Our current understanding of the factors that lead to neurologic complications after peripheral nerve blocks is limited. We report a case of permanent injury to the sciatic nerve after sciatic nerve block through the anterior approach and discuss mechanisms that may have led to the injury.
A previously healthy 51-yr-old woman (height and weight, 150 cm and 60 kg, respectively) was admitted to the hospital for open operative treatment of a nonunion fracture of her distal fibula and tibial malleolus. During the anesthesia interview, she seemed extremely anxious and required premedication (midazolam 4 mg). Twenty minutes later, she was taken to the operating room and received an additional 2 mg of midazolam and 100 μg of fentanyl before placement of a peripheral nerve block (PNB). A single-injection sciatic nerve block was performed through the anterior approach (1,2) using a 15-cm-long 21-gauge needle (Stimuplex®, B. Braun Medical Inc, Bethlehem, PA) connected to a nerve stimulator (Digistim, B. Braun). The sciatic nerve was stimulated at a depth of approximately 12 cm on the third insertion attempt, and a motor response (dorsal flexion of the foot) of the common peroneal nerve (CPN) at a current of 0.38 mA (0.1 ms/2 Hz) was obtained. The resident performing the injection noted high resistance at the beginning of the injection of the local anesthetic (LA). After the forceful injection of the first 1 mL of LA, the administration of the subsequent 29 mL of LA (total, 30 mL) was without resistance. The patient remained comfortable, conversant, and cooperative throughout the injection. A femoral nerve block was also administered for application of the tourniquet using a standard technique (3), and injection of 20 mL of LA after a quadriceps muscle twitch at 0.3 mA had been obtained. Mepivacaine 2% with freshly added sodium bicarbonate 1 mEq/10 mL and epinephrine 1:300,000 was used for both PNBs. The surgical procedure proceeded uneventfully; a thigh tourniquet was used (250 mm Hg) for 92 min.
Twenty-four hours later, the patient had not regained sensation in, or the ability to move, her right foot and complained of pain radiating along the path of the sciatic nerve. On examination, she had absent sensation in the anterolateral aspect of the skin below the knee and was unable to dorsiflex the foot or to extend the great toe; the tibial component of the sciatic nerve was intact. Neurology consultation 48 h later confirmed the diagnosis of sciatic nerve injury with neuropraxia of the right CPN. The patient was discharged 5 days after surgery with the persistent neurologic deficit. Two weeks later, her surgical wound healed nicely; however, the sensory-motor deficits in the CPN territory persisted, as did the radiating pain, which required treatment with acetaminophen with codeine, naproxen (375 mg twice a day), and gabapentin (300 mg every bedtime). The peroneal longus, brevis, and anterior tibialis and extensor hallucis longus were profoundly weak, whereas the gastrocnemius and posterior tibialis were normal. There was a diminished pinprick sensation in the web space between the first and second digits of the right foot and on the lateral aspect of the foot and lower leg. A laboratory workup for metabolic causes of the neurologic deficit was normal.
An electromyography (EMG) study was performed 4 wk after the injury and demonstrated absent right peroneal motor potentials and conduction velocities; EMG of the right tibial nerve was normal. Additionally, EMG of selected right leg muscles showed mild spontaneous activity of the right anterior tibialis, indicating denervation in the territory of the CPN. The injury was determined to be at the level of the thigh, corresponding to the level of needle insertion for the anterior sciatic block. After intensive physical therapy, the patient gradually regained strength and partially recovered; at 12 mo after the injury, the patient had only mild weakness during dorsal flexion but continued to have pain. At 3 yr after the injury, the radiating pain in the distribution of the right sciatic nerve is still present, particularly with ambulation, resulting in a limitation of her daily activities and the need for management of her chronic pain.
Severe neurologic injury is an infrequent but often-feared complication of PNBs and may be present in 0.4% of all nerve block procedures (4,5). Our current understanding of the factors that lead to neurologic complications after PNBs is limited. This is partly the result of our inability to conduct meaningful retrospective studies because of a lack of standard and objective documentation procedures for PNBs. Unfortunately, in the absence of objective data, published discussions of the factors that lead to nerve injury, as well as medico-legal reviews, are often speculative at best.
Intraneural injection of LA is a well established mechanism of neurologic injury associated with PNBs (6,7). However, in current clinical practice, there is no consensus on the techniques or methods that can reduce the risk of intraneural injection. Much of the debate has focused on methods of nerve localization (i.e., paresthesia versus nerve stimulation); however, neurologic injury can occur even with experienced practitioners using either technique (5). Educational material in regional anesthesia suggests that lancinating pain and high injection pressure may portend the intraneural injection of LA (8–11). However, our patient did not report pain during the PNBs. Whereas it can be argued that the administration of sedatives and analgesics in our patient may have blunted the sensation of pain on injection, many patients require proper premedication for comfort before the placement of PNBs, particularly during the placement of more uncomfortable, deep PNBs (3). Furthermore, the severity of pain that results from intraneural injections is believed to be so severe and lancinating that one would have expected it to have been perceived by the conversant patient. However, intraneural injection of LA and neurologic injury has been reported to occur without pain on injection by several other authors (6,12). These publications as well as our report suggest that pain on injection is not a constant or reliable warning sign of impending nerve injury.
Anesthesiologists often rely on a subjective evaluation (termed “syringe feel”) during PNBs to detect abnormal resistance to injection and prevent intraneural injection (10,11,13,14). Indeed, a large animal model study suggested that high injection pressure (>20 psi) is associated with intrafascicular injection and the consequent neurologic injury (15). However, the subjective perception of abnormal resistance and pressure required to inject is impossible to verify because anesthesiologists vary widely in what they perceive as appropriate force and rate of injection during PNBs (16). In addition, resistance to injection also may be affected by variability in needle design (16). These factors conspire to make meaningful assessment, monitoring, and objective documentation of the injection technique difficult. Nerve block injection in our patient was perceived as high resistance; however, because this could not be quantified, the action was not undertaken to help avoid the intraneural injection.
Neuronal ischemia can occur from a variety of sources, including disruption of the neuronal microvasculature, high-endoneurial pressures, addition of vasoconstricting drugs, and exogenous compression from tourniquets (17). The application of a tourniquet over the site of the nerve block may have aggravated the ischemic insult after an intraneural injection (17). However, the paucity of reported severe complications, despite the widespread use of tourniquets during extremity surgery, suggests that peripheral nerves are relatively resistant to ischemia of limited duration and magnitude (18).
It is possible that the use of a relatively large concentration of LA in our patient (mepivacaine 2%) contributed to nerve injury. However, mepivacaine 2% has been in clinical use for decades without reports of neurotoxicity. In addition, application of the identical LA mixture for the femoral block in the same patient did not result in neurologic consequences. Regardless, exposure of the endoneurium (as may occur during intraneuronal injection) to a large concentration of LA, particularly when coupled with intraneural pressure and ischemia, may contribute to the increased vulnerability of the nerve to neurologic injury (9,19).
In summary, neurologic complications of PNBs are uncommon, but they can and do occur, even in the hands of experienced practitioners (5). Our current understanding suggests that needle trauma and intraneural injection may lead to nerve injury. Further studies and improvements in nerve localization and injection monitoring techniques are indicated to further reduce the risk of neurologic complications after PNBs.
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