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Medicine - Cirrhosis + Portal HTN (i) (Cirrhosis (Clinical stages defined…
Medicine - Cirrhosis + Portal HTN (i)
Cirrhosis
end stage of any chronic liver disease
regenerative nodules surrounded by fibrous tissue
can be compensated or decompensated (jaundice, HE, ascites, variceal haemorrhage, portal vein thrombosis)
compensated often asymp - may be tired or more infection prone
decompensated will die without transplant
complications result from 2 clinical syndromes
portal HTN
variceal haemorrhage
ascites
SBP
HRS
liver insufficiency
HE
jaundice
HE is the result of both portal HTN (portosystemic shunting) + liver dysfunction (decreased ammonia metabolism)
Dx
histological
don't bx if
overt signs of decompensation present (clinical dx)
clear evidence of cirrhosis on imaging (imaging dx)
if FibroScan (non-invasive transient elastography) shows significantly elevated liver stiffness
^ however the absence of these features doesn't rule our cirrhosis
bx carries a bleeding risk (portosystemic collats are abnormally formed)
liver looks nodular on US
can also be dxed on 4 phase CT
can be graded - A B C
Clinical stages defined by varices, ascites, bleeding
0: compensated, no varices or ascites (1yr mortality = 1%)
1: compensated, varices but no ascites (1yr mortality = 3%)
2: decompensated, maybe varices definitely ascites (1yr mortality = 20%)
3: decompensated, maybe ascites definitely bleeding (1yr mortality = 57%)
cause of thrombocytopenia
architectural liver disruption -> distorted sinusoids -> pressure backup -> congestive splenomegaly -> secondary hypersplenism -> increased platelet sequestration
splanchnic vasodialation -> increased flow through collats -> variceal growth + eventual rupture
in every cirrhotic patient...
surveillance for HCC, ascites, HE, varices
OGD (oesophago-gastroduodenoscopy) to screen for varices
repeat every 2-3 yrs if -ve
US + AFP every 6 months
find underlying cause + tx it
vaccines: HAV, HBV, pneumovax every 5-10 yrs, annual influenza
Variceal haemorrhage
prophylaxis (prevent 1st one)
propranolol or carvedilol (start low + increase as tolerated, aim to reduce HR by 25%)
B-blockers not effective in preventing development of varices
each episode has a mortality rate of 20% - so try to prevent
can be oeso, gastric, or other
tx of acute haemorrhage
general
bloods to lab for FBC, coag, GXM (cross-matching for blood transfusion), U+E
IV access x2, fluid resuscitation, urinary catheter
blood + other blood products, but do not over transfuse (aim for Hb of 8 g/dL)
consider ICU + intubation to protect airway esp if haematemesis + evidence of ongoing haemorrhage
antibiotics prophylaxis
scrupulous attention to line asepsis
early removal of cannulas/catheters/tubes
consider cover for alcohol withdrawal (Pabrinex + chlordiazepoxidine
ABCDE
specific
IV terlipressin (vasopressor)
endoscopy
ligation
1st suction device to remove blood
then banding - strangulation
controls bleeding in 90%
rebleeding rate = 30%
compared to scleropathy less rebleeding, lower mortality, fewer complications, fewer tx sessions
scleropathy (medication injected into veins to make them shrink)
Sengstaken-Blakemore tube
inflate gastric balloon in stomach under direct vision
last ditch reduce attempt, if ligation unsuccessful
risk of malposition (oeso/bronchus rupture)
TIPSS (transjugular intrahepatic portosystemic shunt)
needle into jugular
stent between portal + hepatic veins
risk of HE - toxins esp ammonia bypass liver + go straight to heart + brain
prevent rebleeding
endoscopic band ligation until obliterated
B blocker
TIPSS as rescue therapy if others fail