In the last post, Dr. Hofmeister discussed his approach to assessment for anesthesia of the patient with liver disease. He made the important distinction between patients who have elevations in liver enzymes and those who have evidence of clinical liver dysfunction. These are two very different types of patients who will usually look different clinically, have vastly different ASA statuses, and require different perianesthetic approaches.
Dr. Hofmeister explained that you can begin to assess the synthetic capacity of the liver by looking at blood values commonly obtained on routine chemistry panels, including blood glucose, albumin, cholesterol and blood urea nitrogen. If signalment (Hello there 5 month old tiny Yorkie who sometimes stares into space!), clinical signs (weight loss, vomiting, jaundice), or blood work results indicate that liver disease might exist, running a pre- and post-prandial bile acid test is a common next step, in addition to ultrasound evaluation and possibly percutaneous fine needle aspirate or biopsy.
Once you have decided that overt liver dysfunction exists, there are 3 main areas to focus on for perianesthetic management:
1) Hepatic synthetic function
2) Hepatic metabolic function
3) Maintenance of hepatic oxygen delivery
Hepatic Synthetic Function: in this respect, I am mainly concerned about some of the things the liver makes that I might need to supplement, including blood glucose, albumin, and coagulation factors.
Blood glucose is an easy one: check the BG on presentation the morning of the procedure and at least once more upon recovery. Even if a patient has been able to maintain their BG previously, fasting them for anesthesia might reveal the inadequate stores of hepatic glycogen and the inability of the liver to keep up with gluconeogenesis. You may need to supplement dextrose during the procedure and I generally start with 1 -2.5 % dextrose added to the IVF.
Hypoalbuminemia can affect anesthesia care in several ways. Most of the anesthetics and sedatives we use are bound by albumin in the blood. Since it is the unbound fraction that is active, when hypoalbuminemia exists, more active drug may be available to cross the blood-brain barrier. It is important to use cautious dosing strategies with highly protein bound drugs and your best bet is titrate injectable drugs intravenously to effect while monitoring the cardiovascular, respiratory, and CNS results. Additionally, moderate to severe hypoalbuminemia will decrease colloid oncotic pressure and may require reduced sodium fluids, synthetic colloids, or albumin transfusions.
Coagulation status can actually be quite complicated because the liver makes both clotting factors and anti-coagulant proteins as well as several fibrinolytic molecules. The coagulopathy of hepatic disease is often referred to as a “balanced coagulopathy” because of this reduction in both pro- and anti-coagulant factors. A traditional clotting factor profile may not reflect the true clinical status of the clotting system in a patient with hepatic disease. For example, in dogs with congenital portosystemic shunts, documented elevations in PTT did not reflect the tendency towards clinical bleeding.1 A method of that allows assessment of the entire clotting process including speed of formation, clot strength, and extent of fibrinolysis, such as thromboelastography (TEG), may provide a better descriptor of the functional coagulation in the patient with advanced liver disease. Point-of-care testing of TEG is used by anesthesiologists in some human operative settings, such as liver transplant, but it is not widely available in veterinary medicine yet.
If traditional clotting factor tests are quite elevated, having access to fresh frozen plasma and possibly packed red cells or fresh whole blood might be warranted prior to highly invasive procedures.
Hepatic Metabolic Function: as Dr. Hofmeister pointed out, if hepatic synthetic function is compromised, it is likely that hepatic metabolic function could be problematic. He covered the major points of drug selection in the last post but the take home message is: avoid high doses of long acting drugs that depend heavily on the liver for clearance and are not reversible.
Additionally, in areas where halothane is still available, it might make sense to avoid this inhalant anesthetic in favor of ones such as isoflurane or sevoflurane that have not been commonly associated with post-anesthesia hepatitis.
One note about NSAIDs in the face of liver dysfunction: the hepatotoxicity of NSAIDs is idiosyncratic – meaning it is not predictable or dose-dependent. Decreased hepatic metabolic capacity does not prevent me from using NSAIDs; however, I reduce the dose and/or frequency of administration so that plasma concentrations do not build up. Put another way, I will prescribe NSAIDs if the patient requires them, I am just conservative on my dosing strategy.
Maintaining Hepatic Oxygen Delivery: in order to avoid deterioration of hepatic function following recovery from anesthesia, we need to try to maintain hepatic blood flow so that the liver cells get the oxygen they need to maintain normal ATP production, Na+/K+ pump function, and cell membrane integrity. Because the liver plays a central role in the immunologic and metabolic response to stress, ischemia and subsequent reperfusion injury to the already compromised liver may lead to severe consequences, including multiple organ dysfunction syndrome and death.