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N935 Advanced Pathophysiology II > Hepatic 2 > Flashcards

Hepatic 2 Flashcards

1
Q

usual causes of acute hepatitis

A
  • viral infection
  • drug reaction
  • exposure to hepatotoxin (alcohol, carbon tetrachloride)
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2
Q

clinical manifestations of acute hepatitis

A
  • 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
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3
Q

acute fulminant hepatic failure

A

rapid, massive necrosis of the liver parenchyma and decrease in liver size

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4
Q

common viral causes of acute hepatitis

A
  • hepatitis A, B and C viruses are the most common

- also D, E, Epstein-Bar, Herpes Simplex, CMV, and coxsackievirus

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5
Q

how is hep A spread?

A

oral fecal route

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6
Q

how are hep B and C spread?

A

percutaneously and by contact with body fluids

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7
Q

hepatitis A

A
  • least severe
  • most recover in weeks to months
  • transmission through fecal contamination
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8
Q

hepatitis E

A
  • similar to A
  • in 3rd word countries where there is not the best sanitation
  • transmission through fecal contamination
  • usually recover well
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9
Q

hepatitis D

A
  • 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
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10
Q

hepatitis B

A
  • 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
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11
Q

hepatitis C

A
  • 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
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12
Q

viral infection associated with acute hepatitis

A
  • 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
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13
Q

drug-induced acute hepatitis causes

A
  • direct dose-dependent toxicity of a drug or metabolite
  • idiosyncratic drug reaction
  • combination of the two
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14
Q

most common cause of drug-induced acute hepatitis

A

alcohol

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15
Q

fatty infiltration of the liver from chronic alcohol ingestion

A
  • impaired fatty acid oxidation (i.e., impaired beta oxidation)
  • increased uptake and esterification of fatty acids
  • diminished lipoprotein synthesis and secretion
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16
Q

common drugs that can cause acute hepatitis

A
  • acetaminophen
  • alcohol
  • salicylates
  • vinyl chloride
  • carbon tetracholoride
  • halothane
  • sulfonamides
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17
Q

Pre-op considerations for acute hepatitis

A
  • 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%)
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18
Q

pre-op labs for acute hepatitis

A
  • 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)
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19
Q

elevated transaminases

A
  • do not correlate well with degree of cellular necrosis (just indicative of hepatocellular dysfunction)
  • ALT>AST with acute hepatitis
  • AST>ALT with alcoholic hepatitis
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20
Q

what is the best indicator of synthetic function of the liver with hepatitis?

A

PT

-prolongation >3-4 seconds (INR > 1.5) following admin of vitamin K is indicative of severe liver dysfunction

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21
Q

Preop evaluation of emergent patient with acute hepatitis

A
  • 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
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22
Q

alcoholics preop eval

A
  • acute toxicity = inappropriate behavior or obtunded patient
  • withdrawal = irritability, tremulousness, HTN, tachy (benzos and thiamine indicated for withdrawal)
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23
Q

goal of intraoperative management of those with acute hepatitis

A
  • preserve existing hepatic function

- avoid factors that may be detrimental to the liver

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24
Q

intraoperative considerations for acute hepatitis

A
  • 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
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25
Q

alcoholic patients intraoperative considerations

A
  • 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
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26
Q

avoid things to reduce hepatic blood flow

A
  • hypotension
  • excessive SNS stimulation
  • high mean airway pressure during controlled ventilation
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27
Q

what is the preferred inhalation agent for liver patients?

A

isoflurane because has the smallest effect on hepatic blood flow

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28
Q

chronic hepatitis

A

persistent hepatic inflammation for longer than 6 months as evidenced by elevated serum aminotransferases

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29
Q

patient classification of chronic hepatitis

A
  • determined by liver biopsy
  • three distinct syndromes
  • chronic persistent hepatitis
  • chronic lobular hepatitis
  • chronic active hepatitis
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30
Q

chronic persistent hepatitis

A
  • 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
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31
Q

chronic lobular hepatitis

A
  • 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
32
Q

chronic active hepatitis

A
  • 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
33
Q

antiviral treatment

A
  • hep B - antivirals + immune modulator drugs (interferon)

- hep C - antiviral can cure more than 95% of affected patients

34
Q

anesthetic management of chronic hepatitis

A
  • chronic persistent or chronic lobular - similar to acute hepatitis
  • chronic active - assumed to have cirrhosis and treated as such
35
Q

cirrhosis

A
  • progressive disease that eventually results in hepatic failure
  • result = hepatocyte necrosis followed by fibrosis and nodular regeneration
36
Q

common causes of cirrhosis

A
  • alcohol abuse
  • NAFLD
  • chronic active hepatitis B and C
  • chronic biliary inflammation or obstruction
37
Q

destruction of liver’s normal cells and vasculature causes…

A
  • obstruction of the portal venous flow leading to PORTAL HTN
  • impairment of normal synthetic and metabolic functions of liver leading to multisystem disease
38
Q

clinical manifestations of cirrhosis

A
  • jaundice
  • ascites
  • spider angiomas
  • palmar erythema
  • gynecomastia
  • spleenomegaly
39
Q

what are the three major complications associated with cirrhosis?

A
  • variceal (esophageal) hemorrhage from portal HTN
  • intractable fluid retention in form of ascites
  • hepatic encephalopathy or coma
40
Q

what do 10% of patients with cirrhosis develop?

A
  • bacterial peritonitis

- hepatocellular carcinoma

41
Q

why are those with cirrhosis at increased risk for deterioration of liver function?

A
  • detrimental effects of anesthesia and surgery on hepatic blood flow
  • already limited hepatic reserve
42
Q

childs-turcotte-pugh scoring system

A
  • estimates severity of hepatic impairment and surgical risk
  • 2 clinical features and 3 lab assessments
  • total bilirubin
  • serum albumin
  • INR
  • ascites
  • hepatic encephalopathy
43
Q

Cirrhosis GI manifestations

A
  • 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
44
Q

medical treatment for esophageal varices

A
  • 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
45
Q

cirrhosis heme manifestations

A
  • anemia
  • thrombocytopenia/coagulopathy
  • leukopenia
46
Q

anemia periop associated with

A
  • blood loss
  • increased RBC destruction
  • bone marrow suppression
  • nutritional deficiencies
47
Q

thrombocytopenia + coagulopathy associated with

A
  • 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
48
Q

leukopenia periop associated with

A

-congestive spleenomegaly due to portal HTN

49
Q

preoperative blood transfusions considerations

A
  • 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
50
Q

cirrhosis circulatory manifestations

A
  • 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
51
Q

Cirrhosis respiratory manifestations

A
  • 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
52
Q

cirrhosis renal manifestations + fluid balance

A
  • ascites, edema, electrolyte abnormalities, hepatorenal syndrome
  • hyponatremia common
  • hypokalemia common
53
Q

mechanisms thought responsible for ascites

A
  • 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
54
Q

patients with cirrhosis and ascites have

A
  • decreased renal perfusion
  • altered intrarenal hemodynamics
  • enhanced proximal and distal tubule Na+ reabsorption
  • impairment of free water clearance
55
Q

hepatorenal syndrome

A

-functional deficit in patients with cirrhosis that usually follows GI bleeding, aggressive diuresis, sepsis, or major surgery

56
Q

characteristics of hepatorenal syndrome

A
  • progressive oliguria
  • avid Na+ retention
  • azotemia (a lot of nitrogen in blood)
  • intractable ascites
  • very high mortality rate
57
Q

treatment of hepatorenal syndrome

A

-supportive and often unsuccessful unless liver transplant

58
Q

intra + preop considerations for renal dysfunction with cirrhosis

A
  • 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
59
Q

cirrhosis CNS manifestations

A
  • 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
60
Q

characteristics of hepatic encephalopathy

A
  • alterations in mental status
  • fluctuating neurological signs (asterixis, hyperreflexia)
  • EEG changes
  • some patients may have increased ICP
61
Q

GI toxins potentially involved in hepatic encephaolopathy

A
  • ammonia
  • methionine metabolites
  • short chain fatty acits
  • phenols
62
Q

factors that precipitate hepatic encephalopathy

A
  • GI bleeding
  • increased dietary protein intake
  • hypokalemiac alkalosis from vomiting or diuresis
  • infection
  • worsening liver function
63
Q

cirrhosis drug response unpredictable due to

A
  • CNS sensitivity
  • Vd changes
  • protein binding
  • drug metabolism
  • drug elimination
64
Q

NMBDs

A
  • greater loading doses (bc higher Vd)

- lower maintenance doses (hepatic elimination decreased)

65
Q

anesthetic technique for cirrhosis

A
  • 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
66
Q

intraop monitoring with cirrhosis

A
  • 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
67
Q

fluid replacement intraop with cirrhosis

A
  • most patients Na+ restricted preop
  • colloids preferred
  • intraabdominal procedures = excessive bleeding and fluid shifts so prepare to give blood and fluids
68
Q

excessive bleeding due to…

A
  • venous engorgement from portal HTN
  • adhesions from previous surgery
  • coagulopathy
69
Q

fluid shifts due to…

A
  • evacuation of ascites fluid (removal of large amounts of ascites fluid may require IV colloids to prevent HypoTN
  • prolonged surgical procedures
70
Q

hepatobiliary disease

A
  • 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)
71
Q

treatment of extrahepatic obstruction

A

SURGICAL

72
Q

treatment of intrahepatic obstruction

A

MEDICAL

73
Q

hepatobiliary disease preop considerations

A
  • 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
74
Q

hepatobiliary disease intraop considerations

A
  • 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)
75
Q

common hepatic surgeries

A
  • repair of lacerations
  • drainage of abscesses
  • resection of tumors
76
Q

how much of the liver can be resected?

A

80-85%

77
Q

post op complications of hepatic surgery

A
  • sepsis
  • bleeding
  • hepatic dysfunction

N935 Advanced Pathophysiology II (16 decks)

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