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Anesthesia for patients with liver disease (Proceedings)
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.
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 surgery.
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 liver disease.
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 instability.
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.
Although opioid metabolism may be prolonged in patients with liver disease, their ability to decrease the dose of induction and maintenance agents, minimal cardiovascular effects, and reversibility make them useful in liver disease. Opioids (and especially mu agonists) should be avoided if increased biliary sphincter tone will be detrimental to the patient. Opioids may decrease heart rate, and this may be problematic in anesthetized patients. However, this side effect is easily treated with anticholinergic drugs (i.e., atropine or glycopyrrolate). Opioids may also cause respiratory depression. This side effect is also handled easily during anesthesia by monitoring exhaled CO2 and ventilating the patient when appropriate.
In general, major tranquilizer use should be minimized due to adverse effects on blood flow (i.e., alpha-two agonists) or prolonged activity (acepromazine).
In patients with mild liver disease, little adjustment in anesthetic protocol needs to be considered. However, in patients with clinically significant liver disease, propofol is the injectable induction drug of choice. It is extensively redistributed, and is metabolized rapidly by hepatic and extrahepatic processes. Etomidate should be considered if severe cardiopulmonary dysfunction is concurrent with liver disease. Etomidate causes minimal cardiovascular dysfunction, is extensively redistributed, and undergoes one-step hepatic biotransformation (Most anesthetic drugs undergo a two-step biodegradative process). Inhalant anesthetics (isoflurane, sevoflurane, or desflurane) may also be used to induce anesthesia. Waste gas pollution, patient stress, and lack of rapid airway control are all significant disadvantages associated with inhalant induction.
Isoflurane, sevoflurane, or desflurane are all suitable for maintaining general anesthesia in patients with liver disease. All of these drugs may cause hypotension, and this should be avoided through appropriate monitoring and treatment with fluids and inotropes. The amount of inhalant anesthetic can be minimized by concurrent administration of opioid drugs, and this strategy is appropriate in many patients with reduced liver function.
Grubb TL. Anesthesia for Patients with Special Concerns. In: Small Animal Anesthesia and Analgesia. Carroll GL, ed. 2008.