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Anesthetic Implications of End-Stage Liver Disease and Liver Transplantation. Todd M. Oravitz, MD Associate Professor Department of Anesthesiology University of Pittsburgh School of Medicine Chief, Liver Transplantation Anesthesia VA Pittsburgh Healthcare System. Lecture objectives.

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Anesthetic Implications of End-Stage Liver Disease and Liver Transplantation


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    1. Anesthetic Implications of End-Stage Liver DiseaseandLiver Transplantation Todd M. Oravitz, MD Associate Professor Department of Anesthesiology University of Pittsburgh School of Medicine Chief, Liver Transplantation Anesthesia VA Pittsburgh Healthcare System

    2. Lecture objectives 1) Discuss the pathophysiology of end-stage liver disease 2) Discuss the management of anesthesia in patients with end-stage liver disease 3) Discuss the perioperative management of patients undergoing liver transplantation 4) Discuss the perioperative management of patients undergoing procedures after liver transplantation

    3. Normal Hepatic Function • Liver plays a role in • Carbohydrate metabolism • Produces/stores glycogen, which can be depleted after 24-48 hours of fasting • Site of gluconeogenesis, with amino acids, glycerol and lactate as substrates

    4. Normal Hepatic Function • Liver plays a role in • Protein metabolism • All plasma proteins, except for immunoglobulins, made in the liver • Albumin helps maintain plasma oncotic pressure and is the primary binding/transport protein for many anesthetic drugs • All coagulation factors, except for factor VIII and von Willebrand factor, made in the liver

    5. Normal Hepatic Function • Liver plays a role in • Drug metabolism • Most medications undergo at least some hepatic degradation or biotransformation, or both • End products either metabolically inactive or more water-soluble for biliary or urinary excretion

    6. Normal Hepatic Function • Drug metabolism • Phase I reactions • Include oxidation/reduction (redox) • Cytochrome p450 • Benzodiazepines and barbiturates degraded via phase I • Phase II reactions • May or may not follow phase I • Involve conjugation to facilitate elimination via bile or urine

    7. Normal Hepatic Function • Drug metabolism • Cytochrome p450 • Ethanol, ketamine capable of enzyme induction, resulting in tolerance to the drugs’ effects • Cimetidine, chloramphenicol can cause prolongation of drug effects by enzyme inhibition

    8. Normal Hepatic Function • Anatomy/physiology • Largest organ in the body, weighing about 1.5kg • Right upper quadrant location • Dual blood supply • Liver blood flow ~1.5L/min • Hepatic artery • Portal vein

    9. Normal Hepatic Function • Dual blood supply • Hepatic artery • Accounts for 25% of blood flow and 50% of O2 delivery • Flow is auto-regulated • Portal vein • Accounts for 75% of blood flow and 50% of O2 delivery • Flow depends on GI and splenic blood flow

    10. End-Stage Liver Disease (ESLD) • The liver has a remarkable capacity for regeneration • The liver has tremendous physiologic reserve • Hepatic disease can develop insidiously and a large proportion of function can be lost before problems become apparent

    11. End-Stage Liver Disease (ESLD) • Common symptoms • Anorexia • Weakness • Nausea/vomiting • Abdominal pain • Common signs • Hepatosplenomegaly • Ascites • Jaundice • Spider angiomas • Encephalopathy

    12. Pathophysiology of ESLD • Hepatic changes • Portal hypertension – high resistance to blood flow through the liver – hallmark of ESLD • Leads to accumulation of blood and increased venous pressure in the vascular beds “upstream” to the liver • Esophagus • Spleen • Stomach and intestines

    13. Pathophysiology of ESLD • Portal hypertension leads or contributes to • Ascites • Esophageal varices • Gastric and other intra-abdominal varices • Splenomegaly

    14. Pathophysiology of ESLD • Esophageal varices • Portal-systemic collaterals that allow splanchnic venous blood to flow from the high-pressure portal system to the low-pressure azygos and hemi-azygous system • Not all patients with ESLD develop varices and not all patients with varices have bleeding • Patients that do bleed have significant morbidity and mortality – up to 30% of initial episodes of bleeding are fatal

    15. Variceal Disease • Treatment • Chronic • Propranolol is a non-selective beta-blocker that decreases portal venous pressure • Reduces risk of primary bleeding • Reduces risk of re-bleed • Banding, ligation, sclerotherapy • Transjugular intrahepatic portosystemic shunt (TIPS)

    16. Pathophysiology of ESLD • TIPS • Improves blood flow through the liver • Percutaneous approach to create a shunt between the portal and hepatic veins • Decreases activity of the sodium-retaining pathways • Improves renal response to diuretics

    17. T I P S

    18. Variceal Disease • Treatment • Acute • Aggressive fluid resuscitation; ± blood • Correct coagulation defects, if present • Airway protection – intubation • Octreotide – reduces portal pressure • Endoscopy with possible intervention – banding • Balloon tamponade – Blakemore tube

    19. Pathophysiology of ESLD • Hepatic changes • Spontaneous bacterial peritonitis (SBP) • Spontaneous infection of ascitic fluid without an intra-abdominal source • Increased intestinal wall permeability allows translocation of bacterial into the conducive media of ascitic fluid

    20. Pathophysiology of ESLD • Hepatic changes • Spontaneous bacterial peritonitis (SBP) • Cefotaxime is the antibiotic of choice for treatment as it covers 95% of the offending flora, including the 3 most common – E coli, Klebsiellaand pneumococcus • Quinolone (e.g. ciprofloxacin) prophylaxis is indicated after an initial episode as there is a 70% recurrence rate in the 1st year and it has a beneficial effect on patient survival • Two year survival after SBP is less than 50%

    21. Pathophysiology of ESLD • Hepatic changes • Hepatic encephalopathy (HE) • Occurs when substances normally metabolized by the liver accumulate due to its dysfunction • Ammonia felt to be most important in HE patients • Increased activity of inhibitory neurotransmitters also may play a role • Increased GABAergic tone • Administration of the benzodiazepine antagonist flumazenil often results in an improvement in the mental status of HE patients

    22. Hepatic Encephalopathy • Often occurs after a precipitating event • Increased ammonia level • Large dietary protein load • GI bleeding • Azotemia • Decreased hepatic perfusion • Anesthesia and surgery with resultant hypotension, hypoxemia and/or hypovolemia • Diuretic administration, paracentesis or GI disturbance such as diarrhea or vomiting

    23. Hepatic Encephalopathy • Other possible precipitating events • Sepsis • Increased ammonia levels due to protein catabolism • Decreased hepatic perfusion • Creation of portal-systemic shunt • TIPS • Results in decreased hepatic metabolism

    24. Hepatic Encephalopathy • Treatment • Remove/minimize, to the extent possible, any/all underlying causes • Decrease blood ammonia levels • Reduce production • Lower dietary protein intake • Neomycin – targets urease-producing bacteria • Reduce GI absorption • Lactulose – non-absorbable disaccharide that decreases large intestinal absorption of ammonia and also promotes growth of non-urease producing bacteria

    25. Pathophysiology of ESLD • Coagulation/hematologic changes • Coagulopathy results mostly from two factors • Impaired synthesis of clotting factors • Thrombocytopenia • Decreased levels of anticoagulants, most notably antithrombin III and protein C, can lead to thrombotic complications • Portal vein thrombosis • Deep venous thrombosis (DVT) • Pulmonary embolism (PE)

    26. Coagulation/Hematologic Changes • Coagulopathy • Impaired synthesis of coagulation cascade proteins • All clotting factors, except von Willebrand factor, made in the liver • Vitamin K dependent factors – II, VII, IX and X – at additional risk • Bile salts needed for intestinal absorption of vitamin K and may be decreased by ESLD • Overall poor nutritional status in many ESLD patients

    27. Coagulation/Hematologic Changes • Coagulopathy • Thrombocytopenia • Portal hypertension-induced splenomegaly • Occurs in 30-60% of ESLD patients • Up to 90% of platelets can be sequestered in the enlarged spleen • Platelet count usually >30K and spontaneous bleeding is fairly uncommon • Associated disease processes can contribute • Poor nutrition – folate deficiency • Chronic alcohol intake

    28. Pathophysiology of ESLD • Cardiovascular changes • Hyperdynamic circulation • Increased cardiac output • Decreased systemic vascular resistance • Normal to decreased blood pressure • Increased heart rate • Normal to increased stroke volume

    29. Pathophysiology of ESLD blood pressure=cardiac output x systemic vascular resistance ↔/↓BP = ↑CO X ↓SVR ↓ −−−−−−−−−−−−−−−−− ↓ ↓ ↑HR X ↔/↑SV cardiac output = heart rate x stroke volume

    30. Pathophysiology of ESLD • Cardiovascular changes • Result from development of vasodilation and abnormal shunting • Blood passes from the arterial to the venous circulation without crossing a capillary bed; an anatomic example of this is a spider angioma • Thought to result from increased plasma levels of glucagon and vasoactive intestinal polypeptide

    31. Pathophysiology of ESLD • Pulmonary changes • Hypoxemia, with PaO2 values of 60-70mmHg, is commonly seen in ESLD patients • Causes include • Underlying cardiopulmonary disease • Intrapulmonary shunting • V/Q mismatch • Decreased diffusion capacity

    32. Pulmonary Changes - Hypoxemia • Underlying cardiopulmonary disease • Congestive heart failure, interstitial lung disease, chronic obstructive pulmonary disease • Intrapulmonary shunting • Pre-capillary or larger arteriovenous communications are the result of intrapulmonary vascular dilatation • Hepatopulmonary syndrome

    33. Hepatopulmonary Syndrome (HPS) • Defined by the clinical triad of • Chronic liver disease • Increased A-a gradient • Evidence of intrapulmonary vascular dilatation • Increased pulmonary nitric oxide production is the likely cause • Usually diagnosed by echocardiography

    34. Hepatopulmonary Syndrome (HPS) • Incidence 5-30% • Decreased survival compared to patients with similar degree of liver disease who do not have HPS • HPS patients with severe preoperative hypoxemia (PaO2 <50mmHg) have increased mortality after liver transplantation • HPS often resolves completely after transplant

    35. Pathophysiology of ESLD • Pulmonary changes • Hepatic hydrothorax • Seen in 5-10% of ESLD patients • Pleural effusion from transfer of ascitic fluid through diaphragmatic defects • Treated by sodium restriction, diuretics and/or thoracentesis

    36. Pathophysiology of ESLD • Pulmonary changes • Pulmonary hypertension • Seen in <5% of ESLD patients • Defined as mean pulmonary artery pressure (MPAP) >25mmHg and increased pulmonary vascular resistance • Patients with MPAP >35mmHg have increased perioperative morbidity/mortality • Patients with MPAP >50mmHg, at VAPHS, are not transplant candidates secondary to greatly increased mortality • Etiology not well understood

    37. Pulmonary Hypertension • Avoid physiologic conditions that increase pulmonary vascular resistance, as acute right-sided heart failure can result • Hypoxemia • Hypercapnia • Acidosis • Important to remember during monitored anesthesia care (MAC) cases

    38. Pathophysiology of ESLD • Renal changes • Impaired free water and sodium excretion • Decreased renal perfusion and glomerular filtration rate (GFR) • Vasodilation, which effectively reduces plasma volume, leads to sympathetic nervous system activation of the renin-angiotension-aldosterone pathway, resulting in enhanced sodium and free water resorption

    39. Pathophysiology of ESLD • Renal changes lead to development of • Edema • Ascites • Long term decrease in renal perfusion and GFR can lead to hepatorenal syndrome (HRS) • HRS occurs in up to 10% of patients with ESLD • Functionally HRS is a pre-renal phenomenon whose hallmark is intense renal vasoconstriction

    40. Hepatorenal Syndrome (HRS) • Type I • Progressive oliguria with rapidly rising creatinine • Often follows an episode of spontaneous bacterial peritonitis (SBP) • Poor outcome – median survival < 1 month without intervention • Treatment with albumin, octreotide, and midodrine has shown some promise

    41. Hepatorenal Syndrome (HRS) • Type II • Usually seen in patients with refractory ascites • Renal impairment is usually more mild than type I • Clinical course is far less progressive than type I

    42. Pathophysiology of ESLD • Ascites • Common complication of ESLD; in fact, nearly 50% of patients develop ascites within 10 years of initial diagnosis • Significant associated mortality – nearly 50% of patients die within 3 years of onset of ascites • Etiology complex, multifactorial and not completely understood • Portal hypertension • Sodium, water retention

    43. Pathophysiology of ESLD • Ascites • Treatment • Sodium restriction and diuretics (spironolactone) • Refractory cases treated with repeated large-volume paracentesis and volume expanders, usually albumin • Transjugular intrahepatic portosystemic shunt (TIPS) also can be used for refractory ascites, but it has not been shown to improve survival compared to repeat paracentesis

    44. Anesthesia and ESLD • Preoperative preparation should focus on optimizing liver-related pathology (if possible) • Volume status • Coagulation – parenteral vitamin K if INR elevated • Renal function • Electrolyte imbalance • Nutritional status

    45. Anesthesia and ESLD • Medications should be scrutinized in the preoperative period, as there are a large number that can cause or worsen underlying hepatic dysfunction • Acetaminophen • Isoniazid • Methyldopa • Phenytoin • Indomethacin

    46. Anesthesia and ESLD • Administration of anesthesia decreases liver blood flow via changes in hepatic perfusion pressure and/or splanchnic vascular resistance • Physiologic reserve is decreased patients with ESLD • Perioperative morbidity and mortality in patients undergoing all but minor procedures is increased

    47. Child-Pugh Classification System

    48. Child-Pugh Class and Mortality • Thirty day mortality in patients undergoing either cholecystectomy, hernia repair, GI or miscellaneous surgery; 25% were emergencies • Class A – 10% • Class B – 30% • Class C – 80% • Highest mortality in GI and emergent procedures

    49. Child-Pugh Class and Mortality • Three month mortality for patients hospitalized with liver complications, but not undergoing surgery • Class A – 4% • Class B – 14% • Class C – 50%

    50. Model for End-Stage Liver Disease (MELD) Score • Originally developed to predict survival in patients with portal hypertension undergoing elective TIPS procedures • Found to be an accurate predictor of survival in patients with a variety of liver diseases • Adopted in 2002 as the rank list criteria for liver transplantation by the United Network of Organ Sharing (UNOS), replacing Child-Pugh