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
Vitamin K requires
24 hours for a full response
These complications eventually develop in most patients with cirrhosis:
jaundice & ascites
3 major complications associated with cirrhosis include:
variceal hemorrhage from portal hypertension
intractable fluid retention in the form of ascites
hepatic encephalopathy or coma
Preoperative considerations for the patient with cirrhosis include
prevent or limit complications
can affect all organ systems: GI, circulatory, pulm, renal, hematological, infectious, metabolic, & neurological
The severity of hepatic impairment & surgical risk can be
estimated using the Childs-Turcotte- Pugh scoring system
-has 2 clinical features & 3 lab assesssments
List what is included in the Childs- Turcotte Pugh score assessment:
total bilirubin, serum albumin, INR, ascites, & hepatic encephalopathy
Gastrointestinal manifestations of cirrhosis include:
extensive venous collateral channels- gastroesophageal
hemorrhoidal, periumbilical, & retroperitoneal
A major source of morbidity & mortality for the patient with cirrhosis is:
massive bleeding from gastroesophageal varices
medical tx. includes balloon tamponade, replace blood loss, vasopressin, somatostatin, & propranolol to reduce rate of blood loss
The hematological manifestations of the cirrhotic patient include
anemia, thrombocytopenia/coagulopathy, & leukopenia (usually due to things backing up in the spleen)
In regards to preoperative blood transfusions, _____ can precipitate encepalopathy
protein breakdown from excessive blood transfusions
Circulatory manifestations of cirrhosis include:
cardiac output is often increased & generalized peripheral vasodilation is present (similar to sepsis)
- AV shunts can develop in the systemic & pulmonary circulation
Cirrhotic cardiomyopathy may be present due
increased cardiac output as a result of above normal filling pressures and below normal SVR
Mechanisms believed to be responsible for ascites include:
portal hypertension, hypoalbuminemia, seepage of protein-rich lymph fluid from the surface of the liver, avid renal sodium (and often water) retention
Respiratory manifestations of cirrhosis include
hyperventilation is common and results in primary respiratory alkalosis
Hypoxemia is frequent due to
right to left shunts
- shunting is due to increase anomalous AV
- Also have V/Q mismatch
- up to 40% of CO is involved
Ascites fluid (resp. issues)
causes an elevation of the diaphragm leading to decreased lung volumes (particularly FRC) resulting in atelectasis
Renal manifestations & fluid balance abnormalities are most severe with
the onset of hepatorenal syndrome
Hepatorenal syndrome is characterized by:
progressive oliguria, avid Na+ retention, azotemia, intractable ascites, & very high mortality rate
Hepatorenal syndrome usually follows
GI bleeding, aggressive diuresis, sepsis, & major surgery
Acute intravascular fluid deficits should be corrected with
colloid infusion
Hepatic encephalopathy is characterized by
alterations in mental status, fluctuating neurological signs (asterixis, hyperreflexia), EEG changes, & increased ICP
________ has been implicated in the development of hepatic encepalopathy
accumulation of toxins originating in the GI tract & normally metabolized in the liver (ammonia, phenols)
Response to drugs is unpredictable due to changes in
CNS sensitivity, volume of distribution, protein binding, drug metabolism, & drug elimination
Volume of distribution of highly ionized NMBAs is increased therefore:
requires greater than normal loading dose
Hepatic elimination of NMBAs is decreased therefore
requires lower than normal maintenance dose
The best thing you can do with your drugs is
titrate them
The cirrhotic liver is very dependent on
hepatic ARTERIAL blood flow due to reduced portal blood flow
Induction with ____ is recommended
propofol
cisatricurium is the NMBA of choice
Removal of large amounts of ascites fluid may require
IV colloid solutions to prevent profound hypotension
Significant transfusions can result in citrate toxicity. IV
Ca2+ is often necessary to reverse the negative inotropic effects of decreased ionized Ca
The most common cause of cholestasis is
extrahepatic obstruction
due to gallstones, stricture, tumor in the common hepatic duct
Cholestasis can also be caused by
intrahepatic obstruction due to
suppression or stoppage of bile flow in the bile canalciulus
results from viral hepatitis or idiosyncratic drug reaction
Treatment of extrahepatic obstruction vs. intrahepatic
extrahepatic- surgical
intrahepatic- medical
Both intrahepatic & extrahepatic produce a
predominantly conjugated hyperbilirubinemia & marked elevation in alk phos
Hepatobiliary disease is characterized by
cholestasis- suppression or stoppage of bile flow