ANESTHESIA FOR HEPATIC DISEASE Flashcards
1
Q
what are the functional units of the liver?
A
- lobule
* acinus
2
Q
name the 8 segments of the liver
A
- I – posterior caudal segment
- II – lateral segment
- III – left anterior lateral segment
- IV – medial segment
- V – anterior medial segment
- VI – right anterior lateral segment
- VII – posterior lateral segment
- VIII – posterior medial segment
3
Q
describe the large vascular capacity of the liver
A
- 25-30ml blood/100gm tissue
- 10-15% of total blood volume
- (70% venous)
4
Q
how much blood flow does the liver receive per minute?
A
total hepatic blood flow = 1200-1400ml/min
* 100ml/min/100gm tissue
5
Q
what percentage of total cardiac output does the liver see?
A
25% of cardiac output
6
Q
what percentage of hepatic blood flow does the portal vein receive? from what organs?
A
portal vein received 70-80% of hepatic blood flow
- intestine (60%)
- stomach (20%)
- pancreas (10%)
- spleen (10%)
7
Q
what percentage of hepatic blood flow does the hepatic artery receive?
A
20-30%
8
Q
blood from the superior mesenteric vein is filtered primarily through which lobe of the liver?
A
right lobe
9
Q
blood from the splenic, gastric, and inferior mesenteric veins is filtered primarily through what lobe of the liver?
A
left lobe
10
Q
describe the hepatic acinus
A
functional microvascular unit, cluster of parenchymal cells formed about a vertical axis, consisting of:
- terminal portal venule
- hepatic arteriole
- bile duct
- lymph vessels and nerves
11
Q
describe hepatic blood flow
A
high flow, low resistance
12
Q
describe the liver as a blood reservoir
A
- normal blood reservoir of 450ml (10% TBV)
* expandable to 0.5-1.0L (CHF)
13
Q
describe lymph flow in the liver
A
- sinusoids are permeable to fluids and proteins
- contain half of all lymph in body
- ascites forms from high hepatic vascular pressure (e.g., cirrhosis, liver disease)
14
Q
describe the hepatic artery buffer system
A
hepatic artery blood flow increases with decreases in portal vein flow to maintain pressure in liver
- hepatic artery can perfuse the entire liver
- dependent on systemic arterial pressure
15
Q
describe hepatic compliance
A
highly compliant
- 2-3ml/mmHg for each 100g of liver weight
- raising venous pressure by 1mmHg results in an increase of 40-50ml
16
Q
define hepatic volumes for unstressed and stressed hepatic compliance
A
- unstressed (0mmHg): 210-250ml
- stressed (8mmHg): 300-350ml
- capacitance is about 600-1000ml
17
Q
intrinsic regulation of hepatic flow is maintained by what two mechanisms?
A
- autoregulation
* metabolic control
18
Q
how does autoregulation maintain intrinsic hepatic flow?
A
hepatic artery vasoconstriction
* myogenic response to smooth muscle stretch
19
Q
how does metabolic control maintain intrinsic hepatic flow?
A
- arterial hypoxemia
- decreased blood pH (acidosis, hypercarbia)
- hyperosmolarity
20
Q
extrinsic regulation of hepatic blood flow is maintained by what two mechanisms?
A
- neural control
* humoral factors
21
Q
how does neural control maintain extrinsic regulation of hepatic flow?
A
- sympathetic stimulation of vagus and splanchnic nerve decreases blood flow
- 500ml can be expelled in seconds
22
Q
how does epinephrine help to maintain extrinsic regulation of hepatic flow?
A
epinephrine – initial vasoconstriction via alpha receptors, then vasodilation via beta-receptors
23
Q
how does glucagon help to maintain extrinsic regulation of hepatic flow?
A
glucagon is a long-lasting arterial vasodilator
24
Q
how does angiotensin II help to maintain extrinsic regulation of hepatic flow?
A
angiotensin II produces profound vasoconstriction
25
how does vasopressin (ADH) help to maintain extrinsic regulation of hepatic flow?
vasopressin produces marked splanchnic vasoconstriction
26
how does anesthesia affect hepatic blood flow?
* all anesthetics and techniques that decrease cardiac output will produce a proportional decrease in total hepatic blood flow
27
how does controlled ventilation affect hepatic blood flow?
* controlled ventilation will decrease portal venous flow
28
how does regional anesthesia affect hepatic blood flow?
* regional anesthesia will decrease hepatic blood flow in parallel with systemic BP
29
how does controlled hypotension affect hepatic blood flow?
* controlled hypotension with sodium nitropresside will not alter hepatic blood flow due to an increased portion of blood flow to the portal vascular bed
30
how does the site of surgery affect hepatic blood flow?
the site of surgery effects hepatic blood flow, with upper abdominal surgery decreasing flow up to 60%
31
which inhalation anesthetic has the least effect on hepatic blood flow? the most?
* least – sevoflurane
| * most – halothane (almost linear sharp decrease in HBF as MAC level increases)
32
describe the metabolic function of the liver
* protein metabolism – except gamma globulin
* produces albumin
* production of all coagulation factors – except factor III, IV, VIII
* amino acid metabolism
* carbohydrate metabolism
* nutrient metabolism
* fat metabolism
* bacterial filtering
33
what is the normal range for serum albumin?
3/5-6g/dl
| * serum albumin is a reliable predictor of chronic liver disease
34
which coagulation factors are vitamin K dependent?
II, VII, IX, X
35
which coagulation factors are non-vitamin K dependent?
V, XI, XII, XIII, fibrinogen
36
what test is a good indicator of acute hepatic dysfunction, as well as vitK dependent coagulation factor deficiencies?
PT (prothrombin time)
37
why must liver function be significantly impaired before coagulation decreases?
only 20-30% of normal levels needed for adequate coagulation
38
describe amino acid metabolism in the liver
* deamination of amino acids in process of energy production
* removal of ammonia in form of urea
* * impaired in both acute and chronic hepatic disease
39
describe carbohydrate metabolism in the liver
"glucose buffer system"
* storage of large amounts of glycogen – converted to glucose as needed
* * glycogen stores exhausted by NPO in 24hr
40
describe the deleterious effects of impaired liver function in terms of nutrient metabolism
in pts with impaired liver function, glucose loads are poorly tolerated, and blood glucose can rise several-fold –> diabetes
41
the majority of cholesterol synthesized in the liver is converted to what?
bile salts, secreted in bile
42
what cells in the liver are responsible for phagocytosis of bacteria that enter through the intestines?
```
Kupffer cells (macrophages)
* liver can trap all but less than 1% of bacteria before it passes into systemic circulation
```
43
describe fat metabolism in the liver
* oxidation of fatty acids for energy
* synthesis of cholesterol and phospholipids
* major source of acetyl-CoA
44
how much bile is produced by hepatocytes daily?
~500ml
45
how much bile can the gallbladder hold?
35-50ml of concentrated bile
46
how is the secretion of bile triggered?
* fat in duodenum triggers cholecystokinin release from duodenal mucosa
* cholecystokinin reaches gallbladder through circulation – stimulates gallbladder contraction
* bile released into small intestine
47
describe the mechanism of fat solubilization by bile
* bile contains bile salts, bilirubin, cholestorol
| * bile salts act as detergent, solubilizing fat to be absorbed
48
describe the formation of bilirubin
* breakdown of hemoglobin (RBCs)
* heme released converted to free, unconjugated bilirubin (lipid soluble), bound to albumin
* conjugated in liver (hydrophilic), secreted into bile
* 300mg produced daily
49
how does jaundice progress?
* results from accumulation of bilirubin in extracellular fluids
* skin coloration (yellow-green) visible with plasma bilirubin = 3x normal value
* result of increased Hgb breakdown or obstruction of bile duct
50
what form of bilirubin are hemolytic and obstructive jaundice associated with?
* hemolytic jaundice – unconjugated (indirect) bilirubin
| * obstructive jaundice – conjugated (direct) bilirubin
51
describe how drugs affect bile formation
* all narcotics increase common bile duct pressure (fentanyl >morphine >demoral)
* attenuated by NTG, nalonone, atropine and glucagon
52
define drug biotransformation
conversion of lipophilic substances to excretable metabolites
* enzymatic responses
53
describe the two phases of biotransformation
* phase I – oxidation, cytochrome P450, >90%
| * phase II – conjugation w/ glucuronic acid to increase water solubility for biliary excretion
54
what factors affect drug metabolism?
* HBF, protein binding, intrinsic hepatic clearance
| * enzyme inducing compounds
55
which liver enzyme lab test is a good indicator of hepatitis?
```
alanine aminotransferase (ALT) – primarily found in liver
* 5-40 IU/L
```
56
which liver enzyme lab test is a good indicator of biliary disease or blockage?
```
alkaline phosphatase (ALP) – primarily found in bile ducts
* 13-39 IU/L
```
57
how is serum albumin assessed for liver function?
albumin levels are decreased in chronic liver disease (cirrhosis)
58
how is coagulation assessed for liver function?
PT – assesses extrinsic pathway of clotting cascade, namely factor VII and is associated with acute liver disease
59
what is the normal range for PT?
9-12, 10-15sec
60
what factors will affect PT?
* liver disease
* coumarin therapy
* heparin therapy
* VitK deficiency
* Factor VII deficiency
61
what effects will low serum albumin levels have? what is the normal range for serum albumin?
* reduced intravascular osmotic pressure
* vascular leaking leading to edema and ascites
* range: 3.9-5.0g/dl
62
coumadin interferes with which coagulation factors?
VitK dependent factors: II, VII, IX, X
63
tissue factor is which coagulation factor and is the sole factor in the extrinsic pathway?
VII
64
trace the intrinsic pathway to factor X
XII –> XI –> IX –> VIII
65
a deficiency of what intrinsic pathway factor leads to hemophilia B/christmas disease?
IX
66
a deficiency of what intrinsic pathway factor leads to hemophilia A and von willebrand disease?
VIII
67
elevated unconjugated (indirect) bilirubin is an indicator of what?
problem upstream of bilirubin excretion
| * hemolysis, hepatitis, cirrhosis can be suspected
68
elevated conjugated (direct) bilirubin is an indicator of what?
problem with bilirubin excretion
| * bile duct obstruction by gallstones or cancer can be suspected
69
what are the ranges for total, direct, and indirect bilirubin?
* total bilirubin – 0.2-1.5mg/dl
* direct (conjugated) – 0.0-0.03mg/dl
* indirect (unconjugated) – 0.2-0.8mg/dl
70
how is hepatitis A transmitted?
via fecal/oral route, contaminated shell fish is common route
71
how does hep A manifest?
clinically manifests as acute viral hepatitis:
* fever
* jaundice
* painfully enlarged liver
72
how is hep B transmitted?
* blood transfusion
* needle sticks
* sexual contact
* across the placenta
73
how does hep B manifest?
* clinically manifests as acute with development to fulminant hepatitis and rapid liver destruction
* 10% develop chronic hepatitis (asymptomatic or chronic)
* complications: primary hepatocellular carcinoma or cirrhosis
74
is there a vaccination for hep B?
yes. should be taken by healthcare workers who are at high risk of potentially contracting it through contaminated needle sticks
75
how is hep C transmitted?
same as hep B
* blood transfusion
* needle sticks
* sexual contact
* across the placenta
76
how does hep C manifest?
clinically manifests as acute hepatitis
77
how does hep C progress?
* 50% of pts will get chronic
* 20% will develop cirrhosis
* increased risk of developing hepatocellular carcinoma
78
describe hep D
* co-infection acquired with hep B
| * acute infection that can progress to fulminant hepatitis or cirrhosis
79
describe hep E
* spread by fecal/oral route due to contaminated water or poor hygiene
* rarely found in US
80
what are the anesthetic considerations for hepatitis?
* assessment of coagulation preoperatively, tx with FFP if indicated
* glucose monitoring
* maintain near normal HBF, avoid hypercarbia
* drug metabolism may be affected – prolonged effect
81
what effects will benzodiazepines have on pts with severe hepatic dysfunction?
* prolonged and more intense effect
| * should be avoided as a pre-med w/ severe hepatic failure
82
how will opioids affect pts with hepatic dysfunction?
* morphine, alfentanil – prolonged effect
| * fentanyl, sufentanil – not so much
83
what effect will non-depolarizing muscle relaxants have on pts with hepatic dysfunction?
* hepatic dysfunction = hypoproteinemia
| * less drug bound to protein, prolonged effect
84
what muscle relaxants are a better choice for hepatic dysfunction?
cis and atracurium
* metabolized by plasma esterases
* best choice if reversal is planned
85
describe cirrhosis
* chronic disease of liver characterized by distortion of the normal hepatic structure or scarring caused by cellular destruction
* interference with intrahepatic circulation and gradual failure of liver function
86
describe cholelitiasis
formation of calculus (stones) in gallbladder, caused by cholesterol crystal precipitation
87
describe cholecystitis
inflammation of gallbladder caused by gallstone in cystic duct that connects to hepatic duct
88
anesthetic considerations for pts presenting for cholecystectomy
* may present with recent history of N/V
* considered full stomach – RSI
* opioids may constrict sphincter of oddi preventing flow of contrast dye from common bile duct
89
what complications should be considered when administering blood to pts with hepatic dysfunction?
* 1u PRBCs contains ~ 250mg bilirubin – increases with age of transferred unit
* an elevation of unconjugated bilirubin can lead to seizures and brain damage (Kernicterus)
* pts with hepatic disease/hyperbilirubin get newest PRBCs possible
90
where do malignant tumors of the liver generally arise from?
* parenchymal cells – hepatocarcinoma (80-90%)
| * bile duct epithelium – cholangio-carcinoma
91
what percentage of malignant tumors of the liver have underlying cirrhosis (primarily alcoholic in origin)
75%
92
what is the most common source of hepatic tumors?
metastasis from another site
93
what is the treatment for hepatic tumors?
chemotherapy and/or surgery if the tumor is isolated to a lobe or segment
94
what are the anesthetic considerations for hepatic resection?
* large bore IV access
* a-line monitoring
* CVP monitoring
* epidural catheter for post-op pain management
* keep pt relatively hypovolemic during resection phase to minimize venous engorgement of liver/blood loss
* T&C for at least 6u blood
95
describe portal hypertension
a sustained elevation of pressure in the portal vein above the normal level of 6-12cmH2O (8-16mmHg)
96
how does portal hypertension manifest clinically?
* increased resistance to blood flow in liver (decreased outflow), increased splanchnic arterial flow (increased inflow) = overflow of portal circulation
97
what comorbidities present with portal hypertension?
* development of collateral channels/varices in attempt to circumvent hepatic obstruction
* splenomegaly caused by back pressure in portal system – partly responsible for accumulation of ascites in abdomen
98
what causes portal HTN in the hepatic vein (posthepatic portal HTN)?
* Budd-Chiari syndrome
* right heart failure
* restrictive cardiomyopathy
* constrictive pericarditis
99
what causes portal HTN in the liver (intrahepatic portal HTN)?
cirrhosis
100
what causes portal HTN in the portal vein (prehepatic portal HTN)?
thrombosis
101
what is the morbid clinical manifestation of portal HTN?
GI bleeding
| * bleeding of varices esp in esophagus means that hepatic obstruction and portal HTN are severe
102
what is the treatment for GI bleeding/portal HTN?
* temporarily stop the hemorrhage
| * attempt to decompress portal venous circulation
103
what are the anesthetic considerations for GI bleeding/portal HTN?
* may require large volume blood transfusion
| * pt may already be coagulopathic from liver disease = high mortality rate
104
describe transjugular intrahepatic portosystemic shunt (TIPS)
* used as a way to decompress portal circulation and buy time in course of underlying liver disease
* often used as a bridge to liver transplant
105
what anesthetic plan is used for TIPS?
GA in the interventional radiology suite
106
describe ascites
* accumulation of serous fluid in the peritoneal cavity
107
what are the anesthetic considerations for draining ascites?
* abdominal viscera are compressed
| * decompression allows expansion of large venous reservoir causing hypovolemia and potentially severe hypotension
108
describe arterial hypoxemia relative to ascites
* PaO2 values of 60-70mmHg common in pts with ascites = supplemental O2
* probably due to impaired movement of diaphragm, right-to-left intrapulmonary shunting as a result of portal HTN, smoking, COPD
109
what is the treatment for ascites?
* drug-induced diuresis with spironolactone
| * max diuresis of ascitic fluid not to exceed 1L/d for fear of hypovolemia
110
how is removal of ascites fluid managed?
* requires venous volume expansion – IV fluids, usually colloids, to prevent/minimize hypotension
* good IV access important – may have to administer large amounts of fluid quickly
111
what are the normal values for PT, PTT, activated clotting time, and thrombin time?
* PT – 10-12sec
* PTT – 25-35sec
* activated clotting time – 90-120sec
* thrombin time – 9-11sec
112
what is the primary treatment of coagulopathy?
FFP
113
in addition to FFP, what may be required to bring coagulopathic pt PT to within 3sec of normal preoperatively?
cryoprecipitate and platelets
114
what is the greatest fear of massive blood loss in the coagulopathic pt?
breakdown of the clotting process (fibrinolysis)
115
how does encephalopathy (hepatic coma) manifest?
* mental confusion/ obtundation
* asterixis – flapping motion of hands at wrist caused by loss of extensor tone
* fetor hepaticus – fruity odor of the breath
116
what are the causes of encephalopathy?
* cerebral intoxication caused by intestinal contents that have not been metabolized by the liver
* protein breakdown products from GI bacteria
* ammonia (normally converted to urea by the liver)
117
how is encephalopathy treated?
* protein restriction
* antibiotics to restrict gut bacteria (neomycin)
* reduce diuretic therapy
* treat hypokalemia
* restrict sedatives, tranquilizers
