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.
Definitions
Rehabilitation is the process of restoring a person with a disability to the fullest possible physical, psychological, social and vocational function. Two key tools are orthoses and prostheses. An orthosis is an external appliance applied to a body part to support, align, correct or improve function of an existing limb (e.g. a caliper or splint), whereas a prosthesis is an artificial device that replaces a missing part (e.g. an artificial limb). The disciplines are orthotics and prosthetics.
Orthosis Prosthesis Purpose Supports/corrects an existing part Replaces a missing part Example AFO, caliper, knee brace, spinal brace Artificial leg/arm, hand Named by region AFO, KAFO, HKAFO, TLSO Trans-tibial, trans-femoral prosthesis Goal Stability, deformity control, function Restore lost function & appearance Orthoses
Orthoses are named by the joints they span: an AFO (ankle-foot orthosis), KAFO (knee-ankle-foot), HKAFO (hip-knee-ankle-foot), and TLSO (thoraco-lumbo-sacral orthosis, a spinal brace). Their functions are to stabilise a flail or unstable joint (e.g. a caliper for a polio limb or foot drop), to correct or prevent deformity (e.g. a scoliosis brace), to relieve pain/off-load a part, and to improve function (e.g. an AFO for foot drop that assists a normal gait).
Prostheses & Amputee Rehabilitation
A limb prosthesis has a socket (the crucial interface with the stump), a suspension mechanism, joints (knee/ankle units), and a terminal device (foot or hand). Successful use depends on a well-shaped, healthy stump, a correctly fitting socket, and gait training. Rehabilitation of an amputee is a multidisciplinary, staged process: pre-operative counselling; post-operative stump care, oedema control and shaping; provision of a temporary then definitive prosthesis; and gait/functional training, alongside psychological and vocational support.
💡Remember the distinction cleanly: an orthosis assists an existing limb (‘ortho’ = to straighten/support), while a prosthesis replaces a missing one. Both are named functionally — e.g. AFO spans the ankle and foot.Principles of Rehabilitation
Effective rehabilitation is goal-oriented, patient-centred and multidisciplinary (surgeon, physiotherapist, occupational therapist, prosthetist/orthotist, social worker, psychologist). It aims to maximise independence in mobility and daily activities, prevent secondary complications (contractures, pressure sores), and support social and vocational reintegration. The WHO framework considers not just the impairment but the resulting activity limitation and participation restriction.
Complications & Practical Points
Poorly fitting appliances cause pressure sores and stump ulceration, and heavy or uncomfortable devices are abandoned, so comfort, weight and cosmesis all affect compliance. Appliances need regular review and adjustment, especially in growing children and as a stump matures or the disease progresses.
Assistive Devices & Mobility Aids
Beyond orthoses and prostheses, rehabilitation makes wide use of mobility and assistive devices that improve independence and safety. Walking aids — sticks, elbow and axillary crutches, and frames (walkers) — offload a painful or weak limb, improve balance and widen the base of support; a stick is conventionally held in the hand opposite the affected leg to reduce load through the painful hip. Wheelchairs restore mobility to those who cannot walk, and a range of aids to daily living (raised toilet seats, grab rails, adapted cutlery, dressing aids) provided by occupational therapists allow patients to manage everyday tasks despite impairment.
💡Keep the vocabulary straight for the exam: an orthosis supports or corrects a limb that is still present and is named by the joints it crosses (AFO, KAFO, TLSO), whereas a prosthesis replaces a part that has been lost — and the success of either depends on comfort, fit and the patient actually using it.Prosthesis replaces; orthosis supports — the fundamental distinction. 🔑KEY POINTS TO REMEMBER- Orthosis supports/corrects an existing limb; prosthesis replaces a missing one.
- Orthoses named by joints spanned: AFO, KAFO, HKAFO, TLSO (spinal).
- Prosthesis = socket + suspension + joints + terminal device; fit & stump health are key.
- Amputee rehab is staged & multidisciplinary: stump care → prosthesis → gait training + support.
- Poor fit → pressure sores; review/adjust regularly (esp. children & maturing stumps).
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.The Normal Gait Cycle
Gait is the manner of walking. The gait cycle is the sequence of events between one heel-strike and the next heel-strike of the same foot, and is divided into two phases: the stance phase (~60%), when the foot is on the ground (heel-strike → foot-flat → mid-stance → heel-off → toe-off), and the swing phase (~40%), when the foot is off the ground and advancing. Normal gait requires intact bones and joints, muscle power, neurological control, balance and sensation.
The gait cycle: stance phase (foot on the ground, ~60%) and swing phase (foot advancing, ~40%). Pathological Gaits
Disorders of any component produce characteristic gaits. An antalgic (painful) gait shortens the stance phase on the painful limb to reduce time bearing weight. A Trendelenburg gait (weak hip abductors — gluteus medius/minimus) drops the pelvis on the opposite (swing) side, and a bilateral/compensated form gives a waddling gait. A high-stepping (steppage) gait (foot drop) lifts the knee high to clear the toes. Other patterns include the short-limb (dipping) gait, the stiff-hip/knee gait, the spastic scissoring gait (cerebral palsy), the ataxic broad-based gait (cerebellar), and the shuffling festinant gait of Parkinsonism.
Gait Cause Antalgic Pain — shortened stance on the affected side Trendelenburg Weak hip abductors → pelvis drops on opposite (swing) side Waddling Bilateral abductor weakness / proximal myopathy / DDH High-stepping (steppage) Foot drop (common peroneal palsy) Scissoring Spasticity (cerebral palsy) Broad-based ataxic Cerebellar / proprioceptive loss 💡The Trendelenburg sign: with weak abductors, standing on the affected leg makes the pelvis drop on the opposite (unsupported) side — ‘the sound side sags’. It reflects abductor weakness, a painful hip, or an unstable/dislocated hip.Clinical Assessment
Gait is examined by watching the patient walk (and, where possible, run), looking at each phase from the front, side and behind. Observation of the abnormal pattern localises the problem (pain, weakness, deformity, stiffness, shortening or neurological cause) and guides further examination (e.g. Trendelenburg test for the hip). Instrumented gait analysis is used to plan surgery in complex cases such as cerebral palsy.
Clinical Relevance
Recognising the gait pattern is a powerful diagnostic short-cut: an antalgic gait signals a painful lower limb, a Trendelenburg/waddling gait points to hip abductor pathology, and a steppage gait to foot drop. Correcting the underlying cause — and providing walking aids or orthoses — restores efficient, safe walking.
🔑KEY POINTS TO REMEMBER- Gait cycle: stance phase (~60%, foot on ground) + swing phase (~40%, foot advancing).
- Antalgic = pain (short stance); Trendelenburg = weak abductors (opposite pelvis drops).
- Steppage = foot drop; scissoring = spasticity; broad-based = cerebellar.
- Watch gait from front/side/behind to localise pain, weakness, deformity or neurological cause.
- Trendelenburg sign: ‘the sound side sags’ with abductor weakness/hip instability.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Purpose
Bone grafting is the transplantation of bone (or use of a bone substitute) to promote healing, fill defects, provide structural support, or achieve fusion. It is used for non-union and delayed union, to fill cavities (after curettage of cysts/tumours), to bridge bone defects (trauma, tumour resection), and to achieve arthrodesis or spinal fusion.
How Grafts Work (Three Properties)
A bone graft may act through three mechanisms: osteogenesis — living cells in the graft directly form new bone (only fresh autograft, especially cancellous, provides this); osteoinduction — factors (e.g. bone morphogenetic proteins) that stimulate host stem cells to differentiate into bone-forming cells; and osteoconduction — the graft acts as a passive scaffold onto which host bone grows. The ideal autograft supplies all three.
Property Meaning Best source Osteogenic Graft’s own cells make bone Fresh cancellous autograft Osteoinductive Stimulates host cells to form bone Autograft, demineralised matrix, BMP Osteoconductive Scaffold for host bone ingrowth Autograft, allograft, ceramics Types of Graft
Autograft (from the patient — e.g. iliac crest, fibula): the gold standard, being osteogenic, osteoinductive and osteoconductive with no immune rejection, but limited in quantity and with donor-site morbidity. Allograft (from another human, e.g. bone bank): available in larger amounts and useful for structural defects, but osteoconductive only (processed), with a small risk of disease transmission and immune response. Bone substitutes — synthetic ceramics (hydroxyapatite, tricalcium phosphate), calcium sulphate, demineralised bone matrix and BMPs — avoid donor-site morbidity and are used alone or as graft extenders. A vascularised graft (e.g. free fibula with its blood supply) is used for large defects.
💡Autograft (iliac crest) is the gold standard because it is the only graft that is simultaneously osteogenic, osteoinductive and osteoconductive. Its limits are the available quantity and donor-site pain, which is why allografts and substitutes are used for large or supplementary needs.Graft Incorporation & Complications
A graft is incorporated by ‘creeping substitution’ — host vessels and osteoclasts invade and gradually replace the graft with new living bone. Success requires a well-vascularised, stable, clean (non-infected) recipient bed. Complications include donor-site pain/morbidity and haematoma (autograft harvest), non-incorporation/graft resorption, infection, and — for allograft — a small risk of disease transmission and immune reaction.
⚠️A bone graft will not ‘take’ in an infected or poorly vascularised, mobile bed. Eradicate infection, ensure a good blood supply and provide rigid fixation before or alongside grafting, or the graft simply resorbs.Choosing & Combining Grafts
In practice the choice of graft is dictated by the size and nature of the defect and by whether structural support is required. A small cavity or a non-union is well served by cancellous autograft, which is rich in osteogenic cells and revascularises quickly; a large segmental defect needing mechanical strength calls for a cortical autograft, structural allograft or vascularised bone transfer; and where autograft is insufficient it is common to extend it with allograft or a synthetic substitute, combining the biological activity of the autograft with the bulk of the substitute. The recipient bed is prepared by freshening the bone ends, and rigid fixation is provided so that the graft heals in a stable, mechanically favourable environment.
💡The one-line summary examiners want: autograft is the gold standard because it alone is osteogenic, osteoinductive and osteoconductive; its only real drawbacks are limited quantity and donor-site pain, which is exactly why allografts and synthetic substitutes exist.Autograft alone provides all three properties. 🔑KEY POINTS TO REMEMBER- Bone grafting promotes healing/fusion and fills or bridges defects.
- Three properties: osteogenic (cells make bone), osteoinductive (stimulate host), osteoconductive (scaffold).
- Autograft (iliac crest) = gold standard (all three); allograft = conductive, structural; substitutes = ceramics/BMP.
- Incorporated by creeping substitution; needs a vascular, stable, non-infected bed.
- Complications: donor-site morbidity, resorption, infection; allograft — small disease-transmission risk.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Anatomy
The knee is stabilised by four main ligaments — the anterior and posterior cruciate ligaments (ACL, PCL) and the medial and lateral collateral ligaments (MCL, LCL) — and cushioned by the medial and lateral menisci. Sports and twisting injuries commonly damage these structures, causing pain, instability and, in the long term, osteoarthritis.
Anterior Cruciate Ligament (ACL) Injury
The ACL prevents anterior translation and rotation of the tibia. It is typically torn by a non-contact twisting/pivoting injury (deceleration with the foot planted), often in sport. The patient may feel or hear a ‘pop’, develops a rapid haemarthrosis (swelling within hours), and complains of the knee giving way on pivoting. Diagnosis is clinical (Lachman’s test — the most sensitive — and the anterior drawer and pivot-shift tests) confirmed by MRI.
Structure Function Key test ACL Resists anterior tibial translation Lachman’s / anterior drawer / pivot-shift PCL Resists posterior tibial translation Posterior drawer / sag sign MCL / LCL Resist valgus / varus stress Valgus / varus stress test Meniscus Load-sharing, shock absorption McMurray’s / joint-line tenderness Meniscal Injuries
The menisci are torn by a twisting force on a flexed, weight-bearing knee (younger patients) or by degeneration (older patients). Features include joint-line pain and tenderness, swelling that develops over a day, and mechanical symptoms — clicking, catching or ‘locking’ (a displaced bucket-handle fragment blocking full extension). McMurray’s test reproduces pain/click; MRI confirms.
💡A knee that swells within a couple of hours of injury has a haemarthrosis — most often an ACL rupture (also osteochondral fracture or patellar dislocation), whereas a meniscal effusion typically develops more slowly, overnight.Management
ACL: not all tears need surgery. Physiotherapy (quadriceps/hamstring rehabilitation) suits lower-demand patients and copers; arthroscopic ACL reconstruction (with a tendon graft) is offered to young, active patients or those with instability, followed by prolonged rehabilitation. Meniscus: a small stable or degenerate tear is treated conservatively; a repairable peripheral (vascular ‘red zone’) tear is repaired to preserve the meniscus, while an irreparable symptomatic tear is treated by limited arthroscopic meniscectomy (preserving as much meniscus as possible). Collateral ligament injuries usually heal with bracing.
⚠️A locked knee (cannot fully extend) after a twisting injury suggests a displaced bucket-handle meniscal tear and needs prompt arthroscopic treatment. Preserve meniscus wherever possible — total meniscectomy accelerates osteoarthritis.Long-Term Consequences & the ‘Unhappy Triad’
A severe valgus-and-rotation injury of the knee can damage three structures together — the ACL, the medial collateral ligament and the medial (or lateral) meniscus — the combination classically termed O’Donoghue’s ‘unhappy triad’. Whatever the pattern, the long-term importance of these injuries lies in the risk of secondary osteoarthritis: an ACL-deficient, unstable knee and, especially, a meniscus-deficient knee wear out prematurely, which is the rationale for restoring stability and for preserving as much meniscus as possible rather than excising it wholesale.
💡Two exam-favourite facts: a knee that fills with blood within a couple of hours (haemarthrosis) after a twist is an ACL rupture until proven otherwise, and a locked knee that will not fully straighten is a displaced bucket-handle meniscal tear — both point you straight to the diagnosis.Immediate haemarthrosis suggests ACL tear. 🔑KEY POINTS TO REMEMBER- ACL/PCL + MCL/LCL stabilise the knee; menisci share load & absorb shock.
- ACL tear: twisting/pivot injury, ‘pop’, rapid haemarthrosis, giving way; Lachman’s most sensitive.
- Meniscal tear: joint-line pain, delayed swelling, clicking/locking; McMurray’s test.
- ACL: physio for copers, reconstruction for active/unstable knees.
- Meniscus: repair peripheral (red-zone) tears, preserve meniscus; a locked knee needs prompt arthroscopy.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Purposes
Traction is the application of a sustained pulling force to a limb or the spine to reduce and hold a fracture or dislocation, overcome muscle spasm, relieve pain, and prevent or correct deformity. Immobilisation (by plaster casts, splints or braces) holds a part still to allow healing. Both are fundamental conservative tools in orthopaedics.
Skin traction Skeletal traction Force applied to Skin (adhesive strapping/foam) Bone (via a pin, e.g. Steinmann/K-wire) Max weight Limited (~4–5 kg; skin damage) Heavier weights possible Duration Short-term Longer-term Example Buck’s / Bryant’s traction Tibial/calcaneal pin traction Risk Skin blistering, pressure Pin-site infection Types of Traction
Skin traction applies the force through adhesive strapping over the skin and is limited to light loads for short periods (e.g. Buck’s traction for a hip fracture pre-op; Bryant’s (gallows) traction for a young child’s femoral fracture). Skeletal traction applies the force directly to bone through a metal pin (e.g. a Steinmann pin through the proximal tibia or calcaneus), allowing heavier, longer-term traction. Traction may be fixed (against a fixed point, e.g. a Thomas splint) or balanced/sliding (using weights and pulleys).
💡The essential distinction: skin traction pulls through the skin (light, short-term) while skeletal traction pulls through a pin in the bone (heavier, longer). Bryant’s (gallows) traction is only for young children (weight limit) because of the risk of vascular compromise in older/heavier patients.Casts, Splints & Their Principles
Plaster (or synthetic) casts immobilise a fracture, usually spanning the joint above and below. Principles: apply well-moulded but not too tight; elevate the limb; and watch for complications. A fresh injury may be put in a backslab / split cast to allow for swelling. Splints (e.g. Thomas splint for a femoral fracture) provide support and traction, particularly for transport.
⚠️A tight cast can cause a compartment syndrome or pressure sores, and a pin site can become infected. Warn the patient about the danger signs of a tight cast (increasing pain, numbness, swelling, colour change) and split or remove a constricting cast immediately rather than waiting.Complications
Traction: skin damage/pressure sores and neurovascular compromise (skin traction), pin-site infection and loosening (skeletal traction), joint stiffness, and the general complications of prolonged bed rest (chest infection, DVT, pressure sores). Casts: tightness (compartment syndrome), pressure sores, joint stiffness, and ‘cast disease’ (stiffness, wasting and osteoporosis from prolonged immobilisation).
Principles of Effective Traction
For traction to work safely it must obey a few principles: there must be an adequate counter-traction (often the patient’s own body weight, achieved by elevating the foot of the bed) to oppose the pull, the line and magnitude of pull must be appropriate to reduce and hold the fracture without over-distraction, and the apparatus (ropes, pulleys and weights) must run freely and hang clear of the floor. The limb’s neurovascular status and the pin or skin sites are checked regularly, and traction is increasingly a temporary or transport measure in modern practice, with most fractures that once needed weeks of traction now treated by early internal or external fixation to allow mobilisation.
💡Remember Bryant’s (gallows) traction is reserved for children under about two years / 12–14 kg, because in a heavier child suspending both legs vertically can compromise the circulation to the feet — a classic safety point.Skin traction is limited to about 5 kg to avoid skin damage. 🔑KEY POINTS TO REMEMBER- Traction = sustained pull to reduce/hold fractures, overcome spasm, relieve pain, correct deformity.
- Skin traction (through skin; light, short; Buck’s/Bryant’s) vs skeletal (pin in bone; heavier, longer).
- Fixed (Thomas splint) vs balanced/sliding traction; Bryant’s only for young children.
- Casts immobilise (span joint above & below); use a backslab for fresh swelling.
- Watch for tight-cast compartment syndrome/pressure sores & pin-site infection; split a tight cast at once.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Tennis elbow (lateral epicondylitis) and golfer’s elbow (medial epicondylitis) are overuse enthesopathies — degeneration and micro-tearing at the origin of the forearm muscles from the epicondyles of the humerus. Tennis elbow affects the common extensor origin (lateral epicondyle); golfer’s elbow affects the common flexor origin (medial epicondyle).
Clinical Features
Tennis elbow: pain over the lateral epicondyle, worse on resisted wrist/finger extension and gripping (the commonest; often in manual workers, not just tennis players). Golfer’s elbow: pain over the medial epicondyle, worse on resisted wrist flexion/pronation. There is local tenderness; the diagnosis is clinical.
💡Simple rule: tennis → lateral → extensors (pain on resisted wrist extension); golfer’s → medial → flexors (pain on resisted wrist flexion).Management
Both are usually self-limiting and treated conservatively: activity modification/rest, analgesia/NSAIDs, physiotherapy (eccentric strengthening), a counterforce brace, and corticosteroid injection for persistent symptoms (short-term relief). A small proportion with refractory symptoms are considered for surgery. Recovery, although sometimes slow, is the rule.
Clinical Note
Although named after sport, these conditions far more often result from occupational and repetitive strain, and both are fundamentally degenerative (‘tendinosis’) rather than truly inflammatory, which is why rest and graded eccentric loading work better than repeated steroid injections — injections give short-term relief but can weaken the tendon origin if overused. Patients are reassured that, although recovery may take many months, the natural history is towards resolution.
💡Aim your examination at the origin: resisted wrist extension hurts in tennis elbow (lateral), resisted wrist flexion hurts in golfer’s elbow (medial) — a two-second bedside distinction.⚠️Beware of injecting the medial epicondyle carelessly in golfer’s elbow: the ulnar nerve lies just behind it in the cubital tunnel and can be injured, and medial elbow pain may itself be due to ulnar neuritis rather than epicondylitis, so the nerve is examined before attributing all medial pain to the tendon origin.Pain on resisted wrist extension versus flexion separates them. 🔑KEY POINTS TO REMEMBER- Overuse enthesopathy of forearm muscle origins at the humeral epicondyles.
- Tennis elbow = lateral (extensor origin); golfer’s elbow = medial (flexor origin).
- Pain on resisted wrist extension (tennis) or flexion (golfer’s); clinical diagnosis.
- Conservative: rest, NSAIDs, physio, brace ± steroid injection; usually self-limiting.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
The rotator cuff is the group of four muscles (supraspinatus, infraspinatus, teres minor, subscapularis — ‘SITS’) whose tendons blend with the shoulder capsule to stabilise the glenohumeral joint and power its movement. Rotator cuff disease ranges from impingement/tendinopathy to partial and full-thickness tears, and is a very common cause of shoulder pain.
Impingement & Tears
In subacromial impingement, the cuff tendons (especially supraspinatus) are compressed beneath the acromion, causing a painful arc (pain in mid-abduction, roughly 60–120°) worse on overhead activity. A cuff tear (degenerative in the older patient, or traumatic) causes weakness — e.g. difficulty initiating abduction (supraspinatus) with a positive ‘drop-arm’ test in large tears.
💡A painful arc (60–120°) suggests subacromial impingement/supraspinatus tendinopathy; an inability to hold the arm abducted (a positive drop-arm test) suggests a significant full-thickness supraspinatus tear.Management
Impingement/tendinopathy: conservative — activity modification, NSAIDs, physiotherapy (cuff strengthening and scapular control) and subacromial corticosteroid injection; refractory cases may need arthroscopic subacromial decompression. Tears: small/degenerate tears are treated conservatively, while significant tears in active patients (or acute traumatic tears) are considered for surgical cuff repair followed by rehabilitation.
Clinical Note
Rotator cuff problems are strongly age-related: impingement and tendinopathy predominate in younger, active patients, whereas degenerate full-thickness tears become common with age and may be surprisingly well tolerated. Distinguishing a stiff, painful shoulder from a genuinely weak one guides management, and imaging (ultrasound or MRI) confirms the presence and size of a tear when surgery is being considered.
💡Let the two signs guide you: a painful arc in mid-abduction means impingement/tendinopathy, whereas a positive drop-arm test means a significant full-thickness tear that may need repair.Painful arc between 60 and 120 degrees of abduction. 🔑KEY POINTS TO REMEMBER- Rotator cuff = supraspinatus, infraspinatus, teres minor, subscapularis (SITS); stabilises the shoulder.
- Impingement: painful arc 60–120°, worse overhead; tear: weakness, positive drop-arm test.
- Supraspinatus most commonly affected.
- Conservative (physio, NSAIDs, injection) first; repair significant/traumatic tears in active patients.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Plantar fasciitis is a common overuse/degenerative condition of the plantar fascia at its origin on the calcaneus (heel), causing inferior heel pain. It is the commonest cause of heel pain in adults.
Clinical Features
The characteristic symptom is heel pain that is worst on taking the first steps in the morning (or after a period of rest), easing a little with walking then worsening again with prolonged activity. There is tenderness over the medial calcaneal tuberosity. Risk factors include prolonged standing, obesity, a tight Achilles tendon and unsupportive footwear. A calcaneal heel spur may be seen on radiographs but is often incidental.
💡The classic story is ‘first-step’ heel pain in the morning with medial calcaneal tenderness. A heel spur on X-ray is usually an incidental finding rather than the cause of pain.Management
Plantar fasciitis is self-limiting in most patients but can be slow to settle. Treatment is conservative: rest/activity modification, calf and plantar-fascia stretching, supportive footwear and heel cushions/orthoses, and analgesia/NSAIDs. Resistant cases may be offered a corticosteroid injection (used sparingly — risk of fat-pad atrophy and fascial rupture) or extracorporeal shock-wave therapy; surgery is rarely needed.
Clinical Note
Because the plantar fascia tightens overnight, much of the treatment is aimed at stretching it and the calf — night splints that hold the ankle in dorsiflexion, and a programme of plantar-fascia and Achilles stretches — alongside cushioning of the heel. Persistent or atypical heel pain should prompt consideration of other causes such as a calcaneal stress fracture or nerve entrapment before repeated injections are given.
💡The diagnosis is usually made on the story alone — first-step morning heel pain with medial calcaneal tenderness — and the heel spur so often seen on the X-ray is a red herring rather than the cause.⚠️Persistent heel pain that is atypical — present at rest, worse with activity in a young athlete, or associated with a limp — should not simply be labelled plantar fasciitis: a calcaneal stress fracture, tarsal tunnel syndrome or a seronegative spondyloarthropathy (enthesitis) must be considered, especially when symptoms fail to settle with standard treatment.Pain is characteristically worst on the first steps in the morning. 🔑KEY POINTS TO REMEMBER- Overuse/degeneration of the plantar fascia origin at the heel; commonest cause of heel pain.
- ‘First-step’ morning heel pain; tenderness over the medial calcaneal tuberosity.
- Heel spur on X-ray often incidental.
- Conservative: stretching, supportive footwear/orthoses, NSAIDs; injection sparingly; usually self-limiting.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
De Quervain’s tenosynovitis is a stenosing tenosynovitis of the first dorsal extensor compartment of the wrist, which contains the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons. Thickening of the sheath causes pain on thumb and wrist movement. It is common in new mothers (lifting the baby) and after repetitive thumb use.
Clinical Features
Pain and tenderness over the radial styloid (the lateral side of the wrist at the base of the thumb), worse on thumb and wrist movement, sometimes with local swelling. Finkelstein’s test — flexing the thumb into the palm and ulnar-deviating the wrist — reproduces the pain and is diagnostic.
💡Finkelstein’s test (thumb tucked into the fist, wrist deviated ulnar-ward) reproduces sharp pain over the radial styloid in de Quervain’s — the key clinical sign.Management
Treatment is usually conservative: a thumb-spica splint, activity modification, NSAIDs, and a corticosteroid injection into the first compartment (highly effective). Persistent cases are treated by surgical release of the first dorsal compartment.
Clinical Note
De Quervain’s is essentially a mismatch between the swollen APL and EPB tendons and the tight fibro-osseous tunnel of the first dorsal compartment, and the condition is especially common in the post-partum period from repeated lifting of the baby with the thumb abducted. A steroid injection accurately placed into the compartment is one of the most reliable non-operative treatments in the hand, and surgical release cures the resistant cases.
💡If Finkelstein’s test reproduces sharp pain at the radial styloid, the diagnosis is de Quervain’s; an accurately placed injection into the first dorsal compartment is one of the most effective treatments in the hand.⚠️A related and easily confused condition is intersection syndrome, felt a little more proximally on the dorsoradial forearm where the first and second compartments cross; distinguishing it matters because the point of tenderness and the site of any injection differ, and mislabelling leads to an injection in the wrong place.Finkelstein test reproduces the pain and confirms the diagnosis. 🔑KEY POINTS TO REMEMBER- Stenosing tenosynovitis of the 1st dorsal compartment (APL & EPB).
- Common in new mothers/repetitive thumb use; pain/tenderness at the radial styloid.
- Finkelstein’s test reproduces the pain (diagnostic).
- Splint, NSAIDs, steroid injection; surgical release if persistent.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Purpose
A systematic set of clinical tests assesses the ligaments and menisci of the injured knee and, together with the history and MRI, guides diagnosis. Each test stresses a specific structure.
Test Structure / meaning Lachman’s ACL (most sensitive) — anterior tibial glide at 20–30° flexion Anterior drawer ACL — anterior glide at 90° flexion Pivot-shift ACL — rotational instability (giving way) Posterior drawer / sag PCL — posterior tibial displacement Valgus / varus stress MCL / LCL McMurray’s Meniscal tear — pain/click on rotation Key Tests Explained
Lachman’s test (the most sensitive for the ACL) assesses anterior tibial translation with the knee flexed ~20–30°. The anterior drawer tests the ACL at 90° and the posterior drawer/sag sign tests the PCL. Valgus and varus stress tests assess the collateral ligaments. McMurray’s test (rotating the flexed knee while extending it) elicits pain or a click with a meniscal tear, supported by joint-line tenderness.
💡Lachman’s test is the most sensitive clinical test for an ACL tear — more so than the anterior drawer, because it is done in slight flexion where hamstring guarding is less.Clinical Note
No single test is perfect, so the structures are examined in combination and always compared with the normal side, since a degree of laxity is individual; guarding from pain and swelling can mask instability in the acute knee, which is why examination is sometimes repeated once the acute phase has settled, and why MRI is a valuable adjunct for confirming ligament and meniscal injury.
💡When you have only one test to trust for the ACL, choose Lachman’s — done in slight flexion, it is the most sensitive because hamstring guarding is minimised.⚠️Because pain and muscle guarding can mask instability in the freshly injured knee, a normal-feeling examination immediately after injury does not exclude a ligament tear; the tests are therefore repeated once swelling settles, and an examination under anaesthesia or MRI is used when clinical doubt persists.Lachman test is the most sensitive for ACL injury. 🔑KEY POINTS TO REMEMBER- Lachman’s (most sensitive) & anterior drawer & pivot-shift → ACL.
- Posterior drawer / sag → PCL; valgus/varus stress → MCL/LCL.
- McMurray’s + joint-line tenderness → meniscal tear.
- Combine tests with history and MRI to localise the injury.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
A ganglion is a benign cystic swelling arising from a joint capsule or tendon sheath, filled with a clear, viscous, gelatinous (mucin-like) fluid. It is the commonest soft-tissue swelling of the hand and wrist, most often on the dorsum of the wrist.
Clinical Features
A smooth, rounded, well-defined swelling, usually painless (occasionally aching), that may fluctuate in size. It is firm and characteristically transilluminates (because it is fluid-filled) — a useful bedside sign. Common sites are the dorsal and volar wrist and the flexor tendon sheath of a finger. It is usually of cosmetic concern or causes mild discomfort.
💡A cystic wrist swelling that transilluminates and is attached to a joint/tendon sheath is almost certainly a ganglion — the transillumination distinguishes a fluid-filled cyst from a solid tumour.Management
Many ganglia are harmless and resolve spontaneously, so reassurance and observation is appropriate for an asymptomatic lesion. Symptomatic ones may be treated by aspiration (± steroid, though recurrence is common) or, for persistent/recurrent or troublesome ganglia, surgical excision (removing the root/stalk to reduce recurrence). The old ‘hitting it with a book’ remedy is not recommended.
Clinical Note
Although the classic teaching is that a ganglion transilluminates and is harmless, an atypical, firm or rapidly enlarging swelling should not be assumed to be a ganglion, and imaging (ultrasound or MRI) is used where the diagnosis is in doubt to exclude other soft-tissue lesions. When a ganglion is excised, removing its stalk and a cuff of the underlying capsule reduces the significant recurrence rate that follows simple aspiration.
💡The bedside clincher is transillumination: a soft, well-defined wrist swelling that glows when a light is held to it is a fluid-filled ganglion rather than a solid tumour.⚠️An important trap is the volar wrist ganglion, which lies close to the radial artery: aspiration or surgery in this location carries a risk of vascular injury, so these are approached with particular care, and Allen’s test and imaging are used to define the anatomy before any intervention.Becomes more prominent on wrist flexion. 🔑KEY POINTS TO REMEMBER- Benign cyst from a joint capsule/tendon sheath with gelatinous fluid; commonest hand/wrist swelling.
- Smooth, well-defined, usually painless, transilluminates; often dorsal wrist.
- Many resolve spontaneously → reassure/observe.
- Aspiration (recurs) or surgical excision (remove stalk) for symptomatic/recurrent lesions.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Overview
The plaster (or synthetic) cast is a mainstay of conservative fracture treatment, but it has important complications, some of which are limb-threatening. Anticipating and recognising them is essential.
Key Complications
A cast that is too tight (or applied to a swelling limb) can cause compartment syndrome and neurovascular compromise — the most dangerous complication. Pressure sores develop over bony prominences from poor moulding or ridges. Nerve palsy can occur from local pressure (e.g. the common peroneal nerve at the fibular neck). Prolonged immobilisation causes ‘cast/fracture disease’ — joint stiffness, muscle wasting and disuse osteoporosis. Other problems include a loose/ineffective cast (allowing fracture displacement), skin maceration/allergy, and thermal injury during setting.
⚠️Warn every patient in a cast about the danger signs of a tight cast: increasing pain, tingling/numbness, swelling, or colour change of the fingers/toes. The response is to split or remove the cast immediately and reassess — never to reassure and wait, as delay risks compartment syndrome and ischaemic contracture.Prevention
Complications are minimised by applying a well-moulded, well-padded cast, using a backslab or split cast for a fresh, potentially swelling injury, elevating the limb, giving clear cast-care instructions, and reviewing the patient to check the cast and neurovascular status.
Clinical Note
The single most important message about casts is that a limb in a fresh cast can develop a compartment syndrome, and the earliest and most reliable warning is pain out of proportion, made worse by passive stretch of the fingers or toes; the correct response is to split the cast and its padding down to skin at once. Regular review, elevation and clear written cast-care advice prevent most other complications.
💡The rule that saves limbs: pain out of proportion, worse on passively stretching the toes/fingers, in a casted limb means compartment syndrome until proven otherwise — split the cast to skin at once, do not reassure and wait.Increasing pain under a cast means split it, do not sedate. 🔑KEY POINTS TO REMEMBER- Cast complications range from nuisance to limb-threatening.
- Most dangerous: tight cast → compartment syndrome / neurovascular compromise.
- Also: pressure sores, nerve palsy, cast disease (stiffness, wasting, osteoporosis), loose cast.
- Warn of tight-cast danger signs (pain, numbness, swelling, colour change) → split cast at once.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.