Chapter 25 Renal, Liver, and Biliary Tract Disease
Renal disease
1. What are some essential physiologic functions of the kidneys?
2. Name some factors that place patients at an increased risk of acute renal failure in the perioperative period.
3. What percent of the cardiac output normally goes to the kidneys? What fraction of this goes to the renal cortex?
4. 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?
5. Even during normal kidney autoregulatory function, what two factors can alter renal blood flow?
6. What is renin? What is the secretion of renin usually in response to? What effect does renin have on renal blood flow?
7. What is the physiologic effect of the secretion of renin?
8. What triggers the release of prostaglandins that are produced by the renal medulla? What is the effect of prostaglandins released by the renal medulla?
9. What is the renal effect of arginine vasopressin released by the hypothalamus?
10. What is glomerular filtration? What is glomerular filtration dependent on?
11. What is the normal hydrostatic pressure of the glomerular capillaries? What is the normal plasma oncotic pressure in the afferent and efferent arterioles?
12. What is the average normal rate of glomerular filtration?
13. About what percent of the fluid shift from glomerular filtration is reabsorbed from renal tubules and ultimately returned to the circulation?
14. How is the GFR influenced by the renal blood flow?
15. What are the three mechanisms upon which the renal clearance of drugs depends?
16. Name some tests used for the evaluation of renal function. How sensitive are tests of renal function?
17. What degree of renal disease can exist before renal function tests begin to indicate possible decreases in renal function?
18. What is the normal level of blood urea nitrogen (BUN)?
19. What factors may influence the BUN level?
20. Why does the BUN concentration increase in dehydrated states? What is the serum creatinine level under these circumstances?
21. What do BUN concentrations higher than 50 mg/dL almost always indicate?
22. What is the source of serum creatinine? How is the serum creatinine level related to the GFR?
23. Why might a normal creatinine level be seen in elderly patients despite a decreased GFR?
24. Why might normal serum creatinine levels not accurately reflect the GFR in patients with chronic renal failure?
25. What is the creatinine clearance a measurement of?
26. Why is the creatinine clearance a more reliable measurement of the GFR than serum creatinine levels? What is a disadvantage of creatinine clearance measurements?
27. What are some nonrenal causes of proteinuria?
28. What are the differences in site of action of thiazide, spironolactone, and loop and osmotic diuretics?
29. What are the differences in pharmacologic action between dopamine and fenoldopam?
30. What are the systemic changes that frequently accompany end-stage renal disease (ESRD)?
31. What are some anesthetic considerations for the anesthetic management of patients with ESRD?
32. Should succinylcholine be avoided in patients with ESRD?
33. What are some causes of prerenal oliguria?
34. What is the treatment for prerenal causes of oliguria?
35. What are some causes of oliguria due to intrinsic renal disease?
36. 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?
Liver and biliary tract disease
38. What are some physiologic functions of the liver?
39. What is the blood supply to the liver? What percent of the cardiac output goes to the liver?
40. What are some determinants of hepatic blood flow?
41. What is hepatic autoregulation? How is hepatic autoregulation affected by surgery and anesthesia?
42. What is the hepatic arterial buffer response? How is this hepatic response affected by anesthesia?
43. What results from sympathetic nervous stimulation of the liver?
44. How does positive pressure ventilation of the lungs affect hepatic blood flow?
45. How does congestive heart failure affect hepatic blood flow?
46. How do changes in cardiac output or myocardial contractility affect hepatic blood flow?
47. How do changes in arterial blood pressure affect hepatic blood flow?
48. How does the liver store glucose?
49. How does the liver maintain glucose homeostasis in times of starvation?
50. Why might patients with cirrhosis be more likely to develop hypoglycemia in the perioperative period?
51. What role does the liver play in blood coagulation? What is the clinical implication of this for the patient with liver disease?
52. How significant must liver dysfunction be before abnormal blood coagulation is noted? How can this be evaluated preoperatively?
53. What is the role of vitamin K in coagulation?
54. How does the liver facilitate the renal excretion of lipid soluble drugs?
55. How does chronic drug therapy affect the metabolism of anesthetic drugs by the liver?
56. How does chronic liver disease impact drug metabolism?
57. Why may hepatic drug metabolism be accelerated after the administration of certain medications?
58. What role does the liver play in the excretion of bilirubin? What is the clinical implication of this for the patient with liver disease?
59. What proteins are synthesized in the hepatocytes?
60. What is the role of the urea cycle in the hepatocytes?
61. What pathophysiologic changes are associated with end-stage liver disease (ESLD)?
62. What are the hemodynamic changes associated with ESLD?
63. What are some consequences of the portal hypertension seen in ESLD?
64. What are some of the symptoms of portal hypertension?
65. What are some complications that can occur as a result of the portal hypertension seen in ELSD?
66. What are some pulmonary complications that can be seen in ESLD?
67. 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?
68. What are some causes of hepatic encephalopathy seen in patients with ESLD?
69. What is the therapy for hepatic encephalopathy? Is it effective?
70. 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?
71. Why is ascites thought to accumulate in patients with hepatic cirrhosis?
72. What are some complications associated with ascites?
73. What is the treatment for ascites?
74. How might renal function be affected in patients with hepatic cirrhosis?
75. What categories of hepatorenal syndrome have been described? Are there any therapies?
76. In the absence of surgical stimulation, how do regional and inhaled anesthetics affect hepatic blood flow?
77. Is there any evidence to suggest one inhaled anesthetic preserves hepatic autoregulation more than others?
78. What is halothane hepatitis? Are pediatric patients or adult patients more likely to develop halothane hepatitis?
79. What is the cause of halothane hepatitis?
80. How is the diagnosis of halothane hepatitis made?
81. Can volatile anesthetics, other than halothane, cause hepatotoxicity?
82. What are some commonly ordered liver function tests? What is the utility of liver function tests in the perioperative period?
83. What are some preoperative findings in patients with liver disease that are associated with increased postoperative morbidity?
84. What monitoring may be useful intraoperatively for patients with hepatic cirrhosis undergoing surgical procedures?
85. Why is the intraoperative maintenance of the arterial blood pressure particularly important in patients with hepatic cirrhosis?
86. 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?
87. What are the most likely causes of postoperative liver dysfunction?
88. What laboratory values indicate an intrahepatic cause of liver dysfunction?
89. What are some causes of postoperative jaundice?
90. What is delirium tremens? How does it usually present?
91. What is the treatment of delirium tremens?
92. What is the mortality associated with delirium tremens? What is the usual cause of death in these patients?
93. What approximate percent of females and males aged 55 to 65 years are believed to have gallstones?
94. What is the potential problem with the use of opioids intraoperatively during a cholecystectomy or common bile duct exploration?
95. How can intraoperative spasm of the sphincter of Oddi be treated?
96. What are some anesthetic considerations for patients undergoing laparoscopic procedures?
Answers*
Renal disease
1. 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. (448)
2. 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. (449, Table 28-1)
3. 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. (448)
4. 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. (448)
5. Even during normal kidney autoregulatory function, renal blood flow can be altered by sympathetic nervous system activity and by circulating renin. (448)
6. 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. (449)
7. 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. (449)
8. 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, norepinephrine, and the renin-angiotensin system on the kidney by maintaining cortical blood flow. Drugs that inhibit prostaglandins, such as nonsteroidal antiinflammatory agents and aspirin, may impair this protective effect of prostaglandins. (449)
9. 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. (450)
10. 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. (449-450)
11. 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. (449)
12. The average normal rate of glomerular filtration is 125 mL/min. (449)
13. 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. (449)
14. The GFR is decreased during times of decreased renal blood flow or decreased mean arterial blood pressure. (449)
15. 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. (450)
16. 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 sensitive. (450-451)
17. 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. (450-451)
18. 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. (450-452)
19. 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. (451)
20. 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. (451)
21. Blood urea nitrogen concentrations higher than 50 mg/dL are almost always a reflection of decreased GFR. (451)
22. 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. (451)
23. 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. (451)
24. 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. (451)
25. The creatinine clearance is a measurement of the excretion of creatinine into the urine after being filtered by the glomerulus. (451-452)
26. 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. (451-452)
27. 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. (452)
28. 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. (452)
29. 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. (453)
30. 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. (453)
31. 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. (453-454)
32. 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. (454)
33. 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. (454, Table 28–6)
34. 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. (454-455)
35. Acute tubular necrosis, glomerulonephritis, and acute interstitial nephritis are intrinsic renal causes of oliguria. (454, 455, Table 28-6)
36. Oliguria due to acute tubular necrosis is characterized by urine that is typically dilute and contains excessive sodium. (454, 455, Table 28-6)
37. 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. (455)
Liver and biliary tract disease
38. Physiologic functions of the liver include protein synthesis, drug metabolism, fat metabolism, hormone metabolism, bilirubin formation and excretion, and glucose homeostasis. (455)
39. 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. (455)
40. 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. (455)
41. 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. (455)
42. 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. (455)
43. 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. (455)
44. 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. (455)
45. Congestive heart failure, particularly right-sided heart failure, decreases hepatic blood flow through its increase in hepatic venous pressure. (455)
46. Decreases in cardiac output or myocardial contractility result in decreases in hepatic blood flow. (455)
47. Decreases in arterial blood pressure result in decreases in hepatic blood flow. (455)
48. The liver stores glucose as glycogen in the hepatocytes. (456)
49. 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. (456)
50. Patients with cirrhosis may be more likely to develop hypoglycemia in the perioperative period as gluconeogenesis may be impaired. (456)
51. 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. (456)
52. Bleeding can be prevented with only 20% to 30% of normal levels of clotting factors, so that abnormal blood coagulation manifests only after significant liver disease. 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. (456)
53. Vitamin K plays an important role in the catalysis of some of the procoagulant proteins to produce factors II, VII, IX, and X. (456)
54. The liver facilitates the renal excretion of lipid soluble drugs by converting the drugs to more water soluble forms via mechanisms such as conjugation. (456)
55. 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). (456)
56. 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. (456)
57. 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. (456)
58. 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. (456)
59. All proteins are synthesized in hepatocytes except for gamma globulins and factor VIII. (456)
60. 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. (456)
61. 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). (457)
62. 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. (457)
63. 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. (457)
64. Some of the symptoms of portal hypertension include anorexia, nausea, ascites, esophageal varices, spider nevi, and hepatic encephalopathy. (457)
65. 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. (457)
66. 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. (457)
67. 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. (457)
68. 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. (457)
69. 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. (457)
70. 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. (456-457)
71. 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. (457)
72. 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. (457)
73. 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. (457)
74. 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 cirrhosis are at risk of developing hepatorenal syndrome, a serious complication that is often fatal. The syndrome is characterized by intravascular fluid depletion, intrarenal vasoconstriction, worsening hyponatremia, hypotension, and oliguria. (457-458)
75. 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. (457-458)
76. 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. (458)
77. There is some evidence to suggest that isoflurane inhibits hepatic autoregulation less than other inhaled anesthetics. (458)
78. 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. (458)
79. 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. (458)
80. 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. (458)
81. 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. (458)
82. 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. (458-459, Table 28-7)
83. 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. (459, Table 28–8)
84. 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 disease. Central venous pressure or pulmonary artery catheter monitoring might be useful in the fluid management of patients with cardiomyopathy and congestive heart failure. The intravascular fluid balance of patients with liver disease and especially ascites can be difficult to manage. Finally, the use of an intraoperative transesophageal echocardiogram may be useful to monitor myocardial function and intravascular fluid status, but in patients with esophageal varices there exists a risk of bleeding with its insertion. (458-459)
85. 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. (459)
86. 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. (458)
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. (457-58)
88. 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. (460, Table 28-9)
89. 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. (459-460, Table 28-9)
90. 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. (460)
91. The treatment of delirium tremens is primarily with the administration of central nervous system depressants, usually a benzodiazepine. If necessary, a β-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. (460)
92. 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. (460)
93. 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. (460)
94. 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. Intraoperative spasm of the sphincter of Oddi can be treated with naloxone, glucagons, or nitroglycerin. (461)
96. 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. (460-461)
