Fulminant hepatic failure (FHF)-the mass destruction of liver cells in a previously healthy liver-progresses from jaundice to coma within a few hours to a few weeks of a liver injury. (1,2) In one case, a 13-year-old girl developed nausea, vomiting, and diarrhea the day after eating wild mushrooms that she and her faniily had gathered to complement their dinner. After being seen in the ED, she was given prochlorperazine (Compazine) and sent home. Three days later, she was brought back to the ED with an enlarged liver. Within two days, she needed a transplant to survive. (3)
Without a transplant, up to 80% of patients with severe FHF die. (1) While trauma, ischemia, and autoimmune disorders can trigger FHF, the three most common causes include viral hepatitis, acetaminophen toxicity, and idiosyncratic drug reactions. (1,4) In fact, therapeutic drugs now account for up to 40% of FHF cases. (4)
Although our focus here is FHF, patients with chronic liver disease-such as Budd-Chiari syndrome, Wilson's disease, or alcoholic cirrhosis-are also at risk for acute liver failure. However, in these cases, the precipitating event is most likely spontaneous peritonitis, GI bleeding, or protein overload. (5'6)
Whatever the cause, patients with a failing liver have a fairly predictable clinical course. Understanding how the liver functions can provide you with a basis for anticipating complications and guiding nursing interventions. To start, we'll briefly review what happens when the liver can no longer do its job, and then discuss the clinical presentation and the supportive care these patients need to survive FHF.
Complications grow as the liver loses function
Acute liver failure is distinguished by a breakdown of the organ's synthetic and detoxification processes--which can occur within two weeks in a liver that previously was functioning normally. (2) All body systems are affected--almost simultaneously. The complications that result can rapidly culminate in multisystem organ failure. The effects of progressive hepatocellular death include:
* Jaundice. Typically, the first synthetic function to fail is the conjugation of bilirubin, the byproduct of red blood cell metabolism. (1,2,4) Normally, liver cells bind with bilirubin, making a water-soluble compound that's excreted in the bile. When this process fails, serum bilirubin builds. A rise in bilirubin above the normal 0.8 mg/dL indicates liver failure. At a level of 3 mg/dL or greater, the patient becomes jaundiced.
* Hemodynamic instability. The liver synthesizes albumin, along with other major blood proteins. Albumin helps keep circulating fluid in the blood vessels. Without albumin, colloid osmotic pressure is lost. Fluid seeps into the interstitial spaces, causing hypovolemia, generalized edema, and ascites. Hypotension results. The systemic vascular resistance plummets, and cardiac output rises, similar to classic sepsis.
* Hepatic encephalopathy and cerebral edema. Over 70% of patients with FHF die from brain herniation secondary to cerebral edema. (2,4) Although overall blood volume is decreased, cerebral blood flow exceeds the brain's metabolic need. (7) Vasoactive peptides alter the blood-brain barrier, allowing neurotoxins, such as ammonia, to accumulate in the brain. Fluid is pulled into the extracellular compartment, accelerating brain stem herniation....
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