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PubMed1998

Role of propofol in refractory status epilepticus.

OBJECTIVE: To provide a review of the proposed mechanism of action, clinical efficacy, adverse effects, and therapeutic considerations associated with the use of propofol in the management of patients with refractory status epilepticus. DATA SOURCES: A MEDLINE database (January 1966-April 1998) was searched for literature pertaining to status epilepticus and propofol. Additional literature was obtained from the references of selected articles identified in the search. Information from all articles published in English was considered for inclusion in the article. DATA SYNTHESIS: Propofol is a unique, nonbarbiturate, anesthetic agent possessing anticonvulsant properties, although the exact anticonvulsant mechanism is unknown. Several case reports and two small, open, uncontrolled studies have described the efficacy of propofol in refractory status epilepticus. Most of these clinical reports discuss the utility of propofol after traditional treatment regimens have failed or are not tolerated. Initiation of propofol usually resulted in termination of seizure activity and/or electroencephalographic burst suppression within seconds that was sustained during the drug's use. Additionally, propofol was well tolerated. Advantages of propofol compared with traditional barbiturate anesthetic agents include better cardiovascular tolerability and a more favorable pharmacokinetic profile, allowing for rapid assessment of efficacy and neurologic assessment upon drug withdrawal. Propofol has been associated with a variety of neuroexcitatory adverse events such as opisthotonos, muscle rigidity, and choreoathetoid movements. Additionally, although the data are inconclusive, propofol has also been reported to cause seizures. CONCLUSIONS: Propofol has shown promising results in the management of refractory status epilepticus when traditional therapies have failed or were not tolerated; however, controlled clinical trials are needed to better assess the comparative efficacy, neurologic adverse effects, and clinical outcome to better define its role in refractory status epilepticus.

Anticonvulsants↗

PubMed2001

Propofol vs midazolam for ICU sedation : a Canadian multicenter randomized trial.

STUDY OBJECTIVES: To determine whether sedation with propofol would lead to shorter times to tracheal extubation and ICU length of stay than sedation with midazolam. DESIGN: Multicenter, randomized, open label. SETTING: Four academic tertiary-care ICUs in Canada. PATIENTS: Critically ill patients requiring continuous sedation while receiving mechanical ventilation. INTERVENTIONS: Random allocation by predicted requirement for mechanical ventilation (short sedation stratum, < 24 h; medium sedation stratum, > or = 24 and < 72 h; and long sedation stratum, > or = 72 h) to sedation regimens utilizing propofol or midazolam. MEASUREMENTS AND RESULTS: Using an intention-to-treat analysis, patients randomized to receive propofol in the short sedation stratum (propofol, 21 patients; midazolam, 26 patients) and the long sedation stratum (propofol, 4 patients; midazolam, 10 patients) were extubated earlier (short sedation stratum: propofol, 5.6 h; midazolam, 11.9 h; long sedation stratum: propofol, 8.4 h; midazolam, 46.8 h; p < 0.05). Pooled results showed that patients treated with propofol (n = 46) were extubated earlier than those treated with midazolam (n = 53) (6.7 vs 24.7 h, respectively; p < 0.05) following discontinuation of the sedation but were not discharged from ICU earlier (94.0 vs 63.7 h, respectively; p = 0.26). Propofol-treated patients spent a larger percentage of time at the target Ramsay sedation level than midazolam-treated patients (60.2% vs 44.0%, respectively; p < 0.05). Using a treatment-received analysis, propofol sedation either did not differ from midazolam sedation in time to tracheal extubation or ICU discharge (sedation duration, < 24 h) or was associated with earlier tracheal extubation but longer time to ICU discharge (sedation duration, > or = 24 h, < 72 h, or > or = 72 h). CONCLUSIONS: The use of propofol sedation allowed for more rapid tracheal extubation than when midazolam sedation was employed. This did not result in earlier ICU discharge.

Aged↗

PubMed2000

Prospective evaluation of propofol anesthesia in the pediatric intensive care unit for elective oncology procedures in ambulatory and hospitalized children.

OBJECTIVES: To evaluate our experience with propofol anesthesia delivered by pediatric intensivists in the pediatric intensive care unit (PICU) to facilitate elective oncology procedures in children performed by pediatric oncologists. METHODS: Elective oncology procedures performed with propofol anesthesia in our multidisciplinary, university-affiliated PICU were prospectively evaluated over a 7-month period. Ambulatory and hospitalized children were prescheduled for their procedure, underwent a medical evaluation, and met fasting requirements before the start of anesthesia. Continuous cardiorespiratory and neurologic monitoring was performed by a pediatric intensivist and a PICU nurse, while the procedure was performed by a pediatric oncologist. Propofol was delivered in intermittent boluses to achieve the desired level of anesthesia. Information studied included patient demographics, procedures performed, induction and total doses of propofol used, the duration of the different phases of the patient's PICU stay, the occurrence of side effects, the need for therapeutic interventions, and the incidence of recall of the procedure. RESULTS: Fifty procedures in 28 children (mean age: 7.5 +/- 4.3 years) were evaluated. Sixty-one percent of patients had established diagnoses. Fifty-four percent of procedures were lumbar puncture with intrathecal chemotherapy administration and 26% of procedures were bone marrow aspirations with biopsy. Induction propofol doses were 2. 0 +/-.8 mg/kg for ambulatory and hospitalized patients, while total propofol doses were 6.6 +/- 2.3 mg/kg and 7.9 +/- 2.4 mg/kg for ambulatory and hospitalized patients, respectively. Induction time was 1.5 +/-.7 minutes, recovery time was 23.4 +/- 11.5 minutes, and total PICU time was 88.8 +/- 27.7 minutes. Transient decreases in systolic blood pressure less than the fifth percentile for age occurred in 64% of procedures, with a mean decrease of 25% +/- 10%. Intravenous fluids were administered in 31% of these cases. Hypotension was more common in ambulatory patients but was not predicted by propofol dose, anesthesia time, or age. Partial airway obstruction was noted in 12% of procedures while apnea requiring bag-valve-mask ventilation occurred in 2% of procedures. Neither was associated with age, propofol dose, or the duration of anesthesia. All procedures were successfully completed and there were no incidences of recall of the procedure. CONCLUSIONS: Propofol anesthesia is effective in achieving patient comfort and amnesia, while optimizing conditions for elective oncology procedures in children. Although transient hypotension and respiratory depression may occur, propofol anesthesia seems to be safe to use for these procedures in the PICU setting. Recovery from anesthesia was rapid and total stay was brief. Under the proper conditions, propofol anesthesia delivered by pediatric intensivists in the PICU is a reasonable option available to facilitate invasive oncology procedures in children.

Adolescent↗

PubMed2006

Influence of atropine on the dose requirements of propofol in humans.

OBJECTIVE: The purpose of this study was to evaluate the effect of atropine on the dose requirement of propofol for induction of anesthesia and propofol concentrations during continuous infusion. METHODS: Study 1: Forty patients were randomly allocated to the control or atropine groups. Induction of anesthesia commenced 3 min following the administration of 0.9% saline or atropine (0.01 mg kg(-1)), using a Diprifuser set to achieve propofol concentration of 6.0 microg mL(-1). The primary end point was the propofol dose per kg at the moment of loss of response to a command. Study 2: Fifteen patients undergoing elective surgery were enrolled. Propofol was administered to all subjects via target-controlled infusion to achieve a propofol concentration at 2.0 microg mL(-1) after intubation. Before and after administration of atropine (0.01 mg kg(-1)), cardiac output (CO) was measured using indocyanine green as an indicator and blood propofol concentration was determined using high-performance liquid chromatography. RESULTS: Study 1: The propofol dose for each group was 2.22+/-0.21 mg kg(-1) for control group and 2.45+/-0.28 mg kg(-1) for atropine, respectively (p=0.014). Study 2: After the administration of atropine, CO was significantly increased from 4.28+/-0.83 to 5.76+/-1.55 l min(-1) (p<0.0001). Propofol concentration was significantly decreased from 2.12+/-0.28 to 1.69+/-0.27 microg mL(-1) (p<0.0001). CONCLUSIONS: Following the administration of atropine, the propofol requirements for the induction of anesthesia were increased and propofol concentrations were decreased during continuous infusion by the administration of atropine.

Adult↗

PubMed1995

Propofol. An update of its use in anaesthesia and conscious sedation.

Propofol is an intravenous sedative hypnotic agent which rapidly and reliably causes loss of consciousness. It is also associated with a quick and 'smooth' recovery, which distinguishes it from many of the more traditional anaesthetic regimens. Like other intravenous agents, propofol is both a cardiovascular and a respiratory depressant; however, the risk of these effects can be lessened by appropriate dosage adjustment or patient management. Anaphylaxis with propofol is rare. Propofol anaesthesia in day case surgery is consistently associated with a quicker early recovery than other intravenous agents and the more traditional anaesthetic regimens. Savings in time to discharge were more variable compared with these regimens, although propofol was commonly associated with less post-operative nausea and vomiting in this period. In the future, the relative benefits of propofol compared with the newer volatile agents (desflurane and sevoflurane) and propofol/volatile agent combinations need to be examined in this clinical setting. There is now clinical experience with propofol in major surgical procedures including cardiac and neurosurgery. Propofol has also been investigated as a sedative accompanying regional or local anaesthesia for diagnostic and therapeutic procedures, and in other clinical settings (ophthalmic surgery, cardioversion and electroconvulsive therapy). The unique antiemetic, antiepileptic and antipruritic effects of propofol may further broaden its appeal. As a result of its favourable recovery profile, propofol holds a central place in day case surgery anaesthesia. Accumulating clinical experience in cardiac and neurosurgery suggests that the full potential of propofol has yet to be realised.

Anesthetics↗

PubMed2004

Propofol: therapeutic indications and side-effects.

Propofol (2, 6-diisopropylphenol) is a potent intravenous hypnotic agent which is widely used for the induction and maintenance of anesthesia and for sedation in the intensive care unit. Propofol is an oil at room temperature and insoluble in aqueous solution. Present formulations consists of 1% or 2% (w/v) propofol, 10% soybean oil, 2.25% glycerol, and 1.2% egg phosphatide. Disodium edetate (EDTA) or metabisulfite is added to retard bacterial and fungal growth. Propofol is a global central nervous system depressant. It directly activates GABA(A) receptors. In addition, propofol inhibits the NMDA receptor and modulates calcium influx through slow calcium ion channels. Propofol has a rapid onset of action with a dose-related hypnotic effect. Recovery is rapid even after prolonged use. Propofol decreases cerebral oxygen consumption, reduces intracranial pressure and has potent anti-convulsant properties. It is a potent antioxidant, has anti-inflammatory properties and is a bronchodilator. As a consequence of these properties propofol is being increasingly used in the management of traumatic head injury, status epilepticus, delirium tremens, status asthmaticus and in critically ill septic patients. Propofol has a remarkable safety profile. Dose dependent hypotension is the commonest complication; particularly in volume depleted patients. Hypertriglyceridemia and pancreatitis are uncommon complications. Allergic complications, which may include bronchospasm, have been reported with the formulation containing metabisulfite. In addition, this formulation has been demonstrated to result in the generation of oxygen free radicals. High dose propofol infusions have been associated with the "propofol syndrome"; this is a potentially fatal complication characterized by severe metabolic acidosis and circulatory collapse. This is a rare complication first reported in pediatric patients and believed to be due to decreased transmembrane electrical potential and alteration of electron transport across the inner mitochondrial membrane.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2026

Intravenous lidocaine reduces the propofol EC50 for loss of consciousness and intraoperative anesthetic consumption in gynecological laparoscopy: A randomized controlled trial.

BACKGROUND: Intravenous lidocaine reduces propofol requirements and procedure-related adverse events. OBJECTIVES: The study aimed to test whether intravenous lidocaine would reduce the effect-site concentration of propofol required to achieve loss of consciousness and decrease propofol consumption during total intravenous anesthesia in gynecological laparoscopy. METHODS: This was a prospective, randomized, double-blind, placebo-controlled trial. Sixty patients were randomly allocated to receive either intravenous lidocaine (1.5 mg·kg-¹ bolus) followed by continuous infusion or an equal volume of saline. Propofol was administered via target-controlled infusion starting at an effect-site concentration of 3.5 μg/mL. The concentration was then adjusted in steps of 0.5 μg/mLaccording to Dixon's up-and-down sequential method: decreased if loss of consciousness was achieved, or increased if not. Loss of consciousness was defined as loss of response to verbal commands. The median effective concentration (EC50) of propofol for inducing loss of consciousness was calculated using the Dixon's up-and-down method. General anesthesia was maintained with propofol and remifentanil, guided by state entropy (target 40-60) and surgical pleth index (target 20-50). Drug consumption was normalized to anesthesia duration and body weight. RESULTS: The estimated EC50 of propofol for inducing loss of consciousness was significantly lower in the lidocaine group than in the saline group (3.32 μg/mL, 95% Confidence Interval (CI): 3.04-3.59 vs. 3.89 μg/mL, 95% CI: 3.50-4.28). Under the study protocol, the lidocaine group also required less propofol (8.62 mg·kg-1·h-1, 95% CI: 8.10-9.15 vs. 9.89 mg·kg-1·h-1, 95% CI: 9.05-10.73) and less remifentanil (0.23 μg·kg-1·min-1, 95% CI: 0.21-0.24 vs. 0.27 μg·kg-1·min-1, 95% CI: 0.24-0.30) compared with the saline group. CONCLUSION: Intravenous lidocaine reduced the propofol EC50 for Loss of Consciousness (LOC) and decreased intraoperative propofol and remifentanil consumptions in patients undergoing gynecological laparoscopy. These findings suggest a propofol- and opioid-sparing effect of intravenous lidocaine in this setting, although confirmation in larger multicenter trials is needed.

Humans↗

PubMed2000

Evaluation of isoflurane and propofol anesthesia for intraabdominal transmitter placement in nesting female canvasback ducks.

Heart rate, occurrence of apnea, body temperature, quality of anesthesia and nest abandonment were compared during either propofol or isoflurane anesthesia of nesting female canvasback ducks (Aythya valisineria) at 15 to 18 days of incubation. One hundred eighteen canvasbacks were assigned randomly to three treatments so that nest abandonment could be compared among treatments from May to July 1995 and 1996. Sterile dummy silicone implants were placed during an abdominal laparotomy while ducks were anesthetized with either propofol or isoflurane, or ducks were flushed from the nest but not captured (control). Propofol was delivered through an intravenous catheter, while isoflurane was delivered in oxygen. Propofol provided smooth, rapid induction and recovery, whereas ducks recovering from isoflurane tended to struggle. At the nest, ducks in the propofol group were given additional boluses until they were lightly anesthetized, whereas birds that received isoflurane were released. All birds survived surgery but one death occurred prior to surgery in 1995 using propofol during a period without ventilation and monitoring. Adequate artificial ventilation is recommended to prevent complications. Heart rate declined significantly in both years during isoflurane anesthesia and in 1995 during propofol anesthesia but not 1996. During both isoflurane and propofol anesthesia, body temperature declined significantly over time. Nest abandonment was significantly different among treatments and occurred in all treatment groups in both years, but propofol (15%) and control groups (8%) had lower than expected abandonment compared to isoflurane (28%). Propofol offers several advantages over isoflurane for field use; equipment is easily portable, lower anesthetic cost, and ambient temperature does not alter physical characteristics of the drug. Advantages over isoflurane, including lower nest abandonment following intraabdominal radio transmitter placement, make propofol a good anesthetic choice for field studies.

Analysis of Variance↗

PubMed1999

The dose effect of propofol on cerebrovascular reactivity to carbon dioxide in rabbits.

BACKGROUND: Propofol has several properties beneficial to intracranial operation such as reduction in cerebral metabolic rate and cerebral blood flow (CBF) in a dose-dependent manner while leaving autoregulation intact. Several studies have demonstrated that the responsiveness of CBF to changes in arterial carbon dioxide tension (PaCO2) is maintained during propofol anesthesia in both humans and animals. These studies showed a significant difference in the CBF-CO2 reactivity slope between awake and propofol anaesthetized groups, but no comparison with different doses of propofol was made. To determine the dose effect of propofol on cerebrovascular CO2 reactivity, we used laser Doppler flowmetry (LDF) to detect the changes of CBF during propofol anesthesia. METHODS: Ten rabbits were studied using LDF on the parietal cortex. After surgical preparation, anesthesia was maintained with 66% N2O in O2, morphine 10 mg/kg and pancuronium. Three experimental conditions were studied sequentially with intravenous administration of the following drugs: (1) normal saline (control), (2) propofol 20 mg/kg/h i.v., (3) propofol 40 mg/kg/h i.v. Mean arterial pressure, rectal temperature and hematocrit were kept constant. The arterial carbon dioxide tension (PaCO2) was adjusted to three levels during each condition: 20-25 mmHg (hypocapnia), 35-40 mmHg (normocapnia) and 45-50 mmHg (hypercapnia). CBF was measured continuously and recorded after the target PaCO2 had been reached. RESULTS: There were no differences among all conditions in mean arterial pressure and heart rate. The changes of CBF as PaCO2 increased at the three different CO2 levels during each of the conditions were significantly different. The slope of CBF-CO2 reactivity among three different propofol doses was not significantly different. CONCLUSIONS: These data indicate that cerebral vasomotor responsiveness to CO2 during propofol anesthesia is preserved and that the slope of CBF-CO2 reactivity is independent of propofol doses as mean arterial blood pressure is maintained.

Anesthetics, Intravenous↗

PubMed2001

Hyperintense signal abnormality in subarachnoid spaces and basal cisterns on MR images of children anesthetized with propofol: new fluid-attenuated inversion recovery finding.

BACKGROUND AND PURPOSE: MR imaging is the method of choice for pediatric neuroimaging. Sedation is often needed to suppress patient motion and ensure diagnostic image quality, and propofol is rapidly becoming the preferred anesthetic. The purpose of this study was to document a new finding on fast fluid-attenuated inversion recovery (fast-FLAIR) MR images of children anesthetized with propofol that can be mistaken for subarachnoid space pathologic abnormality. METHODS: A retrospective analysis was conducted of 55 MR images of the brain for children who ranged in age from 1 week to 12 years. Forty-two patients received chloral hydrate, and 13 received propofol anesthetic. Multiplanar MR images were studied to detect the presence or absence of hyperintense signal (artifact) in the subarachnoid spaces and basal cisterns. The T1 values and null times of chloral hydrate, propofol, and CSF were determined in vitro at room temperature by using an inversion recovery pulse sequence at 1.5 T. RESULTS: The fast-FLAIR images of all 13 patients who received propofol had hyperintense signal abnormality. For 10 (77%) of 13 patients, this artifact was in the basal cisterns and subarachnoid spaces overlying the brain convexity. For three (23%) of 13 patients, this artifact was in the convexity region only. Two patients underwent follow-up MR imaging with a nonpropofol anesthetic agent, and the artifact resolved. None of the images of the children who received chloral hydrate had this artifact. The T1 value of chloral hydrate was 0.2 s, of propofol was 1.86 s, and of CSF was 2.32 s at room temperature. CONCLUSION: The fast-FLAIR images of children anesthetized with propofol have artifactual hyperintense signal in the basal cisterns and subarachnoid spaces, and this artifact mimics disease of the subarachnoid space. The T1 value of propofol approaches that of CSF. Depending on the chosen null time, there may be incomplete nulling of signal coming from propofol. To account for this observation, other possible causes include increased CSF pulsation in children creating motion artifact, changes in arterial oxygen concentration intrinsic to propofol or related to the supplemental oxygen normally administered, or changes in CSF protein levels related to propofol binding to proteins for uptake into CSF.

Anesthesia↗

PubMedDate not supplied

Influence of blood cell transfusion on the presence of propofol in blood components.

BACKGROUND: Understanding propofol distribution in blood is important for optimizing drug usage during TIVA. We studied changes in the propofol concentration in plasma and formed blood elements separated from blood samples taken before and after transfusion of blood cells to patients during TIVA with propofol. MATERIAL AND METHODS: Twelve patients were studied (ASA I-II). Propofol TIVA was performed at infusion rates of 12-9-6 mg x kg(-1) x h(-1). Fentanyl and pancuronium bromide were administered in fractional doses. After tracheal intubation the lungs were ventilated to normocapnia with oxygen-air mixture (FiO2=0.33). Blood samples for propofol analysis were taken 5 min before and 30 min after blood cell transfusion. At that point the propofol infusion rate was 6 mg x kg(-1) x h(-1). Propofol concentrations were measured by means of HPLC. RESULTS: Blood cell transfusion leads to a change in the propofol level in plasma and formed blood elements. The transfusion process lowers the ratio of the plasma propofol concentration to the propofol concentration in formed blood elements. CONCLUSIONS: Formed blood elements show a greater ability to bind propofol after transfusion of 5-15 day erythrocytes.

Adult↗

PubMed2003

[The influences of propofol on different kinds of brain injuries in rat brain slices].

OBJECTIVE: To investigate the effects of propofol on the three kinds of brain injuries induced by metabolic disorder, neurotoxicity of excitatory amino acid, and oxygen-derived free radicals in rat cerebral cortical and hippocampal slices. METHODS: Slices of rat cerebral cortex and hippocampus were made and incubated in normal artificial cerebrospinal fluid (nACSF). Then the rat cerebral cortical and hippocampal slices were divided into 2 categories: propofol group, the slices in which were co-incubated with 5, 50, or 100 micro mol/L propofol for 3 hours, and 3 experimental injury groups. Each experimental injury group was further subdivided into 3 subgroups including the slices of 4 rats. Two hours after normal incubation the slices were co-incubated with 2,3,5-triphenyltetrazolium chloride (TTC). Formazan, the red crystal product were extracted, and ELISA reader was used to read the absorbance at 490 nm (A(490)) so as to quantitatively evaluate the degree of injury. RESULTS: The values of A(490) of the slices co-incubated with propofol of different concentrations were not significantly different. Compared with those of the control subgroups, the values A490 were significantly decreased in the cerebral cortical and hippocampus slices damaged by OGD, glutamate, and H(2)O(2) injuries (all P < 0.01). The values of A(490) in the subgroups of low and middle concentrations (5 and 50 micro mol/L) of propofol plus OGD or glutamate injury were not significantly different from those of the subgroups of OGD or glutamate injury alone, both in cerebral cortical and hippocampal slices. However, the values of A(490) in the subgroups of high concentration of propofol (100 micro mol/L) plus OGD or glutamate injury was further decreased (P < 0.01). The values of A(490) in the subgroups of low and middle concentrations of propofol plus H(2)O(2) injury were significantly higher than those of the injury subgroup (all P < 0.01), however, however, the values of A490 in the high concentration propofol plus H(2)O(2) injury subgroup were significantly lower than those of the control group (all P < 0.01), even lower than that of the subgroup of H(2)O(2) injury alone. CONCLUSION: Propofol has a neuroprotective effect against hydrogen peroxide injury at low and middle concentrations. Propofol of low and middle concentrations does not improve the decrease of the value of A(490). however, propofol of high concentration augments the oxygen-glucose deprivation and glutamate injuries both in the rat cerebral cortical slices and hippocampal slices.

Animals↗

PubMed2003

Propofol in paediatric anaesthesia.

PURPOSE OF REVIEW: In this review we intend to ascertain trends in propofol administration for paediatric anaesthesia and sedation. RECENT FINDINGS: Propofol is being 'discovered' by non-anaesthesiologist practitioners of paediatric sedation. However it appears that the drug is not infrequently administered alone for painful procedures, necessitating large doses that result in uncontrolled general anaesthesia with a high potential for adverse events. An elegant technique comprises small doses of short-acting opioid (e.g. fentanyl 1 mug/kg) with low-dose propofol infusion. This does not result in worsening of pre-existing right-to-left intracardiac shunts. The dilemma is to educate non-anaesthesiologists about propofol pharmacokinetics and pharmacodynamics and in particular about the advantages of combined drug therapy. A paediatric target-controlled system for propofol has undergone preliminary clinical evaluation and it is hoped that administration according to pharmacokinetic principles will refine administration to infants and children. Sporadic cases of the propofol infusion syndrome in patients receiving prolonged sedation in intensive care units continue to be reported (characterized by metabolic acidosis, rhabdomyolysis and myocardial failure). It appears that one mechanism may be a deficiency of mitochondrial oxidative processes possibly induced by a dialyzable substance, perhaps a propofol metabolite. Propofol has been used with some success in treating postoperative laryngospasm and for tracheal intubation without muscle relaxants. SUMMARY: Propofol should be used with extreme caution for prolonged sedation in intensive care unit patients, at dose rates of below 5 mg/kg per h, while maintaining extreme vigilance for signs of developing propofol infusion syndrome. If used correctly propofol is a suitable drug for sedation outside the operating room.

Journal Article↗

PubMed2001

A comparison of propofol and ketamine/midazolam for intravenous sedation of children.

OBJECTIVE: To compare ketamine and propofol sedation in children undergoing diagnostic and therapeutic procedures. DESIGN: Retrospective study. SETTING: A six-bed pediatric intensive care unit and a pediatric hematology oncology clinic. PATIENTS: From 1996 to 1998, 405 procedures were performed on patients between 1 month and 22 yrs of age. INTERVENTIONS: All patients but one were sedated intravenously with either propofol or ketamine; those who received ketamine also received midazolam and either atropine or glycopyrrolate. Vital signs were monitored continuously. Procedures included bone marrow biopsies, lumbar punctures, esophagoduodenoscopies, colonoscopies, and other miscellaneous procedures. A pediatric intensivist performed all sedations. MEASUREMENTS AND MAIN RESULTS: Two hundred sixty-one procedures were conducted with propofol and 144 with ketamine. The mean time (+/-sd) from administration of the first dose of medication until the patient was awake was 36.6 (15.0) mins for the propofol group and 69.2 (43.2) mins for the ketamine group. The mean time to awakening was significantly longer for the ketamine group, even after adjusting for the length of the procedure, American Society of Anesthesiologists score, and setting of procedure (inpatient or outpatient; p =.0001). Only one unplanned endotracheal intubation in the propofol group and two in the ketamine group occurred. Patients were significantly more likely to have airway (p =.01) or hemodynamic (p =.002) effects with propofol than with ketamine, although these effects were essentially minor in nature. CONCLUSIONS: Both propofol and ketamine provided safe and effective sedation for the short, painful procedures performed. Because the patients who received propofol awakened almost twice as quickly as the patients who received ketamine, the sedation service operated more efficiently when propofol was used. The major complication rates for propofol and ketamine were small, and the differences between the two groups were not statistically significant. We conclude that with proper monitoring, intravenous propofol can be used safely and effectively for short procedures in the pediatric setting.

Journal Article↗

PubMed2006

The influence of injection rate on the hypnotic effect of propofol during anesthesia: a randomized trial.

OBJECTIVE: Previous studies suggested that slow injection of propofol may increase the hypnotic effect during induction of anesthesia. The aim of the present study was therefore to investigate whether injection rate of propofol has an influence on its maximum effect. DESIGN: Randomized, single-blind trial. SETTING: This study has been carried out in the operating rooms of a university hospital. An anesthesiologist and a resident performed the study with the aid of changing nursing staff. PARTICIPANTS: We investigated 99 unpremedicated patients aged 18 to 60 years with American Society of Anesthesiologists (ASA) physical status 1-3. INTERVENTIONS: Anesthesia was induced by intravenous injection of propofol (2 mg/kg). Propofol was manually injected in group 1 over a period of 5 s; in group 2 (120-s injection interval), and in group 3 (240-s injection interval), propofol was administered by an injection pump. After loss of consciousness, mask ventilation was performed with 100% oxygen. Bispectral index (BIS) was used to measure the hypnotic effect of propofol. After the decrease of BIS to the minimum value (i.e., maximum hypnotic effect) and the following increase of BIS to 60, the study period was finished and anesthesia was performed according to clinical criteria. OUTCOME MEASURES: We analyzed whether injection speed has an influence on the maximum hypnotic effect of a given dose of propofol (2 mg/kg). RESULTS: BIS(min) marks the maximum electroencephalogram (EEG) effect of the propofol bolus as measured by the BIS. The lowest mean BIS(min) was measured in group 1 (28.7 +/- 10.3). In group 2, BIS(min) was 33.0 (+/-13.9), and in group 3, BIS(min) was 36.4 (+/-11.0). There were no significant differences between group 2 and groups 1 or 3, but there were significant differences between groups 1 and 3. In group 1, BIS(min) was reached after 102.91 s (+/-44.20), in group 2 after 172.33 s (+/-29.76), and in group 3 after 274.21 s (+/-45.40). These differences were statistically significant for all comparisons. In summary, the lowest value for BIS(min) was achieved in the group with the fastest rate of propofol injection (group1, 5 s). The highest BIS(min) was obtained in the group with the slowest rate of injection (group 3, 240 s). The hemodynamic parameters were not significantly different among groups. CONCLUSIONS: The hypnotic peak effect of propofol is lower with extremely slow injection (240 s versus 5 s). For clinically usual injection rates (5 s and 120 s), there was no significant difference in propofol peak effect.

Journal Article↗

PubMed2001

Effect of dexmedetomidine on propofol requirements in healthy subjects.

Dexmedetomidine-propofol pharmacodynamic interaction was evaluated in nine healthy subjects in a crossover design. Dexmedetomidine/placebo was infused using a computer-controlled infusion pump (CCIP) to maintain a pseudo-steady-state plasma concentration of 0.66 +/- 0.080 or 0 ng/mL, respectively. Forty-five minutes after the dexmedetomidine/placebo infusion was started, propofol was infused using a second CCIP to achieve a stepwise logarithmically ascending propofol concentration (1.00 to 13.8 microg/mL) profile. Each propofol step lasted 10 min. Blood was sampled for plasma concentration determination, and pharmacodynamic endpoint assessments were made during the study. Propofol and dexmedetomidine/placebo infusions were terminated when three endpoints (subjects were too sedated to hold a syringe, followed by loss of eyelash reflex, followed by loss of motor response to electrical stimulation) were achieved sequentially. The concentration of propofol associated with 50% probability of achieving a pharmacodynamic endpoint in the absence of dexmedetomidine (EC50; placebo treatment) was 6.63 microg/mL for motor response to electrical stimulation and ranged from 1.14 to 1.98 microg/mL for the ability to hold a syringe, eyelash reflex, and sedation scores. The apparent EC50 values of propofol (EC50APP; concentration of propofol at which the probability of achieving a pharmacodynamic endpoint is 50% in the presence of dexmedetomidine concentrations observed in the current study; dexmedetomidine treatment) were 0.273, 0.544-0.643, and 3.89 microg/mL for the ability to hold a syringe, sedation scores, and motor response, respectively. Dexmedetomidine reduced propofol concentrations required for sedation and suppression of motor response. Therefore, the propofol dose required for sedation and induction of anesthesia may have to be reduced in the presence of dexmedetomidine.

Adolescent↗

PubMed1993

Propofol emulsion reduces proliferative responses of lymphocytes from intensive care patients.

OBJECTIVE: To test propofol lipid emulsion formulation for its immunosuppressive effects. DESIGN: Propofol lipid emulsion and the emulsion alone were tested at increasing concentrations and compared to initial values and between each other. Propofol alone could not be tested due to its insolubility into the culture medium. PATIENTS AND PARTICIPANTS: Lymphocytes from 12 surgical intensive care (ICU) patients (median APACHE score 16 and median TISS score 28) and 12 healthy volunteers. MEASUREMENTS: Phytohaemagglutinin-, concanavalin A- and pokeweed mitogen-induced lymphocyte proliferative responses were measured in the presence of increasing concentrations of propofol lipid emulsion formulation or the lipid emulsion. RESULTS: Lymphocyte proliferative responses from ICU patients were in general on a lower level than in the volunteers. The propofol lipid emulsion formulation (Diprivan) decreased pokeweed mitogen-induced proliferative responses of lymphocytes from ICU patients at propofol concentrations found in the circulation (1-10 micrograms/ml) and the lipid emulsion alon at 100 micrograms/ml triglyceride concentrations while the other mitogen-induced responses were not affected. No changes were observed in the mitogen-induced responses of lymphocytes from healthy volunteers. CONCLUSIONS: Propofol emulsion formulation decreased in surgical intensive care patients pokeweed mitogen-induced lymphocytic responses in vitro at clinically found concentrations, indicating the need for further studies to test B-lymphocyte functions and T-B-lymphocyte co-operation during propofol lipid emulsion administration. (ICU) patients is widespread because of its good control of sedation. Propofol is currently administered in fat emulsion which is considered immunosuppressive during bolus injection or rapid infusion. Therefore, effects of a propofol fat emulsion formulation on proliferative responses of lymphocytes were studied in blood samples obtained from healthy volunteers and ICU patients known to be immunosuppressed.

Adolescent↗

PubMed1993

Action of propofol on central sympathetic mechanisms controlling blood pressure.

This study was done using Wistar rats to determine if the actions of propofol (22 +/- 1, 40 +/- 2, 64 +/- 3 and 103 +/- 3 mg.kg-1 x hr-1) decreased blood pressure and heart rate through depression of brain stem vasomotor centres. All rats were given atropine to block vagal influences on the heart. Propofol decreased renal nerve activity as well as blood pressure and heart rate in a dose-dependent manner. Infusion of the lowest dose of propofol (22 +/- 1 mg.kg-1 x hr-1) had no effect on blood pressure, heart rate and renal nerve activity. Infusion of propofol at 40 +/- 2 mg.kg-1 x hr-1 decreased renal activity by 22 +/- 4% (mean +/- SEM) and at 64 +/- 3 mg.kg-1 x hr-1 it decreased renal nerve activity by 36 +/- 6%. Finally, infusion of the largest dose of propofol (102 +/- 3 mg.kg-1 x hr-1) decreased nerve activity by 50 +/- 5%. The haemodynamic changes observed in our experiments during the infusion propofol paralleled the changes in sympathetic firing, suggesting that hypotension was caused by central actions of propofol to depress sympathetic firing. In experiments with bolus injections of propofol, the renal nerve activity returned to normal before arterial pressure and heart rate recovered. Because decreases in blood pressure and heart rate were longer-lasting than changes in renal nerve activity, a part of the vasodepression and bradycardia caused by propofol likely resulted from direct actions on blood vessels and the heart. Sympathetic and cardiovascular responses to blocking neurons in the ventrolateral medulla with microinjection of glycine were depressed by propofol.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗