Causes of peroneal neuropathy associated with orthopaedic leg lengthening in different canine models

Abstract

Peroneal neuropathy is one of the complications of orthopaedic leg lengthening. Methods of treatment include slowing of distraction and decompression both of which may lead to additional complications. The purpose of this study was to analyse the changes in histologic peroneal nerve structure during experimental orthopaedic lengthening using various modes of manual or automatic distraction. The obtained data provide the basis for better understanding of peroneal neuropathy pathogenesis and refinement of prophylaxis and preventive treatment protocols. Four experimental models of canine leg lengthening using the Ilizarov fixator were studied: 1 (n = 10)—manual distraction—1 mm/day divided into four increments; 2 (n = 12)—automatic distraction—1 mm/day in 60 increments, 3 (n = 9) and 4 (n = 9)—increased rate of high frequency automatic distraction: 3 mm/day in 120 and 180 increments, respectively. In peroneal nerves semi-thin sections cross-sectional fascicular areas, content of adipocytes in epineurium, endoneurial vascularisation, morphometric parameters of nerve fibres were assessed by computerised analysis at the end of distraction and of consolidation periods and 30 days after fixator removal. In Groups 1–2 massive nerve fibre degeneration along with epineural vessels obliteration was revealed in two cases from 22, whereas in Groups 3–4 there were 10 from 18 (p < 0.01). Injuries of perineurium and endoneurial vessels were noted in Group 3, and long-lasting thinning of nerve fascicles in Group 4. The decrease in epineurial fat tissue was revealed in all groups, more drastic in 3. Modifications and injuries of nerve sheaths and blood vessels depending on distraction rate and frequency contribute to peroneal neuropathy. Its mechanical, circulatory and metabolic causes are discussed.