SLR - June 2022 - Kwame N. Doh, DPM, MSReference: Gupta P, Patil B, Gupta P, Mehta R, Gupta R. Peroneal Nerve Dysfunction in Patients with Clubfoot Deformity: Evaluation of Clinical Presentation and Treatment. Clin Orthop Surg. 2021;13(4):558- 563. doi:10.4055/cios20261
Level of Evidence: III
Reviewed by: Kwame N. Doh, DPM, MS
Residency Program: Emory University School of Medicine, Atlanta, GA
Podiatric Relevance: Isolated cases of complete peroneal nerve dysfunction have been reported in the literature with only short-term outcomes. However, there is a lack of information on anatomic development of the affected limb as it matures. This study aims to investigate whether or not patients with complete peroneal nerve injury can be identified earlier at their first clinical presentation and also describe the early to mid-term follow-up. Early identification of this pathology can help plan management of the neurogenic clubfoot.
Methods: This retrospective study included 658 patients with clubfoot deformity between 2014 and 2019. 8 patients in the cohort had unilateral clubfoot at birth with a mean age of 1.3 years. 3 presented initially at birth, while 5 were previously treated with ponseti casting with an average of 9 applied casts. Peroneal nerve dysfunction was suspected in all 8 patients who presented with complete absence of ankle dorsiflexion on physical examination and no history of syndromic involvement or spinal dysraphism. All patients were treated with an average of 4 ponseti casts in addition to an Achilles tenotomy followed by a foot abduction brace once passive dorsiflexion of the ankle joint was achieved. A nerve conduction study confirmed the suspected peroneal nerve dysfunction during the bracing period followed by continuous treatment in insole molded polythene ankle foot orthosis.
Results: Nerve conduction studies results indicated complete neuropathy of the common peroneal nerve of the symptomatic limb in all patients. Additionally, there was a limb length discrepancy of 1.2 cm difference at the level of the tibia. The mean follow-up time was 5.1 years and the final follow-up at 8 years. Other noticeable findings included calf atrophy, prominence of metatarsal heads 3,4,5 dorsally, increased intermetatarsal webbing of lateral 3 or 4 digits; the latter being consistent with initial presentation. Passive ankle joint motion was 5 degree of dorsiflexion and 15 degrees of plantarflexion. Peroneal nerve dysfunction persisted at last follow-up, with 3 patients above the age of 5 y/o opting for a posterior tibialis (PT) tendon transfer which improved active ankle dorsiflexion to neutral allowing them to discontinue the use of ankle foot orthosis and abduction brace. Patients above 5 y/o with no PT tendon transfer continued to use a form of splint or brace.
Conclusion: Nerve conduction studies can help differentiate clubfoot with peripheral nerve involvement from spinal cord dysfunction. Initial screening for peroneal nerve function should be performed before initiation of cast treatment if signs such as the dorsal prominence of metatarsals 3,4,5 and webbing of lateral 3-4 toes without syndactyly are present. These are new clinical findings that were not previously reported in the literature. These patients should also be educated on the possibility of limb shortening early on. Tibialis posterior tendon transfer can be an option for patients at an appropriate age (>5 y/o), even though it does not guarantee satisfactory improvement in gait. Similar observation with further studies will need to confirm the correlation between metatarsals prominence, webbing of lateral digits and peroneal nerve dysfunction in clubfoot deformities.