Portal hypertension is responsible for most of the complications that mark the transition from compensated to decompensated cirrhosis, namely variceal haemorrhage, ascites and hepatic encephalopathy. Portal hypertension also seems to be pathogenetically closely linked to the development of pulmonary complications seen in liver disease: hepatopulmonary syndrome and porto-pulmonary hypertension.
Gastroesophageal varices result almost solely from portal
hypertension, although the hyperdynamic circulation contributes to variceal
growth and rupture. Ascites results from sinusoidal hypertension (portal
hypertension) and sodium retention, which is, in turn, secondary to
vasodilatation and activation of neurohumoral systems. The predictive value of
noninvasive methods such as fibroscan, spleen size, portal vein diameter, and
transient elastography in the diagnosis of oesophagal varices remains to be
established. Hepatorenal syndrome results from extreme vasodilatation with
extreme decrease in effective blood volume and maximal activation of
vasoconstrictive systems, renal vasoconstriction, and renal failure, which is
probably an indirect effect of the changes in splanchnic circulation.
Spontaneous bacterial peritonitis, a frequent precipitant of the hepatorenal
syndrome, results from deficient immunity and mucosal defences, resulting in
pathological gut bacterial translocation. Hepatic encephalopathy results from
portosystemic shunting and hepatic insufficiency, leading to the accumulation
of neurotoxins, mainly ammonia, in the brain. The development of portal
hypertension and its complications has important prognostic value. Management
of portal hypertension needs to be individualised to attain maximum benefit and
appropriate utilisation of scarce resources.
Author (s)
Details
Harshal
Rajekar
Medicover Hospitals, KLE, Bhosari, Pune, India.
Please see the book here:- https://doi.org/10.9734/bpi/msraa/v5/5542
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