Hepatic 2 Flashcards
usual causes of acute hepatitis
- viral infection
- drug reaction
- exposure to hepatotoxin (alcohol, carbon tetrachloride)
clinical manifestations of acute hepatitis
- depends on severity of inflammatory reaction
- may present as asymptomatic elevations in serum transaminases
- also depends on amount of cellular necrosis
- may also present as acute fulminant hepatic failure
acute fulminant hepatic failure
rapid, massive necrosis of the liver parenchyma and decrease in liver size
common viral causes of acute hepatitis
- hepatitis A, B and C viruses are the most common
- also D, E, Epstein-Bar, Herpes Simplex, CMV, and coxsackievirus
how is hep A spread?
oral fecal route
how are hep B and C spread?
percutaneously and by contact with body fluids
hepatitis A
- least severe
- most recover in weeks to months
- transmission through fecal contamination
hepatitis E
- similar to A
- in 3rd word countries where there is not the best sanitation
- transmission through fecal contamination
- usually recover well
hepatitis D
- does not produce hepatitis by itself
- only occurs if there is a co infection with hepatitis B or super infection with chronic hepatitis B
- severe infection in this setting
- transmitted by fecal contamination or body fluids
hepatitis B
- HBsAg = surface antigen part of the virus
- often anicteric (i.e. no jaundice)
- can lead to fulminant hepatic necrosis or chronic hepatitis
- HBsAg disappears with recovery but disease can be diagnosed by presence of hepatitis B antibody
- transmission through sexual contact/blood
hepatitis C
- antibodies not present for long period
- difficult to diagnose - sometimes diagnosis of exclusion
- subclinical nonicteric infection is common
- rarely produces fulminant hepatic failure
- significant number of those who are chronically infected will develop cirrhosis or liver cancer (20% develop cirrhosis/major cause of hepatocellular carcinoma)
- produces asymptomatic carriers
- no effective vaccine currently available
- transmission through blood
viral infection associated with acute hepatitis
- prodromal illness for 1-2 weeks with fatigue, malaise, low-grade fever, N/V
- may or may not be followed by jaundice (typically lasts 2-12 weeks if present)
- complete recovery indicated by normal transaminase levels which takes about 4 months
- clinical manifestations of different viruses overlap so testing needs to be done
- more complicated clinical course with hepatitis B and C
drug-induced acute hepatitis causes
- direct dose-dependent toxicity of a drug or metabolite
- idiosyncratic drug reaction
- combination of the two
most common cause of drug-induced acute hepatitis
alcohol
fatty infiltration of the liver from chronic alcohol ingestion
- impaired fatty acid oxidation (i.e., impaired beta oxidation)
- increased uptake and esterification of fatty acids
- diminished lipoprotein synthesis and secretion
common drugs that can cause acute hepatitis
- acetaminophen
- alcohol
- salicylates
- vinyl chloride
- carbon tetracholoride
- halothane
- sulfonamides
Pre-op considerations for acute hepatitis
- postpone elective surgery until resolved as determined by normal liver function test (will extend injury if surgery because decreased blood flow)
- increased perioperative M&M during acute phase
- risk with alcoholic hepatitis may not be as great, but high mortality rate associated with alcohol withdrawal in periop period (50%)
pre-op labs for acute hepatitis
- BUN, Cr, Bilirubin, Electrolytes, glucose, transaminases (AST, ALT), alk phos, albumin, PT/INR, plts
- serum HBsAg (if worried about hepatitis B)
- blood alcohol level (if alcoholic)
- hypokalemia and metabolic acidosis not uncommon due to vomiting
- hypomagnesemia with chronic alcoholics (think dysrhythmias)
elevated transaminases
- do not correlate well with degree of cellular necrosis (just indicative of hepatocellular dysfunction)
- ALT>AST with acute hepatitis
- AST>ALT with alcoholic hepatitis
what is the best indicator of synthetic function of the liver with hepatitis?
PT
-prolongation >3-4 seconds (INR > 1.5) following admin of vitamin K is indicative of severe liver dysfunction
Preop evaluation of emergent patient with acute hepatitis
- determine cause and degree of hepatic impairment
- record drug exposures - alcohol, recreational drugs, recent transfusions, prior anesthetics
- presence of N/V = RSI
- correct dehydration and lyte abnormalities
- mental status change = severe impairment
- vitamin K may be needed to correct coagulopathy
- premeds generally not given to maintain mental status and decrease drug exposure
alcoholics preop eval
- acute toxicity = inappropriate behavior or obtunded patient
- withdrawal = irritability, tremulousness, HTN, tachy (benzos and thiamine indicated for withdrawal)
goal of intraoperative management of those with acute hepatitis
- preserve existing hepatic function
- avoid factors that may be detrimental to the liver
intraoperative considerations for acute hepatitis
- drug selections and doses should be individualized - TITRATE because may have issues with Vd and drug metabolism
- acute viral hepatitis may produce increased CNS sensitivity to anesthetics
- use fewest number of anesthetic agents possible
- inhalation agents preferred to IV agents because less dependent on hepatic metabolism
- standard induction doses of IV agents can generally be used as their action is terminated by redistribution rather than metabolism/excretion
- prolonged DOA with repeated doses (esp opioids)
- regional can be used if no coagulopathy