Subacute infantile mountain sickness

Abstract

A description is given of a disease of infants occurring in Lhasa, Tibet at an altitude of 3600 m. Typically if affects infants who have been born at low altitude and subsequently brought to residue in Lhasa, and it is usually fatal within a few weeks or months. There is extreme medial hypertrophy of muscular pulmonary arteries and muscularization of pulmonary arterioles, together with dilatation of the pulmonary trunk and massive hypertrophy and dilatation of the right ventricle. The disease is distinct from acute or chronic mountain sickness and appears to be the human counterpart of 'brisket disease' in cattle.

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases

“…Effects of subacute exposure to high altitude Indirect evidence for elevated PAP has been found in infants of Han descent born at low altitude, who died after an average of 2 months of residence in Lhasa [8] and in Indian soldiers, who failed to acclimatise at the very high altitude of 5,800-6,700 m [7]. In infants, autopsy revealed massive hypertrophy and dilatation of the right ventricle, dilatation of the pulmonary trunk, extreme medial hypertrophy of the muscular pulmonary arteries and muscularisation of the pulmonary arterioles [8].…”

“…In infants, autopsy revealed massive hypertrophy and dilatation of the right ventricle, dilatation of the pulmonary trunk, extreme medial hypertrophy of the muscular pulmonary arteries and muscularisation of the pulmonary arterioles [8]. In Indian soldiers, clinical features compatible with an acute congestive right heart failure developed during weeks 3-22, on average 11 weeks after they were stationed at altitudes between 5,800-6,700 m [7].…”

“…It has been reported that infants born at altitudes between 3,500-4,500 m may show persistent near systemic PAP values for some time after birth [43], and that in some cases elevated mean PAP (y40 mmHg) persisted during infancy [44]. These observations may be linked to right heart failure in infants after birth [8] and to chronic high-altitude pulmonary hypertension in adulthood [45].…”

“…Excessive hypoxic pulmonary vasoconstriction, and thus susceptibility to develop a right heart failure within weeks at high altitude, was first described in Colorado cattle [6]. Indian soldiers stationed at an altitude between 5,800-6,700 m [7] and Han infants in Lhasa [8] develop severe congestive right heart failure within weeks or months after arrival at high altitude. An excessively elevated pulmonary artery pressure (PAP) has not only been reported to cause high altitude cor pulmonale within weeks, months, or years in newcomers, but also in high-altitude residents of the Andes and nonacclimatised climbers prone to high-altitude pulmonary oedema (HAPE) [9].…”

“…An excessively elevated pulmonary artery pressure (PAP) has not only been reported to cause high altitude cor pulmonale within weeks, months, or years in newcomers, but also in high-altitude residents of the Andes and nonacclimatised climbers prone to high-altitude pulmonary oedema (HAPE) [9]. The results of these studies suggest that an excessive rise in PAP is a common denominator in HAPE [9], the syndrome described by SUI et al [8] in infants and by ANAND et al [7] in adults at 6,700 m and termed "subacute mountain sickness" (SMS) of the infant and the adult, respectively, and in the illness of the high-altitude residents of the Andes termed "chronic mountain sickness" (CMS) or "Monge9s disease" in its end-stage [10].…”