Randall L. Carpenter

Effects of Perioperative Analgesic Technique on Rate of Recovery after Colon Surgery

Background Choice of perioperative analgesia may affect the rate of recovery of gastrointestinal function and thus duration and cost of hospitalization after colonic surgery.

Incidence and Risk Factors for Side Effects of Spinal Anesthesia

We prospectively studied 952 patients to identify the incidence of hypotension (systolic blood pressure less than 90 mmHg), bradycardia (heart rate less than 50 beats/min), nausea, vomiting, and dysrhythmia during spinal anesthesia. Historical, clinical, and physiologic data were correlated with the incidence of these side effects by univariate and multivariate analysis. Hypotension developed in 314 patients (33%), bradycardia in 125 (13%), nausea in 175 (18%), vomiting in 65 (7%), and dysrhythmia in 20 (2%). Variables conferring increased odds of developing hypotension include peak block height greater than or equal to T5 (odds ratio 3.8, P less than 0.001), age greater than or equal to 40 yr (2.5, P less than 0.001), baseline systolic blood pressure less than 120 mmHg (2.4, P less than 0.001), combination of spinal and general anesthesia (1.9, P = 0.01), spinal puncture at or above the L2-L3 interspace (1.8, P less than 0.001), and addition of phenylephrine to the local anesthetic (1.6, P = 0.02). Variables conferring increased odds of developing bradycardia include a baseline heart rate less than 60 beats/min (odds ratio 4.9, P less than 0.001), ASA physical status classification of 1 versus 3 or 4 (3.5, P less than 0.001), current therapy with beta-adrenergic blocking drugs (2.9, P less than 0.001), and peak block height greater than or equal to T5 (1.7, P = 0.02). Variables conferring increased odds of developing nausea or vomiting include addition of phenylephrine or epinephrine to the local anesthetic (3.0-6.3, P less than or equal to 0.003), peak block height greater than or equal to T5 (odds ratio 3.9, P less than 0.001), use of procaine (2.6-4.4, P less than or equal to 0.003), baseline heart rate greater than or equal to 60 beats/min (2.3, P = 0.03), history of carsickness (2.0, P = 0.01), and development of hypotension during spinal anesthesia (1.7, P = 0.009). Our results indicate that the incidence of side effects during spinal anesthesia may be reduced by 1) minimizing peak block height; 2) using plain solutions of local anesthetics; 3) performing the spinal puncture at or below the L3-L4 interspace; and 4) avoiding the use of procaine in the subarachnoid space.

Fentanyl Prolongs Lidocaine Spinal Anesthesia Without Prolonging Recovery

Lidocaine spinal anesthesia is a popular anesthetic for short procedures due to its brief duration.The addition of fentanyl may improve the quality and duration of lidocaine spinal anesthesia. Eight volunteers received plain lidocaine 5% in dextrose (50 mg) both with and without 20 micro gram of fentanyl in a randomized, double-blind, cross-over fashion. Sensory analgesia was assessed with pinprick, cold, touch, transcutaneous electrical stimulation equivalent to surgical incision, and duration of tolerance of pneumatic thigh tourniquet. Motor block was assessed with isometric force dynamometry. Regression of pinprick, touch, and cold was prolonged with fentanyl. Duration of tolerance of electrical stimulation at the umbilicus, hip, knee, and ankle was increased with fentanyl (181% increase from plain lidocaine on average; P < 0.01). Duration of tolerance of tourniquet-induced pain was increased by an average of 48% with addition of fentanyl (P = 0.02). Neither motor block nor time to void was prolonged with fentanyl. Pruritus occurred in all subjects receiving fentanyl but was treated easily and were well tolerated. We recommend the addition of 20 micro gram of fentanyl to lidocaine spinal anesthesia as a means to improve duration of sensory anesthesia without prolonging recovery of motor function or time to micturition. (Anesth Analg 1995;80:730-4)

Effect of ropivacaine on cutaneous capillary blood flow in pigs

The effect of subcutaneous infiltration of ropivacaine and bupivacaine on local cutaneous blood flow was assessed by the laser Doppler method. One milliliter of each of ten test solutions (ropivacaine 0.25% and 0.75%, bupivacaine 0.25% and 0.75%, and saline, each with and without added epinephrine 5 micrograms/ml) was injected subcutaneously at separate sites on the side of each pig (n = 6). Skin blood flow was measured by laser Doppler at all sites before and 5, 10, 15, and 30 min after injection. Subcutaneous injection of ropivacaine 0.25% or 0.75% decreased cutaneous blood flow by a maximum of 52% +/- 11% and 54% +/- 14% (mean +/- SE), respectively. In contrast, bupivacaine 0.25% or 0.75% increased flow by 90% +/- 32% and 82% +/- 48%, and injection of saline increased blood flow by 32% +/- 17%. Cutaneous blood flow after the injection of ropivacaine was significantly lower than after injection of bupivacaine or saline, and was also lower than at the uninjected control site (P = 0.0009). All of the solutions with epinephrine decreased blood flow to a similar extent (48-73%, P = 0.3). The ability of ropivacaine to produce cutaneous vasoconstriction offers several advantages over the other local anesthetics presently available for infiltration anesthesia.

Comparison of 0.5% Ropivacaine and 0.5% Bupivacaine for Epidural Anesthesia in Patients Undergoing Lower-Extremity Surgery

Ropivacaine is an amide local anesthetic structurally related to, but appearing less cardiotoxic, than bupivacaine. The authors investigation was designed in a randomized, double-blind fashion to compare the clinical effectiveness of ropivacaine and bupivacaine in patients undergoing lower-extremity surgery. Forty-five patients were randomized to receive 20 ml of 0.5% ropivacaine or bupivacaine. Intermittent sensory (pinprick) and motor (Bromage score) measurements were made while the block was in effect, and changes in heart rate, blood pressure and amounts of additional analgesics, sedatives and other medications were also recorded. Presence of tourniquet pain and the quality of anesthesia were also assessed. One patient was excluded from analysis; thus, 22 patients each received ropivacaine or bupivacaine. No differences were found in patient or perioperative characteristics between the groups. The quality and extent of sensory and motor blockade between groups were comparable, although bupivacaine was slightly longer acting. Cardiovascular changes, incidence of tourniquet pain, and the amounts of supplemental medications necessary were also similar between groups. The authors found 0.5% ropivacaine and bupivacaine to be clinically similar in both sensory- and motor-blocking characteristics, with the exception that bupivacaine produced a blockade of slightly longer duration. Because ropivacaine is reported to be less cardiotoxic than bupivacaine in animal studies, the similarity of clinical epidural anesthesia may make ropivacaine the preferred agent.

Oral clonidine prolongs lidocaine spinal anesthesia in human volunteers

Background Premedication with oral clonidine may improve the quality and duration of lidocaine spinal anesthesia, but this effect has not been examined in a quantitative fashion. Methods Eight volunteers received 50 mg lidocaine (1.5% dextrose free) both with and without 0.2 mg oral clonidine 1.5 h before spinal anesthesia in a randomized, double-blind, placebo-controlled, crossover fashion. Sensory block was assessed by pinprick, transcutaneous electric stimulation equivalent to surgical incision, and duration of tolerance to pneumatic thigh tourniquet. Motor block at the quadriceps and gastrocnemius muscles was assessed by isometric force dynamometry. Episodes of bradycardia, hypotension, and sedation were recorded. Results Regression of pinprick was unchanged with clonidine. However, duration of tolerance to electric stimulation was increased at the knee (28 plus/minus 24 min) and ankle (31 plus/minus 28 min) with clonidine (P < 0.05). The duration of tolerance to tourniquet-induced pain was increased with clonidine (14 plus/minus 12 min; P < 0.05). The duration of motor block was increased at the quadriceps (20 plus/minus 13 min) and gastrocnemius (33 plus/minus 24 min) muscle groups with clonidine (P < 0.05). Although clonidine decreased systolic blood pressure (13 plus/minus 4 mmHg, P < 0.003) and heart rate (13 plus/minus 5 beats/min; P = 0.02), no subjects had hypotension or bradycardia. The incidence of sedation was greater with clonidine than with plain lidocaine (50% vs. 0%, P < 0.04). Discussion Premedication with oral clonidine prolonged sensory and motor block from lidocaine spinal anesthesia. The exact mechanism whereby oral clonidine prolongs spinal anesthesia remains to be determined.

Comparison of 5% with Dextrose, 1.5% with Dextrose, and 1.5% Dextrose-Free Lidocaine Solutions for Spinal Anesthesia in Human Volunteers

The use of lidocaine in concentrations less than 5% for spinal anesthesia may be advantageous but has not been carefully studied.Lidocaine 50 mg (1.5% with dextrose and 1.5% dextrose-free) was administered to eight volunteers in a randomized, double blind, cross-over fashion. All of these subjects had previously received 5% lidocaine with dextrose using the same experimental protocol. Sensory analgesia was assessed with pinprick, transcutaneous electrical stimulation (TES) equivalent to surgical incision, and duration of tolerance of pneumatic thigh tourniquet. Motor block was assessed with isometric force dynamometry. Peak dermatomal level was the highest and duration until regression of pinprick the longest with the 5% solution (P < 0.05). Duration of tolerance to TES was increased (33 +/- 10 min) with the 5% solution (P < 0.04). Duration of tolerance to tourniquet pain was increased (11 +/- 3 min) with the 5% solution (P < 0.02). Duration of motor block was increased (45 +/- 9 min) with the 5% and the 1.5% without dextrose solutions (P < 0.04). Time to void was increased (33 +/- 5 min) with the 5% solution (P < 0.03). In conclusion, the use of different solutions of lidocaine for spinal anesthesia results in significant differences in sensory and motor block and time until recovery of micturition. (Anesth Analg 1995;81:697-702)

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.

Lidocaine 0.5% spinal anaesthesia: a hypobaric solution for short-stay perirectal surgery

The efficacy of subarachnoid injection of 8 ml lidocaine 0.5% was assessed in ten outpatients having perirectal surgery in the jackknife position. This solution is hypobaric, with a baricity 0.9985 ± 0.0003 (mean ± SD). Injections were made with the patient in the surgical position (with the upper torso at a 15° downward inclination). Sensory level was tested by pinprick. Times to two-segment regression, to complete resolution of sensory analgesia, to urination, and to discharge from the recovery room were recorded. All injections produced effective anaesthesia for surgery. Lidocaine 0.5% behaves clinically as a hypobaric solution. Dermatomal levels remained low (T11 to L5) while the patients were in the surgical position (head down), but rose two to six dermatomes if the patient’s head was elevated after surgery. Time to two-segment regression was 97 ± 36 min, time until regression to 5y was 116 ± 22 min, time to complete resolution of sensory blockade was 151 ± 23 min, time to urination was 197 ± 64 min, and time to discharge from the recovery room was 205 ± 45 min. Lidocaine 0.5% provides effective spinal anaesthesia of short duration appropriate for outpatient surgical procedures. Dermatomal sensory spread of anaesthesia, and our measurements of specific gravity, indicate that this solution is hypobaric. It appears that changes in position can alter the spread of analgesia for at least one hour after injection and, thus, we caution against elevating the patient’s head in the immediate postoperative period.RésuméOn a étudié l’efficacité d’une injection sous-arachnoïdienne de 8 ml de lidocaïne 0,5% hypobare (baricité de 0,9985 ± 0,0003) chez dix patients admis pour une chirurgie péri-rectale en position de Depage («jacknife position»). L’injection de lidocaïne a été faite chez le patient en position chirurgicale et le niveau d’anesthésie fut mesuré par piquage. Toutes les injections ont entraîné une anesthésie efficace, le niveau n’excédant pas D11 (D11 à L5) tant que le patient est demeuré en position chirurgicale. Le redressement du patient à la fin de la chirurgie a entraîné une augmentation du niveau d’anesthésie de deux à six dermatomes. Le temps de régression de deux segments, le temps de régression à S1 et le temps de résolution complète du bloc sensitif ont été respectivement de 97 ± 36 min, 116 ± 22 min et 151 ± 23 min. Le temps de miction a été de 197 ± 64 min et le temps de départ de la salle de réveil de 205 ± 45 min. La lidocaïne 0,5% procure une anesthésie rachidienne efficace et de courte durée qui convient bien au patient opéré en externe. En raison du caractère hypobare de la solution, on ne devrait élever la tête du patient que plus d’une heure après l’injection.