CIRRHOSIS

By Professor Dr. NellaiappaGanesan

Head of dept.
General Medicine
 CIRRHOSIS
 Cirrhosis is characterized by diffuse hepatic fibrosis and nodule formation.
 Progressive fibrosis and widespread hepatocyte loss lead to distortion of normal liver
architecture disrupts hepatic vasculature, causes portosystemic shunting.

 Histological diagnosis
 Evolves over years
 Any condition leading to persistent, recurrent hepatocyte death causes cirrhosis
 Most common causes worldwide- chronic viral hepatitis, alcohol, NAFLD
ANATOMY
 HISTOLOGICAL TYPES

 Micronodular cirrhosis- small nodules about 1mm ,seen in alcoholic cirrhosis

 Macronodular cirrhosis-larger nodules of various sizes. Large fibrous scars in areas of

previous collapse of liver architecture
NORMAL

BRIDGING NECROSIS

CIRRHOSIS
 CAUSES OF CIRRHOSIS
 Alcohol
 Chronic viral hepatitis B or C
 NAFLD
 IMMUNE: Primary sclerosing cholangitis, autoimmune liver disease
 BILIARY : Primary biliary cholangitis, secondary biliary cirrhosis, Cystic fibrosis
 GENETIC: Haemochromatosis, Wilson’s disease, alpha1 antitrypsin deficiency
 Chronic venous outflow obstruction
 Cryptogenic – 15%
CLINICAL FEATURES
 Highly variable

 Non-specific symptoms-

anorexia, nausea, vomiting, fatigue, weight loss, upper abdomen discomfort

weakness, fatigue, muscle cramps

 Breathlessness- right pleural effusion, hepatopulmonary syndrome

(CONT.)
 Hepatomegaly- alcohol-related, haemochromatosis

Metabolic sequelae
 Jaundice – failure to excrete bilirubin
 Encephalopathy – failure of clearance of metabolic by-products
 Bleeding – impaired clotting factor synthesis
 Ascites – impaired albumin synthesis- reduced oncotic pressure, reduced aldosterone
clearance- Na retention
 Catabolic status- skin thinning- ‘paper-money skin’, loss of muscle bulk, leukonychia
(CONT.)
 Endocrince changes

Males : Reduced oestrogen clearance-loss of body hair, gynaecomastia, impotence, testicular

atrophy
Females : Hirsuitism, irregular menses, breast atrophy, amenorrhea

 Circulatory changes- Palmar erythema- hyperdynamic circulation, Spider angioma, cyanosis

 Portal hypertension- splenomegaly, variceal bleed, collateral vessels
 Pigmentation, digital clubbing, Dupuytren’s contracture
 Synthetic function affected- low albumin, prolonged PT
COMPLICATIONS OF
CIRRHOSIS
 Portal hypertension- variceal bleeding, hypersplenism

Ascites/ spontaneous bacterial peritonitis

 Hepatic encephalopathy
 Coagulopathy- thrombocytopenia(thrombopoietin synthesis impaired),clotting factors
 Hepatocellular carcinoma
 Hepatopulmonary syndrome
 Hepatorenal syndrome (type 1 and 2)
SIGNS OF HEPATIC.
DECOMPENSATION
 Ascites
 Jaundice
 Hepatic encephalopathy
 Variceal bleeding
 Infection

 Child- Pugh and MELD ( Model for End-stage Liver Disease) scores – used to assess
prognosis
PORTAL HYPERTENSION
 Cirrhosis leads to sinusoidal portal vein obstruction – reduction in portal blood flow
 Leads to formation of collateral vessel at various sites between systemic and portal circulation
 Characterised by increased vascular resistance leading to elevated hepatic venous pressure
gradient. Normal – 5-6 mmHg, portal HTN when > 12mmHg
 Cardinal sign – splenomegaly
 Complications – variceal bleed, ascites, hypersplenism, congestive gastropathy(snakeskin/
portal hypertensive), iron deficiency anemia, renal failure, hepatic encephalopathy,SBP
OTHER CAUSES OF PORTAL HYPERTENSION
 SITES OF PORTOSYSTEMIC
SHUNTING
 ACUTE UPPER GI BLEED

 COMMONEST MANIFESTATION OF LIVER DISEASE

 ACUTE MANAGEMENT

-IV fluids to replace ECF loss

-vasopressors- to reduce portal pressure, terlipressin, alternative-octreotide
-prophylactic antibiotics- to reduce SBP incidence
-emergency endoscopy- band ligation – Obliteration of varices
-Balloon tamponade - Sengstaken-Blakemore tube
-PPI- prevent peptic ulcers
-Phophate enema/ lactulose – prevent hepatic encephalopathy
 SENGSTAKEN-BLAKEMORE
TUBE
 Sclerotherapy – cyanoacrylate, thrombin – preferred for gastric varices
 Primary and secondary prevention of variceal bleeding
- beta blockers- nadolol, propranolol
 TIPSS- Stent placed between portal vein and hepatic vein within the liver to provide
portosystemic shunt and reduce portal pressure
 Portosystemic shunt surgery
 Oesophageal transection -rarely done
 ASCITES
 Accumulation of free fluid in the peritoneal cavity
 Splanchnic vasodilatation – most important factor
 Vasodilators released when portal HTN causes shunting of blood – nitric oxide

leads to :
-activation of RAS with secondary aldosteronism,
-increased sympathetic nervous activity
-increased atrial natriuretic hormone secretion
-altered activity of kallikrein-kinin system
 Salt and water retention due to above factors
 Increased intestinal capillary permeability
PATHOGENESIS OF ASCITES
 TRANSUDATE VS.
EXUDATE
 Serum-ascites albumin gradient = Serum albumin-ascitic fluid albumin
 SAAG <11g/L OR >11g/L
MANAGEMENT
 Salt restriction <100mmol/24hrs
 Water restriction 1-1.5 L/day
 Diuretics- aldosterone antagonists-spironolactone/amiloride, loop diuretics
 Paracentesis
 TIPSS- resistant ascites

 Complications

Renal failure – sepsis, vasodilatation or diuretics

Hepatorenal syndrome
Type 1 – progressive oliguria, rapid rise of creatinine
Type 2 – occurs in refractory ascites, stable increase in creatinine, better prognosis
SPONTANEOUS BACTERIAL
PERITONITIS
 Characterised by abdominal pain, absent bowel sounds and fever.
 Paracentesis- Neutrophil count >250 x 10*6/ L , Cloudy fluid
 Most common- E.coli (usually enteric organisms)
 Rx- broad spectrum antibiotics- cefotaxime or Piperacillin/tazobactam
 Prophylaxis- norfloxacin or ciprofloxacin
 HEPATIC
ENCEPHALOPATHY
 Neuropsychiatric syndrome caused by liver disease
 Usually a precipitating factor is found
 FEATURES : Changes in intellect, personality, emotions and consciousness, with or without
neurological signs. Early features maybe mild.
 Severe features: severe apathy, inability to concentrate, delirium, disorientation, drowsiness,
slurring of speech, convulsions, coma

 EXAMINATION : Asterixis, unable to perform simple arithmetic tasks, constructional

apraxia, hyper-reflexia, B/L plantar extensor responses
 Chronic hepatic encephalopathy- hepatocerebral degeneration – cerebellar dysfunction,
parkinsonian syndromes, spastic paraplegia, dementia
 PATH0PHYSIOLOGY

 Accumulation of neurotoxins which are usually metabolized by the liver and excluded from
circulation
 Mainly nitrogenous substances produced in the gut by bacterial action- Ammonia
 Others: GABA, octopamine, amino acids, mercaptans, fatty acids that can act as
neurotransmitters
GRADES OF
ENCEPHALOPATHY
FACTORS PRECIPITATING
ENCEPHALOPATHY
 Increased protein load
 Gastrointestinal bleeding
 Hypoxia
 Electrolyte imbalance- Hypokalemia
 Constipation
 Infection
 Dehydration-diuretics, paracentesis
 Drugs- sedatives, antidepressants
 MANAGEMENT
 Remove precipitating cause
 Lactulose- osmotic laxative, reduces pH of colonic content>>limiting ammonia absorption,
promotes incorporation of nitrogen into bacteria
 Gastric lavage
 Bowel wash
 Rifaximin – non-absorbed antibiotic, reduces bacterial content of bowel
 Chronic encephalopathy- indication of transplantation
 EXAMINATION
HEAD CHEST HAND ABDOMEN
Diminished axillary Asterixis
Pallor/Icterus hair Palmar erythema Ascites
Fetor hepaticus Spider angioma Duputryen’s contracture Striae
Constructional apraxia Gynecomastia Clubbing (only in biliary Umbilical hernia
Drowsiness and confusion cirrhosis) Caput medusae
Parotid gland enlargement Terry’s “half & half” nails Splenomegaly
Spider angiomas
 OTHERS
 Petechiae

 Ecchymosis

 Scratch marks

 Edema

 Testicular atrophy
CASE SCENARIO 1
CASE SCENARIO 2
CASE SCENARIO 3
CASE SCENARIO 4
CASE SCENARIO 5
CASE SCENARIO 6
THANK YOU