Acute onset common peroneal nerve palsy in a child due to fibular head osteochondroma: a case report

INTRODUCTION

Osteochondroma, considered as most common bone tumor, represents 8% of all bone tumors and 34% of benign cartilaginous tumors.^1,2 They are frequently asymptomatic and have low malignant potential when sporadic and solitary. It usually arises from the metaphyseal or metadiaphyseal zones of long bones of the appendicular skeleton and are most commonly seen around the knee.³ Osteochondromas grow during childhood through adolescence, but usually growth ends when the epiphyseal plate closes. Nerve compressions due to osteochondromas are rare and occur in less than 1% of all cases.^4,5 They are more likely to occur with bulky osteochondromas and multiple hereditary osteochondromatosis.

Common peroneal nerve (CPN) is the most commonly involved nerve in compressive neuropathy in the lower extremity and 3rd most common in body after median and ulnar nerve entrapment.^6,7 The most common location of compression of CPN is neck of fibula followed by popliteal fossa and tibial plateau. In terms of etiology of CPN palsy, the most common is trauma and tumor as a cause is responsible in 6% of cases.⁸ Acute onset peroneal nerve palsy due to proximal fibular osteochondroma is extremely rare and only one case of this kind has been reported in an adult. To the best of our knowledge, no previous study has reported an acute onset CPN palsy in a child due to osteochondroma.

The purpose of this study was to report the clinical presentation and outcomes after surgical treatment in a child with CPN palsy due to fibular head osteochondroma. A secondary aim was to review the literature for similar studies.

CASE REPORT

A 7 year-old girl presented with a left foot drop with a high stepping gait since 8 days. While there was no history of trauma, patient gave a history of sleeping over a hard surface in left lateral position on the night preceding her symptoms. On examination, there was grade 0 power for ankle dorsiflexion. There was no sensory loss.

Plain radiographs showed a sessile bony growth at the proximal fibula (Figure 1A and 1B).

Magnetic resonance imaging (MRI) showed a focal osseous outgrowth at the fibular head neck region laterally which had cortical and medullary integrity with the native bone. The surrounding cartilage gap had a thickness of approximately 3.1 mm. MRI images also showed tenting of peroneal nerve at fibular neck by the lateral edge of the osteochondroma (Figure 2A and 2B).

The electrophysiological study reported that the CPN action potential was absent above the knee. Electromyography (EMG) revealed active and severe denervation in left tibialis anterior. Sensory conduction findings were normal.

The patient was operated 15 days after onset of symptoms. The peroneal nerve was surgically decompressed by excising the osteochondroma. Intraoperatively, the tenting of CPN by lateral edge of osteochondroma was found (Figure 3A). The osteochondroma measuring 2.5×2×1.5 cm was excised. The excision surgery was performed by senior author (SK) wherein CPN was further decompressed by perineural neurolysis (Figure 3B).

Postoperatively the patient was given a static ankle foot splint and advised passive range of motion and encouraged for active movements of ankle joint. Patient began regaining ankle dorsiflexion at 4 weeks after surgery. At 3 months, patients regained full power of ankle dorsiflexion. At the final follow up of 1 year, patient was able to perform all daily living and recreational activities.

DISCUSSION

For literature review on the topic, a search was done in Medline database on June 9, 2021. Our search was conducted using the following search words: “proximal fibular osteochondroma” OR “proximal fibular exostosis” OR “fibular head osteochondroma” OR “osteocartilagenous exostosis of fibula” AND “peroneal nerve palsy” OR “foot drop” OR “drop foot” OR “common peroneal nerve palsy” OR “paresis of peroneal nerve” OR “extension loss of great toe”. Inclusion criteria were studies which reported a CPN palsy due to proximal fibular osteochondroma with a diagnosis established through clinical and radiographic findings and reported final status of neurological recovery. Studies were excluded if the studies were unrelated to topic, patients were treated nonoperatively, unavailability of full article text, and incomplete data on clinical presentation and recovery of patients.

The data noted from the previous similar studies were the study design (case report/case series), year of publication, demographics of the patients (age and sex), symptoms and their duration, osteochondroma/s elsewhere in the body, radiographic findings, electrophysiological study findings, intraoperative findings, extent of neural recovery, and duration of final follow up. The demographic variables, symptoms, treatment, and neurological recovery of patients reported in the included studies were presented in a table (Table 1) and as descriptive statistics.

The age of COHORT of patients from previous and current study were presented as mean and standard deviation. Initial search yielded a total of 2006 articles. The title and abstract of these articles were screened independently by two authors for their relevance to subject. 1990 articles were not related to the topic of interest.

Full text of 16 studies were assessed based on exclusion criteria. Out of 16 studies, two were excluded; one due to unavailability of full text and another due to lack of information regarding age, sex, chronicity of symptoms, intraoperative findings and duration of final follow up. Finally, 14 studies were included in the analysis. Of the 14 included studies, 12 were case reports and 2 were case series (Table 1).^6,9-21 A total of 24 patients (including one from this study) were included in the analysis. Mean age and standard deviation of patients were 12 years and 4.7, respectively. There were 14 male (58%) and 10 female (62%) patients. There were 20 children and 4 adults. One adult patient (previous study) and one child (current study) had acute, and rest 22 patients had gradual onset of symptoms. 16 patients complained of only motor symptoms, 3 patients complained of only sensory symptoms, and 5 patients had both. Upon radiography, all the patients had bony overgrowth from proximal fibula either as a sessile or pedunculated lesion. 5 out of 24 (21%) patients had multiple osteochondromatosis.

All the patients underwent surgical removal of osteochondroma. Out of 24 patients (including the one patient of this study), 20 patients (83%) had complete neurological recovery. Incomplete recovery of nerve function after surgery was associated with the duration of symptoms as mean of onset of duration of symptoms was 5 months in patients who had complete recovery as compared to 26 months in patients who had incomplete recovery. This is the first report in literature of a child with acute onset CPN palsy due to osteochondroma. Based on literature review, complete neurological recovery rate after surgical decompression is 83%. This report also highlights the importance of early surgical intervention to decompress the CPN in the setting of compressive neuropathy due to osteochondroma.

An acute onset of CPN palsy without trauma and due to osteochondroma as reported here is an unusual presentation. The reason of acute onset CPN palsy in the child we reported is unclear. We speculate that the possible reason of acute onset of symptoms could be due to patient’s dependent position of the leg while sleeping causing CPN compression similar to saturday night palsy.²² The authors of previous study who reported similar case of acute onset CPN palsy, but in an adult, stated that the palsy developed after the patient was given spinal anaesthesia in dependent lateral position. The size of the osteochondroma in this report was of one of the smallest dimensions among the searched literature (2.5×2×1.5 cm). A relatively smaller sized lesion causing compressive neuropathy of CPN could be explained by the fact that the patient in this report was a child with seemingly less space for the lesion to grow before it starts compressing the CPN.

One of the reasons for complete recovery of CPN after compressive neuropathy in this case was early intervention after presentation. Our analysis of 24 patients included from this and previous studies showed that the patients who recovered completely after surgery had surgery at a mean of 5 months from symptoms compared to those with incomplete recovery who were operated at a mean of 26 months after onset of symptoms. In line with these findings, previous studies indicate that the surgical decompression of CPN with osteochondroma excision should be performed within 3 months of symptoms to optimize chances of complete neurological recovery.^13,14,23-25 This study has several limitations. First, similar to most of the previous relevant studies, the design here is a case report. This limits the ability of our review to suggest conclusive evidence to diagnose and treat this rare condition.

CONCLUSION

We report the first case in literature of acute onset CPN palsy in a child due to osteochondroma who recovered completely after surgical decompression of the nerve. Our own experience and that from the limited available literature suggests that an early surgical decompression of CPN with osteochondroma excision at least 5 months from onset of symptoms is key for complete neurological recovery.

Funding: No funding sources

Conflict of interest: None declared

Ethical approval: Not required

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