Complications of Fractures

Introduction

Fractures do not just fail to heal in isolation - they carry risks to the whole patient as well as to the injured limb, and those risks change with time. Examiners exploit this by asking about complications using two axes: general (affecting the whole patient) versus local (affecting the injured limb), and early (within days) versus late (weeks to months later). Learning complications against this grid, rather than as an unstructured list, makes both revision and exam answers far more efficient.

This article assumes familiarity with fracture classification, reduction and the principles of bone healing, covered in the companion article on [Fractures](../fractures.json). It also touches on compartment syndrome, which has its own dedicated article - here it is covered only as one complication among many, with the detail left to that article.

Early general complications

Haemorrhagic shock

Fractures bleed, and closed long bone or pelvic fractures can cause life-threatening blood loss without any external wound. Blood loss occurs from the fracture surfaces themselves, from surrounding muscle and soft tissue, and, in pelvic fractures, from the extensive presacral venous plexus and adjacent arterial branches. This is a frequently underestimated source of occult haemorrhage in the trauma patient and is checked explicitly in the ATLS primary survey.¹

Management follows standard trauma resuscitation principles - major haemorrhage protocol with balanced blood product transfusion, tranexamic acid within 3 hours of injury, splinting or binding of the fracture to reduce further bleeding, and early surgical or radiological control of the bleeding source.

Fat embolism syndrome

Fat embolism syndrome results from fat globules entering the venous circulation from the marrow of a fractured long bone, embolising to the pulmonary and systemic circulation, and triggering a systemic inflammatory response. Two mechanisms are proposed: the mechanical theory, in which marrow fat is forced directly into torn venous sinusoids by the fracture and any subsequent intramedullary manipulation; and the biochemical theory, in which circulating free fatty acids trigger a systemic inflammatory cascade that damages the pulmonary capillary endothelium and other microvasculature.²

It is classically associated with fractures of the long bones (especially the femur) and the pelvis, and the risk rises with multiple fractures and with intramedullary nailing. Onset is typically 24-72 hours after injury, which distinguishes it from pulmonary embolism, which can occur at any time and is due to a thrombus rather than fat.

Fat embolism syndrome is a clinical diagnosis. Gurd and Wilson's criteria are the classic framework: diagnosis requires at least one major and four minor criteria, together with fat macroglobulinaemia.²

• Major criteria: petechial rash, respiratory symptoms with bilateral chest signs and characteristic chest X-ray changes, cerebral signs unrelated to head injury or other cause
• Minor criteria: tachycardia, pyrexia, retinal changes on fundoscopy (fat or petechiae), renal changes (oliguria or anuria), jaundice, a sudden unexplained drop in haemoglobin or platelet count, high erythrocyte sedimentation rate, and fat globules in the urine or sputum

There is no specific test or treatment. Investigations are supportive - arterial blood gas typically shows hypoxaemia, chest X-ray may show diffuse bilateral pulmonary infiltrates ('snowstorm' appearance), and CT head or MRI may show characteristic changes if cerebral involvement is suspected. Management is entirely supportive: oxygen and, where needed, ventilatory support, haemodynamic support, DVT prophylaxis, and early fixation of the fracture, which reduces the risk. There is no evidence for corticosteroids or specific pharmacological therapy.²

Venous thromboembolism

Orthopaedic trauma patients are at particularly high risk of venous thromboembolism because they combine several of Virchow's triad in one presentation: venous stasis from immobility and the injury itself, endothelial injury from the fracture and any surgery, and a hypercoagulable state from the systemic inflammatory response to trauma. Pelvic and lower limb fractures carry the highest risk, and risk persists into the rehabilitation period, not just the perioperative one.

NICE recommends that VTE risk be assessed for every patient on admission, alongside bleeding risk, and that prophylaxis be reviewed if the clinical situation changes.³ Prophylaxis in trauma combines:

• Mechanical prophylaxis - intermittent pneumatic compression or anti-embolism stockings, used from admission unless contraindicated (e.g. by peripheral arterial disease or an injury to the limb itself)
• Pharmacological prophylaxis - low molecular weight heparin, started once haemostasis is secured and any regional anaesthesia timing is respected, continued through the period of reduced mobility
• Early mobilisation - the single most effective and cheapest measure, and a key reason surgical fixation is preferred over prolonged traction or bed rest where feasible
• Adequate hydration and correction of anaemia, since both influence blood viscosity and perioperative risk
• Extended prophylaxis after major lower limb surgery, for example hip fracture surgery, per NICE guidance

Early local complications

Compartment syndrome

Compartment syndrome occurs when pressure within a closed fascial compartment rises to the point that capillary perfusion is compromised, threatening the muscle and nerves within it. It is most associated with tibial shaft and forearm fractures, but can complicate any fracture, and can also occur after tight casting or circumferential burns without a fracture at all.

Neurovascular injury

Fractures and dislocations can directly injure adjacent nerves or vessels, either at the moment of injury or during manipulation and reduction. A thorough neurovascular examination before and after any reduction is mandatory and should be documented explicitly, since it is both a patient safety and a medicolegal necessity.

Certain fracture patterns are classically paired with injury to a specific nerve because of their close anatomical relationship, and these associations are a favourite exam and OSCE topic:

Vascular injury is a separate but related concern - the brachial artery in supracondylar fractures and the popliteal artery in knee dislocations and proximal tibial fractures are the classic examples, because both vessels are tethered and relatively immobile at those levels. An absent or asymmetric distal pulse, prolonged capillary refill, or a cool, pale limb after a fracture or dislocation is a vascular emergency requiring urgent reduction and reassessment, with imaging (CT angiography) and vascular surgical input if perfusion does not immediately improve.

Infection

Infection risk is far higher in open fractures, where the fracture communicates with the external environment, than in closed injuries. Management follows the principles in BOAST guidance: prompt intravenous antibiotics (ideally within an hour of injury), photography and a clean dressing rather than repeated wound inspection in the emergency department, urgent debridement in theatre (immediately if grossly contaminated or there is a vascular compromise, otherwise within 12-24 hours), and a combined orthoplastic approach for soft tissue coverage.⁴

Closed fractures can still become infected, particularly after surgical fixation, and the risk is higher with implants (plates, nails, screws) because bacteria can form a biofilm on metalwork that is relatively protected from both the immune system and antibiotics. Established implant-related infection often requires a combination of prolonged antibiotics and further surgery, sometimes including removal of metalwork once the fracture has healed enough to allow it.

Late general complications

Many fracture patients, particularly older adults with hip fractures, spend prolonged periods with reduced mobility during recovery. The complications of bed rest and immobility are common, largely preventable, and heavily tested because they are so amenable to good ward-based care.

• Pressure sores - from prolonged pressure over bony prominences (sacrum, heels); prevented by regular repositioning, pressure-relieving mattresses and early mobilisation
• Hospital-acquired (and aspiration) pneumonia - from reduced chest expansion, poor cough effort and reduced mobility; chest physiotherapy and early sitting out help prevent it
• Urinary tract infection - often related to catheterisation, which should be used only where indicated and removed as soon as possible
• Muscle wasting and deconditioning - loss of strength and function that can be disproportionate to the original injury, particularly in frail or older patients, and a major driver of loss of independence
• Ongoing venous thromboembolism risk - persists for as long as mobility remains reduced, not just in the immediate postoperative period
• Constipation and faecal impaction - from immobility, opioid analgesia and reduced oral intake
• Delirium - common in older patients, multifactorial (pain, opioids, unfamiliar environment, infection, constipation), and itself delays mobilisation

Late local complications

Delayed union and non-union

Delayed union means healing is taking longer than expected for that fracture and that patient, but is still progressing. Non-union means healing has stopped altogether, with no radiographic progress over a period of months (commonly defined as no evidence of healing by 6-9 months). Non-union is subdivided by its radiographic appearance and, broadly, its underlying cause:

Risk factors for non-union include smoking, diabetes, NSAID use, poor nutrition, open fractures, infection, excessive fracture gap or soft tissue interposition, inadequate immobilisation, and disruption of the local blood supply, whether from the injury itself or from the surgery performed to fix it.

Investigation is largely radiographic (plain films over serial follow-up appointments; CT if plain films are equivocal), alongside screening for infection (inflammatory markers, and intraoperative sampling if surgery is undertaken) and for correctable systemic causes. Management depends on the type and cause of non-union and typically includes revision fixation to improve mechanical stability, bone grafting to stimulate biology, correction of any deformity, treatment of infection if present, and optimisation of modifiable risk factors such as smoking cessation. Adjuncts such as low-intensity pulsed ultrasound and electrical bone growth stimulation are used in selected cases, though the evidence base is mixed.

Malunion

Malunion is healing in an unsatisfactory position - with angulation, rotation or shortening beyond what is acceptable for that bone and that patient. It can cause deformity, altered limb mechanics, secondary joint pain and, over time, accelerates degenerative change in adjacent joints. Management ranges from acceptance where the deformity is functionally and cosmetically minor, to corrective osteotomy where it is not.

Avascular necrosis

Avascular necrosis (AVN) occurs when a fracture disrupts the blood supply to a fragment of bone, leading to death of that bone and eventual structural collapse. It is a particular risk at sites where the blood supply is retrograde or otherwise precarious, meaning a fracture at a specific point can cut off the only route in.

AVN may not become symptomatic or radiographically visible for months after the injury, so it is a late complication in the true sense - early X-rays can look normal. MRI is the most sensitive investigation for early AVN, before plain film changes (sclerosis, subchondral collapse - the 'crescent sign' - and eventual joint destruction) appear. Management ranges from observation and joint-preserving procedures (e.g. core decompression) in early disease to arthroplasty once collapse has occurred.

Complex regional pain syndrome

Complex regional pain syndrome (CRPS) is a chronic pain condition that can follow even a relatively minor fracture, classically of the wrist or ankle. It is characterised by pain disproportionate to the inciting injury, together with autonomic and trophic changes:

• Continuing pain, often burning in character and out of proportion to the original injury
• Allodynia (pain from a normally non-painful stimulus) and hyperalgesia
• Vasomotor changes - skin colour and temperature asymmetry between the affected and unaffected limb
• Sudomotor changes - abnormal sweating or oedema
• Trophic changes - altered hair or nail growth, and skin texture changes, in longstanding cases
• Reduced range of motion and, over time, motor weakness or tremor

The exact mechanism is incompletely understood but involves an exaggerated and maladaptive inflammatory and neurological response to injury. It is a clinical diagnosis (the Budapest criteria are the most widely used), and management is multidisciplinary - physiotherapy and occupational therapy to maintain function, pain team input for neuropathic analgesia, and psychological support, since chronic pain and reduced function are closely linked to mood.

Post-traumatic osteoarthritis

Any fracture that disrupts an articular surface, or that heals with residual incongruity or malalignment, changes the mechanical loading of that joint and predisposes to premature osteoarthritis. Intra-articular fractures (e.g. tibial plateau, distal radius extending into the joint, acetabular fractures) carry the highest risk, and the risk rises further if anatomical reduction is not achieved. This is a major reason why intra-articular fractures are generally reduced as accurately as possible, even when a small residual step would be tolerated in an extra-articular fracture.

Growth plate injury in children

In children, a fracture through or near the physis (growth plate) can damage the germinal cells responsible for longitudinal and, at some sites, angular growth. The Salter-Harris classification describes the pattern of physeal involvement and broadly predicts the risk of growth disturbance - higher-numbered types generally carry a higher risk, though this is a simplification.⁶

1. Type I - fracture through the physis only
2. Type II - through the physis, exiting through the metaphysis (the commonest type)
3. Type III - through the physis, exiting through the epiphysis into the joint
4. Type IV - through metaphysis, physis and epiphysis
5. Type V - a crush injury to the physis, often radiographically subtle at presentation but carrying the highest risk of growth arrest

Consequences of physeal injury include partial or complete growth arrest, leading to limb length discrepancy if the whole physis is affected, or angular deformity if growth arrest is asymmetric across the plate. Children with a physeal fracture need clinical and radiographic follow-up over subsequent months, since a growth disturbance may only become apparent as the discrepancy or deformity develops with further growth, well after the original fracture has clinically healed.

Approach to the fracture that is not healing

A common exam and clinical scenario is a patient still in pain, or with an X-ray that looks unchanged, at a follow-up appointment weeks after a fracture. A systematic approach avoids missing a treatable cause:

1. Confirm the timeline is actually abnormal - different bones and patients heal at different rates; check what was expected for this fracture, this age and this bone before assuming a problem
2. Look for a mechanical cause - inadequate immobilisation, inadequate fixation, excessive fracture gap, or ongoing weight-bearing against advice
3. Look for a biological cause - smoking, diabetes, NSAID use, poor nutrition, vitamin D deficiency, or a disrupted blood supply from the injury or the surgery
4. Exclude infection - even in a closed fracture, particularly if metalwork was used; check inflammatory markers and for systemic or local signs
5. Reconsider the diagnosis - is this actually non-union, or is the pain from something else entirely - avascular necrosis, CRPS, metalwork irritation, or a missed second injury?
6. Correlate with imaging - repeat plain films to assess progression, and consider CT if plain films are equivocal for union
7. Address modifiable factors before escalating - optimise nutrition, stop smoking, review medications - alongside, not instead of, surgical options

Red flags