Decompensated Chronic Liver Failure

Full update June 2021

Chronic liver failure can lead to several acute complications.5 The chart below defines and reviews signs and symptoms, prophylaxis, and treatment of ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, and variceal bleeding. It also defines and provides a list of meds that should be avoided in patients who develop hepatorenal syndrome (HRS). See our chart, Drug Therapy for Severe Alcoholic Hepatitis, for more on its management. Use our Perioperative Checklist for Patients With Cirrhosis to help care for cirrhosis patients undergoing surgery.


Answer/Pertinent Information

Ascites (the most common complication of cirrhosis): the accumulation of fluid within the abdomen due to sodium retention and high pressure in the veins of the liver.5,10 There are three grades of ascites:12

  • Grade 1: abdominal fluid only detectable by ultrasound.
  • Grade 2: moderate and symmetrical abdominal distention.
  • Grade 3: large volume ascites with gross abdominal distention.

What are complications associated with ascites?

Complications of ascites include:12

  • hyponatremia
  • spontaneous bacterial peritonitis (see below)
  • HRS (see below)

Generally, avoid certain meds in patients with cirrhosis and ascites (e.g., ACE inhibitors, ARBs, and NSAIDs).4

How can the risk of ascites be reduced?

Abstain from alcohol.4,10,12

Some experts recommend limiting sodium intake.10,12 Recommended max intake varies from about 2,000 to 3,000 mg/day.12

Fluid restriction is not routinely recommended in patients with normal serum sodium levels.12

  • Some experts recommend restricting fluid intake in patients with hypervolemic hyponatremia, though more studies are needed to confirm benefit.12

What medications are used to treat ascites?

Chronic therapy: spironolactone, with or without furosemide (to counteract spironolactone-induced hyperkalemia).4,5,11

  • Start with spironolactone 50 to 100 mg once daily. Doses can be adjusted about every three to five days to achieve weight loss of about 0.5 kg/day (no edema present) to ≥1 kg/day (edema present).12
  • The ratio of spironolactone to furosemide is typically 100 mg of spironolactone to 40 mg of furosemide.4,5,12
  • Max recommended doses are spironolactone 400 mg/day and furosemide 160 mg/day.5,10-12
  • Monitor electrolytes and renal function at least weekly during the first month of therapy and as necessary with dosage adjustments, especially for hyponatremia, hypo- or hyperkalemia, or increased serum creatinine.5,11

Amiloride may be an alternative option in patients with intolerable, painful gynecomastia from spironolactone.11

  • Recommend an initial amiloride dose of 20 mg/day. Amiloride can be titrated to a max of 60 mg/day.11

When is paracentesis used to treat ascites?

Paracentesis (removal of fluid from the abdomen with a needle) is recommended for:4,11

  • new onset ascites.
  • suspicion for spontaneous bacterial peritonitis (see below).
  • symptom relief (e.g., abdominal discomfort, ileus, respiratory compromise).

Administer albumin to patients who have >5 L of fluid removed during paracentesis (e.g., large volume paracentesis) to prevent low blood pressure and maintain blood flow to the kidneys.4,10,12,16,24,31

  • Recommend IV albumin 6 to 8 g for each L of fluid removed during paracentesis.4,11,16

When is transjugular intrahepatic portosystemic shunting (TIPS) used to treat ascites?

TIPS involves inserting a shunt to lower hepatic venous pressure. TIPS can be used for ascites refractory to medication and paracentesis therapies.12

TIPS is not routinely recommended, but can be considered for patients requiring frequent paracentesis (e.g., every one to two weeks) or patients who have a Child-Pugh score ≤11.11

  • Avoid TIPS in some patients (e.g., bilirubin >3 mg/dL, Child-Pugh score >11, age >70, heart failure).11

TIPS appears to be more effective than large volume paracentesis [Evidence Level A-1].12

Possible complications associated with TIPS include HE (see below) and stent thrombosis.12

  • HE may occur in up to 25% of patients that receive a TIPS and incidence appears to be higher in patients older than 60 years old.12

Hepatic Encephalopathy (HE): There is no test to diagnose HE.9 HE is a liver failure complication involving high ammonia levels, inflammation, and cerebral hemodynamic dysfunction.7 HE affects about 20% of patients with liver failure each year.8

What are signs and symptoms of hepatic encephalopathy?

Symptoms can be divided into two categories: mental and physical.9

  • Mental symptoms of HE include:9
    • anxiety and confusion.
    • decreased attention span and difficulty with basic or simple math.
    • disorientation or forgetfulness.
    • mood swings or personality changes.
  • Physical symptoms of HE include:9
    • change in sleeping patterns (e.g., sleeping in the day, awake during the night) or extreme sleepiness.
    • difficulty with fine motor skills (e.g., writing, small hand movements).
    • slowed or sluggish movements or speech, can progress to coma.

What things can trigger or worsen hepatic encephalopathy?

Several conditions, medications, or procedures can trigger or worsen HE:9

  • acute alcohol consumption or binge drinking
  • certain medications (e.g., antidepressants, sleeping pills)
  • constipation
  • dehydration
  • gastrointestinal bleeding
  • infections
  • kidney problems
  • surgery
  • transjugular intrahepatic portosystemic shunting (TIPS)

How is lactulose used to treat hepatic encephalopathy?

Lactulose is the cornerstone of treatment of HE, by reducing ammonia levels.4

  • Lactulose reduces HE episodes, but has no impact on survival.4

Lactulose is used to treat acute episodes of and prevent future episodes of HE.8

  • Initial treatment: oral lactulose 10 to 30 g every one to two hours until a bowel movement occurs.4,11
  • Ongoing treatment and prevention: reduce dosing frequency to about twice daily.4,6
    • Monitor patients closely and aim for about three soft bowel movements per day. Adjust doses as needed.4,6

If oral administration is not possible (e.g., coma), lactulose can be given rectally.3,4,6

Dosing: Lactulose 300 mL in 700 mL normal saline given as an enema and retained for 30 to 60 minutes.3,4,6

  • Rectal dosing can be repeated about every four to six hours.3
  • Resume oral therapy as soon as able, giving the first dose before stopping rectal administration.3

How are antibiotics used to treat hepatic encephalopathy?

Rifaximin or neomycin can be added to lactulose therapy in patients with continued HE episodes despite lactulose therapy.4,8 They are proposed to reduce ammonia levels by minimizing ammonia-producing bacteria in the gut.8

  • Rifaximin is used more commonly than neomycin.4,8
    • Dosing options include rifaximin 400 mg three times daily or 550 mg twice daily.4
  • Neomycin (second-line, due to nephrotoxicity, ototoxicity, and neurotoxicity, especially with long-term use.)4
    • Neomycin dosing ranges from 1 to 3 grams given every six hours for about five to six days.3,4

What are long-term considerations with hepatic encephalopathy?

It is no longer recommended to limit dietary protein intake as a way to decrease ammonia production and ultimately reduce the risk of HE.8,11

Instead, encourage patients to get 1.2 to 1.5 g/kg of protein divided in small meals throughout the day and have a late-night snack with complex carbohydrates (e.g., an apple, cereal with milk, whole grain crackers).8

Hepatorenal Syndrome (HRS): Reduced renal blood flow, due to abdominal vasodilation in cirrhosis and ascites, leads to an inability to eliminate toxins and electrolytes.5 HRS is a strong predictor of mortality in patients with cirrhosis, and these patients should be expedited for possible liver transplation.12 The following are required to diagnose HRS in patients with cirrhosis and ascites:5,12

  • serum creatinine >1.5 mg/dL.
  • no improvement in renal function after two days of volume expansion therapy with albumin and without any diuretics.
  • absence of shock.
  • no current or recent nephrotoxic medications and absence of parenchymal kidney disease (e.g., proteinuria, hematuria).

Which medications should be avoided to prevent hepatorenal syndrome?

Stop diuretics.12 However, can use furosemide to maintain urine output and to treat volume overload.12

Avoid drugs that have been associated with precipitating HRS in patients with cirrhosis.14 Examples include:14

  • Blood pressure meds: alpha-blockers (e.g., terazosin), ACE inhibitors (e.g., lisinopril).
  • Meds that reduce kidney perfusion: NSAIDs, including COX-2 inhibitors (e.g., celecoxib), dipyridamole.
  • Nephrotoxic meds: aminoglycosides, amphotericin.

Spontaneous Bacterial Peritonitis: infection of ascitic fluid with a neutrophil count of ≥250 cell/mm3 or an ascitic fluid culture positive for bacteria, without an existing surgically treatable source.2 It affects about 30% of patients with cirrhosis and has a mortality rate of about 20%.4

How should a first episode of spontaneous bacterial peritonitis be prevented?

Consider primary prophylaxis for patients with cirrhosis that are at high-risk for developing spontaneous bacterial peritonitis (e.g., history of variceal bleeding, ascitic fluid protein levels <1 g/dL).1,2

  • First-line: TMP/SMX double-strength tablet orally once daily.1,2
  • Alternative (e.g., allergic or resistance to TMP/SMX): ciprofloxacin 500 mg orally once daily.1
  • Rifaximin has limited data and inconsistent results for use as primary prevention.1
    • Avoid rifaximin unless TMP/SMX and ciprofloxacin are not options (e.g., allergies, adverse effects).1

How is spontaneous bacterial peritonitis diagnosed?

  • Spontaneous bacterial peritonitis should be suspected in patients with ascites and one or more of the following:
    • abdominal pain or tenderness
    • ascitic fluid neutrophil count ≥250 cells/mm3
    • fever (e.g., 100°F [37.8°C])
    • mental status changes


  • patients presenting with variceal bleeding.
  • If possible, perform paracentesis, send ascitic fluid for a neutrophil count and cultures, and draw blood cultures BEFORE starting antibiotics.4
    • Antibiotic therapy is still warranted if spontaneous bacterial peritonitis is suspected (e.g., fever, abdominal pain) and patients have an elevated ascitic neutrophil count, even with negative cultures.2,4

How should spontaneous bacterial peritonitis be treated?

When selecting antibiotic therapy, review antibiograms for coverage of pathogens that commonly cause spontaneous bacterial peritonitis (e.g., Escherichia coli [E.coli], Streptococcus, Klebsiella).

Treat with antibiotics for five days.1,2 Treatment for more than five days has not been shown to improve cure rates, recurrence, or hospital mortality.11,12

Start with empiric antibiotics outlined below and adjust therapy based on cultures and sensitivities.1

  • First-line options for community-acquired spontaneous bacterial peritonitis include:1,2,4
    • cefotaxime 2 g IV every 8 hours.
    • ceftriaxone 1 g IV every 12 hours or 2 g IV every 24 hours.
    • ciprofloxacin 400 mg or levofloxacin 500 to 750 mg IV every 24 hours (patients with penicillin allergies).
  • For hospital-acquired (symptoms begin >48 hours after hospital admission) spontaneous bacterial peritonitis consider:1
    • Piperacillin/tazobactam 3.375 g IV every six hours PLUS vancomycin 1 g IV every 12 hours.
    • For suspected vancomycin-resistant enterococcus consider linezolid 600 mg IV every 12 hours or daptomycin 4 to 6 mg/kg IV every 24 hours.
    • For suspected ESBL Enterobacteriaceae consider meropenem 1 g IV every 8 hours.

Consider transitioning patients that are improving (e.g., afebrile, tolerating oral intake, white blood cells [WBCs] trending down) from IV to oral antibiotics after about 48 hours of IV therapy using cultures and sensitivities.1,11

When should albumin be used in the treatment of spontaneous bacterial peritonitis?

Albumin may reduce renal failure and mortality in some patients with spontaneous bacterial peritonitis.1

  • Albumin is not necessary for all patients with spontaneous bacterial peritonitis.1
  • Albumin WITH antibiotic therapy prevents one renal injury AND in-hospital death for every five patients treated [Evidence Level A-1].13 Recommend albumin for patients with any of the following:1,4,16,24,31
    • serum creatinine >1 mg/dL.
    • total bilirubin >4 mg/dL.
    • blood urea nitrogen (BUN) >30 mg/dL.

When treating patients with spontaneous bacterial peritonitis with albumin, recommend albumin 25% with the following dosing:1,4,24

  • day one (within six hours of diagnosis): 1.5 g/kg
  • day three: 1 g/kg

What are the most appropriate ways to prevent subsequent episodes of spontaneous bacterial peritonitis?

The risk of recurrence of spontaneous bacterial peritonitis is about 70% within two years of initial episode.1

Recommend secondary prophylaxis against spontaneous bacterial peritonitis.1 Options include:1

  • TMP/SMX double-strength tablet orally once daily five to seven days/week.
  • Ciprofloxacin 500 mg orally daily.

Risk factors for recurrent episodes of spontaneous bacterial peritonitis include:1

  • total bilirubin >4 mg/dL.
  • prothrombin ≤45%.
  • low ascitic fluid protein levels (e.g., <1 g/dL).

Acute bleeding: Chronic liver disease leads to decreased levels of both naturally occurring anticoagulants and procoagulants. There can be a balance between bleeding and clotting risks, but sometimes the balance tips to either bleeding or clotting.20 Acute bleeding episodes (e.g., variceal bleeding, nonvariceal upper gastrointestinal bleeding, intracerebral hemorrhage) can be life-threatening complications of cirrhosis.

What tests are used to assess coagulation status in patients with cirrhosis?

Some of the standard tests used to assess coagulation status include prothrombin time and international normalized ratio (PT/INR), activated partial thromboplastin time (aPTT), platelet count, and fibrinogen.25

  • Unfortunately, aPTT and PT/INR are NOT predictive of bleeding in patients with cirrhosis.21,28

TEG is an emerging coagulation test. TEG provides a more comprehensive look at coagulation status, by assessing factors promoting both coagulation and anticoagulation in one test.28 However, TEG may not be readily available in all hospitals. Data are limited using TEG parameters to manage bleeding. However, using TEG seems to lead to similar bleeding control using fewer blood products, compared to using standard coagulation assessments (e.g., INR, platelet counts) [Evidence Level B-1].17,18,28 Some of the parameters that TEG measures and have been used to guide treatment of acute bleeding include:23,26,28

  • Reaction time (R value or R time): the time to the start of clot formation (normal = 5 to 10 minutes). R time >11 minutes indicates a risk of bleeding. R time seems to correlate most closely with the PT and aPTT.26
  • Maximum amplitude (MA): measure of maximum attainable clot strength, and is specific for platelet functionality (normal = 50 to 70). Seems to correlate most closely with platelet count and fibrinogen.26
  • Clot lysis (LY-30): indicates % fibrinolysis in 30 minutes (normal= 0 to 7.5% per manufacturer, but some experts consider 0 to 3% the normal range for patients with cirrhosis). High values (e.g., >3%) may indicate the need for antifibrinolytic therapy (e.g., tranexamic acid). There does not appear to be an equivalent “standard test” comparable to clot lysis.26

What are initial treatment options to control acute bleeding in patients with cirrhosis?

See our chart, Esophageal Variceal Bleeding FAQs, for specifics on prevention and initial treatment options (e.g., endoscopy, octreotide, antibiotics) in patients presenting with an esophageal variceal bleed.

For patients admitted with an acute nonvariceal upper gastrointestinal bleed, an endoscopy should be done within 24 hours of presentation.27

  • Endoscopic therapy (e.g., clips, thermocoagulation) should be used for patients with high-risk bleeds (e.g., active bleeding, visible vessel in the ulcer bed).27
  • Use high-dose proton pump inhibitors (PPIs) in patients with high-risk ulcers after endoscopic therapy (e.g., esomeprazole 80 mg IV loading dose, followed by a 72-hour continuous infusion [8 mg/hr] or intermittent IV doses [40 mg IV every 12 hours], then 40 mg/day orally to complete two weeks of therapy.27,29 See our PPI chart for appropriate indications for long-term PPI use, and risks associated with PPIs.

When additional treatment is needed to control acute esophageal variceal bleeding, nonvariceal upper gastrointestinal bleeding, or other types of nonvariceal bleeding, you can consider the following:

  • Cryoprecipitate can be used to raise fibrinogen levels without significantly increasing plasma volume.21 Cryoprecipitate is preferred over FFP as it has a smaller transfusion volume and is less likely to worsen portal hypertension.18 You can expect weight-based dosing (1 unit of cryoprecipitate/10 kg body weight) to raise fibrinogen levels about 50 mg/dL. A reasonable goal is to raise fibrinogen to >120 mg/dL.18
  • Platelet transfusions (single-donor may be preferred over pooled-donor due to a lower risk of immunologic reactions) can be considered to bring platelet counts up to at least 50,000/mm3.18,21 Expect one infusion (~250 mL) to increase platelet counts by about 5,000 to 10,000/mm3.18
  • Red blood cell (RBC) transfusions (~250 mL) can be considered in patients with severe anemia and uremia to raise the hematocrit (HCT) to ≥25%.18

What other treatment options can be considered to control acute bleeding in patients with cirrhosis?

Tranexamic acid (e.g., 1 g IV every six hours) can be considered if the above options are not working or are not enough, especially if fibrinolysis is suspected and TEG indicates the LY-30 is >3%.18,26

4-factor prothrombin complex concentrate (4-factcor PCC [Kcentra]) can be considered for a life-threatening bleed (especially intracerebral hemorrhage) based on limited evidence [Evidence Level C].18,20 See our chart, Clotting Factors, for more on 4-factor prothrombin complex concentrate and other clotting factors.

  • Using 4-factor PCC in patients with cirrhosis is off-label. There is no established dosing; however, 25 units/kg seems to be the most common dose used and appears to be safe.20

What should generally NOT be used to control acute bleeding in patients with cirrhosis?

FFP takes time to thaw, can lead to transfusion reactions, and requires a large volume which can worsen portal HTN. In addition, FFP also contains anticoagulants, not just clotting factors.18,20,21

There are no good data that vitamin K is helpful to control bleeding in patients with cirrhosis.19,20,22 In addition, vitamin K takes about 12 hours to begin working.18,20 And, there is a rare risk of anaphylaxis with IV administration of vitamin K.18

There is no proof factor VIIa reverses bleeding or improves morbidity or mortality in patients with acute bleeding due to cirrhosis.20 Some data suggest using recombinant factor VIIa may increase thrombotic events.20

There is no proof desmopressin works to control acute bleeding due to cirrhosis. In addition, desmopressin releases von Willebrand factor (VWF), and VWF levels are usually elevated in patients with cirrhosis.18

Hypoalbuminemia(e.g., <3 g/dL): Albumin plays a number of roles in the body, including maintaining oncotic pressure and acting as an anti-inflammatory. Albumin production can be significantly reduced in patients with advanced liver disease.30,31

What is the role for IV albumin in hospitalized patients with decompensated liver disease and hypoalbuminemia?

Generally, avoid routine use of IV albumin in stable hospitalized patients with low albumin levels and new or worsening ascites, HE, or a suspected variceal bleed.15,30

  • Albumin levels <3 g/dL in patients with cirrhosis are linked to immune dysfunction.30 Because of this, some experts recommend daily albumin when levels are <3 g/dL.15 However, data are not strong.15,30
    • In hospitalized patients with decompensated cirrhosis, daily albumin infusions to maintain albumin levels ≥3 g/dL is NOT better than standard of care at preventing the composite endpoint of new infection, kidney dysfunction, or death [Evidence Level B-1].30 Albumin administration may lead to fluid overload and pulmonary edema.30

Abbreviations: ACE = angiotensin converting enzyme; ARB = angiotensin receptor blocker; COX-2 = cyclo-oxygenase-2; ESBL = extended-spectrum beta-lactamase; FFP = fresh frozen plasma; HE = hepatic encephalopathy; HRS = hepatorenal syndrome; NSAID = nonsteroidal anti-inflammatory drug; IV = intravenously; TEG = thromboelastography; TMP/SMX = trimethoprim/sulfamethoxazole.

Levels of Evidence

In accordance with our goal of providing Evidence-Based information, we are citing the LEVEL OF EVIDENCE for the clinical recommendations we publish.



Study Quality


Good-quality patient-oriented evidence.*

  1. High-quality RCT
  2. SR/Meta-analysis of RCTs with consistent findings
  3. All-or-none study


Inconsistent or limited-quality patient-oriented evidence.*

  1. Lower-quality RCT
  2. SR/Meta-analysis with low-quality clinical trials or of studies with inconsistent findings
  3. Cohort study
  4. Case control study


Consensus; usual practice; expert opinion; disease-oriented evidence (e.g., physiologic or surrogate endpoints); case series for studies of diagnosis, treatment, prevention, or screening.

*Outcomes that matter to patients (e.g., morbidity, mortality, symptom improvement, quality of life).

RCT = randomized controlled trial; SR = systematic review [Adapted from Ebell MH, Siwek J, Weiss BD, et al. Strength of Recommendation Taxonomy (SORT): a patient-centered approach to grading evidence in the medical literature. Am Fam Physician 2004;69:548-56.]


  1. Dever JB, Sheikh MY. Review article: spontaneous bacterial peritonitis – bacteriology, diagnosis, treatment, risk factors and prevention. Aliment Pharmacol Ther 2015;41:1116-31.
  2. Perri GA, Khosravani H. Complications of end-stage liver disease. Can Fam Physician 2016;62:44-50.
  3. Clinical Pharmacology powered by ClinicalKey. Tampa (FL): Elsevier. 2021. (Accessed May 17, 2021).
  4. Long B, Koyfman A. The emergency medicine evaluation and management of the patient with cirrhosis. Am J Emerg Med 2018;36:689-98.
  5. McPherson S, Lucey MR, Moriarty KJ. Decompensated alcohol related liver disease: acute management. BMJ 2016;352:i124.
  6. Patidar KR, Bajaj JS. Covert and overt hepatic encephalopathy: diagnosis and management. Clin Gastroenterol Hepatol 2015;13:2048-61.
  7. Lee GH. Hepatic encephalopathy in acute-on-chronic liver failure. Hepatol Int 2015;9:520-6.
  8. Ellul MA, Gholkar SA, Cross TJ. Hepatic encephalopathy due to liver cirrhosis. BMJ 2015;351:h4187.
  9. American Liver Foundation. Diagnosing hepatic encephalopathy. (Accessed May 17, 2021).
  10. University of Michigan. Liver cirrhosis: a toolkit for patients. Revised October 2011. (Accessed May 17, 2021).
  11. Garcia-Tsao G, Lim J, members of the Veterans Affairs Hepatitis C Resource Center Program. Management and treatment of patients with cirrhosis and portal hypertension: recommendations from the Department of Veterans Affairs Hepatitis C Resource Center Program and the National Hepatitis C Program. Am J Gastroenterol 2009;104:1802-29.
  12. Pericleous M, Sarnowski A, Moore A, et al. The clinical management of abdominal ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: a review of current guidelines and recommendations. Eur J Gastroenterol Hepatol 2016;28:e10-8.
  13. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patient with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med 1999;341:403-9.
  14. Davenport A, Ahmad J, Al-Khafaji A, et al. Medical management of hepatorenal syndrome. Nephrol Dial Transplant 2012;27:34-41.
  15. Nanchal R, Subramanian R, Karvellas CJ, et al. Guidelines for the management of adult acute and acute-on-chronic liver failure in the ICU: cardiovascular, endocrine, hematologic, pulmonary, and renal considerations. Crit Care Med 2020;48:e173-91.
  16. Runyon BA, American Association for the Study of Liver Disease. Introduction to the revised American Association for the Study of Liver Disease practice guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology 2013;57:1651-3.
  17. Kumar M, Ahmad J, Maiwall R, et al. Thromboelastography-guided blood component use in patients with cirrhosis with nonvariceal bleeding: a randomized controlled trial. Hepatology 2020;71:235-46.
  18. O’Leary JG, Greenberg CS, Patton HM, Caldwell SH. AGA clinical practice update: coagulation in cirrhosis. Gastroenterology 2019;157:34-43.e1.
  19. Meyer AV, Green M, Pautler HM, et al. Impact of vitamin K administration on INR changes and bleeding events among patients with cirrhosis. Ann Pharmacother 2016;50:113-7.
  20. Pereira D, Liotta E, Mahmoud AA. The use of Kcentra in the reversal of coagulopathy of chronic liver disease. J Pharm Pract 2018;31:120-5.
  21. Northrup PG, Friedman LS, Kamath PS. AGA clinical practice update on surgical risk assessment and perioperative management in cirrhosis: expert review. Clin Gastroenterol Hepatol 2019;17:595-606.
  22. Marti-Carvajal AJ, Sola I. Vitamin K for upper gastrointestinal bleeding in people with acute or chronic liver diseases. Cochrane Database Syst Rev 2015;(6):CD004792.
  23. Bose E, Hravnak M. Thromboelastography: a practice summary for nurse practitioners treating hemorrhage. J Nurse Pract 2015;11:702-9.
  24. European Association for the Study of the Liver. EASL clinical practice guidelines for the management of patients with decompensated cirrhosis. J Hepatol 2018;69:406-60.
  25. Lab tests online. Prothrombin time and international normalized ratio (PT/INR). February 2019. (Accessed May 17, 2021).
  26. Farkas J. EMCrit. PulmCrit – coagulopathy management in the bleeding cirrhotic: seven pearls and one crazy idea. December 2015. (Accessed May 17, 2021).
  27. Barkun AN, Almadi M, Kuipers EJ, et al. Management of nonvariceal upper gastrointestinal bleeding: guideline recommendations from the International Consensus Group. Ann Intern Med 2019;171:805-22.
  28. Rout G, Shalimar, Gunjan D, et al. Thromboelastography-guided blood product transfusion in cirrhosis patients with variceal bleeding: a randomized controlled trial. J Clin Gastroenterol 2020;54:255-62.
  29. Worden JC, Hanna KS. Optimizing proton pump inhibitor therapy for treatment of nonvariceal upper gastrointestinal bleeding. Am J Health Syst Pharm 2017;74:109-16.
  30. China L, Freemantle N, Forrest E, et al. A randomized trial of albumin infusions in hospitalized patients with cirrhosis. N Engl J Med 2021;384:808-17.
  31. Jagdish RK, Maras JS, Sarin SK. Albumin in advanced liver diseases: the good and bad of a drug! Hepatology 2021 Mar 27. doi: 10.1002/hep.31836.

Cite this document as follows: Clinical Resource, Decompensated Chronic Liver Failure. Hospital Pharmacist’s Letter/Pharmacy Technician’s Letter. June 2021. [370616]

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