Sciatic neuropathy is an uncommon mononeuropathy in children [
1]. It can occur due to trauma, tumor, compression, inflammation, or idiopathic causes. Identifying the cause of sciatic neuropathy is crucial for prognosis and treatment. Postoperative sciatic neuropathy is not uncommon and is usually related to factors such as intragluteal injection, gluteal abscess drainage, hip surgery [
2] (e.g., pelvic osteotomy and spica cast application for congenital hip dysplasia), or prolonged lithotomy position during an operation. However, postoperative neuropathies can also be caused by inflammatory mechanisms [
3]. Cases with inflammatory causes are distinct from those with mechanical causes in that inflammatory neuropathies are observed temporally and spatially distant from the time and site of surgery. Herein, we describe a rare case of postoperative non-mechanical sciatic neuropathy in a child.
A 10-year-old girl who had undergone a right cortical mastoidectomy under general anesthesia experienced numbness, pain in her right leg, and difficulty walking on the third postoperative day. The surgery, which lasted 2 hours, concluded without any immediate postoperative complications. No intragluteal injections were administered, and there was no evidence of position-related sciatic nerve compression either during the surgery or in the postoperative period. Examination revealed right foot drop, knee flexor weakness (power score was 3 out of total score of 5), foot invertor weakness (power score was 2 out of total score of 5), an absent ankle reflex, sensory loss over the sole, and a negative straight leg raise test. Based on the clinical examination, possibilities of L5 radiculopathy, lumbosacral plexopathy, and sciatic neuropathy were considered. Routine blood tests, including complete blood count, C-reactive protein, erythrocyte sedimentation rate, and renal and liver function tests, were normal. Motor nerve conduction studies (NCS) of the right tibial and peroneal nerves revealed reduced compound muscle action potential amplitudes, although conduction velocity and distal latency remained normal. Sensory NCS of the sural nerve indicated reduced sensory nerve action potentials. Needle electromyography (EMG) showed denervation potentials in the extensor digitorum brevis and tibialis anterior muscles, consistent with right sciatic neuropathy. Following the NCS, ultrasonography of the gluteal region was performed, revealing thickening and edema of the right sciatic nerve (
Fig. 1). Magnetic resonance imaging (MRI) demonstrated thickening and a T2/short-tau inversion recovery (STIR) hyperintense signal, suggestive of edema in the right sciatic nerve at the level of the proximal thigh. Imaging showed no evidence of nerve compression by any lesion or anatomical variant, including any intrinsic or extrinsic signs of mechanical neuropathy. Based on these imaging findings, a diagnosis of idiopathic inflammatory sciatic neuropathy was made. Electrophysiological studies, such as NCS and EMG, were instrumental in determining the affected nerve and its level. Although electrophysiological studies yield similar results for any cause of sciatic neuropathy, MRI and ultrasonography provide clues about whether the cause of neuropathy is mechanical or inflammatory. Similar to other reported cases of post-surgical inflammatory neuropathies in the literature, our case also exhibited thickening and a T2 hyperintense signal in the involved nerve [
3]. Additionally, thickening and edema of the nerve were noted on ultrasound.
The patient was administered a high dose of methylprednisolone (1 g/day) for 3 days, followed by oral prednisolone at a dosage of 2 mg/kg (the patient weighed 28 kg) for 6 weeks, with a subsequent gradual taper over the next 6 weeks. Alongside this, symptomatic treatment for pain relief and physiotherapy were initiated. The patient demonstrated gradual improvement following the initiation of treatment. At the 3-month follow-up, the foot drop had completely resolved, with dorsiflexors power rated at 5 out of total score of 5, although muscle atrophy in the right lower limb was still apparent. Repeat imaging showed a significant reduction in the thickness of the sciatic nerve (
Fig. 1). Neuromuscular ultrasonography revealed fasciculations in the hamstring muscles, indicative of nerve reinnervation and denervation (
Supplementary Video 1).
The concept of post-surgical inflammatory neuropathy is relatively new. It is characterized by neuropathy that results from inflammatory infiltrates in nerves [
4]. The exact incidence and causes of this condition are still uncertain. It is likely underdiagnosed due to a lack of clinical suspicion, inadequate imaging, the relative scarcity of literature on the topic, and the necessity of a nerve biopsy for diagnosis. Although the contributing factors for post-surgical inflammatory neuropathy remain unclear, several potential triggers have been identified, including surgical stress, underlying medical conditions, genetic predisposition, the use of anesthetic agents, and blood transfusions [
5-
7].
Our case is unique as it underscores the importance of imaging—specifically neuromuscular ultrasonography and magnetic resonance neurography—as complementary tools to clinical examination and electrodiagnostic studies in diagnosing nerve pathology. Although MRI is considered the most effective technique for identifying sciatic nerve pathology [
8], nerve ultrasonography offers a cost-effective and readily available alternative. It can effectively demonstrate nerve thickening, changes in echogenicity, and the fascicular pattern of the nerve. In our case, ultrasound detected nerve thickening associated with inflammatory neuropathy and was also used to identify muscle fasciculations. Notably, ultrasonography has a higher sensitivity for detecting fasciculations than EMG [
9]. Additionally, this case represents one of the few pediatric instances of post-surgical inflammatory sciatic neuropathy reported thus far [
10]. Regarding treatment, cases of post-surgical inflammatory neuropathy are typically managed with either a 5-day course of steroid pulse therapy or a combination of pulse therapy and weekly steroid injections for 12 weeks [
3]. In our case, we administered a 3-day course of steroid pulse therapy followed by oral steroids for 3 months.
This case highlights the concept of post-surgical inflammatory neuropathy of the sciatic nerve and adds value to the literature, which is relatively scarce in this context. Physicians, particularly surgeons and anesthetists, should be aware that although mechanical factors are the most common causes of sciatic neuropathy in the postoperative period, if no mechanical cause can be identified, inflammatory neuropathy could be the reason for the patient's discomfort. These inflammatory neuropathies may be suspected based on their spatial and temporal separation from the time and site of surgery and can be further confirmed by characteristic imaging findings. While MRI features, in the context of appropriate clinical background, help to diagnose the majority of cases, it can occasionally be challenging to differentiate between post-surgical inflammatory and mechanical neuropathies. In such cases, a nerve biopsy can be performed, which may reveal the pathological features of inflammation. Early diagnosis is crucial, as the condition is reversible with prompt and adequate immunosuppressive therapy.
This report presents a pediatric case of post-surgical inflammatory sciatic mononeuropathy, focusing on diagnostic strategies that led to successful management with corticosteroids. It underscores the significance of considering potentially curable inflammatory neuropathies in the post-surgical setting.
The institutional ethical review board granted a waiver for ethical clearance for this report as no ethical issues were found. Informed written consent from the next of kin of the patient was obtained for the publication of this report.