What are CTEV and DDH, and why are they studied together?
Congenital talipes equinovarus (CTEV), or clubfoot, is one of the commonest congenital deformities. The foot is held in a predictable set of contractures — cavus, adductus, varus and equinus — that vary from a mild, postural foot to a severe, rigid one. Recognised early and treated well, it has excellent results.
Developmental dysplasia of the hip (DDH) is abnormal development of the hip in infancy or early childhood. It is a spectrum: hip instability, acetabular dysplasia, subluxation and frank dislocation. It used to be called 'congenital dislocation of the hip'; the word developmental is preferred because not every case is present or detectable at birth.
The two belong on one page because both are newborn screening problems of the lower limb, both are treated non-operatively when caught early, and they travel together: StatPearls notes that children with clubfoot are about 25 times more likely to have DDH, so the hips of every clubfoot baby must be examined.
What are the components of the clubfoot deformity (CAVE)?
The four deformities are remembered as CAVE, which is also the order in which Ponseti casting corrects them: Cavus first, then Adductus and Varus together, and Equinus last.
| Component | Where | What it looks like |
|---|---|---|
| Cavus | Midfoot | High arch; deep medial plantar crease |
| Adductus | Forefoot | Forefoot turned in; curved lateral border of the foot |
| Varus | Hindfoot (heel) | Heel inverted under the talus |
| Equinus | Hindfoot (ankle) | Foot plantarflexed; empty heel; deep posterior crease |
Pathoanatomy. The deformity sits mainly in the tarsal bones, held in maximal flexion and adduction. The talus is medially deviated and plantarflexed; the calcaneus is in varus and rotated medially around the talus; the navicular and cuboid are displaced medially. Histology shows abnormally dense collagen in the medial and posterior structures — chiefly the Achilles tendon, tibialis posterior, and the tibionavicular and calcaneonavicular ligaments.
How common is clubfoot and what is it associated with?
- Incidence: about 0.5–2 per 1000 births (higher in Hawaiian and Maori populations).
- Sex and side: boys are affected about twice as often as girls; about 50% are bilateral; in unilateral cases the right side is more often affected.
- Environment: maternal smoking and maternal diabetes show the strongest association; maternal alcohol may also be linked.
- Genetics: about a quarter have a family history; monozygotic twin concordance is 33% versus 3% in dizygotic twins.
- Idiopathic vs syndromic: about 80% are isolated. About 20% occur with another condition — distal arthrogryposis, myelomeningocele, amniotic band sequence, congenital myotonic dystrophy, trisomy 18, 22q11 deletion.
Diagnosis is clinical. Clubfoot is often picked up on antenatal ultrasound, otherwise at the newborn examination. X-rays add little in the newborn because many tarsal bones have not ossified. In older or relapsed feet, a weight-bearing AP film may show parallel talus and calcaneus (talocalcaneal angle under 20°).
How is clubfoot severity graded with the Pirani score?
The Pirani score is the most widely used grading system because it is simple and reproducible. Six signs are scored 0, 0.5 or 1 each, giving 0 (normal) to 6 (most severe) per foot — three for the hindfoot and three for the midfoot.
| Hindfoot contracture score (HCS) | Midfoot contracture score (MCS) |
|---|---|
| Posterior crease — single deep crease scores 1 | Medial crease — single deep crease scores 1 |
| Empty heel — calcaneum not palpable scores 1 | Curved lateral border — curve at the calcaneocuboid joint scores 1 |
| Rigid equinus — cannot reach plantigrade scores 1 | Lateral head of talus — stays uncovered on correction scores 1 |
A higher starting Pirani score predicts more casts and a greater need for Achilles tenotomy, so the score is used both for counselling parents and for tracking correction cast by cast. As the foot corrects, the lateral head of the talus becomes covered by the navicular.
What are the steps of the Ponseti method?
Developed by Ignacio Ponseti in the 1940s, the Ponseti method is the gold standard. It has two phases — correction (manipulation and serial casting, usually ending with a tenotomy) and maintenance (bracing). StatPearls reports an initial correction rate of about 98%.
- Start early — ideally in the first one or two weeks of life, but the method works up to about 2 years of age.
- Above-knee plaster casts with the knee flexed about 110° (so the cast does not slip), after gentle manipulation. Casts are changed every 5–7 days; usually 5–9 casts are needed.
- Cavus first — elevate the first metatarsal to line up the forefoot with the hindfoot.
- Adductus and varus next — abduct the foot around the head of the talus, which is palpated and used as the fulcrum. Abduction up to about 60° is possible; heel varus corrects through this abduction.
- Never push directly on the heel to correct varus, and never pronate the foot — pronation blocks calcaneal abduction and recreates cavus.
- Equinus last — once abduction is complete, dorsiflex. If dorsiflexion is still less than 10°, do a percutaneous Achilles tenotomy (needed in about 80%), under local anaesthesia in clinic.
- Final cast for 3 weeks after tenotomy, at about 60° abduction and 20° dorsiflexion.
Bracing starts immediately after the final cast: a foot abduction brace (boots and bar) with the boots shoulder-width apart and the affected foot in about 70° of external rotation. It is worn 23–24 hours a day for the first 3 months, then at night (about 12 hours) plus 2–4 hours by day until 4 years of age.
What if clubfoot relapses, and what else can look like it?
- Early relapse — re-manipulate and recast.
- Tibialis anterior tendon transfer to the lateral cuneiform — for a child over 30 months with dynamic supination (tibialis anterior overpowering weak peronei); needed in about 20%.
- Open Achilles lengthening and other procedures for residual deformity.
- Avoid extensive soft-tissue release where possible — it risks stiffness, overcorrection, weakness, arthritis and even avascular necrosis in the long term.
| Condition | Key difference |
|---|---|
| Idiopathic clubfoot (CTEV) | Present at birth; equinus with cavus, adductus and varus |
| Calcaneovalgus foot | Foot in dorsiflexion, not equinus |
| Congenital vertical talus | Foot in dorsiflexion (rocker-bottom), not equinus with cavus |
| Neuromuscular equinovarus (cerebral palsy, spina bifida) | Not present at birth; develops later from muscle imbalance |
In unilateral cases the treated foot may stay 1–2 sizes smaller and the calf thinner — expected findings, not treatment failure. Long-term studies report good or excellent results in about 78% of Ponseti-treated idiopathic clubfeet.
What are the risk factors for DDH?
| Risk factor | What to remember |
|---|---|
| Breech in the last trimester | The single most significant risk factor (odds ratio about 5.5) |
| Female sex | About 4 times commoner in girls — ligamentous laxity from maternal hormones |
| Family history | Recurrence risk about 6% |
| Swaddling with hips adducted and extended | Avoid; hip-healthy swaddling keeps the hips free to flex and abduct |
| In-utero crowding | Oligohydramnios, large-for-gestational-age baby, multiple pregnancy |
| Post-term gestation | Prematurity is not a risk factor |
A PMC review adds that about 60% of affected children are firstborn, the left hip is involved more often than the right, and about 20% are bilateral. The left-sided predominance is linked to the usual left occipito-anterior fetal position, which presses the left hip into adduction against the maternal spine.
How do the Barlow, Ortolani and Galeazzi tests differ?
Both newborn manoeuvres are done with the baby supine, calm and undressed, the hip flexed to 90°. They test opposite things.
| Test | How | Positive finding means |
|---|---|---|
| Barlow | Adduct the flexed hip with gentle backward pressure | A clunk as the hip dislocates — a dislocatable hip |
| Ortolani | Abduct the flexed hip while lifting the greater trochanter forward | A clunk as a dislocated hip reduces — a dislocated but reducible hip |
| Galeazzi | Hips and knees flexed, feet flat on the couch; compare knee heights | Apparent femoral shortening on one side — a later sign, mainly in unilateral dislocation |
| Limited abduction | Abduct both flexed hips | The most important sign after about 4 months |
| Klisic | Line from greater trochanter through ASIS | Line passes below the umbilicus on the dislocated side |
When is ultrasound used for DDH and when is an X-ray better?
The switch-point is ossification of the femoral head. The femoral head nucleus usually appears between 4 and 6 months (range 1.5–8 months). Before that the head is cartilage and is seen only on ultrasound; after it, the X-ray becomes the preferred test.
- Ultrasound (Graf method): the alpha angle (bony acetabular roof) should be more than 60°; the beta angle (cartilaginous roof/labrum) normally less than 55°; the acetabulum should cover at least 50% of the femoral head.
- Timing for at-risk babies: a normal exam with risk factors gets an ultrasound at about 6 weeks (letting physiological laxity settle) — or an X-ray at 4 months.
- CT or MRI confirms position after closed reduction and spica casting.
| Line / angle | Normal |
|---|---|
| Hilgenreiner line (horizontal, through both triradiate cartilages) | Femoral head lies below it |
| Perkin line (vertical, from lateral acetabular edge) | Femoral head lies medial to it (lower inner quadrant) |
| Shenton line (femoral neck to upper border of obturator foramen) | A smooth, unbroken arc |
| Acetabular index | Under 35° at birth, under 25° at 1 year |
| Centre-edge angle of Wiberg | Over 20°; reliable after age 5 |
How is DDH treated at different ages?
| Age | Treatment | Key points |
|---|---|---|
| 0–4 weeks | Observe mild instability; refer dislocatable hips | Most Barlow-positive newborn hips stabilise on their own |
| 1–6 months | Pavlik harness | Worn 23 h/day for at least 6 weeks; ultrasound every 3–4 weeks; switch if not reduced by 3 weeks |
| 6–18 months (or failed harness) | Closed reduction + hip spica under general anaesthesia | 90–100° flexion, 40–50° abduction; main risk avascular necrosis |
| 18 months – 8 years | Open reduction ± femoral shortening ± pelvic osteotomy (Salter, Pemberton, Dega) | Clears obstacles: inverted labrum, pulvinar, hypertrophied ligamentum teres, tight iliopsoas |
| Older child / adolescent | Salvage (e.g. Chiari) or periacetabular osteotomy | For residual dysplasia or subluxation |
How the Pavlik harness works: an anterior strap holds the hip flexed at about 90° and stops extension; a posterior strap prevents adduction. This keeps the femoral head pointing into the acetabulum so both can grow normally. Success is about 90% for Barlow-positive hips; failure is likelier with an Ortolani-positive hip, start after 7 weeks, male sex and associated foot deformity.
Untreated or residual DDH leads to limp, limb-length difference, limited abduction and early arthritis — DDH is the commonest cause of early hip osteoarthritis in women under 40. The aim of screening is to diagnose every case before 6 months.
What are the common exam traps in CTEV and DDH?
- Order of Ponseti correction: cavus → adductus + varus → equinus (CAVE). Equinus is never first.
- Fulcrum for abduction is the head of the talus — not the calcaneocuboid joint.
- Tenotomy is the Achilles tendon, done when dorsiflexion is < 10° after abduction.
- Brace — boots and bar: full-time 3 months, then nights until 4 years.
- Barlow dislocates (adduction); Ortolani relocates (abduction).
- Most important DDH risk factor: breech presentation.
- Investigation: ultrasound before about 4–6 months; X-ray after the femoral head ossifies.
- Treatment under 6 months: Pavlik harness; 6–18 months: closed reduction and spica; over 18 months: open reduction.
Related reading: the upper-limb birth injury in Erb's palsy, the bowed legs of rickets, and newborn assessment in Apgar score. For past papers, see NEET PG orthopaedics PYQs.