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C Cirrhosis: an Evidence-Based Treatment Approach

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C Cirrhosis: an Evidence-Based Treatment Approach 1.5 0.5 CONTACT HOURS CONTACT HOUR eranicle Cirrhosis: An evidence-based treatment approach Abstract: The NP’s role in managing cirrhosis is increasing due to the growing prevalence of the disease. The purpose of this article is to review the pathophysiology, diagnosis, and management of patients with cirrhosis with an emphasis on interdisciplinary collaboration and evidence-based practice. Cirrhosis complications are also discussed. By Kelly Casler, DNP, APRN, FNP-BC, EBP-C, CHSE and Amanda Chaney, DNP, APRN, FNP-BC, FAANP irrhosis is reported to be one of the most chal- and Black patients.2,4 It is the 12th leading cause of lenging chronic conditions healthcare provid- death in the US, causing at least 1 million deaths an- C ers must manage, yet evidence suggests that nually.3,4 Underdiagnosis is common; over two-thirds primary care providers (PCPs) will take on more of of patients are unaware that they have liver disease. the burden of care as the disease becomes more preva- This is concerning given that cirrhosis confers a higher lent.1 Therefore, it is imperative that NPs understand risk of mortality than many other chronic diseases.1,4 the challenges and best practices of managing this Annually, 30 billion dollars are spent on care of pa- common chronic disease. tients with cirrhosis.2 ■ Epidemiology ■ Pathophysiology Cirrhosis prevalence has increased over the last 20 Cirrhosis starts with an initial injury or inciting event years with higher disease rates seen in impoverished to the liver that triggers an infl ammatory response. The Keywords: cirrhosis, collaboration, evidence-based practice, interdisciplinary, NP 16 The Nurse Practitioner • Vol. 45, No. 8 www.tnpj.com Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. Cirrhosis: An evidence-based treatment approach most common inciting events in the US are viral infec- tions (hepatitis B or C), nonalcoholic steatohepatitis Chronic liver conditions that can lead to cirrhosis6 (caused by excess carbohydrates and calories), and al- Most common Less common coholic liver disease (excess alcohol) (see Chronic liver 5,6 Nonalcoholic Primary sclerosing conditions that can lead to cirrhosis). In response to steatohepatitis cholangitis infl ammation, new blood vessels form, extracellular Infectious hepatitis Primary biliary cholangitis matrix proliferates, and new hepatocytes migrate to the area, replicating excessively. Angiogenesis becomes ab- Alcoholic liver disease Autoimmune hepatitis normal and fi brosis develops. The fi brosis coalesces, causing nodules to replace normal liver tissue.7 Fibrosis functions. Additionally, persistent alterations in cellular then advances from mild to severe, with the most severe homeostasis during cirrhosis can lead to increased pro- fi brosis leading to cirrhosis. During this time, the liver pensity for hepatocellular neoplasm.8 attempts to regenerate normal functioning liver tissue Cirrhosis of the liver also alters the hepatic vascu- in between diseased areas and these regenerative nod- lature, which results in portal hypertension, a state of ules give the cirrhotic liver its hallmark lumpy appear- increased pressure in the portal venous system. As the ance (see Progression to cirrhosis and its complications). pressure inside the liver increases, blood fl ow is re- Recovery and regression of early fi brosis is usually pos- stricted, and blood vessels become congested and en- sible if the damaging event is removed. However, liver gorged with blood. As this occurs over months to years, transplant has been traditionally thought of as the only this pressure increase can cause damage to the vessel cure once cirrhosis develops.7 But new research is ex- walls and chronic infl ammation. Ultimately, portal ploring the reversibility of liver cirrhosis.8,9 Since pro- hypertension can lead to complications of esophageal gression toward cirrhosis is slow, taking 2 to 3 decades, varices, portal hypertensive gastropathy, and ascites. cirrhosis is most often diagnosed in the fourth or fi fth Additionally, patients may develop portal vein throm- decade of life. However, recent data reveal that diagnosis bosis that can further complicate blood fl ow to and is occurring at younger ages than in past decades.2,4 from the portal circulation. A healthy liver performs a wide range of functions Cirrhosis is classified as either compensated or including carbohydrate and lipid metabolism; break- decompensated. Compensated cirrhosis is often as- down of medications, ammonia, and bilirubin; and ymptomatic and may therefore go undetected.1 Con- synthesis of albumin and coagulation factors.10 Kupffer versely, decompensated cirrhosis is manifested by cells help with immune system regulation and hepato- complications; the most common are ascites, esopha- cytes produce bile, which is critical for digestion and geal varices, and hepatic encephalopathy. Comorbidi- absorption of fat-soluble vitamins.10 Cirrhosis can cause ties, such as diabetes, predispose a patient to a higher dysfunction affecting one or more of these primary liver likelihood of decompensation.11 Prognosis is poor Progression to cirrhosis and its complications Normal Chronic Hepatitis Cirrhosis HCC/ESLD FPO © MAYO CLINIC Key: HCC, hepatocellular carcinoma; ESLD, end-stage liver disease Used with permission of Mayo Foundation for Medical Education and Research, all rights reserved. www.tnpj.com The Nurse Practitioner • August 2020 17 Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved. Cirrhosis: An evidence-based treatment approach following decompensation.12 While life expectancy referred to as liver enzymes or liver transaminases, estimate for compensated cirrhosis is 12 or more years, since they do not refl ect how well the liver is function- life expectancy for decompensated cirrhosis is ap- ing.14 True “liver function tests” include albumin, proximately 2 years.12 Therefore, when a patient moves prothrombin time (PT)/international normalized from compensated to decompensated cirrhosis, refer- ratio (INR), and bilirubin. However, even these tests ral to a transplant center for liver transplant evaluation may not show variation until late in decompensated is warranted. cirrhosis, at which point albumin levels will be re- duced and PT/INR will be elevated. Thrombocyto- ■ Evaluation of patients with cirrhosis penia can be an early lab clue to cirrhosis, since it can As with any chronic illness, a thorough history, physical occur in the early stages of portal hypertension.12,15 exam, and diagnostic evaluation is important. During Patients should be evaluated for possible cirrhosis this time, the NP may evaluate for signs of cirrhosis, when platelet levels fall below 160,000/mm3.13 identify the underlying etiology of liver disease, and Several diagnostic tests are used in the evaluation intervene for improved outcomes (see Signs and symp- and monitoring of cirrhosis. Ultrasound will often toms of cirrhosis and underlying pathophysiology). For show splenomegaly during cirrhosis and portosystemic collateral veins with worsening cir- rhosis.15 The gold standard to diag- The gold standard to diagnose fi brosis and nose fibrosis and cirrhosis is liver cirrhosis is liver biopsy, but its invasiveness biopsy, but the invasiveness of the limits its usefulness. procedure limits its usefulness. Therefore, transient liver elastogra- phy is frequently used to evaluate for example, treatment of hepatitis C and abstinence from advanced fi brosis.16 Other mechanisms for fi brosis and alcohol can improve complication rates and life expec- cirrhosis diagnosis, such as serum biomarkers, are be- tancy in patients with cirrhosis.8,13 ing studied, but not yet FDA-approved. Two of the most common lab tests to monitor and evaluate cirrhosis are alanine aminotransferase (ALT) ■ Evaluation and management of cirrhosis and aspartate aminotransferase (AST). Although it complications is frequently assumed that both AST and ALT are Ascites, hepatic encephalopathy, and esophageal/gastric elevated in patients with cirrhosis, their levels can be varices are the three most common complications seen normal during compensated cirrhosis and even in decompensated cirrhosis. However, there are several sometimes, decompensated cirrhosis.12,14 Conse- other possible complications that require monitoring quently, although these tests are frequently referred (see Monitoring for complications of cirrhosis). to as “liver function tests,” they should actually be Ascites. Ascites is the most common complication of cirrhosis with almost one half of patients with com- pensated cirrhosis developing it over a 10-year peri- Signs and symptoms of cirrhosis and od.13,17 Sometimes, the diagnosis of ascites is the fi rst underlying pathophysiology53-55 clue to prompt the identifi cation of cirrhosis. Ascites Sign/symptom Underlying pathophysiology is thought to occur due to disrupted equilibrium be- Splenomegaly and Splenic congestion from tween the intravascular and extravascular space when thrombocytopenia portal hypertension portal hypertension results in elevated hydrostatic Caput medusae, dilated Portal hypertension pressure and hypoalbuminemia results in decreased abdominal wall veins, osmotic pressure. As a consequence, fl uid accumulates ascites, peripheral edema in the peritoneal space.10,15 Palmar erythema, spider Increased estrogen levels Evaluation of patients with ascites may show a angiomas, gynecomastia, loss of body hair positive fl uid wave test. A fl uid wave test is performed by having the patient lay supine and push down on the
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