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 & Importance
The pelvis is a rigid osteoligamentous ring formed by the two innominate bones and the sacrum, bound by the strong posterior sacroiliac, sacrospinous and sacrotuberous ligaments. Because it is a ring, a displaced break at one point almost always implies a second break or ligament disruption elsewhere. High-energy pelvic fractures are important because of life-threatening haemorrhage (from the presacral venous plexus and internal iliac branches) and associated urogenital and visceral injuries.
The pelvic ring. An anteroposterior-compression (‘open-book’) injury widens the pubic symphysis and disrupts the anterior sacroiliac ligaments, greatly increasing pelvic volume. Classification
Two systems are used. The Young–Burgess classification is based on the direction of force: anteroposterior compression (APC) — the ‘open-book’ injury that opens the symphysis and increases pelvic volume; lateral compression (LC) — the commonest, impacting the ring; and vertical shear (VS) — the most unstable, with cranial displacement of a hemipelvis. The Tile classification groups fractures by stability: Type A stable, Type B rotationally unstable but vertically stable, Type C both rotationally and vertically unstable.
Young–Burgess Mechanism Key feature APC (open-book) AP force Symphysis widens; ↑ volume; venous bleeding Lateral compression Side impact Commonest; sacral/rami impaction Vertical shear Axial (fall) Most unstable; hemipelvis rides up Combined Mixed Elements of the above Clinical Features
Following high-energy trauma there is pelvic pain, bruising (perineum, scrotum, flanks), and instability on gentle pelvic compression (do not repeatedly ‘spring’ the pelvis — it dislodges clot). Look for signs of urethral injury: blood at the meatus, a high-riding prostate, a scrotal/perineal haematoma, and inability to pass urine. A per-rectal / per-vaginal examination detects open fractures and rectal tears. Assess distal neurovascular status (lumbosacral plexus, sciatic nerve).
⚠️An unstable pelvic fracture with haemodynamic instability is an immediate threat to life. Do not perform urethral catheterisation until urethral injury is excluded (blood at meatus, high-riding prostate) — a retrograde urethrogram is done first if injury is suspected.Investigations
AP pelvic radiograph is part of the primary trauma survey; inlet and outlet views and, definitively, a CT scan (with angiography) define the fracture and any arterial bleeding. A retrograde urethrogram assesses suspected urethral injury; FAST/CT evaluates associated abdominal injuries.
Management
Management follows ATLS priorities because these patients are polytraumatised.
Resuscitation & haemorrhage control: apply a pelvic binder at the level of the greater trochanters to close an open-book injury, reduce pelvic volume and tamponade venous bleeding; give blood/massive transfusion. Persistent arterial bleeding is treated by angio-embolisation or surgical pre-peritoneal packing; an external fixator provides temporary mechanical stability.
Definitive fixation: stable fractures are treated conservatively with early mobilisation; unstable Tile B/C injuries need internal fixation — anterior plating/external fixation of the symphysis/rami and posterior fixation (iliosacral screws) of the sacroiliac disruption. Associated urogenital and rectal injuries are managed jointly.💡The pelvic binder is a simple, life-saving first step: by reducing pelvic volume in an open-book injury it decreases the space for bleeding and helps clot form.Complications
Haemorrhagic shock and death (the leading early cause), urethral and bladder injury (leading to stricture or incontinence), lumbosacral nerve injury, sexual dysfunction, malunion with pelvic obliquity/leg-length discrepancy, and chronic sacroiliac pain.
🔑KEY POINTS TO REMEMBER- Pelvis is a ring — one displaced break implies a second break/ligament injury.
- Young–Burgess: APC (open-book), LC (commonest), vertical shear (most unstable).
- Main killers: haemorrhage; main pitfalls: urethral & bladder injury.
- First aid = pelvic binder at trochanters; then embolisation/packing + external fixator.
- Unstable Tile B/C → anterior + posterior internal fixation.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & the Question of Stability
Thoracolumbar spine injuries most commonly occur at the thoracolumbar junction (T11–L2), the transition between the rigid thoracic and mobile lumbar spine. The central clinical question is whether the injury is stable or unstable — i.e. whether the spine can protect the neural elements and bear physiological loads without further displacement or deformity.
Denis Three-Column Concept
Denis divided the spine into three columns. The anterior column = anterior longitudinal ligament + anterior half of the vertebral body/disc; the middle column = posterior half of the body/disc + posterior longitudinal ligament; the posterior column = the bony neural arch, facet joints and posterior ligamentous complex. Disruption of two or more columns, and especially of the middle column, indicates instability.
Denis three-column model: integrity of the middle column is the key determinant of stability. Patterns of Injury
Compression (wedge) fracture — anterior column failure only; usually stable. Burst fracture — axial load fails the anterior and middle columns, with retropulsion of bone into the canal (potentially unstable, may cause cord/cauda injury). Flexion-distraction (Chance) fracture — a seat-belt injury failing the posterior and middle columns in tension, often with intra-abdominal injuries. Fracture-dislocation — all three columns fail; grossly unstable, high rate of neurological injury.
💡A burst fracture differs from a simple wedge compression by middle-column involvement with bony retropulsion into the canal — hence the neurological risk. CT is needed to see it.Clinical Assessment
Following the ATLS survey, the whole spine is log-rolled and palpated for a tender step or gap. A full neurological examination — motor, sensory (including the sacral segments), reflexes, and per-rectal tone/sensation — is documented and classified (ASIA). Remember associated injuries: a Chance fracture demands abdominal evaluation; a calcaneal/pelvic fracture demands spinal evaluation.
Investigations
CT is the imaging of choice for bony detail, canal compromise and column assessment; MRI is added when there is a neurological deficit or suspected posterior ligamentous / disc / cord injury. Plain radiographs may screen but underestimate the injury.
Management
Stable injuries (simple wedge/compression, minimal loss of height, neurologically intact) are treated conservatively — analgesia, a brace (e.g. TLSO) and early mobilisation. Unstable injuries, significant canal compromise or a neurological deficit require surgical stabilisation and decompression — posterior pedicle-screw instrumentation and fusion, with anterior/posterior decompression of retropulsed fragments as needed. Spinal precautions, prevention of secondary cord injury (maintain oxygenation and perfusion), and rehabilitation are integral.
⚠️Never clear a spine or allow mobilisation on plain films alone in a high-energy injury. Maintain full spinal precautions until the whole spine is cleared clinically and radiologically — 10% of spinal fractures have a second, non-contiguous spinal fracture.🔑KEY POINTS TO REMEMBER- Thoracolumbar junction (T11–L2) is the commonest site.
- Denis three columns; instability = ≥ 2 columns, especially the middle column.
- Wedge (anterior) usually stable; burst (ant+mid, retropulsion) may injure the cord.
- CT for bone/canal; MRI for deficit or ligament/cord injury.
- Stable → brace; unstable/deficit → decompression + instrumented fusion. 10% have a second fracture.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Levels
Spinal cord injury (SCI) is damage to the cord producing motor, sensory and autonomic dysfunction below the level of the lesion. The cord ends at the conus medullaris (~L1); below this the cauda equina (lumbosacral nerve roots) continues. Injury is described by its neurological level and whether it is complete (no motor or sensory function in the lowest sacral segments) or incomplete.
Primary vs Secondary Injury
The primary injury is the mechanical insult at the moment of trauma. Secondary injury is the subsequent cascade of oedema, ischaemia, hypoxia and inflammation over the ensuing hours — and it is preventable. Much of acute SCI care is directed at limiting secondary injury by maintaining oxygenation, blood pressure (cord perfusion) and spinal alignment.
Spinal Shock
Spinal shock is the transient loss of all cord function below the lesion — flaccid paralysis, areflexia and loss of sensation — immediately after injury. Its resolution is heralded by return of the bulbocavernosus reflex (usually within 24–48 h). The neurological examination can only be called ‘complete’ (and prognosticated) once spinal shock has resolved.
Incomplete syndrome Mechanism Hallmark Central cord Hyperextension (elderly, spondylosis) Arms > legs weakness; commonest Anterior cord Flexion / ant. spinal a. injury Loss of motor + pain/temp; dorsal columns spared; poor prognosis Brown-Séquard Hemisection (penetrating) Ipsilateral motor + proprioception loss, contralateral pain/temp; best prognosis Posterior cord Rare Loss of proprioception/vibration Conus / cauda equina L1 region injury Bladder/bowel & saddle anaesthesia 💡Central cord syndrome is the commonest incomplete injury — a hyperextension injury in an elderly patient with cervical spondylosis, causing weakness worse in the arms than the legs (the medially placed arm fibres of the corticospinal tract are most affected).Neurogenic Shock
In injuries above T6, loss of sympathetic outflow causes neurogenic shock: hypotension with bradycardia and warm peripheries (distinguishing it from hypovolaemic shock, which causes tachycardia). It is managed with fluids, vasopressors and atropine for symptomatic bradycardia, while excluding concurrent haemorrhage.
Management
Follow ATLS with full spinal immobilisation. Prevent secondary injury: secure the airway, maintain oxygenation and an adequate mean arterial pressure for cord perfusion, and keep the spine aligned. Perform CT and MRI to define the bony and cord injury. Unstable injuries and compressive lesions with deficit are treated by reduction, decompression and stabilisation (early surgery may benefit selected incomplete injuries). Meticulous supportive care prevents complications: bladder management, bowel care, pressure-area and skin care, DVT prophylaxis, respiratory care (high lesions) and early rehabilitation. High-dose steroids are controversial and not routinely recommended.
Prognosis & Rehabilitation
Prognosis depends chiefly on whether the injury is complete or incomplete and on the neurological level. Incomplete injuries (some sacral sparing) have the best potential for recovery; among the syndromes, Brown-Séquard fares best and anterior cord worst. Rehabilitation is multidisciplinary and lifelong, aiming to maximise function and independence and to prevent the complications of paralysis: pressure sores, contractures, urinary infection and stones, venous thromboembolism, spasticity, and respiratory compromise in high lesions. Bladder and bowel programmes, seating and wheelchair provision, physiotherapy and psychological support are central.
⚠️Watch for autonomic dysreflexia in chronic lesions above T6 — a noxious stimulus below the level (typically a blocked catheter or loaded rectum) triggers a dangerous surge of hypertension with headache and sweating. Treat by sitting the patient up and removing the stimulus urgently.Sacral sparing indicates an incomplete injury — better prognosis. 🔑KEY POINTS TO REMEMBER- Complete = no motor/sensory in the lowest sacral segments; assess after spinal shock resolves.
- Return of the bulbocavernosus reflex marks the end of spinal shock.
- Central cord (commonest, arms>legs) < Brown-Séquard (best prognosis) < anterior cord (worst).
- Neurogenic shock (lesion >T6): hypotension + bradycardia; treat with fluids + vasopressors.
- Prevent secondary injury: oxygenation, perfusion, alignment; decompress/stabilise unstable injuries.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Importance
Cervical spine injuries follow high-energy trauma (RTA, fall, diving) and, in the elderly, low-energy falls onto a spondylotic spine. They are critical because the cervical cord supplies the diaphragm and limbs — a high lesion is immediately life-threatening — and because a missed unstable injury can convert an intact patient into a quadriplegic one. The upper cervical spine (occiput–C2) and the subaxial spine (C3–C7) have distinct injury patterns.
Upper Cervical Injuries
Atlanto-occipital dissociation — usually fatal. Jefferson fracture — a burst fracture of the C1 ring from axial loading (may be stable if the transverse ligament is intact). Odontoid (dens) fractures — classified by Anderson–D’Alonzo (Type II, at the base, is commonest and prone to non-union). Hangman’s fracture — traumatic spondylolisthesis of C2 (bilateral pars fracture) from hyperextension.
Subaxial (C3–C7) Injuries
These include flexion injuries (wedge compression, unstable teardrop fractures, uni- and bi-facet dislocations), burst fractures from axial loading, and extension injuries (especially in the spondylotic elderly, causing central cord syndrome). Facet dislocations frequently injure the cord or nerve roots.
Clinical Features & Assessment
Assume a cervical injury in any patient with head/facial trauma, neck pain, or an altered conscious level. Immobilise with a collar, blocks and tape/board. Examine for midline tenderness and a full neurological deficit. The NEXUS criteria and the Canadian C-spine rule identify low-risk patients who may not need imaging.
⚠️In an unconscious or intoxicated trauma patient, the cervical spine cannot be cleared clinically — maintain immobilisation and obtain CT of the whole cervical spine. Never remove precautions on the basis of inadequate plain films.Investigations
CT of the cervical spine is the standard imaging in significant trauma (far more sensitive than plain radiographs, which must show the occiput to T1). MRI is added for neurological deficit, or suspected ligamentous, disc or cord injury.
Management
Maintain immobilisation and ATLS priorities, preventing secondary cord injury. Stable injuries (e.g. many isolated C1 or minor wedge fractures) are treated in a collar or halo/orthosis. Unstable injuries, facet dislocations and those with cord compression require reduction (traction or closed reduction for locked facets) and surgical stabilisation/fusion with decompression. Type II odontoid fractures may be treated by halo immobilisation or anterior screw/posterior C1–C2 fixation depending on displacement and age. Throughout, the priorities are to prevent secondary cord injury and to achieve a stable, painless, well-aligned spine that protects neural function and permits rehabilitation.
Facet Dislocations
A flexion–distraction force can cause the inferior facet of one vertebra to jump over the superior facet of the one below — a unilateral (~25% translation, rotational deformity) or bilateral (~50% translation, high risk of cord injury) facet dislocation. Treatment is prompt reduction (closed reduction with traction, or open reduction) followed by fusion. Many units obtain an MRI before reduction to exclude a herniated disc that could be driven into the cord during manipulation.
Complications
Spinal cord injury (from the initial trauma or secondary displacement) is the feared complication, with quadriplegia and respiratory failure in high lesions. Others include vertebral artery injury, non-union (notably of type-II odontoid fractures), post-traumatic deformity and instability, and chronic pain.
💡Always image the cervicothoracic junction (C7–T1) — it is the commonest site of a missed injury on plain films because of overlying shoulders; if not seen, obtain a swimmer's view or CT.Clearance & Prevention
A cervical spine is only ‘cleared’ when the patient is alert, unintoxicated, has no distracting injury, no midline tenderness and a normal neurological examination (or a normal CT where imaging is indicated). In the obtunded patient, precautions are maintained until adequate imaging is reviewed. Many sporting cervical injuries (diving, rugby, gymnastics) are preventable through technique and rule changes, and ‘spear-tackling’ with a flexed neck is a recognised cause of catastrophic injury.
Assume injury until cleared clinically or radiologically. 🔑KEY POINTS TO REMEMBER- Immobilise every at-risk patient; a missed unstable injury can cause quadriplegia.
- Upper C-spine: Jefferson (C1 burst), odontoid (type II common, non-union), Hangman's (C2).
- Subaxial: flexion (wedge, teardrop, facet dislocation), burst, extension (central cord).
- CT is the imaging standard; add MRI for deficit or ligament/cord injury.
- Stable → collar/halo; unstable/cord compression → reduction + fusion. Always image C7–T1.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition & Anatomy
An acetabular fracture involves the socket of the hip joint. It is an intra-articular fracture, usually from high-energy trauma transmitted through the femoral head (a dashboard injury with the hip flexed, or a fall). The acetabulum is conceptualised as two columns — the anterior (iliopubic) and posterior (ilioischial) columns, joined by the sciatic-buttress ‘inverted Y’ — the basis of the Judet–Letournel classification.
The acetabulum as anterior and posterior columns joined by the sciatic buttress — the anatomical basis of the Judet–Letournel classification. Mechanism & Associated Injuries
The pattern depends on the position of the femoral head at impact and the direction of force. A dashboard injury with the hip flexed and adducted drives the head posteriorly, producing a posterior wall fracture ± posterior dislocation; force through an abducted hip tends to injure the anterior structures. Because of the high energy, look for associated ipsilateral knee, femoral shaft and neck injuries, and pelvic and abdominal trauma.
Classification
The Judet–Letournel classification divides fractures into elementary (posterior wall, posterior column, anterior wall, anterior column, transverse) and associated patterns (e.g. both-column, T-shaped, transverse + posterior wall). Posterior wall fractures are the commonest and are frequently associated with posterior hip dislocation.
Clinical Features
Hip pain and inability to bear weight after high-energy trauma. Because many acetabular fractures accompany a hip dislocation, assess the limb position and — crucially — the sciatic nerve (especially its peroneal division) in posterior injuries. Screen for the associated pelvic, knee (dashboard) and abdominal injuries.
⚠️A posterior hip dislocation (with or without a posterior wall fracture) is an orthopaedic emergency — reduce it urgently to reduce the risk of avascular necrosis of the femoral head and to relieve sciatic nerve stretch. Check and document nerve function before and after.Investigations
AP pelvis with Judet (oblique) views and, definitively, a CT scan with reconstructions to define the columns, articular comminution, marginal impaction, and any intra-articular fragments or femoral head injury.
Management
The goal is a congruent, stable, pain-free hip. Undisplaced fractures, or those with a congruent joint and an intact weight-bearing dome, are treated non-operatively with protected weight-bearing. Displaced fractures with articular incongruity, an unstable joint or an intra-articular fragment require open reduction and internal fixation (anatomical reduction of the joint surface via the appropriate column approach). In the elderly with severe comminution, acute total hip replacement (sometimes with fixation) is an option.
Complications
Post-traumatic osteoarthritis (the main long-term problem, from articular damage or incongruity), avascular necrosis of the femoral head (especially after dislocation), sciatic nerve injury, heterotopic ossification, and infection after surgery.
🔑KEY POINTS TO REMEMBER- Intra-articular, high-energy; conceptualised as anterior + posterior columns (Judet–Letournel).
- Posterior wall is commonest and often accompanies posterior hip dislocation.
- Reduce a hip dislocation urgently; check the sciatic (peroneal) nerve.
- CT defines the pattern; congruent joint → non-operative, displaced/incongruent → ORIF.
- Main sequelae: post-traumatic OA and femoral head AVN.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Two Distinct Entities
‘Shock’ in spinal injury refers to two entirely different phenomena that are frequently confused. Spinal shock is a neurological phenomenon (loss of cord function), whereas neurogenic shock is a circulatory phenomenon (a form of distributive shock). They may coexist but must be distinguished.
Spinal Shock
Spinal shock is the transient loss of all spinal cord functions below the level of injury immediately after trauma — flaccid paralysis, areflexia, and loss of sensation and autonomic tone. It is temporary; recovery of reflexes begins within 24–48 hours, signalled by return of the bulbocavernosus reflex. The completeness of a cord injury (and hence prognosis) can only be judged after spinal shock has resolved.
Neurogenic Shock
Neurogenic shock occurs with injuries above T6, where loss of sympathetic outflow leaves unopposed vagal tone. The result is hypotension with bradycardia and warm, vasodilated peripheries — a combination that distinguishes it from hypovolaemic shock (which causes tachycardia and cold peripheries).
Feature Spinal shock Neurogenic shock Nature Neurological (cord) Circulatory (haemodynamic) Findings Flaccidity, areflexia Hypotension + bradycardia Level Any complete cord injury Lesion above T6 Recovery marker Bulbocavernosus reflex returns Resolves with sympathetic recovery Treatment Supportive; await resolution Fluids, vasopressors, atropine ⚠️In a trauma patient, always assume hypotension is due to haemorrhage until proven otherwise. Diagnose neurogenic shock only after excluding bleeding; the tell-tale sign is hypotension with bradycardia rather than tachycardia.Why the Distinction Matters
Confusing the two is dangerous. Treating neurogenic shock as pure hypovolaemia leads to over-transfusion and pulmonary oedema, while attributing a fall in blood pressure to the cord injury can cause a fatal missed haemorrhage. Equally, prognosticating a cord injury as ‘complete’ during the phase of spinal shock is invalid, because reflexes and some function may yet return once spinal shock resolves. The safe rule is: resuscitate for haemorrhage first, and judge cord completeness only after spinal shock has passed.
Bradycardia with hypotension distinguishes neurogenic from hypovolaemic shock. 🔑KEY POINTS TO REMEMBER- Spinal shock = neurological (flaccid, areflexic); neurogenic shock = circulatory.
- Bulbocavernosus reflex return marks the end of spinal shock.
- Neurogenic shock (lesion >T6): hypotension + bradycardia + warm peripheries.
- Exclude haemorrhage first; treat neurogenic shock with fluids, vasopressors, atropine.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Cauda equina syndrome (CES) is compression of the lumbosacral nerve roots below the conus medullaris (below ~L1), producing a characteristic pattern of bladder/bowel dysfunction, saddle anaesthesia and lower-limb weakness. It is a surgical emergency because delayed decompression risks permanent sphincter and sexual dysfunction.
Causes
The commonest cause is a large central lumbar disc prolapse (typically L4–L5 or L5–S1); other causes include tumour, epidural abscess or haematoma, spinal stenosis, and trauma.
Clinical Features (red flags)
The warning features are urinary retention with overflow incontinence (or altered bladder sensation), faecal incontinence / loss of anal tone, saddle (perineal) anaesthesia, bilateral sciatica or leg weakness, and sexual dysfunction. Per-rectal examination assesses tone and perianal sensation. Painless urinary retention with a large post-void residual is a particularly ominous sign.
⚠️Bilateral sciatica with any bladder/bowel disturbance or saddle numbness is CES until proven otherwise. Do not wait for ‘complete’ signs — arrange an urgent MRI and emergency decompression; outcome depends on early surgery, ideally before retention becomes established.Management
Urgent MRI of the whole lumbosacral spine confirms the level and cause. Treatment is emergency surgical decompression (e.g. discectomy/laminectomy, or drainage of an abscess/haematoma). The bladder is catheterised; steroids are given if the cause is tumour. Earlier decompression gives better recovery of sphincter function.
Incomplete vs Complete & Prognosis
CES is described as incomplete (CES-I) — altered urinary sensation and difficulty voiding but without painless retention — or complete (CES-R), with painless retention and overflow incontinence. Outcome is markedly better when decompression is performed in the incomplete stage, before painless retention becomes established; this is why urgent recognition and imaging are stressed. Recovery of bladder, bowel and sexual function is the principal determinant of long-term disability.
A surgical emergency — delay causes permanent incontinence. Red flag Finding Saddle anaesthesia Perineal sensory loss Bladder dysfunction Retention with overflow incontinence Bowel dysfunction Loss of anal tone, incontinence Motor Bilateral progressive leg weakness Action Urgent MRI + decompression within 48 hours 🔑KEY POINTS TO REMEMBER- CES = compression of lumbosacral roots below the conus; a surgical emergency.
- Commonest cause: large central lumbar disc prolapse.
- Red flags: retention/incontinence, saddle anaesthesia, bilateral sciatica, ↓ anal tone.
- Urgent MRI + emergency decompression; earlier surgery = better sphincter recovery.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
The atlas (C1) and axis (C2) form a unique upper-cervical complex specialised for rotation and support of the skull. Two classic bony injuries here are the Jefferson fracture of C1 and the Hangman’s fracture of C2.
Jefferson Fracture (C1)
A burst fracture of the ring of the atlas caused by an axial load onto the head (e.g. diving into shallow water), which splays the lateral masses. Stability depends on the transverse ligament: if it is intact the fracture is stable; if disrupted (suggested by lateral-mass overhang > ~7 mm on the open-mouth view) it is unstable. Despite the dramatic radiograph, neurological injury is often absent because the canal is capacious at this level.
Hangman’s Fracture (C2)
A traumatic spondylolisthesis of the axis — bilateral fracture of the pars interarticularis of C2 — from a hyperextension–distraction force (judicial hanging historically; now RTAs). Like the Jefferson fracture, the canal is wide here so cord injury is frequently avoided.
Jefferson (C1) Hangman’s (C2) Mechanism Axial compression Hyperextension–distraction Fracture Burst of the C1 ring Bilateral C2 pars fracture Stability key Transverse ligament Displacement / disc-ligament injury Typical Rx Collar/halo (stable) or fusion Collar/halo; fusion if unstable Management
Both are assessed with CT (and MRI for ligamentous/cord concern). Stable injuries are treated with a rigid collar or halo vest; unstable patterns (disrupted transverse ligament, significant displacement or angulation) require surgical stabilisation/fusion. Immobilisation and prevention of secondary injury apply throughout.
Clinical Features
There is upper neck pain and stiffness after axial or hyperextension trauma, often with the patient guarding or supporting the head. Neurological deficit is frequently absent because the spinal canal is capacious at the C1–C2 level, but a deficit or vertebral artery injury must always be sought. Diving into shallow water, falls onto the vertex and high-speed RTAs are the typical mechanisms. Suspicion plus a low threshold for CT is essential, as plain radiographs readily miss these injuries.
Both are often neurologically intact due to a capacious canal. 🔑KEY POINTS TO REMEMBER- Jefferson = axial-load burst of C1; stability depends on the transverse ligament.
- Hangman’s = hyperextension bilateral C2 pars fracture (traumatic spondylolisthesis).
- Wide canal at C1–C2 → cord injury often avoided despite dramatic films.
- Stable → collar/halo; unstable → fusion. CT is the key investigation.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
The odontoid process (dens) is the peg of the axis (C2) around which the atlas rotates, held by the transverse ligament. A dens fracture results from flexion or extension forces (RTA in the young, a fall in the elderly). It is important because the type-II fracture is prone to non-union and to instability that threatens the cord.
Anderson–D’Alonzo Location Note Type I Tip of the dens (avulsion) Rare; usually stable Type II Base of the dens (junction with body) Commonest; high non-union rate Type III Extends into the C2 body Broad cancellous surface; unites well Clinical Features & Investigations
Neck pain and stiffness, often with the patient supporting the head with the hands; neurological deficit is variable. Diagnosis is by the open-mouth (odontoid peg) radiograph and, definitively, CT; MRI assesses the transverse ligament and cord.
Management
Type I and III fractures generally unite with external immobilisation (collar or halo vest). Type II is problematic: undisplaced fractures may be treated in a halo, but displacement, age > 50 and high non-union risk favour surgical fixation — anterior odontoid screw or posterior C1–C2 fusion.
⚠️The elderly tolerate halo immobilisation poorly and type-II fractures have a high non-union rate in this group — surgical fixation or a well-fitted hard collar is often preferred over prolonged halo treatment, which the frail elderly tolerate badly and which carries its own respiratory and skin risks.Non-union & Its Determinants
The type-II fracture is notorious for non-union because the fracture line lies at the narrow junction of dens and body, a watershed with a poor blood supply and a small cross-sectional area of cancellous contact. Risk factors for non-union include displacement > 5 mm, angulation, advanced age, delayed treatment and posterior displacement. A united type-III fracture, by contrast, has a broad cancellous surface and heals reliably. Non-union may produce chronic instability (os odontoideum-like) threatening the cord.
Type II has the highest non-union rate and often needs fixation. 🔑KEY POINTS TO REMEMBER- Dens fracture around which C1 rotates; flexion/extension mechanism.
- Anderson–D’Alonzo I (tip), II (base — commonest, non-union), III (body — unites well).
- Open-mouth view + CT; MRI for ligament/cord.
- I & III → immobilise; II → halo or surgery (odontoid screw / C1–C2 fusion).
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
A burst fracture is a compression fracture in which an axial load fails both the anterior and middle columns of the vertebra, so that bone is retropulsed into the spinal canal. It typically occurs at the thoracolumbar junction after a fall from height or an RTA, and — unlike a simple wedge compression — carries a risk of neurological injury.
Clinical Features & Investigations
Back pain, a palpable tender step, and a variable neurological deficit (from intact to conus/cauda involvement). Perform a full neurological and sacral examination. CT demonstrates the middle-column failure and canal compromise (retropulsed fragment); MRI is added for a deficit or to assess the posterior ligamentous complex and cord.
💡The feature that separates a burst fracture from a stable wedge compression is middle-column involvement with retropulsion of bone into the canal — assessed on CT and central to management.Management
A neurologically intact, stable burst fracture (acceptable kyphosis and canal compromise, intact posterior ligamentous complex) can be managed conservatively in a TLSO brace with early mobilisation and follow-up imaging. A fracture with a neurological deficit, significant canal compromise, progressive kyphosis or posterior ligamentous injury requires surgical decompression and instrumented stabilisation (posterior pedicle screws ± anterior decompression).
Assessing Stability & Complications
Decision-making is aided by scores such as the Load-Sharing classification (degree of comminution) and the TLICS score, which combine the fracture morphology, the integrity of the posterior ligamentous complex and the neurological status to guide operative versus non-operative treatment. Complications include a neurological deficit (conus or cauda), progressive kyphotic deformity and chronic pain from an inadequately stabilised fracture, and the general risks of surgery and prolonged recumbency.
Follow-up & Outcome
Whichever route is chosen, patients are followed with serial imaging to detect progressive kyphosis or late instability, and with repeated neurological examination. Most neurologically intact stable burst fractures do well with bracing; operative stabilisation reliably restores alignment in unstable injuries but carries surgical risks. Long-term back pain and stiffness are the commonest residual complaints.
Posterior ligamentous complex integrity determines stability. 🔑KEY POINTS TO REMEMBER- Axial load fails anterior + middle columns with retropulsion into the canal.
- Thoracolumbar junction; risk of neurological injury (unlike a simple wedge).
- CT shows middle-column failure/canal compromise; MRI for deficit/ligament/cord.
- Intact & stable → brace; deficit/unstable/canal compromise → decompress + fuse.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.The Problem
An unstable pelvic fracture is a leading cause of preventable death in trauma because of massive haemorrhage. Bleeding is predominantly venous (presacral plexus) and from fracture surfaces, with an arterial source (internal iliac branches) in a minority. Opening the pelvic ring (an open-book injury) increases the volume available for bleeding, so that clot cannot form and tamponade the injury — the rationale for early ring closure.
The Pelvic Binder
The pelvic binder is a simple, immediate, life-saving device applied at the level of the greater trochanters (not the iliac crests). By compressing and closing the ring it reduces pelvic volume, restores bony apposition and promotes tamponade of venous bleeding. It is applied early in the ATLS primary survey in any suspected unstable pelvic injury with haemodynamic compromise.
⚠️Apply the binder over the greater trochanters. Placed too high (over the iliac crests) it fails to close the ring and does not control bleeding. Internally rotate and tie the legs to help close the pelvis.Escalation of Haemorrhage Control
If bleeding continues despite a binder and resuscitation (massive transfusion protocol, tranexamic acid), escalate to: angiography with embolisation for arterial bleeding; pre-peritoneal pelvic packing for surgical control of venous/bony bleeding; and an external fixator or C-clamp for mechanical stability. These are complementary and chosen by the pattern of bleeding and local resources.
Ongoing Care After the Binder
The binder is a temporising measure, not definitive treatment. After application, the patient is resuscitated to a permissive target while the source of bleeding is addressed, and the pelvis is later stabilised definitively (external or internal fixation). Prolonged binder use risks pressure necrosis of the skin over the trochanters and sacrum, so the binder should be released or repositioned once haemorrhage is controlled. Continuous monitoring of haemodynamics, urine output and distal perfusion guides escalation to embolisation or packing. The binder is combined with, not a substitute for, correction of coagulopathy, warming, and calcium replacement as part of damage-control resuscitation.
Binder goes over the trochanters, not the iliac crests. 🔑KEY POINTS TO REMEMBER- Unstable pelvic fracture → life-threatening (mostly venous) haemorrhage.
- Pelvic binder over the greater trochanters closes the ring & tamponades bleeding.
- Too-high placement (iliac crests) fails — apply at the trochanters.
- Escalate: transfusion/TXA → embolisation (arterial) / pre-peritoneal packing → external fixation.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.Definition
Whiplash-associated disorder is a soft-tissue (musculoligamentous) injury of the cervical spine caused by a sudden acceleration–deceleration (‘whiplash’) movement of the neck, classically in a rear-end road-traffic collision. There is no fracture or dislocation, but the neck is hyperextended then flexed, straining the muscles, ligaments and facet joints.
Clinical Features
Symptoms are often delayed by hours and include neck pain and stiffness, occipital headache, reduced range of movement, and referred pain to the shoulders and interscapular region. Dizziness, paraesthesiae and difficulty concentrating may occur. The examination excludes a true neurological deficit or bony injury (the Quebec classification grades severity 0–IV).
Investigations & Management
Radiographs (or CT where the Canadian C-spine rule/NEXUS indicate) are performed to exclude a fracture or dislocation; imaging is normal in whiplash apart from possible loss of the cervical lordosis from muscle spasm. Management is conservative and emphasises reassurance, early mobilisation and return to normal activity, simple analgesia and physiotherapy. Prolonged collar immobilisation is discouraged as it delays recovery and fosters stiffness. Patients are reassured that the great majority recover fully, and are encouraged to keep the neck moving within the limits of pain and to resume work and driving as symptoms allow.
Grading and Prognosis
The Quebec Task Force grades whiplash from 0 (no complaint) through I (pain only), II (pain with musculoskeletal signs) and III (pain with neurological signs) to IV (fracture or dislocation). Most patients in grades I and II recover within a few weeks to months with active management. A minority develop a chronic whiplash syndrome with persistent pain and disability; recognised risk factors include high initial pain intensity, pre-existing neck symptoms and psychosocial stressors. Setting realistic expectations and encouraging early return to normal activity measurably improve outcome.
💡The modern principle is ‘act as usual’: reassurance, analgesia and early active movement give better outcomes than rest and a collar, which prolong stiffness and disability.Collars are avoided — early movement gives better outcomes. 🔑KEY POINTS TO REMEMBER- Soft-tissue acceleration–deceleration injury of the neck (rear-end collision); no fracture.
- Delayed neck pain/stiffness, headache, reduced movement.
- Image to exclude fracture/dislocation; films otherwise normal (± lost lordosis).
- Treat conservatively: reassurance, analgesia, early mobilisation; avoid prolonged collar.
📚SOURCES: Maheshwari's Essential Orthopaedics; Apley & Solomon's System of Orthopaedics and Trauma; AO Principles of Fracture Management.