Poliomyelitis (Orthopaedic Sequelae)

Poliomyelitis is an acute viral infection by poliovirus, an enterovirus, that selectively destroys the anterior horn motor neurons of the spinal cord and sometimes the brainstem motor nuclei. The orthopaedic surgeon almost never sees the acute illness. The work is 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, so proprioception, light touch and pain are normal, and that 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.

Near eradication. Global cases have fallen by over 99% since the Global Polio Eradication Initiative (1988). Wild poliovirus type 1 now circulates endemically only in Afghanistan and Pakistan, and types 2 and 3 are certified eradicated (2015 and 2019 respectively). Rare circulating vaccine-derived poliovirus (cVDPV) outbreaks can still cause new paralytic cases where immunisation coverage is low.

The surviving cohort. Despite near-eradication, millions of polio survivors remain worldwide, and their musculoskeletal sequelae will be encountered for decades to come. The largest number of untreated residual deformities is in low- and middle-income countries, where late presentation with neglected deformity is common.

Why it stays on the exam. Polio is the prototype flaccid paralysis with intact sensation, so it tests whether you can localise a lesion from the examination alone. It is also the classic teaching model for tendon transfer, balancing surgery, osteotomy and arthrodesis, principles that transfer directly to other LMN conditions (peripheral nerve injury, spina bifida, CMT). It overlaps with neuromuscular scoliosis, the paralytic hip, and limb reconstruction with external fixation.

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The neurological insult is static. Poliovirus reaches the CNS and lyses anterior horn cells, and the number of cells destroyed determines the final deficit. During the convalescent phase surviving neurons sprout to re-innervate orphaned muscle fibres, forming enlarged "giant" motor units, which is why power can recover for up to about 2 years.

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The deformity is progressive. As in cerebral palsy, the neurological lesion is static but the musculoskeletal deformity progresses, driven by three forces acting on a growing skeleton:

• Muscle imbalance - a living muscle with no working antagonist pulls the joint into a fixed position; an intact tibialis posterior against a dead tibialis anterior leads to equinovarus
• Growth - imbalance across active physes produces progressive bony deformity and torsion, and the paralysed segment grows poorly, leaving limb-length discrepancy (LLD) and atrophy (reduced muscle pump and vascularity)
• Gravity and posture - habitual postures, gravity and contracture of fascia and capsule convert dynamic imbalance into fixed contracture

The pattern depends on which motors survive.

• Foot and ankle - equinus, equinovarus, calcaneus, cavus or flail foot (set out under Classification)
• Knee - flexion contracture (weak quadriceps, tight hamstrings and ITB), genu recurvatum (weak quadriceps with a fixed plantarflexed foot, below), flail knee
• Hip - flexion-abduction-external rotation contracture, paralytic subluxation or dislocation from 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

History. Establish the age at infection, the limbs affected, the recovery achieved, and previous surgery and bracing. Then current function: walking distance, falls, brace use, pain and fatigue. New weakness, fatigue or pain raises the question of post-polio syndrome, but other causes are excluded first.

Look. Wasting, deformity, scars, posture, brace wear and limb-length discrepancy. The skin is trophic but usually intact, because sensation is preserved.

Feel. Confirm that sensation is intact; it is the diagnostic discriminator. Polio is a pure motor disease, so a sensory deficit means the diagnosis is not polio: think of spina bifida, peripheral neuropathy or spinal cord pathology instead. Palpate for fixed contractures.

Move. Distinguish fixed from correctable deformity, and chart the MRC power of every relevant muscle. The muscle chart is the single most important examination step for planning.

Function and gait. Identify the gait pattern, which localises the paralysed motor; the paralytic gaits are set out in the next section.

The special tests:

• Coleman block test - in 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) against apparent length, identifying the contribution of pelvic obliquity
• Trendelenburg test - abductor competence, relevant to paralytic hip instability

Each paralysed motor has its own compensation, so reading the gait names both the dead muscle and what a brace or transfer must replace.

• Quadriceps (hand-to-thigh) gait - with a weak or absent quadriceps the patient presses a hand on the thigh in stance, or thrusts the knee into extension or recurvatum, to keep it from buckling. It is the signature of quadriceps palsy
• Gluteus maximus lurch - with a weak hip extensor the patient throws the trunk backwards over the hip at heel strike, moving the ground-reaction line behind the hip to lock it in extension
• Gluteus medius (Trendelenburg) lurch - with weak abductors the pelvis drops on the swing side and the patient lurches the trunk over the stance hip; a waddling gait if bilateral
• Calcaneus gait - a weak triceps surae gives no push-off, a heel-only stance and crouch
• High-stepping foot-drop gait - weak dorsiflexors

Diagnosis is clinical. Residual polio rests on the history of an acute paralytic illness in childhood and the characteristic LMN, normal-sensation examination, and no single test proves it. The principal "investigation" for surgical planning is a meticulous MRC muscle chart of the whole limb, which identifies the expendable donors and the muscles driving the deformity.

Plain radiographs document bony deformity, subluxation or dislocation of the hip, arthritis and limb-length discrepancy (scanogram or CT scanogram). The bones of the affected limb are characteristically osteopenic and slender, with a narrow medullary canal, which matters for implant selection. Standing alignment and scoliosis films assess paralytic spinal deformity and pelvic obliquity.

CT plans the correction of complex bony deformity and assesses the narrow canal before nailing.

Electrodiagnostics (EMG/NCS) confirm a chronic neurogenic picture (large-amplitude, long-duration motor units with reduced recruitment) with normal sensory conduction. They are especially useful in the workup of suspected post-polio syndrome, to demonstrate ongoing or active denervation and to exclude alternative causes such as radiculopathy and entrapment neuropathy.

The mechanism. A weak or absent quadriceps forces the patient to lock the knee in hyperextension to stand, and over years the deformity becomes fixed. Two mechanisms are distinguished: a structural (bony) recurvatum from remodelling of the posterior proximal tibia and tibial plateau, and a ligamentous recurvatum from stretching of the posterior capsule. A coexisting fixed equinus compounds both by thrusting the tibia backwards at heel strike.

Assessment. Chart quadriceps power, the underlying cause, measure the arc of hyperextension, and separate correctable from fixed deformity. Then assess the ankle, because an uncorrected equinus will recreate the recurvatum.

Non-operative. A KAFO holding the knee in a few degrees (about 5-10) of flexion blocks the damaging hyperextension and is often definitive. Correcting a coexisting equinus with an AFO or heel raise removes the back-thrust.

Operative. For a disabling fixed deformity, a proximal tibial or supracondylar femoral flexion (extension-blocking) osteotomy restores a few degrees of flexion and a stable stance. The equinus must be corrected at the same sitting, and residual quadriceps weakness (or a substituting KAFO) still sets the functional ceiling.

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PrinciplesNon-OperativeTendon TransferOsteotomy & Arthrodesis

Polio reconstruction reduces to three repeatable principles, applied in order, and the aim is a plantigrade, braceable, energy-efficient limb.

1. Correct the deformity - make the joint supple and the segment aligned: soft-tissue release for fixed contracture, then osteotomy for residual bony or rotational malalignment
2. Stabilise the unstable - provide a stable, plantigrade base: arthrodesis or bracing for a flail joint, or arthrodesis to create a stable foundation before any transfer
3. Balance the muscles - restore a working agonist-antagonist couple by tendon transfer of an expendable, powerful donor onto the deficient action, done last, onto a corrected, stable limb

Never balance a deformed or unstable limb. Correct and stabilise first, then transfer; transferring onto a deformed foot is the classic candidate error. Across a whole limb the steps are often staged or combined, and in adults "limited surgery plus external fixation" can correct multiple deformities efficiently.

Many survivors are managed for life with a well-fitted brace and never need surgery. Physiotherapy maintains range of motion, prevents contracture and strengthens surviving muscles without overuse.

• AFO - controls a flail ankle or foot drop
• KAFO - stabilises a knee with quadriceps insufficiency, allowing safe standing and walking
• Shoe raise - for limb-length discrepancy

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Energy conservation applies especially in post-polio syndrome: pacing, weight management, assistive devices, and avoiding the overuse that accelerates motor-unit failure.

A transfer replaces a paralysed action with an expendable, powerful donor pulling in a straight line. It cannot work in phase if the joint beneath it is unstable or deformed, which is why it is the last step, performed onto a corrected, stable limb.

Mnemonic

SPARETendon Transfer Prerequisites - SPARE

S

Supple joint

The joint must be passively mobile - no fixed contracture left to correct

P

Plantigrade/stable base

Correct bony deformity first; never transfer onto an unstable foundation

A

Adequate power donor

Donor muscle ideally MRC grade 4-5 (loses ~1 grade after transfer)

R

Right direction & line of pull

Straight line of pull; avoid sacrificing the only remaining useful muscle

E

Expendable donor

Removing the donor must not create a new imbalance or deformity

Hook:SPARE the patient a failed transfer - check the prerequisites first.

The classic transfers:

• Foot drop - tibialis posterior through the interosseous membrane to the dorsum, to restore dorsiflexion
• Quadriceps palsy - biceps femoris and semitendinosus to the patella, to restore active knee extension in selected, well-balanced cases
• Flail shoulder - trapezius transfer or shoulder arthrodesis, depending on the remaining motors

Bony surgery sets up the limb so that bracing, or a subsequent transfer, can succeed.

Osteotomy corrects residual angular and rotational malalignment and realigns the mechanical axis. For fixed knee flexion deformity a supracondylar femoral extension osteotomy is a standard option, often combined with hamstring lengthening, to make the limb braceable.

Arthrodesis is the workhorse for a flail joint with no useful motors. Triple arthrodesis stabilises and realigns a flail or deformed foot into a plantigrade position, and knee or hip arthrodesis gives selected adults with a flail joint a stable, weight-bearing limb.

Limb-length discrepancy is managed by contralateral epiphysiodesis, timed in the growing child, or by limb lengthening, often with external fixation, for larger discrepancies.

Arthroplasty. The hip and knee cases below show what replacement meets in a polio limb: weak periarticular muscles, abnormal bone and the risk of instability.

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From the disease. Left alone, the deformities described above progress: fixed contracture and joint deformity, limb-length discrepancy with pelvic obliquity, paralytic hip subluxation or dislocation, paralytic scoliosis and genu recurvatum. Chronic abnormal loading adds degenerative joint disease, and the affected limb becomes osteoporotic, with fragility fractures from low bone density, reduced muscle pull and falls.

From surgery.

• Recurrence or relapse of deformity, especially when operating before skeletal maturity or on an unbalanced limb
• Iatrogenic calcaneus foot after over-lengthening the tendo-Achilles (see Foot Deformity)
• Failed or under-powered tendon transfer - donor too weak, or transfer onto an unstable base
• Implant difficulty in the paralysed femur (below)

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Fractures in the polio femur. The narrow osteopenic canal, a valgus neck-shaft angle and increased anteversion make intramedullary nailing of femoral fractures difficult. Choose implants that allow early weight-bearing: smaller nails, or the fixed-angle plates and sliding hip screws that are often preferred.

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Post-polio syndrome. The late picture adds cold intolerance and, less commonly, dysphagia or respiratory decline to the new weakness, abnormal fatigue and muscle and joint pain, with loss of previously stable function and increasing dependence on orthoses and aids.

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.

Related pages: Cerebral Palsy for the other great paediatric paralytic deformity, and the contrast that defines both - polio is a pure LOWER motor neurone lesion with flaccid weakness, normal tone and intact sensation, while cerebral palsy is an upper motor neurone lesion with spasticity, so tendon transfers behave predictably in polio and unpredictably in spasticity; Neuromuscular Scoliosis for the collapsing C-curve with pelvic obliquity that paralytic trunk muscles produce; Spina Bifida for the paralytic deformity that DOES carry sensory loss, which is why insensate skin and pressure ulceration dominate its management and not this one's; Charcot-Marie-Tooth Disease for the other lower motor neurone cause of cavovarus and foot-muscle imbalance; Clubfoot for the deformity that residual polio equinovarus is mistaken for, and the corrective principles it shares; Limb Length Discrepancy and Epiphysiodesis for the growth inhibition of the paralysed limb; and Limb Lengthening Principles for the circular-fixator techniques that have largely replaced acute correction in the neglected fixed deformities described here.

• 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.