Prolonged Propofol Infusions in Pregnant Neurosurgical Patients


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To JNA Readership:There are few descriptions of prolonged propofol use in pregnancy, and we would like to describe our experience of using propofol for prolonged neurosurgery in 2 such patients.AX was a 32-year-old primigravida at 26 weeks gestation with neurofibromatosis II and a vestibular schwannoma increasing in size and causing neurologic deterioration. Preinduction blood gases showed a respiratory alkalosis consistent with pregnancy. Anesthesia lasted 18.5 hours, and consisted of remifentanil 0.1 to 0.35 μg/kg/min and propofol TCI (Target Controlled Infusion) 3 to 5 μg/mL for 11 hours; this was changed to sevoflurane (ET 0.8% to 1.3%) for the remaining 7 hours. This action was taken because the base excess decreased from 0.1 to −6.2 mmol/L, pH decreased from 7.5 to 7.37 with bicarbonate decreasing from 24.9 to 19.4 mmol/L; although not in the “acidotic” range, the comparative difference was significant. Lactate ranged from 1.4 to 3.7 mmol/L and chloride from 103 to 112 mmol/L.1BX was a 21-year-old primigravida who, at 9 weeks gestation presented with a recurrent vestibular schwannoma. Anesthetic time was 14 hours. The technique used was the same as for AX, with sevoflurane (ET 0.4% to 1.4%) being substituted for propofol after 10 hours due to developing acidosis.In both cases, in view of the deteriorating acid-base status, propofol was changed to sevoflurane and, because chloride was also rising, 0.9% saline was changed to Hartmann's (ringers lactate) solution, reducing the chloride infused from 154 to 111 mmol/L. No further increase in acidosis developed after these changes, although it took 24 hours for the base deficits to normalize.In searching for a cause for these patients' metabolic acidosis, it was important to rule out remediable causes; there was no evidence of renal failure, hypoxemia, impaired hepatic lactate metabolism, sepsis, and CO2 was normal. Generous fluids were given to eradicate hypoperfusion as a cause of acidosis. A “massive” blood transfusion can occasionally cause a metabolic acidosis but AX only received 4 units very slowly.To explain the base deficit being caused by propofol we would have expected an “anion gap metabolic acidosis.”2 The anion gap remained within the normal range (8 to 16 mmol/L) at all times. Although the measured parameters go against these being examples of “propofol infusion” syndromes, in future cases we would use a volatile-based technique from the outset.Metabolism and distribution of propofol is altered in the gravid patient (explained in part by the increased volume of distribution and differences in protein binding) and it may be of interest to readers that during AX's anesthetic, with the propofol TCI set at 4.5 μg/mL, serum concentration was measured as 2 μg/mL, and later with the TCI at 1 μg/mL, serum concentration was 0.6 μg/mL. This alteration in metabolism compounds the notorious difficulty in correctly estimating the weight that should be entered into the TCI algorithm in such patients. We found the use of the Bispectral index monitor invaluable in these 2 cases.There is little data on the effect of propofol infusions and the fate of the unborn child. We are happy to report that both mothers gave birth to healthy full-term babies.

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