Cirrhosis and Its Complications

Maha Almatrafi

Liver cirrhosis is the result of chronic inflammation and damage to liver cells. When the liver cells are damaged
they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver. This fibrosis affects the
structure and blood flow through the liver, which causes increased resistance in the vessels leading in to the liver.
( portal hypertension. ) For cirrhosis to occur
• Cirrhosis is a chronic liver disease characterized by fibrosis, disruption of the liver following an acute liver
architecture, and widespread nodules in the liver. The fibrous tissue replaces disease it must be an acute
damaged or dead hepatocytes. liver insult

Most Common Causes

• Alcoholic liver disease (most common cause)
• Non Alcoholic Fatty Liver Disease
• Hepatitis C (second most common cause)
• Hepatitis B

How the liver disease patient present to you?

• Asymptomatic at early stage then symptoms of the complications

Complications
• Portal Hypertension, Varices and Variceal Bleeding

I
• Ascites and Spontaneous Bacterial Peritonitis (SBP)
• Hepato-renal Syndrome
• Hepatic Encephalopathy
• Hepatocellular Carcinoma
Portal Hypertension and Varices
Liver cirrhosis increases the resistance of blood flow in the liver. As a result, there is increased back-pressure into
the portal system “portal hypertension”. This back-pressure causes the vessels at the sites where the portal
system anastomoses with the systemic venous system to become swollen and tortuous. These swollen, tortuous
vessels are called varices. They occur at the:
• Gastro oesophageal junction
• Ileocaecal junction
• Rectum hemorrhoids
• Anterior abdominal wall via the umbilical vein (caput medusae)
Varices do not cause symptoms or problems until they start bleeding. Due to the high blood flow through varices,
once they start bleeding patients can exsanguinate (bleed out) very quickly.
Treatment of stable varices
• Propranolol reduces portal hypertension by acting as a non-selective beta blocker
• Elastic band ligation of varices
• Injection of sclerosant (less effective than band ligation) Transjugular Intra-hepatic Portosystemic
Shunt (TIPS) is a technique where an
interventional radiologist inserts a wire
Bleeding Portal varices: under xray guidance into the jugular vein,
▪Varices develop in 50-60 % of cirrhotic patients down the vena cava and into the liver via
the hepatic vein. They then make a
▪30% of them develop upper gastrointestinal bleeding UGIB connection through the liver tissue between
▪Risk of rebleeding is high and fatal (2nd bleeding ) 60-70% over the hepatic vein and the portal vein and put
24months a stent in place. This allows blood to flow
directly from the portal vein to the hepatic
▪Death in cirrhotics 1/5 – 1/3 ,due to variceal bleeding vein and relieves the pressure in the portal
▪ Related to increased congestion at Porto-Venous collaterals system and varices. This is used if medical
Presents as hematemesis ,Melena , anemia or circulatory shock. and endoscopic treatment of varices fail or if
there are bleeding varices that cannot be
Management : controlled in other ways.
• Resuscitation
• Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices
• Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors)
• Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality
• Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell
• Urgent endoscopy
• Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
• Elastic band ligation of varices
• Sengstaken-Blakemore Tube is an
inflatable tube inserted into the
oesophagus to tamponade the bleeding
varices. This is used when endoscopy
fails.
 Ascites
Ascites is basically fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out
of the capillaries in the liver and bowel and in to the peritoneal cavity. The drop in circulating volume caused by fluid
loss into the peritoneal space causes a reduction in blood pressure entering the kidneys. The kidneys sense this
lower pressure and release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-
aldosterone system) and reabsorption of fluid and sodium in the kidneys.
Cirrhosis causes a transudative, meaning low protein content, ascites. Clinical Features :
• Abdominal Distention
Management of Ascites
• Low sodium diet • Shifting dullness
• Anti-aldosterone diuretics (spironolactone) • Fluid wave
• Paracentesis (ascitic tap or ascitic drain)
• Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients
with less than 15g/litre of protein in the ascitic fluid
• Consider TIPS procedure in refractory ascites
• Consider transplantation in refractory ascites
Spontaneous Bacterial Peritonitis (SBP)
This occurs in around 10% of patients with ascites secondary to cirrhosis and can have a mortality of 10-20%. It
involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary
to an ascitic drain or bowel perforation).
Presentation
• Can be asymptomatic so have a low threshold for ascitic fluid culture
• Fever
• Abdominal pain
• Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
• Ileus
• Hypotension
Most common organisms
• Escherichia coli
• Klebsiella pnuemoniae
• Gram positive cocci (such as staphylococcus and enterococcus)
Management of SBP
• Take an ascitic culture (paracentesis) prior to giving antibiotics
• Usually treated with an IV cephalosporin such as cefotaxime
Hepatic Encephalopathy
This is also known as portosystemic encephalopathy. Caused by the build up of toxins that affect the brain. In
particularly ammonia, which is produced by intestinal bacteria when they break down proteins and is absorbed in
the gut.
There are two reasons that ammonia builds up in the blood in patients with cirrhosis:
• Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste
products.
• Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver
altogether and enters the systemic system directly.
By giving laxatives we help clear the ammonia from the gut before it is absorbed and by giving antibiotics we reduce
the number of bacteria in the gut producing ammonia.
Acutely, it presents with reduced consciousness and confusion. It can present in a more chronically with changes
to personality, memory and mood.
• Occur in 50% of all cases of cirrhosis with different severity

Precipitants include alkalosis, hypokalemia (due to diuretics) ,sedating drugs, GI bleeding, systemic infection and
hypovolemia

Clinical Features :
• Decreased mental function, confusion, poor concentration, even stupor or coma
• Asterixis ('flapping tremor')
• Rigidity, hyperreflexia
• Musty odor of breath

Management:
• Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3
soft motions daily. They may require enemas initially.
• Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria
producing ammonia. Rifaximin is useful as it is
poorly absorbed and so stays in the GI tract.
• Nutritional support. They may need nasogastric
feeding.
 Hepatorenal Syndrome
Hepatorenal syndrome occurs in liver cirrhosis.
Hypertension in the portal system leads to dilation
of the portal blood vessels, stretched by large
amounts of blood pooling there. This leads to a loss of
blood volume in other areas of the circulation,
including the kidneys. This leads hypotension in the
kidney and activation of the renin-angiotensin
system. This causes renal vasoconstriction, which
combined with low circulation volume leads to
starvation of blood to the kidney. This leads to rapid
deteriorating kidney function. Hepatorenal
syndrome is fatal within a week or so unless
liver transplant is performed.

Clinical features :
• Azotemia, Oliguria, hyponatremia,
hypotension, low urine sodium ( < 10 mEq/
L).

Criteria for diagnosis of HRS ( Hepatorenal syndrome )

1. Serum creatinine > 1.5mg/dl
2. No shock
3. No Nephrotoxic agents exposure.
4. No improvement of renal function ( s.Creat < 1.5mg/dl) after at least 2
days of diuretic withdrawal and volume expansion with albumin at 1g/kg/d
up to a maximum of 100 g/day.
5. No Parenchymal renal disease as defined by proteinuria < 0.5 g/d , No
microhematuria , and normal renal US.
Treatment : Liver transplantation. The prognosis is very poor

Hyperestrinism
Occur due to reduced hepatic catabolism of estrogen
• Spider angiomas : dilated cutaneous arterioles with central red spot and reddish extensions that radiate outward
• Palmar erythema
• Gynecomastia
• Testicular atrophy

Compensated: is the asymptomatic stage.

https://zerotofinals.com/medicine/gastroenterology/cirrhosis/
Compensated patients do not have ascites,
variceal hemorrhage, hepatic encephalopathy,
or jaundice. Decompensated: When your
cirrhosis has progressed to the point that the
liver is having trouble functioning and you start
having symptoms of the disease, you're
considered to have decompensated cirrhosis.