Please enable JavaScript.
Coggle requires JavaScript to display documents.
Acute Liver Failure (ALF) - Coggle Diagram
Acute Liver Failure (ALF)
Definition and Classification
Acute Liver Failure (ALF) is characterized by rapid liver dysfunction, leading to jaundice, coagulopathy, and hepatic encephalopathy in patients without prior liver disease. It is classified based on the time between jaundice onset and encephalopathy:
Hyper-acute: <7 days
Acute: 7–21 days
Sub-acute: 21 days to 26 weeks.
Causes of ALF
ALF can result from various causes, including:
Viral infections (HAV, HBV, HDV, HEV, herpes simplex virus, cytomegalovirus, Epstein-Barr virus)
Drugs and toxins (acetaminophen overdose, NSAIDs, sulfonamides, herbal remedies)
Vascular issues (Budd-Chiari syndrome, portal vein thrombosis, cardiac failure)
Metabolic disorders (Wilson’s disease, acute fatty liver of pregnancy)
Surgery and transplantation complications.
Pathophysiology
ALF leads to multiple physiological disruptions, including:
Jaundice from impaired bilirubin conjugation
Coagulopathy due to reduced clotting factor synthesis
Hypoglycemia from decreased glucose production
Metabolic acidosis from reduced lactate clearance
Hepatic encephalopathy due to toxic substance accumulation
Complications of ALF
ALF affects multiple organ systems, causing:
Increased risk of infection
Fluid and electrolyte imbalances
Ascites due to portal hypertension
Cerebral edema leading to increased intracranial pressure
Coagulopathy and increased bleeding risk
Acute kidney injury (AKI) and hepatorenal syndrome.
Clinical Presentation
Patients typically present with:
Malaise, nausea, vomiting, and abdominal pain
Jaundice and signs of hepatic encephalopathy (confusion, personality changes, coma)
Symptoms of cerebral edema (hypertension, bradycardia, papilledema)
Evidence of bleeding or renal failure.
Diagnostic Studies
Laboratory tests: Prolonged prothrombin time (PT), elevated bilirubin, AST, alkaline phosphatase, serum ammonia; low albumin
Arterial blood gases: Metabolic acidosis or respiratory alkalosis
Imaging: Ultrasound, CT scan for liver structure evaluation.
Management Priorities
ABCs (Airway, Breathing, Circulation) stabilization
Hemodynamic monitoring and fluid management
Ventilatory support for respiratory distress or encephalopathy
Antibiotic therapy for infection prevention.
Reducing Ammonia Levels and Encephalopathy Treatment
Lactulose: Promotes ammonia excretion
Antibiotics (neomycin, rifaximin): Reduce intestinal bacteria that produce ammonia
Avoiding sedatives: To prevent worsening of encephalopathy.
Nutritional Support and Fluid Balance
High-protein diet (1.2–2 g/kg/day) to prevent catabolism
Sodium and fluid restriction (to control ascites and edema)
Nasogastric feeding or TPN in severe cases.
Nursing Care and Prevention of Injury
Monitor for signs of bleeding (petechiae, IV site bleeding)
Limit invasive procedures to minimize bleeding risk
Prevent skin breakdown through regular repositioning
Control intracranial pressure by elevating the head of the bed and minimizing stimulation.