liver failure(redirected from Hepatic failure)
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liver failureClinical medicine Liver insufficiency that results in death, requires a liver transplant, or is characterized by recovery after encephalopathy, or while awaiting a transplant; also defined as a condition with ≥ 3 of following: albumin < 3.5 g/dL; prolonged prothrombin time–PT; jaundice; ascites; PT is expressed as a ratio vs value from pooled normal plasma, is considered prolonged when the values are > the upper limit of normal–ie, 0.84-1.18; jaundice is defined as a BR concentration ≥ 2X upper normal range; ascites is ID'd by ultrasonography Epidemiology 27,000 die/yr–US Etiology Viral hepatitis; drugs–eg, valproic acid, INH, halothane, acetaminophen, mushroom, phosphorous, aspirin, etc; alcohol; idiopathic; myocarditis, heart surgery, cardiomyopathy, Budd-Chiari syndrome; metabolic disorders–eg, galactosemia, tyrosinemia, iron storage, mitochondrial disease, fatty acid oxidation Clinical Jaundice, fatigue, weight loss, if extreme, renal failure, hepatic encephalopathy Complications Cerebral edema, infection, renal failure, bleeding Treatment Symptomatic support; liver transplantation; possibly in the future, bioartificial liver
liver failureThe end stage of severe liver disease in which liver function is so impaired that it cannot meet the metabolic needs of the body. There is JAUNDICE, an accumulation of toxic substances in the blood such as ammonia, fatty acids and nitrogenous compounds causing a sweet musty odour in the breath, nausea and vomiting and brain damage with restlessness, disorientation, coarse tremor of the hands, sometimes aggressive outbursts, convulsions, weakness, coma and death.
|Mean LOS:||7 days|
|Description:||MEDICAL: Disorders of Liver Except Malignancy, Cirrhosis, Alcoholic Hepatitis With Major CC|
Liver (hepatic) failure is a loss of liver function because of the death of many hepatocytes. The damage can occur suddenly, as with a viral infection, or slowly over time, as with cirrhosis. Acute liver failure refers to both fulminant hepatic failure (FHF) and subfulminant hepatic failure. FHF occurs when sudden (within 8 weeks from onset) severe liver decompensation caused by massive necrosis of the liver leads to coagulopathies and encephalopathy. Approximately 2,000 people in the United States develop FHF each year. Subfulminant hepatic failure, also known as late-onset hepatic failure, can take up to 26 weeks before hepatic encephalopathy develops. Hepatic encephalopathy occurs with neurological changes such as personality changes, changes in cognition and intellect, and reduced level of consciousness.
Because of the complex functions of the liver, liver failure leads to multiple system complications. When ammonia and other metabolic byproducts are not metabolized, they accumulate in the blood and cause neurological deterioration. Without normal vitamin K activation and the production of clotting factors, the patient has coagulation problems. Patients are at risk for infections because of general malnutrition, debilitation, impairment of phagocytosis, and decreased liver production of immune-related proteins. Fluid retention occurs because of decreased albumin production, leading to decreased colloidal osmotic pressure with failure to retain fluid in the bloodstream. Renin and aldosterone production cause sodium and water retention. Ascites occurs because of intrahepatic vascular obstruction with fluid movement into the peritoneum.
Complications of liver failure include bleeding esophageal varices (Box 1), hemorrhagic shock, hepatic encephalopathy, hepatorenal syndrome, coma, and even death.Bleeding Esophageal Varices
- Esophageal varices (fragile, distended, and thin-walled veins in the esophagus) occur in patients with liver failure because of portal hypertension. Obstructed blood circulates to low-resistance alternate vessels around the portal circulation in the liver, which is a high-pressure system. One of these routes is through the esophageal veins, which become distended with blood, irritated from pressure, and susceptible to rupture. Treatment of esophageal varices includes the following:
- Surgery. Procedures include placing a portal caval shunt or distal splenorenal shunt, esophageal repair, or devascularization.
- Endoscopic Sclerotherapy. To cause fibrosis of the varices, patients are injected with solutions during an endoscopy procedure. Sodium tetradecyl sulfate or sodium morrhuate are commonly used sclerosants in the United States.
- Esophageal Balloon Tamponade. Endoscopic therapy has replaced balloon tamponade in almost all situations. If balloon therapy is used, it is essential that it is initiated by an experienced clinician. In balloon tamponade, a multilumen gastrointestinal tube with an esophageal and gastric balloon is passed into the upper gastrointestinal tract through the patient’s mouth. The gastric balloon, which is filled with 250 to 300 mL of air, acts as an anchor; the esophageal balloon, which is filled with enough air to cause 20 to 75 mm Hg pressure, compresses the esophageal varices to decrease bleeding. Traction may be inserted by taping the outer portions of the multilumen tube to the face mask of a football helmet.
- Parenteral Therapy. Maintain a large-bore intravenous (IV) line and keep several units of packed cells on call from the blood bank at all times.
- Vasopressin (Pitressin) Therapy. A continuous infusion of this vasoconstrictor causes constriction of the mesenteric circulation and decreased blood flow to the portal circulation.
The leading causes of FHF are viral hepatitis and hepatotoxic drug reactions. Although viral hepatitis can lead to liver failure, fewer than 5% of patients with viral hepatitis actually develop it. Other causes include chronic alcohol abuse, hepatotoxic drug reactions (acetaminophen in particular), acute infection or hemorrhage that leads to shock, fatty liver of pregnancy, prolonged cholestasis (arrest of bile excretion), and metabolic disorders. Many of these lead to cirrhosis, a chronic liver disease that results in widespread tissue fibrosis, nodule formation, and necrosis of the liver tissue.
Autosomal dominant polycystic disease is due to mutations in two genes (AD-PKD1 and AD-PKD2) that increase susceptibility to liver cysts. Isolated liver cysts (the polycystic liver disease) has been linked to the protein kinase C substrate 80K-H (PRKCSH) gene. Some affected persons develop massive hepatic cystic disease that results in liver failure. Wilson’s disease is a genetic disorder (autosomal recessive pattern) leading to a large liver accumulation of copper. About 5% of patients suffer from acute liver failure or fulminant hepatitis.
Gender, ethnic/racial, and life span considerations
Although acute liver failure can occur at any age, infants and children are more likely to have an inherited disease, whereas adult men are more likely to have alcohol-related disease. The poorest outcomes and mortality rates are found in children under 10 years or adults older than 40 years. Cirrhosis is the 12th leading cause of death in the United States and occurs most commonly between the ages of 35 and 55. Women develop acute liver failure at a later age than men and are more likely to have failure related to viral hepatitis E or autoimmune liver disease than men. No data exist regarding racial and ethnic susceptibility.
Global health considerations
The cause of liver failure varies across different nations. Worldwide statistics indicate that postnecrotic cirrhosis is more common in women than men and is the most common type of liver failure worldwide. Acetaminophen overdose is a common cause of liver failure in Western Europe, whereas hepatitis B viral infections are a major cause in developing countries. Hepatitis E virus is associated with liver failure in women who are pregnant, particularly women living or traveling in developing regions in Mexico, India, China, and Northern Africa.
Take a detailed medication history with particular attention to hepatotoxic medications, such as anesthesia agents, analgesics, antiseizure medications, cocaine, alcohol, isoniazid, and oral contraceptives. Ask about any recent travel to China, southeast Asia, sub-Saharan Africa, the Pacific Islands, and areas around the Amazon River, which may have exposed the patient to hepatitis B. Explore the patient’s occupational history for hepatitis exposure; patients who are day-care workers, dental workers, physicians, nurses, or hospital laboratory workers are particularly at risk. Ask the patient if she or he has experienced previous liver or biliary disease. IV drug users and male homosexuals are at risk for hepatitis and therefore liver failure. Those who eat raw shellfish are at similar risk.
Early symptoms include personality changes (agitation, forgetfulness, disorientation), fatigue, anorexia, drowsiness, and mild tremors. Some patients experience sleep disturbance and low-grade fevers. As larger areas of the liver are destroyed, the patient has increasing fatigue, confusion, and lethargy. If the patient has long-standing liver failure, he or she experiences jaundice, dry skin, early-morning nausea, vomiting, anorexia, weight loss, altered bowel habits, and epigastric discomfort. If sudden FHF occurs, the patient may develop encephalopathy (decreased mental status, fixed facial expression), peripheral swelling, ascites, and bleeding tendencies. Urine is often dark from bilirubin, and stools are often light colored because of the absence of bilirubin.
The patient with acute liver failure usually has jaundiced skin and sclera. Fluid retention results in ascites and peripheral edema. The patient’s facial expression appears fixed, her or his movements are hesitant, and speech is slow. Usually, the patient’s mental status is markedly decreased, and you may smell fetor hepaticus, a sweet fecal odor, on the patient’s breath. The patient may have multiple bruises, a bloody nose, or bleeding gums.
The patient’s peripheral pulses are bounding and rapid, indicating fluid overload and a hyperdynamic circulation. You may also palpate peripheral edema, an enlarged firm liver in acute failure and a small hard liver in chronic failure, an enlarged spleen, a distended abdomen, and an abdomen with shifting dullness to percussion and a positive fluid wave because of ascites. As ascites worsens, the patient develops hernias, an everted umbilicus, and an elevated and displaced heart because of a raised diaphragm. Usually, the patient with late disease has neck vein distention, and men develop gynecomastia (enlarged breasts), testicular atrophy, and scant body hair. When you monitor the patient’s vital signs, you may find an elevated temperature and a low-to-normal blood pressure; if the physician initiates hemodynamic monitoring, the cardiac output may be low if ascites is decreasing the right ventricular filling pressure and if the systemic vascular resistance is low.
The patient may feel upset or guilty if he or she contracted the disease while traveling. Use a nonjudgmental approach to elicit the patient’s feelings if the condition is related to alcohol abuse. If the patient is a candidate for a liver transplant, determine the patient’s emotional stability, ability to cope with a complex medical regimen, and ability to rely on significant others.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Prothrombin time||Varies by laboratory; generally 11–13 sec||Prolonged > 15 sec||Prothrombin is formed in the liver and is a vitamin K–dependent glycoprotein necessary for firm clot formation|
|Viral hepatitis seriologies: Hepatitis A virus (HAV); hepatitis B virus (HBV); hepatitis C virus (HCV); hepatitis D virus (HDV); hepatitis E virus (HEV) (see Hepatitis, p. 482)||Negative results||If patient has hepatitis: acute HAV: positive anti-HAV IgM; acute HBV: anti-HBV IgM; HB surface antigen; acute HCV: anti-HCV antibody, HCV RNA; HDV: anti-HDV IgM, HDV antigen; HEV: not available; non-A, non-B: all tests negative||Identify patients with hepatitis; virus leads to markers such as immunoglobulins (IgG and IgM), antigens, antibodies|
|Liver function tests||Alanine aminotransferase (ALT), 4–46 U/L; aspartate aminotransferase (AST), 8–20 U/L; alkaline phosphatase, 32–92 U/L||ALT elevated as high as or higher than 1,000 U/L; AST elevated as high as or higher than 1,000 U/L; alkaline phosphatase mildly elevated||Determine the extent of liver damage|
Other Tests: The most important aspect of the diagnostic work-up is to determine the underlying cause of liver failure. Tests include liver ultrasound, computed tomography, magnetic resonance imaging, drug and alcohol screening, bilirubin, lactate dehydrogenase, complete blood count, serum glucose, serum sodium and potassium, ammonia, albumin, and liver biopsy.
Primary nursing diagnosis
DiagnosisFluid volume excess related to water and sodium retention
OutcomesFluid balance; Hydration; Nutrition management; Nutrition therapy; Knowledge: Treatment regimen
InterventionsFluid/electrolyte management; Fluid monitoring; Medication administration
Planning and implementation
Liver transplantation is the definitive treatment for liver failure. More than 16,000 people are waiting for liver transplantation in the United States, and approximately 7,000 transplants are done each year. A liver transplant is indicated for patients with irreversible progressive liver disease who have no alternatives to transplantation, have life-threatening complications, or have the inability to sustain a normal quality of life.
While waiting for transplantation, if indicated, patients are managed with supportive therapy depending on their symptoms. Maintenance of airway, breathing, and circulation is the highest priority. Fluid and electrolyte imbalances, malnutrition, ascites, respiratory failure, cerebral edema, and bleeding esophageal varices can all occur with liver failure. Unless the patient has clinically significant hyponatremia, the patient usually receives limited IV fluids and food that contains sodium because increased sodium intake makes peripheral edema and ascites worse. Patients with ascites are usually restricted to 500 mg of sodium per day. A paracentesis may be used to remove 4 to 6 L of fluid. If the ascites is refractory, surgical placement of a peritoneal-venous shunt may be needed. Hypokalemia usually needs to be corrected with IV replacements. If the patient has serious fluid imbalances, a pulmonary artery catheter may be inserted for hemodynamic monitoring.
If respiratory failure is present, the patient may need endotracheal intubation and mechanical ventilation with supplemental oxygen. To manage nutrition in patients without evidence of hepatic encephalopathy, a high-calorie, 80- to 100-g protein diet is prescribed to allow for cellular repair. Some patients may need enteral or total parenteral nutrition to maintain calorie and protein levels. Hepatorenal failure is treated by fluid restriction, maintenance of fluid and electrolyte balance, and withdrawal of nephrotoxic drugs. Renal dialysis is generally not used because it does not improve survival and can lead to additional complications.
|Medication or Drug Class||Dosage||Description||Rationale|
|Histamine receptor (H2) antagonists||Varies with drug||Ranitidine and famotidine||Decrease gastric secretion; used as prophylaxis for ulcers|
|Thiamine||100 mg qd for several days or longer, depending on nutritional deficiencies||Vitamin supplement||Reduces risk for neuropathies|
|Vitamin K||Up to 10 mg IV as needed||Vitamin supplement||Needed for prothrombin production|
Other Drugs: Sedatives and acetaminophen are avoided because poor metabolism can precipitate encephalopathy. Aspirin is usually avoided because of the action on platelets, which can lead to increased bleeding. If ascites is present, diuretics, particularly aldosterone antagonists such as spironolactone (Aldactone), may be prescribed and, if ineffective, more potent loop diuretics may be added. Mannitol may be used as an osmotic diuretic to reduce cerebral edema. Barbiturates such as pentobarbital and thiopental may be used for intracranial hypertension. Silibinin is a derivative of silymarin, an active ingredient in herbal preparations that possesses antioxidant properties; its use may benefit liver disease management.
The most common problem for patients with liver failure is fluid volume excess. Measure the patient’s abdominal girth at the same location daily and mark the location as a reference point for future measurements. Notify the physician if the girth increases by 2 inches in 24 hours. Provide the required fluid allotment over the three meals and at night. If the patient desires, reserve some fluids to be used as ice chips. Provide mouth care every 2 hours. Because areas of edema are likely to be fragile and prone to skin breakdown, provide skin care.
One of the most life-threatening complications of liver failure is airway compromise because of neurological or respiratory deterioration. Keep endotracheal intubation equipment and an oral airway at the bedside at all times. Elevate the head of the patient’s bed to 30 degrees to ease respirations and support the patient’s arms on pillows to decrease the work of breathing. It is essential to be at the bedside and to perform serial assessments of all critical systems. Space all activities and limit visitors as needed so that the patient gets adequate rest. To encourage rest, consider nonpharmacologic methods such as diversionary activities and relaxation techniques.
The patient may be anxious, depressed, angry, or emotionally labile. Allow the patient to verbalize anxieties and fears. If needed, refer the patient to a counselor. Evaluate thoroughly anyone who is a candidate for a liver transplant to ensure that she or he has the ability to cope with a complex situation. Answer all questions, and explain the risks and benefits. Refer to an alcohol counselor if appropriate.
Evidence-Based Practice and Health Policy
Garg, H., Kumar, A., Garg, V., Sharma, P., Sharma, B.C., & Sarin, S.K. (2012). Clinical profile and predictors of mortality in patients of acute-on-chronic liver failure. Digestive and Liver Disease, 44(2), 166–171.
- Acute-on-chronic liver failure (ACLF) is characterized by jaundice and coagulopathy that is complicated within 4 weeks by ascites and/or encephalopathy.
- A study among 91 patients with ACLF revealed a 90-day mortality of 63%, with the time to death from admission ranging from 2 to 102 days (median, 15 days).
- Twenty-nine percent of patients had multiorgan failure at the time of admission, and 46% had developed multiorgan failure within 1 week postadmission.
- In this sample, the presence of hepatic encephalopathy increased the risk of mortality by 2.3 times (95% CI, 1.3 to 3.9; p = 0.002), serum sodium less than 133 mEq/L increased the risk of mortality by 1.8 times (95% CI, 1 to 3.1; p = 0.038), and INR of two or more increased the risk of mortality by 2.3 times (95% CI, 1.3 to 4.1; p = 0.005).
- Physical responses: Vital signs, ease of respirations, breath sounds, heart sounds, level of consciousness, gastrointestinal distress, abdominal girth, daily weights, color of skin and sclera
- Nutrition: Tolerance of diet, appetite, ability to maintain body weight or to decrease fluid retention, presence of muscle wasting or signs of malnutrition, albumin level
- Response to therapy: Clearing of mental status, improvement in infection, decreased or stable blood ammonia level
Discharge and home healthcare guidelines
Teach the patient to follow prescribed sodium and fluid restrictions. Assist the patient to individualize a diet plan to maximize personal choices, including a dietitian if necessary. Encourage sodium-restricted patients to read labels on all canned soups, sauces, and vegetables and on all over-the-counter medications. Be sure the patient understands any pain medication prescribed, including dosage, route, action, and side effects. Teach the patient and family the need to limit the rise of infections by good hand washing, avoidance of others with colds, and prompt treatment by a healthcare provider when an infection occurs. Refer the patient to an alcohol support group.