CHAPTER 43 Perioperative Hepatic Dysfunction Matthew J. Fiegel, MD 1 What is the normal physiologic function of the liver? The human liver consists of four anatomic lobes (left, right, caudate, quadrate) and eight surgical lobes (I–VIII). The liver receives approximately 20% to 25% of the cardiac output and contains 10% to 15% of the total blood volume. The portal vein supplies 75% of the blood flow of the liver and 50% of its oxygen requirements. Almost all plasma proteins are synthesized in the liver. These include albumin, α1-acid glycoprotein, pseudocholinesterase, and all coagulation factors except factors III, IV, and VIII. The liver is also involved in carbohydrate, lipid, and cholesterol metabolism and bile synthesis. The liver produces 20% of the body’s heme. The liver possesses an immune function in that hepatic Kupffer cells filter splanchnic venous blood of bacteria. Last, the liver serves as the main organ of drug metabolism and detoxification. Through three hepatic reactions (phases I, II, and III), drugs are metabolized to a more water-soluble form and excreted in the urine or bile. Phase I reactions use the cytochrome P-450 family of proteins and consist of oxidation, reduction, or hydrolysis. Phase II reactions undergo conjugation with substances such as glucuronic acid and amino acids. In phase III reactions, endogenous hepatic proteins use adenosine triphosphate to excrete various substances. Within the liver, nitrogen-containing compounds are degraded to urea. 2 What is the most common cause of acute parenchymal liver disease? Viral infection is responsible for the majority of cases of acute hepatitis. Traditionally hepatitis B (HBV) was the most common form of acute viral hepatitis. However, with the advent of the HBV vaccine, hepatitis A and C are accounting for a larger percent of cases worldwide. Epstein-Barr virus and cytomegalovirus also cause acute hepatitis. Nonviral causes include drugs and toxins. Drug-induced liver injury (DILI) can mimic acute viral hepatitis and is most commonly caused by alcohol, antibiotics, and nonsteroidal anti-inflammatory drugs. DILI causing an elevation in bilirubin carries a 10% mortality rate. 3 What is cirrhosis? Cirrhosis, the most serious sequelae of chronic hepatitis, is characterized by diffuse death of liver cells, causing fibrous tissue formation and nodular regeneration of hepatic tissue. The consequent distortion of the hepatic circulation further propagates cellular damage and results in a progressive reduction of liver cells, which eventually manifests as impairment of liver function. Hepatic synthetic failure, indicated by a prolonged prothrombin time (PT)/international normalized ratio (INR), decrease in serum albumin levels, and impairment of detoxification mechanisms resulting in encephalopathy, is often termed end-stage liver disease (ESLD). 4 Describe the neurologic derangements in patients with cirrhosis Central nervous system dysfunction presents as hepatic encephalopathy, ranging from confusion to coma, and may be secondary to increased dietary protein consumption or gastrointestinal (GI) bleeding. Increased ammonia levels do not correlate with the degree of encephalopathy. Treatment consists of a low protein diet, lactulose, and rifaximin. Acute fulminating liver failure may present with cerebral edema and increased intracranial pressure. 5 What pulmonary changes occur in a patient with cirrhosis? Arterial hypoxemia with compensatory hyperventilation may be secondary to atelectasis from ascites/hydrothorax or hepatopulmonary syndrome (HPS). HPS is caused by intrapulmonary arteriovenous (AV) shunting. Portal hypertension and neovascularization are responsible for these AV shunts. The clinical features of HPS include platypnea (shortness of breath while standing) and orthodeoxia (decreased saturation when upright). They are indicative of the ventilation/perfusion mismatching. Portal pulmonary hypertension (PPH), defined as a mean pulmonary artery pressure greater than 25 mm Hg, is seen in 2% to 4% of patients with cirrhosis. Its etiology is unclear. Severe PPH is a contraindication to liver transplantation. 6 Describe the changes in the cardiovascular system in patients with cirrhosis As liver disease progresses, most patients develop a hyperdynamic circulatory state, characterized by a fall in total peripheral resistance and a compensatory rise in cardiac output. The circulating plasma volume increases in response to vasodilation, and peripheral blood flow is enhanced. Although total body volume is increased, cirrhotic patients possess decreased effective arterial blood volume. The AV oxygen gradient narrows as a result of increased peripheral shunting. Consequently the mixed venous oxygen saturation of blood is higher than normal. The response to vasopressors is decreased with cirrhosis. 7 What is hepatorenal syndrome? How does it differ from acute renal failure in patients with end-stage liver disease? Both types of renal failure occur in patients with cirrhosis and are characterized by oliguria and increases in serum creatinine. The etiology in both cases is renal hypoperfusion. Differentiation is important because treatment and prognosis vary. Hepatorenal syndrome (HRS) occurs in cirrhotic patients with portal hypertension and ascites. HRS is defined as a plasma creatinine of >1.5 mg/dl and a urine sodium <10 mmol/L in the absence of other renal disease. The etiology is thought to be renal hypoperfusion resulting from a decrease in vasodilating prostaglandins and profound splanchnic sequestration of blood. HRS exists in two forms, types I and II. Type I progresses rapidly and requires immediate dialysis and liver transplantation. Type II HRS is less severe and responsive to conservative treatments, including terlipressin and a Transhepatic Intraportal Portosystemic Shunt procedure. Acute renal failure (ARF) is caused by decreased blood flow to the kidneys. It may be the result of hemorrhage (e.g., ruptured varices), splanchnic sequestration of blood, ascites formation, or dehydration. Restoring arterial blood volume typically corrects ARF, but it can progress to acute tubular necrosis. In acute tubular necrosis, the ability to retain sodium is lost. Urine analysis will show sodium of 50 to 70 mmol/L and frequent tubular casts. 8 Describe volume assessment and fluid management in patients with hepatorenal syndrome Optimization of renal blood flow by correction of hypovolemia may prevent further renal injury during surgery in these patients. Volume assessment may be difficult since central venous pressures are often elevated despite relative hypovolemia from increased back pressure in the inferior vena cava from hepatic enlargement or scarring. A trial of volume expansion should be undertaken as the initial treatment of oliguria. Although immediate improvement occurs in more than one third of patients treated, HRS leads to progressive renal failure unless hepatic function improves. 9 What are the gastrointestinal and hematologic derangements that occur with cirrhosis? GIl complications result from portal hypertension (>10 mm Hg). Portal hypertension leads to the development of portosystemic venous collaterals, including esophagogastric varices. Ruptured varices with hemorrhage account for one third of the mortality in patients with cirrhosis. Hematologic disorders include anemia, thrombocytopenia and coagulopathy. Anemia is secondary to GI bleeding, malnutrition, and bone marrow suppression. Thrombocytopenia is caused by splenic sequestration, bone marrow depression, and immune-mediated destruction. Coagulopathy is caused by decreased synthesis of clotting factors, accelerated fibrinolysis, and disseminated intravascular coagulation. 10 Which liver function tests are used to detect hepatic cell damage? Only gold members can continue reading. 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CHAPTER 43 Perioperative Hepatic Dysfunction Matthew J. Fiegel, MD 1 What is the normal physiologic function of the liver? The human liver consists of four anatomic lobes (left, right, caudate, quadrate) and eight surgical lobes (I–VIII). The liver receives approximately 20% to 25% of the cardiac output and contains 10% to 15% of the total blood volume. The portal vein supplies 75% of the blood flow of the liver and 50% of its oxygen requirements. Almost all plasma proteins are synthesized in the liver. These include albumin, α1-acid glycoprotein, pseudocholinesterase, and all coagulation factors except factors III, IV, and VIII. The liver is also involved in carbohydrate, lipid, and cholesterol metabolism and bile synthesis. The liver produces 20% of the body’s heme. The liver possesses an immune function in that hepatic Kupffer cells filter splanchnic venous blood of bacteria. Last, the liver serves as the main organ of drug metabolism and detoxification. Through three hepatic reactions (phases I, II, and III), drugs are metabolized to a more water-soluble form and excreted in the urine or bile. Phase I reactions use the cytochrome P-450 family of proteins and consist of oxidation, reduction, or hydrolysis. Phase II reactions undergo conjugation with substances such as glucuronic acid and amino acids. In phase III reactions, endogenous hepatic proteins use adenosine triphosphate to excrete various substances. Within the liver, nitrogen-containing compounds are degraded to urea. 2 What is the most common cause of acute parenchymal liver disease? Viral infection is responsible for the majority of cases of acute hepatitis. Traditionally hepatitis B (HBV) was the most common form of acute viral hepatitis. However, with the advent of the HBV vaccine, hepatitis A and C are accounting for a larger percent of cases worldwide. Epstein-Barr virus and cytomegalovirus also cause acute hepatitis. Nonviral causes include drugs and toxins. Drug-induced liver injury (DILI) can mimic acute viral hepatitis and is most commonly caused by alcohol, antibiotics, and nonsteroidal anti-inflammatory drugs. DILI causing an elevation in bilirubin carries a 10% mortality rate. 3 What is cirrhosis? Cirrhosis, the most serious sequelae of chronic hepatitis, is characterized by diffuse death of liver cells, causing fibrous tissue formation and nodular regeneration of hepatic tissue. The consequent distortion of the hepatic circulation further propagates cellular damage and results in a progressive reduction of liver cells, which eventually manifests as impairment of liver function. Hepatic synthetic failure, indicated by a prolonged prothrombin time (PT)/international normalized ratio (INR), decrease in serum albumin levels, and impairment of detoxification mechanisms resulting in encephalopathy, is often termed end-stage liver disease (ESLD). 4 Describe the neurologic derangements in patients with cirrhosis Central nervous system dysfunction presents as hepatic encephalopathy, ranging from confusion to coma, and may be secondary to increased dietary protein consumption or gastrointestinal (GI) bleeding. Increased ammonia levels do not correlate with the degree of encephalopathy. Treatment consists of a low protein diet, lactulose, and rifaximin. Acute fulminating liver failure may present with cerebral edema and increased intracranial pressure. 5 What pulmonary changes occur in a patient with cirrhosis? Arterial hypoxemia with compensatory hyperventilation may be secondary to atelectasis from ascites/hydrothorax or hepatopulmonary syndrome (HPS). HPS is caused by intrapulmonary arteriovenous (AV) shunting. Portal hypertension and neovascularization are responsible for these AV shunts. The clinical features of HPS include platypnea (shortness of breath while standing) and orthodeoxia (decreased saturation when upright). They are indicative of the ventilation/perfusion mismatching. Portal pulmonary hypertension (PPH), defined as a mean pulmonary artery pressure greater than 25 mm Hg, is seen in 2% to 4% of patients with cirrhosis. Its etiology is unclear. Severe PPH is a contraindication to liver transplantation. 6 Describe the changes in the cardiovascular system in patients with cirrhosis As liver disease progresses, most patients develop a hyperdynamic circulatory state, characterized by a fall in total peripheral resistance and a compensatory rise in cardiac output. The circulating plasma volume increases in response to vasodilation, and peripheral blood flow is enhanced. Although total body volume is increased, cirrhotic patients possess decreased effective arterial blood volume. The AV oxygen gradient narrows as a result of increased peripheral shunting. Consequently the mixed venous oxygen saturation of blood is higher than normal. The response to vasopressors is decreased with cirrhosis. 7 What is hepatorenal syndrome? How does it differ from acute renal failure in patients with end-stage liver disease? Both types of renal failure occur in patients with cirrhosis and are characterized by oliguria and increases in serum creatinine. The etiology in both cases is renal hypoperfusion. Differentiation is important because treatment and prognosis vary. Hepatorenal syndrome (HRS) occurs in cirrhotic patients with portal hypertension and ascites. HRS is defined as a plasma creatinine of >1.5 mg/dl and a urine sodium <10 mmol/L in the absence of other renal disease. The etiology is thought to be renal hypoperfusion resulting from a decrease in vasodilating prostaglandins and profound splanchnic sequestration of blood. HRS exists in two forms, types I and II. Type I progresses rapidly and requires immediate dialysis and liver transplantation. Type II HRS is less severe and responsive to conservative treatments, including terlipressin and a Transhepatic Intraportal Portosystemic Shunt procedure. Acute renal failure (ARF) is caused by decreased blood flow to the kidneys. It may be the result of hemorrhage (e.g., ruptured varices), splanchnic sequestration of blood, ascites formation, or dehydration. Restoring arterial blood volume typically corrects ARF, but it can progress to acute tubular necrosis. In acute tubular necrosis, the ability to retain sodium is lost. Urine analysis will show sodium of 50 to 70 mmol/L and frequent tubular casts. 8 Describe volume assessment and fluid management in patients with hepatorenal syndrome Optimization of renal blood flow by correction of hypovolemia may prevent further renal injury during surgery in these patients. Volume assessment may be difficult since central venous pressures are often elevated despite relative hypovolemia from increased back pressure in the inferior vena cava from hepatic enlargement or scarring. A trial of volume expansion should be undertaken as the initial treatment of oliguria. Although immediate improvement occurs in more than one third of patients treated, HRS leads to progressive renal failure unless hepatic function improves. 9 What are the gastrointestinal and hematologic derangements that occur with cirrhosis? GIl complications result from portal hypertension (>10 mm Hg). Portal hypertension leads to the development of portosystemic venous collaterals, including esophagogastric varices. Ruptured varices with hemorrhage account for one third of the mortality in patients with cirrhosis. Hematologic disorders include anemia, thrombocytopenia and coagulopathy. Anemia is secondary to GI bleeding, malnutrition, and bone marrow suppression. Thrombocytopenia is caused by splenic sequestration, bone marrow depression, and immune-mediated destruction. Coagulopathy is caused by decreased synthesis of clotting factors, accelerated fibrinolysis, and disseminated intravascular coagulation. 10 Which liver function tests are used to detect hepatic cell damage? Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: 11: Opioids 19: Anesthesia Circuits and Ventilators 71: Lung Isolation Techniques 14: Local Anesthetics 24: Capnography 66: Epidural Analgesia and Anesthesia Tags: Anesthesia Secrets May 31, 2016 | Posted by admin in ANESTHESIA | Comments Off on 43: Perioperative Hepatic Dysfunction Full access? Get Clinical Tree
