Anesthetic Considerations for Hepatic Disease

Chapter 34
Anesthetic Considerations for Hepatic Disease


An organ with some important jobs


Jane Quandt


College of Veterinary Medicine, University of Georgia, USA



  1. Q. What is the main blood supply to the liver?
  2. A. Twenty percent of the cardiac output is delivered to the liver. Of that percentage, 30% of the blood flow and 90% of the oxygen is supplied by the hepatic artery and the remainder is provided by the portal vein [1].
  3. Q. What are clinical signs of hepatic disease or insufficiency?
  4. A. Clinical signs include ascites, depression, seizures, jaundice, hepato-encephalopathy, stunted growth, anorexia, and weight loss. Decreased blood values for albumin, urea nitrogen, glucose, and cholesterol can be seen with poor liver function. Coagulation times of prothrombin, partial thromboplastin can be prolonged and there can be increased fibrinogen values [1].

    Blood ammonia concentration and bile acids are indicators of liver dysfunction. Bile acids are produced by the liver and excreted in the bile. An increase in postprandial bile acid concentration indicates a decrease in hepatic function or the presence of a portosystemic vascular shunt [1,2].


  5. Q. What are four primary functions of the liver that can affect anesthesia?
  6. A. The liver has many functions, but the four primary functions that can impact anesthesia are:

    • glucose homeostasis
    • protein synthesis
    • production of clotting factors
    • drug metabolism and detoxification.

    Glucose homeostasis (including formation, storage, and release) is an essential part of normal liver function. Blood glucose values should be closely monitored in the patient with liver dysfunction as hypoglycemia can be present. Hypoglycemia (less than 50 mg/dl) can result in neurological symptoms as glucose is the obligate energy source for the brain. Bradycardia and circulatory collapse may also occur. Hypoglycemia during anesthesia can result in a prolonged recovery [1,2]. If hypoglycemia is present, dextrose should be added to the crystalloid fluid therapy to maintain a blood glucose within the normal range [1,2,3]. The concentration of dextrose in the crystalloid fluid can be 2.5–5%. If the fluid rate delivery rate is high the concentration should be lower, that is 2.5%, to avoid hyperglycemia. A fluid delivery rate of less than 5 ml/kg/h may require a higher dextrose concentration to achieve normoglyemia. The patient’s blood glucose value should be monitored every 35–40 min during the duration of anesthesia and recovery to avoid hypo- or hyperglycemia. There are specific dog or cat point-of-care glucometers that simplify this monitoring.


    The liver is the only site for albumin synthesis. Low plasma albumin level will result in more free drug being available as there is less drug binding to protein. When administering anesthetic agents a lower dose may be needed to avoid an overdose.


    Albumin accounts for 80% of the colloid oncotic pressure (COP) of plasma. When the albumin concentration is less than 1.5 g/dl the decrease in COP can result in redistribution of fluid to the extracellular spaces, leading to the development of edema. Fluid therapy may need to include a colloid such as hetastarch or plasma to improve the COP [1,4].


    A low COP may contribute to ascites. A large amount of ascites may impinge on lung expansion and pulmonary function. Removal of ascites prior to anesthesia may be considered but should be done slowly as rapid removal of a large amount of fluid may cause a fluid shift from the vascular space to the abdominal cavity as ascites formation continues. This fluid shift can cause serious hypotension and cardiovascular compromise. This can also be seen intra-operatively if the ascites is removed rapidly via surgical suction. Intravenous fluids should be given during ascites removal to avoid cardiovascular collapse [1,2].

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Sep 3, 2017 | Posted by in SMALL ANIMAL | Comments Off on Anesthetic Considerations for Hepatic Disease

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