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Nursing Guide to Adult Jaundice: Nursing Diagnosis, Interventions, & Care Plans

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Updated On 7 Minute Read

Hyperbilirubinemia, also referred to as jaundice, is characterized by yellow discoloration of the skin, sclerae, and mucous membranes. This is due to elevated levels of bilirubin in the bloodstream, known as hyperbilirubinemia. It’s a symptom rather than a disease, indicating underlying hepatic, hematologic, or biliary pathology.  

Nurses are often the first healthcare providers to identify this symptom during patient assessments and help in monitoring, education, and collaborative management. 

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Etiology and epidemiology 

Bilirubin is a byproduct of heme catabolism from aged or damaged red blood cells. Normally, unconjugated bilirubin binds to albumin, is moved to the liver, conjugated with glucuronic acid, and expelled into bile. Jaundice results from an imbalance between bilirubin production and its hepatic processing and excretion, which causes an excess amount of unconjugated bilirubin to collect in one or more physiological ways.   

Disruption at any point in this pathway can result in visible jaundice, which is broadly categorized into three types: 

1. Pre-hepatic (hemolytic) 

  • This form arises from increased bilirubin production due to accelerated breakdown of erythrocytes, overwhelming the liver’s conjugating capacity. Unconjugated (indirect) bilirubin levels become elevated.
  • Common causes include sickle cell anemia, hereditary spherocytosis, thalassemia, transfusion reactions, and parasitic infections like malaria.
  • Clinical features may include anemia, pallor, splenomegaly, and dark urine due to urobilinogen. 

2. Hepatic (hepatocellular) 

  • This type stems from liver parenchymal cell dysfunction, impairing uptake, conjugation, or excretion of bilirubin. Both conjugated and unconjugated bilirubin levels can rise.
  • Etiologies include viral hepatitis (A, B, C, etc.), alcoholic hepatitis, nonalcoholic steatohepatitis (NASH), autoimmune hepatitis, hepatocellular carcinoma, and drug-induced hepatotoxicity (e.g., acetaminophen overdose).
  • Symptoms often include malaise, right upper quadrant pain, nausea, elevated liver enzymes, and signs of chronic liver disease, such as spider angiomas and ascites. 

3. Post-hepatic (obstructive) 

  • This occurs when bile flow is impeded after bilirubin conjugation, leading to the accumulation of conjugated (direct) bilirubin in the blood.
  • Common causes include choledocholithiasis (bile duct stones), pancreatic head carcinoma, biliary atresia, and cholangiocarcinoma.
  • Clinically, patients present with jaundice, pale stools, dark urine, pruritus, and elevated alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT). 

ICD-10 code 

  • R17 — Unspecified jaundice
  • K83.1 — Obstruction of bile duct
  • K76.0 — Fatty (change of) liver, not elsewhere classified 

Nursing care plan 

Nursing care for patients with hyperbilirubinemia is comprehensive and extends beyond symptom management. Nurses help with the early identification of complications, patient safety, and the implementation of targeted interventions.  

Their responsibilities include monitoring physiological parameters, managing discomfort related to skin changes, providing nutritional and hydration support, and reinforcing the treatment plan through patient and caregiver education.  

The individualized nursing care plan should address the specific type and severity of jaundice, as well as any underlying hepatic or systemic conditions contributing to bilirubin elevation. When creating and implementing a care plan, keep the following components in mind: 

Nursing considerations 

  • Assess skin and scleral color.
  • Monitor input, output, and nutritional intake.
  • Watch for neurological changes (e.g., confusion, lethargy).
  • Prevent skin breakdown due to pruritus.
  • Document bilirubin trends and lab findings. 

Assessment 

  • Skin, sclerae, mucosa
  • Urine and stool color
  • Appetite, weight changes
  • Bleeding/bruising
  • Neurological status 

Nursing diagnosis/risk for 

  • Risk for impaired skin integrity
  • Imbalanced nutrition: less than body requirements
  • Risk for fluid volume deficit
  • Fatigue related to liver dysfunction
  • Risk for injury related to altered mental status 

Interventions 

  • Apply soothing lotions for pruritus.
  • Promote small, frequent meals.
  • Administer prescribed medications.
  • Use fall precautions.
  • Educate on disease and lifestyle modifications. 

Expected outcomes 

  • Bilirubin levels stabilize
  • Patient remains alert and oriented
  • Adequate oral intake and hydration
  • Improved understanding of self-care 

Clinical history, examination, and testing 

An accurate clinical history should explore multiple domains to help differentiate between hepatic, pre-hepatic, and post-hepatic causes: 

  • Duration and progression of jaundice: Sudden onset may suggest obstruction or acute hepatitis. A gradual onset may indicate chronic liver disease.
  • Medication and substance use: Hepatotoxic drugs (e.g., acetaminophen, methotrexate), alcohol use, herbal supplements.
  • Infectious exposure: Recent travel to areas endemic for hepatitis A or E; contact with jaundiced individuals.
  • Transfusion history: Risk for viral hepatitis or transfusion reactions.
  • Family history: Inherited hemolytic disorders (e.g., Gilbert's syndrome, G6PD deficiency, Wilson disease). 

Physical exam 

Use the physical examination to assess for signs that correlate with specific etiologies like these: 

  • Scleral icterus: This is one of the earliest and most sensitive signs of hyperbilirubinemia.
  • Hepatomegaly or splenomegaly: This may indicate infiltrative liver disease or hemolysis.
  • Ascites or peripheral edema: This is suggestive of portal hypertension and chronic liver dysfunction.
  • Signs of chronic liver disease: Spider angiomas, palmar erythema, caput medusae, muscle wasting.
  • Bruising or bleeding: This reflects coagulopathy due to impaired hepatic synthesis of clotting factors.
  • Neurological assessment: An altered mental status or asterixis in hepatic encephalopathy. 

Laboratory tests 

The following types of laboratory testing provide biochemical confirmation: 

  • ALT, AST: Elevated levels are markers of hepatocellular injury; AST>ALT in alcoholic hepatitis.
  • ALP, GGT: Elevated in cholestatic or obstructive jaundice; GGT is more liver specific.
  • CBC: Anemia may point to hemolysis; leukocytosis suggests infection; thrombocytopenia is common in portal hypertension.
  • PT/INR: Prolonged times indicate impaired liver synthetic function.
  • Hepatitis serologies: This is essential for diagnosing viral hepatitis (A, B, C).
  • Autoimmune panel: ANA, ASMA for autoimmune hepatitis.
  • Metabolic testing: Ceruloplasmin for Wilson disease; alpha-1 antitrypsin and iron studies for genetic liver disorders. 

Imaging 

Radiologic studies are vital for visualizing hepatic architecture and biliary tree anatomy: 

  • Abdominal ultrasound: This is the first line for evaluating hepatomegaly, biliary dilation, gallstones, or liver masses.
  • CT or MRI: This provides a more detailed assessment of liver parenchyma and surrounding organs
  • Magnetic resonance cholangiopancreatography (MRCP): This is a non-invasive imaging technique beneficial for detecting bile duct obstruction, strictures, or cholangiocarcinoma. 

NANDA-I framework 

Incorporating the North American Nursing Diagnosis Association-International (NANDA-I), nursing diagnoses can guide clinical decision-making and care planning: 

  • Impaired liver function: Related to hepatocellular injury or bile obstruction, as evidenced by jaundice and elevated liver enzymes.
  • Risk for bleeding: Due to reduced hepatic synthesis of clotting factors.
  • Imbalanced nutrition: less than body requirements: Resulting from anorexia, nausea, or malabsorption.
  • Disturbed thought process: Associated with hepatic encephalopathy. 

These nursing diagnoses support comprehensive care planning alongside medical management. 

Management 

Treatment is based on the underlying cause and requires a multidisciplinary approach, involving medical, surgical, and supportive interventions tailored to the type of jaundice. 

Pre-hepatic 

  • Manage hemolysis. In conditions like autoimmune hemolytic anemia, corticosteroids or immunoglobulin therapy may be indicated. In severe anemia, blood transfusions may be necessary. Infections such as malaria require prompt treatment with antimalarial medications.
  • Give supportive care. Ensure adequate hydration to facilitate renal clearance of bilirubin. Oxygen therapy may be needed in anemic hypoxia, and folate supplementation supports increased erythropoietic activity. 

Hepatic 

  • Viral hepatitis: Administer specific antiviral regimens based on the type of virus (e.g., interferon-based or direct-acting antivirals for hepatitis C).
  • Alcoholic liver disease: Requires absolute cessation of alcohol, nutritional rehabilitation including thiamine and multivitamins, and corticosteroids in severe cases such as alcoholic hepatitis with Maddrey score >32.
  • Autoimmune hepatitis: Immunosuppressive therapy with corticosteroids and azathioprine is the mainstay. Long-term monitoring for relapses is essential.
  • Drug-induced liver injury (DILI): Immediate discontinuation of the offending agent is critical. Monitor liver function tests closely and consider N-acetylcysteine in acetaminophen toxicity. 

Post-hepatic 

  • Gallstones: ERCP (endoscopic retrograde cholangiopancreatography) can relieve obstruction, followed by elective cholecystectomy to prevent recurrence.
  • Tumors or strictures: Management may involve biliary stenting, surgical resection, chemotherapy, or palliative care depending on the extent of disease.
  • Cholangitis: Urgent initiation of broad-spectrum antibiotics and biliary drainage via ERCP is required to prevent sepsis. 

Supportive care 

  • Hydration: Maintain euvolemia with oral or intravenous fluids as needed.
  • Nutrition: Promote a high-calorie, balanced diet tailored to hepatic function. Protein intake may be adjusted in advanced liver disease.
  • Monitoring for complications: Regular assessments for hepatic encephalopathy, coagulopathy, ascites, and variceal bleeding. Early intervention improves outcomes and quality of life. 

Individual/caregiver education 

  • Signs of worsening liver function
  • Importance of follow-up lab work and imaging
  • Medication safety: Avoid acetaminophen and alcohol
  • Nutritional guidelines for liver health 

FAQs

Resources 

References 

Headshot of Mary Lynch

Mary Lynch, MSN, RN

Mary E. Lynch, MSN, RN, is a multidisciplinary healthcare leader with over 20 years of experience spanning financial analytics, clinical care, and healthcare education. After nearly a decade in the accounting and finance sectors, Lynch followed her passion for maternal health and pivoted into nursing, specifically postpartum care. She spent over 10 years supporting new moms, babies, and their families through one of life's most vulnerable transitions. Her deep clinical foundation now fuels her work as a Curriculum Designer at Relias.