Cirrhosis

Cirrhosis is the final stage of chronic liver disease (CLD) and it is characterized by regenerative nodules and fibrous septae in liver parenchyma in response to chronic hepatic injury. Cirrhosis is most commonly due to excessive alcohol consumption, metabolic dysfunction-associated steatotic liver disease, or hepatitis C. Other causes include inflammatory or metabolic diseases, such as primary biliary cirrhosis and hemochromatosis. Subsequent hepatic repair mechanisms lead to fibrosis progressing to cirrhosis with abnormal tissue architecture and impaired liver function. Patients can present with a range of symptoms, including ascites; hepatosplenomegaly; and skin manifestations of cirrhosis, such as jaundice, spider angiomata, and/or palmar erythema. Men may also present with signs of feminization (e.g., gynecomastia, hypogonadism). In severe cases, the accumulation of toxic metabolites or involvement of additional organs can lead to complications such as hepatic encephalopathy and hepatorenal syndrome (HRS). Laboratory study findings indicate hepatocyte damage (e.g., elevated liver enzymes, hyperbilirubinemia) and/or impaired hepatic synthetic function (e.g., prolonged prothrombin time, low albumin). Abdominal ultrasound typically shows atrophic, heterogeneous liver parenchyma with a nodular surface. A biopsy is the method of choice for confirming the diagnosis; however, it is usually only performed if the results from other diagnostic modalities are inconclusive. Management consists of treatment of the underlying disease (e.g., avoidance of toxic substances, antiviral drugs), adequate calorie intake, and treating complications, e.g., esophageal varices, hepatocellular carcinoma (HCC). In cases of decompensated cirrhosis, interventional procedures may be used to alleviate symptoms (e.g., paracentesis to drain ascites) or as a bridge until liver transplantation is possible.

For details about pulmonary complications that occur in individuals with cirrhosis (e.g., hepatopulmonary syndrome, portopulmonary hypertension, and hepatic hydrothorax), see "Pulmonary complications of cirrhosis."

• Liver fibrosis: the reversible proliferation of fibroblasts and accumulation of excessive extracellular matrix components (e.g., crosslinked type 1 collagen) in liver parenchyma in response to hepatic injury [1]
• Advanced chronic liver disease (ACLD): suspected cirrhosis in the absence of biopsy, based on liver elastography and platelet count [2]
• Cirrhosis: the final stage of CLD; characterized by regenerative nodules and fibrous septae (usually irreversible) in liver parenchyma in response to hepatic injury [2][3]
• Compensated cirrhosis: the asymptomatic stage of cirrhosis in which complications of portal hypertension (e.g., overt ascites, variceal bleeding, hepatic encephalopathy) are absent; evidence of portal hypertension (e.g., gastroesophageal varices) may be present.
• Decompensated cirrhosis: the development of complications of portal hypertension (e.g., overt ascites, variceal bleeding, hepatic encephalopathy) in a patient with cirrhosis; often triggered by an acute event (e.g., infection, alcohol intake, certain medications) but can also develop gradually (e.g., accumulation of fluid in ascites)

• Prevalence: approx. 0.27% in US adults [4]
• Sex: ♂ > ♀ (2:1) [5]
• Mortality [5]
  • Responsible for approx. 1–2% of all deaths in the US (12^th leading cause of death)
  • Most deaths occur in the fifth to sixth decade of life.

Epidemiological data refers to the US, unless otherwise specified.

See also “Etiology of chronic liver disease.”

• Chronic hepatitis C (most common cause of cirrhosis in the US)
• Chronic alcohol use disorder (AUD)
• Metabolic dysfunction-associated steatotic liver disease (MASLD)
• Autoimmune conditions: e.g., type 1 AIH, PBC, PSC
• Genetic conditions: e.g., hereditary hemochromatosis, Wilson disease, α1-antitrypsin deficiency
• Hepatic vein congestion or vascular anomalies: e.g., Budd-Chiari syndrome, cardiac cirrhosis
• Cryptogenic cirrhosis: cirrhosis of unknown etiology despite adequate diagnostics

Cryptogenic cirrhosis is a diagnosis of exclusion and should only be considered after a complete patient evaluation has ruled out all other possible causes of cirrhosis.

Hepatitis C, alcohol-associated liver disease, and MASLD are the most common causes of cirrhosis worldwide. [6]

• Cirrhosis is characterized by irreversible diffuse fibrosis of the liver (the final common pathway for chronic liver diseases).
• Pathogenesis is multifactorial.
  • Different liver cells and cytokines are involved in the activation and progression of liver fibrosis.
  • Cytokine‑mediated activation of hepatic stellate cells has been identified as a central element for developing fibrosis.
• The following three mechanisms have been described for all types of liver cirrhosis: [7]
  1. Degeneration and necrosis of hepatocytes
     • Activated Kupffer cells destroy hepatocytes, activate hepatic stellate cells, and promote inflammation.
     • Inflammatory cytokines (e.g., TGF-β, PDGF) → hepatocyte apoptosis and hepatic stellate cell activation → excess collagen production
  2. Fibrotic tissue and regenerative nodules replace the liver parenchyma
     • Hepatocyte destruction triggers repair mechanisms → excess formation of connective tissue (fibrosis)
     • Excessive connective tissue in periportal zone and centrilobular zone → regenerative nodules and fibrous septa → compression of hepatic sinusoids and venules → ↑ portal vein hydrostatic pressure → intrasinusoidal hypertension → ↓ functional sinusoids
  3. Loss of liver function: sinusoidal capillarization → loss of fenestration and scar tissue formation→ impaired substrate exchange → loss of normal liver function (exocrine and metabolic)

Cirrhosis can be asymptomatic or manifest with nonspecific features. Symptoms are triggered by an acute event (e.g., infection, certain medications) or due to gradual progression of liver damage.

Nonspecific features

• Patients are often initially asymptomatic.
• Fatigue, malaise, anorexia, and weight loss

Specific features

Dermal features

• Pruritus
• Jaundice
• Telangiectasia: most commonly spider angioma (a central red arteriole with numerous, thin arterial extensions, commonly manifesting on light, sun-exposed skin and the trunk)
• Caput medusae
• Palmar erythema (plantar erythema also possible) [8]
• Nail clubbing
• Petechiae and purpura
• Generally dry and atrophic skin
• White nails with ground-glass opacity (also known as “Terry nails”)
• Lacquered lips, smooth red tongue

Abdominal features

• Nausea, vomiting
• Hepatomegaly (possibly causing dull RUQ pain)
• Splenomegaly
• Ascites

Hormonal disorders

• Hyperestrogenism [9]
  • Changes in the hepatic metabolization of sex hormones cause an imbalance in the estrogen-androgen ratio, resulting in a marked increase in systemic estrogen levels.
  • In men, increased estrogen levels cause feminization.
    • Gynecomastia
    • Hypogonadism; (e.g., testicular atrophy, reduced libido, erectile dysfunction, infertility)
    • Decreased body hair (e.g., loss of chest hair, a female pattern of pubic hair distribution)
  • In women, a massive increase in estrogen can cause amenorrhea.

Other

• Asterixis
• Fetor hepaticus: bad breath with a characteristic sweet, pungent smell caused by an accumulation of dimethyl sulfide
• Dupuytren contracture (in patients with cirrhosis due to AUD) [10][11]
• Peripheral edema [12]
• See also “Clinical features” in “Portal hypertension.”

Specific clinical features due to rare causes

• Hemochromatosis: dark, bronze skin color, and diabetes (bronze diabetes)
• Wilson disease
  • Neurological/psychiatric symptoms (parkinsonism and personality changes)
  • Indirect hyperbilirubinemia due to hemolysis.
• Alpha‑1 antitrypsin deficiency: lung emphysema (typically before 50 years of age) [13]

General principles [14][15]

• Diagnosis is typically based on a combination of typical clinical features, laboratory findings, and features on imaging.
• Initial evaluation
  • Routine laboratory studies and screening for the underlying etiology (e.g., viral hepatitis panel)
  • Abdominal ultrasound to evaluate the liver parenchyma and detect complications
• Additional evaluation (e.g., noninvasive liver fibrosis assessment, liver biopsy) may be needed to stage fibrosis or if the etiology remains unclear.

Patients with cirrhosis are usually either asymptomatic with incidental abnormal findings on laboratory studies or imaging, or present late with features of decompensated cirrhosis.

Laboratory studies

Routine laboratory studies [14][16][17]

Laboratory findings are nonspecific and the presence and degree of abnormality may vary.

• Liver chemistries
  • Transaminases: ↑ ALT and AST
    • ALT > AST: present in most liver diseases (e.g., MASLD, viral hepatitis)
    • AST > ALT: indicative of alcohol-associated liver disease and/or cirrhosis of any etiology
    • Massive AST and/or ALT elevation (> 15 times ULN): Consider differential diagnoses (e.g., acetaminophen toxicity, acute viral hepatitis, autoimmune hepatitis).
  • ↑ Bilirubin (may be normal initially)
  • ↑ ALP
  • ↑ Gamma‑glutamyl transferase (GGT)
• Coagulation studies: ↑ prothrombin time (↑ INR) because of decreased production of coagulation factors
• CBC
  • Thrombocytopenia: due to decreased thrombopoietin production by the liver and/or splenomegaly [16]
  • Anemia: multiple potential causes, e.g., vitamin B₁₂ or folate deficiency , chronic blood loss, splenic sequestration
  • Leukopenia
• CMP
  • ↓ Albumin
  • ↓ Total protein
  • Hyponatremia

Liver chemistries may be normal in early compensated cirrhosis. [14]

Some CBC abnormalities are due to the combination of increased hepatic and splenic sequestration of thrombocytes (portal hypertension leads to splenomegaly with hypersplenism) and decreased production of hematopoietic factors by the liver.

Hepatocyte injury: ↑ AST, ALT, ALP, GGT. Synthetic dysfunction: ↑ bilirubin and PT/INR; ↓ albumin and platelets

Additional laboratory studies [14][17][18][19]

These studies may help to identify the underlying etiology and further evaluate liver function. Modification may be required based on clinical features and the presence of risk factors.

• Viral hepatitis: especially in patients with risk factors
  • Hepatitis B and hepatitis C: HBsAg, IgM anti-HBc, anti-HCV
  • Hepatitis A and hepatitis E: IgM HAV, IgM HEV
• MASLD: fasting lipid levels and HbA1c
• Hemochromatosis: serum iron, ferritin, transferrin saturation
• Alcohol-associated liver disease: assess for alcohol use disorder; consider measuring alcohol biomarkers.
• Autoimmune hepatitis: total IgG or serum electrophoresis (showing hypergammaglobulinemia), ANA, ASMA, anti-LKM-1 antibody, anti-soluble liver antigen antibody
• Alpha-1 antitrypsin deficiency: alpha-1 antitrypsin level and phenotype
• Wilson disease: serum ceruloplasmin, serum total and free copper, urinary copper
• Primary biliary cholangitis: antimitochondrial antibodies (AMA or AMA-M2), ALP, bilirubin
• Primary sclerosing cholangitis: cholestasis parameters (GGT, ALP, and bilirubin), pANCA, IgG
• Other tests [20][21]
  • Ammonia (not routinely indicated) [21]
  • Plasma cholinesterase
  • Serum protein electrophoresis: ↓ albumin band, ↑ gamma band, and unchanged alpha‑1, alpha‑2, and beta globulin fractions [20]

Imaging

Abdominal ultrasound with Doppler [14][22]

• Indications
  • Suspected cirrhosis: best initial test
  • Established cirrhosis: for HCC screening and detecting complications
• Findings
  • Liver form and structure
    • Nodular liver surface
    • Atrophy of the right lobe
    • Loss of structural homogeneity (hyperechoic or variable increase in echogenicity) with fibrous septa
  • Liver size
    • Initially enlarged [23]
    • Atrophy with disease progression [23]
    • Hypertrophy of the caudate lobe and left lobe [22][24]
    • Atrophy of segment IV
  • Other possible findings
    • Changes in liver vasculature
    • Complications of portal hypertension: ascites, splenomegaly, portal vein thrombosis (PVT), increased portosystemic collateral flow [25]

CT abdomen [22][26]

• Indication: patients in whom adequate assessment with ultrasound is not possible (e.g., because of obesity)
• Findings: similar to those on ultrasound
  • Relative hypertrophy of the left lobe and caudate lobe
  • Regenerative nodules
  • Irregular liver surface
  • Indirect findings: ascites, splenomegaly, portosystemic collaterals

Noninvasive liver fibrosis assessment

Blood biomarker-based scores [14][27]

These biomarker-based tools can be used as an adjunct to confirm and stage cirrhosis of certain etiologies.

• AST-to-platelet ratio index (APRI)
  • Indications: chronic hepatitis B and C, MASLD, AIH, and PBC
  • Parameters: AST and platelet count
  • Interpretation: APRI > 1 is suggestive of cirrhosis.
• Fibrosis-4 score
  • Indications: chronic hepatitis B and C and MASLD
  • Parameters: age, platelet count, AST and ALT levels
  • Interpretation: Thresholds for identifying advanced fibrosis depend on the underlying cause.
• NAFLD fibrosis score
  • Indication: MASLD
  • Parameters: age, BMI, AST, ALT, platelet count, albumin, and diabetes (or impaired fasting glucose)
  • Interpretation: A score > 0.676 is predictive of advanced fibrosis in MASLD.

Liver elastography [14][28][29]

• Definition: an imaging technique that measures liver stiffness to help determine the degree of fibrosis
• Indications
  • Diagnosis and staging of liver fibrosis and cirrhosis in adults with chronic HCV, chronic HBV, MASLD, ALD, or chronic cholestatic liver disease [30]
  • Diagnostic confirmation of suspected portal hypertension
• Modalities
  • Transient elastography (most common): uses a device (FibroScan®) that only performs elastography; no direct visualization of the liver [29]
  • Acoustic radiation force impulse: integrated into a conventional ultrasound system, enabling simultaneous elastography and visualization of the liver [31]
  • Magnetic resonance elastography: uses MRI to generate a map of tissue stiffness (i.e., elastogram) according to the propagation of induced shear waves [32]

Liver biopsy [14][17]

• Indications
  • In cases of diagnostic uncertainty (gold standard)
  • Grading and staging of inflammation and fibrosis (e.g., using the IASL score or METAVIR score)
  • Monitoring treatment response (e.g., in autoimmune hepatitis)
  • Evaluation of focal lesions
• Findings: See “Pathology.”

Noninvasive studies can identify mild fibrosis and advanced fibrosis but cannot accurately identify intermediate stages; therefore, invasive studies may be needed.

MELD and Child-Pugh scores are essential for assessing liver disease severity and guiding treatment decisions.

Model for end-stage liver disease score (MELD score) [33]

• Used to predict the three-month mortality rate of patients with cirrhosis
• Primarily used to prioritize patients for liver transplantation [33]
• Patients are given a score from 6 to 40 based on serum bilirubin, INR, and creatinine levels.
• Patients with high scores have the worst prognosis without intervention and should therefore be prioritized for transplantation (if appropriate)

Child-Pugh score [34]

• A prognostic grading scale that assesses survival rate and predicts the likelihood of developing complications based on bilirubin and albumin levels, prothrombin time, and the presence of ascites and encephalopathy
• Can be used as a prognostic scoring system [35]
  • Child‑Pugh class A: one-year survival rate of ∼ 100%
  • Child‑Pugh class B: one-year survival rate of ∼ 80%
  • Child‑Pugh class C: one-year survival rate of ∼ 45%

CHILD's ABCDEs: Albumin, Bilirubin, Coagulation (i.e., ↑ INR), Distended abdomen (i.e., ascites), and Encephalopathy

Treat the underlying condition (e.g., treatment of AUD, antivirals for HCV) and refer to a specialist (e.g., hepatologist) to optimize management.

Supportive care for cirrhosis [3][14][36][37]

• Encourage alcohol abstinence
  • Complete abstinence is recommended.
  • Initiate treatment for alcohol use disorder if present.
• Reconcile medication list
  • Stop hepatotoxic medications.
  • Avoid prescribing medications associated with complications, e.g.: [36]
    • NSAIDs
    • Opioids
    • Benzodiazepines in patients with hepatic encephalopathy
    • Medications that reduce effective arterial volume (e.g., ACE inhibitors, ARBs) in patients with ascites [38]
• Reduce the risk of infection-associated complications, e.g.:
  • Recommended immunizations: pneumococcal (PPSV23), hepatitis A, hepatitis B, influenza, SARS-CoV-2, and tetanus vaccination [39]
  • Avoidance of raw seafood and unpasteurized dairy [14]
• Address nutritional status [37]
  • Routinely assess for malnutrition, including:
    • Micronutrient deficiencies (e.g., zinc deficiency, vitamin D deficiency)
    • Frailty assessment and/or sarcopenia assessment (e.g., hand grip strength, calf circumference)
    • See “Clinical evaluation” and “Diagnosis” in “Unintentional weight loss and malnutrition in adults.”
  • Dietary recommendations
    • Aim for 1.0–1.5 g of protein per kilogram of dry body weight daily; protein restriction is not recommended. [37]
    • Recommend eating frequent small meals.
    • Consider early specialized nutritional support to hospitalized patients with cirrhosis.

Screening for complications

HCC and portal vein thrombosis [2]

• Abdominal ultrasound every 6 months in patients with compensated cirrhosis [2]
• See “Screening for hepatocellular carcinoma” and “Portal vein thrombosis” for details.

Esophageal varices [2][40]

For patients with known varices, see “Monitoring of low-risk varices” in “Esophageal varices.”

• Decompensated cirrhosis: EGD upon diagnosis to assess for varices and high-risk features for esophageal variceal hemorrhage
• Compensated cirrhosis with evidence of CSPH
  • EGD in patients not already treated with a nonselective beta blocker (NSBB) who have both:
    • Liver stiffness > 20 kPa on transient elastography [2]
    • Platelet count ≤ 150,000/mm³ [2]
  • Frequency
    • Every 2 years if ongoing liver injury [2]
    • Every 3 years if no ongoing liver injury [2]
• Compensated cirrhosis without CSPH: annual platelet count and liver stiffness assessment (with transient elastography), or EGD if noninvasive liver fibrosis assessment is unavailable

Do not screen for esophageal varices with EGD if results will not change management (e.g., patients without CSPH who have liver stiffness < 20 kPa AND platelet count > 150,000/mm³, patients already treated with NSBBs). [2]

Management of common complications

• See “Treatment of ascites” for details on:
  • Fluid restriction if hyponatremic [38]
    • Serum sodium level < 125 mmol/L: < 1L/day and cessation of diuretics
    • Serum sodium level < 120 mmol/L: Consider IV albumin and additional fluid restriction.
  • Dietary sodium restriction, e.g., ≤ 2 g/day [38]
  • Pharmacotherapy, e.g., spironolactone (off-label) [38]
  • Paracentesis indications and considerations
  • Management of refractory ascites
• See “Spontaneous bacterial peritonitis” for details on:
  • Prophylaxis for SBP
  • Indications for diagnostic paracentesis in SBP
  • Peritoneal fluid analysis in SBP
  • Empiric antibiotic therapy for SBP
  • Adjunctive therapy, e.g., IV albumin (off-label) [38]
  • Monitoring, e.g., repeat paracentesis after 48 hours to assess response to antibiotics [38]
  • Acute management checklist for SBP
• See “Esophageal varices” for details on:
  • Prophylaxis against variceal bleeding with NSBBs, e.g., carvedilol [2]
  • Management of esophageal variceal hemorrhage
    • Vasoactive medication, e.g., octreotide (off-label) [41]
    • Antibiotic prophylaxis, e.g., ceftriaxone (off-label) [38]
• See “Treatment of hepatic encephalopathy” for details on:
  • Treatment with lactulose
  • Disposition
  • Prevention with lactulose and rifaximin
• See “Hepatorenal syndrome” for details on:
  • Diagnostic criteria for HRS-AKI
  • Treatment for HRS-AKI (e.g., terlipressin, renal replacement therapy)

Liver transplant [42]

• Liver transplant is the only curative treatment option.
• Indications for liver transplant evaluation include:
  • Occurrence of an index complication (i.e., ascites, hepatic encephalopathy, variceal hemorrhage)
  • Hepatocellular dysfunction resulting in a MELD score of ≥ 15

Cirrhosis (decompensated, inpatient management)

Assessment: This is a @AGE@-year-old @SEX@ with a history of cirrhosis secondary to [**alcohol, hepatitis C, MASH] presenting with evidence of decompensation. Current issues include [ascites [**new-onset, refractory, associated with abdominal discomfort]; hepatic encephalopathy [**confusion, asterixis, somnolence]; variceal bleeding [**hematemesis, melena]; infection [**SBP, sepsis]]. Precipitating factors include [**infection, gastrointestinal bleeding, alcohol use, medication nonadherence].

Plan

Disposition

–[ICU admission] (if hemodynamically unstable)

–OR [Inpatient admission] (if hemodynamically stable)

Diagnostics [if not already done]

–Initial labs: CBC, CMP, coagulation studies, blood cultures, ammonia level

–Imaging: abdominal ultrasound with Doppler to evaluate for portal vein thrombosis

–Ascitic fluid analysis (if ascites present)

–Cell count, differential, protein, albumin, and culture

–Serum-ascitic albumin gradient to differentiate causes

Monitoring

–BP: goal MAP ≥ 65 mm Hg

–Daily assessment for hepatic encephalopathy

–Daily BMP, urine output

Ascites

–Sodium restriction: < 2 g/day

–Diuretics: spironolactone 100 mg and furosemide 40 mg (adjust in a 10:4 ratio based on response)

–Goal weight loss: 0.5–1 kg/day

–Tense ascites: large-volume paracentesis with albumin infusion (6–8 g per L of fluid removed)

Hepatic encephalopathy

–Lactulose: 30–45 mL PO every 1–2 hours to induce rapid laxation

–Rifaximin 400 mg PO every 8 hours (add if recurrent or persistent encephalopathy)

Variceal bleeding (if present or suspected)

–GI consult for urgent upper endoscopy within 12–24 hours for suspected bleeding

–Octreotide 50 mcg bolus, then 50 mcg/hour continuous infusion

–Prophylactic antibiotics: ceftriaxone 1 g IV once daily for 7 days

Infection [**SBP or other infections]

–Cefotaxime 2 g IV every 8 hours for suspected SBP

–Treat sepsis with IV fluids and broad-spectrum antibiotics as per source.

Chronic liver disease

–Avoid alcohol, NSAIDs, sedatives, and unnecessary medications.

–Carvedilol for variceal bleed prevention

–Immunizations: pneumococcal, hepatitis A and B, influenza, SARS-CoV-2, and tetanus

Referral for liver transplant evaluation

–Indicated for decompensated cirrhosis or MELD score ≥ 15

–Consult hepatology for evaluation of transplant candidacy.

F/E/N

–Protein intake: 1.0–1.5 g/kg/day; avoid restriction unless encephalopathy is refractory.

–Caloric intake: 25–35 kcal/kg/day

–Fluid restriction (if serum sodium < 120 mmol/L)

• Fibrosis (fibrous septa)
• Replacement of normal liver tissue with collagenous regenerative nodules (histological staging is based on the size of the regenerative nodules) [43]
• Abnormal cell activation with infiltration of inflammatory cells
• Loss of physiological vessel architecture (central vein disappearance)

• See “Alcohol-associated liver disease,” “Hepatitis B,” and “Hepatitis C” for specific pathological findings related to these conditions.

Overview [38]

Cirrhosis-associated ascites and edema and elevated bleeding risk increase the risk for hypovolemic shock.

Vitamin K infusion may improve clotting function in select patients with vitamin K deficiency; it is unlikely to be effective in patients with advanced liver disease and coagulopathy.

We list the most important complications. The selection is not exhaustive.

• Definition: the development of overt ascites, overt hepatic encephalopathy, or variceal bleeding in patients with cirrhosis [2]
• Onset: can be triggered by an acute event (e.g., bleeding, sepsis) or develop gradually (e.g., ascites, encephalopathy) [46][47]
• Common precipitating factors[47]
  • Infection (e.g., spontaneous bacterial peritonitis) or sepsis
  • Alcohol consumption
  • Medications (e.g., NSAIDs)
  • GI bleeding
  • Dehydration
  • Constipation
  • Acute PVT
  • HCC
• Diagnostics: to establish the cause of decompensation
  • CBC, BMP, liver chemistries
  • Magnesium and phosphate levels
  • Coagulation panel
  • Consider type and screen.
  • Paracentesis in patients with ascites
  • CRP, blood cultures, urinalysis and culture, chest x-ray
  • Abdominal ultrasound to assess for PVT
• Acute management: See “Management of acute liver failure.” [3][41][47]
  • Gastroenterology consult
  • Treat the underlying cause and complications (if applicable).
• Prognosis: In patients with decompensated cirrhosis, survival rates are usually poor unless liver transplantation is performed.

Liver cirrhosis in pregnancy [48][49]

• Maternal complications
  • Worsening of liver cirrhosis; pregnancy in individuals with advanced disease is associated with increased risk of:
    • New-onset ascites or worsening of ascites
    • Liver failure
    • Hepatorenal syndrome
    • Variceal bleeding (during pregnancy and/or labor)
  • Increased risk of pregnancy-related complications, including:
    • Gestational diabetes
    • Placental abruption
    • Preeclampsia
    • Postpartum hemorrhage
    • Spontaneous abortion, need of cesarean delivery, preterm delivery
• Fetal complications: associated with increased rates of newborn asphyxia and small size for gestational age

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