OR8.1 | Post-polio Residual Paralysis — Summary & Reflection

KEY TAKEAWAYS

Post-polio residual paralysis results from selective anterior horn cell destruction by poliovirus, producing a pure LMN flaccid paralysis — asymmetric, with wasting, absent reflexes, and preserved sensation. The three stages are acute (supportive care, positioning), convalescent (physiotherapy, orthoses, recovery by collateral re-innervation), and residual (deformity correction and reconstruction). The dominant pathological mechanism is muscle imbalance: the unopposed antagonist of a paralysed muscle drives progressive joint deformity. Management follows a strict hierarchy: physiotherapy → orthoses (AFO, KAFO, Thomas calliper) → soft-tissue corrective procedures → tendon transfer → bony stabilisation (osteotomy, arthrodesis). Tendon transfer requires four prerequisites: donor grade ≥4, supple joint, neurological stability, and correct vector. Common transfers include tibialis posterior through interosseous membrane for equinus, peroneus longus to Achilles for calcaneal deformity, and hamstring transfer to patella for flail knee. Triple arthrodesis corrects rigid hindfoot deformity at skeletal maturity. Post-polio syndrome occurs 15–40 years post-acute illness due to failure of enlarged motor units; it is managed conservatively. The FUNDAMENTAL clinical distinction is LMN-flaccid (PPRP) vs UMN-spastic (cerebral palsy) — absent reflexes and intact sensation confirm the former.

REFLECT

Consider this scenario: A 9-year-old girl presents with equinovarus deformity of the left foot following polio at age 1. Her tibialis posterior is grade 4, peronei grade 2, tibialis anterior grade 1, gastrosoleus grade 4. The equinus is fixed at 20 degrees and the varus is dynamic. What is the sequence of procedures you would plan, and why does the sequence matter? Reflect on how you would counsel the family about functional expectations, the number of surgical stages needed, and the role of orthoses between and after procedures. How would your management differ if the child had spastic equinovarus from cerebral palsy rather than PPRP?