Common Orthopaedic Deformities and Their Patho-Anatomy – A Clinical Guide

A deformity is an abnormal alteration in the shape, alignment, length or rotational relationship of a body segment. In orthopaedics, deformities may arise from congenital abnormalities, growth disturbance, trauma, infection, metabolic disease, neuromuscular imbalance, degenerative disease or abnormal mechanical loading.

Understanding a deformity requires more than simply naming its visible appearance. The orthopaedician must identify the underlying patho-anatomy — which bone, joint, physis, muscle, tendon, ligament or neurological structure has become abnormal and how this produces the observed clinical deformity.

A systematic analysis should determine whether the deformity is:

• Angular.
• Translational.
• Rotational.
• Length-related.
• Joint-related.
• Dynamic or fixed.
• Primary or compensatory.
• Congenital, developmental or acquired.

A deformity should be described anatomically before it is labelled diagnostically.

Deformity can develop through abnormalities affecting one or more components of the musculoskeletal system.

Dynamic Deformity

A dynamic deformity results primarily from abnormal muscle activity, weakness or imbalance and may be corrected passively when the offending muscle force is removed.

Examples include early spastic equinus and dynamic clawing of the toes.

Fixed Deformity

With time, muscle-tendon shortening, capsular contracture, ligament adaptation and bony remodelling may convert a dynamic deformity into a fixed structural deformity.

Many neuromuscular deformities begin dynamically and become structural as the child grows.

Varus and valgus describe the relationship of the distal segment relative to the proximal segment.

• Varus: distal segment deviates toward the midline.
• Valgus: distal segment deviates away from the midline.

Thus:

• Genu varum → distal tibia lies medially relative to femur.
• Genu valgum → distal tibia lies laterally relative to femur.
• Cubitus varus → forearm deviates medially relative to arm.
• Cubitus valgus → forearm deviates laterally relative to arm.

Cubitus varus is a deformity in which the normal carrying angle of the elbow is reduced or reversed. It most commonly develops following malunion of a childhood supracondylar humerus fracture.

Patho-anatomy

Cubitus varus is not simply a coronal-plane deformity. It is typically a three-dimensional deformity involving:

• Varus angulation.
• Internal rotation of the distal fragment.
• Extension deformity.

Medial tilting of the distal humeral fragment produces loss of the carrying angle. Rotational and sagittal components contribute to the characteristic appearance.

Clinical Consequences

• Cosmetic gunstock appearance.
• Altered elbow biomechanics.
• Posterolateral rotatory instability in some patients.
• Rare tardy ulnar nerve or lateral condylar problems.

Cubitus varus is classically a malunion problem rather than a growth-arrest deformity.

Cubitus valgus is excessive lateral deviation of the forearm relative to the arm.

Classic Cause

The classic acquired cause is nonunion or malunion of a lateral condyle fracture of the humerus in childhood.

Patho-anatomy

Failure of union or growth disturbance on the lateral side of the distal humerus alters the distal humeral articular orientation. Progressive valgus may develop with growth.

The increased carrying angle stretches the ulnar nerve behind the medial epicondyle, potentially causing tardy ulnar nerve palsy.

Cubitus valgus + childhood lateral condyle nonunion → think tardy ulnar neuropathy.

Clawing of the fingers is characterised by:

• Hyperextension at the metacarpophalangeal joint.
• Flexion at the proximal and distal interphalangeal joints.

Normal Muscle Balance

The lumbricals and interossei flex the MCP joints while extending the interphalangeal joints through the extensor expansion.

Patho-anatomy

Paralysis of the intrinsic muscles allows:

• Extensor digitorum to hyperextend the MCP joint.
• FDS and FDP to flex the IP joints unopposed.

Partial Claw

Ulnar nerve palsy causes clawing predominantly of the ring and little fingers because the medial lumbricals and interossei are paralysed.

Complete Claw

Combined median and ulnar nerve palsy causes paralysis of essentially all intrinsic muscles, producing clawing of all four fingers.

Ape thumb deformity occurs in severe median nerve palsy due to loss of thenar muscle function.

Patho-anatomy

• Thenar muscle paralysis and wasting.
• Loss of opposition.
• Loss of palmar abduction.
• Thumb lies in the plane of the palm.

The thumb becomes adducted and externally rotated with loss of normal opposition mechanics.

The hand of benediction is best considered a dynamic posture seen when attempting to make a fist in a proximal median nerve palsy rather than a fixed resting deformity.

Patho-anatomy

Paralysis of FDS and the median-innervated part of FDP prevents effective flexion of the index and middle fingers, while the ulnar-innervated FDP to the ring and little fingers remains active.

Wrist drop occurs in radial nerve palsy due to paralysis of the wrist extensors.

Patho-anatomy

Loss of wrist extension permits the wrist to fall into flexion under the influence of gravity and intact wrist flexors.

Loss of MCP extension may also occur depending on the level of radial nerve injury.

Wrist flexion also reduces the mechanical efficiency of finger flexors because of active insufficiency, weakening grip.

Mallet finger is characterised by loss of active extension at the distal interphalangeal joint.

Patho-anatomy

The terminal extensor tendon is disrupted or avulsed from the base of the distal phalanx. This may occur as a purely tendinous injury or with a bony avulsion.

The intact flexor digitorum profundus pulls the DIP joint into flexion, producing the characteristic drooping fingertip.

Swan-neck deformity consists of:

• PIP joint hyperextension.
• DIP joint flexion.

Patho-anatomy

Multiple mechanisms can produce the deformity:

• Volar plate laxity at the PIP joint.
• Intrinsic muscle tightness.
• Excessive pull through the central slip.
• Chronic mallet finger producing extensor mechanism imbalance.

Chronic terminal tendon insufficiency can shift extensor forces proximally and contribute to PIP hyperextension while the DIP remains flexed.

Boutonnière deformity consists of:

• PIP flexion.
• DIP hyperextension.

Patho-anatomy

Rupture or attenuation of the central slip over the PIP joint allows the lateral bands to migrate volarly.

Once positioned volar to the axis of PIP rotation, the lateral bands become PIP flexors. Their distal pull on the terminal extensor mechanism contributes to DIP hyperextension.

Central slip failure → PIP flexion + DIP hyperextension.

Z-thumb is commonly associated with rheumatoid arthritis.

Typical Configuration

• MCP flexion and subluxation.
• IP hyperextension.

Synovitis, capsuloligamentous attenuation, tendon imbalance and joint destruction progressively alter thumb alignment.

Ulnar deviation of the fingers at the MCP joints is a classic deformity of rheumatoid arthritis.

Patho-anatomy

• Chronic MCP synovitis.
• Attenuation of radial collateral structures.
• Volar subluxation of proximal phalanges.
• Ulnar displacement of extensor tendons.
• Intrinsic muscle imbalance.

Once the extensor tendons migrate ulnarly, they themselves generate an ulnarly directed deforming force, worsening the drift.

Genu varum is a coronal-plane deformity in which the knees remain separated when the ankles are approximated.

Patho-anatomy

The deformity may originate from the distal femur, proximal tibia, knee joint itself or a combination of these.

Common Causes

• Physiological infantile bowing.
• Blount disease.
• Rickets.
• Post-traumatic malunion.
• Physeal arrest.
• Medial compartment knee osteoarthritis.

Biomechanical Consequence

The mechanical axis moves medially, increasing the knee adduction moment and loading the medial compartment.

In medial compartment osteoarthritis, this can produce a vicious cycle:

Genu valgum is characterised by lateral deviation of the distal tibia so that the knees approximate while the ankles remain apart.

Common Causes

• Physiological childhood valgus.
• Rickets.
• Post-traumatic deformity.
• Physeal arrest.
• Skeletal dysplasia.
• Lateral compartment knee degeneration.

Biomechanics

The mechanical axis shifts laterally, increasing loading of the lateral tibiofemoral compartment. Significant valgus can also influence patellofemoral tracking and increase lateral vector forces.

Genu recurvatum refers to pathological hyperextension of the knee.

Patho-anatomical Mechanisms

• Anterior physeal arrest of proximal tibia producing posterior tibial slope abnormality.
• Ligamentous laxity.
• Quadriceps weakness causing compensatory knee locking.
• Equinus at the ankle altering the ground-reaction force.
• Neuromuscular imbalance.

In neuromuscular disease, the patient may hyperextend the knee deliberately to create a stable limb when quadriceps control is poor.

A flexion deformity is inability to achieve full knee extension.

Patho-anatomy

• Posterior capsular contracture.
• Hamstring shortening.
• Joint effusion causing a position of comfort in flexion.
• Fixed bony deformity.
• Articular destruction.
• Neuromuscular spasticity.

Flexed-knee posture increases quadriceps demand during standing and can substantially increase energy expenditure.

The varus arthritic knee is one of the most common adult deformities encountered in orthopaedic practice.

Patho-anatomy

• Medial compartment cartilage loss.
• Medial joint-space narrowing.
• Subchondral sclerosis.
• Osteophyte formation.
• Medial tibial bone loss in advanced disease.
• Lateral soft-tissue stretching.
• Medial soft-tissue contracture.

Progressive varus shifts the mechanical axis medially and further increases medial compartment loading.

Patho-anatomy

• Lateral compartment cartilage loss.
• Lateral femoral condylar hypoplasia or bone loss in some cases.
• Contracted lateral soft tissues.
• Attenuated medial structures.
• External tibial rotation may coexist.
• Patellar maltracking may occur.

The common peroneal nerve may be under increased tension when a severe valgus deformity is corrected.

Coxa vara is a reduction in the femoral neck-shaft angle.

Patho-anatomy

A reduced neck-shaft angle increases the bending moment across the femoral neck and changes abductor mechanics.

Consequences

• Relative limb shortening.
• High-riding greater trochanter.
• Reduced abductor lever arm efficiency.
• Trendelenburg gait.
• Increased shear forces across the femoral neck.

Coxa valga refers to an increased femoral neck-shaft angle.

It may be seen in neuromuscular conditions such as cerebral palsy where abnormal loading and altered proximal femoral development contribute to progressive valgus and femoral anteversion.

Consequences

• Reduced femoral head coverage.
• Reduced effective abductor lever arm.
• Increased hip instability in susceptible patients.
• Association with progressive hip displacement in cerebral palsy.

Femoral anteversion describes the angular relationship between the femoral neck axis and the distal femoral condylar axis in the transverse plane.

Excessive anteversion may cause the patient to internally rotate the hip so that the femoral head is more congruently positioned within the acetabulum.

Clinical Appearance

• In-toeing gait.
• Increased hip internal rotation.
• Reduced external rotation.
• Patellae may face inward during walking.

Tibial torsion refers to rotation of the distal tibia relative to the proximal tibia.

Internal Tibial Torsion

Produces an in-toeing foot progression angle despite the patella pointing more anteriorly.

External Tibial Torsion

Produces out-toeing and may contribute to patellofemoral malalignment when combined with proximal femoral abnormalities.

Equinus is limitation of ankle dorsiflexion such that the foot remains relatively plantarflexed.

Patho-anatomy

• Gastrocnemius contracture.
• Combined gastrocnemius-soleus contracture.
• Achilles tendon shortening.
• Spastic plantarflexor activity.
• Posterior capsular contracture.
• Bony impingement in rigid cases.

The Silfverskiöld test helps differentiate isolated gastrocnemius tightness from combined gastrocnemius-soleus restriction.

Pes cavus is an abnormally high medial longitudinal arch. Cavovarus additionally includes hindfoot varus.

Typical Patho-anatomy

• Plantarflexed first ray.
• High medial arch.
• Forefoot pronation relative to hindfoot.
• Compensatory hindfoot varus.
• Claw toes may coexist.

In many neuromuscular cavovarus feet, weakness of tibialis anterior and peroneus brevis with relative preservation of peroneus longus and tibialis posterior produces a plantarflexed first ray and hindfoot varus.

Cavovarus is commonly a muscle-imbalance deformity and should prompt consideration of an underlying neurological disorder.

Pes planovalgus consists of flattening of the medial longitudinal arch associated with hindfoot valgus.

Patho-anatomy

• Hindfoot valgus.
• Talonavicular uncoverage.
• Forefoot abduction.
• Medial arch collapse.
• Relative talar plantarflexion.

In adult acquired flatfoot, posterior tibial tendon dysfunction and progressive failure of medial ligamentous supports can allow increasing hindfoot valgus and forefoot abduction.

Clubfoot is a complex congenital three-dimensional deformity classically described by CAVE:

• Cavus.
• Adductus.
• Varus.
• Equinus.

Patho-anatomy

The deformity is centred around abnormal relationships of the talus, calcaneus, navicular and forefoot.

• Talus is relatively plantarflexed.
• Navicular is medially displaced around the talar head.
• Calcaneus is adducted and in varus beneath the talus.
• Forefoot is adducted.
• First ray plantarflexion contributes to cavus.
• Posteromedial soft tissues are contracted.

Clubfoot is not simply an equinus-varus ankle deformity; it is a complex deformity involving the entire foot.

Hallux valgus consists of lateral deviation of the great toe associated with medial deviation of the first metatarsal.

Patho-anatomy

• Metatarsus primus varus.
• Lateral deviation of proximal phalanx.
• Medial eminence prominence.
• Sesamoid complex becomes relatively displaced laterally.
• Adductor hallucis and flexor/extensor tendons increasingly act as deforming forces.
• Capsular imbalance develops.

As the toe deviates laterally, tendons that normally cross close to the centre of rotation shift laterally, reinforcing the deformity.

Hammer toe is classically characterised by:

• MCP extension.
• PIP flexion.
• DIP may be neutral or extended.

It results from imbalance between intrinsic and extrinsic muscles, often combined with footwear-related pressure and progressive capsular contracture.

Claw toe consists of:

• MTP hyperextension.
• PIP flexion.
• DIP flexion.

It is commonly associated with intrinsic muscle weakness, cavus foot and neuromuscular disease.

Mallet toe primarily consists of flexion deformity of the DIP joint, often resulting from flexor tendon imbalance and progressive contracture.

Charcot neuroarthropathy is a destructive deforming arthropathy occurring in an insensate foot, commonly related to diabetic neuropathy.

Patho-anatomy

• Loss of protective sensation.
• Repetitive unrecognised trauma.
• Bone fragmentation and joint destruction.
• Subluxation and collapse.
• Midfoot collapse may create a rocker-bottom configuration.

Plantar bony prominence may then create areas of extreme pressure and ulceration.

Kyphosis is excessive posterior convexity of the spine in the sagittal plane.

Patho-anatomical Causes

• Vertebral compression fracture.
• Congenital anterior vertebral formation failure.
• Scheuermann disease.
• Spinal tuberculosis.
• Post-traumatic collapse.
• Degenerative sagittal imbalance.

Angular focal kyphosis is often termed a gibbus, particularly when produced by severe anterior vertebral destruction.

Structural scoliosis is a three-dimensional spinal deformity characterised by coronal curvature associated with vertebral rotation.

Patho-anatomy

• Lateral spinal curvature.
• Vertebral rotation.
• Rib rotation producing a rib prominence.
• Sagittal-plane abnormalities may coexist.

As vertebrae rotate toward the convexity, the ribs rotate posteriorly on the convex side, producing the characteristic rib hump on forward bending.

Structural scoliosis is a three-dimensional deformity, not merely a lateral bend of the spine.

Hyperlordosis represents excessive anterior convexity of the lumbar spine.

Possible Mechanisms

• Hip flexion contracture.
• Anterior pelvic tilt.
• Compensation for thoracic kyphosis.
• Neuromuscular disorders.
• Spondylolisthesis-related postural compensation.

A hip flexion contracture may cause anterior pelvic tilt, and lumbar hyperlordosis develops to maintain an upright trunk.

Congenital muscular torticollis results from shortening and fibrosis of the sternocleidomastoid muscle.

Characteristic Deformity

Because the SCM produces ipsilateral lateral flexion and contralateral rotation:

• Head tilts toward the affected side.
• Chin rotates toward the opposite side.

Long-standing cases can develop secondary craniofacial asymmetry and plagiocephaly.

Developmental dysplasia of the hip represents a spectrum from acetabular dysplasia to subluxation and complete dislocation.

Patho-anatomy in Established Dislocation

• Shallow acetabulum.
• Abnormal femoral head position.
• Increased femoral anteversion may be present.
• Capsular elongation.
• Hypertrophied ligamentum teres.
• Inverted or hypertrophied labrum may obstruct reduction.
• Contracture of adductors and iliopsoas.

Persistent abnormal head-acetabulum contact interferes with normal acetabular development, so dysplasia and instability can perpetuate one another.

Crouch gait is characterised by excessive hip and knee flexion during stance, often accompanied by excessive ankle dorsiflexion.

Patho-anatomy

• Hamstring contracture or apparent hamstring tightness.
• Hip flexion contracture.
• Quadriceps weakness.
• Lever-arm dysfunction.
• Excessive tibial torsion.
• Planovalgus foot.
• Weak plantarflexor-knee extension coupling.

Overlengthening of the Achilles tendon can worsen crouch by reducing plantarflexor strength and decreasing the ability of the ankle-foot complex to support knee extension during stance.

Spastic equinus commonly develops due to excessive activity and later contracture of the gastrocnemius-soleus complex.

Initially the deformity may be dynamic. Over time:

Poliomyelitis causes selective lower motor neuron paralysis, producing deformity according to which muscle groups are weak and which antagonists remain functional.

Examples

• Quadriceps paralysis → knee instability and compensatory recurvatum.
• Dorsiflexor paralysis → equinus or foot drop depending on muscle balance.
• Peroneal weakness with preserved invertors → varus foot.
• Hip abductor weakness → Trendelenburg gait.

The final deformity is therefore determined by the pattern of residual muscle imbalance rather than by paralysis alone.

Charcot-Marie-Tooth disease produces a characteristic progressive cavovarus foot through selective muscle weakness and imbalance.

A typical sequence includes:

1. Relative weakness of tibialis anterior and peroneus brevis.
2. Relative preservation of peroneus longus and tibialis posterior.
3. First ray plantarflexion.
4. Forefoot-driven hindfoot varus.
5. Progressive cavus and clawing.

Volkmann ischaemic contracture is a late consequence of untreated or severe forearm compartment syndrome.

Patho-anatomy

Flexor muscles are commonly affected, producing wrist and finger flexion deformity. Median and ulnar nerve injury may coexist.

The deformity often becomes more obvious when the wrist is extended because shortened flexor tendons increase finger flexion.

Malunion occurs when a fracture heals in an abnormal position.

Components

• Angulation.
• Translation.
• Rotation.
• Shortening.
• Combination deformity.

The functional effect depends on the bone involved and the proximity of the malunion to a joint.

Rotational deformity is particularly poorly tolerated in the forearm and lower limb because it alters the orientation of the distal joint and functional axis.

A partial physeal arrest occurs when a portion of the growth plate stops growing while the remaining physis continues longitudinal growth.

Patho-anatomy

The physeal bar acts as a tether. Continued growth on the opposite side progressively produces angular deformity.

A complete physeal arrest, in contrast, predominantly produces limb-length discrepancy rather than progressive angular deformity.

Partial physeal arrest → angular deformity; complete arrest → primarily shortening.

Rickets causes defective mineralisation of growing bone and particularly affects the physis and metaphysis.

Patho-anatomy

• Weak metaphyseal bone.
• Physeal widening and disorganisation.
• Metaphyseal cupping and fraying.
• Mechanical loading produces progressive bowing.

Depending on age and loading pattern, lower-limb deformity may present as genu varum or genu valgum.

Blount disease is a growth disorder affecting the posteromedial proximal tibial physis, producing progressive tibia vara.

Patho-anatomy

• Disordered medial proximal tibial physeal growth.
• Medial metaphyseal depression.
• Progressive varus.
• Internal tibial torsion may coexist.
• Advanced cases develop joint-line deformity and medial plateau depression.

Increased medial loading further suppresses medial physeal growth, creating a vicious cycle of progressive deformity.

Trendelenburg gait is caused by failure of the hip abductors to stabilise the pelvis during single-leg stance.

Patho-anatomical Causes

• Gluteus medius/minimus weakness.
• Superior gluteal nerve palsy.
• Coxa vara reducing abductor efficiency.
• Hip dislocation or dysplasia.
• Greater trochanteric migration.

During stance on the affected side, the contralateral pelvis drops. The patient may compensate by leaning the trunk toward the affected side to reduce the external hip adduction moment.

Foot drop results from weakness or paralysis of ankle dorsiflexors.

Patho-anatomy

Loss of tibialis anterior and other dorsiflexor function causes the foot to plantarflex during swing. To prevent toe dragging, the patient increases hip and knee flexion, producing a high-stepping gait.

Common causes include common peroneal nerve palsy, L4/L5 neurological pathology and neuromuscular disease.

Limb-length discrepancy may be caused by true bony shortening or apparent shortening due to joint position or pelvic obliquity.

Possible Compensations

• Pelvic obliquity.
• Functional scoliosis.
• Equinus of the short limb.
• Knee flexion of the long limb.
• Hip adduction or abduction contracture altering apparent length.

Therefore, the visible deformity may be compensatory rather than located at the site of the primary pathology.

A contracture is a fixed limitation of joint movement caused by shortening or structural change in muscle, tendon, capsule, ligament, skin or fascia.

Examples

• Hip flexion contracture.
• Knee flexion contracture.
• Achilles contracture causing equinus.
• Burn scar contracture.
• Volkmann ischaemic contracture.
• Post-immobilisation capsular contracture.

An important part of deformity analysis is distinguishing the primary deformity from compensation elsewhere.

Example: Hip Flexion Contracture

Example: Limb Shortening

Treating the compensation without recognising the primary deformity may worsen overall alignment.

A deformity should be analysed systematically rather than simply named.

1. Identify the anatomical region.
2. Describe the plane: coronal, sagittal or rotational.
3. Identify the apex and direction.
4. Assess whether the deformity is fixed or flexible.
5. Determine whether it originates from bone, joint or soft tissue.
6. Assess limb length.
7. Assess rotation.
8. Look for compensatory deformities.
9. Evaluate neurological and muscle function.
10. Determine the functional consequence.

Imaging should demonstrate the deformity under conditions relevant to function.

Common Investigations

• Standard AP and lateral radiographs.
• Weight-bearing radiographs.
• Full-length standing alignment films.
• Specialised foot or spine views.
• CT for complex rotational or multiplanar deformity.
• MRI where cartilage, physis, ligament or neural pathology is relevant.

In lower-limb angular deformity, full-length standing radiographs allow assessment of the mechanical axis, joint orientation and location of the deformity.

The Centre of Rotation of Angulation (CORA) is the intersection of the proximal and distal anatomical or mechanical axes in an angular deformity.

CORA analysis helps distinguish where the deformity originates rather than simply observing where the limb appears crooked.

If correction is performed at the CORA, angular correction can occur without creating secondary translation. Correction away from the CORA generally requires translation to restore alignment.

Many clinically important deformities are not confined to one plane.

Examples

• Cubitus varus – coronal, sagittal and rotational components.
• Clubfoot – cavus, adduction, varus and equinus.
• Scoliosis – coronal curvature plus vertebral rotation and sagittal alteration.
• Cavovarus – forefoot and hindfoot components.

Treating only the visually dominant component may leave substantial residual deformity.

Neuromuscular deformity often develops because one muscle group remains active while its antagonist is weak or paralysed.

The active muscle continuously pulls the growing skeleton toward its direction of action.

This concept explains many deformities in cerebral palsy, poliomyelitis, peripheral nerve palsy and hereditary neuropathies.

• Varus and valgus are named according to the distal segment.
• Cubitus varus is usually a three-dimensional malunion following supracondylar humerus fracture.
• Cubitus valgus is classically associated with lateral condyle nonunion and tardy ulnar nerve palsy.
• Claw hand results from intrinsic muscle paralysis: MCP hyperextension with IP flexion.
• Boutonnière deformity = PIP flexion + DIP hyperextension due to central slip failure.
• Swan-neck = PIP hyperextension + DIP flexion.
• Mallet finger results from terminal extensor tendon failure.
• Partial physeal arrest commonly causes progressive angular deformity.
• Complete physeal arrest primarily produces shortening.
• Genu varum shifts the mechanical axis medially and increases medial compartment loading.
• Genu valgum shifts the mechanical axis laterally and increases lateral compartment loading.
• Coxa vara shortens the limb and reduces hip abductor efficiency.
• Excessive femoral anteversion commonly presents with increased hip internal rotation and in-toeing.
• Cavovarus should prompt evaluation for underlying neurological disease.
• Clubfoot is remembered by CAVE: Cavus, Adductus, Varus, Equinus.
• Adult acquired planovalgus may develop through posterior tibial tendon and medial ligament failure.
• Structural scoliosis includes vertebral rotation; it is not simply lateral curvature.
• Volkmann contracture results from ischaemic muscle necrosis followed by fibrosis and shortening.
• In neuromuscular disease, identify the muscle imbalance before planning correction of the visible deformity.
• Fixed deformities often represent the late structural consequence of an initially dynamic abnormality.
• Always distinguish primary deformity from compensatory deformity before surgical planning.

1. Describe before diagnosing: determine the plane, direction, apex, rotation and length abnormality.
2. Identify the anatomical origin: bone, physis, joint, muscle, tendon, ligament or nerve.
3. Determine whether the deformity is dynamic or fixed.
4. Look for muscle imbalance: particularly in neuromuscular disorders.
5. Separate primary deformity from compensation.
6. Assess growth: remaining growth can make physeal deformity progressively worse.
7. Assess mechanics: determine how the deformity changes joint loading and the mechanical axis.
8. Use appropriate imaging: preferably weight-bearing and full-length views where alignment is the clinical question.
9. Recognise multiplanar deformity: correcting one visible plane may be insufficient.
10. Correct the pathology, not merely the appearance.

Every orthopaedic deformity represents an anatomical and biomechanical problem. Successful treatment begins by identifying what structure is abnormal, why the deformity developed, whether it is flexible or fixed, and how it alters the function of the entire limb.