RENAL, LIVER, AND BILIARY TRACT DISEASE Flashcards
1
Q
- What are some essential physiologic functions of the kidneys?
A
- Essential physiologic functions of the kidneys include the excretion of metabolic
wastes; the retention of nutrients; the regulation of water, tonicity, and
electrolyte and hydrogen ion concentrations in the blood; and the production
of hormones that contribute to water regulation and bone metabolism.
2
Q
- Name some factors that place patients at an increased risk of acute renal failure in the perioperative period.
A
- Factors that place patients at an increased risk of acute renal failure in the
perioperative period include advanced age, emergent surgery, liver disease,
high-risk surgery, body mass index, peripheral vascular occlusive disease, and
COPD.
3
Q
- What percent of the cardiac output normally goes to the kidneys? What fraction of this goes to the renal cortex?
A
- Although the kidneys typically constitute only 0.5% of body weight, about 20%
of the cardiac output normally goes to the kidneys. Of the 20%, more than
two-thirds goes to the renal cortex and the remaining blood flow supplies the renal
medulla
4
Q
- Over what range of mean arterial blood pressures do renal blood flow and the
glomerular filtration rate (GFR) remain constant? How is this accomplished by the
kidneys? Why is it important?
A
- Renal blood flow and the GFR remain constant when mean arterial blood pressures
range between 80 and 180 mm Hg. This autoregulatory function of the kidneys
is accomplished by the afferent arteriolar vascular bed. The afferent arterioles are
able to adjust their tone in response to changes in blood pressure, such that
during times of higher mean arterial blood pressure the afferent arterioles
vasoconstrict, whereas the opposite occurs during times of lower mean arterial
blood pressure. This is important for two reasons. The ability of the kidneys to
maintain constant renal blood flow despite fluctuations in blood pressure ensures
continued renal tubular function in the face of changes, especially decreases, in
blood pressure. In addition, autoregulatory responses of the afferent arterioles
protect the glomerular capillaries from large increases in blood pressure during
times of hypertension, as may occur with direct laryngoscopy. When mean arterial
blood pressures are less than 80 mm Hg or greater than 180 mm Hg renal blood
flow is blood pressure dependent
5
Q
- Even during normal kidney autoregulatory function, what two factors can alter renal blood flow?
A
- Even during normal kidney autoregulatory function, renal blood flow can be altered
by sympathetic nervous system activity and by circulating renin.
6
Q
- What is renin? What is the secretion of renin usually in response to? What effect
does renin have on renal blood flow?
A
- Renin is a proteolytic enzyme secreted by the juxtaglomerular apparatus of
the kidney. There are at least three things that stimulate the release of renin
from the endothelial cells of the afferent arteriole:
(1) Sympathetic nervous stimulation;
(2) decreased renal perfusion; and
(3) decreased delivery of sodium to distal convoluted renal tubules.
• Renin increases efferent renal arterial
arteriolar tone at low levels and causes afferent arteriolar constriction at higher
levels.
7
Q
- What is the physiologic effect of the secretion of renin?
A
- Renin is the rate-limiting enzyme in the production of angiotensin II. After its
secretion from the juxtaglomerular apparatus of the kidneys, renin acts on
angiotensinogen. Angiotensinogen is a large glycoprotein released by the liver
to the circulation. After being cleaved by renin, angiotensin I is formed from
angiotensinogen. Angiotensin I is in turn cleaved by angiotensin converting
enzyme in the lungs to form angiotensin II. Angiotensin II stimulates the release of
aldosterone from the adrenal cortex and is a potent vasoconstrictor. It also inhibits
renin secretion as part of a negative feedback loop
8
Q
- What triggers the release of prostaglandins that are produced by the renal medulla?
What is the effect of prostaglandins released by the renal medulla?
A
- Prostaglandins are released from the renal medulla in response to angiotensin II, hypotension and sympathetic nervous system stimulation. Prostaglandins attenuate the actions of the sympathetic nervous system, arginine vasopressin,
9
Q
- What is the renal effect of arginine vasopressin released by the hypothalamus?
A
- Arginine vasopressin (previously known as antidiuretic hormone) release by the
hypothalamus results in the renal tubular conservation of water, an increased urine
osmolality, and a decrease in plasma osmolality. It is typically secreted in
response to small increases in serum osmolality
10
Q
- What is glomerular filtration? What is glomerular filtration dependent on?
A
- Glomerular filtration is the filtration of water and low molecular weight substances from the blood in the renal afferent arterioles into Bowman’s space through
the glomerulus. Glomerular filtration is dependent on two things: the permeability of the filtration barrier (the glomerular membrane) and the net difference
between the hydrostatic forces pushing fluid into Bowman’s space and the
osmotic forces keeping fluid in the plasma. (
11
Q
- What is the normal hydrostatic pressure of the glomerular capillaries? What is the normal plasma oncotic pressure in the afferent and efferent arterioles?
A
- The normal hydrostatic pressure of the glomerular capillaries is about 50 mm Hg.
The normal plasma oncotic pressure in the afferent and efferent arterioles is 25 mm
Hg and 35 mm Hg, respectively. The increase in oncotic pressure between the
afferent and efferent arterioles reflects the effects of filtration.
12
Q
- What is the average normal rate of glomerular filtration?
A
- The average normal rate of glomerular filtration is 125 mL/min. (
13
Q
- About what percent of the fluid shift from glomerular filtration is reabsorbed from renal tubules and ultimately returned to the circulation?
A
- About 90% of the fluids that have been filtered by the glomerulus into
Bowman’s capsule are reabsorbed from renal tubules and ultimately returned
to the circulation
14
Q
- How is the GFR influenced by the renal blood flow
A
- The GFR is decreased during times of decreased renal blood flow or decreased mean
arterial blood pressure
15
Q
- What are the three mechanisms upon which the renal clearance of drugs depends?
A
- The renal clearance of drugs or their metabolites depends on three things:
glomerular filtration (GFR and protein binding), active secretion by the renal
tubules, and passive reabsorption (favors nonionized compounds) by the
tubules
16
Q
- Name some tests used for the evaluation of renal function. How sensitive are tests of renal function?
A
- Tests that are commonly used for the preoperative evaluation of renal function
include a serum creatinine level, a BUN level, creatinine clearance, and urine protein levels. Tests that are commonly used for the preoperative evaluation of renal tubular function include the urine specific gravity, urine osmolarity, and urine sodium excretion. Most tests of renal function are not very sensitiv
17
Q
- What degree of renal disease can exist before renal function tests begin to indicate possible decreases in renal function?
A
- A significant degree of renal disease can exist before it is reflected in renal function tests. It is estimated that more than a 50% decrease in renal function may exist before these tests become abnormal.
18
Q
- What is the normal level of blood urea nitrogen (BUN)?
A
- The normal BUN level in serum varies among individuals, typically ranging between 10 and 20 mg/dL. Urea is freely filtered by the glomerulus of the kidney, but its reabsorption from the tubules varies greatly. Although the BUN varies with changes in GFR, it is influenced by multiple other factors that decrease its utility as a measure of the GFR and of renal function.
19
Q
- What factors may influence the BUN level?
A
- Factors that may influence the BUN level include dietary protein intake,
gastrointestinal bleeding, decreased urinary flow, hepatic function, and increased catabolism as during trauma, sepsis, or febrile illness.
20
Q
- Why does the BUN concentration increase in dehydrated states?
What is the serum creatinine level under these circumstances?
A
- The BUN concentration increases in dehydrated states as a result of the
corresponding decrease in urinary flow through renal tubules. During low urinary
flow rates, a greater fraction of the urea is reabsorbed by the kidney. During
low urinary flow rates the serum creatinine level remains normal, such that the
ratio of serum BUN to creatinine is increased during times of low urinary flow
associated with hypovolemia.
21
Q
- What do BUN concentrations higher than 50 mg/dL almost always indicate?
A
- Blood urea nitrogen concentrations higher than 50 mg/dL are almost always
a reflection of decreased GFR.
22
Q
- What is the source of serum creatinine? How is the serum creatinine level related to the GFR?
A
- Serum creatinine is a product of skeletal muscle protein catabolism. Serum
creatinine levels are dependent on a patient’s total body water, creatinine
generation rate, and creatinine excretion rate. The generation of creatinine is
relatively constant within an individual, making its release into the circulation
relatively constant as well. Serum creatinine levels are believed to be reliable
indicators of the GFR, because its rate of clearance from the circulation is directly
dependent on the GFR.
23
Q
- Why might a normal creatinine level be seen in elderly patients despite a decreased GFR?
A
- Elderly patients may have a normal creatinine level despite a decreased GFR
secondary to the decrease in muscle mass that commonly accompanies aging.
For this reason, even mild increases in the serum creatinine level of elderly patients
may be an indication of significant renal dysfunction
24
Q
- Why might normal serum creatinine levels not accurately reflect the GFR in patients
with chronic renal failure?
A
- Normal serum creatinine levels may not accurately reflect the GFR in patients with chronic renal failure for two reasons. First, patients with chronic renal failure
may have decreased skeletal muscle mass, resulting in a decrease in creatinine
production. Second, the excretion of creatinine occurs via nonrenal means in these patients
25
Q
- What is the creatinine clearance a measurement of?
A
- The creatinine clearance is a measurement of the excretion of creatinine into the
urine after being filtered by the glomerulus. (
26
Q
- Why is the creatinine clearance a more reliable measurement of the GFR than
serum creatinine levels? What is a disadvantage of creatinine clearance
measurements?
A
- The creatinine clearance is a more reliable measurement of GFR than serum
creatinine levels because the clearance does not depend on corrections for age or the
presence of a steady state. A disadvantage of creatinine clearance measurements
is the requirement of accurate, timed urine collections. (
27
Q
- What are some nonrenal causes of proteinuria?
A
- Intermittent proteinuria occurs in healthy individuals after standing for long
periods of time and after strenuous exercise. Proteinuria may also occur during
febrile states and congestive heart failure.
28
Q
- What are the differences in site of action of thiazide, spironolactone, and loop and
osmotic diuretics?
A
- Thiazide diuretics cause diuresis by inhibition of reabsorption of sodium and
chloride ions from the early distal renal tubules. Spironolactone, an aldosterone
antagonist, blocks the renal tubular effects of aldosterone. Spironolactone is a
potassium-sparing diuretic. Loop diuretics inhibit the reabsorption of sodium and
chloride, and augment the secretion of potassium primarily in the loop of Henle.
Osmotic diuretics, such as mannitol, produce diureses by being filtered at the
glomeruli but not reabsorbed by the renal tubules. The excess osmolarity of the renal
tubular fluid leads to excretion of water.
29
Q
- What are the differences in pharmacologic action between dopamine and fenoldopam?
A
- Dopamine dilates renal arterioles by its agonist action at the DA-1 receptor and
causes adrenergic stimulation leading to an increase in renal blood flow and GFR.
Dopamine therapy when used to augment urine output has not been shown to alter
the course of renal failure. Dopamine also potentially leads to tachydysrhythmias,
pulmonary shunting, and tissue ischemia. Fenoldopam is a dopamine analog
which also possesses DA-1 agonist activity, but lacks the adrenergic activity of
dopamine.
30
Q
- What are the systemic changes that frequently accompany end-stage renal disease
(ESRD)?
A
- There are several systemic changes that accompany end-stage renal disease (ESRD).
Cardiovascular disease is the predominant cause of death in patients with ESRD.
Systemic hypertension is very common and can be severe and refractory to therapy.
Acute MI, cardiac arrest/dysfunction and cardiomyopathy account for more than 50% of deaths in patients maintained on dialysis. Diabetes mellitus frequently presents concomitantly with ESRD. Electrolyte abnormalities also occur commonly
as patients develop difficulty excreting their dietary fluid and electrolyte loads.
A normochromic normocytic anemia is frequently present because of decreased erythropoiesis. Uremia-induced platelet dysfunction can lead to clinical coagulopathy.
31
Q
- What are some anesthetic considerations for the anesthetic management of patients
with ESRD?
A
- There are several considerations for the anesthetic management of patients with ESRD. These patients may benefit from extensive monitoring, such as direct arterial
blood pressure monitoring and perhaps central venous pressure monitoring depending on the surgical case, comorbidities, and other factors. Hypotension can commonly occur in patients with ESRD, particularly after hemodialysis.
Patients with arteriovenous fistulas should have the presence of the thrill monitored during positioning and intraoperatively. Patients with gastroparesis should be considered at increased risk for the aspiration of gastric contents. Electrolytes,
especially potassium, should be evaluated preoperatively and intraoperatively if necessary. Finally, drugs or their metabolites that are renally excreted should be administered judiciously or avoided if possible
32
Q
- Should succinylcholine be avoided in patients with ESRD?
A
- Succinylcholine is not contraindicated in patients with ESRD. The increase in serum
potassium after a large dose of succinylcholine is approximately 0.6 mEq/L for
patients both with and without ESRD. This increase can be tolerated without imposing a significant cardiac risk, even in the presence of an initial serum potassium concentration higher than 5 mEq/L
33
Q
- What are some causes of prerenal oliguria?
A
- Prerenal oliguria is indicative of a decrease in renal blood flow, the most common causes of which include a decrease in the intravascular fluid volume and a decrease in the cardiac output. Another cause may be surgical compression of the renal arteries leading to obstructed blood flow to the kidneys, either directly through
clamping or inadvertently through retraction or manual traction. Whatever the cause, the duration of oliguria should be minimized to decrease the risk of acute renal failure.
34
Q
- What is the treatment for prerenal causes of oliguria?
A
- The treatment of prerenal causes of oliguria is dependent on whether the cause is secondary to a decrease in intravascular fluid volume or in cardiac output. A crystalloid fluid bolus would result in a brisk diuresis if in fact the cause was hypovolemia. A lack of response to the fluid bolus would indicate that perhaps the
cause of the oliguria is a decrease in cardiac output or is a result of the secretion of antidiuretic hormone in response to surgical stress. A small dose of furosemide, 0.1 mg/kg intravenously, will lead to diuresis if the cause of the oliguria is antidiuretic hormone secretion. If there is no response to the intravenous administration of furosemide, a determination should be made as to whether the patient remains hypovolemic or there is a decrease in cardiac output. If the patient
is at risk for a decrease in cardiac output, it may be worthwhile to monitor
cardiac filling pressures to guide intravascular fluid replacement. If the cardiac
filling pressures is high, a cause for the decrease in cardiac output should be
sought.
35
Q
- What are some causes of oliguria due to intrinsic renal disease?
A
- Acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis are
intrinsic renal causes of oliguria.
36
Q
- For oliguria that is secondary to renal causes such as acute tubular necrosis, is the urine typically concentrated or dilute? Does the urine typically contain excessive or minimal stores of sodium?
A
- Oliguria due to acute tubular necrosis is characterized by urine that is typically dilute and contains excessive sodium.
37
Q
- What are some causes of postrenal oliguria?
A
- Causes of postrenal oliguria include ureteral obstruction, bladder outlet obstruction, and obstruction or kinking of the Foley catheter. Postrenal causes of oliguria are frequently reversible.
38
Q
- What are some physiologic functions of the liver?
A
- Physiologic functions of the liver include protein synthesis, drug metabolism, fat
metabolism, hormone metabolism, bilirubin formation and excretion, and
glucose homeostasis.
39
Q
- What is the blood supply to the liver? What percent of the cardiac output goes to the
liver?
A
- The liver receives its blood supply via the portal vein (70%) and hepatic artery
(30%). Approximately 25% of the cardiac output goes to the liver. While the portal
vein supplies 70% of hepatic blood supply, it only contributes 50% of the liver’s
oxygen supply. The remaining 50% of the liver’s oxygen supply comes from
the hepatic artery.
40
Q
- What are some determinants of hepatic blood flow?
A
- Total hepatic blood flow is directly proportional to the perfusion pressure across the
liver and is inversely proportional to splanchnic vascular resistance. There are many
determinants of hepatic blood flow. Determinants intrinsic to the liver include
hepatic autoregulation, metabolic control, and the hepatic arterial buffer response.
Determinants extrinsic to the liver include sympathetic nervous system activity,
surgical stimulation, and humoral factors.
41
Q
- What is hepatic autoregulation? How is hepatic autoregulation affected by surgery
and anesthesia?
A
- Hepatic autoregulation refers to the ability of the hepatic artery to alter its resistance
in response to changes in arterial pressure to maintain hepatic artery blood flow.
For example, hepatic artery resistance may decrease to maintain perfusion to
the liver when portal vein flow is reduced. Of note, there does not appear to be
autoregulation of the portal venous system. Instead portal venous blood flow
parallels cardiac output. Surgery and anesthesia impair hepatic autoregulation
and typically result in reduced hepatic perfusion
42
Q
- What is the hepatic arterial buffer response? How is this hepatic response affected by
anesthesia?
A
- The hepatic arterial buffer response refers to the capacity of the liver to increase or
decrease hepatic artery blood flow in response to decreases or increases in portal
venous flow. For example, when portal venous flow decreases, the resistance of
the hepatic artery decreases and hepatic artery blood flow increases. This reciprocal
relationship allows for the hepatic oxygen supply and total hepatic blood flow
to be maintained despite alterations in portal venous flow. This compensatory
mechanism does not completely compensate for changes in portal venous flow,
however. In addition, the hepatic arterial buffer response can be disrupted by several
factors, including neural, humoral, and metabolic changes. This hepatic response
is also disrupted by hepatic cirrhosis and volatile anesthetics.
43
Q
- What results from sympathetic nervous stimulation of the liver?
A
- Innervation of the liver is by both the parasympathetic nervous system and
the sympathetic nervous system. Generalized sympathetic nervous system
stimulation, as can occur with arterial hypoxemia or hypercarbia, pain or surgical
stress, results in an increase in the splanchnic vascular resistance. The increase
in splanchnic vascular resistance yields a decrease in liver blood flow and blood
volume.
44
Q
- How does positive pressure ventilation of the lungs affect hepatic blood flow?
A
- Positive pressure ventilation of the lungs decreases hepatic blood flow through
its increase in hepatic venous pressure. Hepatic blood flow is decreased further
by the application of positive end-expiratory pressure through the same
mechanism.
45
Q
- How does congestive heart failure affect hepatic blood flow?
A
- Congestive heart failure, particularly right-sided heart failure, decreases hepatic
blood flow through its increase in hepatic venous pressure.
46
Q
- How do changes in cardiac output or myocardial contractility affect hepatic blood
flow?
A
- Decreases in cardiac output or myocardial contractility result in decreases in hepatic
blood flow
47
Q
- How do changes in arterial blood pressure affect hepatic blood flow?
A
- Decreases in arterial blood pressure result in decreases in hepatic blood flow.
48
Q
- How does the liver store glucose?
A
- The liver stores glucose as glycogen in the hepatocytes.
49
Q
- How does the liver maintain glucose homeostasis in times of starvation?
A
- Glucose homeostasis is maintained during times of starvation by the breakdown
of the glycogen to glucose in the hepatocytes. Glucose is then released into the
circulation. The glycogen stores of the liver correspond to 24 to 48 hours of glucose
supply during times of starvation. Prolonged starvation that results in the
depletion of the glycogen stores requires that the liver convert lactate, glycerol, and
amino acids to glucose. This is termed gluconeogenesis.
50
Q
- Why might patients with cirrhosis be more likely to develop hypoglycemia in the
perioperative period?
A
- Patients with cirrhosis may be more likely to develop hypoglycemia in the
perioperative period as gluconeogenesis may be impaired.
51
Q
- What role does the liver play in blood coagulation? What is the clinical implication
of this for the patient with liver disease?
A
- A normal liver synthesizes most of the proteins responsible for the coagulation of
blood. A diseased liver may therefore manifest as coagulopathy in the patient
52
Q
- How significant must liver dysfunction be before abnormal blood coagulation is
noted? How can this be evaluated preoperatively?
A
- Bleeding can be prevented with only 20% to 30% of normal levels of clotting
factors, so that abnormal blood coagulation manifests only after significant liverdisease. The coagulation status of a patient can be evaluated preoperatively by
checking the patient’s prothrombin time, partial thromboplastin time, and bleeding
time. Indeed, the prothrombin time is frequently used as an evaluation of the
synthetic function of the liver. (
53
Q
- What is the role of vitamin K in coagulation?
A
- Vitamin K plays an important role in the catalysis of some of the procoagulant
proteins to produce factors II, VII, IX, and X
54
Q
- How does the liver facilitate the renal excretion of lipid soluble drugs?
A
- The liver facilitates the renal excretion of lipid soluble drugs by converting
the drugs to more water soluble forms via mechanisms such as conjugation.
55
Q
- How does chronic drug therapy affect the metabolism of anesthetic drugs by the
liver?
A
- Chronic drug therapy can inhibit anesthetic drug metabolism by inhibiting hepatic
enzymes. Conversely, they can also enhance drug metabolism by inducing
hepatic enzymes (particularly cytochrome P isoforms).
56
Q
- How does chronic liver disease impact drug metabolism?
A
- Chronic liver disease may interfere with the metabolism of drugs because of the
decreased number of enzyme-containing hepatocytes or the decreased hepatic
blood flow that typically accompanies cirrhosis of the liver.
57
Q
- Why may hepatic drug metabolism be accelerated after the administration of certain
medications?
A
- Accelerated drug metabolism may be noted after the administration of certain
drugs such as phenytoin. It is believed that exposure of the microsomal
enzymes to these drugs causes an up-regulation, or induction, of their own
synthesis.
58
Q
- What role does the liver play in the excretion of bilirubin? What is the clinical
implication of this for the patient with liver disease?
A
- The conjugation of bilirubin with glucuronic acid takes place in the liver through
the action of glucuronyl transferase. The conjugation of bilirubin allows it to
become water soluble for renal excretion. Impairment of this function of the liver,
as with liver disease, can lead to increased serum levels of unconjugated bilirubin.
The liver is also responsible for the excretion of conjugated bilirubin into bile.
This explains the elevated serum levels of conjugated bilirubin in the presence of
liver disease.
59
Q
- What proteins are synthesized in the hepatocytes?
A
- All proteins are synthesized in hepatocytes except for gamma globulins and factor
VIII
60
Q
- What is the role of the urea cycle in the hepatocytes?
A
- The urea cycle is used by hepatocytes to convert the end products of amino acid
degradation, such as ammonia and other nitrogenous waste products, to urea
which is readily excreted by the kidneys.
61
Q
- What pathophysiologic changes are associated with end-stage liver disease
(ESLD)?
A
- End-stage liver disease (ESLD) is associated with portopulmonary hypertension,
hepatopulmonary syndrome (shunting due to impairment of hypoxic pulmonary
vasoconstriction), atelectasis, pleural effusions, hepatic encephalopathy,
impaired drug binding, coagulopathy, ascites, and renal dysfunction (due to
various factors including the hepatorenal syndrome).
62
Q
- What are the hemodynamic changes associated with ESLD?
A
- Severe liver disease that has advanced to cirrhosis is associated with a
hyperdynamic circulation. Patients typically have normal to low systemic blood
pressure, increased cardiac output and decreased systemic vascular resistance due to
vasodilation and shunting.
63
Q
- What are some consequences of the portal hypertension seen in ESLD?
A
- Portal hypertension, as seen in ESLD, is the high resistance of blood flow through
the liver. This results in an accumulation of blood in the vascular beds that normally
drain to the liver, and these vessels become dilated and hypertrophy. Vessels
draining the esophagus, stomach, spleen, and intestines are affected, resulting in
varices.
64
Q
- What are some of the symptoms of portal hypertension?
A
- Some of the symptoms of portal hypertension include anorexia, nausea, ascites,
esophageal varices, spider nevi, and hepatic encephalopathy
65
Q
- What are some complications that can occur as a result of the portal hypertension
seen in ELSD?
A
- Complications that can occur as a result of the portal hypertension seen in
ELSD include increased susceptibility to infection, renal failure, mental status
changes, and massive hemorrhage through the rupture of the engorged dilated
submucosal veins. Gastroesophageal varices are at the greatest risk of rupture.
66
Q
- What are some pulmonary complications that can be seen in ESLD?
A
- Pulmonary complications that can be seen in ESLD include pulmonary
arteriovenous communications that are not ventilated, the impairment of hypoxic
pulmonary vasoconstriction, atelectasis, and restrictive pulmonary disease due
to ascites and pleural effusions. In less than 5% of patients with ESLD
portopulmonary hypertension develops, whose cause is not well established.
67
Q
- What are some reasons why a patient with hepatic cirrhosis may have arterial
hypoxemia? Does the administration of supplemental oxygen increase the oxygen
saturation in these patients?
A
- Patients with hepatic cirrhosis may have arterial hypoxemia for several
reasons. Often, patients with hepatic cirrhosis have right-to-left pulmonary
shunting in response to the portal vein hypertension. Patients with ascites
and hepatomegaly may also have impairment of diaphragmatic excursion due
to the weight of the abdominal contents, particularly in the supine position.
In patients with significant ascites, pleural effusions may impair lung expansion.
In the early stages of ESLD, supplemental oxygen may improve arterial
hypoxemia, but as the disease progresses oxygen therapy may not be
effective.
68
Q
- What are some causes of hepatic encephalopathy seen in patients with ESLD?
A
- The cause of hepatic encephalopathy seen in patients with ESLD is multifactorial.
Hepatic encephalopathy is in part due to increased serum concentrations of
chemicals normally cleared by the liver, especially ammonia. Other factors include
disruption of the blood–brain barrier, increased central nervous system inhibitory
neurotransmission, and altered cerebral energy metabolism.
69
Q
- What is the therapy for hepatic encephalopathy? Is it effective?
A
- Therapy for hepatic encephalopathy revolves around reducing the production
and absorption of ammonia. Neomycin is used to reduce ammonia production
by urease-producing bacteria and lactulose is administered to reduce ammonia
absorption. Some symptoms of hepatic encephalopathy are reversible with
flumazenil therapy. These therapies are not completely effective because multiple
other etiologic factors are associated with hepatic encephalopathy. It is also
important to rule out other causes of altered mental status in the patient with
ESLD. Other causes may include intracranial bleeding, hypoglycemia, or a postictal
state.
70
Q
- What role does the liver play in drug binding to serum proteins? What is the clinical
implication of this for the patient with liver disease?
A
- The liver synthesizes albumin, which binds drugs in the plasma. The binding of
drugs to albumin decreases the free, or pharmacologically active, portion of the
drug. When the liver is diseased the synthesis of albumin becomes impaired,
decreasing the albumin available in the plasma for binding. As a result there is
an increased concentration of free, unbound drug in the plasma. Patients
with liver disease may manifest a more pronounced drug effect than patients
with normal liver function after an intravenous injection of a specific drug
dose. Increased drug effect secondary to a decrease in protein binding is more
likely to be seen when the serum albumin concentration is less than 2.5 g/dL.
71
Q
- Why is ascites thought to accumulate in patients with hepatic cirrhosis?
A
- Ascites affects 50% of patients with hepatic cirrhosis. Ascites is thought to
accumulate secondary to a decrease in plasma oncotic pressure, a corresponding
increase in the hydrostatic pressure in the hepatic sinusoids, and an increase in
sodium retention by the kidneys due to increased circulating levels of antidiuretic
hormone.
72
Q
- What are some complications associated with ascites?
A
- Complications associated with ascites include marked abdominal distention that
can lead to atelectasis and restrictive pulmonary disease, spontaneous bacterial
peritonitis, and circulatory instability due to compression of the inferior vena cava
and right atrium
73
Q
- What is the treatment for ascites?
A
- The treatment for ascites is initially fluid restriction, reduced sodium intake, and
diuretic therapy. In severe cases abdominal paracentesis temporarily effectively
reduces abdominal distention and restores hemodynamic stability
74
Q
- How might renal function be affected in patients with hepatic cirrhosis?
A
- Patients with hepatic cirrhosis tend to have a decrease in arterial blood volume,
and consequently a decrease in renal blood flow and the GFR. Because of this
patients with hepatic cirrhosisare at risk of developing hepatorenal syndrome, a seriouscomplication that is often fatal. The syndrome is characterized by intravascular
fluid depletion, intrarenal vasoconstriction, worsening hyponatremia, hypotension,
and oliguria. (
75
Q
- What categories of hepatorenal syndrome have been described? Are there any
therapies?
A
- Two types of hepatorenal syndrome have been described. Type 1 hepatorenal
syndrome presents as rapidly progressing prerenal failure. It is associated with
a poor prognosis in the absence of therapeutic intervention. Type 2 hepatorenal
syndrome presents with a milder degree of renal dysfunction. Treatment with
octreotide, glucagon, and midodrine have shown promise at reversing type 1
hepatorenal syndrome.
76
Q
- In the absence of surgical stimulation, how do regional and inhaled anesthetics
affect hepatic blood flow?
A
- In the absence of surgical stimulation, regional and inhaled anesthetics decrease
hepatic blood flow by 20% to 30%. Changes in hepatic blood flow in response to
regional and inhaled anesthetics are believed to result from decreases in cardiac
output, mean arterial pressure, or both. Volatile anesthetics may also decrease
hepatic blood flow by impairing intrinsic hepatic mechanisms to maintain hepatic
blood flow to varying degrees.
77
Q
- Is there any evidence to suggest one inhaled anesthetic preserves hepatic
autoregulation more than others?
A
- There is some evidence to suggest that isoflurane inhibits hepatic autoregulation
less than other inhaled anesthetics. (4
78
Q
- What is halothane hepatitis? Are pediatric patients or adult patients more likely to
develop halothane hepatitis?
A
- There are two different forms of hepatotoxicity that can result from the
administration of halothane. Halothane hepatitis typically refers to the more
severe hepatotoxicity that can result in hepatic necrosis and death. Halothane
hepatitis is extremely rare. Adult patients are more likely to develop halothane
hepatitis than pediatric patients. Patients most likely to be affected are middle-
aged, obese women who have had repeated administration of halothane
anesthesia.
79
Q
- What is the cause of halothane hepatitis?/
A
- Although the exact cause of halothane hepatitis is unclear, it is believed to be due to
an immunologic response to a toxic metabolite of halothane.
80
Q
- How is the diagnosis of halothane hepatitis made?
A
- The diagnosis of halothane hepatitis is made after other causes of hepatitis
have been excluded. Its rare incidence and the disappearance of halothane in
modern clinical practice make the likelihood of halothane hepatitis extremely
unlikely. (
81
Q
- Can volatile anesthetics, other than halothane, cause hepatotoxicity?
A
- The administration of all volatile anesthetics can result in a mild, self-limited form
of hepatotoxicity. It can be seen in up to 20% of patients, but is associated with
minimal sequelae.
82
Q
- What are some commonly ordered liver function tests? What is the utility of liver
function tests in the perioperative period?
A
- Commonly ordered liver function tests include serum bilirubin, aminotransferase
enzymes, alkaline phosphatase, albumin, and the prothrombin time. Liver tests
are very nonspecific, and significant liver dysfunction must occur before it is
reflected in the majority of tests. Despite this, liver function tests have some utility
in the perioperative period. Liver function tests may be useful preoperatively in
detecting the presence of liver disease. Perioperatively, liver dysfunction may be
classified as prehepatic, intrahepatic, or posthepatic through the evaluation of the
results of the various liver function tests
83
Q
- What are some preoperative findings in patients with liver disease that are
associated with increased postoperative morbidity?
A
- Preoperative findings in patients with liver disease that are associated with
increased postoperative morbidity include marked ascites, markedly elevated
prothrombin time and serum bilirubin level, markedly decreased serum albumin
level, and encephalopathy.
84
Q
- What monitoring may be useful intraoperatively for patients with hepatic cirrhosis
undergoing surgical procedures?
A
- Intraoperative monitoring for patients with hepatic cirrhosis should be guided by
the surgical procedure. In general, monitoring of the arterial blood pressure
with an intra-arterial catheter may be useful. This allows for monitoring of the
arterial blood gases, pH, coagulation status, and glucose as well as the blood
pressure. In addition, the urine output should be closely monitored due to the risk of
postoperative renal dysfunction that can occur in patients with severe liver
85
Q
- Why is the intraoperative maintenance of the arterial blood pressure particularly
important in patients with hepatic cirrhosis?
A
- The intraoperative maintenance of the arterial blood pressure is particularly
important in patients with hepatic cirrhosis because these patients are dependent on
hepatic arterial blood flow to provide oxygen to the hepatocytes. In the presence
of portal hypertension, hepatic arterial blood flow is typically reduced from
normal levels. The addition of anesthetics and the surgical procedure can exacerbate
this reduction in hepatic blood flow and may contribute to postoperative liver
dysfunction
86
Q
- When liver function tests become abnormal postoperatively, what is the most
likely mechanism for the postoperative liver dysfunction? In what patients and
types of surgeries are liver function tests most likely to become elevated
postoperatively?
A
- Liver function tests are most likely to become abnormal secondary to an
inadequate supply of oxygen to the hepatocytes intraoperatively. This is the
most likely mechanism for mild, self-limited postoperative liver dysfunction.
Abnormal postoperative liver function tests are most likely to occur in
patients with preexisting liver disease whose hepatic oxygenation was marginal
preoperatively or after surgery in which the operative site was in close proximity
to the liver.
87
Q
- What are the most likely causes of postoperative liver dysfunction?
A
.87. The most likely causes of postoperative liver dysfunction include drugs, arterial
hypoxemia, sepsis, congestive heart failure, cirrhosis, and a history of preexisting
hepatic viruses
88
Q
- What laboratory values indicate an intrahepatic cause of liver dysfunction?
A
- Elevated aminotransferase enzymes, decreased albumin, and a prolonged
prothrombin time are all indicative of an intrahepatic cause of liver
dysfunction. These alterations are reflective of direct hepatocellular damage.
89
Q
- What are some causes of postoperative jaundice?
A
- Operations on the liver or biliary tract, multiple blood transfusions, resorption
of surgical hematoma, antibiotics and other perioperative drugs and metabolic and
infectious causes can all lead to postoperative jaundice. Rarely, inhaled anesthetic
agents may be implicated.
90
Q
- What is delirium tremens? How does it usually present?
A
- Delirium tremens is a severe withdrawal syndrome in patients with a history of
chronic alcohol abuse. The onset of delirium tremens is typically 48 to 72 hours after
cessation of the ingestion of alcohol. Delirium tremens presents clinically as
tremulousness, hallucinations, agitation, confusion, disorientation, and increased
activity of the sympathetic nervous system. Increased activity of the sympathetic
nervous system in these patients is manifest as diaphoresis, fever, tachycardia,
and hypertension. In severe cases the syndrome may progress to seizures and
death.
91
Q
- What is the treatment of delirium tremens?
A
- The treatment of delirium tremens is primarily with the administration of central
nervous system depressants, usually a benzodiazepine. If necessary, a b-adrenergic
antagonist may be administered to offset sympathetic nervous system
hyperactivity. The trachea may be intubated if indicated for airway protection.
Other treatment is supportive as necessary, including hydration and the correction
of electrolyte disorders.
92
Q
- What is the mortality associated with delirium tremens? What is the usual cause of
death in these patients?
A
- The mortality associated with delirium tremens can be as high as 10%. The usual
cause of death in these patients is cardiac dysrhythmias or seizures.
93
Q
- What approximate percent of females and males aged 55 to 65 years are believed to
have gallstones?
A
- Approximately 20% of women and 10% of men aged 55 to 65 years are believed to
have gallstones. Elevated serum bilirubin and/or alkaline phosphatase levels in
these patients imply the presence of a stone in the common bile duct causing
obstruction to the flow of bile.
94
Q
What is the potential problem with the use of opioids intraoperatively during a
cholecystectomy or common bile duct exploration?
A
- Opioids such as morphine, meperidine, and fentanyl may produce spasm in the
sphincter of Oddi. This increases the pressure in the common bile duct in a
dose-dependent manner and may be painful to an awake patient. The
administration of these medicines intraoperatively could hinder the passage of
contrast medium for exploration of the common bile duct. In clinical practice,
however, the administration of opioids to these patients rarely results in difficulty
with intraoperative cholangiograms. (460
95
Q
- How can intraoperative spasm of the sphincter of Oddi be treated?
A
- Intraoperative spasm of the sphincter of Oddi can be treated with naloxone,
glucagons, or nitroglycerin.
96
Q
- What are some anesthetic considerations for patients undergoing laparoscopic
procedures?
A
- Anesthetic considerations for patients undergoing laparoscopic procedures are
multiple. Included are the insufflation of the abdomen with carbon dioxide and the
possible impairment of ventilation of the lungs in the presence of increased
ventilatory requirements, the probable placement of the patient in the
Trendelenburg position, the risk of puncture of bowel or vessels, and the potential
for nitrous oxide to expand bowel gas.
