Extreme Altitude Chronic Mountain Sickness Misdiagnosed as High Altitude Cerebral Edema

Chronic mountain sickness (CMS) represents a variably reversible asynchronous syndrome of secondary polycythemia along with erythrocytosis, erythrocyte aggregation, hemoglobinemia, hemoconcentration, thrombocytopenia, increased whole blood viscosity, fibrinogenemia, prothrombotic state, pulmonary and systemic hypertension, and congestive heart failure, occurring due to hypobaric hypoxia-anoxia-induced erythropoiesis reported in both native mountain residents and new climbers after prolonged stays at high altitudes. CMS can be accelerated by smokinginduced carboxyhemoglobinemia at high altitudes. The core pathology of polycythemia is both a boon to mountain adaptation and athletic training as well as a bane towards high altitude deterioration (HAD) leading to CMS.1,2 A large number of explorers and adventurers along with 140 million people residing at altitudes above 3000 m/9800 ft are at risk of contracting altitude illness. CMS along with hypoxia, cold, and other physiological extreme altitude stressors can contribute to lassitude, cyanosis, thromboembolic phenomena, right ventricular enlargement, myocardial infarction, cerebral infarction, stroke, and frostbite. CMS can be asymptomatic or oligosymptomatic at extreme altitudes above 5500 m/18 000 ft and may be confused with high altitude cerebral edema (HACE). The case being discussed highlights some important aspects of an insidious presentation of CMS which was confused with HACE at an extreme altitude of 6400 m/21 000 ft in the Karakoram Himalayas.