Cirrhosis of liver
Dr Manoj K Ghoda M.D., M.R.C.P.
Visiting faculty, GCS hospital
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gujarat gastro group
35 yrs old Female
No p.h/o any illness
No h/o drugs like NSAIDs
O/E : Pallor ++
No edema or ascites
P/A: Liver not palpable
Visible veins on
LFT: Bil: 0.8 mg
ALT: 27 i.u.
ALP: 123 i.u.
S. Alb.: 2.9
PT: 18/15 sec
Creat: 1.0 mg
What are the common
causes of GI bleed in
What will you do
In Pediatric pts
Common causes of UGI bleed in India
•Ulcers, including NSAID
What would do you now?
Irrespective of etiology first management step is to
stabilize the patient
A: Airway protection
Your next step?
Next step is to establish the cause of bleeding
Only UGI endoscopy could establish the cause of
bleeding, even when there is established portal HT
as nearly 3rd of patients with portal HT could bleed
from other causes, mainly peptic ulcers.
While waiting to optimize the patient for endoscopy
you may want to obtain evidence of portal HT by
• What is portal hypertension ?
• How does it present ?
• How do we diagnose and manage it ?
Superior mesenteric vein
Portal vein is not a true vein
Measuring Portal vein pressure
HEPATICVEIN PRESSURE GRADIENT
The HVPG is the difference between the wedged hepatic
venous pressure (WHVP) and free hepatic vein pressure
(FHVP). The HVPG has been used to assess portal
hypertension since its first description in 1951,and has
been validated as the best predictor for the development
of complications of portal hypertension.
Normally, the HVPG does not exceed 5 mm Hg. Portal
hypertension exists if the HVPG exceeds this value.
Cirrhosis of Liver:
It is a group of signs and symptoms resulting from altered
architecture of the liver resulting from unregulated
fibrosis in the liver.
It is more of a pathological diagnosis than clinical one as
most, if not all the signs and symptoms produced by cirrhosis
may also be found in chronic liver diseases without cirrhosis.
Pathology and pathogenesis:
Because of repeated insults to hepatic parenchyma and specific
promotion of fibrogenesis in certain conditions, there is unregulated
The liver progressively shrinks in size and nodular cirrhosis develops with
occasional malignant transformation..
Because of fibrosis, there is a loss of elasticity and the liver becomes hard.
Associated with these, there is progressive portal hypertension.
There is widespread fibrosis in the liver, which may encircle the lobule to form
Vascular arrangement of portal vein and hepatic vein radicals is disturbed in such
a way that there is a mismatch.
Telltale sign of the underlying pathology like hepatitis B or alcoholic hepatitis
may be present.
Malignant transformation may be seen.
Clinical features of Cirrhosis:
They vary according to the stage of liver involvement but it is not uncommon to have
practically no specific symptoms or signs even in advanced cirrhosis and it is not
uncommon to see the patient presenting for the first time with one of its complication
like GI bleed or ascites or encephalopathy.
Tiredness, lethargy, depression may be present.
Jaundice may be present.The skin of the exposed part may become black.
There may be ascites and ankle edema.
There may be spider nevi
Liver palms, an erythematous skin in the periphery of the palms may also be seen.
Gynecomastia and soft testis in males, together with reduced pubic hair may be seen
because of failure to metabolise estrogen.
There may be muscle wasting.
Umbilical hernia and visible veins radiating from umbilicus or on the flanks with flow
away from the centre may be seen.
Liver may be enlarged in early cirrhosis and spleen may be enlarged, sometimes
Flapping tremors and signs of encephalopathy may be present.
Esophageal, gastric and rectal varices may be seen at endoscopy.
It is two fold; supportive and specific.
Supportive include use of salt and fluid restriction, high protein diet and albumin
supplement, use of diuretics, frusemide up to 160 mg. and aldesterone antagonists
Spironolactone up to 400 mg. for edema. Non selective B-blockers, like
propranolol may be used for reducing portal hypertension. Lactulose may be used
for relieving constipation.
Specific treatment for encephalopathy, hepatorenal syndrome, Hepatopulmonary
syndrome and GI bleed .
Specific treatment for viral hepatitides,Wilson’s, autoimmune hepatitis and
hemochromatosis as appropriate.
In end sage cirrhosis liver transplant is the treatment of choice.
Unless the underlying etiology could be effectively
treated and that too, at not a very late stage, the
prognosis is dismal and once the decompensation
sets in, mortality could be as high as 75% at 2 years.
Important side effect of portal HT is
development of varices.
If there was no development of Esophageal or
Gastric varices, portal HT would be of little
Main sites of development of varices:
•The squamocolumnar epithelial junctions of the gastrointestinal
tract.These sites are gastroesophageal junction and anorectal
•Esophageal varices are the most important.They are supplied
mainly by an enlarged coronary (left gastric) vein and by the
short gastric veins arising from the splenic bed and drain into
the azygous vein.They are largest 2-3cm above the
•The next most common site for significant varices is the stomach,
either in obvious continuity with esophageal varices or isolated
Other sites of development of varices
The recanalized umbilical vein, which communicates
with the paraumbilical plexus in the abdominal wall.
This gives rise to caput medusae and a Cruveilhier-
Baumgarten venous hum in the epigastrium.
The retroperitoneum.The veins of abdominal viscera are commonly in
contact with the abdominal wall. Retroperitoneal collaterals frequently
communicate with the left renal vein.
Sites of previous abdominal surgery or intra-abdominal trauma.
Ectopic sites in the gastrointestinal tract.These are, the duodenum,
ileum, cecum, and rectum especially in patients who have had previous
Portal hypertension could remain silent for ever in
Upper or lower GI bleeding are the most commonly
recognizable and dreaded symptoms.
If there is advanced decompensated liver diseases
accompanying, then there may be jaundice, ascites,
edema and encephalopathy.
Collaterals may be visible on the abdomen.
Spleen may be enlarged, sometimes grossly.
Investigations and diagnosis:
•USG may show dilated portal vein, splenomegaly
and at times collaterals in splenic hilum and lower
end of esophagus. Underlying etiology like cirrhosis,
portal vein or splenic vein thrombosis and Budd-
Chiari syndrome could be identified. Doppler study
may shoe thrombosis as mentioned above and
reversal of blood flow and collaterals.
•Upper GI endoscopy may show varices and
portal hypertensive gastropathy. Colopathy
changes could be seen on sigmoidoscopy.
Management of Portal HT and its complications:
If there is no cirrhosis/ liver parenchymal damage, esophageal
and gastric varices are the only dreaded complication of portal
•Non selective B-blocker propranolol starting with a dose of 10
mg. twice a day and then titrated to reduce the pulse rate buy
25% is used as primary prophylaxis against bleeding
•In a high risk patients, patients living in remote area or in
selected patients with large esophageal varices of grade 3 or more
could be offered prophylactic endoscopic band ligation(EVL).
•Bleeding is managed as mentioned in the upper GI bleeding.
•Underlying etiology may be corrected with appropriate
Principles of UGI bleed
•While waiting for endoscopy start IV PPI and if portal
HT is suspected Somatostatin or Octreotide.
•Clean stomach with help of a large bore Ryle's tube.
Rule of 18; 18 GVenflon, 18 G Ryle’s tube, and
endoscopy in 18 hours
•Once the diagnosis is confirmed stop one of the two
as per the findings
Prognosis in portal HT:
Depends upon bleeding and underlying liver
In NCPF, the prognosis is excellent if the bleeding
episodes are well managed.
Prognosis is guarded if there is accompanying liver
Dr Manoj K Ghoda M.D., M.R.C.P.
Visiting faculty, GCS Hospital
gujarat gastro group
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