In the United States, about 2,000 people a year suffer acute liver failure. That doesn’t sound like a big number, but of those 2,000 people, 30% to 50% will die from complications. Those are big numbers—especially if you’re caring for one of the 2,000 patients.
Patient outcomes depend on several variables: early recognition of signs and symptoms, the cause of acute failure, the patient’s age, supportive therapy, and sometimes the availability of a liver for transplant. Nurses play key roles in monitoring these patients, identifying early signs and symptoms of complications, and coordinating and delivering the supportive care that allows time for hepatic regeneration or for sufficient improvement before liver transplantation.
Acute liver failure, previously called fulminant hepatic failure or fulminant liver failure, results from a massive impairment of liver cell function. The condition is divided into three types: hyperacute liver failure, acute liver failure, and sub-
acute liver failure (See Classifying acute liver failure in the PDF version by clicking on the download now button.)
What causes acute liver failure?
In the United States, most cases result from acetaminophen toxicity caused by an intentional or unintentional overdose. Unintentional overdoses may occur when a patient mistakenly exceeds the recommended dosage or when a patient takes the recommended dosage of acetaminophen and unknowingly takes more of the drug in a prescribed combination analgesic such as Vicodin (hydrocodone and acetaminophen). Drinking alcohol while taking acetaminophen can also cause acute liver failure. Alcohol alone rarely causes acute failure, though it does cause chronic liver failure and cirrhosis.
For residents of underdeveloped countries and those returning to the United States from underdeveloped countries, viral hepatitis—especially hepatitis A and B—may cause acute liver failure. The risk of acute liver failure is greater in those with hepatitis B and D than in those with hepatitis B alone.
Acute liver failure can also result from idiosyncratic reactions to herbal supplements and drugs, such as bromfenac (Xibrom), isoniazid (Nydrazid), phenytoin (Dilantin), methyldopa, sulfonamides, and nonsteroidal anti-inflammatory drugs.
Less common causes include:
• Amanita poisoning in amateur mushroom gatherers
• exposure to organic solvents—such as fluorinated hydrocarbons found in propellants, solvents, and refrigerants—and the industrial solvent trichloroethylene
• acute fatty liver of pregnancy
• metastatic cancer
• autoimmune conditions
• Wilson’s disease
• Budd-Chiari syndrome.
Monitoring the patient
The initial signs and symptoms are subtle and nonspecific, typically nausea and malaise. These symptoms are followed by jaundice. Your physical examination may reveal hepatic tenderness and enlargement. Ask the patient which drugs he is taking and note the dosages.
Patients with acute liver failure are at risk for hepatic encephalopathy, increased intracranial pressure (ICP), and cerebral edema, which result from hyperammonemia. Normally, ammonia is synthesized by microorganisms in the GI tract and detoxified in the astrocytes in the central nervous system. In those with acute liver failure, detoxification doesn’t occur.
Perform a complete neurologic assessment and ask about recent irritability, insomnia, confusion, or forgetfulness. Also ask about difficulty with handwriting, muscle tremors, or stiffness, which may suggest early encephalopathy. Because neurologic changes can develop rapidly, assess the patient’s neurologic status frequently to detect encephalopathy. (See Stages of encephalopathy in the PDF version by clicking on the download now button.) As encephalopathy develops, the risk of increased ICP rises, so evaluate pupil size and reaction and monitor vital signs for widening pulse pressure, transient increases in systolic blood pressure, and tachyarrhythmias or bradycardia.
The patient may develop nausea and vomiting, confusion, agitation, and aggression. Check his oxygenation status and fluid and electrolyte balance. Electrolyte imbalances—specifically sodium and potassium imbalances—may result from water retention and impaired function of the sodium-potassium pump. Check, too, for signs and symptoms of coagulopathy, which develops from platelet dysfunction, thrombocytopenia, decreased hepatic synthesis of fibrin, deficiencies in coagulation factors, and vitamin K deficiency.
Renal failure may develop from liver failure or cardiovascular changes. Changes in circulation may lead to a compromised cardiovascular status, and some patients may experience renal insufficiency. Hypoglycemia may result from depleted glycogen stores and hyperinsulinemia. And impaired host defense mechanisms increase the risk of infection.
Tests for acute liver failure include:
• liver function tests to check for elevated levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, and bilirubin
• complete blood count and coagulation studies to detect bleeding and coagulation disorders
• blood chemistry panel to identify hypoglycemia, electrolyte imbalances, and renal dysfunction
• lactate and alpha-fetoprotein levels to evaluate liver function and regeneration
• viral serologic and other tests to check for viral infections and metabolic and autoimmune disorders.
Several tests may be used to evaluate the cause and extent of liver dysfunction:
• ultrasound scan to detect liver contour and size, spleen size, bile duct dilation, and ascites
• computed tomography (CT) scan to detect liver contour and size, spleen size, hepatocellular carcinoma, metastatic cancer, ascites, and varices
• magnetic resonance imaging to evaluate the same structures as a CT scan as well as the blood vessels and biliary system
• liver biopsy to determine the cause of liver disease, amount of necrosis, and the presence and amount of fibrosis.
Managing the complications
Some causes of acute liver failure require specific treatments. If the cause is acetaminophen toxicity, for example, the patient should receive N-acetylcysteine within 8 hours of ingestion. If the cause is Amanita poisoning, the patient needs a penicillin and silymarin infusion. Most nursing interventions, however, focus not on the underlying cause but on the complications of acute liver disease.
A leading cause of death in patients with acute liver failure is cerebral edema. To detect it early and manage it, monitor your patient’s ICP and maintain cerebral perfusion pressure. Some patients may require an ICP monitoring device.
High ammonia levels may cause cellular swelling, increased cerebral vasodilation, or increased levels of gamma aminobutyric acid, all of which decrease neurologic function. To eliminate the source of increased ammonia, you’ll likely administer lactulose, a cathartic that will increase bowel movements. Neomycin or metronidazole (Flagyl) may be added to the regimen to decrease ammonia levels by reducing GI flora that produces ammonia as a byproduct. If the patient is going from stage 2 to stage 3 encephalopathy, notify the physician and gather equipment for elective intubation and ventilation.
Neck flexion and jugular vein occlusion can also increase ICP, so position the head of the bed at 30 degrees and use rolled towels to maintain a midline alignment of the patient’s head. If the patient needs sedation, a short-acting drug such as propofol (Diprivan) should be prescribed.
Patients with acute liver failure have an increased risk of infection and sepsis. Gram-positive, gram-negative, or fungal organisms may cause the infection. Common infection sites are the lungs and the urinary tract. Respiratory complications from sepsis, hemorrhage, pleural effusions, atelectasis, and intrapulmonary shunts may contribute to respiratory problems. Some patients develop acute respiratory distress syndrome. To prevent infection, limit I.V. access. If the patient will receive a liver transplant, empiric antibiotics may be prescribed.
Fluid imbalances and renal failure
A patient with acute liver failure may develop fluid overload because of renal dysfunction or fluid shifts caused by fluctuating oncotic pressures. Or the patient may become dehydrated from osmotic diuretic therapy, diabetes insipidus, or high-output renal failure. Evaluate hydration status, using hemodynamic monitoring to assess central venous pressure and maintaining accurate intake and output records. Also, monitor and correct electrolyte imbalances from changes in sodium and potassium levels and acid-base imbalances from changes in lactate levels.
Renal failure, which develops in about 50% of patients with acute liver failure, can result from dehydration or ingestion of a nephrotoxic substance such as acetaminophen. Initially, administer I.V. fluids and diuretics, as prescribed, and avoid administering nephrotoxic drugs. A patient with renal failure may need dialysis or continuous venous-venous hemodialysis.
Abnormal glucose levels and malnutrition
Closely monitor serum glucose levels to prevent hyperglycemia and hypoglycemia. The patient may need I.V. glucose or an insulin drip to maintain glycemic control.
Decreased glycogen stores can lead to malnutrition, and impaired synthetic activity in the liver can cause protein deficiency. Acute liver failure also increases the metabolic rate, increasing the risk of malnutrition. Supplementing a patient’s diet with tube feeding or total parenteral nutrition can help, but closely monitor glucose, lactate, triglyceride, and ammonia levels to evaluate substrate use.
If coagulopathy develops, minimize the number of needle sticks and monitor the patient’s gums, I.V. sites, and urine for signs of bleeding. Therapy for coagulopathy may consist of administering fresh frozen plasma, vitamin K, and coagulation factors, as appropriate. To suppress gastric acid secretion and reduce upper GI bleeding, a physician may order an I.V. proton pump inhibitor.
If a patient’s liver doesn’t regenerate and clinical and biochemical functions don’t improve, the physician will consider transplantation.
If the patient is a good candidate, he or she will receive priority status for transplantation.
Managing a patient with acute liver failure can be complex and challenging. But the goal is pretty simple: Manage the condition and its complications to buy the patient time. Time may not heal all livers in acute failure, but it heals most.
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Stravitz RT, Kramer AH, Davern T, et al. Intensive care of patients with acute liver failure: recommendations of the U.S. Acute Liver Failure Study Group. Crit Care Med. 2007;35(11):2498-2508.
Visit www.AmericanNurseToday.com/journal for a complete list of selected references.
Patricia Radovich is Manager of Nursing Research at Loma Linda University Medical Center in Loma Linda, California.