Published Jan 2020, Update in progress
Authors: Yilin Zhang, MD¹; Brandon Fainstad, MD²
Based on talk developed by Neha Deshpande, MD³; Yilin Zhang, MD¹; Eric Lamotte, MD³
1 Assistant Professor, Department of General Internal Medicine, University of Washington-Valley Medical Center
2 Assistant Professor, Department of Medicine, University of Colorado – Anschutz
3 Assistant Professor, Department of General Internal Medicine, University of Washington
- Differentiate between compensated and decompensated cirrhosis
- Recognize the significance of MELD-Na score
- Evaluate a patient presenting with acute decompensation of cirrhosis
- Evaluate and manage the common complications of cirrhosis including hepatic encephalopathy, ascites, variceal bleeding, hepatorenal syndrome and spontaneous bacterial peritonitis
Plan to spend at least 30-60 minutes preparing for this talk by using the Interactive Board and clicking through the graphics animations to become familiar with the flow and content of the talk. All interactive and clickable elements are represented by a mouse icon.
The anticipated time to deliver this talk is roughly 35-40 min.
This can be presented in two ways:
- Project the “Interactive Board “
- Reproduce a drawing of the presentation on a whiteboard
With either method, print out copies of the Learner’s Handout so learners can take notes as you expand on the evaluation and management of the various complications of decompensated cirrhosis.
Take Home Points
- MELD-Na score predicts 3 month mortality and is used for liver transplant allocation.
- Acute decompensation of cirrhosis occurs when patients have an increase in their MELD-Na score or develop new complications of cirrhosis.
- The precipitants of many of the complications of cirrhosis overlap and include infection/ SBP, GI bleeding or portal vein thrombosis and initial work-up should include diagnostic paracentesis, evaluation for clinical signs of bleeding and potentially a RUQ US with duplex.
- Essentially everyone admitted to the hospital with cirrhosis and ascites should receive a diagnostic paracentesis.
Ge, PS & Runyon, BA. Treatment of Patients with Cirrhosis. NEJM. 2016;375:767-77
Liou, IW. Management of end-stage liver disease. Med Clin North Am. 2014 Jan;98(1):119-52.
Sharma, BG, et al. A Randomnized, Double-Blind, Controlled Trial Comparing Rifaximin Plus Lactulose with Lactulose Alone in Treatment of Overt Hepatic Encephalopathy. The American Journal of Gastroenterology. 2013; 108: 1458-1463.
Rahimi, RS, et al. Lactulose vs polyethylene glycol 3350 –electrolyte solution for treatment of overt hepatic encephalopathy: the HELP randomized clinical trial. JAMA Internal Medicine. 2014; 174(11): 1727-33.
Rahimi, RS & Rockey, DC. Novel Ammonia-Lowering Agents for Hepatic Encephalopathy. Clin Liver Dis. 2015; 19(3): 539-49.
Sachar, H, Vaidya, K & Laine, L. Intermittent vs Continuous Proton Pump Inhibitor Therapy for High-Risk Bleeding Ulcers. JAMA Internal Mediicne. 2014; 174(11): 1755-1762.
Villaneuva, C, et al. Transfusion Strategies for Acute Upper Gastrointestinal Bleeding. NEJM. 2013; 368: 11-2.
Salpeter, SR, et al. Systematic review of noncancer presentations with a median survival of 6 months or less. American Journal of Medicine. 2012, 125(5):512.e1-6.