Intraneural Injection during Anterior Approach for Sciatic Nerve Block

A 75-yr-old woman, 75 kg, 158 cm, American Society of Anesthesiologists physical status III having a history of noninsulin-dependent diabetes mellitus treated with oral hypoglycemic agents was scheduled for transmetatarsal amputation of the right foot because of a severe vasculopathy. The patient gave her written informed consent to perform a continuous sciatic nerve block using the anterior approach.5A CT image confirmed possible access to the sciatic nerve along an anatomical path that avoided contact with other significant structures (fig. 1). After setting up a peripheral blood access line, administering oxygen at a rate of 4 l/m, sedating the patient with 1 mg of midazolam, and anesthetizing the injection site with 3 ml of 1% mepivacaine we inserted the 100 mm stimulation needle (Plexolong®; Pajunk GmbH, Geisingen, Germany). Final position of the needle tip was determined by nerve stimulation. Nerve stimulation (Stimuplex® HNS 11; B Braun Melsungen AG, Melsungen, Germany) performed at a frequency of 2 Hz and pulse duration of 300 μs. The initial stimulation current intensity was set at 1.5 mA, and the needle was advanced until we observed a plantar flexion at a depth of 9 cm. Further advancement of the needle allowed a decrease in intensity to 0.3 mA, an intensity commonly used for administration of anesthetic near the nerve. After needle stabilization, we first administered 2 ml of 1.5% mepivacaine, which induced no pain or discomfort, followed by another 18 ml of mepivacaine to which we had added 1 ml of nonionic, iso-osmolar iodine contrast medium (Iohexol-Omnipaque® 300; Nycomed Ireland, LTD., Cork, Ireland) without resistance or pain. CT images showed contrast medium around the nerve and between nerve fascicles with a small bubble of entrapped air intraepineurally (fig. 2). Contrast medium showed along the entire 9.5-cm length of nerve explored (fig. 3). Normal flat nerve morphology before needle puncture changed to circular morphology after the injection (fig. 2). A catheter was inserted through the needle to a depth of 3 cm. A further dose of 10 ml of 1.5% mepivacaine mixed with 0.5 ml of iodine contrast medium was administered. Further scan sequences showed the catheter inside the epineurium (fig. 4). The catheter was left in place for 3 days after the surgical procedure to administer a continuous infusion of 0.2% ropivacaine at a rate of 5 ml/h. Motor and sensory functions of the foot recovered when the infusion was discontinued.

Similar observations were made in another noninsulin-dependent diabetic woman with distal diabetic polyneuropathy and vasculopathy. She was 69 yr old, 53 kg, 152 cm, and ASA physical status III. In this patient, the depth of the needle was 9.5 cm, and the minimal stimulation intensity was 0.56 mA at pulse duration of 300 μs. The local anesthetic and contrast medium were administered following the same protocol as in the previous patient. A CT scan confirmed the diffusion of the contrast medium inside the nerve and along the entire length of 10 cm of explored nerve. The final administration trough the catheter of 10 ml dose of 1.5% mepivacaine mixed with 0.5 cm of iodine contrast medium showed its intraneural diffusion (fig. 5). At the end of the surgical procedure, motor and sensory functions recovered fully.

Several factors may contribute to postoperative nerve damage after performing peripheral nerve block anesthesia. Modern current nerve stimulators, such as those used in our case studies, allow for the more precise positioning of the needle electrodes and minimize the risk of errors resulting from a possible malfunction of the equipment during nerve stimulation. The electrical current applied to the nerve (electrical charge = nC) will depend on two settings controlled by the nerve stimulator: current intensity and duration of the stimulus (measured in mA and μs, respectively).1,6In the above cases, stimulus duration of 300 μs was used and current intensity was varied. Minimal current intensities to produce motor responses in our patients were 0.3 mA (90 nC) and 0.56 mA (168 nC), which, according to the literature, are in the range of intensities used for infusion of the anesthetic near the nerve6. Finally, a disappearance of muscular twitch with 2 ml of local anesthetic without inducing paresthesia or discomfort and the reappearance with increased voltage (negative Raj test7) indicates correct performance of the technique. However, several tests confirmed that the nerve was punctured and that the anesthetic was actually administered intraepineurally in both patients. CT images showed contrast medium inside the nerve. The contrast occupied the interfascicular space, and the catheter inserted through the stimulator needle was positioned inside the nerve.

The fact that these two patients were diabetic should be taken into account. However, diabetic polyneuropathy would affect the excitability of distal more than proximal parts of the nerve.8Therefore, a proximal approach to the sciatic nerve in a diabetic patient might not be expected to theoretically significantly alter the response to stimulation.8 

Nerve stimulation can induce specific motor responses. Nevertheless, because of the random distribution of nerve fibers into fascicles, the specific muscle group activated may vary among patients. Induction of specific movements may also be the consequence of selective stimulation of nerve fascicles if the needle has been placed intraneurally through the epineurium.

The structure of the sciatic nerve is different from other nerves. It has a thick, well-formed epineurium that covers two main nerve branches, the tibial and the peroneal nerves.9These two nerves are functionally and structurally separate but share a common epineurium. These structural characteristics may explain why, for this specific nerve, to achieve nerve stimulation at the usual clinical intensities, the needle may have to go through the epineurium. As Vloka et al.  9suggest, injecting the anesthetic within the epineural adventitia causes the contrast medium to spread into the epineurium around the perineurium that surrounds the fascicles. This procedure is different from an “intrafascicular” injection, which could indeed induce nerve damage. Vloka et al.  9performed their studies in embalmed cadavers, in which the neural fascia might have suffered structural changes. This intraepineural adventitial administration explains the diffusion of the contrast medium observed in our two patients. The study by Reina et al.  10suggested that by inserting the needle into the epineurium of the sciatic nerve, nerve damage may occur because the fascicles can be “easily touched.” However, the strong sheath of the perineurium is different from the loose tissue framework of the interfascicular epineurium. After puncture of the epineural adventitia the needle probably enters the nerve but separates the fascicles rather than punctures them. CT images showed that the local anesthetic diffused within the intraneural space as well as outside the epineurum. This may be the result of a partial administration of the anesthetic inside and outside because of needle displacement or of the retrograde flow from intraneural space.

The two cases described here demonstrate that, when using a nerve stimulation guided approach, puncture of the sciatic nerve can occur and the local anesthetic can be injected intraneurally (inside the epineurium). Although such procedure did not induce any noticeable nerve damage in the reported patients, intraneural administration of local anesthetic should be avoided. More extensive studies on the sciatic nerve as well as other peripheral nerves are indicated to improve our understanding of this phenomenon.