Propofol infusion rate does not affect local pain on injection

Background: Local pain at the site of an i.v. injection of propofol is a well‐known problem, particularly in infants. This randomised investigator‐blinded crossover study was designed to assess the effect of the i.v. bolus infusion rate on propofol‐induced pain at the site of injection. Methods: Thirty unpremedicated patients scheduled for ear‐nose‐throat or plastic surgery at Malmö University Hospital, Sweden, were given two consecutive 2.0 ml injections of propofol 10 mg/ml (Diprivan^®, AstraZeneca, Sweden/UK), at different infusion rates (0.2 or 1.0 ml/s), immediately before induction of general anesthesia. Half of the patients (n=15) received the first bolus of propofol over 2 s and the second bolus over 10 s, and the other half (n=15) had their injections in reversed order. After each injection, the patient was asked by an investigator to indicate pain intensity on a visual analog scale (VAS) and to report the times of the appearance, maximum point and disappearance of pain. The injections were given approximately 2 min apart. The investigators scoring pain intensity, as indicated by the patients on a 10‐point numerical rate scale, were blinded to the order in which the injections were given, as were the patients themselves. Results: There were no statistically significant differences in the incidence (both 86%) of intensity (median; 25th; 75th percentiles, in VAS units: 3.1; 1.0; 5.3 and 3.3; 1.4; 5.0, respectively) or duration (66±31 and 73±26 s, respectively) of pain between the faster (1.0 ml/s) and slower (0.2 ml/s) bolus infusion rates of propofol studied. Conclusions: We conclude that the i.v. bolus infusion rate of propofol does not influence drug‐induced local pain on injection, at least not within the infusion rate interval studied. Therefore, adjusting i.v. injection speed does not seem to be a clinically useful tool for reducing the intensity or duration of propofol‐induced pain at the site of administration.     

Propofol infusion syndrome

Propofol infusion syndrome has not only been observed in patients undergoing long-term sedation with propofol, but also during propofol anesthesia lasting 5 h. It has been assumed that the pathophysiologic cause is propofol's impairment of oxidation of fatty acid chains and inhibition of oxidative phosphorylation in the mitochondria, leading to lactate acidosis and muscular necrosis. It has been postulated that propofol might act as a trigger substrate in the presence of priming factors. Severe diseases in which the patient has been exposed to high catecholamine and cortisol levels have been identified as trigger substrates. Once the development of propofol infusion syndrome is suspected, propofol infusion has to be stopped immediately and specific therapeutic measures initiated, including cardiocirculatory stabilization and correction of metabolic acidosis. To increase elimination of propofol and its potential toxic metabolites, hemodialysis or hemofiltration are recommended. Due to its possible fatal side effects, the use of propofol for long-term sedation in critically ill patients should be reconsidered. In cases of unexplained lactate acidosis occurring during continuous propofol infusion, propofol infusion syndrome must be taken into consideration.     

Propofol infusion syndrome

The clinical features of propofol infusion syndrome (PRIS) are acute refractory bradycardia leading to asystole, in the presence of one or more of the following: metabolic acidosis (base deficit > 10 mmol.l(-1)), rhabdomyolysis, hyperlipidaemia, and enlarged or fatty liver. There is an association between PRIS and propofol infusions at doses higher than 4 mg.kg(-1).h(-1) for greater than 48 h duration. Sixty-one patients with PRIS have been recorded in the literature, with deaths in 20 paediatric and 18 adult patients. Seven of these patients (four paediatric and three adult patients) developed PRIS during anaesthesia. It is proposed that the syndrome may be caused by either a direct mitochondrial respiratory chain inhibition or impaired mitochondrial fatty acid metabolism mediated by propofol. An early sign of cardiac instability associated with the syndrome is the development of right bundle branch block with convex-curved ('coved type') ST elevation in the right praecordial leads (V1 to V3) of the electrocardiogram. Predisposing factors include young age, severe critical illness of central nervous system or respiratory origin, exogenous catecholamine or glucocorticoid administration, inadequate carbohydrate intake and subclinical mitochondrial disease. Treatment options are limited. Haemodialysis or haemoperfusion with cardiorespiratory support has been the most successful treatment.     

Propofol and alfentanil infusion

In 42 patients undergoing major surgery, anaesthesia was induced by intravenous alfentanil 10 micrograms/kg together with methohexitone 1.5 mg/kg or propofol 2 mg/kg. An infusion of six times these doses per hour was then started; the rate was varied subsequently as indicated by the monitoring of arterial blood pressure, heart rate, EEG and frontalis electromyogram. The mean duration of infusion was 76.7 minutes for propofol and 74.5 minutes for methohexitone and the infusion was stopped about 10 minutes before the end of surgery in each group. The induction dose differed, but the total dose requirement for the two drugs was similar. In every case, anaesthesia was satisfactory. Methohexitone caused a significant rise in mean pulse rate throughout anaesthesia (p less than 0.05, paired t-test). There was no change in mean pulse rate during propofol infusion. The dose of alfentanil used provided excellent control of autonomic reflexes, with negligible respiratory depression. Naloxone was not required. Propofol provided better anaesthesia than methohexitone, with fewer side effects (p less than 0.05, Chi squared test), easier control of the level of narcosis and faster recovery (p less than 0.001, t-test after log transformation).     

A case of suspected non-neurosurgical adult fatal propofol infusion syndrome

A previously healthy woman (20 years old) was admitted to our hospital with several fractures after a car accident. She was sedated with propofol, etc. in doses ranging from 1.4 to 5.1 mg/kg/h for 88 h. She developed multiple organ failure with rhabdomyolysis and died. This case fulfils (except acidosis) the criteria of propofol-infusion syndrome (PRIS) in a young adult.     

Garcin's syndrome--a case report

BACKGROUND: Garcin's syndrome in its complete form is very rare, and hence, this case is reported. CASE DESCRIPTION: A 45-year-old patient presented to us with proptosis of the right eye and progressive weakness of all cranial nerves on the right side without associated features of raised intracranial pressure or long tract dysfunction. He had a bulge in the right buccolabial fold, from which fine needle aspiration cytology was done. Cytology report came as a poorly differentiated carcinoma. CONCLUSIONS: Garcin's syndrome is a very rare neurosurgical entity. The course of the condition depends on the nature of underlying pathology.     

Propofol infusion syndrome in a patient with sepsis

Propofol is widely used for sedation in critically ill patients. Several adult patients, all with acute neurological disorders, have been reported suffering from propofol infusion syndrome, which occurs in patients receiving high-dose propofol and catecholamines and/or steroids. We present a case of a septic patient without neurological illness who developed propofol infusion syndrome.     

Propofol infusion syndrome in children

Department of Anaesthesia, Royal Victoria Infirmary, Queen Victoria Road, Newcastle upon Tyne NE1 4LP, UKThe use of propofol infusions to sedate children in intensive care units has decreased after reports of deaths from myocardial failure. More recently it has been suggested that propofol might have been prematurely condemned. Information about 18 children who had received propofol infusions and suffered serious unwanted effects was used to define their common features. Three of the deaths occurred in one intensive care unit where propofol infusions had been used between 1987 and 1993. During this period 44 children with respiratory tract infections had been admitted to this unit and sedated for at least 48 h. Nine had received long-term (>48 h), high-dose (>4 mg·kg^·1·h^-1) propofol infusions and three had developed progressive myocardial failure and died. There was a significant association between receiving a long-term, high-dose propofol infusion and developing progressive myocardial failure (Fisher's Exact Test, two-tailed hypothesis, P=0.0128) although a causative relationship could not be proved.     

Propofol: bolus or continuous infusion

Forty patients undergoing vaginal termination of pregnancy were randomly allocated to receive a propofol anaesthetic using either a repeat bolus or infusion technique. The Ohmeda 9000 Infusion Pump was used in the study. Patients in the infusion group recorded significantly longer induction times, greater maintenance doses and prolonged immediate recovery characteristics. Both techniques offered cardiovascular stability but no advantages were demonstrated for the infusion technique over a conventional repeat bolus method.     

Propofol infusion anaesthesia for Caesarean section

Two propofol infusion regimens and a standard general anaesthetic were compared in thirty Chinese women undergoing elective Caesarean section. After induction of anaesthesia with propofol 2 mg.kg-1, ten patients received propofol 6 mg.kg-1.hr-1 and nitrous oxide 50 per cent in oxygen while ten were given propofol 9 mg.kg-1.hr-1 with 100 per cent oxygen. The other ten patients received thiopentone 4 mg.kg-1 and nitrous oxide 50 per cent in oxygen with enflurane one per cent. Maternal recovery times and psychomotor performance were recorded. Neonates were assessed by Apgar scores, neurologic and adapative capacity scores (NACS) and umbilical cord blood gas analysis. Haemodynamic changes were similar immediately following induction but the low propofol infusion group had the best haemodynamic stability subsequently. Recovery times were fastest in the low-infusion group but there were no differences in later postbox testing. Neonatal Apgar scores and umbilical blood gas analysis were similar but NACS at two hours were poorer in the high infusion group. A propofol infusion coupled with nitrous oxide appears to be a satisfactory technique for Caesarean section.