With the advancement of medical technology, there are increasing opportunities for new-borns, infants, and pregnant women to be exposed to general anaesthesia. Propofol is commonly used for the induction of anaesthesia, maintenance of general intravenous anaesthesia and sedation of intensive-care children. Many previous studies have found that propofol has organ-protective effects, but growing evidence suggests that propofol interferes with brain development, affecting learning and cognitive function. The purpose of this review is to summarize the latest progress in understanding the neurotoxicity of propofol. Evidence from case studies and clinical studies suggests that propofol has neurotoxicity on the developing brain. We classify the findings on propofol-induced neurotoxicity based on its damage mechanism. We end by summarizing the current protective strategies against propofol neurotoxicity. Fully understanding the neurotoxic mechanisms of propofol can help us use it at a reasonable dosage, reduce its side effects, and increase patient safety.

A 9-year-old African-American girl presented with sudden cardiac arrest a few hours after adenotonsillectomy. She received anaesthesia which included propofol during the procedure. Her electrocardiogram (EKG) showed type 1 Brugada pattern, and genetic testing revealed a variant of unknown significance in desmoplakin (DSP) gene. We discuss the association between propofol, Brugada EKG pattern, and malignant ventricular arrhythmias.

Propofol is a intravenous anaesthetic most commonly used in ultrasound oocyte retrieval. We studied if the use of propofol had an effect on mouse oocyte maturation, pregnancy, childbirth and progeny and investigated the correlation between propofol side effects and reproductive performance in mice. There was no statistical difference in mating, pregnancy, childbirth, litter size, the number of stillbirths and survival between each group (P>0.05). Propofol also had no effect on polar body extrusion in oocyte maturation as well as on pronucleus formation and, subsequently, early embryo development (P>0.05). An increased concentration of propofol had no effect on this result, although propofol at more than 0.01 mg/ml reduced polar body extrusion. Different concentrations of propofol had no effect on oocyte culture in vitro, pronucleus formation and early embryo development.

Introduction: An evidence-based care protocol to treat migraine with low-dose Propofol was implemented in May 2014 at the emergency department (ED) of the CHUL (Québec city). Given potential side effects of Propofol, we aimed to evaluate the safety and effectiveness of this protocol. Methods: We reviewed charts of all patients aged 16 years and older who received Propofol between May 2014 and August 2017 for a migraine headache with or without aura, as defined in the International Headache Society Classification. The care protocol consisted of: 1) administration of intra-venous Propofol 20 mg each 5 to 10 minutes as needed (maximum of 6 doses); 2) sets of vital signs before and after each dose; and 3) continuous cardiac and saturation monitoring. Our primary outcome measures were the incidence (95%CI) of the following side effects: low arterial pressure (< 90 systolic or < 65 mean), desaturation (SaO2<92%), excessive sedation (scores 3 or 4 on the Pasero scale), and any arrhythmia. We also compared the mean reduction (95%CI) of pain pre- and post-treatment (visual analogous scale VAS 0-10) and the proportion (95%CI) of rescue medication among patients who received Propofol as first-line medication to a matched cohort of patients who had Metoclopramide first. The two cohorts were paired for gender, age, triage priority, and month/year of ED visit. Results: Over the 3-year study period, 45 patients with migraine received Propofol through the care protocol, either as a first-line or a rescue therapy. In this cohort, hypotension, bradycardia (<60/min) and desaturation occurred in 17.8% (8.0-32.1), 13.3% (5.1-26.8) and 6.7% (1.4-18.3) of cases respectively; no excessive sedation was reported. An intervention was undertaken in 4 cases [8.9% (2.5-21.2) 3 iv fluid bolus, 1 supplemental oxygen] to palliate the side effects of Propofol. A statistically significant mean reduction of 3.6 points (2.8-4.4) on the VAS scale was observed in patients treated with Propofol as first-line therapy (n=35). However, patients managed with first-line Metoclopramide (n=100) experienced a significantly higher mean reduction of their VAS score [5.3 (4.6-6.0)] than the Propofol group (p=0.003). The proportion of patients requiring the use of rescue medication was higher among patients first treated with Propofol [77.1% (63.2-91.1) vs. 29.0% (20.1-37.9); p<0.001]. Conclusion: Our care protocol to treat migraine with low doses of Propofol appears to be safe and to cause very few side effects prompting corrective interventions. Continuous (as opposed to intermittent) heart and saturation monitoring is probably not indicated. Given the effectiveness of Propofol compared to Metoclopramide, our care protocol will be used as a second-line therapy.

Background: Intraoperative sedation is often used to facilitate deep brain stimulation (DBS) surgery; however, these sedative agents also suppress microelectrode recordings (MER). To date, there have been no studies that have examined the effects of differing sedatives on surgical outcomes and the success of DBS surgery. Methods: We performed a retrospective study to evaluate the effect of differing sedative agents on postoperative surgical outcomes at 6 months in parkinsonian adult patients who underwent DBS surgery, from January 2004 through December 2014, at one academic center. Surgical outcomes of DBS were evaluated using a simplified Unified Parkinson Diseases Rating Score-III and levodopa dose equivalent reduction at baseline and 6 months postoperatively. Results: We analyzed data from 121 of 124 consecutive parkinsonian patients. Propofol, dexmedetomidine, remifentanil, and midazolam were used individually or in combination. All sedatives were routinely discontinued 20 to 30 minutes before MER, in accordance with our institutional protocol. We found no statistically significant association between the use of individual agent or combination of sedative agents and surgical outcomes at 6 months, the success of DBS, duration of MER, duration of stage 1 procedure, and perioperative complications. Conclusions: Our study showed that the choice of sedative agent was not associated with poor surgical outcomes after DBS surgery using MER and macrostimulation techniques in parkinsonian patients.

The influence of propofol on mood was evaluated, considering the potential use of propofol as an anesthetic for electroconvulsive therapy. The mood state of 80 psychologically healthy subjects was assessed before and from 1/2 hour till 4 hours after surgery under anesthesia with either propofol or methohexitone. The mood was assessed with the Profile of Mood States (POMS). The propofol group was more elated from one hour until 4 hours after anesthesia (p<0,01 )(factor 1). 1 hour after anesthesia the propofol group was continuously more composed than the methohexitone group (p<0,01) (factor 4) and after two hours the propofol group was more agreeable (p<0,05) (factor 2). Moreover, patients, who received propofol, were less tired (factor 3) and confused (factor 5). It can be concluded that, compared with methohexitone, propofol has a favorable influence on different aspects of mood.

Background: Children with pulmonary hypertension routinely undergo pulmonary vascular resistance studies to assess the disease severity and vasodilator responsiveness. It is vital that results are accurate and reliable and are not influenced by the choice of anaesthetic agent. However, there are anecdotal data to suggest that propofol and inhalational agents have different effects on pulmonary vascular resistance. Methods: A total of 10 children with pulmonary hypertension were selected sequentially to be included in the study. To avoid confounding because of baseline anatomic or demographic details, a crossover protocol was implemented, using propofol or isoflurane, with time for washout in between each agent and blinding of the interventionalist. Results: Pulmonary and systemic vascular resistance were not significantly different when using propofol or isoflurane. However, the calculated resistance fraction – ratio of pulmonary resistance to systemic resistance – was significantly lower when using propofol than when using isoflurane. Conclusions: Although no difference in pulmonary vascular resistance was demonstrated, this pilot study suggests that the choice of anaesthetic agent may affect the calculation of relative pulmonary and systemic vascular resistance, and provides some preliminary evidence to favour propofol over isoflurane. These findings require replication in a larger study, and thus they should be considered in future calculations to make informed decisions about the management of children with pulmonary hypertension.

Aim: This study aimed to compare the effects of dexmedetomidine–propofol and ketamine–propofol sedation on haemodynamic stability, immobility, and recovery time in children who underwent transcatheter closure of atrial septal defects. Methods: In all, 46 children scheduled for transcatheter closure of atrial septal defects (n = 46) were included. The dexmedetomidine–propofol group (n = 23) received dexmedetomidine (1 μg/kg) and propofol (1 mg/kg) for induction, followed by dexmedetomidine (0.5 μg/kg/hour) and propofol (100 μg/kg/minute) for maintenance. The ketamine–propofol group (n = 23) received ketamine (1 mg/kg) and propofol (1 mg/kg) for induction, followed by ketamine (1 mg/kg) and propofol (100 μg/kg/minute) for maintenance. Results: In all, 11 patients in the dexmedetomidine group (47.8%) and one patient (4.3%) in the ketamine group demonstrated a decrease ≥20% from the baseline in mean arterial pressure (p = 0.01). Heart rates decreased ≥20% from the baseline value in 10 patients (43.4%) in the dexmedetomidine group and three patients (13%) in the ketamine group (p = 0.047). Heart rate values were observed to be lower in the dexmedetomidine group throughout the procedure after the first 10 minutes. The number of patients requiring additional propofol was higher in the dexmedetomidine group (p = 0.01). The recovery times were similar in the two groups – 15.86 ± 6.50 minutes in the dexmedetomidine group and 19.65 ± 8.19 minutes in the ketamine group; p = 0.09. Conclusion: The ketamine–propofol combination was less likely to induce haemodynamic instability, with no significant change in recovery times, compared with the dexmedetomidine–propofol combination. The ketamine–propofol combination provided good conditions for the intervention.