The Liver: Surgery and Anesthesia



The Liver: Surgery and Anesthesia





The liver is the largest internal organ and is the body’s metabolic headquarters (Table 45-1 and Fig. 45-1) (Steadman RH, Braunfeld MY. The liver: surgery and anesthesia. In: Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Ortega R, Stock MC, eds. Clinical Anesthesia. Philadelphia: Lippincott Williams & Wilkins; 2013:1294–1325).


I. Assessment of Hepatic Function



II. Hepatobiliary Imaging



III. Liver Biopsy

Liver biopsy is the method of choice to determine whether liver damage is due to necrosis, inflammation, steatosis, or fibrosis (coagulopathy or thrombocytopenia contraindicates percutaneous liver biopsy).


IV. Hepatic and Hepatobiliary Diseases



  • Liver disease may be the result of a variety of causes, including developmental or genetic defects, metabolic abnormalities, autoimmune diseases, infectious diseases, neoplasm, alcohol, environmental toxins, and drug toxicity.


  • Liver disease can be divided into hepatocellular (parenchymal) or biliary. In hepatocellular diseases, evidence of cholestasis and synthetic dysfunction appear synchronously.


  • Liver disease may also be described as acute (drug toxicity, infection) or chronic (viral hepatitis, alcoholic liver disease, nonalcoholic fatty liver disease [NAFLD]). The most common causes of chronic liver disease are chronic viral hepatitis, alcoholic liver disease, and NAFLD. The most important consequences of chronic liver disease are portal hypertension, cirrhosis, and malignancy.


V. Acute Liver Failure

Acute liver failure (ALF) is defined as the appearance of encephalopathy together with coagulopathy, usually an international normalized ratio (INR) ≥1.5, in a patient who has no previous history of liver disease and who has had an illness of <26 weeks’ duration.





  • Drug-related toxicity accounts for more than half of the cases of ALF in the United States. Of these drug-related cases, more than 80% are the result of acetaminophen ingestion.


  • The natural history of adult ALF in the United States is one of spontaneous recovery in approximately 45% of patients, liver transplantation in 25%, and death without transplantation in 30%.



  • The most serious, and often the proximate cause of death, is acute cerebral edema and intracranial hypertension (Table 45-4).


  • Coagulopathy is a necessary finding for the diagnosis of ALF; however, clinically significant spontaneous bleeding is uncommon. Correction of thrombocytopenia to ≥50,000/mm3 and INR to ≤1.5 are suggested for the bleeding patient or the patient about to undergo an invasive procedure.


  • Hypotension in ALF may be the result of several days of gastrointestinal losses, poor intake, or myocardial dysfunction but likely includes a component of decreased arterial tone as liver necrosis progresses.



    • Vasopressors (norepinephrine, dopamine) may be used to treat either systemic hypotension or to maintain an adequate cerebral perfusion pressure.


    • The use of arginine vasopressin or its analogs cannot be recommended because there is evidence that their use is associated with increases in intrahepatic cholestasis of pregnancy (ICP).






Figure 45-1. Basic structure of a liver lobule showing the cellular plates, the blood vessels, the bile-collecting system and the lymph flow system composed of the spaces of Disse, and the interlobular lymphatics.








Table 45-1 Hepatic Function in Health




Receives 25% of the cardiac output via a dual supply (low-resistance portal vein and hepatic artery that can increase flow by up to 100% to maintain hepatic oxygen delivery)
Can store up to 1 L of blood
Energy production and storage of nutrients (blood glucose regulation)
Synthesizes fat, cholesterol, phospholipids, and lipoproteins
Synthesizes all the plasma proteins
Deaminates amino acids
Clotting factors (exceptions are tissue thromboplastin, calcium, and von Willebrand factor)
Unique ability to regenerate after injury








Table 45-2 Blood Tests and the Differential Diagnosis of Hepatic Dysfunction










































  Bilirubin Overload (Hemolysis) Parenchymal Dysfunction Cholestasis
Aminotransferases Normal Increased (may be normal or decreased in advanced stages) Normal (may be increased in advanced stages)
Alkaline phosphatase Normal Normal Increased
Bilirubin Increased unconjugated Increased conjugated Increased conjugated
Serum proteins Normal Decreased Normal (may be decreased in advanced stages)
Prothrombin time Normal Decreased (may be normal in early stages) Normal (may be prolonged in advanced stages)
Blood urea nitrogen Normal Normal (may be decreased in advanced stages) Normal
Sulfobromophthalein/indocyanine green Normal Retention Normal or retention








Table 45-3 Hepatobiliary Imaging






  • Plain radiography (limited role in evaluation of liver disease)
  • Ultrasonography (primary screening test for hepatic parenchymal disease and extrahepatic disease)
  • Computed tomography (supplements scanning ultrasonography)
  • Magnetic resonance imaging (evaluation of hepatobiliary disease)

    • Need a 20-second breath hold that may require sedation or anesthesia in young or uncooperative patients

  • Percutaneous transhepatic cholangiography (determine the site and cause of biliary obstruction)
  • Endoscopic retrograde cholangiopancreatography: u

    • Uses endoscopy to visualize the ampule of Vater and selectively inject contrast material into the pancreatic and common bile ducts








Table 45-4 General Measures to Reduce Cerebral Edema




Maintain 30-degree head-up position with head in neutral position.
After the patient is intubated, administer muscle relaxants to minimize rises in intracranial pressure from coughing.
Mannitol-induced osmotic diuresis
Response to hyperventilation is short lived
Corticosteroids not indicated
Prophylactic antibiotics to prevent sepsis and minimize inflammatory mediator burden


VI. Acute Hepatitis



  • The most common causes of acute viral hepatitis are, collectively, the five identified viral hepatitides: A (HAV), B (HBV), C (HCV), D (HDV or delta-virus), and E (HEV).



    • HAV and HBV have been well characterized, and vaccines have been developed to prevent their transmission.


    • A vaccine is not available for HCV, but the number of reported new cases is decreasing most likely due to better screening of transfused blood products and the adoption of universal precautions.




  • The diagnosis of acute hepatitis is made on the basis of classic signs (jaundice, fever, arthralgia) and symptoms (may be nonspecific such as fatigue or poor appetite) together with laboratory studies. Many infections are subclinical.


  • Incubation periods can be several weeks to even months, and patients may undergo surgery without awareness of illness. For this reason, viral hepatitis should be part of the differential diagnosis when there is any evidence of postoperative liver injury.


VII. Alcoholic Hepatitis

Alcoholic hepatitis is the syndrome marked by the development of jaundice and liver dysfunction in the setting of heavy alcohol use.


VIII. Drug-Induced Liver Injury

Drug-induced liver injury (DILI) is largely a diagnosis of exclusion and should always be considered when formulating the differential diagnosis of patients presenting with liver abnormalities.



  • DILI is a serious problem for the pharmaceutical industry because it is the most common reason for regulatory actions such as failure of approval, removal from market, or restrictions on indications for use.


  • Nonacetaminophen drug-induced idiosyncratic liver injury accounts for 11% to 13% of cases of ALF, and with a 20% rate of survival with supportive care, it has a poorer than average rate of spontaneous recovery.


  • In anesthesiology, perhaps the best-known potentially hepatotoxic drug is halothane.


IX. Pregnancy-Related Liver Diseases



  • Abnormalities in liver studies occur in 3% to 5% of pregnancies


  • The most common causes are hyperemesis gravidarum, intrahepatic cholestasis of pregnancy, preeclampsia, preeclampsia complicated by hemolysis, low platelet count, and elevated liver enzymes (HELLP syndrome) and acute fatty liver of pregnancy (Table 45-5).


X. Cirrhosis and Portal Hypertension



  • Cirrhosis is the end product of the long course of chronic liver disease, during which there have been either steady or recurrent episodes of parenchymal inflammation and necrosis.



  • Increased resistance to blood flow through the liver leads to portal hypertension. When portal hypertension becomes severe (generally defined as a hepatic venous pressure gradient of >10–12 mm Hg), chronic liver disease becomes a systemic illness, affecting other organ systems as well.








Table 45-5 Distinguishing Features of Intrahepatic Cholestasis of Pregancy (ICP), Hellp Syndrome, and Acute Fatty Liver of Pregnancy (AFLP)
































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Jun 16, 2016 | Posted by in ANESTHESIA | Comments Off on The Liver: Surgery and Anesthesia

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  ICP HELLP AFLP
% Pregnancies 0.1 (United States) 0.2–0.6 0.005–0.01
Onset 25–32 weeks’ gestation Third trimester or postpartum Third trimester or postpartum
Family history Often No Occasionally
  Presence of preeclampsia No Yes 50%
  Typical clinical features Pruritus
Mild jaundice
Elevated bile acids
Decreased vitamin K