Characterized by widespread fibrotic (scarred) bands of connective tissue that disrupt normal liver architecture.
Tissue becomes nodular, obstructing both blood and lymph flow through the liver, leading to increased intrahepatic vascular resistance.
Results in shrinking and hardening of the liver, contributing to various portal complications.
Cirrhosis Types:
Postnecrotic: Often follows severe liver damage or necrosis.
Laennec's (alcoholic): Resulting from chronic alcohol abuse.
Biliary: Due to bile duct obstruction and injury.
Other Conditions:
Hepatitis A, B, C, D, E: Viral infections causing inflammation of the liver.
Liver tumors/cancers: Both primary (like hepatocellular carcinoma) and metastatic cancers.
Portal hypertension: Increased pressure in the portal venous system leading to varices.
Ascites and esophageal varices: Fluid accumulation in the abdominal cavity and swollen veins in the esophagus that can bleed.
Biliary obstruction: Leading to jaundice and potential liver failure.
Hepatic encephalopathy: Impaired brain function due to liver failure, characterized by confusion and altered consciousness.
Potential for liver failure and other severe complications affecting overall health.
Key Interventions for Decompensated Cirrhosis:
Limiting protein intake to lower ammonia production.
Managing nausea and vomiting to ensure nutritional intake.
Monitoring fluid intake and output to prevent fluid overload.
Elevating the head of the bed > 30 degrees to help with breathing and reduce ascites discomfort.
Leading Causes of Cirrhosis:
Hepatitis C (most common in U.S.): One of the major causes due to chronicinfection.
Hepatitis B and D (common causes worldwide): Hepatitis B can lead to cirrhosis if untreated.
Non-alcoholic fatty liver disease (NAFLD): Associated with obesity and metabolic syndrome, another growing concern.
Excessive and prolonged alcohol use: A primary risk factor in many patients.
History:
Age, gender, and employment history (exposure risk to toxins, viruses).
Social and family history, including instances of liver disease and substance use.
Needlestick injuries, especially in healthcare workers.
Physical Assessment:
Signs including fatigue, unintentional weight change, gastrointestinal symptoms like dyspepsia.
Abdominal assessment for presence of ascites and tenderness indicating potential liver enlargement or inflammation.
Psychosocial Assessment:
Assess for alcohol withdrawal symptoms in patients with a history of chronic alcohol use.
Signs include:
Jaundice, spider nevi, pallor, and caput medusae (dilated abdominal veins).
Anemia, leukopenia, thrombocytopenia commonly observed in late-stage disease.
Ascites presenting as abdominal distension, splenomegaly, and testicular atrophy are common physical findings.
Hemorrhagic tendencies due to coagulopathy, altered hair distribution in some cases of hepatic dysfunction.
Key laboratory tests:
ALP, ALT, AST, GGT, serum bilirubin, serum albumin, PT/INR, CBC, ammonia level critical for diagnosis and monitoring.
Normal Liver Functions:
AST: 8-48 U/L
ALT: 7-55 U/L
LDH: 122-222 U/L
ALP: 40-129 U/L
GGT: 8-61 U/L
Bilirubin: 0.1-1.2 mg/dL
Albumin: 3.5-5.0 g/dL
Total protein: 6.3-7.9 g/dL
PT: 11-12.5 seconds
INR: 0.8-1.1
Imaging Assessments:
Abdominal X-rays, CT, MRI to visualize structural changes.
Diagnostic Procedures:
Liver ultrasound for size and blood flow evaluation, transient elastography for stiffness assessment, paracentesis for ascitic fluid analysis, ERCP for biliary tree evaluation.
Fluid Management:
Address fluid overload and manage ascites via paracentesis, where large amounts of fluid are drained.
Management of Hemorrhage:
Use of Sengstaken-Blakemore tube for varices management to control and prevent bleeding.
Preventing Confusion:
Monitor and manage increased serum ammonia levels, initiating therapy as needed.
Self-management education regarding medications such as lactulose and diuretics for symptom control and ascites management.
Avoidance of alcohol, monitoring for signs and symptoms of encephalopathy to prevent worsening conditions.
Beta-Blockers:
To reduce portal inflow and manage bleeding risks effectively.
Expected outcomes include:
Decreased or no ascites with fluid therapy.
Normal electrolyte levels and balanced nutritional intake.
No occurrences of hemorrhage with effective management and intervention.
Successful abstinence from alcohol, as determined by patient self-reports and clinical evaluation.
Types of Viral Hepatitis:
HAV, HBV, HCV, HDV, HEV noted for their public health impact.
Etiology of Hepatitis:
HAV: Shellfish contamination, poor food handling practices, especially in endemic areas.
HBV: Transmitted through unprotected sex, needle sharing, blood transfusions (pre-1992), and more.
HCV: Primarily through illicit IV drug use and occupational exposure risks.
HDV: Requires HBV to replicate and is primarily seen in high-risk IV drug users.
HEV: Waterborne infection prevalent in certain geographic regions during poor sanitation conditions.
Vaccination for HAV and HBV to prevent infections.
Infection control education, especially for healthcare workers, to mitigate transmission risks.
Successful management and understanding of the complications and treatment options for liver diseases are crucial for patient outcomes, emphasizing the importance of early detection and intervention.