AMS factors (Grocott and Montgomery 2008) are some

AMS can
progress to HACE in as little as 12 hours, but normally requires at least 3
days.  Fortunately, the incidence of HACE
is relatively rare, and occurs in less than 1% of all individuals exposed to hypoxic
environments (Armstrong 2000).  Fluid
accumulation in the brain may be caused by cytotoxic edema (cell swelling due
to increased intracellular osmolarity), vasogenic oedema (leak of the
blood-brain barrier with extravasation of proteins and fluid into the
interstitial space), or both.  It is
crucial that HACE is treated at the first signs of a change in consciousness
and ataxia.  Rapid descent is critical
for treatment, as well as supplemental oxygen and the drug Dexamethasone (West 2012).  High-altitude
pulmonary edema (HAPE) is another potentially fatal form of high altitude
illness that occurs in otherwise healthy unacclimatized sea level soujorners
who 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 (Durmowicz
et 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 in
breathing, typically develops 2-4 days after arrival at high altitude and as
the disease progresses frothy pink sputum develop which is the hallmark of
HAPE.  HAPE begins as individuals collect
a small amount of extra fluid in alveolar walls when traveling to altitude.  Previous studies have shown exaggerated,
unsustainable and non-uniform

pulmonary
vasoconstriction, leading to mechanically induced breaks at blood-gas barrier, to
be concomittant with HAPE (West 2000).  Clinical investigations suggest that the increased
pulmonary vascular permeability and pulmonary hypertension possibly due to
inhomogeneous hypoxic pulmonary vasoconstriction (HPV) (Maggiorini et al 2001),
(Hopkins et al 2005), (Dehnert et al 2006), transarteriolar leakage (Whayne et
al 1968), which leads to vascular leakage through over perfusion, capillary stress
failure, resulting in high concentration of vascular proteins and red blood cells
in the alveolar fluid are known to be causally linked to HAPE.  Augmented hypoxic pulmonary vasoconstrictor (HPV) response to hypoxia (Bartsch
1997), (Stream and Grissom 2008) and increased pulmonary artery systolic pressure
(PASP) during exercise in normoxia (Grunig et al 2000) have also been reported
in susceptible individuals.  Beside
hypoxia induced damage to endothelial cells-derived vasodilator nitric oxide
(NO) (Duplain et al 2000), (Busch et al 2001), cell adhesion molecules, activation
of cytokines and chemokines  may involve in
lung inflammatory response (West 2000).  Notably, individuals who develop
HAPE run a significant risk of recurrence suggesting involvement of genetic
component in its etiology although little is known about the genetic basis of
HAPE.  If left untreated, HAPE can be
fatal within 12 hours (Armstrong 2000).  Genetic
predisposition and individual susceptibility in cases of HAPE has been
postulated (Schoene RB 2004).  It is
considered a multifactorial condition whose inception and progression are
governed both by genetic and environmental factors (Patel and Peacock 2001).  Ascending slowly, climbing and sleeping at low
altitudes and restricting physical activity can prevent HAPE.  Although the exact mechanism underlying the development
of HAPE remains unclear.  

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