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Biomedical subjects

R A Stevens

Publications and source records attributed to R A Stevens.

At least 37 records · Page 2Linked to original sources

The efficacy of epinephrine test doses during spinal anesthesia in volunteers: implications for combined spinal-epidural anesthesia.

Epinephrine test doses may be administered during combined spinal-epidural anesthesia to determine intravascular placement of epidural catheters. This study was designed to determine systolic blood pressure (SBP) and heart rate (HR) responses to intravenous injection of epinephrine (15 microg) during spinal anesthesia. Twelve volunteers received three spinal anesthetics (lidocaine 100 mg, tetracaine 15 mg, and bupivacaine 15 mg) in a randomized, double blind, cross-over fashion. Epinephrine was administered prior to spinal anesthesia (control), 30 min after injection of spinal anesthesia, and at regression of sensory block to T-10. SBP was measured with a radial arterial catheter and HR with an electrocardiogram. Positive responses were defined as peak increase in SBP > or = 15 mm Hg or HR > or = 20 bpm after injection of epinephrine. Compared with control, peak SBP responses decreased by a mean of 12 mm Hg during spinal anesthesia with tetracaine and bupivacaine (P < 0.05). Peak HR responses decreased by 11 bpm during all three spinal anesthetics (P < 0.05). Incidences of detection of intravenous injection by positive SBP and HR responses ranged from 50% to 100% and were not significantly affected by spinal anesthesia. Spinal anesthesia reduces hemodynamic responses to intravenous epinephrine injection but is unlikely to reduce detection by positive SBP and HR criteria.

Adult↗

Hyperbaric dye solution distribution characteristics after pencil-point needle injection in a spinal cord model.

BACKGROUND: The flow-rate limiting and directional characteristics of caudally directed microcatheters, which lead to intrathecal maldistribution of hyperbaric 5% lidocaine, are believed to have contributed to at least 11 cases of cauda equina syndrome. The authors investigated the distribution characteristics of hyperbaric dye solutions via caudally directed side port needles at various rates of injection in a spinal cord model to determine the potential for maldistribution. METHODS: Using a digital video image processing technique, we injected a hyperbaric solution of phthalocyanine blue dye through caudally directed side-port needles into a supinely oriented transparent spinal canal model filled with simulated cerebrospinal fluid. Injections via commonly used spinal needles (24-gauge and 25-gauge Sprotte, and 25-gauge and 27-gauge Whitacre) were recorded using five injection rates (2, 4, 6, 8, and 16 ml/min). RESULTS: For all needles tested, injection rate had a significant effect on the peak dye concentration (P < 0.0001). Injection rates > or = 6 ml/min (2 ml/20 s) resulted in peak dye concentrations of less than 168 mg/1 (extrapolated concentration of 1% lidocaine). Injection via the 24-gauge Sprotte needle, which has a larger orifice area and internal diameter, resulted in significantly lower peak dye concentrations than via the smaller Whitacre needles tested (P < 0.05). CONCLUSIONS: Sacral maldistribution could be minimized by using injection rates > or = 6 ml/min (2 ml/20 s), for all of the side-port spinal needles used in this model study. When very slow injection rates (2 ml/min) are used, peak dye concentrations varied inversely and significantly with needle internal diameter and orifice area.

Anesthetics, Local↗

Transient neurologic deficit after spinal anesthesia: local anesthetic maldistribution with pencil point needles?

Recent reports of transient neurologic deficits have raised concern about the potential toxicity of single-dose spinal 5% lidocaine in 7.5% dextrose. Two cases of volunteers who experienced minor local sensory deficits after slow (60 s) injections of 2 mL 5% lidocaine via Whitacre needles are described. One case was a result of a double injection because of a "failed" block. It seemed possible that the neurologic deficit in these cases resulted from neurotoxicity associated with maldistribution of local anesthetic. Using an in vitro spinal model, we investigated drug distribution resulting from injections through side-port spinal needles to determine whether the use of these needles could result in high local concentrations of hyperbaric solutions. A spinal canal model was fabricated using human magnetic resonance measurements. The model was placed in a surgical supine position and filled with lactated Ringer's solution to simulate the specific gravity of cerebral spinal fluid at 22 degrees C. A hyperbaric solution of phthalocyanine blue dye and dextrose (SG 1.042), simulating the anesthetic, was injected through three different needles (27-gauge 4 11/16-in. Whitacre, 25-gauge 3 1/2-in. Whitacre, 25-gauge 3 1/2-in. Quincke). Triplicate injections were done at rapid (2 mL/10 s) and slow (2 mL/60 s) rates, with needle side ports oriented in a sacral and cephalad direction. At slow rates of injection, using 27- or 25-gauge sacrally directed Whitacre needles, injections showed evidence of maldistribution with extrapolated peak sacral lidocaine concentrations reaching 2.0%. In contrast, distribution after slow injection through sacrally directed Quincke needles was uniform.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Does spinal anesthesia result in a more complete sympathetic block than that from epidural anesthesia?

BACKGROUND: Spinal and epidural injection of local anesthetics are used to produce sympathetic block to diagnose and treat certain chronic pain syndromes. It is not clear whether either form of regional anesthesia produces a complete sympathetic block. Spinal anesthesia using tetracaine has been reported to produce a decrease in plasma catecholamine concentrations. This has not been demonstrated for epidural anesthesia in humans with level of anesthesia below C8. One possible explanation is that spinal anesthesia results in a more complete sympathetic block than epidural anesthesia. To examine this question, a cross-over study was performed in young, healthy volunteers. METHODS: Ten subjects underwent both spinal and epidural anesthesia with lidocaine (plain) on the same day with complete recovery between blocks. By random assignment, spinal anesthesia and epidural anesthesia were induced via lumbar injection. Before and 30 min after local anesthetic injection, a cold pressor test (CPT) was performed. Blood was obtained to determine epinephrine and norepinephrine plasma concentrations at four stages: (1) 20 min after placing peripheral catheters, (2) at the end of a 2-min CPT (before conduction block), (3) 30 min after injection of epidural or spinal lidocaine, and (4) at the end of a second CPT (during anesthesia). Mean arterial pressure, heart rate, noninvasive cardiac index, and analgesia to pin-prick were monitored. RESULTS: Neither spinal nor epidural anesthesia changed baseline resting values of catecholamines or any hemodynamic variable, except heart rate, which was slightly decreased during spinal anesthesia. Median level of analgesia was T4 during spinal and T3 during epidural anesthesia. CPT before conduction block reliably increased heart rate, mean arterial pressure, cardiac index, epinephrine, and norepinephrine. Conduction block attenuated the increase in response to CPT only in mean arterial pressure (spinal and epidural) and cardiac index (spinal only). Neither technique blocked the increase in heart rate, norepinephrine, or epinephrine to CPT. CONCLUSIONS: Spinal anesthesia did not result in a more complete attenuation of the sympathetic response to a CPT than did epidural anesthesia. In response to the CPT, spinal anesthesia blocked the increase in cardiac index, and epidural anesthesia resulted in a decrease in total peripheral resistance compared to the pre-anesthesia state. The differences between the techniques are not significant and are of uncertain clinical implications.

Adult↗

International medical education and the concept of quality: historical reflections.

After offering reflections on the words "global" and "international," this paper presents examples supporting the observations that physicians have long crossed national boundaries in a quest for learning and that dominant nations have long brought their perceptions of quality to institutions of medicine elsewhere. It then discusses cross-cultural issues in defining quality in medicine and in medical education; although some technical aspects of medicine span national boundaries, medical practice has a large cultural component. Tension is noted between forces favoring international standardization in medicine--for example, the communication revolution and the desire for international control of infectious diseases--and forces favoring variation among cultures.

Cross-Cultural Comparison↗

Back pain after epidural anesthesia with chloroprocaine.

BACKGROUND: Chloroprocaine has been associated with severe back pain after epidural anesthesia. Factors proposed to contribute to this problem are: 1) the preservative disodium ethylenediaminetetraacetic acid (EDTA), 2) large volumes of chloroprocaine, 3) low pH of chloroprocaine, and 4) local infiltration with chloroprocaine. METHODS: Using a prospective, balanced, randomized study design, 100 patients aged 18-65 yr who were undergoing outpatient knee surgery during continuous epidural anesthesia received one of five local anesthetics (all containing epinephrine 1:200,000). Group I received a bolus of 30 ml 2% lidocaine, followed by 10 ml every 45 min. Group II received 15 ml of 3% chloroprocaine (containing EDTA), plus 5 ml every 45 min. Group III received 30 ml of 3% chloroprocaine plus 10 ml every 45 min. Group IV received 30 ml of 3% chloroprocaine (containing metabisulfite as the preservative but no EDTA) plus 10 ml every 45 min. Group V received 30 ml of 3% chloroprocaine with the pH adjusted to 7.3, plus 10 ml every 45 min. After the anesthesia dissipated and before any analgesic agents were given, the patients were asked to rank maximum knee and back pain on a visual analog scale (0-10) and to give a description of back pain. A telephone interview was conducted 24 h after surgery to determine if back pain returned. Back pain scoring was assessed using a verbal analog scale. RESULTS: After dissipation of anesthesia, the back pain reported by patients fell into two distinct categories. Type 1 pain was described commonly as superficial and localized to the site of needle insertion. There was no difference among groups in incidence of type 1 pain. Type 2 pain was described as deep, aching, burning, and poorly localized in the lumbar region (5% of the patients in group I, 10% in groups II and IV, 50% in group III, and 25% in group V). The incidence of type 2 pain was significantly greater in group III than in groups I, II, or IV. Group III also had a significantly greater mean visual analog scale pain score (types 1 and 2) than all other groups. CONCLUSIONS: Large doses (> or = 40 ml) of chloroprocaine containing EDTA resulted in a greater incidence of deep burning lumbar back pain. Using 25 ml or less of the same solution resulted in an incidence of both types 1 and 2 postepidural anesthesia back pain similar to that in the lidocaine control group.

Adolescent↗

Does the choice of local anesthetic affect the catecholamine response to stress during epidural anesthesia?

BACKGROUND: Previous work has established that 2-chloroprocaine epidural anesthesia has no effect on circulating plasma epinephrine concentrations in young, healthy, resting volunteers, and results in a decrease in norepinephrine concentration only when a level of analgesia to pinprick of C-8 is reached. The current study was performed to evaluate the possibility that this finding is unique to 2-chloroprocaine. METHODS: Nine healthy volunteers were studied on three occasions at least 48 h apart; each received three local anesthetics (0.75% bupivacaine, 2% lidocaine, and 3% 2-chloroprocaine, all without epinephrine). After placement of lumbar epidural and central venous catheters, blood samples were drawn from the central venous catheter at the following stages: (1) 20 min after catheter placement (baseline), (2) during the first cold pressor test (CPT; hand held in an ice water bath for 90 s), (3) 20 min after reaching epidural analgesia to T-1 level of analgesia, and (4) during a second CPT (epidural analgesia to T-1). Monitoring consisted of noninvasive cardiac output (impedance), noninvasive blood pressure, and EKG. RESULTS: Extensive epidural block (stage 3) altered measured variables only minimally with respect to resting baseline state. During stage 2 (first CPT), mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), epinephrine, and norepinephrine increased. During stage 4 (second CPT), increases in HR and CI were not attenuated by any of the three local anesthetics. Increases in MAP were attenuated by epidural anesthesia with all three local anesthetics. Bupivacaine and 2-chloroprocaine epidural anesthesia significantly attenuated increases in plasma catecholamines, but lidocaine epidural anesthesia did not. CONCLUSIONS: Epidural anesthesia with all three local anesthetic agents tested resulted in an incomplete sympathectomy in the resting state in healthy young men, judged by plasma catecholamine concentrations and cardiovascular variables minimally changed from resting baseline. Lidocaine epidural anesthesia did not attenuate the catecholamine response to CPT, indicating decreased blockade of sympathetic efferent neural traffic compared with bupivacaine and chloroprocaine epidural anesthesia.

Adult↗

Redistribution of sufentanil to cerebrospinal fluid and systemic circulation after epidural administration in dogs.

Due to its higher lipid solubility, sufentanil may be less likely than morphine to migrate rostrally in the cerebral spinal fluid (CSF) and cause delayed respiratory depression following epidural administration. However, early respiratory depression has been reported in patients after relatively large doses of epidural sufentanil. This has been attributed to systemic drug uptake. We used a dog model to investigate the pharmacokinetics and rostral spread of epidural sufentanil in CSF. Sampling catheters were placed in the lumbar subarachnoid space, the cisterna magna, and femoral arteries of six mongrel dogs. Samples of cisternal CSF, lumbar CSF, and blood were drawn at 0, 1, 5, 15, 30, 60, 90, 120, and 180 min after lumbar epidural sufentanil injection. We measured sufentanil concentrations by gas chromatography-mass spectrometry and used the least squares method to a fit tri-exponential function to each sufentanil concentration versus time data set. Paired t-test was used to test for statistical significance. After epidural sufentanil, lumbar CSF concentrations were significantly higher than plasma or cisternal CSF sufentanil concentrations at all assessment times. Sufentanil concentrations were significantly higher in cisternal CSF than in plasma at 30 and 60 min after injection. Sufentanil appeared rapidly in lumbar CSF, reaching a maximum concentration (Cmax) of 57 ng/mL at 6.5 min. In cisternal CSF, a Cmax of 1.2 ng/mL was reached at 21 min, and Cmax in plasma was 0.35 ng/mL at 6 min. The area under the concentration-time curve (AUC) of sufentanil in cisternal CSF was approximately six times higher than the plasma AUC (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Changes in human plasma catecholamine concentrations during epidural anesthesia depend on the level of block.

To test the hypothesis that increasing levels of epidural analgesia will produce progressive decreases in circulating catecholamines, we sequentially produced three levels of analgesia, T8, T4, and C8, to pin prick in young, healthy volunteers. Three percent chloroprocaine (plain) was used as the local anesthetic. The epidural analgesia was allowed to dissipate following the T8 and T4 levels of block. After the C8 level the block was reinforced to study the effect of a "top-up" dose. Blood samples were drawn from a central venous catheter. Plasma concentrations of norepinephrine and epinephrine were determined by the single isotope radioenzymatic method. Despite extensive block, hemodynamic alterations were minimal, and no significant decrease in plasma epinephrine was observed as the level of analgesia was raised to the C8 dermatome. When the level of analgesia was raised above T8, there was a trend for norepinephrine to decrease, but this decrease did not become statistically significant until analgesia reached the C8 dermatome. Reinforcing the epidural block at the C8 level of analgesia resulted an insignificant decrease in epinephrine and norepinephrine NE. Under the conditions of the present study, epidural block with a sensory analgesia level as high as C8 did not significantly decrease the plasma concentration of epinephrine in unstressed volunteers. The plasma concentration of norepinephrine significantly decreased only when the level of sensory analgesia was approximately C8.

Adult↗

Epidural anaesthesia attenuates the catecholamine response to hypoventilation.

The effect of a high epidural block on the catecholamine response to hypoventilation was studied in six unanesthetized dogs given intravenous sufentanil (15 micrograms.kg-1). Sufentanil alone resulted in a increase of norepinephrine (NE) concentration from 108 +/- 73 pg.ml-1 to 843 +/- 399 pg.ml-1 and epinephrine (E) from 279 +/- 80 pg.ml-1 to 2010 +/- 1416 pg.ml-1. At least one week later, an epidural block to T1 was achieved using 8-10 ml, two per cent lidocaine. Plasma NE and E decreased after EA to about 50 per cent of resting baseline measurements. The addition of sufentanil increased NE and E levels to reach approximately the resting base-line levels. In all dogs intravenous sufentanil resulted in bradypnoea, bradycardia, hypoxaemia, and hypercarbia. Intravenous lidocaine infusions had no significant effect on plasma catecholamine levels when plasma lidocaine levels ranged from 1.7 micrograms.ml-1 to 5.3 micrograms.ml-1. We conclude that a high two per cent lidocaine epidural block attenuates the catecholamine response to hypoventilation in dogs, but the persistence of baseline plasma levels of NE and E suggests that the efferent sympathetic block by high EA is incomplete.

Anesthesia, Epidural↗

pH-adjustment of 2-chloroprocaine quickens the onset of epidural anaesthesia.

The effect of pH-adjustment of three per cent 2-chloroprocaine (2-CP, Nesacaine MPF) on the onset, duration, and spread of epidural analgesia and anaesthesia was studied in patients undergoing lower extremity surgery. Forty ASA physical status I and II patients were randomized to two groups. In a double-blinded fashion, patients in both groups received an epidural injection of 15 ml of local anaesthetic (LA) solution via a Tuohy needle at the L3-4 interspace. Local anaesthesia for Group I was prepared by adding 3 mEq NaHCO3 to 27 ml three per cent 2-CP and for Group II was prepared by adding 3 ml 0.9 per cent NaCl to 27 ml three per cent 2-CP. Both solutions contained epinephrine (1:200,000). The pH of commercially prepared Nesacaine MPF was 3.19 +/- 0.02. The pH of the solutions used for Group I and Group II patients were 7.32 +/- 0.01 and 3.27 +/- 0.02, respectively. Times to analgesia and anaesthesia at the L2 dermatome were significantly decreased in Group I patients by 2.5 and 6.6 minutes, respectively. Likewise, pH-adjustment accelerated the attainment of maximum level of block by 2.8 min. No statistical differences were found between groups in the maximum level of epidural block, or in time to 2-segment regression. No precipitation of LA was observed in pH-adjusted solutions of 2-CP after 24 hours. We recommend the use of pH-adjusted three per cent 2-CP (Nesacaine MPF) to accelerate the onset of epidural block.

Adult↗

Successful treatment of dural puncture headache with epidural saline infusion after failure of epidural blood patch. Case report.

A case is presented of a 30-year-old female with a 4-month history of post-lumbar puncture headache (PLPHA) resulting from an accidental dural puncture during an attempted epidural anesthetic for cesarean section. Epidural blood patches were attempted at 4 days and 3 months post-lumbar puncture, but were unsuccessful. At 4 months post-lumbar puncture, a 24-h epidural saline infusion relieved the PLPHA for 48 h, but the headache returned. Finally, a second epidural saline infusion was done, followed by an epidural blood patch, which permanently cured the PLPHA. Follow-up to 4 months showed no return of the PLPHA. The rationale for epidural blood and saline patches is discussed.

Adult↗