Hepatic Pathophysiology and Anesthesia Complications Flashcards
1
Q
acute hepatitis is the result of (3)
A
viral infection
drug reaction
exposure to hepatotoxin ex) alcohol
2
Q
acute fulminant hepatic failure pathophysiology (general)
A
rapid, massive necrosis of liver and a decrease in liver size
3
Q
how is hepatitis A transmitted
A
oral fecal
4
Q
how is hepatitis B and C transmitted
A
primarily percutaneously (needles/blood) and by contact with body fluids
5
Q
hep a
severity
recovery
A
least severe
most recover in weeks to months
6
Q
hep e
where it is found
transmission
A
found in 3rd world countries (similar to hep A)
transmission through fecal contamination
7
Q
hep D
only occurs as (2 consideration)
transmission
A
only occurs as co infection with acute hep B or super infection with chronic hep B
transmission through fecal contamination/body fluids
8
Q
HBsAg
A
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
9
Q
what can hep B lead to
A
fulminant hepatic necrosis or chronic hepatitis
10
Q
hep C and diagnosis considerations
A
antibodies not present for long period, therefore difficult to diagnose.
produces asymptomatic carriers
11
Q
hep C and possible progressive pathophysiology of the liver
A
rarely produces fulminant hepatic failure
significant number will develop cirrhosis or liver cancer
12
Q
hep C vaccine
A
none available currently
13
Q
acute hepatitis early clinical signs
A
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.
14
Q
acute hepatitis recovery
A
usually takes 4 months, evidenced by normal serum transaminase
15
Q
how to diagnose type of hepatitis
A
have to do serological testing or biopsy since s/sx overlap
16
Q
chronic active viral hepatitis can be seen with
A
hep b and c
17
Q
how to take precaution against infectious patients
A
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
18
Q
drug induced acute hepatitis results from
A
direct dose dependent toxicity of a drug or metabolite
idiosyncratic drug reaction
combination of the two
19
Q
most common cause of hepatitis
A
drug induced
20
Q
chronic alcohol ingestion can result in fatty infiltration as a result of (3)
A
impaired fatty oxidation (beta oxidation)
increased uptake and esterification of fatty acids
diminished lipoprotein synthesis and secretion
21
Q
toxic drug induced acute hepatitis offenders (4)
A
alcohol
acetaminophen
vinyl chloride (inhalation for a brief time)
carbon tetrachloride
22
Q
idiosyncratic drug induced acute hepatitis offnders
A
volatile anesthetics
sulfonamides
23
Q
toxic and idiosyncratic acute drug induced hepatitis
A
amiodarone
24
Q
acute hepatitis preoperative considerations
A
postpone elective surgery until resolved as determined by LFT’s
25
alcohol withdrawal during surgery associated with mortality rate as high as
90%
26
patients with hepatitis are at risk for these 3 things during perioperative period
encephalopathy
coagulopathy
hepatorenal syndrome
27
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
```
28
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
29
does elevated transaminase correlated with the degree of cellular necrosis
no, AST/ALT does not correlate well
30
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
31
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
32
goal of intraoperative management of hepatitis
preserve existing hepatic function
| avoid factors that may be detrimental to the liver
33
acute viral hepatitis and anesthetics
may produce increased CNS sensitivity to anesthetics
34
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)
35
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
36
volatile agent of choice for hepatic issues
isoflurane, least effect on hepatic blood flow
37
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
38
try to avoid these responses intraoperatively with hepatitis patients that decrease hepatic BF
hypotension
excessive SNS stimualtion
high mean airway pressures during controlled ventilation
39
regional anesthesia and liver abnormalities
can be used in the absence of coagulopathy
40
chronic hepatitis definition
defined as persistent hepatic inflammation for longer than 6 months as evidenced by elevated serum aminotransferase
41
classification of chronic hepatitis based on 3 distinct syndromes via liver biopsy
chronic persistent hepatitis
chronic lobular hepatitis
chronic active hepatitis
42
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
43
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
44
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
45
treatment of hep B
ARV + immune modulator drugs (interferon)
46
treatment of hep C
ARV can cute more than 95% of these infected patients
47
anesthetic management of patients with chronic persistent of chronic lobular hepatitis
treat like those with acute hepatitis
48
anesthetic management of patients with chronic active hepatitis
assume cirrhosis, treat them as such
49
most common causes of cirrhosis (4)
alcohol abuse
NAFLD
chronic active hep B and C
chronic biliary inflammation or obstruction
50
result of cirrhosis
hepatocyte necrosis followed by fibrosis and nodular regeneration
51
cirrhosis eventually results in
hepatic failure. is a progressive disease
52
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
53
4 manifestations related to cirrhosis
spider angiomas
palmar erythema (due to volume distribution issue)
gynecomastia
splenomegaly
54
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
55
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
56
major cause of morbidity and mortality in cirrhotic patients
massive bleeding from esophageal varices
57
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
58
hematological considerations for a patient with cirrhosis
may present with anemia, thrombocytopenia/coagulopathy, leukopenia
59
anemia related to cirrhosis associated with
blood loss
increased RBC destruction
bone marrow suppression
nutritional deficiencies
60
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
61
leukopenia related to cirrhosis associated with
congestive splenomegaly due to portal HTN
62
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
63
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
64
cirrhotic cardiomyopathy may be present due to
AV shunts or decreased blood viscosity
| contribute to increased CO, above normal filling pressures, below normal SVR
65
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
66
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
67
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)
```
68
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
69
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
```
70
hepatorenal syndrome tx
supportive, often unsuccessful unless liver transplantation performed
71
intraoperative fluid administration: colloids or crystalloids?
colloids
72
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
73
hepatic encephalopathy is characterized by
alterations in mental status
fluctutating neurological signs (asterixis, hyperreflexia)
EEG changes
some patients also have increased ICP
74
toxin accumulation in GI tract that can be attributed to hepatic encephalopathy include
ammonia, methionine metabolites, short chain fatty acids, phenols (like cleaning agents)
75
factors known to precipitate hepatic encephalopathy include
GI bleeding, increased dietary protein intake, hypokalemia alkalosis from vomiting or diuresis, infections, worsening liver function
76
encephalopathy and sedatives
recommended to avoid, try to tx enceophalopathy preoperatively
77
drug response to agents is unpredictable in cirrhosis due to changes in
```
CNS sensitivity
Vd
protein binding
drug metabolism
drug elimination
TITRATE
```
78
Vd of highly ionized NMBA's is ________ in cirrhosis patents, therefore
increased
| requires greater than normal loading doses
79
hepatic elimination of NMBA's is _________ in cirrhosis patients therefore
decreased
| requires lower than normal maintenance doses
80
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
81
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
82
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
83
patient with right to left shunts and cirrhosis, intraoperative consideration
may not tolerate N2O, may require PEEP to treat VQ inequalities and subsequent hypoxemia
84
most patients should have aline monitoring with cirrhosis as a result of these possibilities
excessive bleeding
rapid intercompartmental fluid shifts
surgical manipulations
85
need these monitors for patients with cirrhosis
```
cellsaver
blood warrmer
fluid
blood in room
CVC
many large bore IV's
aline
urinary catheter
```
86
cirrhosis and fluid replacement
colloids intraop still take precedence over the Na restriction to manage intravascular fluid volume
87
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)
```
88
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
89
hepatobilitary disease characterized by
cholestasis, suppression of stoppage of bile flow
90
most common cause of cholestasis
extrahepatic obstruction of biliary tract (obstructive jaundice) due to gallstones, stricture, tumor in common hepatic duct
91
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
92
treatment of extra hepatic obstruction
surgical
93
treatment of intra hepatic cholestasis
medical
94
extra hepatic obstruction and intrahepatic cholestasis two dx labs
predominately conjugated hyperbilirubinemia and marked elevation in alk phos
95
cholangitis
concomitant chills or high fever from ascending bacterial infection of biliary systems
96
how gallstones can cause acute pancreatitis
can obstruct pancreatic duct
97
sx that presents with cholelithiasis
biliary colic secondary to obstruction of cystic duct
98
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
99
treatment for acute cholecystitis
nasogastric suction
IV fluids
abx
opioid analgesics
100
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
101
high levels of this lab may be associated with renal failure, esp in hepatobiliary disease patients
bilirubin levels
102
long standing extra hepatic biliary obstruction is associated with
secondary biliary cirrhosis and portal hypertension
103
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
104
sphincter of oddi spasm can be treated with
glucagon, naloxone
105
common hepatic surgeries include
repair of lacterations
drainage of abcesses
resection of tumors
106
how much liver can be resected
80-85%
107
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)
108
postop complications of hepatic surgery include
bleeding, sepsis, hepatic dysfunction
| postop mechanical ventilation may be necessary in patients undergoing extensive resection
