Anesthesia for Liver Disease

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Anesthesia for the Patient with Liver Disease:

Anesthesia for the Patient with Liver Disease University of New England School of Nurse Anesthesia


Hepatitis Acute and Chronic Viral- Type A, B, C, D, E Chronic may follow acute viral hepatitis Hepatic disease following EBV, CMV Drug or toxin induced


Viral All are similar Infections range from asymptomatic to jaundiced or flu like symptoms Types determined by serologic testing May require liver bx


Symptoms Dark urine Nausea Fatigue Anorexia Abdominal discomfort Fever Emesis Pruritis Light colored stool

Drug Induced Hepatitis:

Drug Induced Hepatitis Can be due to drug reactions from: analgesics anticonvulsants volatile anesthetics antibiotics antihypertensives tranquilizers

Acetaminophen Overdose:

Acetaminophen Overdose Causes profound hepatocellular necrosis Hepatic glutathione typically conjugates toxic metabolites High doses of acetaminophen deplete stores of hepatic glutathione and toxicity increases and destroys liver cells N acetylcysteine may decrease the toxicity ETOH may decrease hepatic glutathione and cause toxicity with standard doses

Volatile Anesthetics:

Volatile Anesthetics May produce mild postop liver dysfunction Caused by anesthetic induced decrease in hepatic oxygen delivery relative to demand Any anesthetic that decreases hepatic flow may interfere with hepatic oxygenation α-glutathione S- tranferase (α-GST) , a sensitive marker of hepatocellular damage Levels increase transiently after volatile anesthetics

Immune-Mediated Hepatoxicity Associated with Volatile Anesthetics:

Immune-Mediated Hepatoxicity Associated with Volatile Anesthetics Rare, life threatening hepatic dysfunction following volatile anesthetic-esp. halothane Thought to be auto-immune response in genetically susceptible patients Patients with this syndrome have elevated IgG antibodies Trifluoroacetyl halide metabolite of halothane effect microsomal proteins on surface of hepatocytes A highly specific anti- trifluoroacetyl antibody test confirms diagnosis as they do not appear in other liver disease 1:10,000 to 1:30,000 adults having had halothane

Volatile Agents:

Volatile Agents Ethrane, isoflurane, and desflurane may form trifluoroacetyl metabolites Degree of metabolism is much less, therefore much less likely to occur A patient with genetic predisposition could be sensitized by halothane, then have hepatic dysfunction following a different volatile agent Sevo does not undergo trifluoroacetyl metabolism

Chronic Hepatitis:

Chronic Hepatitis Encompasses a group of diseases Long term elevation of liver chemistries (greater than 6 months) Evidence of hepatocellular inflammation with liver bx Autoimmune hepatitis, HBV with or without HDV, HCV, drug induced hepatitis, Wilsons disease,α1 antitrypsin defiency, or primary biliary cirrhosis, or primary sclerosing cholangits

Signs and Symptoms:

Signs and Symptoms Range from mild increase in aminotransferace to rapid progression to fulminant hepatic failure Most common symptoms are fatigue, malaise, mild abdominal pain May have arthralgia, arthritis , glomerulonephritis , rash, amenorrhea, thyroiditis


Labs Increased liver enzymes May or may not have elevated bilirubin levels Viral hepatitis causes increase gamma globulin levels Decreased serum albumin Prolonged prothrombin times Hepatomegaly with/without splenomegaly


Cirrhosis Typically the result of chronic etoh or chronic HBV, HCV Scarring of the liver causes regenerating nodules to form Liver bx establishes definitive dx Bx in pts on if INR is no more than 1.5 and PT no longer than 10 secs over normal, plts higher than 50,000 UGI endoscopy confirms varices

Signs and Symptoms:

Signs and Symptoms Fatigue and malaise Palmer erythema Spider nevi Gynecomastia Testicular atrophy Evidence of portal htn

Portal HTN:

Portal HTN Fibrotic changes increase resistance to hepatic flow through the portal vein Liver is enlarged with left lobe palpable below xyphoid process Decreased serum albumin and prolonged PT are typical Increased liver enzymes (alkPtase,aminotransferases)

Complications of Liver Cirrhosis:

Complications of Liver Cirrhosis Portal vein htn Varices Ascites Hyperdynamic circulation Cardiomyopathy Anemia coagulopathy

Complications of Cirrhosis:

Complications of Cirrhosis Arterial hypoxemia Hepatorenal syndrome Hypoglycemia Duodenal ulcer Gallstones Spontaneous bacterial peritonitis Hepatic encephalopathy Primary hepatocellular carcinoma

Anesthesia Management:

Anesthesia Management Consider the trauma patient and the relationship to alcohol (1/2 of all traumas are related to ETOH consumption) ETOH abusers have increased likely hood of ascites, sepsis, COPD Increased morbidity and mortality with surgery in this population

Preoperative Preparation:

Preoperative Preparation

Morbidity /Mortality:

Morbidity /Mortality Identify and manage comorbidities Cardiorespiratory function,coagulation status,renal function,fluids and electrolytes,nutrition Vit K for prolonged PT (severe hepatocellar disease if Vit K does not improve PT) Thrombocytopenia, administer platelets Hypoglycemia, give perioperative glucose soln Preop diuresis indicates adequate hydration

Chronic ETOH Ingestion:

Chronic ETOH Ingestion Increased requirement of inhaled anesthetics Increased requirement for induction agents Presence of cardiomyopathy may make them sensitive to cardiodepressant effects Decreased response to catecholamines Decreased protein binding increases free fraction Jaundiced patients may develop acute renal failure, sepsis. Suggest Mannitol, antibiotics preop.

Intraoperative Management:

Intraoperative Management No secret formula for anesthetic plan Remember decreased hepatic flow secondary to inhaled agents, liver manipulation Limit doses of inhaled anesthetics , combine with N 2 O, opiods to avoid decrease MAP Cumulative drug effects slow metabolism Likely to have postop liver dysfunction increased despite agents used Regional anesthetics when possible

Muscle Relaxants:

Muscle Relaxants Consider role of liver in clearance of the particular relaxant Succinylcholine, acceptable but may be prolonged due to decreased level of plasma cholinesterases Increase volume of distribution may require bigger dose of nondepolarizing agent, this may prolong block if dependant on hepatic clearance

Nondepolarizing Agents:

Nondepolarizing Agents Atracurium, cisatracurium , T½β not altered Vecuronium, T½β not unfluenced until dose exceeds .1mg/kg Short to intermediate acting relaxants are the drugs of choice


Monitoring ABG, PH, urine output Give exogenous glucose Hypoxemia may occur due to vasodilation of portal system and intrapulmonary shunting Administration of glucose and glucose monitoring Consider citrate levels in stored blood with the diseased liver’s diminished clearance of citrate


Monitoring Consider PA catheter, CVP Maintain UO to decrease likelyhood of post op renal failure. ( Mannitol may be necessary) Avoid esophogeal instrumentation with patients with varices

Post op Management:

Post op Management Expect postop liver dysfunction in patients with liver disease Cholestasis may cause jaundice Sepsis is more prevelant with liver dysfunction Consider etoh withdrawl, (48-72 hrs after cessation)

Sober Alcoholic Patients:

Sober Alcoholic Patients Consider effects of cirrhosis, chronic liver disease Postop morbidity, mortality is increased

Intoxicated Alcoholic Patients:

Intoxicated Alcoholic Patients Requires less anesthetic Less able to manage stress or blood loss Decreases brain tolerance to hypoxia More prone to regurgitation of stomach contents (slows gastric emptying, diminishes sphincter tone) Alters platelet function Increases plasma catecholamines may lead to arrythmias

Acute Liver Failure:

Acute Liver Failure Altered mental state Impaired coagulation Fulminant liver failure is present when hepatic encephalopathy occurs within 8 wks of clinical illness. Most often acute liver failure is secondary to viral hepatitis or drug induced liver injury

Signs and Symptoms:

Signs and Symptoms Malaise, nausea is a previously healthy person Development of jaundice Rapid alteration of mental state Coma Rapid progression of symptoms, coma may develop in 2-10 days Hallmarks are altered mentation and coagulopathy


Labs Increased serum aminotransferase Hypoglycemia Respiratory alkalosis


Features Abrupt onset of encephalopathy Presence of cerebral edema Hypertension and bradycardia Jaundice Oliguric renal failure Hypotension Increased risk of sepsis

Acute Fatty Liver of Pregnancy:

Acute Fatty Liver of Pregnancy Microscopic fat in hepatocytes ½ of patients have Pregnancy induced htn, HELLP syndrome Initial sx include Nausea,vomiting, right upper quad pain,viral like sydrome followed in 7-14 days, jaundice. Treat by delivering baby, untreated progresses to acute liver failure, death

Treatment of Acute Liver Failure:

Treatment of Acute Liver Failure No definitive, specific treatments are proven Give antidotes for acetaminophen or mushroom poisoning early Manage hypoglycemia with glucose and careful monitoring Manage intravascular volume with PA catheter and fluid management Vasopressors tend to be inefffective and may impair hepatic oxygen delivery Only cure is liver transplant

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