Search

Intravenous lipid emulsion has been suggested as treatment for local anaesthetic toxicity, but the exact mechanism of action is still uncertain. Controlled studies on the effect of lipid emulsion on toxic doses of local anaesthetics have not been performed in man. In randomized, subject-blinded and two-phase cross-over fashion, eight healthy volunteers were given a 1.5 ml/kg bolus of 20% Intralipid(®) (200 mg/ml) or Ringer's acetate solution intravenously, followed by a rapid injection of lidocaine 1.0 mg/kg. Then, the same solution as in the bolus was infused at a rate of 0.25 ml/kg/min. for 30 min. Electroencephalography (EEG) was recorded, and 5 min. after lidocaine injection, the volunteers were asked to report subjective symptoms. Total and un-entrapped lidocaine plasma concentrations were measured from venous blood samples. EEG band power changes (delta, alpha and beta) after the lidocaine bolus were similar during lipid and during Ringer infusion. There were no differences between infusions in the subjective symptoms of central nervous system toxicity. Lidocaine was only minimally entrapped in the plasma by lipid emulsion, but the mean un-entrapped lidocaine area under concentration-time curve from 0 to 30 min. was clearly smaller during lipid than Ringer infusion (16.4 versus 21.3 mg × min/l, p = 0.044). Intravenous lipid emulsion did not influence subjective toxicity symptoms nor affect the EEG changes caused by lidocaine., (© 2014 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).)

Reports on the efficacy and pharmacokinetics of local anesthetics in uremic patients have been controversial. Our study involved 29 uremic and 28 nonuremic patients. We performed axillary block with ropivacaine 300 mg (50 mL). Venous blood samples were drawn for 24 h for assay of total and unbound plasma ropivacaine, 3-hydroxyropivacaine, pipecoloxylidide (PPX), and serum alpha(1)-acid glycoprotein (AAG). Block quality was similar in both groups. No toxicity occurred. Plasma clearance of ropivacaine was smaller and the area under the concentration-time curve of ropivacaine, 3-hydroxyropivacaine, and PPX larger in the uremic patients. The plasma concentration of PPX increased until 24 h in uremic patients whose AAG concentrations were also larger throughout the study. The free fraction of ropivacaine in plasma was smaller in the uremic group when measured 60 min and 12 h after the block, but the unbound concentration of ropivacaine was larger in the uremic group at 12 h. Enhanced absorption of ropivacaine into circulation, increased binding to AAG, and probably reduced urinary excretion of the metabolites lead to larger total plasma concentrations of ropivacaine and its main metabolites in uremic patients.

Background and Objectives: Major complications after spinal or epidural anesthesia are extremely rare. The occurrence of less serious and transient sequelae and complaints may be underestimated if there is no established organization for the systematic and continuous surveillance of patients after anesthesia. This study was designed to evaluate the possible relationship between various block-related occurrences and the intra- and postoperative side effects and complaints., Methods: This prospective study included 3,230 orthopedic patients operated on under neuraxial block. The block was performed by single-dose (single-shot spinal anesthesia [SPIN], 80.6%), continuous spinal anesthesia (CSA, 10.3%), or combined spinal and epidural anesthesia (CSE, 9.1%) technique. The patient position during surgery and a detailed description of block performance and equipment, as well as all intraoperative problems, were immediately recorded. Every patient was given a standardized questionnaire to be completed and returned after 1 week., Results: The overall incidence of paresthesia was 12.8%, being most frequent during spinal catheter insertion with multiple attempts. Postoperative sensory disturbances (numbness, dysesthesia) occurred unrelated to paresthesia elicited by the puncture or catheterization. The failure rates (SPIN, 1.0%; CSA, 1.5%; and CSE, 1.0%) were quite low. Asystole with successful resuscitation, occurred in 1 patient with CSE but, overall, hemodynamic perturbations were more common with the continuous techniques. On the first postoperative day, decreased sensation of the skin was significantly more frequent after the continuous techniques, still present in 6.5% of SPIN patients, 6.1% of CSA patients, and 17.2% of CSE patients 1 week after surgery. These disturbances were also related to the use of a tourniquet and lateral position of the patient during surgery. The frequency of postdural puncture headache (PDPH) was similar for the different techniques (SPIN, 0.9%; CSA, 1.5%; and CSE, 1.7%). About one third of the patients reported strong postoperative pain on the day after the operation, and 5.6% continued to report this at 1 week., Conclusions: Although sensory changes were quite frequent, they were mild and transient. Rather than having been caused by the anesthetic technique, per se, a "nonanesthetic" reason (position, tourniquet, immobilization) should also be considered as their origin. Sensory disturbances, as well as strong pain for at least a week, were reported by several patients, and to become aware of these problems and improve the quality of treatment, a universal regional anesthesia follow-up system is recommended.

Background and Objectives: The use of thin single-hole pencil-point (SHPP) spinal needles may be a reason for subarachnoid maldistribution of local anesthetic. A new double-hole pencil-point (DHPP) needle may be preferable because of a theoretic more uniform initial distribution of local anesthetic., Methods: This was a prospective, double-blinded study of 50 patients randomly selected to have spinal anesthesia using either single-hole 27-gauge (B. Braun, Melsungen, Germany) or double-hole 26-gauge (A.L.B. Medical Inc., U.S.A.) pencil-point needles. The former were inserted with the side port directed caudally and the latter with openings in both caudal and cranial direction. Two milliliters of hyperbaric 0.5% bupivacaine were injected in 1 minute, and sensory and motor block were studied at regular intervals during spinal anesthesia. All patients were interviewed on the first (personal) and the seventh (mailed questionnaire) postoperative day. Furthermore, microscopic inspection of the spinal needles was performed., Results: There were no statistically significant differences in sensory or motor block levels between the two needle types at any time during spinal anesthesia. Likewise, there was no difference in the duration of spinal block. The postanesthetic side effects (headache, backache, pricking, numbness, weakness) were similar in both groups. Light and electron microscopic examination showed resistance of the SHPP needles to tip damage. On the other hand, the DHPP needle tips seemed to be distorted quite frequently, and, even in unused needles, the tip was blunt and asymmetric., Conclusion: There was no difference between the spread of analgesia using either SHPP or DHPP spinal needles. The DHPP needles appear to be vulnerable to tip damage from mechanical contact.

The purpose of this study was to compare the perioperative effects of the intramuscular (i.m.) alpha 2 agonist, dexmedetomidine (DEX), and midazolam (MID) premedication. The study comprised 192 women (64 per group) scheduled for abdominal hysterectomy. The doses of the study drugs were chosen to obtain equal sedative effects. The three groups were: 1) i.m. DEX (2.5 micrograms/kg) and intravenous (i.v.) placebo (DexPla group), 2) i.m. DEX and i.v. fentanyl (FENT) (1.5 micrograms/kg) (DexFent group), and 3) i.m. MID (0.08 mg/kg) and i.v. FENT (MidFent group). I.m. drugs were administered 45-90 min before induction of anesthesia. Preoperative sedation and anxiolysis after DEX was comparable to that after MID. The maximum arterial blood pressure response to endotracheal intubation was blunted in the DexFent group, while in the two other groups blood pressure increased 30-34 mm Hg after endotracheal intubation. The mean isoflurane concentration during surgery was 0.14% in the DexFent group, 0.24% in the DexPla group, and 0.34% in the MidFent group (P < 0.001). During surgery, bradycardia (heart rate < 40 bpm) was observed in 6.2% of DEX patients, and no MID patients, whereas postoperatively 14.1% of DEX patients and 1.6% of MID patients had bradycardia. Fewer patients suffered from postoperative shivering after DEX (10%) than after MID (52%). We conclude that DEX has many desirable effects, but side effects such as bradycardia may limit its routine use in ASA physical status I-II patients.

A randomized study was designed to compare eltanolone (pregnanolone) and propofol anesthesia in 60 unpremedicated women undergoing outpatient termination of pregnancy. The initial doses for induction of anesthesia were 0.8 mg/kg for eltanolone and 2 mg/kg for propofol followed by an additional 25% increment if necessary. The doses required for successful induction were 0.82 +/- 0.06 and 2.1 +/- 0.3 (mean +/- SD) mg/kg for eltanolone and propofol, respectively. Discomfort or pain on injection occurred in none of the patients given eltanolone and in 20% of those receiving propofol (P < 0.05). To maintain satisfactory anesthesia, 29% of the patients given eltanolone and 70% of the patients given propofol needed extra bolus doses of the study drug (P < 0.01). Excitation (twitching of extremities or slight hypertonus) occurred in 29% of the patients in the eltanolone group compared to none in the propofol group (P < 0.05). Both clinical (opening eyes, orientation, walking, tolerating oral fluids, voiding) and psychomotor recovery (Maddox Wing test and Digit Symbol Substitution test) returned to baseline more slowly after eltanolone than after propofol. Overall home readiness was achieved later in the eltanolone group [median 57 min (range 41-190 min)] compared to the propofol [37 (32-100 min)] group. We conclude that recovery from anesthesia is more rapid from propofol as compared to eltanolone anesthesia.

The treatment of bupivacaine-induced cardiovascular toxicity with amiodarone or bretylium was studied using anesthetized pigs (n = 30). The pigs were given ketamine, glycopyrrolate, enflurane, and pancuronium and made hypoxic (FiO2, 12%; N2O, 88%) and hypercarbic (end-tidal CO2, 7.3-8.0%) before the administration of bupivacaine (4 mg/kg i.v.). The animals were then treated, in a randomized and double-blind fashion, with either amiodarone (n = 10) 10 mg/kg in 5% dextrose solution i.v. followed by a constant infusion of 15 mg/hour, bretylium (n = 10) 20 mg/kg in 5% dextrose solution i.v. followed by a constant infusion of 90 mg/hour, or 5% dextrose solution (n = 10). The animals were resuscitated, if required. After 30 minutes of recovery, the animals that survived were made hypoxic and hypercarbic again and given a second injection of bupivacaine (2 mg/kg IV). Bupivacaine caused marked changes in the ECG; polymorphic ventricular tachycardia (20 cases) or severe bradycardia that resulted in asystole (10 cases). Nine animals out of ten treated with amiodarone survived (stable sinus rhythm, arterial blood pressure at near control level, normocarbia), whereas six animals in the bretylium group and four in the control group died. The difference in survival between the groups was not, however, statistically significant.

The analgesic effect of topical application of local anaesthetics on the gingival mucosa and the absorption of the local anaesthetics into the blood were investigated in healthy volunteers by using a 5% eutectic mixture of the local anaesthetics lignocaine (100 mg) and prilocaine (100 mg) plus emulsifier (EMLA) or 10% lignocaine (200 mg) spray (Xylocain). The pain threshold on labial gingiva was measured by using the stimulator of an EMG-apparatus and a pair of stimulating electrodes, specially constructed for this purpose. There were no differences between the two methods in producing analgesia which was at its maximum in 13 to 14 minutes, on average. Sensation of the gingiva (pain thresholds), had usually returned to normal within 30 minutes. In the dosages used, the absorption of the local anaesthetics was more rapid after the mixture application than after spray application. No toxic reactions occurred.

Continuous interscalene brachial plexus block with a single dose of 0.75% bupivacaine (150-210 mg) with adrenaline, continued with an infusion of plain 0.25% bupivacaine 0.25 mg/kg/h, was performed on 20 patients to provide analgesia during shoulder surgery and in the postoperative period. The control group included 20 patients who were given general anaesthesia for surgery after starting a continuous interscalene brachial plexus block; test dose of 0.75% bupivacaine (22.5 mg) with adrenaline, continued with an infusion of 0.25% bupivacaine 0.25 mg/kg/h. Surgery was performed successfully under regional anaesthesia in 16/20 patients; 4/16 were given one dose of fentanyl during the surgery, and diazepam or midazolam as supplementary sedation were given in 13/16 cases. For postoperative analgesia 35/40 patients had a fully functioning catheter for 20-26 hours and the need for oxycodone i.m. during that time was 1.5 +/- 0.4 doses after regional anaesthesia (n = 14) and 1.8 +/- 0.4 doses after general anaesthesia (n = 18). There was a statistically significant difference in the mean plasma bupivacaine concentrations between the groups, concentrations in the regional anaesthesia group being higher at 5, 30, 60 min and 3 h (maximum 2.3 micrograms/ml at 60 min), but there was no difference between the values at 24 h. One infusion of local anaesthetic was discontinued because of probable treatment-related side-effects (breathing difficulties, nausea). Mild local anaesthetic toxicity (dizziness, tinnitus) was noticed in four patients.

Blocking efficacy and acute toxicity of prilocaine (15 ml of 10 mg/ml prilocaine) was examined in 35 (16 + 19) patients by using blocks of the radial, ulnar and median nerves in the elbow region (Group 1), or the haematoma block method (Group 2) for the manipulation of Colles' fracture. In Group 1 vs Group 2, the reposition was painless in 44% (7/16) vs 68% (13/19), moderate pain occurred in 38% (6/16) vs 21% (4/19), and severe pain in 19% (3/16) vs 11% (2/19). At 15 minutes there was a higher degree of block, on average, at the median and ulnar nerve innervation areas in Group 1. Complete motor block at peripheral innervation regions of all three nerves was achieved in only one patient in Group 1 and in no case in Group 2. Despite this, the surgeons assessed the relaxation at the wrist satisfactory for reposition of the fracture in all but one patient (Group 2). The highest individual prilocaine plasma concentration in Group 1 was 0.68 microgram/ml at ten minutes, whereas the highest individual value in Group 2 was 0.77 microgram/ml at ten minutes. Systemic toxicity from the local anaesthetic did not occur.

The present investigation was designed to study the interaction of temperature, lidocaine, and ischemia during intravenous regional anesthesia (IVRA) of the arm. Five volunteers were studied during exposure of one of their arms to four different experimental conditions: hypothermia and ischemia; hypothermia, ischemia, and lidocaine; normothermia and ischemia; normothermia, ischemia, and lidocaine. Each subject was tested on four different occasions with only one test condition imposed per occasion and with 3 or more days between experiments. Somatosensory evoked responses (SERs) and muscle responses to ulnar nerve stimulation were measured, and sensory testing was done to determine whether the neural effects of the particular treatments differed. Anesthesia developed sooner and was more extensive when local anesthetic was injected. A 5-10 degrees C decrease in tissue temperature did not accentuate the anesthetic effects of lidocaine as determined by time to loss of pinprick and touch sensation. With ischemia alone, anesthesia of the finger tips with preservation of sensation on the arm was observed in all subjects 20 min after tourniquet inflation. Anesthesia at all cutaneous test sites was achieved in 7 of 10 lidocaine experiments; no systematic order of sensory loss, such as progression from distal to proximal sites, was observed. Decrease in limb temperature slowed the development of lidocaine effects on evoked responses and recovery from the effect. Under conditions of ischemia, deterioration of sensation generally began earlier under cold rather than warm conditions. Primary differences between changes in the SERs and muscle responses under condition of ischemia versus ischemia and lidocaine were the rate and magnitude of change of potential latency and amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)