (5.200 m) observamos un descenso de la CVF y del VEMS, sin cambios en la relación VEMS/CVF por ciento. La CVF no mejoró tras la presurización en una cámara hiperbárica. Un mes después, la CVF se había normalizado. La caída de la CVF se corelacionó con la aparición de mal agudo de montaña y con la pérdida de peso. La SaO2 en reposo mejoró con la aclimatación y se correlacionó con la respuesta ventilatoria a la hipoxia, tanto antes como después de la aclimatación. La aclimatación corrigió la caída de la SaO2 por el ejercicio. La permanencia a gran altitud disminuyó la fuerza en ambas manos, pero no redujo la PIM ni la PEM. CONCLUSIONES: Durante la ascensión a una montaña de más de 8.000 m, apreciamos una alteración restrictiva que mejora con la aclimatación, atribuible más a edema pulmonar subclínico que a incremento del volumen vascular. Pese al deterioro muscular de la gran altitud, no hallamos debilidad de la musculatura respiratoria (AU)

Neuropathic pain and dysesthesia of the feet after Himalayan expeditions.

High altitude peripheral nerve disease secondary to frostbite or trauma is a well-recognized medical problem during mountaineering expeditions. However, in our experience as medical professionals on 19 expeditions to the Himalayas in the years 1977 to 2000, an unusual syndrome of neuropathic pain and/or dysesthesia in both feet apparently unrelated to frostbite or trench foot was observed in 8 (4.8%) of 165 European mountaineers. Mountaineers complained of persistent and continuous pain, which was consistently described as a "corky" sensation in their feet, associated with severe lancinating exacerbations. Pain improved with cold and worsened with heat and gentle pressure. Symptoms were incapacitating in a third of the cases. Treatment with carbamazepine was effective, and the disorder evolved to total resolution in 4 to 8 weeks. We present the case of a patient who had this syndrome and in whom complete work-up studies done on his arrival home, 14 days after its presentation, were unrevealing. The paucity of information regarding this particular variety of neuropathic pain of the feet may be due to lack of clinical suspicion in the field, favorable outcome, and difficulties for further study and evaluation.