Gale E. Thompson

Functional Anatomy of the Brachial Plexus Sheaths

The brachial plexus sheath was examined in cadavers by suing a combination of anatomic dissection, histologic preparations, and x-rays made after injection of x-ray contrast media, and in surgical patients by using computed tomography (CT) dye studies. The connective tissue forming the sheath was organized more densely proximally near its origin and became loosely organized distally as it ended by joining the medial intermuscular septum of the arm. The connective tissue forming the sheath extends inward, forming septa between components of the plexus. Thus, the sheath is a multicompartmented structure, formed by the thin connective tissue sheath surrounding the plexus and by the septa which extend inward from the sheath. A fascial compartment is created for each nerve, and this compartment serves to define the anatomic limits of that nerve. These compartments have potential clinical importance and implication in the techniques for brachial plexus block. They serve functionally to limit the circumferential spread of injected solutions of local anesthetics. These studies also indicate that injected anesthetic solutions spread easily in a longitudinal manner up and down the nerve and remain compartmentalized. The data presented here provide a rational explanation for the not uncommon occurrence of a profound block of rapid onset in one nerve, yet partial or absent block in other nerves, following any of the techniques of brachial plexus anesthesia.

Hypotensive anesthesia for total hip arthroplasty: a study of blood loss and organ function (brain, heart, liver, and kidney).

The authors attempted to determine whether hypotensive anesthesia or the method of inducing hypotension has any effect on postoperative brain, liver, or kidney function and myocardial status following total hip arthroplasty. Thirty patients were anesthetized with halothane–nitrous oxide for total hip arthroplasty and randomly assigned to one of three groups. In two groups mean arterial blood pressure was decreased to 50 torr by high inspired concentrations of halothane (n = 9) or sodium nitroprusside (n = 12). In the third group (n = 9) mean blood pressure was maintained within 20 per cent of control. Intraoperative blood losses decreased from 1,183 ± 172 ml in the normotensive group to 406 ± 102 ml and 326 ± 41 ml in the halothane and nitroprusside hypotensive groups, respectively. Neither method of inducing hypotension nor hypertensive technique affected the results of postoperative tests of cerebral, hepatic, or renal function and myocardial status. These tests were performed before anesthesia and operation and at intervals in the postoperative course. In this small group of patients, deliberate hypotension for total hiparthroplasty added no morbidity and significantly shortened operating time, decreased blood loss, and decreased the number of blood transfusions needed.

A comparison of epidural levobupivacaine 0.75% with racemic bupivacaine for lower abdominal surgery.

Levobupivacaine, the S(−) isomer of bupivacaine, is less cardiotoxic than racemic bupivacaine. In this prospective, randomized, double-blinded study of epidural anesthesia, the onset, extent, and duration of sensory and motor block produced by 0.75% levobupivacaine (20 mL, 150 mg) was compared with that of 0.75% racemic bupivacaine in 56 patients undergoing elective lower abdominal surgery. The time to onset of adequate sensory block (T10 dermatome) was similar in both treatment groups (13.6 ± 5.6 min for levobupivacaine and 14.0 ± 9.9 min for bupivacaine), with an average peak block height of T5 reached at 24.3 ± 9.4 and 26.5 ± 13.2 min, respectively. Time to complete regression of sensory block was significantly longer with levobupivacaine (550.6 ± 87.6 min) than bupivacaine (505.9 ± 71.1 min) (P = 0.016). Abdominal muscle relaxation was adequate for the scheduled procedure in all patients, and there were no significant differences between the groups in rectus abdominis muscle scores (P = 0.386) and quality of muscle relaxation as determined by the surgeon and anesthesiologist (P = 0.505 and 0.074, respectively). In conclusion, both 0.75% levobupivacaine and 0.75% bupivacaine produced effective epidural anesthesia and their effects were clinically indistinguishable. Implications: The results of this study indicate that the sensory and motor block produced by 0.75% levobupivacaine is equivalent to that of 0.75% racemic bupivacaine. Both local anesthetics are well tolerated and effective in producing epidural anesthesia for patients undergoing lower abdominal surgery.

Systemic Absorption of Mepivacaine in Commonly Used Regional Block Procedures

Arterial plasma level-versus-time profiles of mepivacaine were determined for 70 surgical patients undergoing epidural, caudal, intercostalnerve, brachial-plexus, and sciatic/femoral-nerve blocks. A single dose of 500 mg of mepivacaine HCl was used. The conditions studied were route of injection, concentration of drug solution (1 and 2 per cent), and presence or absence of epinephrine, 1:200,000, in the injected solution. Each condition tested resulted in significant changes in maximum plasma levels (Cpmax), time to occurrence of Cpmax (tmax), and areas under plasma level-versus-time curves (∫Cp.dt). The highest plasma concentrations (5–10 µg base/ml) were seen after intercostal-nerve blocks using plain solutions, but addition of epinephrine caused these to become comparable to peak levels after the other blocks (2–5 µg base/ml). For those blocks studied at both concentrations, use of the 2 per cent solution was always associated with the higher Cpmax and ∫Cp.dt values. Mean values of tmax using plain solutions ranged from 9 min (intercostal block) to 30 min (sciatic/femoral) and were increased two-to-threefold by the addition of epinephrine. No systemic toxic reactions were encountered, indicating the safety of the dosage used under the conditions of the study. Addition of epinephrine, 1:200,000, to mepivacaine solutions is recommended for the nerve blocks investigated, especially for intercostal-nerve block.

Distribution of local anesthetic in axillary brachial plexus block : A clinical and magnetic resonance imaging study

Background There is an unsettled discussion about whether the distribution of local anesthetic is free or inhibited when performing brachial plexus blocks. This is the first study to use magnetic resonance imaging (MRI) to help answer this question. Methods Thirteen patients received axillary block by a catheter–nerve stimulator technique. After locating the median nerve, a total dose of 50 ml local anesthetic was injected via the catheter in four divided doses of 1, 4, 15, and 30 ml. Results of sensory and motor testing were compared with the spread of local anesthetic as seen by MRI scans taken after each dose. The distribution of local anesthetic was described with reference to a 20-mm diameter circle around the artery. Results Thirty minutes after the last dose, only two patients demonstrated analgesia or anesthesia in the areas of the radial, median, and ulnar nerve. At that time, eight of the patients had incomplete spread of local anesthetic around the artery, as seen by MRI. Their blocks were significantly poorer than those of the five patients with complete filling of the circle, although incomplete blocks were also present in the latter group. Conclusion This study demonstrated that MRI is useful in examining local anesthetic distribution in axillary blocks because it can show the correlation between MRI distribution pattern and clinical effect. The cross-sectional spread of fluid around the brachial–axillary artery was often incomplete–inhibited, and the clinical effect often inadequate.

Pharmacokinetics of Ropivacaine and Bupivacaine for Bilateral Intercostal Blockade in Healthy Male Volunteers

BackgroundIntercostal blockade produces the highest serum local anesthetic concentrations of all regional anesthetic techniques. The purpose of this study was to determine the pharmacokinetic properties of ropivacaine and bupivacaine after bilateral intercostal blockade. MethodsThe pharmacokinetics of ropivacaine (n = 7) and bupivacaine (n = 7) were determined in adult human volunteers from venous samples drawn over 24 h after bilateral intercostal blockade of T5-T11 with 140 mg of either drug (0.25% plain solutions, 56 ml). Sensory (pinprick, temperature, and touch) and motor blockade (RAM-test and integrated electromyography) were assessed every 2 h. ResultsThere was no significant difference between the maximum plasma concentrations (Cmax) obtained for either drug (ropivacaine 1.1 ± 0.4 μg/ml, bupivacaine 0.9 ± 0.2 μg/ml, P= 0.39), and there were no toxic signs observed in the obtained plasma concentration ranges. Plasma concentrations tended to peak (tmax) earlier with ropivacaine (21 ± 9 versus 30 ± 8 min, P = 0.09). The terminal half-life (t1/2β) of ropivacaine (2.3 ± 0.8 h) was significantly less than that for bupivacaine (4.6 ± 2.6 h, P = 0.04).Sensory blockade measured by pinprick was of shorter duration with ropivacaine (6.0 ± 2.5 h versus bupivacaine 10.0 ± 3.0 h; P < 0.001). Likewise, motor blockade was less Intense and of shorter duration for ropivacaine by RAM-test (P = 0.02). ConclusionsThe results of this pharmacokinetic study indicate that 0.25% ropivacaine and 0.25% bupivacaine (56 ml, 140 mg) produce peak plasma levels less than those considered toxic when used in bilateral intercostal blockade. Studies of ropivacaine for intercostal blockade in surgical patients are necessary before the optimum concentration for efficacy and anesthetic/analgesic duration is identified.

Effect of Midazolam and Diazepam Premedication on Central Nervous System and Cardiovascular Toxicity of Bupivacaine in Pigs

To determine the effect of benzodiazepine premedication on central nervous system and cardiovascular effects of bupivacaine, the authors administered toxic doses of bupivacaine to awake spontaneously breathing pigs after intravenous premedication with midazolam (0.06 mg/kg), diazepam (0.15 mg/kg), or saline. Five minutes after administration of one of these solutions, they began an infusion of bupivacaine at 2 mg.kg-1.min-1. The bupivacaine infusion was continued until cardiovascular collapse. They then attempted to resuscitate the animals via open chest cardiac massage and a standard resuscitation protocol. Premedication with midazolam or diazepam significantly delayed the onset of ventricular dysrhythmias (P less than 0.05), decreased the incidence of seizures (P less than 0.05), and prevented the increase in blood pressure and heart rate following bupivacaine infusion (P less than 0.05). Benzodiazepine premedication did not affect the dose of bupivacaine or the blood concentration required to produce cardiovascular collapse. The ability to resuscitate animals premedicated with midazolam did not differ from control; however, significantly fewer animals premedicated with diazepam were resuscitated (P less than 0.05). A clinically relevant observation was that almost all animals premedicated with a benzodiazepine progressed directly to cardiovascular collapse without first manifesting seizures.

Effect of Epinephrine on Central Nervous System and Cardiovascular System Toxicity of Bupivacaine in Pigs

To determine what effect the addition of epinephrine has on bupivacaine toxicity, toxic doses of bupivacaine were administered to awake spontaneously breathing pigs. Twenty animals were randomized to one of two groups. One group received an infusion of bupivacaine with epinephrine (5 micrograms/ml) at a rate of 2 mg.kg-1.min-1; the other received an infusion of plain bupivacaine at the same rate. Bupivacaine infusion was continued until cardiovascular collapse. Following cardiovascular collapse we attempted to resuscitate the animals via open chest cardiac massage and a standardized resuscitation protocol. The addition of epinephrine to bupivacaine significantly increased blood pressure and systemic vascular resistance but not heart rate or cardiac output early in the bupivacaine infusion. Epinephrine had no effect on the dose of bupivacaine that caused cardiovascular collapse (P = 0.1), on the plasma concentration of bupivacaine at collapse (P = 0.9), or on the ability to resuscitate animals following cardiovascular collapse. The addition of epinephrine decreased the dose of bupivacaine required to initiate cardiac dysrhythmias (P = 0.003). The first dysrhythmia experienced by the epinephrine group was second degree heart block, which contrasts with the premature ventricular and atrial dysrhythmias experienced by the plain group. The dose of bupivacaine that produced seizures was also reduced by the addition of epinephrine (P = 0.006). The addition of epinephrine to bupivacaine did not alter the dose of bupivacaine that caused cardiovascular collapse in awake spontaneously breathing pigs but did decrease the dose of bupivacaine that caused seizures and dysrhythmias.

Factors determining dosages of amide-type local anesthetic drugs.

The physical status of the patient (sex, age, weight, height, and underlying disease) has been thought to influence the dosage of local anesthetic drugs that can be injected without causing a systemic toxic reaction, but this belief is not supported by statistically significant data. Furthermore, previous studies of plasma levels of bupivacaine and mepivacaine showed no correlation between dosage and physical status, even when maximum dosages recommended by pharmaceutical companies were exceeded. This study of 9,287 regional blocks, using the statistical tests of multiple regression and chi square, substantiates that the occurrence of systemic toxic reactions in adults does not correlate with dosages and/or physical status of the patient when 400 mg or less of bupivacaine, 450 mg or less of etidocaine, or 500 mg or less of mepivacaine is used. Therefore, the study questions the maximum dosages established for certain local anesthetic drugs, as well as the method by which such dosages were established.

Commentary: neurotoxicity of local anesthetics--an issue or a scapegoat?

Background and Objectives. To evaluate the etiologies of cauda equina syndrome (CES) and transient radicular irritation (TRI) or transient neurologic symptoms (TNSs) following hyperbaric spinal anesthesia. Methods. A review of recent (since 1991) and prior (since 1941) investigations regarding CES and TRI (TNSs) was conducted. Results. Recent publications fail to recognize significant prior information regarding CES and TRI (TNSs). Conclusions. Cauda equina syndrome is, in all probability, explainable. Further investigation to pinpoint the etiology of TRI (TNSs) is needed.