Liver
Copyright Information
Copyright © 2016, 2013, 2010, 2006, 2002 by Saunders, an imprint of Elsevier Inc.
Copyright © 2021, Elsevier Inc. All Rights Reserved.
Objectives
Recall the concept of nutrition.
Review pathophysiology of liver disease.
Compare and contrast the risk factors for liver disease.
Discuss the complications of liver disease.
Explain the comprehensive assessment for a client suffering from liver disease.
Interpret the expected assessment findings for a client suffering from liver disease to determine actual and potential consequences.
Identify client goals and determine expected outcomes for a client suffering from liver disease.
Describe nursing and collaborative interventions required to treat and monitor a client suffering from liver disease.
Identify pharmacological therapy used to treat liver disease and associated considerations.
Discuss client considerations for various age groups and cultures.
Concepts
Priority Concepts for Liver Disease:
Cellular regulation
Nutrition
Interrelated Concepts:
Fluid and electrolyte balance
Inflammation
Pain
Functions of the Liver
Metabolism:
Converts excess glucose to glycogen.
Breaks down old red blood cells;
Kupffer Cells (phagocytes) break down hemoglobin into iron and bilirubin.
Bilirubin is excreted in bile and eliminated in stool (brown color).
Breaks down fats and synthesizes cholesterol.
Protein Metabolism:
Ammonia is a byproduct of protein metabolism.
The liver converts ammonia to urea (BUN).
Detoxification:
Filters blood to remove toxins and pathogens (e.g., alcohol, medications, hormones such as estrogen).
Produces:
Bile: Helps carry away waste and break down fats.
Albumin: Keeps water in the capillaries, binds to calcium (Ca+).
Clotting Factors: Fibrinogen and prothrombin.
Cholesterol and Lipoprotein: Regulate cholesterol levels.
Thrombopoietin: Signals bone marrow to produce platelets.
Stores:
Glycogen.
Minerals: Iron and copper.
Vitamins: A, C, D, E, K, B12.
Liver Disease Pathophysiology
Cirrhosis:
Definition: Extensive, irreversible scarring of the liver.
Development: Typically slow, progressive, prolonged.
Causes: Usually chronic reaction to hepatic inflammation and necrosis.
Inflammation caused by toxins or disease leading to destruction of hepatocytes.
Characterized by widespread fibrotic (scarred) bands of connective tissue.
Tissues become nodular, leading to decreased blood and lymph flow.
Early disease: Enlarged, firm liver.
Later stages: Liver shrinks in size and hardens, leads to decreased liver function.
Results in end-stage liver disease.
Types of Cirrhosis
Postnecrotic Cirrhosis:
Caused by viral hepatitis, certain drugs or toxins.
Laennec’s (Alcoholic) Cirrhosis:
Caused by chronic alcoholism.
Biliary Cirrhosis (Cholestasis):
Caused by biliary obstruction or autoimmune disease.
Cirrhosis: Etiology and Genetic Risk Factors
Major Causes:
Hepatitis C: Leading cause of cirrhosis and liver cancer in the U.S.
Hepatitis B and D: Most common causes of cirrhosis worldwide.
Non-Alcoholic Fatty Liver Disease (NAFLD): Affects 30% of Americans.
Non-Alcoholic Steatohepatitis (NASH): Linked to obesity, type 2 diabetes, metabolic syndrome.
Genetic Risk:
PNPLA3 Gene: Latinos at the highest risk.
Alcohol Use:
Excessive and prolonged use has a direct toxic effect on hepatocytes.
Leads to inflammation, destruction, scarring, and cellular necrosis.
Other Causes:
Drugs and chemical toxins, autoimmune hepatitis, gallbladder disease, metabolic causes, cardiovascular disease.
Some systemic viral infections can induce acute hepatitis.
Common Complications of Liver Disease
Portal Hypertension:
Ascites:
Esophageal Varices: Life-threatening;
Portal Hypertensive Gastropathy:
Splenomegaly:
Results in destruction of platelets and red blood cells (RBC).
Thrombocytopenia & Anemia:
Biliary Obstruction:
Decreased Vitamin K: Leads to increased bleeding.
Jaundice: Often accompanied by pruritus.
Hepatic Encephalopathy:
Chronic liver disease and cirrhosis are common causes of death in the U.S.
Hepatic Encephalopathy (HE)
Definition:
A condition where toxins from the gut bypass the liver and impair brain function.
Grades of HE:
Grade 4: Coma.
Grade 3: Sleepy, hard to get attention.
Grade 2: Confused, goofy, stumbling.
Grade 1: Poor attention, mood changes, often referred to as minimal HE.
Key Point: Not dementia, can be reversible with treatment (e.g., lactulose).
Stages of Hepatic Encephalopathy
Stage I:
Subtle manifestations may go unrecognized:
Personality changes.
Behavioral changes (agitation, belligerence).
Emotional lability (euphoria, depression).
Impaired thinking.
Inability to concentrate.
Fatigue, drowsiness.
Slurred or slowed speech.
Sleep pattern disturbances.
Stage II:
Continuing mental changes:
Mental confusion.
Disorientation to time, place, or person.
Asterixis (hand flapping).
Stage III:
Progressive deterioration:
Marked confusion, stuporous but arousable.
Abnormal electroencephalogram (EEG) tracing.
Muscle twitching, hyperreflexia, asterixis (hand flapping).
Stage IV:
Unresponsiveness leading to death:
Unarousable, obtunded, no response to painful stimulus.
No asterixis, positive Babinski sign, muscle rigidity.
Fetor hepaticus: Characteristic liver breath (musty, sweet odor).
Seizures.
HE can develop slowly in chronic liver disease or rapidly in acute liver dysfunction.
Other Complications of Liver Disease
Hepatorenal Syndrome:
Poor prognosis, often cause of death; sudden decrease in urine, elevated BUN and creatinine, increase in urine osmolarity.
Spontaneous Bacterial Peritonitis (SBP):
Symptoms: fever, chills, abdominal pain, tenderness.
Diagnosed by paracentesis where leukocyte count exceeds 250.
Hepatopulmonary Syndrome:
Caused by excessive ascitic volume, leading to dyspnea from intra-abdominal pressure.
Cirrhosis: Assessment - Recognize Cues
History Assessment:
Factors to consider:
Age, gender, employment history (especially exposure).
History of needlestick injuries, sexual, family, and social histories.
Physical Assessment/Signs and Symptoms:
Common symptoms include fatigue, weight change, gastrointestinal symptoms, abdominal pain.
Conduct thorough abdominal assessments.
Psychosocial Assessment:
Evaluate for alcohol withdrawal using CIWA scale.
Laboratory Assessment for Cirrhosis
Chemistry Tests:
Elevated AST, ALT, LDH (may be normal with advanced liver damage).
Increased alkaline phosphatase and GGT with biliary obstruction.
Increased serum bilirubin; decreased serum albumin with severe/chronic liver disease.
Prolonged PT/INR.
CBC:
Low platelet count, low RBC, anemia, potential thrombocytopenia; WBC may be decreased.
Ammonia Level: Elevated in advanced liver disease.
Serum Creatinine: Elevated indicates decreased kidney function.
Imaging and Diagnostic Assessment
Types of Imaging:
Abdominal X-rays, CT, MRI.
Other Diagnostic Methods:
Liver ultrasonography, liver biopsy (most definitive), US transient elastography, arteriography, EGD, ERCP.
Analysis: Analyze Cues and Prioritize Hypotheses
Potential Diagnoses:
Fluid overload due to third spacing of abdominal and peripheral fluid.
Potential for hemorrhage due to portal hypertension.
Acute confusion and other cognitive changes from elevated serum ammonia levels and/or alcohol withdrawal.
Pruritus due to increased serum bilirubin and jaundice.
Planning and Implementation: Generate Solutions and Take Action
Intervention Strategies:
Managing fluid volume.
Preventing or managing hemorrhage.
Preventing or managing confusion.
Managing pruritus.
Esophageal Varices Treatment
Emergency Treatment Tools:
Sengstaken-Blakemore tube for hemorrhage from esophageal varices, equipped with three openings for:
Gastric aspiration.
Inflation of the esophageal balloon.
Inflation of the gastric balloon.
The esophageal balloon is inflated to maintain a pressure of 20 to 40 mmHg, monitored closely.
Evaluation: Assess Outcomes for Clients
Expected Outcomes:
Have a decrease in or no ascites.
Maintain electrolytes within normal limits.
No hemorrhage or effectively managed bleeding.
No development of encephalopathy or effectively managed if it occurs.
Successfully abstain from alcohol or drugs if these contributed to the disease.
Liver Transplantation
Considerations for Patients:
Indications: End-stage liver disease (ESLD) or acute liver failure.
Preventative Measures:
Awareness of transplantation complications.
Interventions post-transplant.
Evaluate psychosocial impact.
Awareness of side effects related to immunosuppressive drugs.
Emphasis on long-term management of post-transplant care.
Practice Questions and Answers
Question 1: Which assessment finding requires immediate nursing intervention in a client with severe ascites?
Options:
Confusion
Temperature 38.2º C
Tachycardia (rate 110 beats/min)
Shallow respirations (rate 32 breaths/min)
Answer: D - Shallow respirations, as ascites can significantly impair lung function.
Question 2: What is the priority nursing intervention in the management of a client with decompensated cirrhosis?
Options:
Limiting protein intake
Managing nausea and vomiting
Monitoring fluid intake and output
Elevating the head of bed >30 degrees
Answer: B - Preventing nausea and vomiting due to the risk of bleeding esophageal varices.
Question 3: Which food item will the nurse remove from the dietary tray of a client with hepatic encephalopathy?
Options:
Salad
Apple
Bread
Legumes
Answer: D - Legumes (high protein) can worsen hepatic encephalopathy.
References
Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2021). In Medical-Surgical Nursing: Concepts for Interprofessional Collaborative Care (10th ed.), Elsevier.
Mayo Foundation for Medical Education and Research. (2023, June 21). Liver disease. Retrieved from https://www.mayoclinic.org/diseases-conditions/liver-problems/symptoms-causes/syc-20374502
Tapper, E. B., & Curry, M. P. (2018). Hepatitis Caused by Other Viruses. In Handbook of Liver Disease, 78–83. https://doi.org/10.1016/B978-0-323-47874-8.00006-7