Liver Failure Flashcards
What are the criteria for diagnosing acute liver failure?
- INR > 2.0
- Hepatic encephalopathy
- Transaminases > 1,000
What are the complications of acute liver failure?
- Cerebral edema
- Infection (bacterial, fungal)
- AKI
- High-output hyperdynamic heart failure (low SVR)
- Coagulopathy and bleeding complocations
- Catabolism and nutritional failure
When do you give gastric lavage and activated charcoal therapy?
In the setting of a toxic ingestion when:
When within 1 hour of ingestion
OR
When within 4 hours of large ingestion
OR
When the exact timing of the ingestion is uncertain.
West Haven grading of hepatic encephalopathy
- Trivial lack of awareness and shortened attention span, no asterixis
- Lethargy or apathy, disoriented to time and place, inappropriate behavior, asterixis
- Somnolence or semi-stupor, but with response to verbal stimuli. Marked confusion and disorientation.
- Comatose and unresponsive to verbal or noxious stimuli. Decorticate or decerebrate posturing.
Liver support systems
Acellular systems that utilize albumin dialysis or bioartificial liver support systems.
May be used in severe cases of acute liver failure. Increase 30 day survival of patients with ALF.
King’s College Hospital (KCH) criteria
Most widely applied criteria for picking patients with acute liver failure for liver transplantation, particularly in the setting of acetominophen toxicity. 70% sensitive and 92% specific for identifying patients who will die without liver transplant.
- pH < 7.30 after resuscitation irrespective of encephalopathy
- PT > 100 s AND Cr > 300 umol/L if the patient has grade III or IV encephalopathy
Where are the stem cells of the liver located?
Along the portal tracts/triads
So, if the portal tracks are relatively preserved in the setting of acute liver injury, the prognosis for liver recovery is good.
Amanita poisoning
Type of mushroom that is more common in Western Europe and coastal Pacific Northwest US.
Amanita poisoning presents with vomiting, crampy abdominal pain, and diarrhea within 10-12 hours of ingestion. Clinical and laboratory findings with acute liver injury often do not manifest until 2 days after ingestion.
Of note, these toxins enter the enterohepatic circulation and recirculate. They are responsible for >90% of mushroom-ingestion-related deaths.
Treatment includes: Evacuation of duodenal contents (irrespective of time, as toxins recirculate). Sodium bicarbonate if within 2 hours of ingestion. Hemodialysis.
Prognosis is poor.
Acute fatty liver of pregnancy
Metabolic abnormality in the fetus causes maternal liver injury.
Typically occurs in the 3rd trimester. Rapid progression of jaundice and liver failure. 50% of cases associated with preeclampsia.
Delivery is the treatment of choice for most patients. Plasma exchange therapy is of some benefit in these patients.
Nutrition for a patient with liver failure
Grade 1 encephalopathic patients can still take food PO, but once they are Grade 2 they should have an enteral tube placed.
Protein intake should be limited to 1g/kg/d to minimize excess ammonia production, and supplemental glutamine should be avoided as this contributes to excessive ammonia production and astrocyte toxicity/cerebral edema.
Patient presents with acute liver failure. They are lucid when they arrive. They are started on standard treatments/supportive care. Shortly thereafter, the patient’s mental status deteriorates to Grade 3 hepatic encephalopathy.
What is the next step in management?
CT scan of the head
You need to know if this patient has cerebral edema, and if so you need to treat it to make sure they don’t herniate.
Why are patients with chronic alcohol ingestion more at risk for acetominophen toxicity?
Chronic alcohol ingestion stimulates CYP2E1 ativity and inhibits the rate of glutathione synthesis.
This, in turn, increases NAPQI production i/s/o acetominophen overdose.
