Hepatic Pathophysiology and Anesthesia Complications Flashcards
acute hepatitis is the result of (3)
viral infection
drug reaction
exposure to hepatotoxin ex) alcohol
acute fulminant hepatic failure pathophysiology (general)
rapid, massive necrosis of liver and a decrease in liver size
how is hepatitis A transmitted
oral fecal
how is hepatitis B and C transmitted
primarily percutaneously (needles/blood) and by contact with body fluids
hep a
severity
recovery
least severe
most recover in weeks to months
hep e
where it is found
transmission
found in 3rd world countries (similar to hep A)
transmission through fecal contamination
hep D
only occurs as (2 consideration)
transmission
only occurs as co infection with acute hep B or super infection with chronic hep B
transmission through fecal contamination/body fluids
HBsAg
surface antigen part of the hep B virus. a lipoprotein layer that the virus sheds that can be measured.
this lipoprotein antibody disappears with recovery
what can hep B lead to
fulminant hepatic necrosis or chronic hepatitis
hep C and diagnosis considerations
antibodies not present for long period, therefore difficult to diagnose.
produces asymptomatic carriers
hep C and possible progressive pathophysiology of the liver
rarely produces fulminant hepatic failure
significant number will develop cirrhosis or liver cancer
hep C vaccine
none available currently
acute hepatitis early clinical signs
often have prodromal illness for 1-2 weeks with fatigue, malaise, low grade fever, nausea and/or vomiting.
period may or may not be followed by jaundice for 2-12 weeks.
acute hepatitis recovery
usually takes 4 months, evidenced by normal serum transaminase
how to diagnose type of hepatitis
have to do serological testing or biopsy since s/sx overlap
chronic active viral hepatitis can be seen with
hep b and c
how to take precaution against infectious patients
avoid direct contact with blood and secretions
immunization highly effective against hep B
no vaccine for hep C and prior exposure does not create immunity
post exposure prophylaxis with hyperimmune globulin is effective for hep b but not c
do have ARV for hep C
drug induced acute hepatitis results from
direct dose dependent toxicity of a drug or metabolite
idiosyncratic drug reaction
combination of the two
most common cause of hepatitis
drug induced
chronic alcohol ingestion can result in fatty infiltration as a result of (3)
impaired fatty oxidation (beta oxidation)
increased uptake and esterification of fatty acids
diminished lipoprotein synthesis and secretion
toxic drug induced acute hepatitis offenders (4)
alcohol
acetaminophen
vinyl chloride (inhalation for a brief time)
carbon tetrachloride
idiosyncratic drug induced acute hepatitis offnders
volatile anesthetics
sulfonamides
toxic and idiosyncratic acute drug induced hepatitis
amiodarone
acute hepatitis preoperative considerations
postpone elective surgery until resolved as determined by LFT’s
alcohol withdrawal during surgery associated with mortality rate as high as
90%
patients with hepatitis are at risk for these 3 things during perioperative period
encephalopathy
coagulopathy
hepatorenal syndrome
preoperative labs to get if the patient has acute hepatitis includes
BUN creatitnine bilirubin electrolytes glucose transaminases alk phos albumin prothrombin time (INR) platelet count serum HBsAg blood alcohol level if alcoholic
two electrolyte deficits you may see preoperatively during hepatitis
hypokalemia and metabolic alkalosis usually d/t vomiting. consider ABG
hypomagnesemia may exist in chronic alcoholics which predisposes to dysrhythmias
does elevated transaminase correlated with the degree of cellular necrosis
no, AST/ALT does not correlate well
best indicator of synthetic function of liver with hepatitis
PT.
prolongation >3-4 seconds (>1.5 INR) following administration of vitamin K indicative of severe liver dysfunction
preoperative evaluation of the emergent patient with acute hepatitis should include
cause and degree of impairment
exposure recording including alcohol intake, recreational drug use, recent transfusions, prior anesthetics
presence of n/v (RSI?)
correction of dehydration and electrolyte abnormalities
mental status changes suggest severe hepatic impairment
alcoholics: look for acute toxicity or withdrawal
vitamin K may be necessary to correct coagulopathy
goal of intraoperative management of hepatitis
preserve existing hepatic function
avoid factors that may be detrimental to the liver
acute viral hepatitis and anesthetics
may produce increased CNS sensitivity to anesthetics
alcoholic patients and intraoperative considerations
display cross tolerance to IV and volatile anesthetic agents
require CV monitoring due to: additive depressant effects of anesthetics and alcohol.
possible presence of cardiac myopathy (eccentric remodeling)
acute hepatitis and intraoperative considerations, IV or inhaled anesthetic?
inhalation agents are preferred to IV agents due to dependence on liver metabolism and alimentation. fewest number of anesthetic agents should be used
volatile agent of choice for hepatic issues
isoflurane, least effect on hepatic blood flow
induction doses of IV agents and hepatitis
can use standard induction doses generally as their action is terminated by redistribution versus metabolism. however, prolonged duration may occur if repeated doses of agents, particularly opioids, are administered
try to avoid these responses intraoperatively with hepatitis patients that decrease hepatic BF
hypotension
excessive SNS stimualtion
high mean airway pressures during controlled ventilation
regional anesthesia and liver abnormalities
can be used in the absence of coagulopathy
chronic hepatitis definition
defined as persistent hepatic inflammation for longer than 6 months as evidenced by elevated serum aminotransferase
classification of chronic hepatitis based on 3 distinct syndromes via liver biopsy
chronic persistent hepatitis
chronic lobular hepatitis
chronic active hepatitis
chronic persistent hepatitis
present with acute hepatitis (usually B or C)
eventually resolves
characterized by chronic inflammation of portal tracts (all tracts including ducts, veins, arteries, canniculi, etc) with preservation of the normal cellular architecture (which sets it apart)
usually does NOT progress to cirrhosis
chronic lobular hepatitis
present with cute hepatitis that resolves but followed by recurrent exacerbation
characterized by foci of inflammation and cellular necrosis in the lobiles
usually does not progress to cirrhosis
chronic active hepatitis
occurs most commonly as a sequela of hep b or c
characterized by chronic hepatic inflammation with destruction of cellular architecture- “more global”
evidence of cirrhosis present initially or eventually develops
treatment of hep B
ARV + immune modulator drugs (interferon)
treatment of hep C
ARV can cute more than 95% of these infected patients
anesthetic management of patients with chronic persistent of chronic lobular hepatitis
treat like those with acute hepatitis
anesthetic management of patients with chronic active hepatitis
assume cirrhosis, treat them as such
most common causes of cirrhosis (4)
alcohol abuse
NAFLD
chronic active hep B and C
chronic biliary inflammation or obstruction
result of cirrhosis
hepatocyte necrosis followed by fibrosis and nodular regeneration
cirrhosis eventually results in
hepatic failure. is a progressive disease
destruction of livers normal cellular and vascular architecture produces
obstruction of portal venous flow leading to portal HTN
impairment of normal synthetic and metabolic functions leading to multi system disease
4 manifestations related to cirrhosis
spider angiomas
palmar erythema (due to volume distribution issue)
gynecomastia
splenomegaly
3 major complications associated with cirrhosis
vatical hemorrhage from portal HTN (esophageal hemorrhages)
intractable fluid retention in the form of ascites
hepatic encephalopathy or coma
child turcotte pugh score
severity of hepatic imparment and surgical risk estimated with this. considers 3 lab values (total bilirubin, serum albumin, INR) and 2 clinical evaluations (ascites, hepatic encephalopathy)
-then classes you A, B, or C which correlates with survival. C being the worst survival rate
major cause of morbidity and mortality in cirrhotic patients
massive bleeding from esophageal varices
medical treatment of variceal bleeding includes
replace blood loss with IV fluids and blood products
vasopressin, somatostatin, propranolol (slow HR, slow CO to liver) to reduce the rate of blood loss
balloon tamponade (hope they form a clot)
endoscopic sclerosis or ligation of the varicose
bleeding continues or recurs emergency surgery is indicated
hematological considerations for a patient with cirrhosis
may present with anemia, thrombocytopenia/coagulopathy, leukopenia
anemia related to cirrhosis associated with
blood loss
increased RBC destruction
bone marrow suppression
nutritional deficiencies
thrombocytopenia/coagulopathy related to cirrhosis associated with
congestive splenomegaly due to portal HTN
decreased hepatic synthesis of clotting factors
enhanced fibrinolysis due to reduced elimination of factors that activate the fibrinolytic system
leukopenia related to cirrhosis associated with
congestive splenomegaly due to portal HTN
preoperative blood transfusion considerations related to cirrhosis
protein breakdown from excessive blood transfusions can precipitate encephalopathy (protein breakdowns causes nitrates/ammonia)
despite this risk coagulopathy should be corrected before surgery
should replete clotting factors with FFP and cryo
platelet transfusion should be considered immediately prior to surgery if platelet count <100,000
cirrhosis preop considerations and circulatory manifestations
cirrhosis typically associated with hyper dynamic circulatory state
CO often increased and generalized peripheral vasodilation (looks like hypovolemia)
arteriovenous shunts can develop in the systemic and pulmonary circulation
superimposed alcoholic cardiomyopathy readily leads to CHF
cirrhotic cardiomyopathy may be present due to
AV shunts or decreased blood viscosity
contribute to increased CO, above normal filling pressures, below normal SVR
cirrhosis preop considerations and respiratory manifestations
hyperventilation common and results in primary respiratory alkalosis
hypoxemia frequent due to right to left shunts
shunting due to increased anomalous AV communication
also have VQ mismatch
decreased lung volumes (particularly FRC) due to ascites and diaphragm elevation
results in atelectasis
get CXR and ABG, maybe paracentesis
cirrhosis preop considerations and renal manifestations and fluid balance
alterations in fluid and electrolyte balance are manifested as: ascites, edema, electrolyte abnormalities, hepatorenal syndrome
patients with cirrhosis and ascites have decreased renal perfusion, altered infrarenal hemodynamics, enhanced proximal and distal tubules Na+ reabsorption, impairment of free water clearance
dilutional hyponatremia is common
hypokalemia is common (secondary to hyperaldosteronism and diuretics)
abnormalities are most sever with onset of hepatorenal syndrome
mechanisms believed to be related to ascites include
portal HTN (increased hydrostatic pressure favors fluid transudation) seepage of protein rich lymph fluid from the surface of the liver "sweating" (secondary to distortion and obstruction of lymphatic channels) avid renal sodium (and often water) retention (hepatorenal syndrome)
hepatorenal syndrome definition and causes
functional deficit in patients with cirrhosis that usually follows GI bleeding, aggressive diuresis, sepsis, major surgery. all can be iatrogenic
hepatorenal syndrome is characterized by
progressive oliguria (<400ml/day) avid Na reabsorption azotemia (alto of nitrogenous material in blood) intractable ascites very high mortality rate
hepatorenal syndrome tx
supportive, often unsuccessful unless liver transplantation performed
intraoperative fluid administration: colloids or crystalloids?
colloids
diuresis of ascites and edema fluid should be done how?
accomplished over several days. loop directive should only be used after bed rest, sodium restriction, and spironolactone therapy have failed
hepatic encephalopathy is characterized by
alterations in mental status
fluctutating neurological signs (asterixis, hyperreflexia)
EEG changes
some patients also have increased ICP
toxin accumulation in GI tract that can be attributed to hepatic encephalopathy include
ammonia, methionine metabolites, short chain fatty acids, phenols (like cleaning agents)
factors known to precipitate hepatic encephalopathy include
GI bleeding, increased dietary protein intake, hypokalemia alkalosis from vomiting or diuresis, infections, worsening liver function
encephalopathy and sedatives
recommended to avoid, try to tx enceophalopathy preoperatively
drug response to agents is unpredictable in cirrhosis due to changes in
CNS sensitivity Vd protein binding drug metabolism drug elimination TITRATE
Vd of highly ionized NMBA’s is ________ in cirrhosis patents, therefore
increased
requires greater than normal loading doses
hepatic elimination of NMBA’s is _________ in cirrhosis patients therefore
decreased
requires lower than normal maintenance doses
cirrhosis and the anesthetic technique
cirrhotic liver is very dependent on hepatic arterial blood flow due to decreased portal blood flow. therefore, avoid anesthetic agents that reduce arterial blood flow
get an aline
regional anesthesia can be used without thrombocytopenia and coagulopathy, take great care fo avoid hypotension
propofol induction with isoflurane maintenance most commonly used
cisatracurium probably NMDA of choice
opioid supplementation reduces volatile agent requirement but have prolonged elimination time
usually RSI if have preop n/v/GIB/andominal distention
CV unstable patients and those with active bleeding and intubation
should have awake intubation or RSI with cricoid pressure using ketamine or etomidate and succ
cirrhosis and montioring
monitor 5 lead EKG esp due to coronary vasoconstriction in patients receiving vasopressin for esophageal varices
supplemental pulse ox with ABG to eval acid base status
patient with right to left shunts and cirrhosis, intraoperative consideration
may not tolerate N2O, may require PEEP to treat VQ inequalities and subsequent hypoxemia
most patients should have aline monitoring with cirrhosis as a result of these possibilities
excessive bleeding
rapid intercompartmental fluid shifts
surgical manipulations
need these monitors for patients with cirrhosis
cellsaver blood warrmer fluid blood in room CVC many large bore IV's aline urinary catheter
cirrhosis and fluid replacement
colloids intraop still take precedence over the Na restriction to manage intravascular fluid volume
intraabdominal procedures in cirrhotic patients are often associated with
increased bleeding (venous engorement from portal HTN, adhesions from previous surgery, coagulopathy( fluid shifts (evacuation of ascites fluid, may need to give colloids. prolonged surgical procedure)
citrate toxicity and blood transfusion in cirrhotic patients
citrate is normally metabolized by the liver
cirrhosis impairs citrate metabolism
citrate binds to serum Ca and leads to hypocalcemia
IV Ca is often necessary to reverse negative inotropic effects of decreased ionized Ca
hepatobilitary disease characterized by
cholestasis, suppression of stoppage of bile flow
most common cause of cholestasis
extrahepatic obstruction of biliary tract (obstructive jaundice) due to gallstones, stricture, tumor in common hepatic duct
cholestasis can also be caused by intrahepatic obstruction due to
suppression or stoppage of bile flow at the level of the hepatocyte or bile canaliculus. most commonly results from vital hepatitis or idiosyncratic drug reaction
treatment of extra hepatic obstruction
surgical
treatment of intra hepatic cholestasis
medical
extra hepatic obstruction and intrahepatic cholestasis two dx labs
predominately conjugated hyperbilirubinemia and marked elevation in alk phos
cholangitis
concomitant chills or high fever from ascending bacterial infection of biliary systems
how gallstones can cause acute pancreatitis
can obstruct pancreatic duct
sx that presents with cholelithiasis
biliary colic secondary to obstruction of cystic duct
hepatobiliary disease-preoperative considerations
most commonly present to OR for cholecystectomy
patients with acute cholecystitis should be treated medically
patients suffering from serious complications may require emergency cholecystectomy
treatment for acute cholecystitis
nasogastric suction
IV fluids
abx
opioid analgesics
patients with extra hepatic biliary obstruction from any cause develop this deficiency (and 2 considerations)
vitamin K deficiency
should be given vitamin K (requrires 24h for full response)
failure of PT to correct prior to surgery may necessitate FFP
high levels of this lab may be associated with renal failure, esp in hepatobiliary disease patients
bilirubin levels
long standing extra hepatic biliary obstruction is associated with
secondary biliary cirrhosis and portal hypertension
hepatobiliary disease-intraoperative considerations
drugs that depend on biliary excretion
lap chole accelerates recovery
use of opioids can be problematic when intraoperative cholangiogram is to her performed
-opioid induced spasm of sphincter of Odd may theoretically result in false positive cholangiogram
some clinicians withheld opioids until after cholangiogram has been performed
in patients with biliary tract obstruction expect a prolonged DOA of drugs that are dependent on biliary excretion (ketamine, prop)
agents dependent on renal excretion are preferable
UOP with indwelling catheter preferable
maintenance of periop diuresis desirable
sphincter of oddi spasm can be treated with
glucagon, naloxone
common hepatic surgeries include
repair of lacterations
drainage of abcesses
resection of tumors
how much liver can be resected
80-85%
hepatic surgery general intraoperative considerations
administration of antifibrinolytics may reduce blood loss (aprotonin, aminocaproic acid, tranexamic acid)
hypoglycemia may occur following large liver resections
drainage of abcess may be complicated to peritoneal contamination (may repeatedly come back to OR for washout)
postop complications of hepatic surgery include
bleeding, sepsis, hepatic dysfunction
postop mechanical ventilation may be necessary in patients undergoing extensive resection
