Prolonged Propofol Anesthesia Is Not Associated with an Inc

rease in Blood Lactate

Anesth Analg 2009;109:1105–10

BACKGROUND

Propofol Infusion Syndrome (PRIS) prolonged (>48 h) high-dose (>5 mg/kg) propofol in

fusion metabolic acidosis lipemia fatty infiltration of liver myocardial dysfunction (rhabdomyolysis) renal failure

BACKGROUND

Lactic acidosis is considered an early sign of propofol infusion syndrome.

Case reports of PRIS developing even after short-term infusion in children and adults during anesthesia in operating rooms or sedation in intensive care units.

An increase in lactate and development of metabolic acidosis was apparent early, within 2–5 h after initiation of the propofol infusion.

BACKGROUND

In this study, we investigated the changes in lactate and pH with propofol versus volatile anesthesia (VA) of long duration.

METHODS

Data Collection

demographic data age, gender, body weight, ASA classification, medical history, chr

onic medications

intraoperative data surgical time, type of surgery, number of vertebral levels instrum

ented, anesthesia duration, dose of anesthesia medications, systolic blood pressure (SBP) every 5 min

Collection oflaboratory variables

Baseline within 2 h of anesthesia start time

T8 8 h after “start of anesthesia” ± 60 min

RESULTS

RESULTS

RESULTS

RESULTS

RESULTS

DISCUSSION

We observed higher lactate levels during VA when compared with propofol anesthesia, and suggesting that the propofol-based general anesthesia is less likely to cause lactic acidosis than VA.

DISCUSSION

An alternative explanation for the difference in blood lactate levels between VA and propofol groups may be a different effect of these anesthetics on lactate metabolism, particularly on 1) lactate production, 2) lactate clearance via the liver or kidney, or 3) imbalance between both.

DISCUSSION Release of catecholamines increases lactat

e production and decreases lactate clearance by decreasing hepatic blood flow and activation of Na-K-ATP pumps, provoking glycolysis.

A potential explanation of an increase in lactate over time with isoflurane and sevoflurane would be an impaired liver clearance of lactate, because both VAs cause a dose-dependent decrease in hepatic blood flow.

DISCUSSION On the other hand, propofol might be expected to

decrease lactate levels as it contains 10% soybean oil, which is a 10% intralipid emulsion containing a mixture of triglycerides, predominantly unsaturated fatty acids.

An infusion of free fatty acids for 2 h has been reported to inhibit glycolysis and stimulate neoglycogenesis in healthy men and diabetic patients.

Similarly,an increase of free fatty acids in blood with intralipids has been demonstrated to profoundly inhibit intrahepatic glycogenolysis and stimulate neoglycogenesis, thereby increasing intrahepatic uptake and use of lactate.

DISCUSSION Decreased oxygen delivery due to hypovolemia, hy

potension, and/or anemia during anesthesia may contribute to hypoperfusion and hypoxemia of peripheral tissues, causing anaerobic metabolism and, as a result, an increase in blood lactate.

The incidence of intraoperative hypotension was similar. Although there was a small difference in baseline SBP between the propofol and VA groups, because the incidence of chronic arterial hypertension and its treatment were similar in both groups.

DISCUSSION

Patients in the VA group were slightly older (58 ± 14 yr) than in the propofol group (52 ± 15 yr).

However, age per se is not known to affect blood lactate levels.

DISCUSSION In the propofol group, patients received

about one-half of the daily caloric intake. This significant caloric intake, compared

with the “fasting” VA group, may play a positive role in neoglucogenesis and use of lactate, thereby maintaining blood lactate levels within the normal range.

CONCLUSIONS During prolonged spine surgery 8 h, VA was

associated with higher serum lactate, when compared with propofol infusion.

However, the exact mechanisms of our findings cannot be ascertained, and prospective studies are needed to elucidate the physiology of lactate production and elimination, and the role of propofol as a nutrient during anesthesia of long duration.

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