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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.

Chronic Liver Disease

Authors

Ashish Sharma1; Shivaraj Nagalli2.

Affiliations
1 Yuma Regional Medical Center
2 Yuma Regional Medical Center

Last Update: July 5, 2020.

Introduction
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. CLD is a continuous process of inflammation, destruction, and regeneration of liver parenchyma, which leads to
fibrosis and cirrhosis. The spectrum of etiologies is broad for chronic liver disease, which includes toxins, alcohol
abuse for a prolonged time, infection, autoimmune diseases, genetic and metabolic disorders. Cirrhosis is a final stage
of chronic liver disease that results in disruption of liver architecture, the formation of widespread nodules, vascular
reorganization, neo-angiogenesis, and deposition of an extracellular matrix. The underlying mechanism of fibrosis
and cirrhosis at a cellular level is the recruitment of stellate cells and fibroblasts, resulting in fibrosis, while
parenchymal regeneration relies on hepatic stem cells. Chronic liver disease is an extremely common clinical
condition, and the focus is done on the common etiologies, clinical manifestations, and management.

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 in East Asia and Sub-
Saharan Africa. There are various genotypes of hepatitis C. In Europe and North America, genotype 1a and 1b are
more prevalent, while in Southeast Asia, genotype 3 is more common. A molecular epidemiological study revealed a
high prevalence of HCV genotype 4, subtype 4a among Egyptian patients living in Sharkia governorate, Egypt.

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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. Here due to a mutation
involving the HFE gene that regulates the iron absorption from the intestine, 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

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.

Other Causes of Chronic Liver Disease

Drugs - amiodarone, isoniazid, methotrexate, phenytoin, nitrofurantoin.

Vascular. Budd-Chiari syndrome.

Idiopathic/cryptogenic, around 15%

Epidemiology
Chronic liver disease is one of the frequent causes of death, especially in the developing world. The increasing
prevalence of chronic liver disease has been noted in recent times. The majority of chronic liver diseases in the
developed world include alcoholic liver disease, chronic viral hepatitis, including hepatitis B and C, non-alcoholic
fatty liver disease (NAFLD), and hemochromatosis.[1] In the United States, according to the National Vital Statistics
Report 2017 from the Center for Disease Control and Prevention, approximately 4.5 million adults had chronic liver
disease and cirrhosis, which is 1.8 percent of the adult population. There were 41,473 deaths (12.8 deaths per 100,000
population) from chronic liver disease and cirrhosis.

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Pathophysiology
The chronic liver disease represents a continuous and progressive process of hepatic fibrosis, liver tissue architectural
distortion, and regeneration nodule formation. While fibrosis is usually irreversible, but it can be reversible in the
initial stage of development. The transition time point of reversible fibrosis to irreversible fibrosis is still not
completely understood. In chronic liver disease, if not treated, the endpoint is usually irreversible fibrosis,
regeneration nodule formation, and development of cirrhosis liver. The development rate of fibrosis is dependent on
the underlying etiologies, environmental, and host factors. The evolution of liver fibrosis was studied in 4852 patients
with different underlying etiology in one study. The author observed significant differences in the rate of development
of fibrosis and its progression. The rate was most rapid in patients with coinfection with HIV- HCV, while primary
biliary cirrhosis was the slowest. Fibrosis progression rate was higher with increasing age, and females demonstrated
a more gradual progression of liver fibrosis in all but alcoholic liver disease.[2] Similarly, in another study, genetic
polymorphism was attributed as an underlying factor for the difference in fibrosis rate progressions and the
development of more severe disease in some individuals compared to others with the same underlying etiology.[3]

Hepatic fibrosis is the deposition of extracellular matrix (ECM) in response to chronic liver injury by any etiology.
The common pathway is initiated by hepatic stellate cells (HSC), which usually are vitamin A storing dormant cells
found in space between sinusoids and hepatocytes. In response to chronic liver injury, HSC gets activated into
proliferative fibrogenic myofibroblast and upregulate expression of inflammatory receptors such as chemokine
receptors, ICAM-1, and other inflammatory mediators by releasing chemokines and other leukocyte chemoattractants.
This pro-inflammatory phase or initiation phase also changes gene and phenotypic expression of the liver cells,
making them more responsive to these inflammatory cytokines, and perpetuation of activated HSC cells results in the
accumulation of ECM and progressive fibrosis.[4]

Histopathology
The stellate cells are thought to be the source of collagen in pathological conditions. Chronic liver injury activates
hepatic stellate cells, which are activated and transformed into a myofibroblast-like phenotype. They then lay down
the extracellular matrix. Chronic inflammation, cytokine production by damaged parenchymal cells, and disruption of
the extracellular matrix are well-characterized stimuli to stellate cells.

The etiology affects the patterns of liver fibrosis. Chronic hepatotropic virus infection causes portal expansion
followed by periportal fibrosis, septal (bridging) fibrosis, and cirrhosis. Alcoholic liver disease and adult non-
alcoholic fatty liver disease cause fibrosis, starting with a centrilobular perivenular distribution and sinusoidal
fibrosis. Pediatric fatty liver disease is similar to hepatotropic virus infection with a periportal distribution.
Perisinusoidal or perivenular fibrosis is usually not apparent.

Biliary tract disease cirrhosis is characterized by feathery degeneration of periseptal hepatocyte leasing to the
presence of prominent “halos” and irregular-shaped nodules (“jigsaw” micronodular pattern). Fibrosis progressively
links the adjacent central veins and portal tracts in venous outflow obstruction, resulting inveno-portal cirrhosis or
veno-centric (“reversed lobulation” cirrhosis).[5]

History and Physical

Clinical Manifestations

Signs and symptoms of CLD can be nonspecific, such as fatigue, anorexia, weight loss, or depend upon the

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complication that the patient has developed. The three significant complications are because of portal hypertension
(esophageal varices, ascites), hepatocellular insufficiency (e.g., jaundice, hepatic encephalopathy), and hepatocellular
carcinoma. 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 as 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

Rectal hemorrhoids

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.

Hepatocellular Insufficiency

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 the 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.

According to AASLD guidelines, depending upon the severity of the disease, there are different grades of hepatic
encephalopathy.[6]

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.

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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 eyes, skin, and mucous membrane because of overproduction or under
clearance of bilirubin. Metabolism of hemoglobin or myoglobin produces bilirubin in the spleen. Bilirubin then
circulates in the body, bound to albumin. The liver dissociates this complex and converts unconjugated bilirubin to
conjugated bilirubin. Jaundice is clinically visible when total bilirubin is greater than 2 mg/dl. As in chronic liver
disease, there is the destruction of liver parenchyma, and it does not conjugate bilirubin, which deposits in various
tissues of the body. There is pruritus because of the accumulation of bile salts.

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:

Chronic liver disease with portal hypertension or advanced liver failure

Continuous rising in creatinine, usually more than 0.3 mg/dl within 48 hours or doubling from baseline within
seven days.

Oliguria with the absence or minimal proteinuria

Urine sodium less than 10 meq/L

Failure to improve with volume expansion and stopping the diuretics.

Absence of shock

No recent use of the nephrotoxic drug

Absence of renal parenchymal disease

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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. Hence, PT/INR (intrinsic pathway) and APTT (extrinsic pathways)
are prolonged.

Evaluation
The diagnosis of chronic liver disease depends upon the etiology and complications of the disease. An outline
regarding the diagnosis for various CLD appears below.

Viral hepatitis B and C: Serology, PCR (quantitative and qualitative) with genotype

Alcoholic liver disease: Elevated levels of AST>ALT with a history of chronic alcohol intake. Usually, AST:
ALT ratio is 2 to 1 in alcoholic liver disease.

Hemochromatosis: Raised serum iron, ferritin, decreased TIBC, and liver biopsy. Genetic testing can detect a
mutation in the HFE gene, especially C282Y.

Wilson disease: Raised urine copper, decreased serum ceruloplasmin, and liver biopsy. Genetic testing for the
ATP7B gene.

Non-alcoholic fatty liver disease: Diagnosis of exclusion and ALT>AST. Ultrasonography of the liver is
informative.

Autoimmune hepatitis: Raised ANA, ASMA, and LKM-1

Alpha 1 antitrypsin deficiency: Decreased levels of alpha one antitrypsin

Primary biliary cirrhosis: Markedly raised alkaline phosphatase levels with an antimitochondrial antibody

Budd-Chiari and veno-occlusive disease: CBC, clotting profile, and imaging studies like ultrasound doppler or
computed tomography with contrast study

Laboratory Findings

In chronic liver disease, there is inflammation and destruction of hepatocytes that leads to the release of aspartate
aminotransferase (AST) and alanine aminotransferase (ALT), hence the high levels of these markers in the blood.
Other parameters (ALP and GGT) of LFTs also appear elevated in cholestatic conditions like PBC. AST and ALT are
usually elevated two to three times of normal limit, but normal levels of these markers do not rule out cirrhosis.[8] As
in compensated, CLD LFTs may be normal in cirrhosis. Bilirubin (unconjugated> conjugated) levels are elevated in
jaundice. There is reduced production of clotting factors leading to raised PT/INR and APTT.

Because of hepatocellular insufficiency in cirrhosis, albumin level drops, and ammonia raises, causing ascites and
hepatic encephalopathy. The increased concentration of ammonia, tryptophan metabolites, short-chain fatty acids,
octopamine, mercaptans, increased oxidative stress, and increase intracellular osmolality are among many which have
been proposed as the mechanism of developing hepatic encephalopathy.[9][10][11][12][13] In a case of ascites,
diagnostic paracentesis is an investigation of choice to see whether ascites are because of raised portal pressure or
another cause. By doing a biochemical and cytological analysis of ascitic fluid, we calculate the serum ascites
albumin gradient (serum albumin-ascitic fluid albumin). If this gradient is greater than 1.1, then portal hypertension is

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a likely cause, but if it is less than 1.1, portal hypertension is unlikely. WBC greater than 500/microliter or PMN
greater than 250/microliter and fluid cultures will be positive in patients with SBP.[14] Ultrasound of the abdomen
and serum AFP levels can help diagnose the presence of hepatocellular carcinoma. In hepatorenal syndrome,
creatinine usually is elevated to more than1.5 g/dl. Thrombocytopenia is an indirect measure of splenomegaly, which
occurs in CLD because of raised portal pressure.

Radiologic Investigations

It includes an abdominal ultrasound, CT scan, fibro scan, hepatic wedge pressure, endoscopy, EEG, TIPS, triphasic
CT, and Doppler scan.

Ultrasound abdomen is one of the most common and affordable imaging studies in a 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. It can also detect cardiovascular damage in
patients with NAFLD.[15] It works on two physical principles; strain displacement and shear wave imaging and
quantification. The latter includes point shear wave elastography. It measures the velocity of low frequency (50
Hz) elastic shear wave propagating through the liver. The stiffer the tissue, the faster elastic shear wave
propagates. It can easily work on an ultrasound machine. According to the European association of study for
the Liver (EASL), TE is the most effective approach to diagnose cirrhosis in chronic liver disease.

Wedge hepatic venous pressure measures portal venous pressure in CLD.

Doppler scan can help in diagnosing Budd-Chiari and portal vein thrombosis.

EEG shows delta waves in hepatic encephalopathy.

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 laparoscopically, transjugular, or percutaneously.

Treatment / Management
Treatment and Prophylaxis

The treatment goal is to stop the progression of the disease and complications and require a multidisciplinary
approach. The principle of management is mainly underlying cause correction, Portal hypertension management, and
specific treatments for individual disease. A brief outline regarding treatment for various CLD and related
complications is given below. For more comprehensive details, please see individual topics in the Statpearls glossary.

General Management

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Patients of chronic liver disease mostly present with one of the complications.

Esophageal varices - Varices related bleeding are one of the deadly complications, and the treatment includes
aggressive fluid resuscitation, vasopressors (octreotide, terlipressin), and endoscopy. Endoscopic band ligation and
injection sclerotherapy are the usual modalities to treat variceal bleed in an emergency. In some patients, early
transjugular intrahepatic portosystemic shunt (TIPS) can increase the survival rate. Propranolol is used for primary
and secondary prophylaxis for esophageal varices. Diuretics (furosemide, spironolactone) and sodium restriction are
essential treatment options for ascites. For tense ascites, therapeutic paracentesis is done. Albumin infusion can also
be considered. Initially, broad-spectrum antibiotics are the treatment of choice for SBP and then specific antibiotics
after culture.

Hepatic encephalopathy - The basic principle of treatment is to address the precipitating factors. Patients with hepatic
encephalopathy usually improve with precipitating cause correction along with rifaximin and lactulose.[16][17]
Lactulose acts by converting ammonia to ammonium ion and decreases its absorption from the gastrointestinal tract.
Lactulose also relieves constipation through its osmotic effect, which further helps to ease the symptoms of hepatic
encephalopathy. Rifaximin is used to decrease ammonia production by gut flora. Liver transplant is the curative
treatment in patients with hepatorenal syndrome.

Hepatorenal syndrome - HRS based on severity divided into two categories. HRS 1 is more severe compared to HRS
2 (less severe). The primary goal is to correct underlying cause correction to reverse acute kidney injury. Treatment
modalities depend on the severity and location of the patient. Treatment modalities include norepinephrine or
terlipressin with albumin infusion or midodrine, octreotide with albumin infusion. TIPS procedure in some patients
can help and liver transplantation the only definite treatment in the patient who fails to respond to all other treatments.
[18][19][20]

Hepatocellular carcinoma (HCC) - Treatment is based on the Barcelona clinic liver cancer staging system in the
management of HCC:

Initial stage (single HCC lesion): Resection and ablation.

Intermediate stage: Transarterial chemoembolization and radio-embolization.[21]

Metastatic disease: Sorafenib[22]

Specific Treatment

Viral Hepatitis

Continuous viral suppression with nucleoside and nucleotide analogs

Direct-acting antivirals achieving HCV eradication

Interferon-alpha

Alcoholic liver disease: Alcohol abstinence

Non-alcoholic fatty liver disease: Treatment of metabolic syndrome components

Autoimmune hepatitis: Corticosteroids and other immunosuppressive drugs

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Hereditary hemochromatosis: Phlebotomy, iron-chelators

Copper overload (Wilson disease): Copper chelators

Alpha-1-antitrypsin deficiency: Transplant

Drugs and toxins: Identify and stop the factor

Primary biliary cholangitis (PBC): Ursodeoxycholic acid (UDCA)[23]

Primary sclerosing cholangitis: Transplant

Budd-Chiari syndrome: Anticoagulation, thrombolysis or angioplasty with or without stenting, TIPS, or liver
transplant

Differential Diagnosis

Constrictive pericarditis

Cor-pulmonale

Dilated cardiomyopathy

Inferior vena cava thrombosis

Nodular regenerative hyperplasia

Sarcoidosis

Schistosomiasis

Staging
Stages of liver disease

1. Hepatitis or steatosis or hepatosteatosis

2. Fibrosis

3. Cirrhosis

4. Hepatocellular carcinoma (HCC)

Prognosis
Compensated chronic liver disease (who has not developed significant complications) usually carry a better prognosis
than decompensated liver cirrhosis. Decompensated liver cirrhosis patients (who have developed variceal bleeding,
ascites, HCC, SBP, and hepatorenal syndrome) have a poor prognosis. Mean survival of about six months if Child-
Pugh score of 12 or greater or MELD score of 21 or higher.

There are various scoring systems used to asses the severity of chronic liver disease.

1. The Child-Pugh score uses ascites, bilirubin, albumin, PT, and encephalopathy.

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Class A (score 5-6): well-compensated disease.

Class B (score 7-9): functional compromise.

Class C (score 10-15): decompensated disease.

2. MELD (model of end-stage liver disease) uses bilirubin, serum creatinine, and INR. The MELD score was initially
used to predict mortality within three months after the TIPS procedure and now used to prioritize patients for receipt
of a liver transplant.

Complications
The following are the complications of chronic liver disease.

Variceal bleeding

Ascites and spontaneous bacterial peritonitis (SBP)

Hepatic encephalopathy

Hepatorenal syndrome

Hepatopulmonary syndrome

Hepatocellular carcinoma (HCC)

Consultations

Gastroenterology/hepatology consultation for patients with decompensated chronic liver disease

Nephrology consultation in patients with hepatorenal syndrome

Dietician consultation for advice on the diet

Referral to a transplant center in patients needing a liver transplant

Deterrence and Patient Education

Patient education is one of the critical factors that can play a pivotal role in the prevention of chronic liver disease.
Most of the causative factors of chronic liver disease damage the liver over a long period; therefore, it is necessary to
stop its progression to avoid cirrhosis and its complications.

Recommendations for 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.

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Maintain a good lipid profile to avoid metabolic syndrome and NAFLD.

Pearls and Other Issues

To prevent complications, patients with chronic liver disease will need surveillance. These patients should undergo
routine monitoring of their CBC, CMP, and prothrombin time at least 3 to 4 times per year.

Routine diagnostic endoscopy should be performed for asymptomatic esophageal varices, and a follow-up endoscopy
should be done in 2 years if varices are not present. Treatment with a nonselective beta-blocker to reduce heart rate by
25% in patients with esophageal varices, offers primary prophylaxis with variceal bleeding.[24] Patients with large
esophageal varices should have prophylactic endoscopic variceal banding to avoid the risk of rupture and bleeding.

The incidence of hepatocellular carcinoma has risen in the United States, and patients with cirrhosis should
undergo surveillance with ultrasonography every six months.[25] A 4-phase CT scan or an MRI scan should be
done to rule out hepatocellular carcinoma in patients with a liver nodule on the ultrasound.

Enhancing Healthcare Team Outcomes

An interprofessional team that provides a holistic and integrated approach is needed for a patient with chronic liver
disease to achieve the best possible outcomes. The earlier signs and symptoms of a complication are identified, the
better is the prognosis and outcome. The team consists of primary care physicians, gastroenterologists/hepatologists,
dieticians as needed, and a social worker and community nurses who can monitor the patient and make referrals as
necessary to prevent the development of complications. Routine labs and endoscopy and the ultrasound as appropriate
are required. The liver transplant team should closely monitor patients who are transplant candidates.

Questions
To access free multiple choice questions on this topic, click here.

References
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