Does Propofol Affect The Enzymes In The Liver?

Propofol, a sedative medication, has been linked to rare instances of acute liver injury and the “Propofol infusion syndrome”, which is characterized by bradyarrhythmias, metabolic acidosis, rhabdomyolysis, hyperlipidemia, and an enlarged or fatty liver. Patients with liver disease often require surgery, and are at increased risk of intraoperative complications and postoperative morbidity and mortality. Studies have shown that isoflurane and propofol have mild effects on liver enzymes in patients without documented evidence of liver disease. Propofol is generally considered safe, but it can cause acute hepatitis, the seventh published case. A study by Oh et al. demonstrated that sevoflurane for maintenance of anesthesia resulted in higher postoperative liver enzyme levels. Propofol anesthesia was associated with changes in lipid profile, pancreatic and liver function indices, which should be considered in clinical practice. In summary, propofol has fewer effects on liver enzymes compared to halothane. Propofol-induced acute liver injury is a rare outcome, and genetic variations can lead to clinically relevant alterations of propofol metabolism. Both agents had varying effects on liver enzymes, with isoflurane resulting in a significantly higher increase in 24 hours post-operative. Reports of intraoperative lipemia during propofol anesthesia are rare but raise concerns about the safety of prolonged propofol infusion.

What can falsely elevate liver enzymes?

Common causes of elevated liver enzymes include: Nonprescription pain medicines, particularly acetaminophen (Tylenol, others). Certain prescription medicines, including statins, which are used to control cholesterol. Drinking alcohol.

Can anesthesia cause high liver enzymes?

Anesthesia and surgery may deteriorate liver function in patients with elevated liver enzyme levels; therefore, in these patients, choosing anesthetics with less hepatotoxicity may be important.

Background. Anesthesia and surgery may deteriorate liver function in patients with elevated liver enzyme levels; therefore, in these patients, choosing anesthetics with less hepatotoxicity is important.

Methods. This retrospective study investigated the effect of total intravenous anesthesia (TIVA) versus inhalation anesthesia (INHA) on the postoperative liver function in patients with preoperatively elevated liver enzyme levels (aspartate transaminase (AST) or alanine transaminase (ALT) 40 U/L) who underwent non-hepatic surgery under general anesthesia. We compared the changes in enzyme levels within 24 hrs before and after surgery.

Results. In 730 patients (TIVA: n=138; INHA: n=592), the baseline characteristics were comparable, except for higher comorbidity rates in the TIVA group. The median anesthesia and operation times were significantly longer in the TIVA group because approximately 50% of the TIVA group (vs 19. 7% of the INHA group) underwent neurosurgery, which had a relatively longer operation time than other surgeries. Intraoperative hypotensive events and vasopressor use were more frequent in the TIVA group. After 1:4 propensity score matching (TIVA: n=94; INHA: n=376), the baseline characteristics and surgical variables were comparable, except for longer anesthesia time. Before matching, postoperative AST and ALT changes were significantly lower in the TIVA group than in the INHA group. After matching, only the ALT change was significantly lower after TIVA than after INHA (median (interquartile range), −16. 7 (−32 to −4) % vs −12. 0 (−28. 6–6. 5) %, P =0. 025).

Does propofol affect liver enzymes?

Propofol anesthesia is generally safe for patients with cirrhosis and minimal hepatic encephalopathy, but isolated case reports of hepatitis arising within days or weeks after anesthesia have been published. The pattern of serum enzyme elevations is usually hepatocellular, with some instances accompanied by jaundice and prolongation of prothrombin time activity. Immunoallergic features and autoantibodies during the liver injury are absent.

Prolonged infusions of propofol can result in a distinctive clinical syndrome known as the propofol infusion syndrome, which is marked by cardiac bradyarrhythmias, metabolic acidosis, rhabdomyolysis, hyperlipidemia, renal insufficiency, and death from cardiovascular collapse. The syndrome generally arises after 2 to 3 days of sedation in association with higher doses of propofol (3-5 mg/kg/hour). Early termination of the propofol infusion can result in reversal of the syndrome, but the mortality rate in published series has been greater than 50.

On autopsy, patients with the propofol infusion syndrome may have hepatic microvesicular steatosis, explaining the lactic acidosis that frequently accompanies muscle and heart abnormalities. However, jaundice and marked elevations in typical liver-associated enzymes in this syndrome are uncommon. A mild form of this syndrome may occur earlier during infusions, as shown by lactic acidosis arising within 2 to 24 hours of starting propofol, which is rapidly reversed upon stopping.

Is anesthesia safe for liver?

Several general anesthetics have been implicated in causing liver injury, usually arising within 1 to 14 days of their administration. Most commonly implicated was halothane, the initial halogenated inhalational general anesthetic which was introduced into practice in the 1950’s. Shortly thereafter, case reports followed by case series were published of severe liver injury attributed to halothane. The liver injury arose within days or a few weeks of the exposure and was typically associated with a hepatocellular pattern of injury accompanied by fever and signs of hypersensitivity. Halothane hepatitis was often severe and, although rare, led to a decrease in its use, particularly with the development of better tolerated and safer halogenated gases for anesthesia such as enflurane, isoflurane, desfurane, and sevoflurane. Drug induced liver injury can occur with the newer agents, but is extremely rare.

The other general anesthetics have not been definitely implicated in causing drug induced liver injury, at least when given in conventional anesthetic doses and for limited periods of time. Nitrous oxide, for instance, has not been convincingly linked to liver injury despite wide scale use for many decades. Two more recently developed anesthetics, however, have been implicated in causing unusual and rare forms of liver injury: propofol and ketamine.

Propofol, which has become the most common general anesthetic in general use, can cause a distinctive and life threatening syndrome (the “propofol infusion syndrome”) when given for prolonged periods, a syndrome that can be accompanied by lactic acidosis and liver dysfunction. Ketamine can cause an unusual form of liver injury when used on a regular basis (as with ketamine abuse), marked by recurrent abdominal pain, biliary strictures and cholestatic liver injury.

Each of the general anesthetics is discussed separately with case examples and references.

Which anesthesia drugs to avoid in liver failure?

Inhalation anesthetics, such as Halothane and Isoflurane, should be avoided in hepatic patients due to their potential decrease in hepatic blood flow, oxygen supply, and postoperative dysfunction. Sevoflurane and Desflurane, newer volatile anesthetics, have not been extensively studied, but they may have some advantages over others. Nitrous Oxide has been used successfully in patients with advanced hepatic disease without complications, but its sympathomimethic effects may jeopardize oxygenation.

Opioids have been successfully used in hepatic patients, but they can have pharmacological consequences like delayed drug clearance and prolonged half-life. Fentanyl is considered the preferred opioid for these patients because it does not decrease hepatic oxygen and blood supply, nor prevent increases in hepatic oxygen requirements. Spasm induction of the Oddi sphincter can be treated with various drugs, including Atropine, Naloxane, Glucagon, Nitroglycerin, volatile anesthetics, and other drugs.

When administering drugs, anesthetists must consider the pharmacokinetics of other anesthetic drugs, such as lidocaine and Benzodiazepines, which may increase in half-life in patients with liver disease. Drugs with high affinity to albumin may have a decline in volume of distribution, so doses should be reduced. Propofol is the preferred intravenous anesthetic drug for patients with liver disease, as it has a short half-life even in patients with decompensated Cirrhosis. However, many drugs may increase the volume of distribution due to edema or increased Gamma Globulin, necessitating an increase in the first effective dose.

Can propofol damage kidneys?

Abstract. Propofol infusion syndrome has been increasingly recognized as a syndrome of unexplained myocardial failure, metabolic acidosis, and rhabdomyolysis with renal failure. It has been described only with acute neurologic injury or acute inflammatory diseases complicated by severe infections or sepsis. It appears to develop in the context of high-dose, prolonged propofol (100 microg/kg/min) treatment in combination with catecholamines and/or steroids. This was first noted in children but is increasingly recognized in adults. This is a case report of 2 patients (a 42-year-old man and a 17-year-old girl) who had acute renal failure associated with use of propofol in the appropriate clinical setting. It examines the pathophysiology and the possible mechanisms of this condition and illustrates the need to consider it as the cause of rhabdomyolysis and acute renal failure in critically ill patients.

Trampitsch E, Oher M, Pointner I, Likar R, Jost R, Schalk HV. Trampitsch E, et al. Anaesthesist. 2006 Nov;55:1166-8. doi: 10. 1007/s00101-006-1085-5. Anaesthesist. 2006. PMID: 17021888 German.

Propofol infusion syndrome: a case of increasing morbidity with traumatic brain injury.

What is the number 1 side effect of propofol?

Transient local pain at the injection site is the most common adverse reaction. This may be decreased by administering IV lidocaine before propofol bolus.

Occasionally has been seen to cause EKG changes (QT interval prolongation). This is rarely clinically significant.

Discolored urine (a green tint); this adverse event is exceedingly rare.

What is the liver clearance of propofol?

Results. Hepatic clearance of propofol was approximately 60% of total body clearance. The hepatic extraction ratio of propofol was 0. 87 ± 0. 09. There was no significant difference in the concentration of propofol between the radial, pulmonary arteries and internal jugular vein. However, a high level of propofol extraction in the kidneys was observed – the renal extraction ratio being 0. 70 ± 0. 13.

Conclusions. We have demonstrated substantial renal extraction of propofol in human. Metabolic clearance of propofol by the kidneys accounts for almost one-third of total body clearance and may be the major contributor to the extrahepatic elimination of this drug.

Keywords: Propofol, kidneys, metabolism, lungs, brain.

What is the most common side effect of propofol?

Adverse Effects Transient local pain at the injection site is the most common adverse reaction. This may be decreased by administering IV lidocaine before propofol bolus. Occasionally has been seen to cause EKG changes (QT interval prolongation). This is rarely clinically significant.

Continuing Education Activity. Propofol is an intravenous anesthetic used for procedural sedation, during monitored anesthesia care, or as an induction agent for general anesthesia. It may be administered as a bolus or an infusion, or some combination of the two. Propofol is prepared in a lipid emulsion which gives it the characteristic milky white appearance. Strict aseptic technique must be used when drawing up propofol as the emulsion can support microbial growth. It has both approved and off-label uses. This activity outlines the indications, mechanism of action, methods of administration, important adverse effects, contraindications, monitoring, and toxicity of propofol, so providers can direct patient anesthesia where it is indicated, as part of the interprofessional team.

Summarize the approved and off-label indications for using propofol.

Review the appropriate monitoring and toxicity of propofol.

How long do liver enzymes stay elevated after surgery?

Decreased hepatic clearance secondary to hepatic hypoperfusion can also cause hepatic dysfunction. Cardiogenic shock due to congestive heart failure can lead to ischemic hepatitis. This condition is characterized by rapid elevations in serum levels of AST, ALT, and LDH, often 10-fold above normal limits and potentially associated with jaundice and prolongation of prothrombin time. These elevations may last 3–11 days and rapidly return to normal thereafter. Noncardiogenic shock, such as septic shock, can also lead to hepatic dysfunction. Accidental ligation of the hepatic artery or its branches can occur during cholecystectomy, resulting in…

What organs does propofol affect?

However, prolonged and high-dose infusions of propofol can lead to a serious condition called propofol infusion syndrome (PRIS), which can result in renal, cardiac, and circulatory failure.

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