AMS factors (Grocott and Montgomery 2008) are some

AMS canprogress to HACE in as little as 12 hours, but normally requires at least 3days.

 Fortunately, the incidence of HACEis relatively rare, and occurs in less than 1% of all individuals exposed to hypoxicenvironments (Armstrong 2000).  Fluidaccumulation in the brain may be caused by cytotoxic edema (cell swelling dueto increased intracellular osmolarity), vasogenic oedema (leak of theblood-brain barrier with extravasation of proteins and fluid into theinterstitial space), or both.  It iscrucial that HACE is treated at the first signs of a change in consciousnessand ataxia.

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 Rapid descent is criticalfor treatment, as well as supplemental oxygen and the drug Dexamethasone (West 2012).  High-altitudepulmonary edema (HAPE) is another potentially fatal form of high altitudeillness that occurs in otherwise healthy unacclimatized sea level soujornerswho rapidly ascend to high altitude (above 3000 m).  A prior history of HAPE (Bartsch et al 1991), rapid ascent to high altitude(Bartsch 1999), strenuous exercise at high altitude (Grissom  2006), preexisting respiratory infection (Durmowiczet al 1997) and genetic factors (Grocott and Montgomery 2008)  are some of the proposed reasons for HAPE.Symptoms of HAPE,characterised by tightness in chest, cough, gurgling sound, difficulty inbreathing, typically develops 2-4 days after arrival at high altitude and asthe disease progresses frothy pink sputum develop which is the hallmark ofHAPE.  HAPE begins as individuals collecta small amount of extra fluid in alveolar walls when traveling to altitude.  Previous studies have shown exaggerated,unsustainable and non-uniformpulmonaryvasoconstriction, leading to mechanically induced breaks at blood-gas barrier, tobe concomittant with HAPE (West 2000).  Clinical investigations suggest that the increasedpulmonary vascular permeability and pulmonary hypertension possibly due toinhomogeneous hypoxic pulmonary vasoconstriction (HPV) (Maggiorini et al 2001),(Hopkins et al 2005), (Dehnert et al 2006), transarteriolar leakage (Whayne etal 1968), which leads to vascular leakage through over perfusion, capillary stressfailure, resulting in high concentration of vascular proteins and red blood cellsin the alveolar fluid are known to be causally linked to HAPE.  Augmented hypoxic pulmonary vasoconstrictor (HPV) response to hypoxia (Bartsch1997), (Stream and Grissom 2008) and increased pulmonary artery systolic pressure(PASP) during exercise in normoxia (Grunig et al 2000) have also been reportedin susceptible individuals.

 Besidehypoxia induced damage to endothelial cells-derived vasodilator nitric oxide(NO) (Duplain et al 2000), (Busch et al 2001), cell adhesion molecules, activationof cytokines and chemokines  may involve inlung inflammatory response (West 2000).  Notably, individuals who developHAPE run a significant risk of recurrence suggesting involvement of geneticcomponent in its etiology although little is known about the genetic basis ofHAPE.  If left untreated, HAPE can befatal within 12 hours (Armstrong 2000).

 Geneticpredisposition and individual susceptibility in cases of HAPE has beenpostulated (Schoene RB 2004).  It isconsidered a multifactorial condition whose inception and progression aregoverned both by genetic and environmental factors (Patel and Peacock 2001).  Ascending slowly, climbing and sleeping at lowaltitudes and restricting physical activity can prevent HAPE.  Although the exact mechanism underlying the developmentof HAPE remains unclear.  

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