Version July 2025
INTRODUCTION —
Cirrhosis represents a late stage of progressive hepatic fibrosis characterized by distortion of the hepatic architecture and the formation of regenerative nodules. It is generally considered to be irreversible in its advanced stages, at which point the only treatment option may be liver transplantation. However, reversal of cirrhosis (in its earlier stages) has been documented in several forms of liver disease following treatment of the underlying cause. Patients with cirrhosis are susceptible to a variety of complications, and their life expectancy is markedly reduced. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'Prognosis'.)
This topic will review the etiologies, clinical manifestations, and diagnosis of cirrhosis. An overview of the complications, prognosis, and general management of cirrhosis is discussed separately. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis".)
ETIOLOGIES AND CLASSIFICATION —
There are numerous causes of liver disease that can result in cirrhosis, either by causing chronic hepatic inflammation or cholestasis. In resource-abundant countries, common causes of cirrhosis include [1,2]:
●Alcohol-associated liver disease
●Metabolic dysfunction-associated steatotic liver disease
●Chronic viral hepatitis (hepatitis B, C virus infection)
Less common causes include:
●Hemochromatosis
●Autoimmune hepatitis
●Primary biliary cholangitis
●Primary (and secondary) sclerosing cholangitis
●Wilson disease
●Alpha-1 antitrypsin deficiency
●Granulomatous liver disease
●Right-sided heart failure
●Veno-occlusive disease
CLINICAL MANIFESTATIONS —
The clinical manifestations of cirrhosis may include nonspecific symptoms (eg, anorexia, weight loss, weakness, fatigue, pruritus, muscle cramps, sexual dysfunction) or signs and symptoms of hepatic decompensation (jaundice, signs of upper gastrointestinal bleeding, abdominal distension from ascites, confusion or altered executive function due to hepatic encephalopathy) (table 1). Physical examination findings may include jaundice, spider angiomata, gynecomastia, ascites, splenomegaly, palmar erythema, and asterixis. Laboratory abnormalities may include elevated serum bilirubin, abnormal aminotransferases, elevated alkaline phosphatase/gamma-glutamyl transpeptidase, a prolonged prothrombin time/elevated international normalized ratio (INR), hyponatremia, hypoalbuminemia, and thrombocytopenia.
Symptoms — Patients with compensated cirrhosis may be asymptomatic or they may report nonspecific symptoms. Patients with decompensated cirrhosis may present with jaundice, upper gastrointestinal bleeding (hematemesis, melena, hematochezia), abdominal distension from ascites, or confusion due to hepatic encephalopathy. Patients with cirrhosis may experience muscle cramps, which can be severe [3-7].
Patients should be asked about lower extremity edema, weight loss, pruritus, increasing abdominal girth, muscle cramps, falls, confusion, or sleep disturbances (possibly indicating encephalopathy).
In females, chronic anovulation is common, which may manifest as amenorrhea or irregular menstrual bleeding [8]. Clinical manifestations of sexual dysfunction include decreased sexual interest and dyspareunia [9]. Some of the abnormalities may be due to variations in testosterone, estradiol, prolactin, and luteinizing hormone levels in patients with cirrhosis compared with normal controls [10].
Males with cirrhosis may develop hypogonadism. It is manifested by impotence, infertility, loss of sexual drive, and testicular atrophy. This is especially common in patients with alcohol-associated cirrhosis. More than one mechanism appears to be involved. In some cases, primary gonadal injury appears to be more prominent, as suggested by increased serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) concentrations, whereas in others, suppression of hypothalamic or pituitary function appears to have a primary role, as suggested by serum LH concentrations that are not elevated. The toxic effects of alcohol or iron may also contribute to its development [11]. (See "Causes of primary hypogonadism in males".)
Patients with cirrhosis may also present with a diverse range of signs and symptoms that reflect the pivotal role that the liver has in the homeostasis of many different bodily functions. In addition, they may have features related to the underlying cause of cirrhosis such as cryoglobulinemia from hepatitis C, diabetes mellitus and arthropathy in patients with hemochromatosis, or extrahepatic autoimmune diseases (such as hemolytic anemia or thyroiditis) in patients with autoimmune hepatitis.
Physical examination — A number of physical findings have been described in patients with cirrhosis, including jaundice, spider angiomata, gynecomastia, ascites, splenomegaly, palmar erythema, and asterixis.
Decreasing blood pressure — As cirrhosis progresses, patients often have a decrease in mean arterial pressure [12]. Patients who were previously hypertensive may become normotensive or hypotensive. The decrease in mean arterial pressure contributes to the development of hepatorenal syndrome and is an important predictor of survival. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'Decompensated cirrhosis' and "Hepatorenal syndrome: Clinical presentation and diagnosis", section on 'Pathogenesis'.)
Skin findings — Patients with cirrhosis frequently develop jaundice and spider angiomata. Jaundice is a yellow coloring of the skin and mucous membranes that results from increased serum bilirubin. It is usually not detectable until the bilirubin is greater than 2 to 3 mg/dL. Hyperbilirubinemia may also cause the urine to appear dark or "cola" colored. (See "Diagnostic approach to the adult with jaundice or asymptomatic hyperbilirubinemia".)
Yellow skin discoloration can also be caused by excessive consumption of carotene (such as in patients who consume large quantities of carrots). Yellowing of the skin in carotenemia can be distinguished from jaundice by the absence of yellow discoloration in the sclera in the former.
Spider angiomata (also referred to as spider telangiectasias) are vascular lesions consisting of a central arteriole surrounded by many smaller vessels. They are most frequently found on the trunk, face, and upper limbs. The body of the lesion (the central arteriole) can be seen pulsating when compressed with a glass slide. Blood fills the central arteriole first before traveling to the peripheral tips of each "leg" after blanching. There are usually multiple radiating legs and surrounding erythema that may encompass the entire lesion or only its central portion.
The pathogenesis of spider angiomata is incompletely understood, but they are believed to result from alterations in sex hormone metabolism. One study suggested that the presence of spider angiomata in males was associated with an increase in the estradiol-to-free testosterone ratio [13]. Acquired spider angiomata are not specific for cirrhosis since they may also be seen during pregnancy (picture 1) and in patients with severe malnutrition. They can also be seen in otherwise healthy people, who usually have fewer than three small lesions. As a general rule, the number and size of spider angiomata correlate with the severity of liver disease [14,15]. Patients with numerous, large spider angiomata may be at increased risk for variceal hemorrhage.
Head and neck findings — Head and neck findings in patients with cirrhosis may include parotid gland enlargement and fetor hepaticus. Parotid gland enlargement is typically seen in patients with alcohol-associated liver disease and is probably due to alcohol, not cirrhosis per se. Enlargement is usually secondary to fatty infiltration, fibrosis, and edema rather than a hyperfunctioning gland [16].
Fetor hepaticus refers to a sweet, pungent smell to the breath of a patient with cirrhosis. It is caused by increased concentrations of dimethyl sulfide, the presence of which suggests underlying severe portal-systemic shunting [17].
Chest findings — Gynecomastia is seen in up to two-thirds of patients with cirrhosis. It is possibly caused by increased production of androstenedione from the adrenals, enhanced aromatization of androstenedione to estrone, and increased conversion of estrone to estradiol [18]. Males may also develop other features reflecting feminization, such as loss of chest or axillary hair and inversion of the normal male pubic hair pattern. Gynecomastia can be seen in a variety of conditions other than cirrhosis. (See "Epidemiology, pathophysiology, and causes of gynecomastia".)
Gynecomastia is defined histologically as a benign proliferation of the glandular tissue of the male breast and is diagnosed on exam as a palpable mass of tissue (usually underlying the nipple). The evaluation of gynecomastia is discussed separately. (See "Clinical features, diagnosis, and evaluation of gynecomastia in adults".)
Abdominal findings — Findings on abdominal examination include hepatomegaly, splenomegaly, ascites, caput medusae, and a Cruveilhier-Baumgarten murmur.
Ascites — Ascites is the accumulation of fluid in the peritoneal cavity. Physical findings in patients with ascites include abdominal distension, a fluid wave, and flank dullness to percussion. The accuracy of physical findings is variable, depending on the amount of fluid present, the technique used to examine the patient, and the clinical setting (eg, detection may be more difficult in patients who are obese). In one study, the absence of flank dullness was the most accurate predictor against the presence of ascites; the probability of ascites being present was less than 10 percent in such patients [19]. However, approximately 1500 mL of fluid had to be present for flank dullness to be detected. (See "Evaluation of adults with ascites".)
Hepatomegaly — The cirrhotic liver may be enlarged, normal sized, or small. While the presence of a palpable liver may indicate liver disease, a non-palpable liver does not exclude it. When palpable, the cirrhotic liver has a firm and nodular consistency. The liver is the largest internal organ in humans and typically spans 21 to 23 cm horizontally and 14 to 17 cm vertically. The size of the normal liver varies depending on sex, height, and body habitus.
Physical examination of the liver can be helpful for assessing its shape, its consistency, and whether there is tenderness of the liver edge. It is less useful for assessing its size since assessment of liver size by physical examination correlates poorly with radiologic assessment [20]. Nevertheless, the liver span can be estimated using percussion techniques or the scratch test. The scratch test uses auscultation while lightly scratching the skin. The intensity of the scratching sound increases when the liver is encountered with the scratching finger. A normal liver span in the mid-clavicular line by physical examination is 7 to 10 cm.
In healthy people, the liver is generally not palpable because it lies posterior to the rib cage. By contrast, an enlarged liver can often be palpated below the costal margin. However, there are exceptions in which a normal-sized liver can be palpated below the costal margin including patients with emphysema, a thin-body habitus, the presence of a hypertrophied caudate lobe (such as seen in patients with Budd-Chiari syndrome), or Riedel's lobe (an anatomical variant in which there is an extension of the right-lobe downward and lateral toward the gallbladder). (See "Overview of the evaluation of hepatomegaly in adults".)
Splenomegaly — Splenomegaly is common, especially in patients with cirrhosis from nonalcohol-related etiologies [21]. It is believed to be caused primarily by congestion of the red pulp resulting from portal hypertension. However, splenic size does not correlate well with portal pressures, suggesting that other factors may be contributing [22]. The differential diagnosis of splenomegaly includes several other disorders. (See "Splenomegaly and other splenic disorders in adults".)
Caput medusae — The veins of the lower abdominal wall normally drain inferiorly into the iliofemoral system, while the veins of the upper abdominal wall drain superiorly into the veins of the thoracic wall and axilla. When portal hypertension occurs as the result of cirrhosis, the umbilical vein, normally obliterated in early life, may open. Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins, causing them to become prominent. This appearance has been said to resemble the head (caput) of the mythical Gorgon Medusa.
Dilated abdominal veins can also be seen in the inferior vena cava syndrome [23] and the superior vena cava syndrome (if obstruction includes the azygous system) [24]. In these conditions, collateral veins tend to be more prominent in the lateral aspect of the abdominal wall. One maneuver that has been proposed to distinguish vena caval obstruction from portal hypertension is to pass a finger along dilated veins located below the umbilicus to strip them of blood and determine the direction of blood flow during refilling. In portal-systemic collateral veins, the blood flow should be directed inferiorly, away from the umbilicus, whereas vena caval collateral vein flow should be cephalad. However, the actual ability of this maneuver to discriminate between the two is limited, since in both conditions the dilated veins may lack valves and thus have bidirectional blood flow [25].
Cruveilhier-Baumgarten murmur — The Cruveilhier-Baumgarten murmur is a venous hum that may be auscultated in patients with portal hypertension. It results from collateral connections between the portal system and the remnant of the umbilical vein. It is best appreciated when the stethoscope is placed over the epigastrium. The murmur is augmented by maneuvers that increase intraabdominal pressure, such as the Valsalva maneuver, and diminished by applying pressure on the skin above the umbilicus [26].
Genitourinary findings — Males with cirrhosis may have testicular atrophy due to the development of hypogonadism. (See 'Symptoms' above.)
Extremity findings — Findings on examination of the extremities of a patient with cirrhosis may include palmar erythema, nail changes, and Dupuytren's contracture [27].
Palmar erythema is an exaggeration of the normal speckled mottling of the palm and is believed to be caused by altered sex hormone metabolism [22]. It is most frequently found on the thenar and hypothenar eminences, while sparing the central portions of the palm. Palmar erythema is not specific for liver disease and can be seen in association with pregnancy, rheumatoid arthritis, hyperthyroidism, and hematologic malignancies.
Nail changes include Muehrcke nails and Terry nails. Muehrcke nails are paired horizontal white bands separated by normal color. The exact pathogenesis is unknown, but it is believed to be caused by hypoalbuminemia [28]. They are not specific for cirrhosis since they may also be seen in other conditions associated with a low serum albumin, such as nephrotic syndrome. In patients with Terry nails, the proximal two-thirds of the nail plate appears white, whereas the distal one-third is red (picture 2). This finding is also believed to be secondary to a low serum albumin [28].
Clubbing and hypertrophic osteoarthropathy are two additional but uncommon findings in patients with cirrhosis. Clubbing is present when the angle between the nail plate and proximal nail fold is greater than 180 degrees (figure 1). Hypertrophic osteoarthropathy (HOA) is a chronic proliferative periostitis of the long bones that can cause considerable pain. Neither feature is specific for liver disease. Lung cancer and other pulmonary diseases are more commonly associated with hypertrophic osteoarthropathy, and these issues are discussed separately. (See "Overview of nail disorders", section on 'Clubbing' and "Malignancy and rheumatic disorders", section on 'Hypertrophic osteoarthropathy'.)
Dupuytren's contracture results from the thickening and shortening of the palmar fascia, which causes flexion deformities of the fingers (picture 3). Pathologically, it is characterized by fibroblastic proliferation and disorderly collagen deposition with fascial thickening. The pathogenesis is unknown but may be related to free radical formation generated by the oxidative metabolism of hypoxanthine [29]. It is relatively common in patients with alcohol-associated cirrhosis, in whom it may be found in as many as one-third of patients [30]. However, it can also be seen in several other conditions, including in workers exposed to repetitive handling tasks or vibration, and patients with diabetes mellitus cigarette smoking, alcohol consumption, and Peyronie's disease. (See "Dupuytren's contracture".)
Neurologic findings — Asterixis (bilateral but asynchronous flapping motions of outstretched, dorsiflexed hands) is seen in patients with hepatic encephalopathy. Asterixis may also be seen in patients with uremia and severe heart failure. (See "Hepatic encephalopathy in adults: Clinical manifestations and diagnosis".)
Laboratory findings — Several laboratory abnormalities may be seen in patients with cirrhosis. In addition, because it is common for panels of serum chemistries to be sent for screening or evaluation of specific complaints, laboratory abnormalities may be the first indication that a patient has cirrhosis. Common abnormalities include elevated serum bilirubin, abnormal aminotransferases, elevated alkaline phosphatase/gamma-glutamyl transpeptidase, a prolonged prothrombin time/elevated international normalized ratio (INR), hyponatremia, and thrombocytopenia. (See "Approach to the patient with abnormal liver tests".)
Liver enzymes and liver function tests — Although the term "liver function tests" (LFTs) is commonly used, it is imprecise since many of the tests reflecting the health of the liver are not direct measures of its function. The most common laboratory measures classified as LFTs include the enzyme tests (principally the serum aminotransferases, alkaline phosphatase, and gamma-glutamyl transpeptidase), the serum bilirubin, and tests of synthetic function (principally the serum albumin concentration and prothrombin time).
●Aminotransferases – Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are usually moderately elevated in patients with cirrhosis. AST is more often elevated than ALT. However, normal aminotransferases do not preclude a diagnosis of cirrhosis [31]. Most forms of chronic hepatitis other than alcohol-associated liver disease have a ratio of AST/ALT less than one. However, as chronic hepatitis progresses to cirrhosis, the ratio of AST to ALT may reverse [32,33]. (See "Approach to the patient with abnormal liver tests", section on 'AST to ALT ratio'.)
●Alkaline phosphatase – Alkaline phosphatase is usually elevated in the setting of cirrhosis, but is less than two to three times the upper normal limit. Higher levels may be seen in patients with underlying cholestatic liver disease such as primary sclerosing cholangitis or primary biliary cholangitis. (See "Enzymatic measures of hepatic cholestasis (alkaline phosphatase, 5'-nucleotidase, gamma-glutamyl transpeptidase)".)
●Gamma-glutamyl transpeptidase – Gamma-glutamyl transpeptidase (GGT) levels correlate reasonably well with alkaline phosphatase in liver disease but are nonspecific [34]. Levels of GGT are typically much higher in cirrhosis from alcohol than other causes. This may be the result of alcohol-inducing hepatic microsomal GGT [35] or alcohol causing GGT to leak from hepatocytes [36]. (See "Enzymatic measures of hepatic cholestasis (alkaline phosphatase, 5'-nucleotidase, gamma-glutamyl transpeptidase)".)
●Bilirubin – Bilirubin levels may be normal in well-compensated cirrhosis. However, they rise as the cirrhosis progresses
●Albumin – Albumin is synthesized exclusively in the liver. Albumin levels fall as the synthetic function of the liver declines with worsening cirrhosis. Thus, serum albumin levels can be used to help grade the severity of cirrhosis. Hypoalbuminemia is not specific for liver disease, since it may be seen in many other medical conditions such as heart failure, nephrotic syndrome, protein losing enteropathy, or malnutrition. (See "Tests of the liver's biosynthetic capacity (eg, albumin, coagulation factors, prothrombin time)".)
●Prothrombin time – Most of the proteins involved in the coagulation process are produced in the liver. Thus, the prothrombin time reflects the degree of hepatic synthetic dysfunction. The prothrombin time increases as the ability of a cirrhotic liver to synthesize clotting factors diminishes. It is important, however, to recognize that prothrombin time does not by itself reflect the patient's risk of bleeding. (See "Tests of the liver's biosynthetic capacity (eg, albumin, coagulation factors, prothrombin time)".)
Serum chemistries — Hyponatremia is common in patients with cirrhosis and ascites and is related to an inability to excrete free water. [37]. Hyponatremia often becomes severe as cirrhosis progresses [38]. (See "Hyponatremia in patients with cirrhosis".)
As cirrhosis progresses, patients may develop hepatorenal syndrome, with a progressive rise in serum creatinine. (See "Hepatorenal syndrome: Clinical presentation and diagnosis".)
Hematologic abnormalities — Patients with cirrhosis commonly have a number of hematologic abnormalities, including varying degrees of cytopenia. Thrombocytopenia is the most common hematologic abnormality, while leukopenia and anemia develop later in the disease course [39].
Thrombocytopenia is mainly caused by portal hypertension with attendant congestive splenomegaly. An enlarged spleen can result in temporary sequestration of up to 90 percent of the circulating platelet mass. However, this uncommonly results in platelet counts less than 20,000/mL, and unless complicated by coexisting coagulopathy, it is rarely a clinical problem [34]. Decreased thrombopoietin levels may also contribute to thrombocytopenia. (See "Clinical applications of thrombopoietic growth factors" and "Hemostatic abnormalities in patients with liver disease", section on 'Physiologic effects of hepatic dysfunction'.)
Anemia is usually multifactorial in origin; acute and chronic gastrointestinal blood loss, folate deficiency, direct toxicity due to alcohol, hypersplenism, bone marrow suppression (as in hepatitis-associated aplastic anemia), the anemia of chronic disease (inflammation), and hemolysis may all contribute. (See "Diagnostic approach to anemia in adults".)
Leukopenia and neutropenia are due to hypersplenism.
Other abnormalities — Globulins tend to be increased in patients with cirrhosis. This may be secondary to shunting of bacterial antigens in portal venous blood away from the liver to lymphoid tissue, which induces immunoglobulin production [40].
In addition to deficiency of coagulant proteins, patients may develop varying degrees of fibrinolysis with high levels of fibrinolytic markers and low fibrinogen levels, all of which may contribute to bleeding. (See "Hemostatic abnormalities in patients with liver disease".)
Radiologic findings — Radiologic studies such as abdominal ultrasound, computed tomography (CT) scan, and magnetic resonance imaging (MRI) may suggest the presence of cirrhosis. Findings may include a liver that appears shrunken, irregular, and nodular as well as caudate lobe hypertrophy. Imaging studies may also show evidence of varices (including umbilical vein recanalization) and ascites in patients with portal hypertension. At early stages, radiologic studies are roughly 80 percent sensitive and 80 percent specific for the presence of cirrhosis. (See 'Imaging studies' below.)
DIAGNOSIS —
In patients suspected of having cirrhosis, abdominal imaging (typically ultrasound) is obtained to evaluate the liver parenchyma and to detect extrahepatic manifestations of cirrhosis. A liver biopsy is required to definitively confirm the diagnosis. However, it is generally not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and the results would not alter the patient's management. Noninvasive serologic and radiographic methods for diagnosing cirrhosis are also being developed. (See "Noninvasive assessment of hepatic fibrosis: Overview of serologic tests and imaging examinations".)
When to suspect cirrhosis — Cirrhosis is often suspected in patients with [41]:
●Stigmata of chronic liver disease discovered on physical examination (table 1) (see 'Physical examination' above)
●Evidence of cirrhosis on laboratory or radiologic testing or by direct visualization while undergoing a surgical procedure
●Evidence of decompensated cirrhosis, which is characterized by the presence of complications, such as variceal hemorrhage, ascites, spontaneous bacterial peritonitis, or hepatic encephalopathy
A meta-analysis found that the factors with the best ability to predict cirrhosis in adults with known or suspected liver disease included [42]:
●Presence of ascites (likelihood ratio [LR] 7.2)
●Platelet count <160,000/mm3 (LR 6.3)
●Spider angiomata (LR 4.3)
Laboratory tests — Several noninvasive tests for the diagnosis of cirrhosis have been proposed, but none has yet emerged as a standard. Examples include the Fibrosis [FIB]-4 index, AST to platelet ratio index and FibroTest/FibroSure. Nevertheless, they can provide adjunctive information to conventional laboratory testing. (See "Noninvasive assessment of hepatic fibrosis: Overview of serologic tests and imaging examinations".)
Imaging studies — Abdominal imaging is typically obtained in patients suspected of having cirrhosis, though radiographic imaging alone is not adequately sensitive or specific to diagnose cirrhosis. The findings must be viewed in light of other signs of cirrhosis, such as physical examination or laboratory test findings. In addition to evaluating the liver, abdominal imaging may reveal hepatocellular carcinoma or extrahepatic findings suggestive of cirrhosis, such as ascites, varices, splenomegaly, and hepatic or portal vein thrombosis. Abdominal ultrasound is typically the first radiologic study obtained because it is readily available, provides information about the appearance of the liver and blood flow within the portal circulation, is less expensive than other imaging modalities, and does not expose patients to intravenous contrast or radiation.
In rare instances, radiographic findings suggest the etiology of cirrhosis. A hypertrophied caudate lobe discovered on computed tomographic (CT) scanning, for example, suggests Budd-Chiari syndrome [43]. Decreased signal intensity on magnetic resonance imaging may indicate iron overload from hereditary hemochromatosis (image 1) [44].
●Ultrasonography – Ultrasonography is routinely used during the evaluation of cirrhosis. It is noninvasive, well tolerated, widely available, and provides valuable information. In decompensated cirrhosis, the liver may appear small and nodular. Surface nodularity and increased echogenicity with irregular appearing areas are consistent with cirrhosis but can also be seen with hepatic steatosis [45,46]. There is typically atrophy of the right lobe and hypertrophy of the caudate or left lobes.
Ultrasonography may also be used as a screening test for hepatocellular carcinoma and portal hypertension. The finding of nodules on ultrasonography warrants further evaluation since benign and malignant nodules can have similar ultrasonographic appearances. Findings of portal hypertension include an increased diameter of the portal vein, the presence of collateral veins, and decreased flow within the portal circulation on Doppler imaging [2,47]. Ultrasonography is also useful for detecting splenomegaly, ascites, and portal vein thrombosis.
●Computed tomography – CT is not routinely used in the diagnosis and evaluation of cirrhosis. It provides similar information to ultrasonography, but at the expense of radiation and contrast exposure. CT findings of hepatic nodularity, atrophy of the right lobe and hypertrophy of the caudate or left lobes, ascites, or varices suggest the presence of cirrhosis, but they are not diagnostic. Patency of the portal vein can be demonstrated with CT portal phase imaging, but the direction of blood flow cannot be determined.
●Magnetic resonance imaging – The role of magnetic resonance imaging (MRI) in the diagnosis of cirrhosis is unclear. Despite much enthusiasm about the potential of MRI in the evaluation of patients with cirrhosis, its use is limited by expense, poor tolerance of the examination by some patients, and the ability to obtain information provided by MRI through other means.
●Elastography – Increasing scarring of the liver is associated with increasing "stiffness" of the tissue. Several methods have been developed to assess liver stiffness. These include standalone tests (vibration-controlled transient elastography) or add-ons to ultrasound and MRI. (See "Noninvasive assessment of hepatic fibrosis: Overview of serologic tests and imaging examinations", section on 'Imaging examinations'.)
Liver biopsy — The gold standard for diagnosing cirrhosis is examination of an explanted liver, either at autopsy or following liver transplantation, because the architecture of the entire liver can be appreciated. Cirrhosis can be diagnosed with a liver biopsy (picture 4), during which a sample of the liver is obtained by either a percutaneous, transjugular, laparoscopic, or endoscopic approach. The method for obtaining the biopsy will depend on the clinical setting [48]. The sensitivity and specificity of a liver biopsy for cirrhosis is in the range of 80 to 100 percent, depending on the method used, and the size and number of specimens obtained. (See "Approach to liver biopsy" and "Transjugular liver biopsy".)
However, liver biopsy is not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and if the results would not alter the patient's management. An example would be a patient with a history of heavy alcohol use who has ascites, severe coagulopathy, and a shrunken, nodular-appearing liver on ultrasonography.
In addition to demonstrating that cirrhosis is present, a liver biopsy can sometimes suggest the cause. This is especially true for metabolic causes of cirrhosis such as hereditary hemochromatosis (picture 5), metabolic-associated steatohepatitis (picture 6), Wilson disease (picture 7), and alpha-1 antitrypsin deficiency. (See "Approach to the patient with suspected iron overload", section on 'Liver biopsy' and "Wilson disease: Clinical manifestations, diagnosis, and natural history", section on 'Diagnostic evaluation' and "Clinical features and diagnosis of metabolic dysfunction-associated steatotic liver disease (nonalcoholic fatty liver disease) in adults".)
DETERMINING THE CAUSE OF CIRRHOSIS —
Many causes of chronic liver injury can lead to cirrhosis (table 2), and a specific etiology can be determined in 85 to 90 percent of patients [49]. Determining the etiology of cirrhosis is important because it may influence treatment decisions, permit counseling of family members, and help predict the patient's prognosis. The initial evaluation includes obtaining a history, performing a physical examination, and obtaining routine blood tests (ie, liver biochemical and function tests and a complete blood count). The findings from the initial evaluation are then used to guide additional testing. (See "Approach to the patient with abnormal liver tests", section on 'Initial evaluation'.)
If the initial evaluation does not help guide the evaluation (eg, in a patient with an unremarkable history and normal laboratory tests), testing for common causes of cirrhosis should be performed. An overview of the approach to determining the cause of a patient's liver disease is discussed in detail elsewhere. In addition, detailed discussions of the diagnosis of specific disorders can be found in their respective topic reviews. (See 'Etiologies and classification' above and "Approach to the patient with abnormal liver tests".)
WHEN TO REFER TO A SPECIALIST —
Referral to a hepatologist should be considered in patients suspected of having cirrhosis if the diagnosis remains unclear after noninvasive testing (eg, imaging and laboratory tests). In particular, referral should be considered prior to obtaining a liver biopsy. It is also reasonable to refer to a specialist to aid with determining the cause of the cirrhosis if common etiologies are ruled out (eg, hepatitis C) or to aid with management. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis", section on 'When to refer to a specialist'.)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cirrhosis".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Cirrhosis (The Basics)")
●Beyond the Basics topics (see "Patient education: Cirrhosis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Etiology – There are numerous causes of liver disease that can result in cirrhosis, either by causing chronic liver inflammation or cholestasis (table 2). (See 'Etiologies and classification' above.)
Determining the etiology of cirrhosis is important because it may influence treatment decisions, permit counseling of family members, and help predict the patient's prognosis. The initial evaluation includes obtaining a history, performing a physical examination, and obtaining routine blood tests (ie, liver biochemical and function tests and a complete blood count). The findings from the initial evaluation are then used to guide additional testing. (See "Approach to the patient with abnormal liver tests", section on 'Initial evaluation'.)
●Clinical manifestations – The clinical manifestations of cirrhosis may include nonspecific symptoms (eg, anorexia, weight loss, weakness, falls, fatigue, pruritus, muscle cramps, and sexual dysfunction) or signs and symptoms of hepatic decompensation (jaundice, signs of upper gastrointestinal bleeding, abdominal distension from ascites, confusion due to hepatic encephalopathy) (table 1). Physical examination findings may include jaundice, spider angiomata, gynecomastia, ascites, splenomegaly, palmar erythema, and asterixis. Laboratory abnormalities may include elevated serum bilirubin, abnormal aminotransferases, elevated alkaline phosphatase/gamma-glutamyl transpeptidase, a prolonged prothrombin time/elevated international normalized ratio (INR), hyponatremia, and thrombocytopenia. (See 'Laboratory findings' above.)
●When to suspect cirrhosis – Cirrhosis is often suspected in patients with (see 'When to suspect cirrhosis' above):
•Stigmata of chronic liver disease discovered on physical examination (see 'Physical examination' above)
•Evidence of cirrhosis on laboratory or radiologic testing or by direct visualization while undergoing a surgical procedure
•Evidence of decompensated cirrhosis, which is characterized by complications such as variceal hemorrhage, ascites, spontaneous bacterial peritonitis, or hepatic encephalopathy
●Radiographic imaging – In patients suspected of having cirrhosis, abdominal imaging is typically obtained, though radiographic imaging alone is not adequately sensitive or specific to diagnose cirrhosis. The findings must be viewed in light of other signs of cirrhosis such as physical examination or laboratory test findings. In addition to evaluating the liver, abdominal imaging may reveal hepatocellular carcinoma or extrahepatic findings suggestive of cirrhosis such as ascites, varices, splenomegaly, and hepatic or portal vein thrombosis. (See 'Imaging studies' above.)
Abdominal ultrasound is typically the first radiologic study obtained because it is readily available, provides information about the appearance of the liver and blood flow within the portal circulation, is less expensive than other imaging modalities, and does not expose patients to intravenous contrast or radiation.
●Methods for establishing the diagnosis – Noninvasive serologic and radiographic methods for establishing cirrhosis are discussed in detail separately. (See "Noninvasive assessment of hepatic fibrosis: Overview of serologic tests and imaging examinations".)
A liver biopsy can be performed to definitively confirm the diagnosis of cirrhosis. However, it is generally not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis and the results would not alter the patient's management. (See 'Liver biopsy' above.)
