Fulminant hepatic failure is another name for acute liver failure. Acute means it has a rapid onset and follows a short, severe course. The liver performs many important functions, including the production of bile, which helps change substances in the foods we eat into proteins, fats, and carbohydrates, and the absorption of harmful substances such as chemicals, drugs, and alcohol from the body. If liver cells are damaged and die, the remaining cells are not able to perform all of the liver’s functions. As toxins build up, the patient’s health begins to fail.
Risk group
Fulminant hepatic failure is more common in infants and children with certain diseases and metabolic defects that damage and destroy liver tissue. Children who take immunosuppressive drugs or have a disease that compromises the immune system are also at higher risk for liver failure as a complication of the herpes virus.
Causes
Fulminant hepatic failure in infants under four weeks old can be caused by viruses such as herpes simplex; adenovirus, which causes conjunctivitis and upper respiratory tract infections; or enteroviruses, which affect the gastrointestinal tract. Other causes in very young infants include neonatal iron storage disease, certain metabolic disorders such as tyrosinemia and galactosemia, fructose intolerance, familial erythrophagocytic histiocytosis, peroxisomal diseases, and defects in respiratory chain and fatty acid oxidation or synthesis of bile acid. Older infants and children are more likely to develop fulminant hepatic failure from viral hepatitis (HBV, HEV, NANBNC) or parvovirus (which causes fifth disease). Other causes of liver failure in older children can include Wilson’s disease, fatty liver, acetaminophen overdose, chronic alcohol abuse, exposure to toxins (such as poisonous mushrooms), leukemia, Reye’s syndrome, cardiomyopathy, and autoimmune hepatitis. In some cases, the cause of liver failure is unknown.
Symptoms
Symptoms of fulminant hepatic failure include a build up of fluid in the abdomen, which causes swelling called ascites; a yellowish tone to the skin, called jaundice; light-colored bowel movements; a tendency to bruise or bleed easily; fever; abdominal pain; itchy skin; dark urine; nausea; loss of appetite; fatigue; and weakness. As the condition progresses, it causes confusion and erratic behavior as the build up of toxins in the blood affects brain function. This is called liver encephalopathy. Liver failure can also cause kidney failure, coma, and death.
Acute Care Patient Management
Nursing Diagnosis: Deficient fluid volume related to ascites secondary to hypoalbumineia, bleeding secondary to decreased clotting factors or variceal hemorrhage, and diuretic therapy.
Patient Monitoring
Treatment for fulminant hepatic failure is based upon the cause and the symptoms. The child will receive intravenous (IV) fluids to carefully balance fluids, electrolytes, and glucose levels. If the child is comatose, he or she may need to be intubated to help with breathing. Medications, blood transfusions, and hemodialysis can be used to remove toxins from the body. However, liver damage cannot be reversed. The most effective treatment is liver transplant. The survival rate for patients who receive a liver transplant is higher than those who do not.
Comprehensive care
If your child has been diagnosed with fulminant hepatic failure, work with your doctor to learn all you can about your child’s condition. You will find that knowledge is your best defense and will help you make the right decisions for your child. When your child comes home from the hospital, carefully follow your doctor’s orders for diet and medication to keep your child as healthy as possible.
Diagnostic Assessment
Nursing care plan assessment and physical examination
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 distension, 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.
Nursing care plan primary nursing diagnosis: Fluid volume excess related to water and sodium retention.
Nursing care plan intervention and treatment plan Patients are managed with supportive therapy, depending on their symptoms. Fluid and electrolyte imbalances, malnutrition, ascites, respiratory failure, 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.
Fulminant hepatic failure is more common in infants and children with certain diseases and metabolic defects that damage and destroy liver tissue. Children who take immunosuppressive drugs or have a disease that compromises the immune system are also at higher risk for liver failure as a complication of the herpes virus.
Causes
Fulminant hepatic failure in infants under four weeks old can be caused by viruses such as herpes simplex; adenovirus, which causes conjunctivitis and upper respiratory tract infections; or enteroviruses, which affect the gastrointestinal tract. Other causes in very young infants include neonatal iron storage disease, certain metabolic disorders such as tyrosinemia and galactosemia, fructose intolerance, familial erythrophagocytic histiocytosis, peroxisomal diseases, and defects in respiratory chain and fatty acid oxidation or synthesis of bile acid. Older infants and children are more likely to develop fulminant hepatic failure from viral hepatitis (HBV, HEV, NANBNC) or parvovirus (which causes fifth disease). Other causes of liver failure in older children can include Wilson’s disease, fatty liver, acetaminophen overdose, chronic alcohol abuse, exposure to toxins (such as poisonous mushrooms), leukemia, Reye’s syndrome, cardiomyopathy, and autoimmune hepatitis. In some cases, the cause of liver failure is unknown.
Symptoms
Symptoms of fulminant hepatic failure include a build up of fluid in the abdomen, which causes swelling called ascites; a yellowish tone to the skin, called jaundice; light-colored bowel movements; a tendency to bruise or bleed easily; fever; abdominal pain; itchy skin; dark urine; nausea; loss of appetite; fatigue; and weakness. As the condition progresses, it causes confusion and erratic behavior as the build up of toxins in the blood affects brain function. This is called liver encephalopathy. Liver failure can also cause kidney failure, coma, and death.
Acute Care Patient Management
Nursing Diagnosis: Deficient fluid volume related to ascites secondary to hypoalbumineia, bleeding secondary to decreased clotting factors or variceal hemorrhage, and diuretic therapy.
Patient Monitoring
- Obtain pulmonary artery pressure, central venous pressure, and blood pressure until the patient’s condition is stable, then hourly.
- Continuously monitor ECG for lethal dysrhythmias that may result from electrolyte and acid-base imbalances.
- Monitor fluid volume status. Measure intake and output hourly.
Treatment for fulminant hepatic failure is based upon the cause and the symptoms. The child will receive intravenous (IV) fluids to carefully balance fluids, electrolytes, and glucose levels. If the child is comatose, he or she may need to be intubated to help with breathing. Medications, blood transfusions, and hemodialysis can be used to remove toxins from the body. However, liver damage cannot be reversed. The most effective treatment is liver transplant. The survival rate for patients who receive a liver transplant is higher than those who do not.
Comprehensive care
If your child has been diagnosed with fulminant hepatic failure, work with your doctor to learn all you can about your child’s condition. You will find that knowledge is your best defense and will help you make the right decisions for your child. When your child comes home from the hospital, carefully follow your doctor’s orders for diet and medication to keep your child as healthy as possible.
Diagnostic Assessment
- Review serial serum ammonia, albumin, bilirubin, platelet count, PT, PTT and ALT to evaluate hepatic function.
- Review serial serum electrolytes.
- Review urine electrolyte, BUN, and creatinine to evaluate renal function.
- Administer intravenous crystalloids as ordered.
- Administer potassium as ordered. Validate adequate urine output before potassium administration.
- Sodium restriction of 0.5 g/day and fluid restriction to 1000 ml/day may be ordered.
- Vitamin K or fresh frozen plasma (FFP) may be required to promote the clotting process.
- Institute bleeding precautions. Avoid razor blades and use soft-bristled toothbrushes.
- Paracentesis may be performed if abdominal distention is severe.
- Prepare the patient and family for liver transplant, as indicated.
Nursing care plan assessment and physical examination
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 distension, 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.
Nursing care plan primary nursing diagnosis: Fluid volume excess related to water and sodium retention.
Nursing care plan intervention and treatment plan Patients are managed with supportive therapy, depending on their symptoms. Fluid and electrolyte imbalances, malnutrition, ascites, respiratory failure, 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.
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