Carol A. Stephenson

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.

Prospective study of the incidence of transient radicular irritation in patients undergoing spinal anesthesia.

Background There is considerable controversy regarding the role of subarachnoid 5% hyperbaric lidocaine in the syndrome transient radicular irritation (TRI). This randomized, double‐blinded, prospective study was designed to determine the incidence of TRI and identify factors possibly contributing to its development. Methods One hundred fifty‐nine ASA physical status 1 or 2 patients undergoing outpatient knee arthroscopy or unilateral inguinal hernia repair were prospectively randomized to receive spinal anesthesia with 5% hyperbaric lidocaine with epinephrine (60 mg with 0.2 mg epinephrine for arthroscopy or 75 mg with 0.2 mg epinephrine for hernia repair), 2% isobaric lidocaine without epinephrine (60 mg for arthroscopy or 75 mg for hernia repair), or 0.75% hyperbaric bupivacaine without epinephrine (7.5 mg for arthroscopy or 9.0 mg for hernia repair) in a double‐blinded fashion. On the 3rd postoperative day, patients were contacted by a blinded investigator and questioned regarding the incidence of postoperative complications including TRI, defined as back pain with radiation down one or both buttocks or legs occurring within 24 h after surgery. Postoperatively, time from injection to block resolution, ambulation, voiding, and ready for discharge were recorded by a postanesthesia care unit nurse blinded to the group assignment. Results The incidence of TRI was greater in patients receiving lidocaine than in those receiving bupivacaine (16% vs. 0%; P = 0.003). There was no difference in the incidence of TRI between the patients receiving 59% hyperbaric lidocaine with epinephrine and those receiving 2% isobaric lidocaine without epinephrine (16% vs. 16%; P = 0.98). The incidence of TRI was greater in patients undergoing arthroscopy than in those undergoing hernia repair (13% vs. 5%; P = 0.04). There was no difference in discharge times in patients receiving bupivacaine versus those receiving hyperbaric lidocaine with epinephrine (292 vs. 322 min; P = 0.61). Conclusions The incidence of TRI is greater with lidocaine than bupivacaine, decreasing the lidocaine concentration to 2% does not prevent TRI, and surgical position may be an important contributing factor. Discharge times at our institution are not different when equipotent doses of 0.75% hyperbaric bupivacaine or 5% hyperbaric lidocaine with 0.2 mg epinephrine are used in ambulatory patients undergoing spinal anesthesia.

Hyperbaric Spinal Ropivacaine A Comparison to Bupivacaine in Volunteers

Background: Ropivacaine is a newly introduced local anesthetic that may be a useful alternative to low-dose bupivacaine for outpatient spinal anesthesia. However, its relative potency to bupivacaine and its dose-response characteristics are unknown. This double-blind, randomized, crossover study was designed to determine relative potencies of low-dose hyperbaric spinal ropivacaine and bupivacaine and to assess the suitability of spinal ropivacaine for outpatient anesthesia. Methods: Eighteen healthy volunteers were randomized into three equal groups to receive one spinal administration with bupivacaine and a second with ropivacaine, of equal-milligram doses (4, 8, or 12 mg) of 0.25% drug with 5% dextrose. The duration of blockade was assessed with (1) pinprick, (2) transcutaneous electrical stimulation, (3) tolerance to high tourniquet, (4) electromyography and isometric force dynamometry, and (5) achievement of discharge criteria. Differences between ropivacaine and bupivacaine were assessed with linear and multiple regression. P < 0.05 was considered significant. Results: Ropivacaine and bupivacaine provided dose-dependent prolongation of sensory and motor block and time until achievement of discharge criteria (R 2 ranges from 0.33-0.99; P values from < 0.001 through 0.01). Spinal anesthesia with ropivacaine was significantly different from bupivacaine and was approximately half as potent for all criteria studied. A high incidence of back pain (28%; P = 0.098) was noted after intrathecal ropivacaine was given. Conclusion: Ropivacaine is half as potent and in equipotent doses has a similar profile to bupivacaine with a higher incidence of side effects. Low-dose hyperbaric spinal ropivacaine does not appear to offer an advantage over bupivacaine for use in outpatient anesthesia.

dilution of Spinal Lidocaine Does Not Alter the Incidence of Transient Neurologic Symptoms

BACKGROUND Although it has been suggested that the dilution of 5% hyperbaric lidocaine before injection for spinal anesthesia may decrease the incidence of transient neurologic symptoms, previous studies have not noted a decreased incidence between 5% and 2% lidocaine. The aim of the current study was to determine whether the incidence of transient neurologic symptoms could be altered by further diluting spinal lidocaine from 2.0% to 0.5%. METHODS One hundred nine patients with American Society of Anesthesiologists physical status 1 or 2 undergoing outpatient knee arthroscopy were randomized in a double-blind fashion to receive 50 mg hyperbaric spinal lidocaine as a 2.0%, 1.0%, or 0.5% concentration. On the third postoperative day, patients were contacted by a blinded investigator and questioned regarding the incidence of postoperative complications, including transient neurologic symptoms, defined as pain or dysthesia in one or both buttocks or legs occurring within 24 h of surgery. RESULTS The incidence of transient neurologic symptoms did not differ among patients receiving 2.0% (incidence of 15.8%), 1.0% (incidence of 22.2%), and 0.5% (incidence of 17.1%) lidocaine (P = 0.756). CONCLUSIONS For ambulatory patients undergoing arthroscopy, the incidence of transient neurologic symptoms is not reduced by decreasing spinal lidocaine concentrations from 2.0% to 1.0% or 0.5%. The incidences of transient neurologic symptoms with the 0.5%, 1.0%, and 2.0% solutions are similar to previously reported incidences for 5.0% lidocaine, suggesting that dilution of lidocaine from 5.0% to 0.5% does not change the incidence of these symptoms.

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.

Spinal nerve function in five Volunteers experiencing transient neurologic symptoms after lidocaine subarachnoid anesthesia

The etiology of transient neurologic symptoms (TNS) after 5% lidocaine spinal anesthesia remains undetermined. Previous case reports have shown that patients acutely experiencing TNS have no abnormalities on neurologic examination or magnetic resonance imaging. The aim of our study was to determine whether volunteers with TNS would exhibit abnormalities in spinal nerve electrophysiology. Twelve volunteers with no history of back pain or neurologic disease underwent baseline electromyography (EMG), nerve conduction studies, and somatosensory-evoked potential (SSEP) testing. Then, the volunteers were administered 50 mg of 5% hyperbaric lidocaine spinal anesthesia and were placed in a low lithotomy position (legs on four pillows). The next day, all volunteers underwent follow-up EMG, nerve conduction, and SSEP testing and were questioned and examined for the presence of complications including TNS (defined as pain or dysthesia in one or both buttocks or legs occurring within 24 h of spinal anesthesia). Volunteers who had TNS underwent additional EMG testing 4–6 wk later. Five of the 12 volunteers reported TNS. No volunteer had an abnormal EMG, nerve conduction study, or SSEP at 24 h follow up, nor were there any changes in EMG studies at delayed testing in the five volunteers experiencing TNS. On statistical analysis, the right peroneal and the right tibial nerve differed significantly for all volunteers from pre- to postspinal testing. When comparing pre- and postspinal testing of the TNS and non-TNS volunteers, statistically significant changes occurred in the nerve conduction tests of the right peroneal and left tibial nerve. There was no difference in measurements of F response, H reflex latency, amplitude, or velocity for either leg. Multivariate analysis of variance showed no significant difference between TNS and non-TNS volunteers for the changes in the nine nerve conduction tests when considered together (P = 0.4). We conclude that acute TNS after lidocaine spinal anesthesia did not result in consistent abnormalities detectable by EMG, nerve conduction studies, or SSEP in five volunteers. Implications: Electrophysiologic testing in volunteers experiencing transient neurologic symptoms is not abnormal.

Hyperbaric spinal ropivacaine: a comparison to bupivacaine in volunteers

BACKGROUND Ropivacaine is a newly introduced local anesthetic that may be a useful alternative to low-dose bupivacaine for outpatient spinal anesthesia. However, its relative potency to bupivacaine and its dose-response characteristics are unknown. This double-blind, randomized, crossover study was designed to determine relative potencies of low-dose hyperbaric spinal ropivacaine and bupivacaine and to assess the suitability of spinal ropivacaine for outpatient anesthesia. METHODS Eighteen healthy volunteers were randomized into three equal groups to receive one spinal administration with bupivacaine and a second with ropivacaine, of equal-milligram doses (4, 8, or 12 mg) of 0.25% drug with 5% dextrose. The duration of blockade was assessed with (1) pinprick, (2) transcutaneous electrical stimulation, (3) tolerance to high tourniquet, (4) electromyography and isometric force dynamometry, and (5) achievement of discharge criteria. Differences between ropivacaine and bupivacaine were assessed with linear and multiple regression. P < 0.05 was considered significant. RESULTS Ropivacaine and bupivacaine provided dose-dependent prolongation of sensory and motor block and time until achievement of discharge criteria (R2 ranges from 0.33-0.99; P values from < 0.001 through 0.01). Spinal anesthesia with ropivacaine was significantly different from bupivacaine and was approximately half as potent for all criteria studied. A high incidence of back pain (28%; P = 0.098) was noted after intrathecal ropivacaine was given. CONCLUSION Ropivacaine is half as potent and in equipotent doses has a similar profile to bupivacaine with a higher incidence of side effects. Low-dose hyperbaric spinal ropivacaine does not appear to offer an advantage over bupivacaine for use in outpatient anesthesia.

Prolonged PR Interval Is a Risk Factor for Bradycardia During Spinal Anesthesia

Background and Objectives. Bradycardia occurs during 9%‐13% of spinal anesthetics and may lead to cardiac arrest. Several risk factors for the development of bradycardia have been identified, but the risk conferred by presence of abnormalities detected on preoperative electrocardiogram (ECG) has not been examined. The authors undertook the study to correlate abnormal ECG findings with the incidence of bradycardia. Methods. The database was previously collected from 952 patients undergoing spinal anesthesia. Patient records were reviewed and 537 had ECGs performed within 6 months of surgery. Intraoperative bradycardia was defined as a heart rate <50 bpm (plus >10% decrease from baseline). Abnormalities recorded from the ECG were prolonged PR interval (PR > 0.2 sec), atrial‐ventricular conduction abnormalities, evidence of chamber hypertrophy, ischemia, and infarction. The findings were compared with incidence of bradycardia using contingency tables. Significant correlations were then evaluated with logistic regression. Significance was defined as P < .05. Results. The incidence of bradycardia in this population was 12%. Patients with a prolonged PR interval had an increased incidence of bradycardia (25%, P = .01). Other ECG abnormalities did not correlate with increased incidence of bradycardia. Duration of PR interval did correlate significantly (P = .001) but poorly (r2 = 0.014) with baseline heart rate. However, logistic regression demonstrated that prolonged PR interval was a significant and independent predictor for bradycardia (odds ratio = 3.2, P = .01). Conclusions. Risk factors previously identified for the development of bradycardia during spinal anesthesia include: baseline heart rate <60 bpm, ASA physical status 1 versus 3 or 4, use of beta‐blocking drugs, sensory block height ≥T5, and age <50. The results demonstrate that prolonged PR interval on the preoperative ECG is another significant and independent predictor for bradycardia.