Propofol Infusion Syndrome Research Articles

Therapeutic Aspects of Lipofilling, Abdominoplasty in Combination with Body Liposuction and Bariatric Surgery

This review article is dedicated to the therapeutic aspects of various plastic surgery procedures. Nowadays, improving appearance and quality of life through plastic surgery is becoming increasingly popular. Managing patients after lipofilling and abdominoplasty combined with liposuction is an interdisciplinary challenge. Intraoperative risks in plastic surgery are associated with anesthesia and comorbidities. The immediate response of the cardiovascular and respiratory systems to the administration of anesthetic agents and the anesthesiologist's qualifications determines the immediate success of the operations. The duration of the surgery, volumetric disturbances, reduction of body surface area, and changes in metabolic and immunological status after mechanical impact on adipose tissue significantly alter the rate of compensatory-adaptive reactions of the body. In the long-term period after lipofilling, abdominoplasty, liposuction, and augmentation mammoplasty, systemic complications are often observed. These include insomnia, chronic kidney disease, protein-energy malnutrition, arthropathies, nonspecific interstitial lung lesions, unverified hepatitis, lupus-like syndrome, antibodies to transplanted fats and silicone materials, idiopathic limb edema, as well as autoinflammatory syndromes. The presented work also provides data on propofol infusion syndrome and the clinical-prognostic significance of vascular endothelial growth factor in plastic surgery. The authors’ team also presents their own clinical data on obesity and associated diseases. To maintain the aesthetic effect and prevent long-term complications after lipofilling, liposuction, augmentation mammoplasty, blepharoplasty, and rhinoplasty, it is recommended to follow a hypoallergenic and low-calorie diet for the next 3-6 months, avoid night work, excessive physical exertion, simultaneous intake of antibiotics and anti-inflammatory drugs, sun exposure, trips to mountainous areas, and long flights.

A case of pediatric Perthes’ disease with unexplained hyperlactatemia at the time of initial surgery and anesthetic management with remimazolam for the subsequent surgery

BackgroundThe causes of perioperative hyperlactatemia vary, but they are generally associated with hypoperfusion. Here, we report the case of a pediatric patient who developed unexplained hyperlactatemia during anesthesia with propofol and sevoflurane, which recurred during a second surgery under anesthesia with remimazolam.Case presentation.An 8-year-old boy with Perthes disease and no remarkable past or family history was scheduled for an osteotomy. Anesthesia was induced with propofol and rocuronium and then maintained with sevoflurane and remifentanil. The patient developed lactic acidosis without hemodynamic instability during anesthesia, with a normal lactate/pyruvate ratio after surgery, suggesting a lack of hypoperfusion. We used remimazolam instead of propofol during the second surgery 6 months later, considering the possibility of drug-induced lactic acidosis, including malignant hyperthermia and propofol infusion syndrome, where the unexplained hyperlactatemia recurred.ConclusionsDistinguishing the causes of hyperlactatemia, particularly in the absence of other symptoms, is challenging. The lactate/pyruvate ratio during episodes of hyperlactatemia can provide insights into the underlying pathology.

Fospropofol disodium versus propofol for long-term sedation during invasive mechanical ventilation: A pilot randomized clinical trial

Study objectiveFospropofol disodium is a propofol prodrug that is water-soluble and has a reduced risk of bacterial contamination and hypertriglyceridemia compared with propofol. Prior to implementing a large randomized trial, we investigated the feasibility, initial efficacy, and safety of fospropofol disodium compared with propofol in long-term mild-to-moderate sedation in intensive care units (ICUs). DesignSingle-centered, prospective, unblind, randomized, parallel-group clinical trial. SettingThe general ICU of university-affiliated teaching hospital. PatientsAdult patients (n = 60) expected to have mechanical ventilation for >24 h were enrolled and randomly assigned to the fospropofol or propofol group.Interventions: The fospropofol group received continuous fospropofol disodium infusions and the propofol group received continuous propofol infusions. The sedation goal was a score of −3 to 0 on the Richmond Agitation and Sedation Scale (RASS). MeasurementsThe primary outcome was the percentage of time spent in the target sedation range without rescue sedation. Safety outcomes were based on adverse events. Blood samples were collected to measure formate concentration in plasma. Main resultsThe median dose was 4.33 (IQR, 3.08–4.94) mg/kg/h in the fospropofol group and 1.96 (IQR, 1.44–2.94) mg/kg/h in the propofol group. The median percentage of time spent in the target RASS range without rescue sedation was identical in both groups, with 83.33% (IQR, 74.43%–100.00%) in the fospropofol group and 83.33% (IQR, 77.45%–100.00%) in the propofol group (p = 0.887). At least one adverse event was identifed in 23 (76.7%) fospropofol patients and 27 (90.0%) propofol patients. The most common adverse events were tachycardia and hypotension. No paresthesia, catheter-related bloodstream infection or propofol infusion syndrome in both groups was reported. Three patients in the fospropofol group had mild hypertriglyceridemia, and nine patients in propofol group had hypertriglyceridemia (mild in eight patients and moderate in one patient) (10% versus 30%, p = 0.104). The formate concentration in plasma was very low, and no significant difference was identified at any time point between the two groups. ConclusionsFospropofol disodium appears to be a feasible, effective and safe sedative for patients receiving invasive mechanical ventilation with long-term sedation.

Overdose with the anesthetic propofol causes hematological cytotoxicity and immune cell alteration in an experimental ex vivo whole blood culture model

Propofol, an anesthetic characterized by its benefits of rapid induction, maintenance, and recovery times, may cause cytotoxic effects, resulting in propofol infusion syndrome (PRIS). In addition to causing dyslipidemia in PRIS, our previous works showed that propofol overdose induced phagocyte apoptosis. This study, using an experimental ex vivo model of propofol treatment, investigated the possible cytopathology in the blood. A complete blood count examination showed the deregulating effects of propofol overdose 24 h postinoculation, characterized by mononuclear cell increase (lymphocyte and monocyte subsets) and granulocyte decrease. Advanced marker-based flow cytometric analysis confirmed these findings, although there was no change in CD14+ monocytes. Blood smear staining showed the deregulating effects of propofol overdose 24 h postinoculation, characterized by cytosolic vacuolization and cytotoxicity, particularly in neutrophils. Immune cell profiling of caspase-3 activation demonstrated the induction of cell apoptosis following propofol overdose treatment, particularly in granulocytes. Using multiparameter flow cytometry, this study further analyzed the changes in the profile of immune cells, showing a notable increase in CD4 + HLA-DR-CD62L- helper T cells. These studies explored an ex vivo model of cytopathogenic propofol overdose and its special immune-deregulating effects on peripheral blood cells.

Propofol for Anesthesia in Pediatric Patients With Epilepsy on the Ketogenic Diet: A Single-Center Experience

BackgroundPropofol use is contraindicated in patients on ketogenic diet (KD) due to higher risk of propofol infusion syndrome (PIS). This study is intended to provide a descriptive analysis of our experience with propofol bolus and short infusions for anesthetic care in patients on the KD and to evaluate if any signs of PIS were observed. MethodsAll patients on the KD who underwent anesthesia with propofol between 2012 and 2022 were reviewed. Anesthetic encounters and charts were studied for type of surgical procedure; signs of PIS, including new cardiac arrhythmias, acidosis, or rhabdomyolysis in the periprocedural period; hypoglycemia; unplanned admissions within 24 hours of the procedure; if procedure was unexpectedly aborted; and increased seizure frequency within one week. ResultsWe identified 65 patients, aged from one to 20 years who underwent 165 anesthetic encounters with propofol, of which 123 were boluses and 42 were infusions.In bolus dosing, the average dose was 2.8 mg/kg (0.7 to 12.8 ± 1.8 mg/kg). Of these, four encounters developed acidosis, one developed rhabdomyolysis, and one developed increased seizures. With infusions, the average infusion rate was 9 mg/kg/hour, with mean infusion duration of 83 minutes (10 to 352 ± 75 minutes). Of these, one developed acidosis and one increased seizures. No cases of PIS were identified. None of the adverse effects were attributed to propofol. ConclusionsBoluses and brief infusions of propofol for anesthetic use in patients on the KD did not cause PIS in our cohort.

Propofol infusion syndrome as a cause for CRRT circuit malfunction: a case report with literature review

BackgroundPropofol is commonly used for sedation in the Intensive Care Unit (ICU). When administered in high doses and for a prolonged time, it can cause a rare but hazardous complication: Propofol Infusion Syndrome (PRIS). Along with other findings, PRIS can cause lipemia and clotting of the Continuous Renal Replacement Therapy (CRRT) circuit.Case presentationA 62-year-old woman admitted to the ICU after an acute ischemic stroke was sedated with Propofol for neuroprotection. On the sixteenth day of infusion (mean daily dose: 4 mg/kg/h), she presented with hyperlactatemia (7.7 mg/dL), acute kidney injury, metabolic acidosis (pH: 7.23 / HCO3–: 12.2 mEq/L), hyperkalemia (6.9 mEq/L), and hypotension requiring high doses of norepinephrine. CRRT and corticosteroids were initiated. After 15 min of CRRT, the blood in the circuit had a milky color, and the therapy was interrupted because of high transmembrane pressure, despite adequate anticoagulation with heparin. Laboratory tests showed hypertriglyceridemia (782 mg/dL), increased transaminases, and creatine phosphokinase (5008 U/L), suggesting the rare and fatal PRIS.ConclusionThere is no established guideline for treating PRIS other than early discontinuation of Propofol and supportive care. Although CRRT is an important tool in managing PRIS, hypertriglyceridemia can cause circuit malfunction. Clinical hypervigilance and serial monitoring in at-risk patients are advised to minimize potentially lethal complications.

Effects of coenzyme Q10 in a propofol infusion syndrome model of rabbits.

Coenzyme Q (CoQ) might be the main site of interaction with propofol on the mitochondrial respiratory chain in the propofol infusion syndrome (PRIS) because of the structural similarity between coenzyme Q10 (CoQ10) and propofol. To investigate the effects of CoQ10 on survival and organ injury in a PRIS model in rabbits. Sixteen male New Zealand white rabbits were divided into 4 groups: (1) propofol infusion group, (2) propofol infusion and CoQ10, 100 mg/kg was administered intravenously, (3) sevoflurane inhalation was administered, and (4) sevoflurane inhalation and CoQ10, 100 mg/kg intravenously, was administered. Arterial blood gas and biochemical analyses were repeated every 2 h and every 12 h, respectively. Animals that were alive on the 24th hour after anesthesia induction were euthanized. The organ damages were investigated under light and transmission electron microscopy (TEM). The propofol infusion group had the highest troponin T levels when compared with the other three groups at the 12th hour. The propofol + CoQ10 group had lower troponin T levels when compared with the propofol and sevoflurane groups (P < 0.05). Administration of CoQ10 decreased total liver injury scores and total organ injury scores both in the propofol and sevoflurane groups. The propofol and sevoflurane organ toxicities were attenuated with CoQ10 in liver, gallbladder, urinary bladder, and spleen. The addition of CoQ10 to propofol and sevoflurane anesthesia prevented the propofol-associated increase in troponin T levels at the 12th hour of infusion and decreased anesthetic-induced total liver and organ injury scores.

Trigger-free anesthesia : Indications and safe application

The safe anesthesiological care of patients with neuromuscular diseases poses aparticular challenge for anesthetists. Only asmall group of muscle diseases and syndromes are associated with an increased risk of malignant hyperthermia and therefore require trigger-free anesthetic procedures avoiding volatile anesthetics and succinylcholine. These diseases are frequently associated with mutations in the RYR1, CACNA1S or STAC-3 genes. In other neuromuscular diseases, anesthetic-induced rhabdomyolysis can occur. Therefore, volatile anesthetics should be avoided in these patients in addition to the contraindication for succinylcholine. In other neuromuscular diseases the risk of a propofol infusion syndrome or myotonic crises can be elevated or the duration of the effect of non-depolarizing muscle relaxants can be changed in an incalculable way. In every case an individual anesthetic aproach including the avoidance of potential pharmacological or non-pharmacological triggers is essential for the safety of the patients.

Propofol in ICU Settings: Understanding and Managing Anti-Arrhythmic, Pro-Arrhythmic Effects, and Propofol Infusion Syndrome.

Propofol has revolutionized anesthesia and intensive care medicine owing to its favorable pharmacokinetic characteristics, fast onset, and short duration of action. This drug has been shown to be remarkably effective in numerous clinical scenarios. In addition, propofol has maintained an overwhelmingly favorable safety profile; however, it has been associated with both antiarrhythmic and proarrhythmic effects. This review concisely summarizes the dual arrhythmic cardiovascular effects of propofol and a rare but serious complication, propofol infusion syndrome (PRIS). We also discuss the need for careful patient evaluation, compliance with recommended infusion rates, and vigilant monitoring.

Propofol-associated serious adverse events: an analysis of the FAERS database

ABSTRACT Propofol is an ultra-fast-acting intravenous anesthetic, which is rapidly metabolized primarily into inactive compounds in the live and then excreted in the urine. The purpose of this study is to explore the risk signals of propofol based on the US FDA Adverse Event Reporting System database. The risk signals of propofol-related adverse reactions in adverse event (AE) reports from 2004 to 2021 in the US FAERS were mined using ratio-report method (ROR) and the ratio-report ratio method (PRR) methods. We screened out 1651 pairs AE reports using propofol as primary suspect (PS) drugs. ROR, PRR, BCPNN and MGPS methods were used to calculate respectively, there are 363 positive preferred terms (PT) signals with 9549 cases. Among them, the top 3 adverse reactions associated with using propofol from the FAERS database were anaphylactic shock, hypotension and propofol infusion syndrome. The top 3 systems of the body associated with adverse reaction of propofol from the FAERS database were General disorders, Cardiac disorders and administration site conditions and Respiratory, thoracic and mediastinal disorders. The top 4 indication of using propofol from the FAERS database, including anaesthesia, induction of anaesthesia, sedation, general anaesthesia. There are many adverse reactions that are not included in the drug insert of propofol and involve a wide range of organs and/or systems. Caution should be exercised in the clinical use of propofol.

Propofol infusion syndrome: a systematic review

Introduction: propofol infusion syndrome (SIP) is a rare but extremely serious condition that can occur following the administration of high doses (&gt;2 - 5 mg/kg/h) of propofol for prolonged periods (&gt;48 hours). However, cases of SIP have also been reported after low-dose or short-duration propofol infusion. The condition is characterized by metabolic acidosis, cardiovascular and renal disturbances, rhabdomyolysis, as well as electrocardiographic abnormalities, etc. Objective: to describe the main characteristics, prevention, diagnosis, and management of SIP. Methods: a literature search and selection of articles published in the last 5 years on SIP in critically ill patients were carried out in English, Spanish, and Portuguese. This was done through the Pubmed, TRipDatabase, SciELO, and Google Scholar databases, following the PRISMA methodology. Results: 26 articles were included, which analyzed the definition, general characteristics, epidemiology, risk factors, pathophysiology, clinical manifestations, prevention, and treatment. Conclusions: the literature found reports that SIP is very rare but potentially fatal. The best treatment is prevention and early diagnosis. It is important to be aware that patients receiving propofol infusion are at risk of developing SIP. Therefore, greater monitoring and knowledge of patient clinical profiles is recommended. If SIP is suspected, propofol use should be discontinued and replaced with an alternative hypnotic agent, and management should be initiated. This includes immediate discontinuation of propofol infusion and problem-oriented management, such as hemodialysis, hemodynamic support, and extracorporeal membrane oxygenation in refractory cases. Further research is needed on SIP to obtain more data on its diagnosis, pathophysiology, and incidence

Effect of noradrenaline on propofol-induced mitochondrial dysfunction in human skeletal muscle cells

BackgroundMitochondrial dysfunction is a hallmark of both critical illness and propofol infusion syndrome and its severity seems to be proportional to the doses of noradrenaline, which patients are receiving. We comprehensively studied the effects of noradrenaline on cellular bioenergetics and mitochondrial biology in human skeletal muscle cells with and without propofol-induced mitochondrial dysfunction.MethodsHuman skeletal muscle cells were isolated from vastus lateralis biopsies from patients undergoing elective hip replacement surgery (n = 14) or healthy volunteers (n = 4). After long-term (96 h) exposure to propofol (10 µg/mL), noradrenaline (100 µM), or both, energy metabolism was assessed by extracellular flux analysis and substrate oxidation assays using [14C] palmitic and [14C(U)] lactic acid. Mitochondrial membrane potential, morphology and reactive oxygen species production were analysed by confocal laser scanning microscopy. Mitochondrial mass was assessed both spectrophotometrically and by confocal laser scanning microscopy.ResultsPropofol moderately reduced mitochondrial mass and induced bioenergetic dysfunction, such as a reduction of maximum electron transfer chain capacity, ATP synthesis and profound inhibition of exogenous fatty acid oxidation. Noradrenaline exposure increased mitochondrial network size and turnover in both propofol treated and untreated cells as apparent from increased co-localization with lysosomes. After adjustment to mitochondrial mass, noradrenaline did not affect mitochondrial functional parameters in naïve cells, but it significantly reduced the degree of mitochondrial dysfunction induced by propofol co-exposure. The fatty acid oxidation capacity was restored almost completely by noradrenaline co-exposure, most likely due to restoration of the capacity to transfer long-chain fatty acid to mitochondria. Both propofol and noradrenaline reduced mitochondrial membrane potential and increased reactive oxygen species production, but their effects were not additive.ConclusionsNoradrenaline prevents rather than aggravates propofol-induced impairment of mitochondrial functions in human skeletal muscle cells. Its effects on bioenergetic dysfunctions of other origins, such as sepsis, remain to be demonstrated.

The incidence of propofol infusion syndrome in critically-ill patients.

PRIS is a potentially fatal syndrome characterized by various clinical symptoms and abnormalities. Experts suggest that propofol treatment duration ≥48 h or dose ≥83 μg/kg/min is associated with developing PRIS. We hypothesized PRIS might be underdiagnosed due to the overlap of PRIS clinical manifestations with critical illnesses. Multihospital, retrospective study of adult patients who received continuous propofol infusion ≥48 h or dose ≥60μg/kg/min for >24 h since admission were assessed for the development of PRIS. The incidence of PRIS was 2.9% with a PRIS-associated mortality rate of 36.8%. In PRIS patients, propofol was administered at a median dose of 36.4 μg/kg/min and over a median duration of 147.0 h. The development of PRIS was observed at a median of 125.0 h post-propofol initiation and a cumulative dose of 276.5 mg/kg. The development of metabolic acidosis (78.9%), cardiac dysfunction (52.6%), hypertriglyceridemia (100%), and rhabdomyolysis (26.3%) were observed in our PRIS patients. PRIS can often be overlooked and underdiagnosed. It is important to monitor for early signs of PRIS in patients who are on prolonged propofol infusion. Prompt recognition and interventions can minimize the dangers resulting from PRIS.

Could Hydroxocobalamin Be of Use in the Treatment of Lactate Acidosis Induced by Propofol Infusion Syndrome? - A Case Report

Could Hydroxocobalamin Be of Use in the Treatment of Lactate Acidosis Induced by Propofol Infusion Syndrome? - A Case Report

Successful recording of direct cortical motor-evoked potential from a pediatric patient under remimazolam anesthesia: a case report

BackgroundIntraoperative motor-evoked potential (MEP) monitoring reduces postoperative motor deficits. Propofol-based total intravenous anesthesia is the gold standard for intraoperative myogenic MEPs. Although there is no contraindication to administering propofol in adults with peanut, soy, or egg allergies, its safety in children with these allergies remains unclear.Case presentationA 12-year-old girl required general anesthesia under intraoperative direct cortical MEP (dc-MEP) monitoring due to supratentorial glioma. Remimazolam-based anesthesia was selected, instead of propofol, due to the patient’s egg hypersensitivity. Stable myogenic MEPs were recorded throughout the surgery with remimazolam at 0.9 mg/kg/h and remifentanil at 0.35 μg/kg/min, following adjustments of stimulation intensity and titration of remimazolam infusion. Neither intraoperative memory nor motor deficits were present after surgery.ConclusionsWe present a pediatric case whose dc-MEP was recorded under remimazolam anesthesia. The cardiovascular stability and avoidance of propofol infusion syndrome with remimazolam were superior to propofol.

Propofol in the Pediatric Intensive Care Unit, a Safe and Effective Agent in Reducing Pain and Sedation Infusions: A Single-Center Retrospective Study.

IntroductionPropofol has long been used as an anesthetic agent during pediatric surgery. Its use in pediatric intensive care units has been largely controversial. A beneficial use of propofol is to facilitate weaning of other pain and sedation infusions such as opiates and benzodiazepines. However, some have advocated to not use propofol due to fear of possible adverse effects including propofol infusion syndrome and hemodynamic instability. The purpose of this study was to determine both the safety of propofol infusions in critically ill pediatric patients, as well as the change in the requirement of other pain and sedation infusions by use of a propofol infusion.MethodsSingle-center, retrospective data (January 2011 to January 2020) was obtained manually using a study-specific data extraction tool created for electronic medical records. The data obtained included variables of interest that measured physiological parameters and pain/sedation infusion (morphine, fentanyl, hydromorphone, midazolam, and dexmedetomidine) rates during three time periods: before propofol initiation, immediately after discontinuation, and four hours after discontinuation. The physiological parameters were then compared to the pain and sedation infusion rates using paired Wilcoxon signed-rank tests.ResultsThere was a total of 33 patients with an average age of 11.1 years who were given a median initial propofol infusion of 50 mcg/kg/min with a peak dose of 75 mcg/kg/min over an average of eight hours. Age had a weak and insignificant correlation with initial rate and duration and a moderate and significant correlation with peak rate and duration. Physiological parameters did not vary at any time point measured. There was a significant reduction in other pain and sedation infusions after discontinuation of propofol.ConclusionPropofol infusions are hemodynamically tolerated and the majority of patients who are on other pain and sedation infusions tolerate complete discontinuation of these infusions following propofol discontinuation.

Modeling propofol-induced cardiotoxicity in the isolated-perfused newborn mouse heart.

Infants and children are vulnerable to developing propofol infusion syndrome (PRIS) and young age is a risk factor. Cardiac involvement is often prominent and associated with death. However, the mechanisms of pediatric PRIS are poorly understood because of the paucity of investigation and lack of a gold standard animal model. Unfortunately, in vivo modeling of PRIS in a newborn mouse is not feasible and would be complicated by confounders. Thus, we focused on propofol‐induced cardiotoxicity and aimed to develop an ex‐vivo model in the isolated‐perfused newborn mouse heart. We hypothesized that the model would recapitulate the key cardiac features of PRIS seen in infants and children and would corroborate prior in vitro observations. Isolated perfused newborn mouse hearts were exposed to a toxic dose of propofol or intralipid for 30‐min. Surface electrocardiogram, ventricular contractile force, and oxygen extraction were measured over time. Real‐time multiphoton laser imaging was utilized to quantify calcein and tetramethylrhodamine ethyl ester fluorescence. Propidium iodide uptake was assessed following drug exposure. A toxic dose of propofol rapidly induced dysrhythmias, depressed ventricular contractile function, impaired the mitochondrial membrane potential, and increased open probability of the permeability transition pore in propofol‐exposed hearts without causing cell death. These features mimicked the hallmarks of pediatric PRIS and corroborated prior observations made in isolated newborn cardiomyocyte mitochondria. Thus, acute propofol‐induced cardiotoxicity in the isolated‐perfused developing mouse heart may serve as a relevant ex‐vivo model for pediatric PRIS.

Review of remimazolam and sedatives in the intensive care unit.

Remimazolam is a novel intravenous ultra-short acting benzodiazepine that has the potential of being a safe and effective new sedative for use in intensive care unit (ICU) settings. Because remimazolam metabolizes rapidly by being hydrolyzed to an inactive metabolite (CNS 7054) through non-specific tissue esterase activity, specific dosing adjustment for older adults and for patients with renal or hepatic impairment patients (except for those with severe hepatic impairment) is not required. In addition, research has shown that remimazolam may be reversed by administration of flumazenil, as its half time was sufficiently short compared to flumazenil. It shows a lower incidence of cardiorespiratory depression, less injection pain, and no fatal complications such as propofol infusion syndrome and malignant hyperthermia of inhalational anesthetics. Future studies to study the suitability of remimazolam for managing the sedation of ICU patients who need sedation for a long time over several days is required.

Propofol: use, toxicology and assay features

The study objective is to review the literature on the use, pharmacological properties, toxicology, and assay methods for intravenous anesthetic propofol. The scope and forms of propofol use, its pharmacokinetics, biotransformation features, which occurs more than 90% in the liver, and side effects associated with propofol use for anesthesia, are addressed. Propofol infusion syndrome (also known as PrIS) and deaths from propofol overdose due to medical errors, abuse, suicide attempts, and homicide are reported. Propofol identification and assay methods based on high-performance liquid chromatography (HPLC), gas chromatography with mass spectrometry (GC-MS), and liquid chromatography (LC) are described. The features of the methods performance are outlined; biological materials (the study objects) are listed: mainly blood and plasma, as well as urine, bile, hair, etc. The relevance of a comprehensive forensic chemical study of propofol is indicated, though there are few forensic studies of propofol.

Restarting propofol following successful management of propofol infusion syndrome: a case report

: Propofol infusion syndrome (PRIS) is a rare and potentially fatal complication seen in high-dose (>5 mg/kg/h) or prolonged (>48 h) propofol infusions. PRIS presents as a constellation of symptoms, including anion-gap metabolic acidosis, elevated lactate, cardiogenic shock, rhabdomyolysis, arrhythmia, among other biochemical abnormalities. The current standard of care focuses on early recognition, propofol cessation, and supportive management. Case reports have shown evidence for several novel therapeutic interventions, including plasmapheresis, dialysis, and extracorporeal membrane oxygenation. There has yet to be a documented case demonstrating a trial of reinitiating propofol following successful PRIS management. We present the case of a previously healthy 20-year-old male that presented to the emergency department with new-onset refractory status epilepticus, secondary to suspected autoimmune encephalitis. Despite multiple immunomodulators, anesthetic therapies, and anti-epileptic agents, he exhibited ongoing refractory seizure activity on continuous electroencephalogram monitoring. Propofol boluses were the only therapy to offer seizure burst suppression, prompting uptitration of the infusion. The patient subsequently developed hemodynamic instability and multiple biochemical abnormalities consistent with PRIS. He was managed with one round of plasmapheresis, later followed by a session of sustained-low efficiency dialysis (SLED). This therapeutic combination was successful in managing PRIS and restoring hemodynamic stability. After stopping the propofol infusion, he developed near constant electrographic seizures, with breakthrough clinical seizures despite multiple other therapeutic interventions. Propofol was later restarted for seizure control, with no further recurrence of PRIS. This case provides support for novel therapeutic modalities, plasmapheresis and SLED, when managing PRIS. This case also marks the first successful attempt at restarting propofol following PRIS.