Winnie et al. (1) first described a posterior approach for lumbar plexus block. Inadvertent epidural (2) and spinal (3) anesthesia have occurred with this approach, and this has led to concerns regarding its use (4). Bilateral anesthesia has also complicated alternative approaches to lumbar plexus or psoas compartment block (PCB) as described by Chayen et al. (5) and Dekrey (6).
The invariable medial needle redirection with Winnie's technique to locate the lumbar plexus may be a factor in bilateral anesthesia (1,7). Capdevila et al. (7) revisited Winnie's landmarks and modified the approach to permit maintenance of a perpendicular needle orientation. They found no cases of bilateral anesthesia. A radiographic study of this technique demonstrated epidural spread of contrast medium in only 2% of patients (8). This incidence is less than the commonly quoted incidences of 10%–20% for Winnie's approach (9). Comparison of quoted incidences of bilateral anesthesia secondary to PCB in the literature suggests that the incidence is dependent on the approach used (10).
However, accurate determination of the incidence of bilateral anesthesia after PCB is complicated by a number of factors. Assessment of bilateral blockade has been variable in terms of timing and extent (2,6,7). Radiographic imaging does not provide an indication of spread over time (8). Finally, incidences of bilateral anesthesia compare PCB performed by different operators. Identification of anatomical surface landmarks is extremely variable among anesthesiologists (11,12).
The increasing use of nerve stimulation in peripheral nerve block techniques has resulted in a modification of Winnie's original technique, and stimulation of the femoral nerve, rather than paresthesia, is now sought (2,13). We therefore performed a modified Winnie technique, seeking femoral nerve stimulation, and standardized our medial needle redirection as 15°. Our aims were to compare a modified Winnie technique with Capdevila's approach for PCB performed by the same operator in terms of incidence of contralateral spread, extent of lumbar plexus blockade, and efficacy of postoperative analgesia after primary total hip or knee arthroplasty.
With institutional ethics committee approval and written informed consent, 60 ASA I–III patients scheduled for primary hip or knee arthroplasty were enrolled. Exclusion criteria were contraindications to regional anesthesia, contraindications to nonsteroidal antiinflammatory drugs, or scoliosis on clinical examination.
Before the induction of anesthesia, a 16- to 18-gauge cannula was placed, followed by routine monitoring that consisted of electrocardiography, pulse oximetry, and noninvasive arterial blood pressure recorded at 5-min intervals (AS3; Datex Instrumentarium Corp., Finland). Baseline arterial blood pressure was recorded. Patients received midazolam 2–3 mg IV, and Hartmann's solution 10 mL/kg was administered. Patients were assigned to 1 of 2 groups by using a random number table with restricted randomization in blocks of 10. The primary investigator was given the randomization group in a sealed envelope. Patients in the Capdevila group (group C) had PCB performed according to the modified surface landmarks of Capdevila et al. (7). In the Winnie group (group W), PCB was performed as described by Winnie et al. but was modified to include a nerve-stimulation technique with a standardized medial needle redirection (1). A single operator (SM) equally experienced with both techniques performed all blocks. The two techniques for PCB differ primarily in terms of the skin site for needle insertion. Patients were positioned in the lateral position with the operative side uppermost. Lidocaine 3 mL 1% was injected subcutaneously. The skin was prepared with chlorhexidine. A Stimuplex A® 100-mm needle (B. Braun Medical, Melsungen, Germany) was inserted and connected to a nerve stimulator (Stimuplex S®; B. Braun Medical) with a starting output of 1.5 mA and 2 Hz. The needle was advanced until quadriceps twitches were elicited or bony contact (assumed to be transverse process) was made. If bone was encountered for either approach, the needle was withdrawn, directed caudad under the transverse process, and advanced until twitches were elicited with currents between 0.3 and 0.5 mA. After negative aspiration, 0.4 mL/kg levobupivacaine 0.5% (Chirocaine®; Abbott Laboratories, Dublin, Ireland) was injected for approximately 3 min. The duration of the procedure was defined as the time from skin preparation to commencement of local anesthetic administration, to the nearest half minute. The time at which all the local anesthetic solution had been injected was taken as Time 0. Patients were returned to a semirecumbent position with head up of 30°–45°, and diclofenac 75 mg was administered IV.
The bony landmarks used in both groups were similar. A line was drawn connecting the iliac crests (intercristal line). The spinous processes (SP) were marked, and the posterior superior iliac spine (PSIS) was identified. A line through the PSIS was drawn parallel to a line joining the SP. In group C, the point of needle insertion was at the junction of the lateral third and medial two-thirds of a line between the SP and the PSIS and 1 cm cephalad to the intercristal line (Fig. 1). The needle was inserted perpendicular to all planes. In group W, the point of insertion was at the intersection of the intercristal line and the line through the PSIS. For Winnie's approach, needle advancement was initially perpendicular to all planes with a 15° medial redirection if the lumbar plexus was not encountered.
A second investigator unaware of group allocation evaluated sensory and motor function 15, 30, and 45 min after block completion. Sensory blocks of the femoral nerve (anterior thigh), the lateral cutaneous nerve (lateral thigh), and the S1 root (sole of foot) were evaluated by using ethyl chloride spray and compared with the contralateral leg. Sensation was scored as follows: 0, no difference; 1, less cold; and 2, not cold. Blockade of the obturator nerve was evaluated by the degree of thigh adductor motor block and was scored as follows: 0, normal power; 1, weakness in adduction; and 2, paralysis of adduction. Bilateral anesthesia defined as diminished sensation of the contralateral side, was sought by using ethyl chloride spray bilaterally from the T4 to S5 dermatomes, and was recorded as present or absent. Contralateral lower limb motor function was grossly evaluated as follows: 0, normal power; 1, weakness; and 2, paralysis. Hypotension and bradycardia were defined as decreases in systolic blood pressure from baseline of ≥20% and heart rate <60 bpm, respectively.
Patients were returned to the original lateral position and scheduled for spinal anesthesia 45 min after completion of PCB. A 25-gauge Whitacre or 22-gauge Yale needle was used to administer 17.5 mg of bupivacaine 0.5% intrathecally. Rectal acetaminophen 1 g was administered. Midazolam 1–2 mg IV was titrated to a maximum 10 mg for anxiety as clinically indicated. Maintenance and replacement fluids consisted of Hartmann's solution and were administered at the discretion of the attending anesthesiologist.
General anesthesia was administered instead of spinal anesthesia if bilateral anesthesia secondary to PCB resulted in significant hypotension (systolic blood pressure of 30% less than baseline). General anesthesia was induced with 2 mg/kg propofol IV, and a laryngeal mask was inserted. Anesthesia was maintained with 1%–2% sevoflurane end-tidal concentrations in 50% oxygen and nitrous oxide with spontaneous respiration.
After surgery, the following variables were recorded 3, 6, 12, and 24 h after performance of PCB, by nursing staff unaware of group allocation: pain scores at rest, nausea/vomiting, time to first morphine analgesia, and 24-h cumulative morphine consumption. Patients were cared for in a 5-bed recovery ward for 24 h after surgery. Pain was assessed with a verbal rating score (VRS) for all patients, with 0 = “no pain” and 10 = “worst pain you could imagine.” Pain was assessed only at rest, to avoid the risk of prosthesis dislocation. Nausea or vomiting was recorded as present or absent. Antiemetic administration (cyclizine 50 mg IM every 8 h as needed) in the 24-h period was recorded.
Nursing staff administered acetaminophen 1 g every 6 h and diclofenac 75 mg every 12 h irrespective of pain status. Patients with pain scores >3 were administered morphine 0.15 mg/kg IM every 4 h as required. Duration of analgesia was defined as the time from completion of block injection (Time 0) to the time of first administration of morphine. At 24 h after surgery, cumulative morphine consumption was noted.
Based on α = 0.05 and β = 0.2 and seeking a difference of 25% in the proportion of patients with contralateral spread between groups, a sample size of 27 per group was required. Statistical analysis was performed with GraphPad Prism version 4.00 for Windows (GraphPad Software, San Diego, CA). Parametric data were analyzed by using Student's unpaired t-test. Nonparametric data were analyzed by using the Mann Whitney U-test. Proportional data were analyzed with Fisher's exact test. Data are presented as mean ± sd or median (range). P < 0.05 was taken as statistically significant.
The two groups were similar in terms of age, sex, weight, ASA classification, and surgery type (Table 1). Two patients in each group underwent general anesthesia. In group W, medial orientation of the needle was necessary to locate the lumbar plexus in 28 patients. In group C, the needle orientation was maintained perpendicular in all patients.
Twelve patients (40%) in group W and 10 patients (33%) in group C developed contralateral spread (P = 0.8). Distribution of bilateral anesthesia was either thoracic to lumbar dermatomes (8 in group W and 5 in group C), thoracic to sacral (4 in group W and 3 in group C), or lumbar dermatomes only (0 in group W and 2 in group C). In both groups, the highest dermatome reached was T4, and the lowest was S5. Equal bilateral dermatomal distribution occurred in 6 patients in group W and 7 patients in group C. Distribution of spread was unequal bilaterally in 6 patients in group W and 3 patients in group C, ranging from 1 to 5 dermatomes greater on the operative side or 2 to 4 dermatomes more on the contralateral side. No patient in either group had complete motor block of the contralateral lower limb (score, 2). Four patients in group W and 5 patients in group C had a partial motor block (score, 1). In 6 patients (3 in each group), contralateral spread developed 15 min after lumbar plexus block had occurred, and in 1 patient (group W), contralateral spread occurred 30 min later.
Hemodynamic changes occurred in 3 patients in group W and 4 patients in group C and comprised hypotension (2 in group W and 4 in group C) and bradycardia (2 in group W and 1 in group C). Two patients in each group were effectively treated with ephedrine 12 mg IV for a decrease in systolic blood pressure of 30%. All hemodynamic changes occurred in patients who developed bilateral T4 block, except for two patients in group C who had hypotension after developing bilateral T9 to S5 anesthesia.
PCB procedure duration, the duration to first morphine analgesia, and 24-h cumulative morphine requirements were similar in the two groups (Table 2). Similarly, there were no differences between groups in postoperative VRS 3, 6, 12, and 24 h after the block (Table 3).
The extent of lumbar plexus and first sacral (S1) root spread at 45 min after procedure completion was similar in both groups (Table 4). Every patient developed at least partial femoral, lateral cutaneous, and obturator neural block, except for one patient in each group who did not develop obturator nerve block. Nausea or vomiting occurred in 3 patients in group W and 5 patients in group C.
Our findings demonstrate that Winnie's and Capdevila's approaches for PCB are similar in terms of lumbar plexus blockade and the incidence of contralateral spread. Our results demonstrate that the incidence of bilateral anesthesia after PCB via these approaches is more frequent than previously recorded.
Neither Winnie and colleagues' original description (1) nor Chayen et al.'s (5) subsequent article on PCB described bilateral anesthesia as a complication, although Chayen et al. (5) did report a case of dural puncture before local anesthetic administration. The first reported case of bilateral anesthesia after posterior lumbar plexus block was by Muravchick and Owens (14), who used an L4-5 approach. In a recent survey of complications of regional anesthesia, the occurrence of bilateral anesthesia was the most common cause of adverse effects with PCB (4).
It has been postulated that bilateral anesthesia after posterior lumbar plexus block may result from puncture of the epidural sleeves extending along the femoral nerve (13) or may be a result of medial orientation of the needle leading to direct epidural or subarachnoid injection of local anesthetic solution (7). Capdevila et al.'s (7) modification of Winnie's original landmarks was based on computer tomographic imaging of the lumbar plexus in relation to the psoas muscle and the bony landmarks of the iliac crests, PSIS, and SP. Their re-evaluation permits perpendicular maintenance of the needle. On the basis of these mechanisms, it was postulated that avoidance of medial needle orientation toward the neuraxial column should therefore prevent or significantly reduce the likelihood of bilateral anesthesia (7). Our findings clearly demonstrate that this is not so and indicate that bilateral anesthesia after PCB is most likely as a result of solution spread from the psoas compartment rather than from direct epidural administration.
Although diffusion of solution into the epidural space via the intervertebral foramen is possible (6), this is unlikely to be the only mechanism for bilateral anesthesia. Contralateral spread of solution after thoracic paravertebral block (PVB) (15), as well as cases of bilateral anesthesia after lumbar PVB (16), suggest that bilateral spread after PCB may be via similar mechanisms. Gray (17) demonstrated that there is a connection between the thoracic fascia and lumbar fascia surrounding the psoas muscle by reporting the passage of a mediastinal tubercle abscess into the groin via the psoas sheath. Ipsilateral spread of solution occurs from the thoracic paravertebral space into the lumbar paravertebral region along the endothoracic fascia, which is continuous with the fascia transversalis and blends with the psoas fascia (18,19). Contralateral spread of solution in the lumbar region may occur anterior to the vertebral bodies via areolar connective tissue within the subserous fascial layer, as described after PVB in the thoracic region (10,15).
Bilateral anesthesia may also occur as a result of subdural spread of solution. The subdural space is the potential space between the dura and arachnoid mater. The dura can extend into the paravertebral space, and this may facilitate the spread of solution (20). Spread of solution into the subdural space may explain the delayed onset, as well as the extent of sensory but variable motor block, that we recorded (21).
The other important finding of our study was the more frequent incidence of contralateral spread than previously reported with these two approaches. Capdevila et al. described no cases of contralateral spread with their approach. However, their assessment occurred at one hour postblock, assessed only T8 to L1 sensory distribution, and did not include patients with partial sensory block, and a more dilute local anesthetic solution (ropivacaine 0.2%) was administered, followed by continuous infusion (7). Stevens et al. (2) performed PCB via Winnie's approach by using bupivacaine 0.5% with epinephrine with volumes (0.4 mL/kg) similar to those in our and Capdevila et al.'s studies. They demonstrated bilateral anesthesia in 11% of their patients. Their patients underwent general anesthesia followed by PCB and then subsequent hip arthroplasty. Sensory assessment therefore occurred after surgery at variable times in the postanesthesia care unit, was nonspecific for which thoracic and lumbar dermatomes, and did not define partial or complete block; also, possible hemodynamic effects were obscured by the concurrent administration of general anesthesia. Farny et al. (22), performing Winnie's technique, detected contralateral spread in 9% of their patients, whereas Parkinson et al. (6) found an incidence of 16% after PCB performed via Dekrey's L3 approach. In both of these studies, assessment of contralateral spread was by motor testing only. It is likely that the incidence of contralateral spread after PCB, regardless of approach, has been underestimated (Table 5). No previous studies have specifically sought or defined bilateral anesthesia after PCB. These inconsistencies, in terms of the extent and timing of assessment of sensory and motor block, may explain the less frequent incidence, especially because patients with more subtle anesthesia would have had normal hemodynamics and been able to move their lower limbs. When “care was taken to screen for potential bilateral extension of sensory block,” Biboulet et al. (23) demonstrated a 25% incidence of contralateral spread after an L3 approach to PCB.
Our study demonstrates that the extent of lumbar plexus blockade after Capdevila's and Winnie's approaches for PCB was similar, providing very effective three-in-one block. The extent of three-in-one blockade compares favorably to the findings of Parkinson et al. (6), who compared an L3 and L4–5 approach. The equivalent degree of lumbar plexus block of the two groups was supported by clinical findings of similar pain scores and 24-hour morphine consumption. An average 12-hour pain-free interval and a median VRS of 0 at all data time points for 24 hours after surgery demonstrate the efficacy of an analgesic multimodal approach incorporating PCB in this surgical setting.
Radiographic imaging has been used to examine the spread of contrast media after PCB (8); however, it may not provide a complete assessment of local anesthetic spread. Radiographic imaging is unable to provide an indication of spread over time unless repeated or continuous imaging is used. As our results show, this would have to occur for 30 minutes after PCB, because almost one-third of cases of contralateral spread (7 of 22) developed 15 minutes after the onset of lumbar plexus anesthesia. Radiography provides two-dimensional images only, but the use of imaging techniques such as computer tomographic or magnetic resonance imaging was not practical in this surgical setting. Finally, the spread of contrast medium does not necessarily correlate with the extent of sensory block (24).
Large volumes (30–40 mL) have been used for PCB, although our recent clinical experience indicates that 20 mL is sufficient. The fascial interconnections between the psoas compartment and the paravertebral, subdural, and epidural spaces facilitate the spread of local anesthetic solution. Therefore, use of smaller volumes may reduce the risk of bilateral spread, especially in female or elderly patients, in whom the volume of the psoas muscle is less (E. Touhy, personal communication, Department of Anatomy, National University of Ireland, Cork). Patient positioning may also reduce bilateral spread. Jankowski et al. (9) performed PCB with patients lying on the side to be blocked and had no cases of bilateral anesthesia after unilateral PCB despite using 40 mL of local anesthetic.
In conclusion, we found no difference in the incidence of contralateral spread comparing two approaches for PCB. The incidence of bilateral anesthesia is 20%–30% more with these approaches than previously reported. Both Winnie's and Capdevila's approaches for PCB result in successful lumbar plexus in more than 90% of patients. Finally, our findings support investigating factors other than approach as causes of contralateral spread after PCB.
We thank the nursing staff of Block 9, St. Mary's Orthopaedic Hospital, for their time and assistance with postoperative data collection.
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© 2005 International Anesthesia Research Society
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