CIRRHOSIS OF LIVER

Cirrhosis is a condition in which the liver

slowly deteriorates and malfunctions due to
chronic injury. Scar tissue replaces healthy
liver tissue, partially blocking the flow of
blood through the liver. Scarring also
impairs the liver’s ability to
control infections, remove bacteria and
toxins from the blood and process nutrients,
hormones, drugs and
make proteins that regulate blood clotting.
Liver produces bile to help absorb fats—
including cholesterol—and fat-soluble
vitamins
A healthy liver is able to regenerate most
of its own cells when they become damaged.
With end-stage cirrhosis, the liver can no
longer effectively replace damaged cells. A
healthy liver is necessary for survival.
 VARICEAL HEMORRHAGE
A type of varicose vein that develops in
veins in the linings of the esophagus and
upper stomach when these veins fill with
blood as result of collateral circulation
due to portal hypertension. They get swollen
due to an increase in blood pressure in the
portal veins and tend to rupture. Bleeding
occurs in 1/3 patients with varices and
tendency to bleed increases with large
varices, high pressure, more sever disease.
Patients of variceal bleeding present with
painless but massive hematemesis with or
without melena. Proper history and
examination is required to exclude other
causes like peptic ulcer, portal hypertensive
gastropathy and gastritis. In absence of
previous history, the presence of
spleenomegaly, reduced liver span.
Investigations include: Blood CP(to measure
initial level of hemoglobin and platelate
count), PT & APTT, LFT, Serum electrolytes,
Endoscopy(for detection of varices).
Prophylactic measures include administration
of non-selective beta-blocker as propranolol
and the patients who cannot tolerate beta
blockers should be administered isosorbide
mononitrate. Prophylactic sclerotherapy is
not indicated because of increased mortality.
however binding in high risk individuals can
reduce the incidence
 MANAGEMENT OF ACTIVE
BLEEDING
 INITIAL RESUSCITATION
 monitor the blood pressure and pulse
 pass IV canula and give plasma
expander{gelafundin or haemaccel} to restore
circulation and arrange for blood and blood
products such as fresh frozen plasma
 fresh frozen plasma is administered if
patent’s plasma PT is greater than 1.5 times
of normal.
 Platelates should be infused if count is
less than 50,000 per microlitre.
 Pass nasogastric tube to evacuate the
stomach to reduce nausea and vomiting and to
monitor bleeding
 URGENT ENDOSCOPY

 Urgent endoscopy is performed after the

patient has become hemodynamically stable
that usually takes 2-12 hours. Endoscopic
examination is performed to
 exclude other causes of GI bleeding as
peptic ulcer and congestive gastropathy.
 For endoscopic treatment of varices with
either banding or sclerotherapy
 Banding
 Varices are sucked and rubber band is
dislodged over the varices
 Repeated banding sessions are
performed at interval of 1-2 weeks
until varices are oblitered.
 Banding varices lower the rate of
rebleeding and complications and
death than sclerotherapy, so
therefore is treatment of choice.
Injection sclerotherapy:

Varices are injected with sclerosing

agent ethanolamine tetradecyl sulfate
that arrests bleeding by producing
vessel thrombosis. A needle is passed
down the biopsy channel of endoscope
and sclerosing agent is injected into
varices, and repeatedly the session is
performed at interval of 3-7 days
followed by 1-3 weeks until varices are
obliterated. Complications include
chest pain, fever, bacteremia,
espophageal ulceration, perforation and
stricture.
PHARMACOLOGICAL THERAPY

 Because of lack of facilities in our hospitals

the vasoconstrictor therapy is indicated to
reduce the portal pressure. Octereotide is
treatment of choice and vasopressin can also
be used. Octereotide reduces the splanchnic
and hepatic blood flow and portal pressure in
cirrhosis patients and is comparable in
efficacy to sclerotherapy. It provides acute
control of variceal bleeding. Vasopressin is
non selective vasoconstrictor and and reduces
splanchnic blood flow but the complications
include angina, arrhythmia, and MI, so it is
contraindicated in patients with ischemic
heart disease.
OTHER MEASURES TO STOP BLEEDING
 Ballon temponade
 Transjugular intrahepatic portocaval shunt
 Lactulose and vitamin K
 Emergency surgery
 Ballon temponade
 IT IS USED WHEN SCLEROTHERAPY HAS FAILED OR
UNAVAILABLE or vasoconstrictor therapy has
failed or contraindicated. The sangstaken
blackmore tube is passed into stomach and
balloon is inflated with air and pulled back
which exerts pressure on lower esophagus and
gastric fundus to stop bleeding. The
complications include aspiration pneumonia,
esophageal rupture and mucosal ulceration.
 Transjugular intrahepatic
portocaval shunt
 Is performed when when pharmacologic and
endoscopic therapies are failed. A guided
wire is passed from jugular vein into
liver and an expandable metal stent is
forced over it into the liver mass to form
post systemic shunt between portal and
hepatic vein. Complication include stent
stenosis or thrombosis.
 Emergency surgery

 PERFORMED WHEN OTHER MEASURES ARE FAILED

or if tips is not available particularly
if bleeding is from gastric fundal
varices. The most common surgical
technique is transaction of esophagus and
ligation of feeding vessel to bleeding
varices.
 lactulose and vitamin K
 Lactulose management is to prevent
encephalopathy precipitated by large bleed.
Vitamin K should be administered in
patients with prolonged PT
 MEASURES TO STOP REBLEEDING

 Repeated banding or scleropathy, beta

blockers or nitrates and the shunts.
 ASCITES

ASCITES ARE PATHOLOGICAL ACCUMMULATION OF

FLUID IN PERITONEAL CAVITY. Ascitic fluid
may be exudate or transudate. Ascites are
common complication of cirhosis of liver.
Assessment of ascites

Grade 1 — mild; Detectable only by US

Grade 2 — moderate; Moderate symmetrical
distension of the abdomen
Grade 3 — large or gross asites with marked
abdominal distension
Pathogenesis

oHypokalemia and Sodium and water retention

due to stimulation of renin angiotensin
system that develops as result of low
perfusion pressure of kidney in cirrhosis,
this retained fluid causes portal
hypertension and ultimately the ascites.
Nitric oxide is the vasodilator that causes
low perfusion pressure. Other agents are
prostaglandins and natriuretic peptide.

oPortal hypertension that exerts local

hydrostatic pressure causing transudation of
fluid in peritoneal cavity.
oLow serum albumin as result of poor
synthesis by liver causing reduced plasma
osmotic pressure and resulting in in
transudation of fluids in peritoneal cavity

clinical features

abdominal distension wih fullness in flank

diffuse abdominal pain

features of the cause(commonly the chronic

liver disease)

Dehydration
INVESTIGATION OF ASCITES

investigation of ascitic fluid

cirrhosis-----clear straw coloured or

light green

malignant disease-----bloody

infections-----cloudy

biliary communication-----heavy bile

stating

lymnphatic obstruction-----milky white

 cell count
neutrophil count is more than 250 per mm cube

albumin and total protein

SAAG
SAAG is best is best single test to
classify the ascites according to their
cause by portal hypertenion and non-portal
hypertension

SAAG more than 1.1 g/dl suggests that

underlying portal hypertension and less
than it suggests non-portal hypertension
in 4% of patients High SAAG is due to
mixed ascites(portal hypertension and
malignancy), so high SAAG indicated portal
hypertension but donot excludes malignancy

ascitic fluid protein level less than 1

g/dl predispose the patient toward
spontaneous bacterial peritoniti
culture and gram stain
performed to identify infection of ascitic
fluid
neutrophil count is more tha 250/mm cube

Other test
RBC greater than 50000/micro litre denotes
hemorrhaic ascites which is due to
malignancy, TB, and trauma
Glucose is low in TB peritonitis
amylase is high in pancreatic ascites
ULTRASOUND ABDOMEN

confirms the presence of ascites

distinguishes between portal and non portal

cause of ascites.

shows the liver architecture and size of

portal vein
 SPECIFIC MEASURES
DIURESIS
Spironolactone and furesimideL:
spironolactone is diuretic of choice , it
antagonizes aldosterone and prevents salt and
water reabsorption from kidney as secondary
hyperaldosteronism is major factor in salt
and water retention in cirrhosis. Side
effects are gynecomastia and hyperkalemia.
Furesimide is high potency loop diuretic and
should be added to spironolactone if response
to spironolactone high doses is poor.
Therapeutic paracentesis
in patients with massive ascites causing
respiratory distress or ascites refractory to
diuretic therapy large volume paracentesis
over 1-2 hours is effective. However there is
risk of hypovolumoa as ascitic fluid
reaccumulates at expanse of circulating volume
leading to shock. This problem can be overcome
by administration of salt free albumin
concomitantly at dosage of 10g/l of ascitic
fluid removed to protect intravascular volume.
If the patient is non affording then use
plasma expanders such as gelatin infusion
125ml/l of ascitic fluid removed.
LeVeen Shunt and TIPS
its a procedure in which a catheter is
introduced from peritoneal cavity into
internal jugular vein incorporating a one way
valve and allowing the passage of ascitic
fluid directly into circulation. COMPLICATIONS
ARE superior vena caval thrombosis, pulmonary
edema, and bleeding from esophageal varices.
TIPS is better than LeVeen shunt.
 HEPATORENAL FAILURE
PATHOGENESIS
Hepatorenal syndrome is renal failure in absence of shock with
end stage liver disease.
Occurs typically in patients with advanced cirrhosis with
jaundice and ascites. It presents as low urine output, raised urea
and creatinine. Low urinary sodium and hypotension.
This is pre-renal type renal failure in which kidneys remain
histologically normal and if transplanted to non-cirrhotic patient
then they function normally.
Types of hepatorenal failure:

Type 1:doubling of serum creatinine to a level greater than

2.5mg/dl in less than 2 weeks

Type 2: is more slowly progressive and chronic

PATHOGENESIS

Hepatorenal syndrome develops due to

reduced blood flow as result of low
peripheral resistance which leads to
increased secretion of vasoconstrictors
such as nor adrenaline, angiotensin,
aldosterone and vasopressin that cause
vasoconstriction of renal vasculature
resulting in reduced GFR that leads to
extremely low sodium excretion and
there may be decreased production of
renal vasodilators prostaglandinE2
PRECIPITATING FACTORS
Overvigrous diuretic therapy
Diarrhea
GI bleeding
Sepsis
Large paracentesis

MANAGEMENT
The patient should be treated for pre renal
failure, the diuretic should be stopped and
intravascular hypovolemia is corrected with
salt free albumin. The dopamine infusion is
ineffective. TIPS may improve the
condition.
 HEPATOPULMONARY SYNDROME

Hepatopulmonary syndrome occurs occurs

due to chronic liver disease and manifest
as dyspnea in upright position
(orthodeoxia) that is relieved by
recumbency.

PATHOGENESIS

Hypoxia and dyspnea develops due to right

to left intrapulmonary shunt because the
liver is unable to clear the circulatory
pulmonary vasodilators.
INVESTIGATION
Pulse oximetry shows oxygen saturation less
than 92%

Contrast echocardiography is sensitive

screening test for detecting intrapulmonary
shunts.

Macroaggregated albumin lung perfusion

scanning is more specific and used to confirm
the diagnosis.

High resolution CT scan of chest shows

dilated pulmonary vessels
MANAGEMENT

No specific treatment is available however

IV methylene blue may improve oxygenation in
patients by inhibiting nitric oxide induced
vasodilation. TIPS may provide palliation in
patients awaiting liver transplantation.