Epidural fentanyl speeds the onset of sensory and motor blocks during epidural ropivacaine anesthesia

In this study we examined the onset times of sensory and motor block during epidural ropivacaine anesthesia with and without the addition of fentanyl to the epidural solution. Forty-five young male patients undergoing knee arthroscopic surgery were randomly allocated into 3 groups of 15 patients each: epidural fentanyl (EF; epidural administration of 15 mL of 1% ropivacaine plus 100 mug fentanyl followed by IV injection of 2 mL of normal saline); IV fentanyl (IF; epidural administration of 15 mL of 1% ropivacaine plus 2 mL of normal saline followed by IV injection of 100 mug fentanyl); and control (C; epidural administration of 15 mL of 1% ropivacaine plus 2 mL of normal saline followed by IV injection of 2 mL of normal saline). The sensory and motor blocks were assessed by pinprick and modified Bromage scale, respectively. The hemodynamic changes, postepidural shivering, and side effects of epidural fentanyl were also recorded. There was no difference in the distribution of age, weight, and height among the 3 groups. The onset time of sensory block to the T10 dermatome was significantly more rapid in the EF group (13.0 +/- 3.0 min) than in the IF group (16.2 +/- 3.5 min, P < 0.05) or C group (17.7 +/- 3.6 min, P < 0.05). The onset times of motor block up to Bromage scale 1 and 2 were significantly more rapid in the EF group (11.9 +/- 4.6 and 24.4 +/- 5.9 min) than in the IF group (16.9 +/- 4.7 and 30.8 +/- 5.6 min, P < 0.05) or C group (18.3 +/- 4.9 and 32.7 +/- 5.7 min, P < 0.05). There was no difference in the incidence of shivering among the three groups. Pruritus was observed in three patients of the EF group and one patient of the IF group. No nausea, vomiting, respiratory depression, urinary retention, or hypotension was observed in any patient. We conclude that epidural administration of the mixture of 100 mug fentanyl and 1% ropivacaine solution accelerated the onset of sensory and motor blocks during epidural ropivacaine anesthesia without significant fentanyl-related side effects.     

Epidural morphine delays the onset of tourniquet pain during epidural lidocaine anesthesia

We conducted a randomized, double-blinded study to examine the onset time of tourniquet pain during epidural lidocaine anesthesia either with or without morphine in the epidural solution. Forty-five patients undergoing knee surgery with a thigh tourniquet were randomly allocated into 3 groups of 15 patients each: epidural morphine (EM; epidural administration of 17 mL of 2% lidocaine plus 2 mg of morphine, followed by IV injection of 0.2 mL of normal saline), IV morphine (IVM; 17 mL of 2% lidocaine plus 0.2 mL of normal saline, followed by IVM 2 mg IV), and control (17 mL of 2% lidocaine plus 0.2 mL of normal saline, followed by 0.2 mL of normal saline IV). The onset time of tourniquet pain was recorded. The level of sensory block was determined by the pinprick method at the occurrence of tourniquet pain. Hemodynamic changes and side effects of EM were also recorded. The onset time of tourniquet pain from both the epidural injection and the tourniquet inflation were significantly longer in the EM group (103 +/- 15 min and 80 +/- 15 min, respectively) compared with the IVM group (74 +/- 12 min and 50 +/- 12 min, respectively; P < 0.05) and the Control group (67 +/- 9 min and 45 +/- 9 min, respectively; P < 0.05). The level of sensory block at the onset of tourniquet pain and hemodynamic changes were not different among the three groups. Only two and three patients in the EM group complained of nausea/vomiting and pruritus, respectively. Respiratory depression was not observed in any patient. We conclude that epidural injection of the mixture of 2 mg of morphine and 2% lidocaine solution delayed the onset of tourniquet pain during epidural lidocaine anesthesia without significant morphine-related side effects. IMPLICATIONS: We examined the effect of epidural morphine on the onset of tourniquet pain during epidural lidocaine anesthesia. We found that the addition of 2 mg of morphine to epidural 2% lidocaine significantly delayed the onset of tourniquet pain without increasing morphine-related side effects.     

The addition of epinephrine increases intensity of sensory block during epidural anesthesia with lidocaine

BACKGROUND AND OBJECTIVES: Little is known about the effect of adding epinephrine to local anesthetic solutions on the intensity of sensory block during epidural anesthesia. This study examined development of sensory block during lumbar epidural anesthesia using a cutaneous current perception threshold (CPT) quantitative sensory testing device. METHODS: Twenty ASA I patients who were randomly divided to receive 10 mL 1% lidocaine with (group E) or without (group P) epinephrine 1:200,000. Current perception threshold at 2,000, 250, and 5 Hz stimulation at the trigeminal (V), ninth thoracic (T9), and second lumbar (L2) dermatomes, and the dermatomal levels of block of light touch, temperature, and pinprick discrimination were measured before and every 5 minutes, until 60 minutes after injection of epidural lidocaine. RESULTS: After epidural administration of lidocaine with epinephrine, all CPT significantly increased at T9 and L2, whereas no increase was detected after epidural plain lidocaine. Areas under the curves, calculated to express overall magnitude and duration of CPT values, were significantly larger in group E than those in group P at 2,000 and 250 Hz at T9. No differences were observed in the maximal levels of loss of cold, pinprick, and touch sensations between both groups. CONCLUSIONS: These results suggest that lumbar epidural anesthesia using 10 mL 1% lidocaine with epinephrine produces a more intense block of both large and small diameter sensory nerve fibers than that with plain lidocaine. It appears, therefore, that the addition of epinephrine improves the quality of sensory block during epidural anesthesia with lidocaine.     

Epidural fentanyl improves the onset and spread of epidural mepivacaine analgesia

Purpose

To determine the extent of enhanced blockade by the combined use of epidural fentanyl and mepivacaine. We compared the onset of hypoalgesia, analgesia and the threshold of pressure pain.

Methods

Thirty patients were randomly divided into three groups. The fentanyl group received 10 ml saline containing 0.1 mg fentanyl, mepivacaine group received 10 ml mepivacaine 1% and a mixed group received 10 ml mepivacaine 1% with 0.1 mg fentanyl. All solutions, without epinephrine, were injected through an epidural catheter at T_5–6 to T_6–7. The change in sensation, loss of pin-prick and pain threshold sensation, measured by pressure algometer, were assessed at 2.5-min intervals for 15 min at the T₄ dermatome. Spread of analgesia was determined at 15 min.

Results

Loss of pinprick was more rapid in the mixed, 11.0 ± 2.7 (SD) min, than in the mepivacaine group, 15.0 ± 2.9 min, (P < 0.05), although there was no difference in change of sensation. Pressure pain threshold increased with time in the mepivacaine (P < 0.05) and mixed (P < 0.05) groups. It was higher in the mixed than in the fentanyl and mepivacaine groups at 5, 7.5 and 10 min (P < 0.05). The lower level of analgesia was lower in the mixed than in the mepivacaine groups (P < 0.05). Blood pressure was unchanged in the three groups, but heart rate decreased at 7.5, 10, 12.5, and 15 min in the mepivacaine and mixed groups (P < 0.05).

Conclusions

The addition of fentanyl to mepivacaine accelerates the onset of analgesia and enhances the analgesic effect of epidural block.     

Differential sensory block: spinalvs epidural with lidocaine

PURPOSE: In this study we sought to determine if and when a difference exists with regards to differential sensory blockade between spinal and epidural anaesthesia using lidocaine. METHODS: Ten healthy volunteers were randomly assigned to receive both spinal and epidural anaesthesia. Non-epinephrine containing solutions of lidocaine, 100 mg lidocaine 5% with 7.5% dextrose (spinal) and 600 mg lidocaine 2% (epidural), were used to establish sensory blockade. At five minute intervals, for a total of 65 min, the following sensory modalities were tested: anaesthesia (complete loss of sensation to pinprick), analgesia (loss of an equally sharp sensation to pinprick compared with that at an unblocked dermatome), cold sensation (complete loss of cold temperature discrimination). RESULTS: At all times, except at time = 0 during spinal anaesthesia, the levels of analgesia and cold sensation were more cephalad than the level of anaesthesia for both spinal and epidural anaesthesia. Multiple comparison testing among the three dermatomal response levels showed that, during epidural anaesthesia, the level of analgesia was more cephalad than the level of cold sensation at the following times: 25 min, 30 min, and from 40 to 60 min. In contrast, the level of analgesia was not different from the level of cold sensation during spinal anaesthesia. CONCLUSIONS: Spinal and epidural anaesthesia with lidocaine produce a similar degree of differential sensory blockade. Epidural anaesthesia produces a detectable difference between the level of analgesia and cold sensation at various times, whereas spinal anaesthesia did not reliably do so in this study.     

Epidural phenylephrine attenuates hypotension induced by alkalinized lidocaine epidural anesthesia.

In this double-blinded, randomized study, we examined the hemodynamic effects of lumbar epidural injection of alkalinized lidocaine with phenylephrine in 81 patients undergoing inguinal herniorrhaphy. Patients assigned to four equal groups received 20 mL of alkalinized lidocaine (17 mL of 2% lidocaine + 3 mL of 7% sodium bicarbonate) with one of four doses of phenylephrine: 0 (Group 1), 50 (Group 2), 100 (Group 3), or 200 microg (Group 4) injected via a lumbar epidural catheter. Blood pressure, heart rate, and skin temperature on the foot were recorded every 5 min for 1 h after injection and were compared among groups. Hypotension was defined as mean arterial pressure < 80% of baseline. The incidence of hypotension was 45%, 55%, 35%, and 15% in Groups 1-4, respectively. Patients in Group 4 showed the smallest reduction in blood pressure compared with Groups 1 and 2 (one-sided Fisher's exact test, P < 0.05). We conclude that the 200-microg dose of epidural phenylephrine (1:100,000 concentration) reduced the incidence of hypotension after epidural anesthesia with alkalinized lidocaine. IMPLICATIONS: Hypotension after epidural anesthesia is common in general clinical practice. Phenylephrine administered epidurally in combination with alkalinized lidocaine may reduce the incidence of hypotension.     

Effect of epidural saline washout on regression of sensory and motor block after epidural anaesthesia with 2% lidocaine and fentanyl in elderly patients

Seventy elderly males received lumbar epidural anaesthesia with 12 ml of 2% lidocaine containing fentanyl 50 μg. At the end of transurethral surgery, the washout group ( n  = 33) received an epidural bolus of 30 ml saline while the control group ( n  = 34) did not. Mean (SD) times to 1-grade (17.2 (11.9) vs 32.7 (11.3) min) and 2-grade regression (23.8 (12.2) vs 56.0 (23.9) min) of motor block, 3-dermatomal sensory regression (31.4 (11.6) vs 42.2 (14.4) min for cold and 30.8 (15.6) vs 40.6 (14.2) min for pinprick), and regression to S1 (57.7 (16.1) vs 76.2 (20.2) min for cold and 56.8 (17.3) vs 69.2 (16.2) min for pinprick) were significantly shorter in the washout group than the control group. There were no differences in postoperative pain scores and side effects between the two groups. We concluded that epidural washout facilitates regression of both motor and sensory block following epidural anaesthesia without reducing the postoperative analgesic benefit.     

Pharmacokinetics and the lung uptake of lidocaine during epidural anesthesia

In order to investigate the pharmacokinetics of lidocaine especially the lung uptake during epidural anesthesia, we measured the lidocaine concentrations of arterial and central venous blood simultaneously using a homogeneous enzyme immunoassay. Then the lung extraction ratio was calculated as (1-arterial lidocaine concentration/central venous lidocaine concentration) X 100%. With only epidural anesthesia, the lung uptake of lidocaine was above 30% during the first 40 minutes, but was less after additional administration. After general anesthesia with thiamylal, enflurane, nitrous oxide and oxygen, the lung uptake was 30 approximately 40% following initial and additional administrations. There was a positive correlation between the lung extraction ratio and the central venous lidocaine concentration 5 minutes after the initial administration. Having used laryngotracheal lidocaine spray during endotracheal intubation, the lung extraction ratio could not be calculated since this resulted in direct lidocaine administration to the lungs. In conclusion, the lung plays an important role in keeping the arterial lidocaine concentration low.     

Propofol does not inhibit lidocaine metabolism during epidural anesthesia

Propofol is sometimes used in combination with epidural anesthesia with lidocaine. In this study, we investigated the effect of propofol on the plasma concentration of lidocaine and its principal metabolites during epidural anesthesia with lidocaine. Thirty-two patients were randomly allocated to receive either propofol or sevoflurane anesthesia (n = 16 each). In the propofol group, anesthesia was maintained with a target concentration of propofol of 4 microg/mL. In the sevoflurane group, anesthesia was maintained with 1.5% sevoflurane. Lidocaine was administered epidurally in an initial dose of 5 mg/kg, followed by a continuous infusion at 2.5 mg x kg(-1) x h(-1). Free components of plasma lidocaine and its metabolites-monoethylglycinexylidide (MEGX) and glycinexylidide (GX)-were measured 30, 60, 120, and 180 min after the initiation of continuous epidural injection by using high-performance liquid chromatography. Free lidocaine, MEGX, and GX were separated from 2 mL of plasma by ultrafiltration filter units. Hemodynamic data were similar between groups. The plasma concentrations of free lidocaine were not significantly different between groups. The ratios of free MEGX to free lidocaine and free GX to free MEGX were not different between groups. In conclusion, propofol does not alter the metabolism of epidural lidocaine compared with sevoflurane.     

Epidural fentanyl delayed emergence from anesthesia

An 83-year-old man (158 cm, 42 kg) was scheduled for cholecystectomy. He had a history of hypertension and atrial fibrillation. The patient received no premedication. An epidural catheter was inserted via the T9-10 interspace and 2% mepivacaine 7 ml was injected, producing a sensory block from T4 to T12. Anesthesia was induced with propofol and remifentanil, and was maintained with propofol, remifentanil, and nitrous oxide in oxygen. Rocuronium was given to provide neuromuscular block. Just before the completion of surgery, a bolus epidural injection of 2% mepivacaine 2 ml with fentanyl 50 microg was performed. Then epidural solution of ropivacaine 0.1% with fentanyl 6.25 microg x ml(-1), and droperidol 25 microg x ml(-1) was infused at 4 ml x hr(-1). Soon after the surgery, the patient developed atrial fibrillation that was treated with external electrocardioversion with 100 watt x sec. After the restoration of sinus rhythm, anesthetics were discontinued. The patient did not emerge from anesthesia though he breathed spontaneously Doxapram was slightly effective, but he did not respond to the verbal command. Epidural infusion was stopped and the patient was transferred to the ward. The patient fully recovered from anesthesia after 2 hours. Epidural infusion was restarted 17 hours later, and the patient fell asleep. He woke up after stopping epidural infusion. Epidurally administered fentanyl must have been the cause of delayed recovery from anesthesia. He could have been highly sensitive to fentanyl. Patient controlled epidural anesthesia may have been useful for this patient.     

Clinical manifestations and serum fentanyl concentrations during epidural high dose fentanyl anesthesia]

Twelve elective abdominal surgeries were performed under epidural anesthesia with high dose fentanyl. An epidural catheter was inserted at Th9-Th12 interspace and fentanyl 10 micrograms.kg-1 with [E (+)] or without [E(-)] epinephrine 1:100,000 was given for each group of 6 patients. After the administration of epidural fentanyl, arterial blood was sampled at 5, 10, 15, 30, 60, 120, 180, 240 minutes. The serum concentrations of fentanyl were measured by gas chromatography. The peak concentration of serum fentanyl was observed in the E (-) group, while that was not seen in the E (+) group. The time of reach maximum serum concentration after epidural fentanyl administration in the E (-) group was from 10 to 15 minutes. In two cases of E (-) group, the plasma concentration-time course could be fitted to two-compartment model. The others could be fitted neither to a two-compartment nor to a three-compartment model. In both groups, we could maintain anesthesia with enflurane of less than 0. 4%, and N2O, 66%. It is suggested that analgesic effect of fentanyl on opioid receptor of spinal cord plays a major role in this anesthesia method.     

肾上腺素对利多卡因硬膜外麻醉时血流动力学的影响

目的 观察肾上腺素对利多卡因硬膜外麻醉时血流动力学的影响.方法 择期行骨科下肢手术患者40例,ASA Ⅰ或Ⅱ级,随机均分为肾上腺素(E)组和生理盐水(S)组,分别采用2%利多卡因加5 μg/ml肾上腺素或等容生理盐水进行硬膜外麻醉.采用阻抗心动图记录注药前即刻(T0)、注药后5、10、15、20、25、30 min(T1～T6)的MAP、HR、心脏指数(CI)、外周血管阻力指数(SVRI)和加速指数(ACI).结果 与T0时比较,E组在T1～T6时MAP和SVRI降低、CI和ACI升高、HR增快(P<0.05),而S组血流动力学差异无统计学意义.结论 肾上腺素加入利多卡因用于硬膜外麻醉可引起MAP和SVRI下降、CI和ACI升高、HR增快等血流动力学改变.     

Free lidocaine concentrations during continuous epidural anesthesia in geriatric patients

BACKGROUND AND OBJECTIVES: To evaluate the effects of aging on lidocaine pharmacokinetics, the plasma concentrations of total and free lidocaine and its metabolites were measured during continuous thoracic epidural anesthesia in middle-aged (age 41 +/- 9 years, n = 7) and elderly (age 72 +/- 2 years, n = 7) male patients. METHODS: After establishment of general anesthesia, 7 mL 1.5% lidocaine with epinephrine 1:200,000 was injected into the epidural space and subsequently infused at a rate of 5 mL/h for 5 hours. Plasma concentrations of total and free lidocaine, monoethylglycinexylidide (MEGX), and glycinexylidide (GX) were measured at 10, 15, 20, 30, 45, 60, 90, 120, 150, 180, 240, and 300 minutes after initial lidocaine injection using high-performance liquid chromatography (HPLC) with ultraviolet (UV) detection. RESULTS: The elderly group showed a stronger upward trend in the corrected free lidocaine concentrations and lower corrected total MEGX concentrations than the middle-aged group. CONCLUSIONS: Lidocaine metabolite activity in the elderly male patients was lower than that in the middle-aged male patients. Free lidocaine concentration is prone to increase in elderly patients. Caution must be exercised during continuous thoracic epidural anesthesia combined with general anesthesia in geriatric patients.     

Quantitative and selective assessment of sensory block during lumbar epidural anaesthesia with 1% or 2% lidocaine

We have examined sensory block during lumbar epidural anaesthesia using a cutaneous current perception threshold (CPT) sensory testing device in 20 patients who received 10 ml of either 1% or 2% lidocaine (lignocaine). CPT at 2000, 250 and 5 Hz stimulation at the trigeminal (V), ninth thoracic (T9) and second lumbar (L2) dermatomes, and dermatomal levels of block to light touch, temperature and pinprick discrimination were measured before and every 5 min until 60 min after epidural lidocaine. There were significant differences between 1% and 2% epidural lidocaine in all CPT at T9 and L2, in addition to maximal cephalad spread of the three sensory modalities. After 2% lidocaine, all CPT increased significantly at T9 and L2. In contrast, only at 250 and 5 Hz for L2 did epidural block with 1% lidocaine produce significant increases in CPT. Maximal level of loss of touch sensation after 1% lidocaine was significantly lower than that of cold and pinprick sensations. We conclude that the dose of lidocaine affected intensity of sensory block during lumbar epidural anaesthesia. In addition, differential neural block resulting from epidural anaesthesia appeared to be associated with a differential effect on nerve fibres of different sizes.