Long-bone fractures, fat embolism and dislocations

• A long-bone shaft fracture is not just a broken bone: in the femur and tibia it can bleed enough to cause shock, and moving fragments can release fat that blocks the lungs and brain.
• Fix the big problems first: airway, breathing, circulation, then image, then plan fixation. Cover open wounds with saline-soaked gauze and keep the bone's blood supply and soft tissue in mind.
• Fat embolism syndrome appears one to three days after injury as breathlessness, confusion and a petechial rash; no criterion is validated, so think of it early in any deteriorating trauma patient.
• A swollen, painful limb after trauma needs repeated neurovascular checks; a pulseless deformed limb is realigned and splinted immediately, not imaged first.
• Common dislocations are reduced under analgesia or sedation, with imaging before and after reduction; a dislocated hip is an orthopaedic emergency because of avascular necrosis.

By the end of this page you should be able to:

1. Recognise and prioritise femoral, tibial and humeral shaft fractures, including their fixation options and the soft-tissue rules for open fractures.
2. Diagnose fat embolism syndrome, apply its criteria and imaging, and know what is supportive care versus prevention.
3. Carry out and document a neurovascular examination, and state when to image, reduce and refer.
4. Reduce and manage shoulder, hip, elbow and knee dislocations, including aftercare and recurrence.
5. State the BOAST, AO and other guideline editions used for these conditions, and the limits of the evidence.

Long-bone fractures, fat embolism syndrome and dislocations sit together in the emergency department because they are all "stop and think" injuries. A fractured femoral shaft can bleed enough into the thigh to cause shock; a displaced fracture can quietly embolise fat to the lungs; a deformed limb can be losing its blood supply while everyone looks at the X-ray first. The page is about the first 24 hours: what kills, what saves the limb, and what must not be missed.

This page does not cover every fracture and dislocation. Paediatric fractures are in the Pediatrics chapter. Pelvic and hip fractures as bony injuries are addressed elsewhere; this page covers hip dislocation. Paediatric supracondylar fractures of the elbow have their own standard (see the British Orthopaedic Association Standards for Trauma, referenced below). Joint-specific arthroplasty and complex ligament reconstruction are beyond its scope.

A shaft fracture of a long bone is one that lies in the diaphysis, between the proximal and distal metaphyses. Whatever the bone, the sequence is the same: resuscitate, examine the limb, image, temporise, then definitively fix.

Examination. Document motor and sensory function in the limb and the pulses, before and after any manipulation, and note the skin: open or closed, the size and cleanliness of the wound, swelling, deformity and muscle compartments. The British Orthopaedic Association Standard for Trauma (BOASt) for open fractures requires that the examination include assessment and documentation of vascular and neurological status, repeated systematically, particularly after reduction manoeuvres or splinting.^{[8] [5]}

Imaging. Plain radiographs of the bone in two planes, including the joints above and below the fracture, are the baseline. In a high-energy injury the trauma series of imaging helps exclude the associated injuries.

Temporising care. Realign gently and splint the limb, give analgesia and antibiotics if the fracture is open, and obtain senior (orthopaedic and, where relevant, vascular or plastic surgical) input early. For open fractures the BOASt sets debridement urgency by contamination and energy: immediately for highly contaminated wounds (agricultural, aquatic, sewage) or when vascular compromise or compartment syndrome is present; within 12 hours for other solitary high-energy open fractures; and within 24 hours for all other low-energy open fractures.^{[8] [5]}

Femoral shaft fractures have a bimodal pattern: young adults in high-energy trauma, and older adults after low-energy falls, often on osteoporotic bone. They bleed. The priority after resuscitation is pain control, imaging and decision on fixation. The AO Surgery Reference groups these fractures as simple (spiral, oblique, transverse), wedge and multifragmentary patterns.^[10]

In fit adults the standard treatment is operative. Intramedullary nailing, locked to control rotation and length, is the usual definitive fixation; locking plates and external fixation are reserved for problems such as severe open injury, infection, associated vascular injury or very proximal and distal patterns where nailing is less suited. A Cochrane review of methods of intramedullary nailing for femoral shaft fractures exists, but the choice between reamed and unreamed nailing is made by the treating team. In the multiply injured patient the timing depends on physiology: early definitive fixation when the patient is stable, and damage-control external fixation when they are not, converting to an intramedullary nail later.

Tibial shaft fractures are the commonest long-bone fracture in many trauma series. The skin over the medial border is thin, so open fractures are common, and the compartment syndrome risk is real. The AO Surgery Reference groups these as simple, wedge and multifragmentary patterns and highlights open fractures, infection and compartment syndrome as the key concerns.^[9]

Intramedullary nailing is again the commonest definitive fixation for adults, with plates for selected patterns (for example metaphyseal extension) and external fixation for open injuries or temporary damage control. Reamed and unreamed nail techniques both have a role; suprapatellar and infrapatellar approaches are chosen by surgeon experience and anatomy. After fixation, pay attention to rotational alignment, because malrotation is a recognised complication.

Humeral shaft fractures are common in both high- and low-energy trauma. The radial nerve runs in the spiral groove on the posterior aspect of the shaft and can be injured by the fracture or by surgery. Most isolated, non-displaced or minimally displaced fractures can be managed non-operatively in a functional brace, with acceptable union rates. Displaced fractures, open fractures, associated vascular injury, pathological fractures and failures of conservative care are indications for operative fixation, usually plating, with intramedullary nailing used for selected patterns. The AO Surgery Reference prompts a neurovascular assessment and attention to open fractures in the humeral shaft section.^[10]

• Intramedullary nail. Splints the bone from the inside, controls length and rotation with proximal and distal locking, allows early weight-bearing in the lower limb and has low infection rates in closed fractures. It is the workhorse for femoral and tibial shafts.
• Plate and screws. Gives direct, anatomic reduction and is favoured around the ends of the bone, for segmental or highly comminuted patterns unsuited to nailing, and for the humeral shaft. The cost is more soft-tissue dissection and a higher infection risk in open fractures.
• External fixation. Pins above and below the fracture, outside the body. Used for damage control in unstable polytrauma, severe open injury awaiting debridement and soft-tissue cover, infected non-union and vascular injury. It is converted to internal fixation when the soft tissues permit.

Open fractures need antibiotics early: the BOASt states intravenous prophylactic antibiotics should be administered as soon as possible, ideally within 1 hour of injury.^[8] Tetanus prophylaxis follows local guidance. Definitive soft-tissue closure or coverage should be achieved within 72 hours if it cannot be done at the first operation.^{[8] [5]}

A neurovascular examination has three parts and should be recorded, not remembered.

• Motor. Test the nerves that cross the injured level: radial nerve (wrist and finger extension), median (finger flexion, index-thumb pinch), ulnar (finger abduction), common peroneal (ankle dorsiflexion and great-toe extension), tibial (ankle plantarflexion).
• Sensation. Test the autonomous zones: radial (first dorsal web space), median (index tip), ulnar (little finger tip), common peroneal (first web space of the foot), tibial (sole).
• Circulation. Pulses, capillary refill, skin colour and temperature, and, if in doubt, Doppler and an ankle-brachial index (ABI). The EFORT review of multiligament knee injuries states that vascular injury may be present despite palpable pulses, and an ABI under 0.9 has high sensitivity for arterial injury.^[6]

Repeat the check after every manipulation, splinting and pillow change. If the pulses are lost after realignment, assume arterial injury until imaging proves otherwise; the BOASt for arterial injury requires revascularisation to commence within one hour of arrival where possible.^[4]

Fat embolism syndrome (FES) is a complex and potentially life-threatening condition in which fat particles enter the circulation and injure the lungs, brain and skin through a mix of mechanical embolisation and inflammation.^[1] It remains one of the classic "1% that matters" complications of long-bone and pelvic trauma, and the diagnosis is easy to miss because it looks like other things.

FES was first described in 1861 when fat emboli were found in the lung capillaries of a trauma patient who died.^[1] The patient in the first recorded clinical diagnosis had a femoral fracture with breathlessness, cyanosis and coma about 60 hours after injury.^[1]

The numbers today are lower than the autopsy figures. Before modern criteria and routine internal fixation, fat emboli were seen at autopsy in 40 to 100% of cases after trauma.^[1] With modern care the syndrome is clinically apparent after long-bone or pelvic fracture in roughly 1.4 to 12.5% of cases.^[1] A US national hospital discharge analysis from 1979 to 2005 found FES recorded in only 0.004% of 928 324 trauma admissions, more often in men and in patients aged 10 to 39 years.^[1] Multiple femoral shaft fractures carried a higher rate than single fractures (1.29% versus 0.54%).^[1] Where hypoxaemia accompanies a long-bone or pelvic fracture the rate can be around 11%.^[1] Cerebral fat embolism has been reported in about 0.04% of hospital trauma admissions.^[1]

Risk factors include long-bone and pelvic fractures, multiple and open fractures, delay to fixation, and non-traumatic causes such as fat grafting, sickle cell disease vaso-occlusive crisis, acute pancreatitis and bone marrow biopsy. Men and the second and third decades of life are over-represented.

Two ideas explain FES and the syndrome probably involves both.

• Mechanical theory. Force raises pressure inside the medullary cavity, so fat droplets are forced into the venous system; they lodge first in the pulmonary microvasculature and reach the arterial circulation through right-to-left shunts such as a patent foramen ovale or arteriovenous shunts. Bone marrow emboli found in the lungs support this. A patient with a femoral fracture and breathlessness, cyanosis and coma days later fits the classic picture.^[1]
• Biochemical theory. Fat in the pulmonary vasculature triggers a microvascular inflammatory response, with raised plasma phospholipase A2, pro-inflammatory cytokines and free radicals. This explains why symptoms are often delayed by hours to days after the injury, rather than immediate.^[1]

The clinical triad reflects the organs most often hit: lungs (respiratory distress), brain (neurological dysfunction) and skin (petechiae). It does not usually appear all at once.

Symptom onset is typically one to three days after injury.^[1] Many patients are sedated or ventilated by then, which delays recognition.

• Respiratory. Dyspnoea, tachypnoea, hypoxaemia, cough, often progressing to diffuse infiltrates. Severe cases develop acute respiratory distress syndrome; about 44% need invasive ventilation.^[1]
• Neurological. Confusion, agitation, restlessness, seizure or coma out of proportion to any head injury. Focal deficit is unusual early on.
• Cutaneous. Petechiae over the chest, axillae, conjunctivae and palate; present in fewer than half of cases and often overlooked.
• Systemic. Fever, tachycardia, anaemia, thrombocytopenia, lipiduria. Cardiovascular collapse in severe cases.

Brain MRI is the key investigation for cerebral fat embolism. The "starfield" pattern of tiny scattered lesions on diffusion-weighted imaging is the best known finding, but it is non-specific and often reversible. Chest imaging is non-specific: radiograph abnormalities occur in roughly 30 to 50% of cases as bilateral diffuse or patchy infiltrates.^[1]

No diagnostic criterion for FES has been prospectively validated. The three commonly quoted ones are compared below. Treat them as an aid to thinking, not a diagnosis.

There is no disease-specific therapy. Management is supportive intensive care: oxygen, cautious fluid, lung-protective ventilation (invasive ventilation is needed in up to 44% of cases), escalation to prone positioning or extracorporeal membrane oxygenation in severe acute respiratory distress syndrome, and management of brain injury (raised intracranial pressure monitoring and imaging; craniotomy only in selected cases).^[1] Corticosteroids are controversial: meta-analyses suggest they may reduce the incidence of FES and hypoxaemia, but they show no mortality benefit and may increase infection risk, so they are not standard care.^[1]

FES is prevented as much as treated. Early stabilisation of long-bone fractures, ideally within 24 hours, is the most effective preventive strategy: it reduces acute respiratory distress syndrome and improves mobilisation.^[1] In unstable polytrauma the damage-control orthopaedic approach (external fixation now, definitive fixation later) improves survival, at the cost of a staged operation and longer stay. In the EFORT review of multiligament knee injuries, knee-spanning external fixation is similarly used for fracture-dislocations and soft-tissue compromise, with reconstruction three to six weeks later.^[6]

A dislocation is an emergency of the joint and of its neurovascular bundle. The principles run across shoulders, hips, elbows and knees:

1. Analgesia or sedation first, with early discussion of pain-relief options with the patient; procedural sedation and analgesia is first choice when reduction fails without it.^[2]
2. Image before if feasible (two orthogonal views), reduce promptly, then image again to confirm reduction and exclude fracture.
3. Neurovascular examination before and after every manipulation, documented; repeat after splinting. A pulseless deformed limb is realigned and splinted first, not scanned first.^[4]
4. Reduction technique chosen from what you know: traction-based, leverage, or biomechanical (scapular) techniques are all effective with small differences in pain.^[2]
5. Aftercare with brief immobilisation, early guided movement and rehabilitation, plus attention to recurrence risk.

The British Orthopaedic Association, through its trauma standards, has published dislocation-related guidance including first-time lateral patellar dislocation (December 2024) and, in the field of neurovascular safety, the standards for arterial injuries and compartment syndrome.^[3]

Anterior shoulder dislocation is the commonest major joint dislocation, with an incidence of 12 to 26 per 100 000 person-years, usually after a blow or fall. Males dislocate during sport, females more often at home. Prompt arrival matters: one guideline notes that delay to reduction is associated with higher failure rates.^[2]

Clinical picture. The arm is held slightly abducted and externally rotated; the squared-off shoulder and palpable humeral head anteriorly are characteristic. Beware the elderly patient where pain and reluctance to move mask a dislocation, and always look for a concurrent rotator cuff tear or fracture of the greater tuberosity.

Imaging. Radiographs in at least two orthogonal planes before and after reduction; CT when uncertainty persists. An AP view plus a scapular Y view is conventional; ultrasound is not a substitute for radiographs because it misses concomitant fractures. Post-reduction images matter because about 15% of fractures seen after reduction were not visible beforehand.^[2]

Reduction. Use a technique you are confident in; biomechanical (scapular) reduction is recommended as the first method. If the first attempt fails, image to exclude complications, try again under procedural sedation, and resort to open reduction rarely. Realign promptly to limit neurovascular stretch.^[2]

Aftercare. A sling as needed for one week, then early restoration of rotator cuff function, coordination and proprioception. Males and patients under 40 years are at higher risk of recurrence (a 3-fold and 13-fold increase respectively).^[2] In a large registry, recurrent dislocation ranged from 29% in men aged 10 to 19 down to 9 to 12% in patients over 50. Greater tuberosity fracture-dislocation is paradoxically associated with lower recurrence. Discuss surgical stabilisation in patients under 40, in contact-sport athletes and where there is significant bone loss, since a meta-analysis of early Bankart repair showed 8.9% recurrence versus 49% with non-operative care.^[2]

Complications of the mass. Iatrogenic fracture is most often seen in women over 40 with a concomitant greater tuberosity fracture; neurological injury (axillary nerve) and rotator cuff tears are common, so document motor and sensory findings and repeat them. ^[2]

Traumatic hip dislocation usually occurs when the knee strikes the dashboard in a road-traffic collision, often with associated knee ligament injury as well. It is a true orthopaedic emergency: hip dislocation requires immediate reduction as soon as the patient is stable, and avascular necrosis of the femoral head becomes much more likely if reduction is delayed by more than six hours.^[7]

Posterior dislocation (about 90%). The limb is shortened, flexed, adducted and internally rotated; scrub or "tailor's" deformity. The sciatic nerve is commonly injured, especially its peroneal division, so check ankle dorsiflexion and sensation in the first web space carefully; in fracture-dislocations about 4% of limbs develop sciatic palsy, with 60 to 70% recovering spontaneously.^[7] Reduction is by in-line longitudinal traction in the line of the deformed limb, with an assistant providing counter-traction; modest flexion and internal rotation may need to be recreated before traction brings the head back over the rim. Open reduction is required if closed reduction fails or if a femoral neck fracture coexists.

Anterior dislocation. More rare. The limb is shortened, flexed, abducted and externally rotated. Reduction mirrors the deformity. Watch for associated femoral head and acetabular fracture.

Aftercare. Image the hip before and after reduction in two planes; CT is needed to exclude intra-articular fragments and acetabular fracture. If a femoral head fracture is present, management depends on the Pipkin pattern: non-displaced Pipkin I or II fractures may be managed conservatively with partial weight-bearing in adduction and internal rotation for four to six weeks, while displaced fragments usually need open reduction and internal fixation, and elderly Pipkin III injuries may need arthroplasty.^[7] Avascular necrosis, heterotopic ossification (most after anterior approaches) and post-traumatic arthritis are the late complications to discuss with the patient. Early infection occurs in about 3%.^[7]

Simple (pure) posterior elbow dislocation is the second commonest major dislocation in adults. The forearm is shortened and the olecranon prominent posteriorly; the joint is grossly unstable to valgus and varus stress. The mechanism is usually a fall on the outstretched hand or a throwing injury. Because the elbow is a hinge with tight collateral ligaments, the force needed to dislocate it can tear the ligaments and fracture the coronoid process, radial head or capitellum: this is the "terrible triad" (dislocation plus radial head fracture plus coronoid fracture) and it is unstable by definition.

Management. Analgesia or procedural sedation, then closed reduction by traction in line with the forearm with the elbow slightly flexed, followed by gentle extension; a valgus stress and forearm pronation counter the brachialis and flexors. Image before (AP and lateral) and after; CT is used when fracture is suspected, because coronoid fractures can be occult. After reduction, test for stability through a range of movement and assess the coronoid and radial head on imaging. Early active movement within a stable range is encouraged, with the arm in a hinged brace; chronic instability or a terrible triad needs surgical fixation and ligament repair.

Neurovascular traps. The brachial artery and the median and ulnar nerves are at risk; check the compartments of the forearm after reduction and remember that posterior dislocation can stretch the ulnar nerve running behind the medial epicondyle. The BOASt for diagnosis and management of arterial injuries applies: suspected vascular injury means mandatory consultant input, CT angiography if needed and revascularisation as an emergency.^[4]

Knee dislocation is uncommon but limb-threatening. It is a multiligament injury that may reduce spontaneously before the patient reaches hospital, so suspect it from mechanism, deformity, a large effusion, or unexplained pain and instability even when the knee looks normal.

Vascular risk is the story. Vascular injury occurs in roughly 18% of multiligament knee injuries and can be present despite palpable distal pulses; an ankle-brachial index under 0.9 is highly sensitive for arterial injury. The common peroneal (fibular) nerve is injured in 10 to 40% of cases.^[6] The EFORT review recommends serial vascular examinations, selective CT angiography and careful neurological assessment for all.^[6] Urgent reduction in line with the deformity, immobilisation in extension, and reassessment of pulses come before any definitive plan.

Aftercare. Knee-spanning external fixation is indicated for vascular injury, open or fracture-dislocation and persisting instability, with ligament reconstruction commonly delayed three to six weeks; there is no clear superiority of early versus delayed reconstruction for function, though early surgery carries a higher stiffness risk. Arthrofibrosis complicates about 10% of cases.^[6]

• Infection in open fractures and after nailing is prevented by early antibiotics, adequate debridement and timely soft-tissue cover. Staphylococcus aureus and gram-negative organisms are typical.
• Compartment syndrome is the emergency: pain out of proportion, pain on passive stretch, tense swelling; measure pressures if equivocal and fasciotomise promptly.
• Malunion, non-union and malrotation, particularly after tibial nailing; some malrotation changes gait and function.
• Avascular necrosis of the femoral head after hip dislocation, especially with reduction delayed beyond six hours.^[7]
• Sciatic nerve palsy after posterior hip dislocation, mostly peroneal-division, with 60 to 70% spontaneous recovery.^[7]
• Recurrent instability after shoulder and (less commonly) knee dislocation; discussed above.
• Fat embolism syndrome is itself a major complication of long-bone fractures, described above.

Children. Paediatric fractures, including supracondylar humeral fractures and paediatric femoral and tibial shaft fractures, are covered in the paediatrics chapter and have their own standards (the BOAST for paediatric forearm fractures and for supracondylar humeral fractures).^[3] Adults' growth-plate and remodelling biology does not apply: predictable remodelling is a paediatric property. For a child with a long-bone fracture, follow the paediatrics pathway rather than adult fixation algorithms.

Pregnancy. Trauma in pregnancy should be managed by the standard trauma survey with obstetric input; long-bone fixation is not contraindicated where indicated, and fetal monitoring should be arranged. Operative timing and drug choices need individual planning.

Older adults. Low-energy fragility fractures of the femoral shaft or distal femur occur in osteoporotic bone and may need implant choices that suit poor bone quality; recurrent dislocation is less frequent in older patients after a first shoulder dislocation.

• Everything starts with the examination. In facilities without imaging, document neurovascular status, realign, splint and transfer. A pulseless limb is realigned before the X-ray.
• Open fractures. Give antibiotics as soon as possible (within 1 hour if you can) and debride by urgency; clean wounds within 24 hours if transfer is needed.
• Fixation. Intramedullary nails are comparatively cheap and robust where radiography and theatre are available; external fixation with a simple frame works when soft tissues or infection forbid internal fixation and when skills for complex reconstruction are not available.
• Fat embolism. Suspect it on clinical grounds: deterioration two to three days after a long-bone fracture with new hypoxaemia and confusion. Management is oxygen, ventilation and supportive care; early fracture stabilisation is the best prevention and is also the treatment.
• Dislocations. Reduction under sedation using biomechanical or traction techniques is low-resource and effective. Pre- and post-reduction radiographs can be replaced by careful clinical assessment when X-ray is unavailable, but beware occult fracture. Educate patients and families on recurrence and on early movement.
• Hip dislocation must be reduced promptly even where theatre and imaging are limited: delay improves the chance of avascular necrosis.

• Fracture principles, open fractures and compartment syndrome: fracture-principles-open-fractures-compartment-syndrome
• Pelvic and hip fractures, and trauma resuscitation: pelvic-and-hip-fractures; initial-trauma-assessment-primary-survey; trauma-resuscitation-and-massive-transfusion
• Orthopaedic paediatric injuries are in the pediatrics chapter, including paediatric-orthopaedic-injuries
• Avascular necrosis, compartment syndrome and regional anaesthesia are covered elsewhere