Hepatic pearls Flashcards
acute hepatitis is the result of
viral infection, drug reaction, & exposure to hepatotoxin
Hep C produces
asymptomatic carriers
no effective vaccine is currently available
Infectious carriers pose a major health threat to OR personnel:
avoid direct contact with blood & secretions
immunization is highly effective against hep B infection
No vaccine for hep C is available and prior infection does not confer immunity upon re-exposure
post-exposure prophylaxis with hyperimmune globulin is effective for Hep B not C
Most common cause of drug-induced hepatitis is
Alcohol induced
Patients with hepatitis are at risk for further hepatic dysfunction & hepatic failure:
encephalopathy
coagulopathy
Hepatorenal syndrome
Acute hepatitis preop labs that should be addressed include:
Bilirubin, albumin, prothrombin time
In acute hepatitis, (describe what happens with transaminases)
elevated transaminases do not correlate well with the degree of cellular necrosis
Prolongation with INR >1.5 following administration of Vitamin K is indicative of
severe liver dysfunction
Preoperative evaluation of the emergent patient with acute hepatitis should include:
- determination of the cause & degree of hepatic impairment
- record drug exposures including- alcohol intake, rec drug use, recent transfusions, & prior anesthetics
- presence of N/V
- correct dehydration & electrolyte abnormalities
- mental status changes suggest severe hepatic impairment
- alcoholics- signs of withdrawal vs. signs of acute toxicity
- premeds like benzos are generally not given to minimize drug exposure & confounds encephalopathy
Goal of intraoperative management for the acute hepatitis patient is
preserve existing hepatic function
avoid factors that may be detrimental to the liver
The volatile agent of choice due to the least effect on hepatic blood flow is
isoflurane
“Standard” induction doses of IV agents can generally be used as
their action is terminated by redistribution versus metabolism or excretion
If large or repeated doses of IV agents are administered to the patient with hepatitis,
prolonged duration of action may occur (particularly w/ opiods)
Avoid the following things that are known to reduce hepatic blood flow:
sympathetic stimulation, hypotension, high mean airway pressures
Chronic hepatitis is defined as
persistent hepatic inflammation for longer than 6 months as evidenced by elevated serum aminotransferases
Patient classification of chronic hepatitis is determined by
liver biopsy
syndromes include- chronic persistent hepatitis, chronic lobular hepatitis, & chronic active hepatitis
Chronic persisitent hepatitis
eventually resolves
usually does not progress to cirrhosis
characterized by chronic inflammation of the portal tracts with preservation of the NORMAL cellular architecture
Chronic lobular hepatitis is
resolves but followed by recurrent exacerbations
characterized by foci of inflammation & cellular necrosis in the lobules
usually does not progress to cirrhosis
Chronic active hepatitis
chronic hepatic inflammation with destruction of cellular architecture
evidence of cirrhosis present initially or eventually develops
Describe the anesthetic management for patients with chronic persistent, chronic lobular, and chronic active hepatitis
chronic persistent & chronic lobular should be treated similar to those with acute hepatitis
chronic active hepatitis should be assumed to have cirrhosis and treated as such
Most common causes of cirrhosis include:
alcohol abuse
NALFD
chronic active hepatitis (B & C)
chronic biliary inflammation or obstruction
Regardless of the cause of cirrhosis, the result is
hepatocyte necrosis followed by fibrosis & nodular regeneration