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
alcoholic patients intraoperative considerations
- display cross-tolerance to IV and volatile anesthetic agents
- require CV monitoring due to additive depressant effects of anesthetics + alc and the possible presence of alcoholic cardiomyopathy
avoid things to reduce hepatic blood flow
- hypotension
- excessive SNS stimulation
- high mean airway pressure during controlled ventilation
what is the preferred inhalation agent for liver patients?
isoflurane because has the smallest effect on hepatic blood flow
chronic hepatitis
persistent hepatic inflammation for longer than 6 months as evidenced by elevated serum aminotransferases
patient classification of chronic hepatitis
- determined by liver biopsy
- three distinct syndromes
- chronic persistent hepatitis
- chronic lobular hepatitis
- chronic active hepatitis
chronic persistent hepatitis
- present with acute hepatitis (b or c usually) that has a protracted course but eventually resolves
- characterized by chronic inflammation of portal tracts with preservation of the normal cellular architecture
- usually does NOT progress to cirrhosis
chronic lobular hepatitis
- present with acute hepatitis that resolves but followed by recurrent exacerbations
- characterized by foci of inflammation and cellular necrosis in the lobules
- usually does NOT progress to cirrhosis
chronic active hepatitis
- occurs most commonly as a sequela of hepatitis b or c
- characterized by chronic hepatic inflammation with destruction of cellular architecture
- evidence of cirrhosis present initially or eventually develops
antiviral treatment
- hep B - antivirals + immune modulator drugs (interferon)
- hep C - antiviral can cure more than 95% of affected patients
anesthetic management of chronic hepatitis
- chronic persistent or chronic lobular - similar to acute hepatitis
- chronic active - assumed to have cirrhosis and treated as such
cirrhosis
- progressive disease that eventually results in hepatic failure
- result = hepatocyte necrosis followed by fibrosis and nodular regeneration
common causes of cirrhosis
- alcohol abuse
- NAFLD
- chronic active hepatitis B and C
- chronic biliary inflammation or obstruction
destruction of liver’s normal cells and vasculature causes…
- obstruction of the portal venous flow leading to PORTAL HTN
- impairment of normal synthetic and metabolic functions of liver leading to multisystem disease
clinical manifestations of cirrhosis
- jaundice
- ascites
- spider angiomas
- palmar erythema
- gynecomastia
- spleenomegaly
what are the three major complications associated with cirrhosis?
- variceal (esophageal) hemorrhage from portal HTN
- intractable fluid retention in form of ascites
- hepatic encephalopathy or coma
what do 10% of patients with cirrhosis develop?
- bacterial peritonitis
- hepatocellular carcinoma
why are those with cirrhosis at increased risk for deterioration of liver function?
- detrimental effects of anesthesia and surgery on hepatic blood flow
- already limited hepatic reserve
childs-turcotte-pugh scoring system
- estimates severity of hepatic impairment and surgical risk
- 2 clinical features and 3 lab assessments
- total bilirubin
- serum albumin
- INR
- ascites
- hepatic encephalopathy
Cirrhosis GI manifestations
- portal HTN leads to extensive venous collateral channels (gastroesophageal, hemorrhoidal, periumbilical, retroperitoneal)
- Sign of portal HTN = dilated abd vein walls
- MASSIVE bleeding from esophageal varices = major cause of M&M
medical treatment for esophageal varices
- replace blood loss
- vasopressin, somatostatin, propranolol to reduce rate of blood loss
- balloon tamponade
- endoscopic sclerosis or ligation of varices/about 90% effective
- bleeding continues or recurs = emergency surgery
cirrhosis heme manifestations
- anemia
- thrombocytopenia/coagulopathy
- leukopenia
anemia periop associated with
- blood loss
- increased RBC destruction
- bone marrow suppression
- nutritional deficiencies
thrombocytopenia + coagulopathy associated with
- congestive spleenomegaly due to portal HTN
- decreased hepatic synthesis of clotting factors
- enhanced fibrinolysis due to reduced elimination of factors that activate the fibrinolytic system
leukopenia periop associated with
-congestive spleenomegaly due to portal HTN
preoperative blood transfusions considerations
- protein breakdown from excessive blood transfusions can precipitate encephalopathy
- despite this coagulopathy should be corrected before surgery
- clotting factors should be replaced with blood like FFP and cryo
- plt transfusion should be considered immediately prior to surgery if plt count < 100,000
cirrhosis circulatory manifestations
- typically associated with hyperdynamic circulatory state
- CO often increased and generalized peripheral vasodilation present
- AV shunts can develop in systemic and and pulmonary circulation
- circulatory may be present due to the above –> above normal filling pressures and below normal SVR
Cirrhosis respiratory manifestations
- hyperventilation is common and results in primary resp alkalosis
- hypoxemia frequent due to R to L shunts (due to increase in AV communication)
- decrease in lung volume (particularly FRC) due to ascites fluid elevation of diphragm - results in atlectasis
- paracentesis considered for ascites that induces pulmonary compromise
cirrhosis renal manifestations + fluid balance
- ascites, edema, electrolyte abnormalities, hepatorenal syndrome
- hyponatremia common
- hypokalemia common
mechanisms thought responsible for ascites
- portal HTN = favors fluid transudation across intestine and peritoneum
- hypoalbuminemia = decreases plasma oncotic pressure and favors fluid transudation
- seepage of protein rich lymph fluid from the surface of the liver
- avid renal sodium retention
patients with cirrhosis and ascites have
- decreased renal perfusion
- altered intrarenal hemodynamics
- enhanced proximal and distal tubule Na+ reabsorption
- impairment of free water clearance
hepatorenal syndrome
-functional deficit in patients with cirrhosis that usually follows GI bleeding, aggressive diuresis, sepsis, or major surgery
characteristics of hepatorenal syndrome
- progressive oliguria
- avid Na+ retention
- azotemia (a lot of nitrogen in blood)
- intractable ascites
- very high mortality rate
treatment of hepatorenal syndrome
-supportive and often unsuccessful unless liver transplant
intra + preop considerations for renal dysfunction with cirrhosis
- judicious fluid management
- preservation of renal function
- diuresis of ascites and edema accomplished over several days (bed rest, sodium restriction and spironolactone FIRST; then loop diuretics)
- AVOID overzealous preop diuresis
- acute intravascular fluid deficit corrected with colloids
cirrhosis CNS manifestations
- hepatic encephalopathy
- metabolic encephalopathy may be related to the amount of hepatocellular damage and the degree of shunting of portal blood directly into the systemic circulation
characteristics of hepatic encephalopathy
- alterations in mental status
- fluctuating neurological signs (asterixis, hyperreflexia)
- EEG changes
- some patients may have increased ICP
GI toxins potentially involved in hepatic encephaolopathy
- ammonia
- methionine metabolites
- short chain fatty acits
- phenols
factors that precipitate hepatic encephalopathy
- GI bleeding
- increased dietary protein intake
- hypokalemiac alkalosis from vomiting or diuresis
- infection
- worsening liver function
cirrhosis drug response unpredictable due to
- CNS sensitivity
- Vd changes
- protein binding
- drug metabolism
- drug elimination
NMBDs
- greater loading doses (bc higher Vd)
- lower maintenance doses (hepatic elimination decreased)
anesthetic technique for cirrhosis
- dependent on hepatic arterial blood flow due to reduced portal blood flow (preserving this is ESSENTIAL)
- regional anesthesia can be used if no thrombocytopenia or coagulpathy but be caution to avoid HypoTN
- prop induction with iso maint = common
- cis = NMBD of choice
- opioid supplement leads to decreased volatile requirement but caution with repeat doses (resp depression)
- preop N/V or GI bleed or Abd distention = RSI
- CV unstable or those with active bleeding = awake intubation or RSI with etomidate or ketamine and succ
intraop monitoring with cirrhosis
- 5 lead ECG to detect ischemia due to coronary constriction in those getting vaso
- supplement pulse ox with ABGs to evaluate acid-base status
- large R to L shunt may not tolerate nitrous and may need PEEP to treat V/Q mismatch
- art line due to rapid changes in BP from bleeding, rapid fluid shifts, and surgical manipulations
- CVP or PAP monitoring may be necessary because intravascular volume difficult to assess
- foley for UOP; mannitol for low UOP
fluid replacement intraop with cirrhosis
- most patients Na+ restricted preop
- colloids preferred
- intraabdominal procedures = excessive bleeding and fluid shifts so prepare to give blood and fluids
excessive bleeding due to…
- venous engorgement from portal HTN
- adhesions from previous surgery
- coagulopathy
fluid shifts due to…
- evacuation of ascites fluid (removal of large amounts of ascites fluid may require IV colloids to prevent HypoTN
- prolonged surgical procedures
hepatobiliary disease
- characterized by suppression or stoppage of bile flow
- most common cause of cholestasis is extrahepatic occlusion of biliary tract due to gallstones, stricture, tumor in common hepatic duct
- also caused by intrahepatic obstruction due to suppression or stoppage of bile at level of hepatocyte or bile canaliculus (d/t viral hepatitis or idiosyncratic drug reaction)
treatment of extrahepatic obstruction
SURGICAL
treatment of intrahepatic obstruction
MEDICAL
hepatobiliary disease preop considerations
- patients commonly present to OR with cholecystectomy
- patients with acute cholecysitis should be treated medically before coming to the OR (NG suction, IV fluids, Abx, opioids)
- patients with serious complications may require emergent cholecystectomy
- extrahepatic biliary obstruction readily develop vit k deficiency
- high bilirubin associated with renal failure
- long standing extrahepatic biliary obstruction associated with secondary biliary cirrhosis and portal HTN
hepatobiliary disease intraop considerations
- laproscopy chole accelerates recovery
- opioids = problem when chholangiogram performed (sphincter of oddi spasm may theoretically result in false positive)
- prolonged DOA in drugs with biliary excretion
- agents with renal excretion preferred (UOP monitored with foley, and maintain periop diuresis)
common hepatic surgeries
- repair of lacerations
- drainage of abscesses
- resection of tumors
how much of the liver can be resected?
80-85%
post op complications of hepatic surgery
- sepsis
- bleeding
- hepatic dysfunction
