High-dose Propofol Research Articles

Effects of ketamine and propofol on motor evoked potentials elicited by intracranial microstimulation during deep brain stimulation.

Few preclinical or clinical studies have evaluated the effect of anesthetics on motor evoked potentials (MEPs), either alone or in the presence of conditioning stimuli such as deep brain stimulation (DBS). In this study we evaluated the effects of two commonly used anesthetic agents, propofol and ketamine (KET), on MEPs elicited by intra-cortical microstimulation of the motor cortex in a rodent model with and without DBS of the dentatothalamocortical (DTC) pathway. The effects of propofol anesthesia on MEP amplitudes during DTC DBS were found to be highly dose dependent. Standard, but not high, dose propofol potentiated the facilitatory effects of 30 Hz DTC DBS on MEPs. This facilitation was sustained and phase-dependent indicating that, compared to high dose propofol, standard dose propofol has a beta-band excitatory effect on cortical networks. In contrast, KET anesthetic demonstrated a monotonic relationship with increasing frequencies of stimulation, such that the highest frequency of stimulation resulted in the greatest MEP amplitude. KET also showed phase dependency but less pronounced than standard dose propofol. The results underscore the importance of better understanding the complex effects of anesthetics on cortical networks and exogenous stimuli. Choice of anesthetic agents and dosing may significantly confound or even skew research outcomes, including experimentation in novel DBS indications and paradigms.

Dynamic Repertoire of Intrinsic Brain States Is Reduced in Propofol-Induced Unconsciousness

The richness of conscious experience is thought to scale with the size of the repertoire of causal brain states, and it may be diminished in anesthesia. We estimated the state repertoire from dynamic analysis of intrinsic functional brain networks in conscious sedated and unconscious anesthetized rats. Functional resonance images were obtained from 30-min whole-brain resting-state blood oxygen level-dependent (BOLD) signals at propofol infusion rates of 20 and 40 mg/kg/h, intravenously. Dynamic brain networks were defined at the voxel level by sliding window analysis of regional homogeneity (ReHo) or coincident threshold crossings (CTC) of the BOLD signal acquired in nine sagittal slices. The state repertoire was characterized by the temporal variance of the number of voxels with significant ReHo or positive CTC. From low to high propofol dose, the temporal variances of ReHo and CTC were reduced by 78% ± 20% and 76%± 20%, respectively. Both baseline and propofol-induced reduction of CTC temporal variance increased from lateral to medial position. Group analysis showed a 20% reduction in the number of unique states at the higher propofol dose. Analysis of temporal variance in 12 anatomically defined regions of interest predicted that the largest changes occurred in visual cortex, parietal cortex, and caudate-putamen. The results suggest that the repertoire of large-scale brain states derived from the spatiotemporal dynamics of intrinsic networks is substantially reduced at an anesthetic dose associated with loss of consciousness.

Ketogenic diet therapy is effective in encephalitis with refractory seizures

Objective and importance:Although ketogenic diet therapy is effective in refractory seizures in childhood, its effect on adult encephalitis with similar refractory seizures and prolonged encephalopathy has not been well reported.Clinical presentation:We report here a case of a 22-year-old man with acute encephalitis with refractory repetitive partial seizures (AERRPS).Intervention:Partial seizures of the face developed to repeated generalized convulsions, which were refractory against anti-epileptic drugs and a high dose of propofol. After struggling for 9 months, he dramatically recovered after ketogenic diet therapy.Conclusion:Ketogenic diet therapy may be an important tool to help cure AERRPS.

Use of propofol for short duration procedures in children with long chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) or trifunctional protein (TFP) deficiencies

The medication propofol, commonly used for anesthesia, has been avoided in patients with mitochondrial fatty acid oxidation disorders (FAODs) due to concerns that it contains long-chain fatty acids (LCFAs), and because of reports of severe side effects in some critically ill patients receiving high-dose propofol infusions that mimic some of the symptoms regularly found in FAOD patients. In this secondary analysis, we examined the outcomes of 8 children with long-chain 3-hydroxyacyl CoA dehydrogenase (LCHAD) deficiency or trifunctional protein (TFP) deficiency who were repeatedly sedated for an electroretinogram (ERG) as part of a longitudinal study of the progression of chorioretinopathy commonly found in this population. A total of 39 sedated ERG procedures were completed using propofol for sedation. The propofol dosing, estimated total energy needs of the subject, and inpatient dietary intake recording were completed in 32 of these procedures. The LCFAs in the propofol provided approximately 1.0% of the average total daily energy needs. The sedation with propofol resulted in no adverse side effects and was safely used in this short duration procedure.

Effects of different doses of propofol on traumatic brain injury in rats

Objective To evaluate the effects of different doses of propofol on traumatic brain injury in rats .Methods Forty-eight healthy male Sprague-Dawley rats , aged 7-8 weeks , weighing 270-320 g , were randomly divided into 6 groups （ n=8 each ） using a random number table ：sham operation group （group S ） , traumatic brain injury group （group I） ,fat emulsion group （group F） and low-dose propofol group （group L） , medium-dose propofol group （group M ） ,and high-dose propofol group （group H ） .Traumatic brain injury model was established according to the method described by Feeney .In group S ,0.9% normal saline was infused into the left femoral vein at 3.49 ml·kg-1 ·h-1 .In I ,F ,L ,M and H groups ,0.9% normal saline ,20% fat emulsion 3.49 ml·kg-1 ·h-1 ,and propofol 17.46 ,34.92 and 69.84 mg·kg-1 ·h-1 were infused into the left femoral vein ,respectively .Blood samples were collected from the right common carotid artery at 15 and 60 min of infusion （T1-2 ） for determination of serum S100β protein concentrations . The rats were then sacrificed after collecting blood samples at T2 and brains were removed for microscopic examination of the pathological changes of the cerebral cortex （light microscope ） and ultrastructure of neurons in the cerebral cortex （transmission electron microscope） .Results The serum S100β protein concentrations were significantly higher at T1 ,2 in the other five groups than in group S （ P〈0.05 ） .Compared with I and F groups ,the serum S100βprotein concentrations were＆nbsp;significantly decreased at T1 ,2 in L ,M and H groups （ P〈0.05） .Compared with group L ,the serum S100βprotein concentrations were significantly decreased at T2 in M and H groups , and the serum S100β protein concentrations were increased at T1 in H group （ P〈 0.05 ） . The serum S100β protein concentrations were significantly higher at T1 ,2 in H group than in group M （ P〈0.05 ） .Light microscopic examination showed that nucleus condensation , cell necrosis , and cell edema were significantly attenuated in L ,M , and H groups as compared with group I;normal neurons could be found in group M .Transmission electron microscopic examination showed that the severity of neuronal damage was significantly attenuated in L ,M ,and H groups as compared with group I .Conclusion Different doses of propofol can reduce traumatic brain injury in rats . Key words: Propofol; Brain injuries

Comparison between the effect of propofol and midazolam on picrotoxin-induced convulsions in rat

Propofol is a short acting intravenous anesthetic that has been used in the treatment of status epileptics. However, the occurrence of seizures in epileptic and non-epileptic patients during recovery from propofol induced anesthesia suggests that propofol may have proconvulsant effects. We have previously shown that propofol displays anticonvulsant effects against picrotoxin (PTX) induced seizures during its peak sedative effects. The purpose of the present study was to compare the time course of the effect of intravenous administration of various doses (2.5, 5, and 10mg/kg) of propofol and midazolam on PTX-induced seizures in adult female Sprague–Dawley rats. The latency to onset of clonic seizures induced by intraperitoneal injection of PTX was significantly increased by the highest dose of propofol and all doses of midazolam, suggesting that both agents display anticonvulsant effects. The anticonvulsant effects of propofol (10mg/kg) lasted about 20min and PTX-induced clonic seizures were observed thereafter and peaked within 30min post drug administration. Clonic seizures progressed rapidly to tonic seizures leading to high rate of PTX-induced mortality. In midazolam (10mg/kg) treated rats, clonic seizures were observed 25min after drug administration and the number of rats exhibiting clonic seizures was highest within 40min. However, clonic seizures did not progress into tonic seizures and thus, PTX-induced seizure related mortality was significantly reduced. In conclusion, this study provides further evidence for the anticonvulsant effects of propofol and midazolam against PTX-induced seizures. Furthermore, the data of the current study showed that midazolam was more effective than propofol against PTX-induced tonic seizures.

Successful anesthesia in a patient with a history of cardiac arrest following rocuronium injection.

Successful anesthesia in a patient with a history of cardiac arrest following rocuronium injection.

Effects of Propofol on Electrocardiogram Measures in Mice

We investigated the anesthetic effects of propofol on the electrocardiogram (ECG) in mice. We also compared the effects of isoflurane (2%) inhalation anesthesia, intraperitoneal propofol (50 or 100 mg/kg), and pentobarbital (50 mg/kg) on ECG in mice. Isoflurane inhalation and pentobarbital anesthesia were both associated with an acceptable heart rate (HR) range (ca. 450 - 500 bpm). In contrast, high-dose propofol anesthesia significantly decreased the HR. Importantly, propofol anesthesia led to significantly reduced responses to propranolol, a β-blocker, suggesting that it affects sympathetic tonus and is not suitable for the evaluation of cardiovascular or sympathetic function. Propofol also reduced the response to atropine, indicative of suppression of mouse parasympathetic nerve activity. Our data suggest that propofol anesthesia should not be the first choice for cardiovascular analysis in mice.

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Introduction: Benzodiazepines (BZDs) are commonly used as first-line agents for the management of alcohol withdrawal syndrome (AWS). A subset of withdrawal patients do not respond to treatment despite escalating doses of BZDs. Resistant alcohol withdrawal (RAW) has been defined as the requirement of greater than a benzodiazepine-equivalent of 40 mg of diazepam in one hour for management of AWS. RAW has been associated with a higher incidence of mechanical ventilation and nosocomial pneumonia and a longer intensive care unit stay. Strategies that have been studied to manage RAW include high dose BZDs, dexmedetomidine, ketamine, phenobarbital and propofol. The objective of this study is to characterize the pharmacological management of RAW to help formalize a protocol for the management of these patients. Methods: A retrospective study was completed at a single center in a large, academic medical center. The cohort of patients was identified utilizing ICD-9 codes for severe alcohol withdrawal. Patients were included if they met the criteria for RAW. Data on pharmacologic management were collected for seven days after meeting RAW criteria, including the initial, median and maximum maintenance doses for newly added medications, incidence of specialty consultation and the time to documented resolution of RAW. Results: A total of 447 patients with an ICD-9 code for severe alcohol withdrawal were screened for RAW criteria. One-hundred patients (22.4%) meeting RAW criteria were evaluated. A total of seventeen individual medications and multiple combinations were used for patients meeting RAW criteria, varying from BZDs to antipsychotics for management of agitation. Not surprisingly, BZDs were utilized to treat 100% of patients for AWS and lorazepam was the most commonly was BZD (n = 76). Propofol was the most commonly used adjunct agent (n = 66) after determination of RAW, with a median initial dose of 30 mcg/kg/min and median maintenance dose of 29.55 mcg/kg/min. Dexmedetomidine was utilized in fifteen patients, with a median initial dose of 0.4 mcg/kg/hour and a median maintenance dose of 0.54 mcg/kg/hour. The median maximum maximum dose of dexmedetomidine was 0.7 mcg/kg/hour, which was consistent with the dosing recommendations at our institution. The addition of phenobarbital (n = 9) was considered only with the addition of a toxicology consult. Specialty consultations were obtained in 37 patients and all patients were managed by the critical care team. The median time to resolution of RAW was 7 days. Conclusions: The management of patients meeting RAW criteria indicates that prescribing patterns are quite variable. The introduction of a formalized protocol for the management of RAW patients may be beneficial for streamlined management. Future directions include the comparison of different medications on clinical outcomes.

Ketamine Continuous Infusion for Refractory Status Epilepticus in a Patient With Anticonvulsant Hypersensitivity Syndrome

Refractory status epilepticus (RSE) requires aggressive management with multiple antiepileptic drugs (AEDs) often requiring the initiation of continuous infusions of propofol, midazolam, or pentobarbital to achieve adequate control in addition to intermittent agents. Ketamine has been implicated in several case reports as a successful agent for treating RSE given that it blocks the N-methyl-D-aspartate receptor, which is overexpressed in prolonged status epilepticus. We describe a previously healthy 27-year-old woman who presented with prolonged RSE requiring the initiation of multiple AEDs, including high-dose propofol and midazolam continuous infusions. As a result of hypotension from propofol and inadequate seizure control with midazolam, the patient was successfully transitioned to a pentobarbital infusion in combination with multiple AEDs. Although the patient achieved control of her RSE, her course was complicated by the development of an anticonvulsant hypersensitivity syndrome (AHS) with transaminitis. Limited with the options of AED that could have been used, it was decided to initiate the patient on a continuous ketamine infusion plus midazolam and slowly wean the patient off pentobarbital as well as to avoid further use of phenytoin and phenobarbital. The patient was successfully transitioned off pentobarbital to a ketamine infusion plus midazolam with complete seizure control after several dose escalations. Her AHS and transaminitis resolved on a ketamine infusion for a total of 12 days, and she was successfully discharged from the hospital after 60 days in the ICU. This is the first case report to describe a successful transition to a ketamine infusion in a patient with AHS and transaminitis.

Effects of propofol on renal ischemia/reperfusion injury in rats

Renal ischemia/reperfusion injury (IRI) is a major cause of acute renal failure. The aim of this study was to investigate whether propofol pretreatment in a rat model protects kidney tissue against IRI. Thirty-two Wistar rats were equally divided into four groups: a sham-operated group, untreated renal IRI group, and low-dose (5 mg/kg) and high-dose (10 mg/kg) propofol-treated groups which were treated with propofol prior to the induction of IRI. The rats were subjected to renal ischemia by bilateral clamping of the pedicles for 50 min, followed by reperfusion. The low-dose and high-dose propofol treatment groups were pretreated via femoral vein injection with a propofol suspension prior to the induction of ischemia/reperfusion. The untreated IRI group showed significantly higher serum creatinine (SCr), blood urea nitrogen (BUN), interleukin 6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α), and malondialdehyde (MDA) levels compared with the sham-operated rats. Superoxide dismutase (SOD) levels were significantly reduced following IRI; however, they significantly increased following propofol administration. Bone morphogenetic protein 2 (BMP2) levels were significantly increased in the propofol-treated groups compared with the untreated IRI group. These results suggest that propofol reduces renal oxidative injury and facilitates repair following IRI. Propofol may play a protective role by regulating BMP2 expression in renal IRI.

Deleterious impact of propofol on in vitro fertilization. a prospective randomized trial

Propofol is widely used for anesthesia in oocyte transvaginal aspiration. In vitro studies on animal models have shown that propofol could be deleterious for fertilization and embryo development in a dose- and time-dependent manner. The purpose of this study was to analyse the potential negative effects of propofol on human in vitro fertilization outcomes. Prospective-double blind, randomized trial. 144 patients with more than four metaphase II oocytes retrieved were enrolled in this study and randomly separated. Two protocols of anesthesia were used. Group A: (GA, n=74) received intravenous (IV) propofol 2 mg/kg, midazolam 0.015 mg/kg and fentanyl 1 μg/kg. Group B: (GB, n=74) IV propofol 1.5 mg/kg, midazolam 0.05 mg/kg and fentanyl 1.5 μg/kg. Maintenance of anesthesia was achieved by intermittent IV bolus when required. Quantity of propofol, duration and quality of anesthesia, number of oocytes, embryo quality and pregnancy rate were evaluated. Mean doses of propofol were GA: 0.277 ± 0.080 mg/kg.min and GB: 0.195 ± 0.055 mg/kg.min (p< .01). No significant differences were found among anesthetics parameters, patient age, number of oocytes retrieved, fertilization rate and embryo quality in both groups. A significative difference was found in clinical pregnancy rate between groups (GA: 27.0% vs GB: 43.3%, p < .05). Our findings suggest that the administration of high doses of propofol produces a negative late effect on human embryo development. The use of lower doses of propofol and the consistent lower exposure of the oocytes to the drug, show an improvement in clinical pregnancy rate, maintaining quality of anesthesia and optimal postoperative recovery. According to our results, we postulate that the reduction of propofol could improve the results of in vitro fertilization treatments.

Propofol Infusion Syndrome: A Case Report

Propofol is an ultra-short acting intravenous sedative/hypnotic agent commonly used for sedation in the intensive care unit (ICU) and operating room (OR). Up until recently, no severe systemic side effects were apparent but more recently severe and potentially lethal side effects have been sporadically reported and termed propofol-infusion syndrome (PRIS). Herein we describe a case of a 23 year s old previously healthy male admitted to the ICU secondary to trauma. Due to excessive agitation and failure of other agents, he was sedated on high dose propofol ( > 100 µ g/Kg/min) for several days. Following this he developed rhabdomyolysis, worsening renal failure, hyperkalemia, refractory acidosis, and eventually expired secondary to cardiovascular collapse. PRIS was attributed as the cause of death. Since its introduction in the 1980s propofol has been widely used for sedation in the ICU. PRIS has become an increasingly recognized phenomenon where propofol infusions have been used for prolonged periods of time. It is characterized by progressive rhabdomyolysis, renal failure, hyperkalemia, metabolic acidosis, Brugada-like pattern changes on ECG, cardiovascular collapse and finally death, all characteristics present in our patient. Several important risk factors for this condition exist such as prolonged propofol infusion, young age, head trauma, airway infection, increased catecholamine and glucocorticoid levels and malnutrition. The mechanism of PRIS remains incompletely understood but it is thought to be due to mitochondrial dysfunction with propofol serving to uncouple the respiratory chain; as such treatment involves stopping the medication and supportive care. In the vast majority of patients, propofol is safe with few side effects but given its potential for lethal complications heightened vigilance is required for its continued use. In particular, to minimize the potential for the development of PRIS, dose limitations and daily re-evaluation as to the necessity of its continued use are required. Further, PRIS must be considered when patients develop unexplained organ dysfunction with metabolic acidosis, increased creatinine phosphokinase and hemodynamic instability. Awareness of the early clinical manifestations of PRIS leading to prompt termination of propofol infusion and appropriate supportive care may improve its outcome if it does develop. doi: http://dx.doi.org/10.4021/jmc1269w

Clinical evaluation of propofol as sedative for endotracheal intubation in neonates

To determine the effects of propofol for endotracheal intubation in neonates in daily clinical practice. We prospectively studied the pharmacodynamic effects of intravenous propofol administration in neonates who needed endotracheal intubation at the neonatal intensive care unit. Propofol was used for 62 intubations in neonates with postmenstrual ages ranging from 24+3weeks to 44+5weeks and bodyweights ranging from 520 to 4380g. A 2mg/kg bodyweight propofol starting dose was sufficient in 37% of patients; additional propofol was needed less often on the first postnatal day. The mean amount of propofol used was 3.3 (±1.2) mg/kg. The success rate of intubation depended on the experience of the physician and was related to the total administered amount of propofol. Hypotension occurred in 39% of patients and occurred more often at the first postnatal day. In 15% of procedures, propofol mono therapy was insufficient. This study shows that high doses of propofol are needed to reach effective sedation in neonates for intubation, with hypotension as a side effect in a considerable percentage of patients. Further research in newborn patients needs to identify optimal propofol doses and risk factors for hypotension.

Significance of Feeder-based Evaluation of Brain Arteriovenous Malformations

Background: Functional evaluation of the feeder vessels of the arteriovenous malformations (AVMs) through the super-selective cerebral angiography route reveals which tolerable and intolerable arteries are safe for embolization. Propofol is another agent, in place of amobarbital, for the provocative test. The purpose of this study was to show our experience using high doses of propofol as a reliable and effective drug in the neuroendovascular treatment of AVMs. Patients and Methods: A series of 23 patients with 54 feeder arteries were embolized using neuroendovascular techniques. All patients were embolized under general anesthesia. Preembolization neurological examination was performed following a 20 mg dose of propofol injected through an intra-arterial route following microcatheter placement, in or near the AVM nidus. Results: Among these 54 arteries, 4 vessels developed temporary neurological deficits after propofol injection, which were not occluded. None of the feeder arteries passing the provocative test showed a false tolerable result after embolization. Conclusions: Embolization of cerebral AVMs by means of a feeder provocative test with high-dose propofol has yielded reliable results in this series, in which the feeder artery tolerability allows an increase in the safety of the procedure and reduces complications.

Case Scenario: Hypotonia in Infancy

NFANTS with hypotonia of unknown etiology pose a unique challenge as many of the potential diagnoses have major, often conflicting, anesthetic management implications. The differential diagnosis of hypotonia is long and includes possibilities such as Duchenne muscular dystrophy, central core disease, and multiminicore disease. Intravenous anesthetic techniques are recommended because hyperkalemia or malignant hyperthermia is associated with the use of volatile anesthetics. However, the differential diagnosis of infants with hypotonia also includes mitochondrial disorders. In children with mitochondrial disorders, an intravenous anesthetic technique that includes propofol could lead to metabolic decompensation because propofol alters mitochondrial electron transfer. This dilemma is often encountered when hypotonic infants require anesthesia for diagnostic tests such as magnetic resonance imaging and muscle biopsies for definitive diagnosis.

High-Dose Propofol Reduces S-100β Protein and Neuron-Specific Enolase Levels in Patients Undergoing Cardiac Surgery

In a variety of experimental models, propofol has been shown to protect the brain. It was hypothesized that a clinically achievable high dose of propofol would induce cerebral protective effects in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). The authors investigated the effects of different target plasma concentrations of propofol on cerebral injury by measuring serum S-100β protein and neuron-specific enolase (NSE) levels in patients undergoing single-valve replacement with CPB. A prospective, randomized study. A university hospital. Forty-two patients undergoing single-valve replacement with CPB. Patients were randomly divided into 3 groups (n = 14 each). Each group received a target-controlled infusion of propofol with plasma concentrations of 1.8 μg/mL (low dose, Group-L), 2.4 μg/mL (medium dose, Group-M), or 3.2 μg/mL (high dose, Group-H). The propofol target concentrations were unchanged throughout the surgery. In all 3 groups of patients, at all time points after CPB, the plasma S-100β protein and NSE levels, which served as biochemical markers of brain damage, were significantly higher than the preoperative levels (p<0.05). Group-H showed significant decreases in S-100β protein and NSE compared with Group-L (p< 0.05). In the range of commonly used clinical concentrations, administration of a high dose of propofol during CPB attenuated the biochemical markers of brain damage as compared with low-dose propofol anesthesia.

Effects of propofol on airway hyperresponsiveness and airway inflammation of asthmatic mice

Objective To investigate the immunoregulatory effects of propofol on airway hyperresponsiveness,airway inflammation and Thl/Th2 ratio in the asthmatic mice.Methods One hundred female BALB/c mice,aged 6-8 weeks,weighing 18-20 g,were randomly divided into 5 groups (n =20,each):control group (normal saline i.p.,group C),asthma group (group A),low-dose propofol (50 mg/kg i.p.,group LP),medium-dose propofol (100 mg/kg i.p.,group MP) and high-dose propofol (150 mg/kg i.p.,group HP).Mice of groups A,LP,MP and HP were sensitized with ovalbumin (OVA),mice of group C were sensitized with normal saline.24 h after the last challenge,animals were sacrificed by lethal dose of pentobarbital sodium.Blood and bronchoalveolar lavage fluid (BALF) were collected for determination of serum OVA-specific IgE and the levels of cytokines (IL-4,IL-5 and IFN-γ) in the BALF.Airway responsiveness was measured by the forced-oscillation technique and histological inflammation scores were measured by staining with hematoxylin and eosin.Results Propofol (group LP and group MP) attenuated airway hyperresposiveness to the muscarinic agonist methacholine in OVA-induced asthma.Different doses of propofol (group LP,group MP and group HP) decreased eosinoplils influx in lungs.In addition,propofol treatment reduced expression of IL-4,IL-5 and serum OVA-specific IgE and increased the ratio of IFN-γ/IL-4.Conclusion The study demonstrates a potential protective value of propofol in alleviating airway inflammation,up-regulating Th1/Th2 ratio and attenuating airway hyperresposiveness in the asthmatic mice. Key words: Asthma; Propofol ; Respiratory hypersensitivity ; Inflammation

Propofol-Related Infusion Syndrome in an Adult Patient Using Propofol Coma Therapy to Control Intracranial Pressure

Propofol-related infusion syndrome (PRIS) is a rare but fatal complication. Unexplained metabolic acidosis, rhabdomyolysis, hyperkalemia, myocardial dysfunction, cardiovascular collapse and acute kidney injury are the main characteristics of PRIS. Herein, we report a case of PRIS in a neurosurgical adult patient, who had received high-dose propofol continuous infusion in order to control intracranial pressure in an intensive care unit. She manifested severe metabolic acidosis, rhabdomyolysis, acute kidney injury and myocardial dysfunction. As soon as PRIS was diagnosed, propofol infusion was stopped. Conservative treatments, such as vasopressors and inotropics, continuous renal replacement therapy and extracorporeal membrane oxygenation were used to treat PRIS. However, she finally expired. This case report suggests that a great caution to PRIS is needed in a situation with high-dose propofol continuous infusion.

Les médicaments de l’anesthésie et le tonus vasomoteur en CEC : les anesthésiques IV

Anaesthesia during CBP is frequently provided using intravenous anaesthetic drugs, particularly propofol. The effects of the different drugs have been studied during CPB. These drugs have an arterial and venous vasodilator effect during CPB which is dose dependent and is more pronounced for propofol. High doses of propofol or thiopental reduce cerebral blood flow but provide no additional neurological protection.