Seizures and loss of vision in a patient with systemic lupus erythematosus.

Posterior reversible encephalopathy syndrome (PRES) is a rare neurological condition identifiable by clinical presentation and MRI appearance.1 Patients present with headache, seizures, loss of vision and altered mental function. The pathogenesis of the syndrome is poorly understood. One hypothesis is that cerebral vasospasm results in cerebral ischaemia and subsequent development of T2 hyperintensity, and the other is a temporary failure of the autoregulatory capabilities of the cerebral vessels, leading to hyperperfusion, breakdown of the blood-brain barrier, and consequent vasogenic oedema. It is believed that a rapid rise in blood pressure overcomes cerebral autoregulatory mechanisms with abrupt dilatation of cerebral arterioles. We report a patient with systemic lupus erythematosus and PRES after recurrent spontaneous abortion.

Pain on injection of propofol: comparison of metoprolol with lidocaine.

BACKGROUND AND OBJECTIVE: Pain is often experienced when propofol is injected, and intravenous lidocaine is often effective in preventing such pain. We decided to determine whether metoprolol, given before the injection of propofol, is as effective as lidocaine in reducing the incidence and severity of the pain. METHODS: Ninety patients scheduled for elective surgery under general anaesthesia were randomly allocated to one of three groups to receive either metoprolol 2 mg, lidocaine 20 mg or saline 2 mL before any propofol was injected. Each patient was given one of these agents intravenously via a 20-G cannula on the dorsum of the hand whilst the venous drainage was occluded manually, at the middle of the forearm, for 45 s. After the occlusion was released, propofol 2.0-2.5 mg kg(-1), at room temperature, was injected at 2 mL (20 mg) every 4 s. Pain was assessed verbally and scored as none (0), mild (1) or severe (2). RESULTS: The incidence of severe pain in the control group (56.7%) was significantly higher than in the metoprolol and lidocaine groups (16.6 and 10%, respectively). The number of patients who were free of pain was significantly higher in those who had been given either metoprolol or lidocaine. CONCLUSIONS: Pretreatment with intravenous metoprolol was equally as effective as lidocaine in reducing the pain associated with propofol injection.

Effects of adding alfentanil or atracurium to lidocaine solution for intravenous regional anaesthesia.

BACKGROUND AND OBJECTIVE: The addition of alfentanil or atracurium to lidocaine solution for intravenous regional anaesthesia of the arm may have advantages with respect to improved muscle relaxation and better analgesia. The study investigates these possibilities. METHODS: We investigated 33 patients. Plain lidocaine solution was administered to Group 1 (n = 11). Alfentanil (0.5 mg) and atracurium (3 mg) were added to the lidocaine solution in Groups 2 (n = 11) and 3 (n = 11), respectively. The onset of sensory and motor block, intra- and postoperative pain scores, and the duration of postoperative analgesia were evaluated. RESULTS: There was a significant difference in the speed of the onset of sensory block in the hand, but not at the tourniquet site. The onset of the motor block, intra- and postoperative pain scores, and the duration of postoperative analgesia were similar in all groups. CONCLUSIONS: No clinical benefits of adding alfentanil or atracurium to lidocaine solution for intravenous regional anaesthesia of the arm could be shown.

Candida colonization in mechanically ventilated patients.

The diagnosis of pulmonary candidosis is controversial. We undertook a prospective study on 50 mechanically ventilated (>48 h) patients who were hospitalized (>72 h) in the intensive care unit (ICU) with the aim of assessing the incidence of the isolation of Candida species from endotracheal aspirates (EA). Patients were categorized as individuals already colonized with Candida spp. on admission, individuals becoming colonized during hospitalization, or patients with no colonization. Patients in the ICU were hospitalized for a mean of 23 days. The percentage of patients already colonized with Candida was low (six of 50; 12%), the incidence of Candida isolation from EA in critically ill, mechanically ventilated patients in ICU was also low (six of 50; 12%). Age, duration of hospitalization, pre-treatment with antimicrobials or immunosuppressive agents and occurrence of underlying disease were not risk factors in our study. Both antifungal usage and neutropenia were more common in already colonized patients. No risk factors were determined for patients colonized during hospitalization. As all the isolates identified were C. albicans. It appears that at present, colonization and/or infection by more resistant Candida species is not a problem in our unit.

Comparison of intravenous metoprolol, verapamil and diltiazem on the attenuation of haemodynamic changes associated with tracheal extubation.

Changes in heart rate, systolic, diastolic and mean blood pressure were measured after extubation in 60 ASA Grade I and II patients to assess the effects of diltiazem (0.2 mg kg-1), verapamil (0.05 mg kg-1) and metoprolol (0.02 mg kg-1) given as a bolus 2 min before tracheal extubation. All the haemodynamic variables measured increased significantly after extubation in the control and diltiazem groups when compared with the base-line recordings (P < 0.05). Metoprolol effectively blocked the increases in heart rate after extubation and the increase in blood pressure in this group was less when compared with the control group (P < 0.05). Verapamil alleviated the increase in both heart rate and blood pressure. However, profound hypotension and bradycardia requiring therapy, occurred in the verapamil group. For this reason, careful observation is necessary when using verapamil and the routine use of this drug in patients with coronary artery disease requires further studies.

Pharmacokinetics of phenprobamate after oral administration to healthy subjects.

Phenprobamate (CAS 673-31-4) is a centrally acting skeletal-muscle relaxant agent. There are only two studies in the literature about the pharmacokinetics of phenoprobamate in man. The inconsistency between the results of these studies can be attributed partly to the different analytical methodologies used. A sensitive, specific and reproducible HPLC-assay, which may increase the reliability of the pharmacokinetic studies of phenprobamate in plasma, has been developed recently. The objective of this investigation was to assess the single-dose kinetics of phenprobamate in human and to determine the pharmacokinetic parameters of clinical and regulatory concern. The plasma pharmacokinetics of phenprobamate have been investigated following single oral administration at a dose of 800 mg in eleven healthy volunteers.

The effects of verapamil and nimodipine on bupivacaine-induced cardiotoxicity in rats: an in vivo and in vitro study.

UNLABELLED: The purpose of this in vivo and in vitro study was to compare the effects of verapamil or nimodipine pretreatment on bupivacaine-induced cardiotoxicity. In the in vivo study, the dose-response curve for the 50% lethal dose (LD50) of bupivacaine was determined for rats. Two separate groups of rats were pretreated with i.v. verapamil 150 microg/kg (n = 35) or i.v. nimodipine 200 microg/kg (n = 35). Each pretreatment group was then subdivided into four groups of at least four rats each. Three minutes after pretreatment, bupivacaine was administered to each of four groups in doses of 2.5, 3.0, 3.25, and 3.5 mg/kg, respectively. Both verapamil and nimodipine pretreatment increased the LD50 and 95% confidence intervals for bupivacaine and increased survival. In the in vitro study, the effects of verapamil or nimodipine perfusion on bupivacaine cardiotoxicity (negative chronotropic, negative inotropic, and arrhythmogenic effects) and coronary perfusion pressure (CPP) were investigated in isolated, perfused rat heart preparations. Depression of heart rate, contractile force, and CPP, and the incidence of arrhythmias caused by bupivacaine alone were similar to those caused by bupivacaine after verapamil pretreatment. In contrast, bupivacaine induced less negative chronotropic effects (P < 0.05, paired t-test) and arrhythmias (P < 0.05, chi2 analysis) after nimodipine pretreatment. The results of this study demonstrate that both verapamil and nimodipine pretreatment decrease bupivacaine-induced cardiotoxicity in vivo, whereas only nimodipine pretreatment decreased bupivacaine-induced cardiotoxicity and arrhythmias in vitro. IMPLICATIONS: In this experimental study consisting of two stages (in vivo and in vitro), we compared the effects of two calcium channel-blocking drugs (verapamil and nimodipine) on bupivacaine toxicity. Bupivacaine is a local anesthetic frequently used in clinical practice, and cardiotoxicity is one of its severe side effects. Verapamil and nimodipine were both effective in decreasing bupivacaine cardiotoxicity in this rat model.

Interactions of calcium channel blockers with non-depolarising muscle relaxants in vitro.

The effects of two calcium channel blockers (verapamil and nicardipine) on indirectly elicited muscle twitch and possible interactions between these drugs and non-depolarising muscle relaxants (vecuronium, atracurium, pancuronium) were investigated using isolated rat phrenic nerve-hemidiaphragm preparations. Both verapamil 10(-5) M and nicardipine 10(-6) M caused significant depression of twitch amplitude. Verapamil significantly increased vecuronium- and atracurium-induced neuromuscular block, but not that produced by pancuronium. Nicardipine potentiated atracurium-induced neuromuscular block but had no effect on pancuronium- and vecuronium-induced twitch depression. Neostigmine 10(-6) M did not produce any significant changes in the maximal recovery of twitch depression induced with calcium channel blockers and muscle relaxants combinations; also, neostigmine had no effect on maximal recovery time of twitch depression.

Complement (C3, C4) and C-reactive protein responses to cardiopulmonary bypass and protamine administration.

Complement activation has been deemed responsible for the damaging effects of cardiopulmonary bypass (CPB) in patients undergoing open heart surgery. We studied C3, C4 and C-reactive protein (CRP) in 22 patients undergoing CPB. In Group 1 (11 patients), protamine was given intravenously and in Group 2 (11 patients), via the aortic root after CPB. Significant decreases were observed in C3 and C4 during CPB in both groups indicating complement activation primarily by the classic pathway. Protamine did not lead to further activation of the complement system. In both groups, C3 levels gradually returned toward baseline within 24 hours but C4 levels were still lower than baseline 24 hours postoperatively. CPB and protamine administration did not cause any significant changes in CRP levels, but CRP increased abruptly 24 hours after operation. Although activation of complement system during CPB is expected to invoke an acute phase response, we conclude that this period is not long enough to induce an increased production of CRP in response to tissue injury or inflammation.