Rosemary Hickey

A Comparison of Ropivacaine 0.5% and Bupivacaine 0.5% for Brachial Plexus Block

This study compared the effectiveness of 0.5% ropivacaine and 0.5% bupivacaine for brachial plexus block. Forty-eight patients received a subclavian perivascular brachial plexus block for upper-extremity surgery. One group (n = 24) received ropivacaine 0.5% (175 mg) and a second group (n = 24) received bupivacaine 0.5% (175 mg), both without epinephrine. Onset times for analgesia and anesthesia in each of the C5 through T1 brachial plexus dermatomes did not differ significantly between groups. Duration of analgesia and anesthesia was long (mean duration of analgesia, 13-14 h; mean duration of anesthesia, 9-11 h) and also did not differ significantly between groups. Motor block was profound, with shoulder paralysis as well as hand paresis developing in all of the patients in both groups. Two patients in each group required supplemental blocks before surgery. Ropivacaine 0.5% and bupivacaine 0.5% appeared equally effective in providing brachial plexus anesthesia.

Autoregulation of spinal cord blood flow: is the cord a microcosm of the brain?

The autoregulatory capability of regional areas of the brain and spinal cord was demonstrated in 18 rats anesthetized with a continuous infusion of intravenous pentothal. Blood flow was measured by the injection of radioactive microspheres (Co57, Sn113, Ru103, Sc46). Blood flow measurements were made at varying levels of mean arterial pressure (MAP) which was altered by neosynephrine to raise MAP or trimethaphan to lower MAP. Autoregulation of the spinal cord mirrored that of the brain, with an autoregulatory range of 60 to 120 mm Hg for both tissues. Within this range, cerebral blood flow (CBF) was 59.2 +/- 3.2 ml/100 g/min (SEM) and spinal cord blood flow (SCBF) was 61.1 +/- 3.6. There was no significant difference in CBF and SCBF in the autoregulatory range. Autoregulation was also demonstrated regionally in the left cortex, right cortex, brainstem, thalamus, cerebellum, hippocampus and cervical, thoracic and lumbar cord. This data provides a coherent reference point in establishing autoregulatory curves under barbiturate anesthesia. Further investigation of the effects of other anesthetic agents on autoregulation of the spinal cord is needed. It is possible that intraspinal cord compliance, like intracranial compliance, might be adversely affected by the effects of anesthetics on autoregulation.

Plasma concentrations of ropivacaine given with or without epinephrine for brachial plexus block

The purpose of this study was to determine the pharmacokinetic properties of the local anaesthetic ropivacaine used with or without epinephrine for brachial plexus block. Seventeen ASA physical status I or II adult patients undergoing elective orthopaedic surgery received a single injection of 33 ml ropivacaine for subclavian perivascular block and 5 ml to block the intercostobrachial nerve in the axilla. One group (n =8) received 0.5 per cent ropivacaine without epinephrine (190 mg) and the other (n =9) received 0.5 per cent ropivacaine with epinephrine 1:200,000 (190 mg). Plasma ropivacaine concentrations were measured from peripheral venous blood samples taken for 12 hr after drug administration. Ropivacaine base was determined in plasma using gas chromatography and a nitrogen-sensitive detector. The mean peak plasma concentration (Cmax) was 1.6 ± 0.6 mg· L−1 and 1.3 ± 0.4 mg· L−1 after administration of ropivacaine with and without epinephrine. The median time to peak plasma concentration (tmax) was 0.75 hr and 0.88 hr and the mean area under the plasma concentration curve AUC0-12h was 7.7 ± 3.6 and 7.0 ± 3.4 mg · 1 hr−1. The differences were not statistically significant. The terminal phase of the individual plasma concentrationtime curves showed a varying and sometimes slow decline possibly indicating a sustained systemic uptake of ropivacaine from the brachial plexus. No central nervous system or cardiovascular symptoms attributed to systemic plasma concentrations of the drug were observed, with the dose (1.90–3.28 mg · kg−1) of ropivacaine used. It is concluded that the addition of epinephrine does not alter the pharmacokinetic properties of ropivacaine when used for subclavian perivascular brachial plexus block.RésuméLe but de cet étude était de déterminer la pharmacocinetique de l’anesthésique local ropivacaine utilisé avec ou sans épinéphrine pour un bloc de plexus brachiale. Dixsept patients adultes ASA I ou 2 devant subir des chirurgies orthopédiques électives out reçu une injection unique de 33 ml de ropivacaine pour un bloc perivasculaire sous claviere 5 ml afin de bloquer le nerf intercostal brachial à I’aisselle. Un groupe (n =8) a reçu 0.5 pour cent de ropivacaine sans épinéphrine (190 mg) et l’autre (n =9) a reçu 0.5 pour cent de ropivacaine avec epinephrine 1:200,000 (190 mg). Les concentrations plasmatiques de ropivacaine out été mesurées à partir d’échantillons veineux périphériques 12 heures apres l’administration de la drogue. La base de ropivacaine a été déterminee dans le plasma utilisant la chromotographie et un détecteur sensible à l’azote. Les concentrations plasmatiques moyennes les plus élevées (Cmax) était de 1.6 ± 0.6 mg · L−1 et 1.3 ± 0.4 mg· L−1 après administration de ropivacaine avec ou sans épinéphrine. Le temps moyen pour atteindre la concentration plasmatique maximale (tmax) était de 0.75 heures et 0.88 heures vu la moyenne de la surface sous la courbe de concentration plasmatique AUC0–12h était de 7.7 ± 3.6 et7.0 ± 3.4 mg ·1 hr−1−1. Les differences n’ ètaient pas statistiquement significatives. La phase terminale des courbes des concentrations plasmatiquestemps out demontre un declin variable el des fois lent indiquant possiblement une rétention systemique soutenue ds ropivacaine a partir du plexus brachial. Aucun symptome cardiovasculaire ou nerveux central attribue aux concentrations plasmatiques de la drogue furent observe avec des doses de (1.90–3.28 mg · kg−1)de ropivacaine utilisée. On conclut que l’addition d’épinéphrine n’allère pas la pharmacocinetique de la ropivacaine lorsqu’utilisée pour un bloc de plexus brachial.

Tracheal intubation using alfentanil and no muscle relaxant: is the choice of hypnotic important?

Administration of alfentanil followed by propofol intravenously (IV) without neuromuscular blockade for induction of anesthesia provides adequate conditions for tracheal intubation.Other hypnotic drugs have not been thoroughly investigated in this regard. Accordingly, 140 ASA physical status I and II premedicated outpatients were randomly assigned to one of seven groups (n = 20/group). Patients in Groups I-VI received alfentanil 40 micro g/kg followed by etomidate 0.3 mg/kg, propofol 2 mg/kg, or thiopental 4 mg/kg. One half of these patients (Groups II, IV, VI) also received lidocaine 1 mg/kg IV prior to the administration of the above drugs. Patients in group VII received d-tubocurarine 3 mg followed by thiopental 4 mg/kg and succinylcholine 1 mg/kg. Ninety seconds after induction, laryngoscopy and endotracheal intubation were attempted and graded. Patients in Group V (alfentanil/thiopental) were significantly (P < 0.05) more likely to have a clinically unacceptable response to intubation (55%) (e.g., vigorous coughing, purposeful movement, or requirement for succinylcholine to complete intubation) compared with patients who received propofol (35%) or etomidate (20%). Alfentanil/etomidate yielded intubation conditions comparable to those achieved with alfentanil/propofol and d-tubocurarine/thiopental/succinylcholine. Lidocaine appeared to improve intubating conditions, although this improvement did not reach statistical significance. The results suggest that healthy, premedicated patients with favorable airway anatomy who have received alfentanil 40 micro g/kg can be reliably tracheally intubated 90 s after administration of propofol 2 mg/kg or etomidate 0.3 mg/kg. (Anesth Analg 1997;84:1222-6)

A comparative study of 0.25% ropivacaine and 0.25% bupivacaine for brachial plexus block

The present study compares the effectiveness of 0.25% ropivacaine and 0.25% bupivacaine in 44 patients receiving a subclavian perivascular brachial plexus block for upper extremity surgery. The patients were assigned to two equal groups in this randomized, double-blind study; one group received ropivacaine 0.25% (112.5 mg) and the other, bupivacaine 0.25% (112.5 mg), both without epinephrine. Onset times for analgesia and anesthesia in each of the C-5 through T-1 brachial plexus dermatomes did not differ significantly between the two groups. The mean onset time for analgesia ranged from 11.2 to 20.2 min, and the mean onset time for anesthesia ranged from 23.3 to 48.2 min. The onset of motor block differed only with respect to paresis in the hand, with bupivacaine demonstrating a shorter onset time than ropivacaine. The duration of sensory and motor block also was not significantly different between the two groups. The mean duration of analgesia ranged from 9.2 to 13.0 h, and the mean duration of anesthesia ranged from 5.0 to 10.2 h. Both groups required supplementation with peripheral nerve blocks or general anesthesia in a large number of cases, with 9 of the 22 patients in the bupivacaine group and 8 of the 22 patients in the ropivacaine group requiring supplementation to allow surgery to begin. In view of the frequent need for supplementation noted with both 0.25% ropivacaine and 0.25% bupivacaine, we do not recommend using the 0.25% concentrations of these local anesthetics to provide brachial plexus block.

Brachial plexus block with a new local anaesthetic: 0.5 percent ropivacaine

A new local anaesthetic, ropivacaine hydrochloride, was used in a concentration of 0.5 per cent in 32 patients receiving a subclavian perivascular block for upper extremity surgery. One group (n = 15) received 0.5 per cent ropivacaine without epinephrine and a second group (n = 17) received 0.5 per cent ropivacaine with epinephrine in a concentration of 1:200,000. Anaesthesia was achieved in 87 per cent of the patients in both groups in all of the C5 through T1 brachial plexus dermatomes. Motor block was profound with 100 per cent of patients in both groups developing paresis at both the shoulder and hand and 100 per cent developing paralysis at the shoulder. There was a rapid initial onset of sensory block (a mean of less than four minutes for analgesia) with a prolonged duration (a mean of greater than 13hr of analgesia). The addition of epinephrine did not significantly affect the quality or onset of sensory or motor block. The duration of sensory block was reduced by epinephrine at T1 for analgesia and at C7, C8, and T1 for anaesthesia. The duration of sensory block in the remaining brachial plexus dermatomes as well as the duration of motor block was not effected by epinephrine. There was no evidence of cardiovascular or central nervous system toxicity in either group with a mean dose of 2.5– 2.6 mg · kg− 1 ropivacaine.RésuméAfin de permettre une intervention chirugicale sur le membre supérieur, nous avons fait chez 32 patients un bloc périvasculaire par approche sous- clavière en utilisant une solution de 0,5 pour cent d’hydrochlorure de ropivacaïne. Cette solution était employée seule (groupe I, n = 15) ou enrichie d’adrénaline à 1:200 000 (groupe II, n = 17). Nous avons obtenu une anesthésie de tous les dermatomes entre C5 et D1 chez 87 pour cent des patients des deux groupes. Le bloc moteur était intense avec une paralysie de l’épaule et au moins une parésie de la main chez tous les patients. Le bloc sensitif s’installait rapidement et durait longtemps (l’analgésie survenait en moins de quatre minutes et durait plus de 13 heures en moyenne). L’addition d’adrénaline n’eut en général pas d’effet sur la latence, la qualité et la durée des blocs moteurs et sensitifs sauf celui d’abréger l’analgésie dans le territoire de D1 et l’anesthésie dans celui de C7 à D1. Avec des doses moyennes de 2,5 et 2,6 mg· kg− 1 de ropivacaine, nous n’avons noté de signe de toxicité centrale ou cardiovasculaire dans aucun des deux groupes.

Subclavian perivascular block: Influence of location of paresthesia

Subclavian perivascular block of the brachial plexus was used in 156 adult patients undergoing orthopedic hand and forearm surgery. The location of the elicited paresthesia prior to deposition of 30 ml of a solution containing 1% mepivacaine, 0.2% tetracaine and 1·200,000 epinephrine was recorded. Twenty minutes later the quality of the block in the distribution of the superior, middle and inferior trunks of the brachial plexus was evaluated. Anesthesia in each of the three trunks was compared with the three sites where the paresthesia was elicited (superior, middle, or inferior trunk). A middle trunk paresthesia was the most successful in producing surgical anesthesia of all three trunks. A superior trunk paresthesia was the paresthesia most often elicited. It resulted in a significantly lower incidence of inferior trunk anesthesia than did a middle or inferior trunk paresthesia. Complications included arterial puncture (25.6%), Homers syndrome (64.1%), and recurrent laryngeal nerve block (1.3%), with no instances of symptomatic phrenic block or symptomatic pneumothorax.

Long thoracic nerve block

Seven patients with intractable pain of the lateral chest wall under the axilla appeared to have pain originating from spasm of the serratus anterior muscle. A long thoracic nerve block to interrupt selectively the innervation to this muscle could confirm this diagnosis, but a review of the literatu

PROTECTING THE INJURED BRAIN AND SPINAL CORD

Traumatic injury is a major health problem in the United States, both in terms of human death and disability as well as financial costs. It is estimated that approximately 40% of the health care dollar is consumed by direct or indirect medical costs of injury. Injuries to the head and spinal cord result in disabilities that supercede, particularly in social impact, injuries to any other system. 20 Most of these injuries are preventable. For example, over 70% of motor vehicle accidents are due to human factors and greater than 90% of the spinal cord injuries (SCI) that result from motor vehicle accidents occur in unrestrained passengers. 20 Alcohol is also a major contributing factor. Preventative efforts, therefore, are the most logical approach to this problem. In the absence of prevention, we must attempt to limit further injury by interrupting the cascade of cellular ischemia and destruction and also prevent damage by complicating factors such as hypoxia, inadequate perfusion pressure, and intracranial hypertension. This article reviews the pathophysiology of central nervous system (CNS) injury, including the primary and secondary injury processes, and discusses treatment modalities aimed at preventing further neurologic injury.

Autoregulation of spinal cord flow: Is the cord a microcosm of the brain?

SUMMARY The autoregulatory capability of regional areas of the brain and spinal cord was demonstrated in 18 rats anesthetized with a continuous infusion of intravenous pentothal. Blood flow was measured by the injection of radioactive microspheres (Co 57 , Sn 113 , Ru 103 , Sc 4 *). Blood flow measurements were made at varying levels of mean arterial pressure (MAP) which was altered by neosynephrine to raise MAP or trimethaphan to lower MAP. Autoregulation of the spinal cord mirrored that of the brain, with an autoregulatory range of 60 to 120 mm Hg for both tissues. Within this range, cerebral blood flow (CBF) was 59.2 ± 3.2 ml/100 g/min (SEM) and spinal cord blood flow (SCBF) was 61.1 ± 3.6. There was no significant difference in CBF and SCBF in the autoregulatory range. Autoregulation was also demonstrated regionally in the left cortex, right cortex, brainstem, thalamus, cerebellum, hippocampus and cervical, thoracic and lumbar cord. This data provides a coherent reference point hi establishing autoregulatory curves under barbiturate anesthesia. Further investigation of the effects of other anesthetic agents on autoregulation of the spinal cord is needed. It is possible that intraspinal cord compliance, like intracranial compliance, might be adversely affected by the effects of anesthetics on autoregulation. Stroke Vol 17, No 6, 1986 HEMODYNAMIC AUTOREGULATION, a mechanism intrinsic to the cerebrovascular system, and also present in many other tissues, maintains tissue blood flow within a narrow range despite changes in perfusion pressure. It has been firmly established as the primary blood flow regulatory mechanism in the brain and constitutes a physiological adjustment that is of major importance in maintenance of a homeostatic internal environment of the brain. The first observation of cerebral autoregulation was made by Fog in 1934. 1 - 2 He observed the responses of pial vessels of cats through a cranial window under conditions of varying arterial blood pressure and noted dilation with a fall in blood pressure and constriction with a rise in blood pressure. Lassen, in his review in 1959, established the concept of cerebral autoregulation based on actual measurements of blood flow during blood pressure alterations. 3 Since that time, cerebral autoregulation has been extensively investigated and it has been found that under normotensive conditions mean arterial blood pressure can be varied from a lower limit of 60 mm Hg to an upper limit of 130 mm Hg without any measurable change in blood flow. 4 Below these limits, cerebral blood flow markedly falls, and above these limits, forced dilation of arterioles occurs which is associated with disruption of the blood brain barrier and edema formation. 5 Spinal cord autoregulation has been less extensively investigated. Many of the therapeutic principles applied to spinal cord injured patients have been made on the basis of a parallelism between brain and spinal cord