Liver Flashcards
acute hepatic failure, acute liver failure(ALF), or fulminant hepatic failure (FHF) are all the same things, t or f
true
**what does fulminant mean
a disease that has rapid and sudden onset
normal functioning of the liver
neutralizes toxins and waste and the cleaning of blood throughout the entire body
when we have pressure on the diaphragm due to inflammation of the liver, what is the pt predisposed to
respiratory problems
someone in acute liver failure has other dysfunctions what are they
hemodynamic instability - coagulopathies - high risk of bleeding making them predisposed to shock (hypo-volemic shock)
high risk for respiratory insufficiency/failure
risk for perfusion abnormalities
risk for renal failure
high risk for impaired immune responses and infection making them at high risk for infection then sepsis
why is the liver different r/t where it receives it blood supply
most vital organs get blood from arterial system
the liver gets it blood supply from arterial system (1/3) and venous system (2/3) making it a low pressure organ
what does we mean by a low pressure organ (liver)
inflammatory process causes decreased perfusion to the liver resulting in hypo-perfusion and high risk portal hypertension
+ ascites causes pressure on diaphragm causing resp problems - high risk for intravascular fluid depletion - decreased circulating blood volume due to low albumin causing fluid shift into abdomen - hypovolemia with ascites
if the liver fails acutely what are we going to have problems with
shock - sepsis - hypovolemia and bleeding
Acute hepatic failure defined as
Rapid deterioration of liver functioning (includes coagulopathies)
Coagulopathies result in bleeding and hemorrhage
Changes in mental status r/t decreased albumin and increased ammonia - increased ammonia levels cross the blood-brain barrier and causes severe confusion
Acute onset - no previous hx of chronic liver dysfunction
number 1 cause of acute hepatic failure
acetaminophen (Tylenol) overdose
additional cause of fulminant liver failure
Hep B or C exposure (second leading cause) or “Viral”
Tylenol overdose
ingestion of wild mushrooms thought to be edible
what is the antidote to Tylenol overdose
acetylcysteine N (Mucomyst)
Intervention for ALL HEPATIC FAILURE REGARDLESS OF CAUSE
acetylcysteine N (Mucomyst) - shown to improve outcomes
what should we ask a pt w/chg in LOC, bruising and bleeding with no previous hx of cirrhosis or liver dysfunction and the pt may be jaundice
assess exposure to all prescription and OTC meds (amoxicillin and ampicillin in children)
exposure to HEP B and C
what have they eaten - were they in Europe
assess alcohol consumption
definitive treatment for fulminant hepatic failure (FHF)
*liver transplant
mars is used as a bridge to transplantation
necrosis of cells results in
high risk for SIRS likely to result in MODS and ARDS - within 3-8 weeks - rapid process
what do we base fluid resuscitation on
BP - MAP
manifestations of acute hepatic failure
Destruction of liver cells - coagulopathies - PT60-100 - INR - 1.5 or > super high-risk of bleeding
Hyperbilirubinemia (definitive dx tool) - jaundiced - unconjugated because the liver conjugates bilirubin
Hypoglycemia - depression of glucose synthesis
Decreased lactate clearance - worsens metabolic acidosis - give NORMAL SALINE
normal lab values r/t liver fxn tests (lab)
INR - 0.8 - 1.2
PT - 10-14 sec
clotting factors are not normal in FHF
how do we assess coagulopathies in liver failure
PT and INR
FHF fulminant hepatic failure occurs over this period of time
1-3 weeks - confusion, bruising
hepatic encephalopathy (chg in mental status) can occur
as soon as 2 weeks after the onset of disease
within 6-8 weeks of onset of FHF patients are
in a coma, dead or in need of a transplant
in hepatic encephalopathy there are how many stages
4
