Liver failure can be acute or chronic, with chronic being more common. Chronic liver failure progresses from cirrhosis to portal hypertension and its complications like variceal bleeding. Cirrhosis occurs after prolonged liver injury and scarring replaces liver tissue. Portal hypertension occurs when pressure in the portal vein exceeds 10 mmHg, increasing risk of bleeding from esophageal varices. Treatment of liver failure focuses on supportive care in intensive care units, managing complications like encephalopathy, and liver transplantation for severe cases.

1. Liver failure

2. • Aims
• • Define liver failure
• • Know the different types of liver failure.
• • Define cirrhosis and its complications.
• • Define portal hypertension and its complication.
• • Gain knowledge about the management of variceal bleeding
.
• • Identify the different mechanisms by which hepatic failure
• produce its effects on the body.

3. What is liver failure ?
• Liver failure occurs when there is insufficient
metabolic
and synthetic function for the needs of the patient.
• It can be divided into acute and chronic(which is the
most common)
• Can have dramatic effect on survival and quality of life
.
• Many causes are involved

4. • Acute type
• • Uncommon
• • Acute viral hepatitis is the most common cause worldwide
• • In a patient with pre-existing chronic liver disease, the
additional acute insult needed to precipitate liver failure is
much less.
• • in a patient whose liver was previously normal (fulminant
liver failure), the level of injury
• needed to cause liver failure, and thus the patient risk, is very
high.

6. Treatment
Patients with acute liver failure should be treated in a high-
dependency or intensive care unit as soon as progressive
prolongation of the PT occurs or hepatic encephalopathy is
identified
1. Airway protection
2. Management of Encephalopathy and Cerebral Edema
3. Intracranial pressure monitoring
4. Hemodynamic Monitoring
5. Management of Coagulopathy
6. Prevent complications
7. Liver Transplantation
N.B. : N-acetylcysteine therapy may improve outcome,
particularly in patients with acute liver failure due to
paracetamol poisoning.

7. Chronic type
The usual sequence :
• Liver failure
• Portal hypertension
• Cirrhosis

8. • Cirrhosis
• • Cirrhosis is a histological diagnosis represents the end stage of
• chronic liver disease, in which much of the functional liver tissue has
• been replaced by fibrous tissue
• • the most common causes are prolonged excessive alcohol
• consumption, chronic viral hepatitis, and NAFLD, but any condition
• leading to persistent or recurrent hepatocyte death may lead to
• cirrhosis.
• • Following liver injury, stellate cells in the space of Disse are
activated by cytokines produced by Kupffer cells and hepatocytes

9. • Portal hypertension
• • Clinically significant portal hypertension
• is present when the hepatic venous
• pressure gradient (HVPG) exceeds 10
• mmHg and risk of variceal bleeding
• increases beyond a gradient of 12
• mmHg.
• • The HVPG is defined as the difference
• in pressure between the portal vein and
• the inferior vena cava.
• • Major complication of cirrhosis

10. • Splenomegaly is a cardinal finding and a diagnosis of portal
hypertension is unusual when splenomegaly cannot be
detected.
• Ascites(result of renal sodium retention and portal hypertension)
• oesophagus and stomach varicosed
veins.
• caput medusae.
• Haemorrhoids .
• Fetor hepaticus.

11. • • The most important consequence of portal
hypertension is variceal bleeding.
• • commonly arises from oesophageal varices located
• within 3–5 cm of the gastro-oesophageal junction, or
• from gastric varices.
• • The size of the varices, endoscopic variceal features
• such as red spots and stripes, high portal pressure and
• liver failure are all general factors that predispose to
• bleeding.
• • Drugs capable of causing mucosal erosion, such as
• salicylates and NSAIDs, can also precipitate bleeding.
• • Investigation of choice:endoscopy

12. • • The management of portal hypertension
•
• is largely focused on the prevention and/or control of variceal
• haemorrhage.
• • β-adrenoceptor antagonist (β-blocker) therapy with
• propranolol (80–160 mg/ day) or nadolol (40–240
• mg/day) is effective in reducing portal venous
• pressure.
• • In the Management of acute variceal bleeding The
• priority is to restore the circulation with blood and
• plasma, not least because shock reduces liver blood
• flow and causes further deterioration of liver function

13. • Hepatic failure
• • The most severe clinical consequence of liver disease is hepatic
• failure.
• • It may result from sudden and massive liver destruction, as in
• fulminant hepatitis, or be the result of progressive damage to the
• liver, as occurs in alcoholic cirrhosis.
• • Whatever the cause, 80% to 90% of hepatic functional capacity
must
• be lost before liver failure occurs.
• • The manifestations of liver failure reflect the various synthesis,
• storage, metabolic, and elimination functions of the liver .

14. Treatment
• • The treatment of liver failure is directed toward:
• eliminating alcohol intake when the condition is caused by
alcoholic cirrhosis.
• preventing infections.
• providing sufficient carbohydrates and calories to prevent protein
• breakdown.
• correcting fluid and electrolyte imbalances, particularly
Hypokalemia
• decreasing ammonia production in the gastrointestinal tract by
• controlling protein intake.
• • In many cases, liver transplantation remains the only
• effective treatment.

15. Thank you for
listening