JOSEPH COTTEN, MD, PHD MANUEL PARDO, JR., MD
overview
■ Definition: hepatic encephalopathy & coagulopathy in the setting of acute hepatic disease. Time from onset of jaundice until onset of encephalopathy distinguishes fulminant (within 8 wks) from subful- minant (within 26 wks) liver failure.
■ Pts w/ fulminant hepatic failure (FHF) are usually critically ill & do not undergo elective procedures. Urgent procedures that may involve the anesthesia provider include central line placement, dialysis line placement, tracheal intubation for airway protection, GI endoscopy, ICP monitor placement, head CT scan, or liver transplantation.
■ Causes
➣
Viral hepatitisr Most commonly A or B
r Occasionally cytomegalovirus, Epstein-Barr virus, herpes viruses are implicated
➣
Drugsr Predictably toxic drugs (eg, acetaminophen; typically >12 g ingestion, less in the presence of alcohol or starvation) r Idiosyncratic reactions to inhaled anesthetics, sulfonamides,
phenytoin, oral hypoglycemics (troglitazone), others
➣
Toxinsr Organic solvents: trichloroethylene, tetrachlorethane r Herbal remedies: kava kava
r Toxins from the “death cap” mushroom (Amanita phalloides)
➣
Vascularr Myocardial infarction, cardiac arrest, cardiomyopathy, pul- monary embolism, metastatic or infiltrative cancer, amyloi- dosis, veno-occlusive disease (Budd-Chiari, chemotherapy)
➣
Miscellaneous causesr Fatty liver of pregnancy (third trimester; frequently w/ pre- eclampsia)
r Reye’s syndrome
r Wilson’s disease (acute liver failure can be first presentation)
■ Important: Understand the multiple organ system complications of FHF. The most significant complications include
Acute Liver Failure (Fulminant Hepatic Failure) 11
➣
CNS: cerebral edema, hepatic encephalopathy➣
Hematologic: bleeding➣
ID: infection, sepsis➣
Renal: acute renal failure➣
Cardiovascular: hypotension➣
Metabolic: hypoglycemia, lactic acidosis, electrolyte abnormali- tiesCNS
■ Cerebral edema & hepatic encephalopathy are two different condi- tions that can occur together & have the same presenting symptoms in FHF.
➣
Signs & symptoms can includer Agitation, delusions, hyperkinesis, coma, pupillary abnormal- ities, increased muscle tone, decerebrate posturing, seizures, hypertension, bradycardia.
➣
Cerebral edema is rare in chronic liver failure but occurs in about 75% of pts w/ FHF & stage IV encephalopathy.➣
Cerebral edema is the leading cause of death & is due to loss of cell membrane integrity & alterations in the blood-brain barrier.➣
Cerebral herniation is associated w/ an untreated ICP>20 mm Hg & occurs in 25% of pts w/ grade 4 encephalopathy.➣
Cerebral edema treatment r Mannitol 0.3–0.4 g/kg IVr Elevate head of bed 30 degrees to promote venous drainage. r Maintain cerebral perfusion pressure by balancing MAP,
ICP & cerebral oxygen consumption (vasopressors, pentobar- bital coma).
r Unlike some other types of cerebral edema, dexamethasone & hyperventilation are of minimal value.
■ Grading scale for hepatic encephalopathy, based on level of con- sciousness
➣
Grade 1: restlessness, sleep abnormalities➣
Grade 2: lethargy➣
Grade 3: confused, somnolent but arousable➣
Grade 4: coma■ Conditions that can worsen encephalopathy
➣
Hypoxemia➣
Hypoglycemia12 Acute Liver Failure (Fulminant Hepatic Failure)
➣
Hypokalemia➣
Hyponatremia➣
GI bleeding■ Pts w/ grade 3 or 4 coma are generally intubated for airway protec- tion.
■ Subdural or epidural ICP monitor may be placed to follow ICP.
Hematologic
■ Decreased levels of factors II, V, VII, IX, X cause prolonged prothrom- bin time & partial thromboplastin time & predispose to bleeding complications.
■ Platelet counts are commonly<100,000/mm3& platelet function is
altered.
■ Laboratory values are difficult to distinguish from DIC.
■ GI bleeding common
■ Routine correction of coagulopathy w/ FFP does not lead to improved outcome.
➣
FFP & platelets often administered for active bleeding, or imme- diately prior to invasive procedures to minimize bleeding risk.ID
■ Up to 80% of pts develop bacterial infection (mostly gram-positive) & 30% develop fungal infection.
■ Pt may be receiving broad-spectrum antibiotics.
Renal
■ Renal failure may be due to acute tubular necrosis, hepatorenal syn- drome, or intravascular dehydration.
➣
Can also be secondary to a toxin (eg, acetaminophen)■ Conventional hemodialysis can be complicated by hypotension & bleeding & may worsen cerebral edema.
➣
Pt may receive continuous dialysis therapy, which has less impact on hemodynamics.Cardiovascular
■ Hypotension is common & usually related to very low systemic vas- cular resistance (SVR).
➣
Low SVR may be resistant to alpha agents.■ Cardiac index is increased secondary to decreased systemic vascular resistance (SVR) by A-V shunting & vasodilation.
■ Elevated ICP may cause cardiac dysfunction.
■ Arrhythmias may occur from electrolyte abnormalities or elevated ICP.
Acute Liver Failure (Fulminant Hepatic Failure) 13
Pulmonary
■ Pulmonary complications may occur in up to 50% of cases sec- ondary to aspiration, infection, or noncardiogenic pulmonary edema (ARDS).
■ Respiratory alkalosis is common, secondary to cerebral edema or encephalopathy.
■ Ascites in subfulminant liver failure may affect ventilation & lung volumes.
Metabolic
■ Hypoglycemia is very common. Pts require dextrose 10% infusion.
➣
Occurs secondary to diminished gluconeogenesis & decreased insulin uptake■ Lactic acidosis can occur secondary to poor tissue perfusion/oxygen extraction & altered oxygen-hemoglobin dissociation characteris- tics.
■ Hyponatremia occurs from water retention & intracellular sodium shift.
■ Hypokalemia related to respiratory alkalosis may be profound.
preop
Issues/Evaluation
■ ICU management is mandatory. Therapy is largely supportive & a bridge to transplant or recovery of native liver function.
■ Prognosis should be determined quickly so that pt can be referred for liver transplant evaluation.
■ Specific toxin antidotes may be administered.
➣
Penicillin and silymarin are antidotes to Amanita mushroom poisoning.➣
N-acetyl cysteine improves acetaminophen toxicity & is benefi- cial up to 36 hours after toxin ingestion.What To Do
■ Evaluate pt carefully for the multiple organ system manifestations of FHF.
➣
Recheck pertinent laboratory values, as they can change quickly.➣
Type & cross-match for PRBC & consider FFP or platelet transfu- sion to reduce bleeding risk of invasive procedures.■ Since pts are generally critically ill, consider the complexity & risks of transport.
intraop
14 Acute Liver Failure (Fulminant Hepatic Failure) Acute Renal Failure
Management
■ General issues
➣
If pt not already intubated, consider rapid sequence intubation.➣
Obtain adequate IV access to manage bleeding.➣
Arterial access useful to facilitate BP monitoring & lab studies➣
Monitor labs frequently, includingr Glucose: dextrose infusion may be required, or dose may need to be adjusted
r Coagulation studies r Acid-base balance
r Electrolytes: in particular, FFP transfusion may lead to hypocalcemia; PRBC transfusions may lead to hyperkalemia
■ CNS issues
➣
Maintain cerebral perfusion pressure (CPP)>50 mmHg. r Avoidexcesselevationofheadofbed.AlthoughthismayreduceICP, it may further reduce MAP & CPP.
➣
Anticipate prolonged or unpredictable drug effects because of liver & renal dysfunction.➣
For pt w/ cerebral edema, use precautions to minimize ICP rise during tracheal intubation.■ Renal issues
➣
Consider intraop continuous dialysis therapy if fluid, acid-base, or electrolyte management becomes difficult.postop
■ Plan for postop intubation.
■ Continue ICU mgt.
■ Re-evaluate fluid & electrolyte status & consider potential need for dialysis.