OR12.1 | Congenital Lesions — Graded Quiz

Correct. Positive Barlow (subluxatable) + negative Ortolani = located but unstable hip. Up to 80% of neonatal unstable hips stabilise by 3 weeks. Confirm with USG and use Pavlik harness if instability persists. Spica casting and traction are not first-line here.

A positive Barlow test (hip subluxates posteriorly, reduces spontaneously) with negative Ortolani indicates an unstable but located hip (Graf Type IIb/IIc equivalent). Management: double diapering is no longer recommended; a Pavlik harness is initiated after confirmatory ultrasound. Many neonatal unstable hips stabilise spontaneously by 2–3 weeks.

A positive Ortolani (not Barlow) indicates a dislocated hip being reduced. A positive Barlow means the hip is currently located but can be subluxated — less severe. Confirm with USG; Pavlik harness if still unstable at 2–3 weeks.

Correct. MRI is the most sensitive investigation for early AVN detection after DDH reduction. Plain X-ray changes (irregular ossification, fragmentation) appear later. Clinically, AVN manifests as loss of femoral head height over months to years.

AVN is the most serious complication of DDH treatment, caused by excessive abduction (>60°) compressing the blood supply. MRI is the most sensitive early modality for detecting AVN of the femoral head before radiographic changes appear. Plain X-rays are used for longer-term follow-up (irregular ossification, fragmentation).

MRI is most sensitive for early AVN (marrow signal changes). X-ray is used for monitoring but picks up AVN late (bony changes). Bone scan is less specific in young children with open growth plates.

Correct. In high dislocation (Crowe III/IV) the displaced femoral head shortens the abductor mechanism. The gluteus medius cannot maintain pelvic level, producing Trendelenburg sign and compensatory trunk lean (Duchenne lurch) to the affected side.

In untreated DDH in a walking child, the dislocated femoral head shortens the effective lever arm of the gluteus medius (which inserts into the greater trochanter). With the femoral head riding high, the abductors are ineffective, causing a Trendelenburg lurch — the trunk shifts to the dislocated side during stance phase to compensate.

The Trendelenburg sign in DDH is biomechanical: the dislocated femoral head migrates superiorly, shortening the gluteus medius lever arm and abductor efficiency — not a nerve injury.

Correct. Persistent CMT after 12–18 months requires bipolar SCM release (both sternal and clavicular heads distally + mastoid process proximally). The spinal accessory nerve (CN XI) runs in the posterior triangle close to the SCM and must be identified and protected.

Surgical treatment of persistent CMT (>12–18 months, failed physiotherapy) involves bipolar (proximal + distal) release of the sternocleidomastoid. The key intraoperative precaution is protecting the accessory nerve (CN XI) which runs superficial to the SCM in the posterior triangle — injury causes trapezius weakness.

Bipolar release achieves better correction than unipolar. The spinal accessory nerve (CN XI), which innervates the trapezius and SCM, is the critical structure at risk during SCM release in the posterior triangle.

Correct. After Ponseti casting corrects C, A, V, residual equinus persisting beyond 10° is addressed by percutaneous Achilles tenotomy (in ~80% of cases). A 3-week final cast allows tendon healing, after which the foot abduction brace (FAB) is worn full-time for 3 months, then nights until age 4.

After correcting C, A, V with serial casts, ~80% of CTEV cases require a percutaneous Achilles tenotomy (PAT) to correct the residual equinus. PAT is performed under local anaesthesia in the clinic; a short final cast is applied for 3 weeks. Definitive correction is maintained with a foot abduction brace (FAB/Denis Browne boots-and-bar) until age 4.

Continued casting alone will not correct rigid equinus (tight Achilles). Percutaneous Achilles tenotomy is the standard next step; posterior surgical release is reserved for resistant/relapsed cases.

Correct. Ponseti sequence: C (cavus) first by supinating forefoot → A+V (adduction and varus corrected simultaneously by abducting the forefoot with the thumb on the talar head) → E (equinus corrected last, usually by tenotomy). Correcting equinus first causes rocker-bottom foot.

Ponseti method corrects deformities in a specific sequence: first Cavus (by supinating the forefoot to align with the hindfoot), then Adduction and Varus simultaneously (by abducting the forefoot with the thumb on the talar head as a fulcrum — never on the calcaneus), and finally Equinus (by dorsiflexion after Achilles tenotomy). Correcting equinus before adduction/varus is a common error causing a rocker-bottom foot.

Ponseti sequence is CAVE corrected as C first, then A+V together, then E last. Addressing equinus before correcting the mid/forefoot creates a rocker-bottom deformity.

Correct. Cobb 52° + Risser 4 meets the surgical threshold. Bracing is ineffective at Risser ≥ 3 and is not indicated for curves > 45°. Posterior spinal fusion with pedicle screw instrumentation (Harrington → Cotrel-Dubousset → modern segmental systems) achieves 50–70% correction.

For curves > 45–50° in patients who are near skeletal maturity (Risser 4) or who have failed bracing, posterior spinal fusion with instrumented correction is indicated. Bracing is ineffective at Risser ≥ 3 (near mature) and for curves > 45°. Curves > 50° in adults progress at ~1° per year and cause restrictive lung disease if thoracic.

Curves > 45–50° require surgical correction regardless of Risser grade. Bracing is contraindicated at Risser 4 and for curves already beyond 45°. Observation alone risks continued progression (1°/year in adults) and eventual cardiopulmonary compromise.

Correct. L2 level (hip flexors intact, no knee extensors/ankle/toe movement): household/therapeutic ambulation possible with RGOs or KAFOs; community ambulation is unlikely long-term without significant orthotic support. Wheelchair is the primary mobility for community distances.

Ambulatory prognosis in myelomeningocele depends on the functional neurological level: L2 (hip flexors + adductors) = community ambulation unlikely without extensive bracing (KAFO/RGO); L3 (knee extensors) = community ambulation possible with KAFOs; L4 (ankle dorsiflexors) = community ambulation with AFOs; L5-S1 = near-normal ambulation. This child has L2 function — household ambulation at best with reciprocating gait orthosis.

L2 myelomeningocele prognosis: intact hip flexion but no knee extension, ankle, or toe movement. Functional level determines orthosis: L2=KAFO/RGO for household use; wheelchair for community.

Correct. The scoliometer (inclinometer) is placed at the apex of the rib hump during Adam's forward bend test. > 7° trunk rotation = referral for full-spine AP X-ray and Cobb angle measurement. It is the standard school-screening tool for scoliosis.

The scoliometer (inclinometer) is placed at the apex of the rib hump during Adams forward bend test to measure trunk rotation in degrees. A reading > 7° warrants referral for X-ray and measurement of Cobb angle. It is a simple school-screening tool.

The scoliometer is specifically designed to measure angle of trunk rotation in scoliosis screening (Adam's forward bend test). > 7° warrants X-ray referral.

Correct. Syringomyelia (fluid-filled central cord cavity) causes progressive asymmetric neurological deficits below the syrinx level. Asymmetric trunk and paraspinal muscle function produces rapid scoliosis progression. Neurosurgical drainage/decompression is required before spinal correction.

Congenital/neurogenic scoliosis in spina bifida is often driven by muscle imbalance (flaccid paralysis below lesion level). Rapidly progressive scoliosis with syringomyelia suggests tethered cord syndrome or hydromyelia, where progressive cord distension causes asymmetric muscle function. Neurosurgical decompression should precede or accompany orthopaedic spinal surgery.

Rapidly progressive scoliosis in spina bifida + syringomyelia = cord distension causing asymmetric paraspinal muscle function. Neurosurgical decompression of the syrinx must precede spinal surgery.