Sciatic Nerve Injury after an Intramuscular Injection into the Gluteal Region

Article information

J Electrodiagn Neuromuscul Dis. 2023;26(3):53-57

Publication date (electronic) : 2024 December 26

doi : https://doi.org/10.18214/jend.2024.00024

Sangpil Son, Sol Lee, Jae In You, Minji Chae

Department of Rehabilitation Medicine, Daejeon Eulji Medical Center, Eulji University School of Medicine, Daejeon, Korea

Corresponding author: Minji Chae Department of Rehabilitation Medicine, Daejeon Eulji Medical Center, Eulji University School of Medicine, 95 Dunsanseo-ro, Seo-gu, Daejeon 35233, Korea Tel: +82-42-611-3630 Fax: +82-42-259-1125 E-mail: drcherry0911@eulji.ac.kr

Received 2024 July 1; Revised 2024 August 8; Accepted 2024 August 20.

Abstract

Introduction

The sciatic nerve originates from the L4 to S3 spinal nerve roots and provides innervation to various muscles of the lower extremities. It directly innervates the posterior thigh muscles, including the biceps femoris, semimembranosus, and semitendinosus. Distally, it branches into the tibial and peroneal nerves, which further provide motor and sensory branches to the lower leg and foot [1]. Like other nerve injuries, sciatic nerve injury can result from stretching, compression, or ischemia [2]. These injuries are often linked to traumatic events such as falls and vehicle accidents, and are frequently associated with acetabular fractures or posterior hip dislocation [3]. Additionally, cases of iatrogenic sciatic nerve injury due to improperly placed intramuscular gluteal injections have been infrequently reported worldwide. The severity of symptoms from a misplaced injection injury can vary, depending on the extent of nerve involvement and the neurotoxicity of the administered medication [4]. We present a case of a patient with a sciatic nerve injury suspected to have occurred following an intramuscular gluteal injection of diclofenac.

Case Report

A 5-year-old female with no significant past medical history presented at the emergency department with persistent fever and sore throat. Following an evaluation that included a simple X-ray and laboratory tests, such as C-reactive protein levels and white blood cell count, she was diagnosed with acute pharyngotonsillitis and admitted to the department of pediatrics. After reviewing the examination results, a 23-gauge needle was used to administer a prescribed dose of diclofenac into her left buttock via intramuscular injection for fever control. Approximately 30 minutes after the injection, she began to show motor weakness in her left ankle and toes, along with a dragging of her left foot while walking. The muscle strength in her left ankle dorsiflexor and big toe extensor was rated 2/5 according to the Medical Research Council grade. No motor weakness was observed in the other muscles of the left lower extremity. A sensory evaluation was also conducted to check for possible nerve injury, during which the patient reported hypesthesia in the lateral area of her left lower leg. She exhibited no bladder or bowel symptoms, and her deep tendon reflexes were normal.

An electrodiagnostic examination was conducted 3 weeks after the onset of symptoms to ensure more accurate results. At the time of the electrodiagnostic study, there were no neurological changes, including sensation and muscle strength, compared to the initial onset of symptoms. Sensory nerve conduction studies showed no response in the left sural nerve and the left superficial peroneal nerve. In motor nerve conduction studies, no response was observed in the left common peroneal nerve when recorded at the left extensor digitorum brevis muscle. Recording at the left tibialis anterior muscle revealed reduced amplitudes of compound muscle action potential. Similarly, reduced amplitudes of compound muscle action potential were also observed in the left tibial nerve when recorded at the left abductor hallucis muscle. Furthermore, the conduction velocity of the left common peroneal nerve was mildly slower compared to the opposite side (Table 1). In needle electromyographic studies, denervation potential was detected in the left tibialis anterior and peroneus longus muscles. A reduced recruitment pattern was also observed during voluntary contraction of these muscles (Table 2). Overall, the findings suggested an incomplete lesion of the left sciatic nerve with axonal loss, with the peroneal division being more affected. Four weeks after the onset of symptoms, magnetic resonance imaging of the left hip was performed to confirm the nerve lesion. The magnetic resonance imaging revealed diffuse thickening of soft tissue and increased signal intensity on the T2-weighted image at the lateral side of the left sciatic nerve (Fig. 1). No space-occupying lesions, such as a hematoma or cyst, were observed.

Table 1.

Initial and Follow-up Findings of Nerve Conduction Studies

Table 2.

Initial and Follow-up Findings of Needle Electromyography

Fig. 1.

Magnetic resonance imaging of the hip revealed an enlarged diameter of the left sciatic nerve and increased signal intensity in the peroneal portion of the left sciatic nerve on T2-weighted images (arrows). (A) Coronal view. (B) Axial view.

The patient was transferred to the Department of Rehabilitation Medicine after 2 weeks of management for acute pharyngotonsillitis and underwent a follow-up evaluation for sensory and motor deficits. A new weakness in ankle eversion was detected, with a strength of 3/5 according to the Medical Research Council grade. The muscle strength of the left ankle dorsiflexor and big toe extensor had slightly improved to a 3/5 Medical Research Council grade. She exhibited a circumduction gait due to ankle dorsiflexion weakness. Additionally, during gait training, she tended to invert her ankle due to the weakness and decreased endurance of the ankle evertor. To correct the impaired gait pattern, visual and verbal cueing was used. Gait training was conducted barefoot, taking into account the weak dorsiflexor power of the ankle. Electrical stimulation therapy was administered to the left tibialis anterior, peroneus longus, and brevis muscles. Initially, the electrical stimulation therapy was applied to the left tibialis anterior; however, as the ankle dorsiflexion power rapidly recovered, the focus shifted to the peroneus longus and brevis. After several weeks of treatment, the patient was discharged in a significantly improved functional condition, capable of independent gait. Clinically, sensory deficits had fully resolved, and the muscle strength of the left ankle dorsiflexor and the left big toe extensor improved to 4/5 Medical Research Council grade. Follow-up electrodiagnostic studies were conducted about three months later. Given the patient's age and cooperation, only nerves that had shown abnormalities in previous tests were examined. The follow-up sensory nerve conduction study showed no response in the left superficial peroneal nerve, whereas the left sural nerve, which previously showed no response, now demonstrated sensory nerve action potential. In the motor nerve conduction study, there were reduced amplitudes of compound muscle action potential in the left peroneal nerve when recorded at the extensor digitorum brevis and tibialis anterior. Compared to the initial study, the left peroneal nerve now showed compound muscle action potential when recorded at the extensor digitorum brevis muscle. The needle electromyography results no longer showed denervation potential, indicating recovery (Tables 1, 2).

This study was approved by the Institutional Review Board of Daejeon Eulji Medical Center (IRB No.: 2024-06-010).

Discussion

We report a case of a sciatic nerve lesion initially diagnosed through an electrophysiological study, likely induced by an intramuscular injection. In this instance, the peroneal division of the sciatic nerve was predominantly affected, with clinical symptoms presenting solely as damage to the common peroneal nerve. Sensory changes were noted in the dermatome of the superficial peroneal nerve, and muscle weakness was observed in the ankle dorsiflexor, evertor, and big toe extensor. The initial needle electromyographic results showed no abnormal findings in the medial gastrocnemius and the long head of the biceps femoris, suggesting that the peroneal division was primarily affected. The short head of the biceps femoris muscle, which is innervated by the peroneal division of the sciatic nerve, is a critical muscle in the electrodiagnostic evaluation of sciatic neuropathy. However, the needle electromyographic examination of the short head of the biceps femoris muscle in this patient revealed no denervation potential. Considering the somatotopic organization, it can be hypothesized that the injection injury selectively affected only specific fascicles of the sciatic nerve. This hypothesis is further supported by the absence of motor impairment in the short head of the biceps femoris muscle in this patient.

The peroneal portion of the sciatic nerve, characterized by larger funiculi and less supporting connective tissue, is more susceptible to injury compared to the tibial division [5]. This vulnerability was similarly observed in our case. Identifying the cause and location of the nerve damage was relatively straightforward in this instance. However, when the etiology and location of the damage are not clearly defined, there is a risk of misdiagnosis. Therefore, performing electrodiagnostic tests should be considered to accurately determine both the location and the cause of the nerve damage, as injuries to the proximal portion may present symptoms similar to those of injuries solely to the distal portion.

The sciatic nerve exhibits variability in its course, taking several forms. In most individuals, it typically runs beneath the piriformis muscle. However, in some cases, it bifurcates and passes above the muscle, and there are instances where the nerve traverses through or emerges between muscles [6]. Sciatic nerve injection injuries most frequently occur when the needle insertion site deviates medially or inferiorly from the recommended position in the upper outer quadrant of the buttock in normal individuals [4,7]. The proximity of the injection to the nerve is considered the most critical factor in determining the extent of nerve damage. Direct injection into the nerve is associated with the most severe outcomes [7]. Therefore, it is crucial to ensure precise injection into the upper outer quadrant, which is anatomically distant enough from the nervous structures, for intramuscular injections to the buttocks.

Nerve injuries associated with injections can result not only from direct physical damage caused by needlesticks but also from the injection of material into the surrounding tissue [8]. The drug may be injected between the nerve and its sheath or between the fascicles, making the neurotoxicity of the drug a relevant factor in the extent of the damage [9,10]. A histopathological study revealed that the neurotoxic effects of diclofenac on the sciatic nerve were more significant than those caused by other commonly used injection drugs, such as pethidine or morphine [10]. Therefore, physicians should consider alternative treatments, such as oral agents or intravenous drugs, for first-line symptom control. Additionally, further research could be beneficial in identifying more suitable alternative injection sites for diclofenac.

Electrodiagnostic examinations have clinical significance in both confirming the severity of neural damage and predicting the clinical prognosis. In cases where symptoms are mild, conservative treatment usually spans several weeks to months for neurapraxia. However, severe axonotmesis or neurotmesis, characterized by significant motor weakness and neuropathic pain, may require surgical intervention [7,9]. Alongside history taking, physical examination, and imaging studies, electrodiagnostic testing plays a crucial role in forecasting recovery patterns and identifying potential neurological complications.

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