Poliomyelitis (Orthopaedic Sequelae)

What is it? Poliomyelitis is an acute viral infection (poliovirus, an enterovirus) that selectively destroys the anterior horn motor neurons of the spinal cord (and sometimes brainstem motor nuclei). The orthopaedic surgeon almost never sees the acute illness; we manage the lifelong residual paralysis and deformity it leaves behind.

The defining lesion:

• Loss of anterior horn cells produces a lower motor neuron (LMN) picture: flaccid, areflexic, wasted muscles.
• The sensory system is untouched - proprioception, light touch and pain are normal. This is the single most useful examination fact.
• Paralysis is asymmetric and patchy - the virus does not respect anatomical groups, so one muscle may be dead while its neighbour is normal.

Epidemiology and global picture:

• Near eradication: Global cases have fallen by over 99% since the Global Polio Eradication Initiative (1988). Wild poliovirus type 1 now circulates in only a small number of endemic regions; types 2 and 3 are certified eradicated.
• A huge surviving cohort: Despite eradication of transmission, millions of polio survivors remain worldwide. Survivors and their musculoskeletal sequelae will be encountered for decades to come - very much a "living history" exam topic.
• Burden shifts to limited-resource settings: The largest number of untreated residual deformities is in low- and middle-income countries, where late presentation with neglected deformity is common.
• Vaccine-derived polio: Rare circulating vaccine-derived poliovirus (cVDPV) outbreaks can still cause new paralytic cases where immunisation coverage is low.

Why it stays on the exam: Polio is the prototype flaccid paralysis and the classic teaching model for the principles of tendon transfer, balancing surgery, osteotomy and arthrodesis - principles that transfer directly to other LMN conditions (peripheral nerve injury, spina bifida, CMT).

1. The neurological insult (static):

• Poliovirus reaches the CNS and lyses anterior horn cells.
• The number of cells destroyed determines the final deficit; surviving neurons sprout to re-innervate orphaned muscle fibres (enlarged "giant" motor units) during the convalescent phase, which is why power can recover for up to ~2 years.

2. The musculoskeletal sequelae (progressive): Like cerebral palsy, the neurological lesion is static but the MSK deformity is progressive, driven by three forces acting over a growing skeleton:

• Muscle imbalance: A living muscle with no working antagonist pulls the joint into a fixed position (for example, intact tibialis posterior with a dead tibialis anterior leads to equinovarus).
• Growth: Imbalance acting across active physes produces progressive bony deformity and torsion. The paralysed segment also grows poorly, producing limb-length discrepancy (LLD) and atrophy (reduced muscle pump and vascularity).
• Gravity and posture: Habitual postures, gravity, and contracture of fascia/capsule convert dynamic imbalance into fixed contracture.

3. Predictable patterns of deformity:

• Foot and ankle: Equinus, equinovarus, calcaneus, cavus, flail foot - depending on which motors survive.
• Knee: Flexion contracture (weak quadriceps, tight hamstrings/ITB), genu recurvatum (weak quadriceps with a fixed plantarflexed foot), flail knee.
• Hip: Flexion-abduction-external rotation contracture, paralytic hip subluxation/dislocation (abductor and extensor weakness), and apparent LLD from pelvic obliquity.
• Spine: Paralytic (neuromuscular) scoliosis, often a long C-shaped curve with pelvic obliquity when the trunk musculature is involved.
• Upper limb: Less common; flail shoulder, paralytic elbow, intrinsic-minus hand.

4. Genu recurvatum - the classic biomechanics question: A weak/absent quadriceps forces the patient to lock the knee in hyperextension to stand. Over years, the posterior capsule and tibial plateau remodel, producing fixed genu recurvatum. A coexisting fixed equinus contributes by driving the tibia backwards on heel strike.

History:

• Age at infection, limbs affected, recovery achieved, previous surgery and bracing.
• Current function: walking distance, falls, brace use, pain, fatigue.
• New symptoms? New weakness, fatigue or pain raises the question of post-polio syndrome (but exclude other causes).

The "look, feel, move, function" of the paralysed limb:

• Look: Wasting, deformity, scars, posture, brace wear, skin (trophic but usually intact because sensation is preserved), limb-length discrepancy.
• Feel: Confirm sensation is intact (the diagnostic discriminator). Palpate for fixed contractures.
• Move: Distinguish fixed vs correctable deformity. Chart power of every relevant muscle (MRC grade) - this is the single most important examination step for planning.
• Function/gait: Identify the gait pattern (for example, the hand-on-thigh / quadriceps gait of an isolated quadriceps palsy, where the patient pushes the thigh to lock the knee).

Key clinical tests:

• Coleman block test: For the cavovarus foot - distinguishes a flexible (forefoot-driven) from a fixed hindfoot varus, deciding whether a calcaneal osteotomy is needed.
• Thomas test: Fixed flexion deformity of the hip.
• Limb-length measurement: True (ASIS to medial malleolus) vs apparent length; identify the contribution of pelvic obliquity.
• Trendelenburg test: Abductor competence (relevant to paralytic hip instability).

1. Diagnosis is clinical and historical: The diagnosis of residual polio rests on the history of an acute paralytic illness in childhood and the characteristic LMN, normal-sensation examination. No single test "proves" residual polio.

2. Muscle charting:

• A meticulous MRC muscle chart of the whole limb is the principal "investigation" for surgical planning. It identifies expendable donors and the deformity-driving muscles.

3. Imaging:

• Plain radiographs: Document bony deformity, joint subluxation/dislocation (hip), arthritis, and limb-length discrepancy (scanogram/CT scanogram). Bones are characteristically osteopenic, slender, with a narrow medullary canal in the affected limb - important for implant selection.
• Standing alignment / scoliosis films: For paralytic spinal deformity and pelvic obliquity.
• CT: For complex bony deformity planning and assessing the narrow canal before nailing.

4. Electrodiagnostics (EMG/NCS):

• Confirms a chronic neurogenic picture (large-amplitude, long-duration motor units; reduced recruitment) with normal sensory conduction.
• Especially useful in the workup of suspected PPS, to demonstrate ongoing/active denervation and to exclude alternative causes (radiculopathy, entrapment neuropathy).

Disease-related (natural history):

• Progressive fixed contracture and joint deformity.
• Limb-length discrepancy and pelvic obliquity.
• Paralytic hip subluxation/dislocation and paralytic scoliosis.
• Osteoporosis of the affected limb with fragility fractures (low bone density, reduced muscle pull, falls).
• Genu recurvatum and degenerative joint disease from chronic abnormal loading.

Surgery-related:

• Recurrence/relapse of deformity, especially when operating before skeletal maturity or on an unbalanced limb.
• Iatrogenic calcaneus foot after over-lengthening the tendo-Achilles in a weak triceps surae.
• Failed/under-powered tendon transfer (donor too weak, transfer onto an unstable base).
• Implant difficulty: Narrow osteopenic canal, valgus neck and increased anteversion complicate nailing of femoral fractures; fixed-angle plates and sliding hip screws are often preferred, with an emphasis on constructs permitting early weight-bearing.

Late (post-polio syndrome):

• New weakness, abnormal fatigue, muscle and joint pain, cold intolerance, and (less commonly) dysphagia or respiratory decline.
• Loss of previously stable function and increasing dependence on orthoses/aids.

Why examiners love polio:

• It is the cleanest teaching model of flaccid (LMN) paralysis with intact sensation, so it tests whether you can localise a lesion from the examination alone.
• It forces you to articulate the three principles - correct, stabilise, balance - in the right order. Getting the order wrong (for example, transferring onto a deformed foot) is the classic candidate error.
• It overlaps with high-yield neighbours: tendon transfer principles (also peripheral nerve injury, CMT), neuromuscular scoliosis, paralytic hip, and limb reconstruction / external fixation.

The five sentences that score marks:

1. "Polio is a pure lower motor neuron disease with normal sensation - that is how I separate it from spina bifida."
2. "I would delay reconstruction until the residual phase (around two years) once recovery has plateaued."
3. "My principles are to correct deformity, stabilise the joint, and only then balance with a transfer."
4. "A tendon transfer needs a supple joint, a stable base, and a grade 4-5 expendable donor."
5. "New weakness decades later is post-polio syndrome - a diagnosis of exclusion."

• Hamstring-to-patella transfer for quadriceps palsy: Can restore active knee extension in selected, well-balanced limbs, but risks creating a flexion deformity or recurvatum and has variable, often modest, active power - patient selection is everything.
• Joint preservation vs arthrodesis: In the ageing survivor with degenerative change, when to fuse a flail joint versus continue bracing is individualised; there are no high-level trials.
• Arthroplasty in polio limbs: Hip and knee replacement can relieve pain but face instability (abductor/quadriceps insufficiency) and fixation challenges in osteopenic, deformed bone; evidence is limited to small series.
• Optimal management of PPS: No disease-modifying therapy is proven; the balance between activity (to avoid disuse) and rest (to avoid overuse) remains pragmatic and individualised.

Global epidemiology:

• Eradication trajectory: Wild poliovirus cases have fallen by more than 99% since 1988 (Global Polio Eradication Initiative). Wild type 2 and type 3 are certified eradicated; wild type 1 persists in a small number of endemic regions, with sporadic vaccine-derived (cVDPV) outbreaks elsewhere.
• Surviving cohort: Millions of polio survivors remain worldwide; large surgical databases (for example, tens of thousands of sequelae cases in single high-volume centres) confirm that an ageing survivor population will need orthopaedic care for decades.
• Geographic burden: Untreated, neglected residual deformity is concentrated in low- and middle-income settings; high-income settings now mainly manage ageing survivors and post-polio syndrome.

Guidance and frameworks:

• WHO / Global Polio Eradication Initiative: Drives immunisation, surveillance and the endgame strategy - the upstream prevention that determines future caseload.
• March of Dimes post-polio criteria: The widely cited clinical framework for diagnosing post-polio syndrome (prior paralytic polio, stable interval, new persistent weakness, exclusion of alternatives).
• Rehabilitation principles: International rehabilitation guidance for PPS centres on energy conservation, individualised exercise that avoids overuse, orthotic optimisation, and multidisciplinary symptom management.

Registries and data sources:

• No dedicated international polio-sequelae implant registry exists; outcome data come from large single-centre surgical series and national rehabilitation cohorts rather than arthroplasty registries.