A sedative-hypnotic. Useful for induction. Reduces cerebral metabolism, CBF and ICP. Has been described for cerebral protection and for sedation. Short half-life permits rapid awakening which may be useful for awake craniotomy. Not analgesic.
The exact mechanism of action unknown. Short half-life with no active metabolites. May be used for induction and as a continuous infusion during total intravenous anesthesia (TIVA). It causes a dose-dependent decrease in mean arterial blood pressure (MAP) and ICP.
It is more rapidly cleared than and has largely replaced thiopental.
Dexmedetomidine (Precedex®). Alpha 2 adrenergic receptor agonist, used for control of hypertension postoperatively, as well as for its sedating qualities during awake craniotomy either alone or in conjunction with propofol.
Propofol (INN, marketed as Diprivan by Fresenius Kabi) is a short-acting, intravenously administered hypnotic/amnestic agent. Its uses include the induction and maintenance of general anesthesia, sedation for mechanically ventilated adults, and procedural sedation. Propofol is also commonly used in veterinary medicine. It is approved for use in more than 50 countries, and generic versions are available.
Chemically, propofol is not related to barbiturates and has largely replaced sodium thiopental (Pentothal) for induction of anesthesia because recovery from propofol is more rapid and “clear” when compared with thiopental. Propofol is not considered an analgesic, so opioids such as fentanyl may be combined with propofol to alleviate pain.
Propofol has been referred to as milk of amnesia (a play on words of milk of magnesia), because of the milk-like appearance of its intravenous preparation.
It is on the World Health Organization's List of Essential Medicines, the most important medications needed in a health system.
Level II: propofol may control ICP after several hours of dosing, but it does not improve mortality or 6 month outcome. ✖ Caution: high-dose propofol (total dose > 100 mg/kg for > 48 hrs) can cause significant morbidity (see propofol infusion syndrome).
℞: 0.5 mg/kg test dose, then 20–75 mcg/kg/min infusion. Increase by 5–10 mcg/kg/min q 5–10 minutes PRN ICP control (do not exceed 83 mcg/kg/min = 5 mg/kg/hr).
Side effects include propofol infusion syndrome. Use with caution at doses > 5 mg/kg/hr or at any dose for > 48 hrs.
Propofol, an established hypnotic anesthetic agent, has been shown to ameliorate neuronal injury when given after injury in a number of experimental brain studies. We tested the hypothesis that propofol pretreatment confers neuroprotection against SBI and will reduce cerebral edema formation and neurobehavioral deficits in our rat population. Sprague-Dawley rats were treated with low- and high-dose propofol 30 min before SBI. At 24 h post injury, brain water content and neurobehavioral assessment was conducted based on previously established models. In vehicle-treated rats, SBI resulted in significant cerebral edema and higher neurological deficit scores compared with sham-operated rats. Low- or high-dose propofol therapy neither reduced cerebral edema nor improved neurologic function. The results suggest that propofol pretreatment fails to provide neuroprotection in SBI rats. However, it is possible that a SBI model with less magnitude of injury or that propofol re-dosing, given the short-acting pharmacokinetic property of propofol, may be needed to provide definitive conclusions 2).
Malekmohammadi et al. from the Department of Neurosurgery, University of California, Los Angeles, collected local field potentials (LFPs) in 12 awake and anesthetized PD patients undergoing DBS implantation. Spectral power of β (13-35 Hz) and high-frequency oscillations (HFOs: 200-300 Hz) was compared across the pallidum.
Propofol suppressed GPi power by > 20 Hz while increasing power at lower frequencies. A similar power shift was observed in GPe; however, power in the high β range (20-35 Hz) increased with propofol. Before anesthesia both β and HFO activity were significantly greater at the GPi (χ2 = 20.63 and χ2 = 48.81, p < 0.0001). However, during anesthesia, we found no significant difference across the pallidum (χ2 = 0.47, p = 0.79, and χ2 = 4.11, p = 0.12).
GPi and GPe are distinguishable using LFP spectral profiles in the awake condition. Propofol obliterates this spectral differentiation. Therefore, LFP spectra cannot be relied upon in the propofol-anesthetized state for functional mapping during DBS implantation 4).
We analyzed 231 neurosurgery patients. In all patients, propofol was used for standard anesthesia induction. Patient demographics, medical histories, fasting duration, percentage weight loss, baseline blood pressure, and PPV during normal tidal volume breathing and that during forced inspiratory breathing (PPVfi) were recorded. Hemodynamic changes within 10 minutes of intubation were observed. Patients developing hypotension and severe hypotension were determined; lowest mean arterial pressure (MAP) and systolic arterial pressure (SAP) values were recorded, and their differences relative to baseline values were calculated. RESULTS: The incidence of hypotension was 18.6%. Both percentage weight loss and PPVfi were correlated with the changes in MAP and SAP. A PPVfi>14 identified all observed hypotensive episodes with 86% sensitivity and 86.2% specificity, whereas percentage weight loss >1.75% identified all observed hypotensive episodes with 81.4% sensitivity and 70.7% specificity. Furthermore, PPVfi>16.5 identified severe hypotension with 85% sensitivity and 90.5% specificity, whereas percentage weight loss >1.95% identified severe hypotension with 85% sensitivity and 73% specificity. CONCLUSIONS: Percentage weight loss and PPVfi are good predictors of hypotension after anesthesia induction and, thus, may allow anesthesiologists to adopt preventative measures and ensure safer anesthesia induction 5).