Chronic liver disease (CLD) is a progressive deterioration of liver functions for more than six months,

which includes synthesis of clotting factors, other proteins, detoxification of harmful products of
metabolism, and excretion of bile.

Etiology
The following are the most common etiologies:

Alcoholic Liver Disease

Alcoholic liver disease is a spectrum of disease which includes alcoholic fatty liver with or without
hepatitis, alcohol hepatitis (reversible because of acute ingestion) to cirrhosis (irreversible). Patients
with severe alcohol use disorder mostly develop chronic liver disease; this is the most frequent
cause of CLD.

Non-alcoholic Fatty Liver Disease (NAFLD/NASH)

NAFLD has an association with metabolic syndrome (obesity, hyperlipidemia, and diabetes mellitus).
Some of these patients develop non-alcoholic steatohepatitis, which leads to fibrosis of the liver. All
the risk factors of metabolic syndrome can aggravate the disease process.

Chronic Viral Hepatitis

Chronic hepatitis B, C, and D infections are the most common causes of chronic liver disease. Chronic
hepatitis C, if not treated, may lead to hepatocellular carcinoma.

Genetic Causes
 Alpha-1 antitrypsin deficiency: This is the most common genetic cause of CLD among
children.
 Hereditary hemochromatosis: It is an autosomal recessive disorder of iron absorption.
excessive iron is absorbed from the gastrointestinal tract. As a result, there is a pathological
increase in total body iron (such as ferritin and hemosiderin). This process leads to the
generation of hydroxyl free radicals, which in turn causes organ fibrosis.
 Wilson disease: Autosomal recessive disorder leading to copper accumulation
disease is an inherited disorder in which excessive amounts of copper accumulate in the
body, particularly in the liver.

Autoimmune Causes
Autoimmune hepatitis is a rare disease in which there is the destruction of liver parenchyma by
autoantibodies. Most of the patients who present with this disease have already developed cirrhosis.
Females are more commonly affected than males.

Primary biliary cirrhosis (PBC): This is an autoimmune and progressive disease of the liver, which is
the destruction of intrahepatic biliary channels and portal inflammation and scarring. It leads to
cholestatic jaundice and fibrosis of liver parenchyma. PBC is more common in middle-aged women.
Alkaline phosphatase levels increase in PBC.
Primary Sclerosing Cholangitis (PSC): commonly associated with ulcerative colitis. This condition is
characterized by a decrease in the size of intrahepatic and extrahepatic bile ducts due to
inflammation and fibrosis.
Autoimmune hepatitis (AIH): This is a form of chronic inflammatory hepatitis, more common in
women than men, and is characterized by elevated autoantibodies such as antinuclear antibodies,
anti-smooth muscle antibodies, and hypergammaglobulinemia.

Decompensated chronic liver disease can present with one of the following complications.
Portal Hypertension
Portal hypertension is a result of resistance to portal blood flow because of cirrhotic and
noncirrhotic etiology. A portal venous pressure above seven mmHg is considered portal
hypertension; however, clinical features or complications do not develop until portal pressure is
higher than 12 mmHg. Portal hypertension causes can divide into prehepatic (e.g., portal vein
thrombosis), hepatic (e.g., cirrhosis), and post hepatic (e.g., Budd Chiari syndrome). Cirrhosis and
hepatic schistosomiasis remain the most common cause of portal hypertension, with cirrhosis being
more common in developed countries.
The following are the consequences of long-standing portal hypertension.

 Esophageal varices: It presents with melena or upper GI bleed. Cirrhosis of the liver leads to
raised portal pressure, which can cause esophageal or gastric varices. Esophageal variceal
bleeding is the most common life-threatening complication of CLD.
 Caput medusae usually related to liver disease, which eventually causes liver scarring, or
cirrhosis.
 Ascites: It is an accumulation of fluid in the peritoneal cavity because of raised portal
pressure (increased hydrostatic pressure), decreased albumin (reduced oncotic pressure),
and splanchnic vasodilation (due to the release of nitric oxide). Most of the patients develop
ascites in the later stages of cirrhosis. Clinical findings in such patients are abdominal
distension, shifting dullness, and a fluid wave. Tense ascites can lead to shortness of breath
or early satiety.

Hepatic Encephalopathy
This is a neuropsychiatric syndrome caused by hepatic dysfunction. Detoxification of harmful
products of metabolism, e.g., ammonia, occurs in the liver. In a patient with cirrhosis, the removal of
these substances from the body is impaired, leading to an increased level of ammonia. Raised levels
of ammonia can impair consciousness. Almost 50% of patients with DCLD can develop hepatic
encephalopathy.
Depending upon the severity of the disease, there are different grades of hepatic encephalopathy.

Grade 0/Minimal: Subclinical, normal mental status with minimal changes in memory, coordination,
intellectual function, concentration.
Grade 1: Trivial lack of awareness, euphoria or anxiety, shortened attention span, impairment of
addition or subtraction, altered sleep rhythm.
Grade 2: Lethargy or apathy, disorientation to time, personality change, inappropriate behavior,
dyspraxia, asterixis.
Grade 3: Somnolence to semi-stupor, responsive to stimuli, confused, gross disorientation, bizarre
behavior.
Grade 4: Coma
The patient can present in any of these symptoms. Most of the patients with hepatic
encephalopathy present with altered sensorium. Infections, GI bleed, hyperkalemia, TIPS[7],
sedating agents, and alkalosis can aggravate hepatic encephalopathy.

Jaundice
Jaundice is a yellowish discoloration of the eyes, skin, and mucous membrane because of
overproduction or under clearance of bilirubin.
Spontaneous Bacterial Peritonitis (SBP)
It is one of the acute and painful complications of chronic liver disease. Bacteria (E. coli, Klebsiella,
Streptococcus pneumonia) seep through the gastrointestinal tract and infect the ascitic fluid. The
infection spread through the fluid to the peritoneal membrane, causing inflammation. SBP presents
with fever, generalized abdominal pain, tenderness, and absent bowel sounds.
Hyperestrinism
In chronic liver disease, the catabolism of estrogen becomes impaired, resulting in excess estrogen in
the body. This manifests as palmar erythema, spider angiomas (dilated cutaneous arterioles with a
central red spot and red extensions that radiate outward like a spider's web in the territory of SVC),
gynecomastia (enlarged tender subareolar tissue), and testicular atrophy.
Hepatorenal Syndrome (HRS)
Hepatorenal syndrome is a functional renal failure as kidneys are normal, where there is a gradual
loss of renal function. It is a diagnosis of exclusion. Vasoconstrictors are released in CLD, which is
responsible for the narrowing of renal vessels. The following criteria have been described:

Coagulopathy
The liver produces clotting factors, so the patients with CLD have coagulopathies and manifest or
contribute to easy bruising and bleeding per gastrointestinal tracts.

Ultrasound abdomen is one of the most common and affordable imaging studies in the case of
chronic liver disease. Ultrasound detects the size, echogenicity nodularity of the liver, thereby
diagnosing liver cirrhosis. Other benefits of ultrasound in CLD include measurement of portal vein
diameter as portal vein diameter increases in portal HTN and assessment of a clot in the hepatic vein
(Budd-Chari) and portal vein in portal vein thrombosis.
Computed tomography scan can show a lesion in the liver or obstruction of biliary channels in a
more precise way, but triphasic CT is the test of choice in diagnosing hepatocellular carcinoma.
Transient elastography (TE) detects early stages of cirrhosis.
An upper endoscopy can diagnose and treat esophageal varices. On endoscopy, we can measure the
size of varices. Small varices are less than 5 mm, and large varices are greater than 5 mm.
A liver biopsy can confirm the diagnosis of chronic liver disease. Various techniques to perform a
liver biopsy are by laparoscope, transjugular, or percutaneously.
Blood tests. A group of blood tests called liver function tests can be used to diagnose liver disease.
Other blood tests can be done to look for specific liver problems or genetic conditions.

Preventive Care in Chronic Liver Disease

 Avoid various types of alcohol (wine, liquor, mixed drinks, beer).
 Regular screening for hepatitis B and hepatitis C
 Vaccination against hepatitis A and B
 Avoid iron supplementation unless there is an iron deficiency.
 Avoid over-the-counter painkillers (aspirin, acetaminophen) and other hepatotoxic drugs.
 Maintain a good lipid profile to avoid metabolic syndrome and NAFLD.

Medical Management
Pharmacological
 Potassium-sparing diuretic spironolactone (Aldactone)-use to decreased ascites and pleural
effusion.
 Lactulose(Cholac)-used to eliminate the ammonia from the blood into the bowel. Tap water
enemas may also be ordered to help the body eliminate the ammonia.
 Propranolol hydrochloride(Inderal)- an antihypertensive medication may be ordered to
lower portal hypertension.

Nursing Management
 Monitor vital signs, intake and output, and electrolyte levels to determine fluid volume
status.
  Maintain some periods of rest with legs elevated to mobilize edema and ascites—alternate
rest periods with ambulation.
 To assess fluid retention, measure, and record abdominal girth every shift. Weight the
patient daily and document his weight.
 Administer diuretics,potassium, and protein or vitamin supplements as ordered. Restrict
sodium and fluid intake as ordered.
 Observe and document for bleeding gums,ecchymoses,epitaxis,petechiae and degree of
sclerae, skin jaundice. Remain with the patient during the hemorrhagic episodes.
 Inspect stools for amount, color, and consistency. Test stools and vomitus for occult blood as
ordered.
 Watch for signs of anxiety, epigastric fullness, restlessness, and weakness.
 Observe closely for signs of behavioral or personality changes. Report increasing stupor,
lethargy, hallucinations, or neuromuscular dysfunction. Arouse the patient periodically to
determine the level of consciousness. Watch for asterixis, a sign of developing
encephalopathy.

Liver Transplant