Orthopaedics
Trauma and orthopaedics for the Indian MBBS final-year exam — fractures, dislocations, bone and joint infection, tumours, the spine, arthritis, paediatric and regional orthopaedics. Full-length explanation-first answers with diagrams.
Definition
Developmental dysplasia of the hip (DDH) is a spectrum of abnormal development of the hip in which the femoral head and acetabulum have an abnormal relationship — ranging from a shallow dysplastic but located hip, through a subluxatable/dislocatable hip, to a frankly dislocated hip. Early detection is vital because timely treatment gives an excellent outcome, whereas late diagnosis leads to permanent deformity and early osteoarthritis.
Risk Factors
The classic associations (remembered as the ‘6 Fs’-type list) include a positive family history, female sex (much commoner in girls), firstborn, breech presentation, oligohydramnios, and other ‘packaging’ disorders (congenital torticollis, metatarsus adductus). The left hip is more often affected.
Neonatal screening manoeuvres: Barlow’s test dislocates an unstable hip; Ortolani’s test relocates a dislocated hip with a palpable ‘clunk’. Clinical Features & Screening
In the neonate, screening uses Ortolani’s test (abduct and lift the flexed hip to relocate a dislocated head — a palpable clunk) and Barlow’s test (adduct and gently push to dislocate an unstable hip). In the older infant, signs are limited hip abduction, asymmetrical skin/thigh creases, apparent femoral shortening (Galeazzi/Allis sign) and, once walking, a painless limp or waddling (Trendelenburg) gait.
💡Ortolani relocates, Barlow dislocates. After about 3 months these dynamic tests become unreliable as the hip becomes fixed; the key sign then is limited abduction of the flexed hip.Investigations
Under 6 months the femoral head is unossified, so ultrasound is the investigation of choice (Graf technique assesses acetabular morphology and stability). After the head ossifies (around 4–6 months), a plain radiograph is used, assessing Shenton’s line, the acetabular index and the position of the head relative to Perkin’s and Hilgenreiner’s lines.
Management
Treatment depends on age. 0–6 months: a Pavlik harness holds the hips flexed and abducted to allow the acetabulum to develop and the hip to stabilise. 6–18 months (or Pavlik failure): closed reduction and hip spica under anaesthetic, sometimes with adductor tenotomy and arthrogram. Older / irreducible / late hips need open reduction, often combined with femoral and/or pelvic osteotomy to correct the bony deformity. The earlier the treatment, the better the result.
⚠️Avascular necrosis of the femoral head is the most serious complication of treatment, caused by forced or extreme abduction. Reduction must be gentle and held in the ‘safe (human) position’ of moderate flexion and abduction.Age Test / investigation Neonate Ortolani (reduces), Barlow (dislocates) 3–6 months Limited abduction, Galeazzi sign Walking child Trendelenburg gait, limb shortening Under 6 months Ultrasound (Graf method) Over 6 months Radiograph — Perkin, Hilgenreiner, Shenton lines 🔑KEY POINTS TO REMEMBER- Spectrum from dysplasia to dislocation; early diagnosis gives excellent outcomes.
- Risk: female, firstborn, breech, family history, oligohydramnios; left hip commonest.
- Ortolani relocates, Barlow dislocates; after 3 months → limited abduction is the key sign.
- Ultrasound <6 months, radiograph after ossification.
- Pavlik harness (0–6 mo) → closed reduction/spica → open reduction ± osteotomy; beware AVN.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Congenital talipes equinovarus (CTEV, clubfoot) is a common congenital deformity in which the foot is turned downwards and inwards and cannot be passively corrected to normal. It may be idiopathic (the majority), syndromic/teratologic (associated with conditions such as arthrogryposis or spina bifida), or postural (a mild, fully correctable positional deformity). It is commoner in boys and is bilateral in about half of cases.
Components of the Deformity
The deformity has four components, remembered as ‘CAVE’: Cavus (a high medial longitudinal arch), forefoot Adductus, hindfoot Varus (inverted heel), and ankle Equinus (fixed plantarflexion). The calf is often thin and the foot smaller than normal.
The four components of clubfoot — Cavus, Adductus, Varus and Equinus (‘CAVE’). Clinical Assessment
The diagnosis is clinical at birth. The key distinction is between a rigid true CTEV (cannot be passively over-corrected) and a flexible postural deformity (fully correctable). Severity is graded (e.g. the Pirani or Dimeglio score) to guide and monitor treatment. Examine for associated abnormalities (spine, hips) that suggest a syndromic cause.
💡A true clubfoot is rigid and not fully passively correctable, unlike a postural deformity which corrects easily — this distinction determines whether active treatment is needed.Management — the Ponseti Method
Treatment should begin soon after birth while the tissues are supple. The gold standard is the Ponseti method: serial weekly manipulation and casting that sequentially corrects the deformity in a set order (cavus, then adductus and varus, and finally equinus), usually followed by a percutaneous Achilles tenotomy to correct the residual equinus. Correction is then maintained with a foot abduction (boots-and-bar) brace for several years to prevent relapse. Neglected, relapsed or resistant (often syndromic) feet may need soft-tissue release or bony surgery.
⚠️The commonest cause of relapse after successful Ponseti correction is non-compliance with the abduction bracing. Emphasise to parents that faithful brace wear for the recommended years is essential to a lasting result.Complications & Outcome
With early, well-conducted Ponseti treatment the outlook is excellent: most children achieve a supple, plantigrade, painless and functional foot that fits normal footwear. The principal problem is relapse, usually from inadequate bracing, which is managed by repeat casting and, if a dynamic supination persists, a tibialis anterior tendon transfer. Neglected clubfoot presenting late, and rigid syndromic feet (e.g. arthrogryposis), are much harder to treat and may require extensive soft-tissue release or bony surgery, sometimes with gradual correction using an Ilizarov frame.
💡Two anchors for clubfoot: recognise the deformity by ‘CAVE’, and treat it by Ponseti serial casting with an Achilles tenotomy, then a boots-and-bar brace — begun early, this non-surgical method gives a supple, functional foot in the great majority.CAVE component Deformity Cavus High medial arch (midfoot) Adductus Forefoot adduction Varus Hindfoot inversion Equinus Ankle plantarflexion Treatment Ponseti serial casting, then tenotomy and bracing 🔑KEY POINTS TO REMEMBER- Foot turned down and in; components ‘CAVE’: Cavus, Adductus, Varus, Equinus.
- Distinguish rigid true CTEV from a correctable postural deformity.
- Idiopathic (commonest), syndromic/teratologic, or postural; often bilateral.
- Gold standard = Ponseti serial casting + Achilles tenotomy, then boots-and-bar bracing.
- Relapse usually from poor brace compliance; neglected/resistant feet may need surgery.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Perthes disease (Legg–Calvé–Perthes disease) is idiopathic avascular necrosis of the femoral head epiphysis in a child, followed by revascularisation and remodelling over a period of years. If the head reossifies while deformed, incongruity and premature osteoarthritis result. It typically affects boys aged 4–8 years and is usually unilateral.
Pathology & Stages
The natural history passes through recognised stages: an initial avascular (necrosis) phase; a fragmentation phase (resorption of dead bone); a reossification (healing) phase as new bone forms; and a final remodelling phase. The central concept guiding treatment is ‘containment’ — keeping the softened, biologically plastic head well seated within the acetabulum so it remodels into a congruent, spherical shape.
Clinical Features
A child with an insidious limp and pain in the hip, groin, thigh or (referred) knee, often intermittent. Examination shows an antalgic gait, muscle wasting and restricted movement, especially abduction and internal rotation. The child is systemically well.
⚠️A child presenting with knee or thigh pain must always have the hip examined — hip pathology (Perthes, SCFE) classically refers pain to the knee, and the true source is easily missed if only the knee is assessed.Investigations
Plain radiographs (AP and frog-lateral) show the sequence of changes — early increased density and a smaller epiphysis, a subchondral fracture line (the crescent sign), fragmentation, and later reossification and any deformity/subluxation. MRI is more sensitive in the early stages. Prognostic classifications (Catterall, Herring lateral-pillar) assess the extent of head involvement.
Management
The aims are to relieve pain, maintain hip movement and contain the femoral head so it remodels spherically. Many young children with limited involvement do well with observation, activity limitation, physiotherapy to preserve range, and symptomatic treatment. Containment — by bracing or, more effectively, by femoral or pelvic osteotomy — is used for older children or those with more extensive head involvement or loss of containment. Prognosis is better in younger children and with less femoral head involvement.
💡Two prognostic principles: the younger the child and the less of the femoral head involved, the better the outcome — because a young hip has far more remodelling potential. Treatment revolves around containment.Differential Diagnosis
A limping child with hip pain has a broad differential that must be considered before settling on Perthes: transient synovitis (benign, post-viral, self-limiting), septic arthritis and osteomyelitis (febrile, toxic, raised inflammatory markers), SCFE (older, often obese adolescent), juvenile idiopathic arthritis, and, rarely, a bone tumour. Age, systemic features, inflammatory markers and imaging distinguish these; bilateral symmetrical ‘Perthes-like’ changes should prompt thought of an epiphyseal dysplasia or hypothyroidism rather than true Perthes.
Complications
The central risk is a deformed, non-spherical femoral head (coxa magna, coxa plana) that is incongruent with the acetabulum, leading to stiffness, hinge abduction and early osteoarthritis in adult life. Loss of containment and lateral subluxation during the fragmentation phase worsen the deformity, which is precisely what containment treatment sets out to prevent.
💡Perthes hinges on two ideas: it is a self-limiting AVN that passes through necrosis → fragmentation → reossification → remodelling, and the whole of treatment is aimed at containment so the plastic head remodels into a round, congruent shape. Younger children with less head involvement need little more than observation.⚠️Because a stiff, irritable hip in a child can equally be septic arthritis, never attribute an acutely painful, febrile hip to Perthes without excluding infection first — the two are managed completely differently and a missed septic hip is disastrous.Containment of the head in the acetabulum guides treatment. 🔑KEY POINTS TO REMEMBER- Idiopathic AVN of the femoral head epiphysis; boys 4–8 y; usually unilateral.
- Stages: necrosis → fragmentation → reossification → remodelling.
- Insidious limp + hip/thigh/knee pain; ↓ abduction & internal rotation; systemically well.
- X-ray shows the sequence; ‘containment’ is the guiding treatment principle.
- Younger child + less head involvement = better prognosis; osteotomy for containment when needed.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Slipped capital femoral epiphysis (SCFE / SUFE) is a disorder of the adolescent hip in which the femoral head epiphysis slips (displaces) posteriorly and inferiorly relative to the femoral neck through the growth plate (physis). It is essentially a Salter–Harris type-I fracture through a weakened physis and is the commonest hip disorder of adolescence.
Epidemiology & Associations
It typically affects the overweight adolescent around the pubertal growth spurt (boys ~10–16, girls ~10–14 years). Associations include obesity and endocrine disorders (hypothyroidism, hypogonadism, growth-hormone treatment, renal osteodystrophy) — which should be considered, especially in a thin or atypically young/old child.
In SCFE the epiphysis slips posteroinferiorly; on the AP film Klein’s line (drawn along the superior femoral neck) fails to intersect the epiphysis as it normally should. Clinical Features
Hip, groin, thigh or knee pain with a limp; the classic sign is that the affected leg lies in external rotation, and on flexing the hip it moves into obligatory external rotation and abduction (Drehmann sign). Slips are classified by duration (acute, chronic, acute-on-chronic) and, importantly, by stability — a stable slip allows weight-bearing (better prognosis), an unstable slip does not (high risk of AVN).
⚠️Up to a quarter of cases present with pain only in the knee or thigh. Always examine and image the hip in an adolescent with knee pain — missing a SCFE risks progression to a severe slip and avascular necrosis.Investigations & Management
AP and frog-lateral radiographs of both hips; the lateral view is most sensitive for early slips. Klein’s line (along the superior neck) normally intersects the epiphysis; in SCFE it does not. Treatment is urgent surgical stabilisation — usually in-situ fixation with a single cannulated screw to prevent further slip; the contralateral hip is fixed prophylactically in high-risk (endocrinopathy, young) cases. Forceful reduction of a chronic slip is avoided because it precipitates AVN.
💡SCFE is fixed ‘in situ’ — the slip is pinned where it lies rather than reduced, because forceful manipulation dramatically increases the risk of avascular necrosis and chondrolysis.Complications
The two feared complications are avascular necrosis of the femoral head (much higher after an unstable slip or after forceful reduction) and chondrolysis (acute cartilage loss with a stiff, painful hip). Both can lead to permanent damage and early osteoarthritis. Because of the risk to the other hip — particularly in younger children and those with an endocrinopathy — the contralateral side is monitored closely and often pinned prophylactically. Severe residual deformity may later require a corrective osteotomy.
💡The three rules of SCFE: think of it in an adolescent with knee or thigh pain and an externally rotated leg, get a frog-lateral radiograph and check Klein’s line, and treat by urgent in-situ screw fixation without forceful reduction.🔑KEY POINTS TO REMEMBER- Adolescent (often obese) hip; epiphysis slips posteroinferiorly (Salter–Harris I).
- Consider endocrinopathy if atypical (thin, very young/old, bilateral).
- Pain (often referred to knee) + limp; leg externally rotated; obligatory ER on flexion.
- Frog-lateral X-ray; Klein’s line fails to cut the epiphysis; classify by stability.
- Urgent in-situ screw fixation; avoid forceful reduction (AVN); consider prophylactic other side.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Cerebral palsy (CP) is a non-progressive disorder of movement and posture caused by a static lesion of the immature (developing) brain. Although the brain lesion itself does not progress, its musculoskeletal consequences — spasticity, contractures, deformity and hip displacement — do progress with growth, which is where orthopaedic care is central.
Classification
CP is classified by the type of movement disorder — spastic (the commonest, upper-motor-neuron), dyskinetic/athetoid, ataxic or mixed — and by the anatomical distribution (hemiplegia, diplegia, quadriplegia). Functional ability is graded by the Gross Motor Function Classification System (GMFCS, I–V), which strongly guides expectations and management.
Musculoskeletal Problems
Spasticity produces characteristic patterns: at the hip, flexion, adduction and internal rotation with a tendency to progressive hip subluxation/dislocation (which must be monitored by ‘hip surveillance’ radiographs); at the knee, flexion contractures and a crouch gait; at the ankle/foot, equinus and equinovarus/valgus; and, in the spine, neuromuscular scoliosis. Fixed contractures follow chronic spasticity.
⚠️Hip surveillance is essential in non-ambulant children (GMFCS IV–V): the hip can silently subluxate and dislocate as the child grows, causing pain and difficulty with sitting and hygiene. Regular examination and radiographic monitoring of the migration percentage allow timely intervention.Management
Care is multidisciplinary and lifelong, aimed at maximising function, comfort and independence rather than ‘cure’. It includes physiotherapy and occupational therapy, orthoses (e.g. ankle-foot orthoses), and spasticity management (botulinum toxin injections, oral agents, intrathecal baclofen, and selective dorsal rhizotomy in selected children). Orthopaedic surgery — soft-tissue releases/lengthenings, tendon transfers, bony osteotomies for hip displacement, and scoliosis correction — addresses fixed deformities, often performed together as single-event multilevel surgery in ambulant children.
💡The brain lesion in CP is static, but the orthopaedic deformities progress with growth — so treatment is about monitoring and managing the changing musculoskeletal consequences over the child’s development.Aetiology & Associated Problems
The static brain lesion of cerebral palsy may arise antenatally (the majority — prematurity, intrauterine infection, malformation), perinatally (hypoxic-ischaemic injury, birth asphyxia) or postnatally (kernicterus, meningitis, head injury in early life). Beyond the motor disorder, affected children commonly have associated impairments — learning difficulty, epilepsy, visual and hearing deficits, speech and feeding difficulties, and gastro-oesophageal reflux — which is why care is delivered by a broad multidisciplinary team and orthopaedic decisions are made in the context of the whole child.
Assessing Gait & Function
In ambulant children, systematic assessment (including instrumented gait analysis where available) identifies which deformities are the true drivers of dysfunction, distinguishing dynamic spasticity from fixed contracture. This underpins the modern strategy of single-event multilevel surgery, correcting all significant levels in one operative episode to limit repeated anaesthetics and rehabilitation, and preserving energy-efficient walking.
⚠️The orthopaedic hazard that is most often missed is silent hip displacement in the non-ambulant child: it produces no acute complaint yet progresses to a painful dislocation that ruins sitting balance and perineal care. Structured hip surveillance with the migration percentage catches it early, when a simple soft-tissue release or osteotomy can still preserve a located, comfortable hip.💡Remember the paradox at the heart of CP management: the brain lesion is fixed but the deformities grow, so orthopaedic care is a long-term programme of monitoring and timely, function-directed intervention rather than a one-off cure.The brain lesion is static but the musculoskeletal deformity progresses. 🔑KEY POINTS TO REMEMBER- Non-progressive brain lesion → progressive musculoskeletal deformity with growth.
- Classified by movement type (spastic commonest) & distribution; function graded by GMFCS.
- Hip subluxation, contractures, equinus foot, neuromuscular scoliosis; do hip surveillance.
- Multidisciplinary lifelong care; spasticity management + orthoses + selective surgery.
- Aim is function & comfort, not cure; single-event multilevel surgery for fixed deformities.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
The Salter–Harris classification describes fractures involving the growth plate (physis) in children. It is important because physeal injuries can disturb growth, and the type predicts both the risk of growth arrest and the treatment.
Salter–Harris types I–V (red = fracture line/injury). The mnemonic ‘SALTR’ aids recall. Type Mnemonic (SALTR) Line I S – Slip(ped) Through the physis only II A – Above Physis + metaphysis (commonest) III L – Lower Physis + epiphysis (intra-articular) IV T – Through Metaphysis + physis + epiphysis V R – Ram(med)/cRush Crush injury of the physis 💡Use ‘SALTR’: I Slipped, II Above, III Lower, IV Through, V cRush. Type II is the commonest; types III–V (especially V) carry the highest risk of growth arrest and joint problems.Management & Prognosis
Type I and II injuries are usually treated by closed reduction and immobilisation and generally have a good prognosis. Type III and IV are intra-articular and often need anatomical (open) reduction and fixation to restore the joint surface and physis. Type V is frequently diagnosed retrospectively and has the worst prognosis for growth disturbance. All physeal injuries warrant follow-up for growth arrest (angular deformity or limb-length discrepancy from a physeal bar).
🔑KEY POINTS TO REMEMBER- Classifies growth-plate fractures; predicts growth-arrest risk and treatment.
- SALTR: I Slipped, II Above (commonest), III Lower, IV Through, V cRush.
- I–II → closed reduction; III–IV (intra-articular) → anatomical/open fixation.
- Type V worst prognosis; follow up all physeal injuries for growth arrest.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definitions
Genu varum (‘bow legs’) is outward bowing of the legs so the knees are apart when the ankles touch; genu valgum (‘knock knees’) is the opposite — the knees touch and the ankles are apart. Both are often physiological and part of normal development, but may occasionally be pathological.
Physiological Development
There is a normal, well-recognised sequence: infants are mildly bow-legged (varum) up to about 2 years, swing to knock-knees (valgum) that is maximal around 3–4 years, and then settle to the adult alignment by about 6–7 years. This physiological pattern is symmetrical, painless and resolves spontaneously, needing only reassurance and observation.
⚠️Suspect a pathological cause if the deformity is severe, progressive, asymmetrical, painful, outside the expected age range, or associated with short stature. Causes include rickets, Blount’s disease (tibia vara), skeletal dysplasias, and physeal injury.Assessment & Management
Measure the intercondylar (in varum) or intermalleolar (in valgum) distance and observe over time; investigate atypical cases (radiographs, and biochemistry for rickets). Physiological deformity needs only reassurance; pathological deformity is treated by addressing the underlying cause and, if severe or persistent, by guided growth (hemiepiphysiodesis) or corrective osteotomy.
Blount’s Disease
Blount’s disease (tibia vara) is an important pathological cause of genu varum: a growth disorder of the posteromedial proximal tibial physis producing a sharp, progressive varus angulation localised to the upper tibia (unlike the smooth, generalised bowing of physiological varum). It occurs in an infantile form (often bilateral, associated with early walking and obesity) and an adolescent form, and is confirmed radiographically by the abnormal medial physis and metaphyseal beaking. Treatment is by bracing in early cases and guided growth or osteotomy for progressive deformity.
💡The reassuring rule: symmetrical, painless bowing or knock-knee that fits the normal age pattern needs only observation; asymmetry, pain, progression, short stature or deformity outside the expected age demands investigation for rickets, Blount’s disease or a dysplasia.Physiological variation follows a predictable age pattern. 🔑KEY POINTS TO REMEMBER- Varum = bow legs (knees apart); valgum = knock knees (ankles apart).
- Normal sequence: varum <2 y → valgum ~3–4 y → adult alignment by ~7 y.
- Red flags: severe, progressive, asymmetrical, painful, short stature.
- Pathological causes: rickets, Blount’s disease, dysplasias; treat cause ± guided growth/osteotomy.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Osgood–Schlatter disease is a common traction apophysitis (an overuse injury) of the tibial tuberosity, where the patellar tendon inserts. Repetitive traction from the powerful quadriceps on the immature apophysis causes microavulsion, inflammation and pain. It typically affects active adolescents during the growth spurt (boys ~12–15, girls ~8–12 years), often those who play running/jumping sports.
Clinical Features
Pain and a tender, prominent swelling over the tibial tuberosity, worse with activity (running, jumping, kneeling, climbing stairs) and relieved by rest. It is frequently bilateral. The diagnosis is clinical; radiographs, if taken, may show fragmentation or a prominent tuberosity but are mainly used to exclude other pathology.
💡A self-limiting condition: it is essentially a growth-related overuse problem that resolves once the apophysis fuses at skeletal maturity. Reassurance is a large part of treatment.Management
Treatment is conservative and reassuring: activity modification / relative rest from aggravating sports, ice and simple analgesia, and quadriceps and hamstring stretching. Symptoms settle with time and the condition resolves at maturity; a residual bony prominence may persist. Surgery (rarely) is reserved for a persistently symptomatic unfused ossicle in adults.
Related Apophysitis – Sever’s Disease
A useful companion condition is Sever’s disease (calcaneal apophysitis), the equivalent traction/overuse apophysitis at the insertion of the Achilles tendon on the calcaneus, causing activity-related heel pain in the same active-child age group. Like Osgood–Schlatter, it is benign and self-limiting and is managed with rest, heel cushioning, calf stretching and reassurance, resolving as the apophysis matures. Recognising these as growth-related overuse problems avoids unnecessary investigation.
⚠️Persistent, severe or night pain, or pain not clearly related to activity, should prompt reconsideration of the diagnosis — tumours and infection, though rare, must not be dismissed as ‘growing pains’.💡Osgood–Schlatter is a benign, self-limiting growth-related overuse problem of the tibial tuberosity — the mainstay is reassurance and relative rest, and it resolves when the apophysis fuses at skeletal maturity.Occurs in active adolescents; resolves when the apophysis fuses. 🔑KEY POINTS TO REMEMBER- Traction apophysitis of the tibial tuberosity (patellar tendon insertion).
- Active adolescents in the growth spurt; often bilateral.
- Activity-related anterior knee pain + tender prominent tuberosity; clinical diagnosis.
- Self-limiting → rest, ice, analgesia, stretching; resolves at maturity.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Congenital muscular torticollis (‘wry neck’) is a deformity present in infancy in which contracture/fibrosis of the sternocleidomastoid (SCM) muscle causes the head to tilt towards the affected side and rotate (chin) to the opposite side. It is the commonest cause of torticollis in infants and is often associated with a difficult/breech delivery and with DDH.
Clinical Features
The characteristic head posture is noticed in the first weeks of life; a firm, non-tender ‘sternomastoid tumour’ (a fibrous swelling in the muscle) may be palpable and then gradually disappears. Persistent deformity can lead to plagiocephaly (facial and skull asymmetry). Always examine the hips (associated DDH) and exclude other causes of a tilted head.
⚠️Not all torticollis is muscular. Consider and exclude other causes — ocular (squint), neurological/posterior fossa lesions, atlanto-axial or vertebral anomalies, and infection — particularly if it appears later, is painful, or the SCM is not tight.Management
Most cases resolve with conservative treatment: gentle passive stretching of the tight SCM, positioning and physiotherapy, started early. The great majority improve within the first year. Surgical release of the sternocleidomastoid is reserved for the minority with a persistent contracture (typically after about 1 year of failed conservative treatment) to prevent fixed deformity and facial asymmetry.
Plagiocephaly & Positional Care
Persistent torticollis holds the infant’s head consistently to one side, and the resulting sustained pressure can produce positional plagiocephaly — flattening and asymmetry of the skull and face. Early treatment of the torticollis, together with positioning strategies (encouraging the baby to turn towards the restricted side during play and feeding, and supervised tummy time), corrects the neck tightness and allows the skull to remodel, so that most children end up with normal head shape and full neck movement.
💡The classic posture points to the side of the lesion: the head tilts towards the tight sternocleidomastoid and the chin turns away from it. Early stretching and positioning correct the great majority and prevent the facial and skull asymmetry of untreated cases.Early stretching physiotherapy is usually curative. 🔑KEY POINTS TO REMEMBER- Fibrosis/contracture of sternocleidomastoid; head tilts to same side, chin to opposite side.
- Palpable ‘sternomastoid tumour’; associated with breech delivery and DDH (check hips).
- Exclude ocular, neurological and vertebral causes.
- Early stretching/physiotherapy resolves most; surgical release if persistent.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Transient synovitis (irritable hip) is a common, benign, self-limiting inflammation of the hip synovium in young children, often following a recent viral upper respiratory infection. It is the commonest cause of acute hip pain and limp in children aged 3–8 years. Its importance lies chiefly in distinguishing it from septic arthritis.
Clinical Features
A child with acute limp and hip/thigh/knee pain, mild restriction of movement, but who is systemically well, afebrile (or only mildly febrile) and can usually bear weight — in clear contrast to the toxic, febrile child of septic arthritis. Inflammatory markers are normal or only mildly raised.
⚠️The crucial task is to exclude septic arthritis. Apply the Kocher criteria (non-weight-bearing, fever >38.5°C, ESR >40, WCC >12); where doubt remains, ultrasound and joint aspiration are used, because missing a septic hip is far more harmful than a negative tap.Management
Once septic arthritis is excluded, transient synovitis is treated with rest, analgesia/NSAIDs and observation; it settles within 1–2 weeks. Follow-up ensures resolution and that a Perthes disease (which can present similarly) is not evolving.
Diagnosis of Exclusion
Transient synovitis is fundamentally a diagnosis of exclusion: the same presentation — a limping, hip-painful child — can be produced by conditions that are far more serious, above all septic arthritis and osteomyelitis, and also early Perthes disease. Ultrasound typically shows a small effusion; blood tests are reassuringly normal. Because the consequences of missing a septic hip are severe, clinicians keep a low threshold for aspiration and for review if symptoms fail to settle in the expected week or two.
💡The whole clinical task in an ‘irritable hip’ is a single question: is this benign transient synovitis or a septic joint? A systemically well, weight-bearing child with normal inflammatory markers reassures; fever, toxicity and raised markers demand urgent aspiration.Kocher criteria distinguish it from septic arthritis — the critical decision. 🔑KEY POINTS TO REMEMBER- Benign self-limiting hip synovitis, often post-viral; children 3–8 y; commonest cause of childhood limp.
- Systemically well, afebrile, usually weight-bearing — unlike septic arthritis.
- Exclude septic arthritis (Kocher criteria ± aspiration).
- Rest, NSAIDs, observation; resolves in 1–2 weeks; follow up to exclude Perthes.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Flat foot (pes planus) is a loss of the medial longitudinal arch so that the sole appears flat and the hindfoot is in valgus. In children it is usually flexible and physiological; the crucial distinction is between a flexible flat foot (arch restored when non-weight-bearing) and a rigid flat foot (arch absent in all positions), which suggests underlying pathology.
Flexible vs Rigid
Flexible flat foot — common, usually asymptomatic, the arch reappears on tiptoeing or great-toe dorsiflexion (Jack’s test) and when the foot hangs free. It is a normal variant needing only reassurance. Rigid flat foot — the arch does not reform; causes include a tarsal coalition (an abnormal bony/fibrous bridge, often presenting with a painful ‘peroneal spastic’ flat foot in older children), congenital vertical talus, or inflammatory/neurological disease.
💡The key clinical test: if the arch reforms on tiptoe (or with Jack’s test), the flat foot is flexible and benign; if it stays flat, it is rigid and warrants investigation for a tarsal coalition or other cause.Management
Flexible, painless flat feet need only reassurance — no orthoses or special shoes are required to ‘create’ an arch. Symptomatic flexible flat feet may benefit from arch supports, stretching and supportive footwear. Rigid or painful flat feet are investigated (radiographs, CT for coalition) and treated according to the cause, occasionally surgically (e.g. resection of a symptomatic coalition).
Tarsal Coalition
Tarsal coalition — an abnormal bony, cartilaginous or fibrous bridge between tarsal bones (commonly calcaneonavicular or talocalcaneal) — is the classic cause of a rigid, painful (‘peroneal spastic’) flat foot that becomes symptomatic in later childhood or adolescence as the bridge ossifies and restricts subtalar movement. It is confirmed on oblique radiographs or CT and treated first conservatively (orthoses, activity modification, immobilisation for flares) and, if that fails, by surgical resection of the coalition or, in advanced cases, arthrodesis.
💡One test settles most cases: if the arch reappears on tiptoe (or Jack’s test), the flat foot is flexible and benign and needs only reassurance; a foot that stays flat in every position is rigid and warrants a search for a tarsal coalition or other cause.The tiptoe test separates flexible from rigid flat foot. 🔑KEY POINTS TO REMEMBER- Loss of the medial longitudinal arch; usually flexible & physiological in children.
- Flexible: arch reforms on tiptoe/Jack’s test — reassure; rigid: arch fixed — investigate.
- Rigid causes: tarsal coalition, congenital vertical talus, inflammatory/neurological disease.
- Painless flexible feet need no treatment; treat symptomatic/rigid feet by cause.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Obstetric brachial plexus palsy is injury to the brachial plexus during difficult delivery (shoulder dystocia, large baby, breech). The commonest form is Erb’s palsy, an injury to the upper roots C5–C6 (± C7), causing paralysis of the shoulder abductors/external rotators and elbow flexors.
Clinical Features
The affected arm hangs in the classic ‘waiter’s tip’ position: adducted and internally rotated at the shoulder, extended at the elbow, pronated forearm and flexed wrist. The Moro and biceps reflexes are absent on that side while grasp is preserved (the hand is spared). In contrast, Klumpke’s palsy (lower roots C8–T1) affects the intrinsic hand muscles (claw hand) and may show a Horner’s syndrome.
💡Erb’s = upper roots (C5–C6), ‘waiter’s tip’, hand spared; Klumpke’s = lower roots (C8–T1), claw hand ± Horner’s. Erb’s is much commoner and has the better prognosis.Management
Most Erb’s palsies recover spontaneously. Early management is gentle physiotherapy — maintaining a full passive range of movement to prevent contractures — while awaiting recovery. If there is no meaningful recovery of biceps function by about 3 months, referral for consideration of microsurgical nerve repair/grafting is indicated. Later, secondary procedures (tendon transfers, osteotomies) may correct residual deformity.
Assessment & Prognosis
Careful serial examination documents which movements are recovering; return of biceps (elbow flexion) function is the key milestone and the main determinant of the decision to operate. The overall prognosis for Erb’s palsy is good — the majority recover useful function — whereas total (pan-plexus) injuries and those with a Horner’s syndrome (implying a lower-root, often preganglionic, avulsion) carry a worse outlook. Throughout, the priority is to keep the joints supple with passive movement so that a recovering nerve meets a mobile, not a contracted, limb.
💡Distinguish the two birth palsies at a glance: Erb’s (upper C5–C6) gives the ‘waiter’s tip’ arm with a spared hand and a good prognosis, whereas Klumpke’s (lower C8–T1) gives a claw hand, sometimes with Horner’s syndrome, and a worse outlook.Most recover spontaneously; explore if no biceps function by 3 months. 🔑KEY POINTS TO REMEMBER- Birth injury to the brachial plexus; Erb’s = upper roots C5–C6 (± C7).
- ‘Waiter’s tip’ posture; absent Moro/biceps reflex; hand (grasp) spared.
- Klumpke’s (C8–T1) = claw hand ± Horner’s (rarer, worse).
- Most recover; physiotherapy to prevent contractures; nerve surgery if no biceps by ~3 months.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.