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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 alcoholic 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 [17].
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 [18].
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 [19]. Men 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" and "Clinical features,
diagnosis, and evaluation of gynecomastia".)
Gynecomastia is defined histologically as a benign proliferation of the glandular tissue of
the male breast and clinically by the presence of a rubbery or firm mass extending
concentrically from the nipple(s). Fat deposition without glandular proliferation is termed
pseudogynecomastia (often seen in obese men). These two entities can be distinguished
by having the patient lie on his back with his hands behind his head. The examiner then
places his or her thumb and forefinger on each side of the breast, and slowly brings them
together (figure 1).
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 in part 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
[20]. 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 [21]. 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 "Hepatomegaly: Differential diagnosis
and evaluation".)
Splenomegaly Splenomegaly is common, especially in patients with cirrhosis from
nonalcoholic etiologies [22]. 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 [23]. The
differential diagnosis of splenomegaly includes several other disorders. (See "Approach
to the adult patient with splenomegaly and other splenic disorders".)
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 [24] and
the superior vena cava syndrome (if obstruction includes the azygous system) [25]. 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 poor, since in both conditions the dilated veins may lack valves and thus have
bidirectional blood flow [26].
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 [27].
Genitourinary findings Men 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, clubbing, hypertrophic
osteoarthropathy, and Dupuytren's contracture.
Palmar erythema is an exaggeration of the normal speckled mottling of the palm and is
believed to be caused by altered sex hormone metabolism [23]. 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 hematological 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
the 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 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 2). When severe, the distal finger has a "drum
stick" appearance. Hypertrophic osteoarthropathy (HOA) is a chronic proliferative
periostitis of the long bones that can cause considerable pain. Clubbing is more common
in biliary causes of cirrhosis (particularly primary biliary cirrhosis), while hypertrophic
osteoarthropathy can be seen with various causes of liver disease [29,30]. Neither
feature is specific for liver disease. The pathogenesis of clubbing and hypertrophic
osteoarthropathy is not well understood. The most frequent cause of hypertrophic
osteoarthropathy is lung cancer, which should be sought in the appropriate setting. (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 [31]. It is relatively common in
patients with alcoholic cirrhosis, in whom it may be found in as many as a third of
patients [32]. 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, reflex sympathetic dystrophy, cigarette smoking and 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 biochemical and function tests".)
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 [33]. Most forms of chronic hepatitis other than alcoholic 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 [34,35]. (See "Approach to the patient with abnormal
liver biochemical and function tests", section on 'AST to ALT ratio'.)
'Liver biopsy' and "Epidemiology, clinical features, and diagnosis of nonalcoholic fatty
liver disease in adults", section on 'Role of liver biopsy' and "Wilson disease: Diagnostic
tests", section on 'Liver biopsy'.)
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 [65]. 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 biochemical
and function 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
biochemical and function 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'.)
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 10 th 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 information: Cirrhosis (The Basics)")
Beyond the Basics topics (see "Patient information: Cirrhosis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
There are numerous causes of liver disease that can result in cirrhosis, either by
causing chronic hepatic inflammation or cholestasis (table 2). The two most common
causes of cirrhosis in the United States are alcoholic liver disease and hepatitis C, which
together accounted for approximately one-half of patients on the liver transplantation
wait list in 2011. (See 'Etiologies and classification' above.)
Ascites
Spontaneous bacterial peritonitis
Hepatic encephalopathy
Hepatocellular carcinoma
Hepatorenal syndrome
Hepatopulmonary syndrome
Once these complications develop, patients are considered to have decompensated
cirrhosis. Multiple factors can predispose to decompensation in a patient with cirrhosis.
Risk factors for decompensation include bleeding, infection, alcohol intake, medications,
dehydration, and constipation [3-5]. In addition, patients with obesity are at increased
risk for decompensation [6]. Once decompensation has developed, patients should be
considered for liver transplantation. (See "Liver transplantation in adults: Patient
selection and pretransplantation evaluation" and "Liver transplantation in adults: Patient
selection and pretransplantation evaluation", section on 'Cirrhosis'.)
Other major complications of cirrhosis include portal vein thrombosis and
cardiomyopathy. However, patients with these complications alone are not considered to
have decompensated cirrhosis.
This section provides an overview of the complications of cirrhosis. The individual
complications are discussed in detail in their respective topic reviews.
Complications of portal hypertension Many of the complications of cirrhosis are the
result of portal hypertension (increased pressure within the portal venous system). This
can lead to the formation of venous collaterals (varices) as well as circulatory, vascular,
functional, and biochemical abnormalities that contribute to the pathogenesis of ascites
and other complications. (See "Portal hypertension in adults" and "Pathogenesis of
ascites in patients with cirrhosis", section on 'Portal hypertension'.)
Complications of portal hypertension include:
Ascites
Hepatic encephalopathy
Variceal hemorrhage
Spontaneous bacterial peritonitis
Hepatorenal syndrome
Portal hypertensive gastropathy
Hepatic hydrothorax
Hepatopulmonary syndrome
Portopulmonary hypertension
Cirrhotic cardiomyopathy
Variceal hemorrhage Patients with variceal hemorrhage typically present with
hematemesis and/or melena. It is typically treated with endoscopic variceal band
ligation. Other treatments include endoscopic sclerotherapy and placement of a
transjugular intrahepatic portosystemic shunt (TIPS). (See "General principles of the
management of variceal hemorrhage".)
Variceal hemorrhage is associated with high mortality rates. In the past, the mortality
rate of a single variceal hemorrhage was 30 percent, and only one-third of patients
survived for one year [7,8]. Although survival has improved with modern techniques for
controlling variceal hemorrhage, mortality rates remain high (15 to 20 percent 30-day
mortality) [9].
Portal hypertensive gastropathy Portal hypertensive gastropathy (congestive
gastropathy), while extremely common in patients with portal hypertension, is an
uncommon cause of significant bleeding in these patients. When portal hypertensive
gastropathy is the sole cause of bleeding, there is diffuse mucosal oozing with no other
lesions, such as varices, to account for the GI bleeding and anemia. The mucosa is
friable, and bleeding presumably occurs when the ectatic vessels rupture. The severity of
gastropathy is related to the level of portal pressure, the level of hepatic vascular
resistance, and the degree of reduction in hepatic blood flow (See "Uncommon causes of
upper gastrointestinal bleeding in adults", section on 'Portal hypertensive gastropathy'.)
Ascites Ascites is the accumulation of fluid within the peritoneal cavity. It is the most
common complication of cirrhosis. The first step leading to fluid retention and ultimately
ascites in patients with cirrhosis is the development of portal hypertension. Patients
without portal hypertension do not develop ascites or edema. Those with ascites have
several circulatory, vascular, functional, and biochemical abnormalities that contribute to
the pathogenesis of fluid retention. (See "Pathogenesis of ascites in patients with
cirrhosis".)
Ascites is typically treated with a combination of diuretics and sodium restriction, though
some patients require repeated therapeutic paracenteses or TIPS placement. Among
patients with refractory ascites or spontaneous bacterial peritonitis, the use of
nonselective beta blockers may be associated with increased mortality [10,11]. This may
occur because failure to maintain an adequate mean arterial blood pressure is strongly
correlated with survival in patients with advanced cirrhosis. (See "Ascites in adults with
cirrhosis: Initial therapy" and "Ascites in adults with cirrhosis: Diuretic-resistant ascites",
section on 'Discontinuing beta blockers' and 'Decompensated cirrhosis' below and
"Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis", section on
'Discontinue nonselective beta blockers'.)
Spontaneous bacterial peritonitis Spontaneous bacterial peritonitis (SBP) is an
infection of preexisting ascitic fluid without evidence for an intra-abdominal secondary
source, such as a perforated viscus. SBP is almost always seen in the setting of end-stage
liver disease. Clinical manifestations of SBP include fever, abdominal pain, abdominal
tenderness, and altered mental status. Some patients are asymptomatic and present
with only mild laboratory abnormalities. (See "Spontaneous bacterial peritonitis in adults:
Clinical manifestations".)
The index of suspicion for SBP must be high with a low threshold for diagnostic
paracentesis. The diagnosis is established by a positive ascitic fluid bacterial culture
and/or an elevated ascitic fluid absolute polymorphonuclear leukocyte count (250
cells/mm3). Without early antibiotic treatment, mortality is high. (See "Spontaneous
bacterial peritonitis in adults: Diagnosis" and "Spontaneous bacterial peritonitis in adults:
Treatment and prophylaxis".)
nonselective beta blocker or endoscopic variceal ligation, which reduces the risk of
variceal bleeding. (See "Primary and pre-primary prophylaxis against variceal
hemorrhage in patients with cirrhosis".)
Hepatocellular carcinoma: Patients with cirrhosis should undergo surveillance with
ultrasonography every six months. (See "Prevention of hepatocellular carcinoma and
recommendations for surveillance in adults with chronic liver disease", section on
'Surveillance methods'.)
Spontaneous bacterial peritonitis: The risk of spontaneous bacterial peritonitis
(SBP) can be reduced by efforts to judiciously diurese patients since diuresis
concentrates ascitic fluid, thereby raising ascitic fluid opsonic activity. Early recognition
and aggressive treatment of localized infections (eg, cystitis, cellulitis) can also help to
prevent bacteremia and SBP. Proton pump inhibitor use has been associated with an
increased risk of SBP, so proton pump inhibitors should only be given to patients who
have clear indications for their use. Finally, prophylactic antibiotics aimed at
decontaminating the gut have a role in specific clinical settings. (See "Spontaneous
bacterial peritonitis in adults: Treatment and prophylaxis".)
Hepatic encephalopathy: Patients with cirrhosis should be evaluated regularly for
hepatic encephalopathy, the earliest features of which can be subtle. Events that can
precipitate hepatic encephalopathy include the development of variceal bleeding,
infection (such as SBP), the administration of sedatives, hypokalemia, and hyponatremia,
all of which should be corrected/avoided whenever possible (table 4). (See "Hepatic
encephalopathy in adults: Clinical manifestations and diagnosis" and "Hepatic
encephalopathy in adults: Treatment".)
Portal vein thrombosis: Enoxaparin may be effective for preventing portal vein
thrombosis (PVT) in patients with cirrhosis, though it is not used routinely. If it is to be
used, we suggest eradication of varices (if present) prior to initiation of anticoagulation
when possible. (See "Chronic portal vein thrombosis in adults: Clinical manifestations,
diagnosis, and management", section on 'Prevention in patients with cirrhosis' and
"Primary and pre-primary prophylaxis against variceal hemorrhage in patients with
cirrhosis", section on 'Endoscopic variceal ligation'.)
Hepatorenal syndrome: Nephrotoxic agents (such as aminoglycosides) and vigorous
diuresis should be avoided in patients with cirrhosis since they can precipitate renal
failure. (See "Hepatorenal syndrome".)
Secondary infections: Patients with cirrhosis who are hospitalized often acquire
infections while in the hospital. Factors that have been associated with hospital-acquired
secondary infections in patients with cirrhosis include the use of urinary catheters,
mechanical ventilation, and the placement of central lines [43]. Many of these
interventions are performed routinely (such as placement of urinary catheters to
measure urine output). However, avoiding these interventions unless they are absolutely
necessary may decrease the risk of acquiring an infection while in the hospital, and it is
our practice to only use these interventions when clearly indicated.
In a study of 207 patients with cirrhosis who were admitted with or developed an
infection during hospitalization, 50 (24 percent) developed a second infection during
hospitalization [43]. Respiratory infections were the most common (14 patients), followed
by urinary tract infections (13 patients), and Clostridium difficile. Of the urinary tract
infections, 6 (46 percent) were related to the use of bladder catheters. Other factors
associated with second infections included intensive care unit admission, the use of
central lines, mechanical ventilation, shock, renal replacement therapy, and hepatic
encephalopathy. Overall mortality was 39 percent, but it was 48 percent for those who
developed a second infection during admission.
Among patients with cirrhosis and severe septic shock, administration of hydrocortisone
may improve outcomes [49]. (See "Treatment of adrenal insufficiency in adults", section
on 'Glucocorticoid regimens'.)
Other factors associated with poor survival in patients with decompensated cirrhosis
included hepatopulmonary syndrome, rapidly progressive hepatorenal syndrome, and
intensive care unit admission for complications of liver disease along with hypotension
requiring pressor support, serum creatinine >1.5 mg/dL, or jaundice.
Patients with decompensated cirrhosis often require liver transplantation. For those who
are not candidates, hospice care can be considered for patients with predicted survival of
6 months. (See "Liver transplantation in adults: Patient selection and pretransplantation
evaluation" and "Palliative care: Benefits, services, and models of care".)
Predictive models Multiple studies have attempted to predict the prognosis of patients
with cirrhosis based on clinical and laboratory information. Two commonly used models
are the Child-Pugh classification and the Model for End Stage Liver Disease (MELD).
Child-Pugh classification The Child-Pugh classification (table 5) has been used to
assess the risk of non-shunt operations in patients with cirrhosis (calculator 1 and
calculator 2) [50]. It is a modification of the Child-Turcotte classification which
incorporated five variables that were designed to stratify the risk of portacaval shunt
surgery in patients with cirrhosis. The variables included the serum albumin and bilirubin,
ascites, encephalopathy, and nutritional status (table 6) [51]. The Child-Pugh
classification replaces nutritional status with prothrombin time. The score ranges from 5
to 15. Patients with a score of 5 or 6 have Child-Pugh class A cirrhosis (well-compensated
cirrhosis), those with a score of 7 to 9 have Child-Pugh class B cirrhosis (significant
functional compromise), and those with a score of 10 to 15 have Child-Pugh class C
cirrhosis (decompensated cirrhosis).
In a review of 92 patients with cirrhosis who underwent abdominal surgery, the mortality
rate was 10 percent for patients with Child-Pugh class A cirrhosis, 30 percent for patients
with Child-Pugh class B cirrhosis, and 82 percent for patients with Child-Pugh class C
cirrhosis [52]. Other studies have validated the utility of the Child-Pugh classification for
the assessment of surgical risk [53]. (See "Assessing surgical risk in patients with liver
disease".)
The Child-Pugh classification system also correlates with survival in patients not
undergoing surgery; one-year survival rates for patients with Child-Pugh class A, B, and C
cirrhosis are approximately 100, 80, and 45 percent, respectively [54,55]. Child-Pugh
class is also associated with the likelihood of developing of complications of cirrhosis. As
an example, patients with Child-Pugh class C cirrhosis are much more likely to develop
variceal hemorrhage than those with Child-Pugh class A cirrhosis [56].
MELD score Another model to predict prognosis in patients with cirrhosis is the Model
for End Stage Liver Disease (MELD) score. It is based upon bilirubin levels, creatinine,
INR, and the etiology of cirrhosis (calculator 3 and calculator 4). The MELD score has
been adopted for use in prioritizing patients awaiting liver transplantation and has an
expanding role in predicting outcomes in patients with liver disease in the nontransplantation setting. (See "Model for End-stage Liver Disease (MELD)".)
WHEN TO REFER TO A SPECIALIST Referral to a hepatologist is recommended if the
patient develops decompensated cirrhosis or major complications of cirrhosis. Patients
with a MELD score 10 should be referred to a liver transplantation center for evaluation.
In addition, referral to a hepatologist should be considered if the patient requires
treatment for the underlying cause of the cirrhosis (eg, hepatitis C, autoimmune
hepatitis) or if the clinician managing the patient would like the assistance of a
Slowing or reversing the progression of liver disease (see 'Slowing or reversing the
progression of liver disease' above)
Preventing superimposed insults to the liver (see 'Preventing superimposed insults to
the liver' above)
Identifying medications that require dose adjustments or should be avoided entirely
(table 2 and table 3) (see 'Medication adjustments' above)
Managing symptoms and laboratory abnormalities (see 'Management of symptoms and
laboratory abnormalities' above)
Preventing and treating the complications of cirrhosis (see 'Preventing and identifying
complications' above)
Determining the appropriateness and optimal timing for liver transplantation (see 'Liver
transplantation' above)
The prognosis of cirrhosis is highly variable since it is influenced by a number of factors,
including etiology, severity, presence of complications, and comorbid diseases. Once
decompensation occurs (eg, the patient develops variceal bleeding, hepatic
encephalopathy, or spontaneous bacterial peritonitis), mortality rates are high. (See
'Decompensated cirrhosis' above.)