The liver is integral to the production of clotting factors and albumin, and the metabolism of proteins, carbohydrates, fats.
In addition, a variety of other endogenous and exogenous substances are metabolized in the liver. Indeed, the liver plays
a role in the elimination of most anesthetic drugs. Thus, when hepatic disease is associated with altered hepatic function,
a patient must be evaluated closely, and prepared carefully prior to surgery. In addition, an anesthetic management plan should
be formulated that will have minimal detrimental effects on liver function, and that is unlikely to result in prolonged depression
as a result of altered drug metabolism.
Anesthesia and surgery is usually associated with an increase in blood glucose concentration. However, patients with liver
dysfunction may be unable to maintain normoglycemia. Thus monitoring of blood glucose pre-, intra-and post-operatively should
be considered. In those patients with hypoglycemia, 50% dextrose (0.5-1 mL/kg into a central catheter) may be given intravenously.
Alternately, glucose may be added to intravenous fluids (0.5-2.5% final concentration) that are being administered during
Albumin is synthesized in the liver, and its synthesis may be decreased in liver disease. Low plasma albumin concentration
results in decreased volume of distribution of some anesthetic drugs. Hypoalbuminemia also associated with decreased plasma
volume. Therapy with colloidal fluids should be considered in patients with a serum albumin concentration of < 2.0 g/dL or
a total plasma protein concentration of < 4.0 g/dL. Dextran 70, hydroxyethyl starch, and Oxyglobin are three synthetic colloids
that may be administered to expand plasma volume. Dextran solutions and hydroxyethyl starch are given at a maximal rate of
20 mL/kg/day, and provide volume expansion for ~24 h after administration. Bolus administration (4-5 mL/kg) may be given during
anesthesia for rapid blood pressure support. Neither dextran nor hydroxyethyl starch solutions provide drug binding sites,
and both may dilute existing clotting factors. Dextran solutions may be more likely than hydroxyethyl starch to affect clotting/coagulation.
Colloidal solutions are usually co-administered with crystalloid solutions. In general, any of the commercially available
isotonic replacement solutions are appropriate in the perioperative period for patients with mild liver disease. However,
in patients with moderate to severe liver dysfunction, lactate containing solutions are usually avoided (i.e., lactated Ringer's
solution) due to diminished hepatic lactate metabolism. Balanced replacement fluids that contain acetate as the physiological
buffering agents may be used instead.
The rate and volume of colloidal and crystalloid fluid administration should be based upon assessment of vascular volume.
Central venous pressure or pulmonary artery wedge pressure are the most objective measures of vascular preload, but heart
rate, capillary refill time and arterial blood pressure may also indirectly reflect vascular volume.
Animals with liver disease may be predisposed to bleeding due to decreased synthesis of clotting factors, impaired vitamin
K absorption, or consumption of coagulation factors (i.e., disseminated intravascular coagulation). Plasma (fresh or fresh
frozen), cryoprecipitate, or vitamin K therapy may all be indicated prior to anesthetizing a patient with liver disease. Prothrombin
time (extrinsic and common coagulation pathways) and activated partial thromboplastin time or activated clotting time (intrinsic
and common coagulation pathways) should be performed prior to any surgical or invasive diagnostic procedure in a patient with
Ascites may form in patients with liver disease due to hypoalbuminemia, portal hypertension, hepatic inflammation, or hepatic
neoplasia. Large amounts of fluid may impair respiratory movement. Rapid removal of ascitic fluid may be associated with hemodynamic
Principles of anesthesia in the patient with liver disease:
This is one of the most important principles of anesthetic management of patients with liver disease. Nutritional status,
vascular volume, coagulation, acid-base balance, and serum electrolytes should be assessed and abnormalities corrected prior
to surgery, if at all possible.
Avoid drugs whose actions are significantly prolonged by liver disease, drugs that are known to be heptatoxic, and drugs that
significantly diminish hepatic blood flow or oxygenation. Due to altered volume of distribution and increased sensitivity,
drugs doses may frequently be decreased in animals with liver disease.
Maximize hepatic oxygen delivery:
Hepatic oxygenation should be maximized by maintaining blood flow and blood pressure, and by optimizing arterial oxygen content.