Complications from fractures

How common are complications from fractures?

Fractures are common: many people will experience at least one during a lifetime. With modern medical and surgical care, most heal without problems or significant loss of function. However, fractures are associated with a range of complications.

Acute complications are generally those occurring as a result of the initial trauma and include neurovascular and soft tissue damage, blood loss and localised contamination and infection.

Delayed complications may occur after treatment or as a result of initial treatment and may include malunion, embolic complications, osteomyelitis and loss of function.

The risk of complications varies with the particular fracture, its site, circumstances and complexity, with the quality of management, with patient-specific risk factors such as age and comorbidities, and with post-fracture activities such as air travel and immobility.

Risk factors

Fracture complications are often variably defined, and there is a lack of consensus in their assessment, which makes their incidence difficult to estimate. Complications clearly vary with fracture site and nature and with quality of surgery but many also vary with patient attributes such as:

• Age.

• Nutritional status.

• Smoking status.

• Alcohol use.

• Diabetes (type 1 or type 2).

• Use of non-steroidal anti-inflammatory drugs (NSAIDs) within 12 months.

• A recent motor vehicle accident (one month or less prior to fracture).

• Oestrogen-containing hormone therapy (although this may be a proxy for osteoporosis).

Normal fracture healing

The process of normal fracture healing involves:

• Inflammation - with swelling, lasting 2-3 weeks.

• Soft callus formation - a decrease in swelling as new bone formation begins, fracture site stiffens. This takes until week 4-8 post-injury and is not visible on X-ray.

• Hard callus formation as new bone bridges the fracture site. This is visible on X-ray and should fill the fracture by weeks 8-12 post-injury.

• Bone remodelling - the bone remodels to correct deformities in the shape and loading strength. This can take several years, depending on the site.

For healing to happen the site needs adequate stability, a blood supply and adequate nutrition. Healing rates vary by person, and are likely to be compromised by the risk factors above and by age and comorbidity.

Fracture complications such as excessive bleeding or soft tissue compromise, infection, neurovascular injury, the presence of complex bone injury, such as crushing or splintering, and severe soft tissue trauma will clearly prolong and possibly hinder or prevent this healing process.

Early complications of fractures

Life-threatening complications

• These include vascular damage such as disruption to the femoral artery or its major branches by femoral fracture, or damage to the pelvic arteries by pelvic fracture.

• Patients with multiple rib fractures may develop pneumothorax, flail chest and respiratory compromise.¹

• Hip fractures, particularly in elderly patients, lead to loss of mobility which may result in pneumonia, thromboembolic disease or rhabdomyolysis.

Local

• Vascular injury.

• Visceral injury causing damage to structures such as the brain, lung or bladder.

• Damage to surrounding tissue, nerves or skin.

• Haemarthrosis.

• Compartment syndrome (or Volkmann's ischaemia).²

• Wound Infection - more common for open fractures.

• Fracture blisters.³

Systemic

• Fat embolism.⁴

• Shock.

• Thromboembolism (pulmonary or venous).

• Exacerbation of underlying diseases such as diabetes or coronary artery disease (CAD).

• Pneumonia.

Compartment syndrome

See the separate Compartment Syndrome article.

Fat embolism

See the separate Fat Embolism Syndrome article.

Fracture blisters

These are a relatively uncommon complication of fractures in areas where skin adheres tightly to bone with little intervening soft tissue cushioning. Examples include the ankle, wrist, elbow and foot.

Fracture blisters form over the fracture site and alter management and repair, often necessitating early cast removal and immobilisation by bed rest with limb elevation. They are believed to result from large strains applied to the skin during the initial fracture deformation, and they resemble second-degree burns rather than friction blisters. They may be clear or haemorrhagic, and they may lead to chronic ulcers and infection, with scarring on eventual healing.

Management involves delay in surgical intervention and casting. Silver sulfadiazine seemed in one review to promote re-epithelialisation.

Risk factors, other than site, include any condition which predisposes to poor skin healing, including diabetes, hypertension, smoking, alcohol excess and peripheral arterial disease.

Late complications of fractures

Local

• Delayed union (fracture takes longer than normal to heal).

• Malunion (fracture does not heal in normal alignment).

• Non-union (fracture does not heal).

• Joint stiffness.

• Contractures.

• Myositis ossificans.⁵

• Avascular necrosis.

• Algodystrophy (or Sudeck's atrophy).

• Osteomyelitis.

• Growth disturbance or deformity.

Systemic

• Gangrene, tetanus, septicaemia.

• Fear of mobilising.

Problems with bone healing (non-union, delayed union and malunion)

Delayed union is failure of a fracture to consolidate within the expected time - which varies with site and nature of the fracture and with patient factors such as age. Healing processes are still continuing, but the outcome is uncertain.

Non-union occurs when there are no signs of healing after >3-6 months (depending upon the site of fracture). Non-union is one endpoint of delayed union. The distinction between delayed union and non-union can be slightly arbitrary: whilst fractures can generally be expected to heal in 3-4 months, this will vary in the case of open fractures and those associated with vascular injury, and also in the presence of patient risk factors described below. However, non-union is generally said to occur when all healing processes have ceased and union has not occurred.

Malunion occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction.

Factors predisposing to delayed union⁶

• Severe soft tissue damage.

• Inadequate blood supply.

• Infection.

• Insufficient splintage.

• Excessive traction.

• Older age.

• Severe anaemia.

• Diabetes.

• Low vitamin D level.

• Hypothyroidism.

• Medications including NSAIDs and steroids.

• Complicated/compound fracture.

• Osteoporosis.

Factors disposing to non-union
Delayed union and non-union occurs in approximately 5-10% of all fractures but is more common in open long bone fractures (17% non-union) or where there is motion at the fracture site.⁷ Risk factors are all of those above and also:

• Too large a space for bony remodelling to bridge.

• Interposition of periosteum, muscle or cartilage.

• Bony site with a limited blood supply: some sites are more vulnerable to compromise of blood supply by the fracture (eg, scaphoid, femoral head and neck, and tibia).

Presentation of non-union

• Pain at fracture site, persisting for months or years.

• Non-use of extremity.

• Tenderness and swelling.

• Joint stiffness (prolonged >3 months).

• Movement around the fracture site (pseudarthrosis).

• Palpable gap at fracture site.

• Absence of callus (remodelled bone) or lack of progressive change in the callus suggests delayed union.

• Closed medullary cavities suggest non-union.

• Radiologically, bone can look inactive, suggesting the area is avascular (known as atrophic non-union) or there can be excessive bone formation on either side of the gap (known as hypertrophic non-union).

Management of non-union
Non-surgical approaches:

• Early weight bearing and casting may be helpful for delayed union and non-union.

• Bone stimulation can sometimes be used. This delivers pulsed ultrasonic or electromagnetic waves to stimulate new bone formation. It needs to be used for up to an hour every day, and may take several weeks to be effective.

• Medical treatments such as teriparatide (unlicensed use in the UK) have also been used to promote fracture healing, particularly in patients with osteoporosis.⁷

Surgical approaches:

• Debridement to establish a healthy infection-free vascularity at the fracture site.

• Bone grafting to stimulate new callus formation. Bone may be taken from the patient or may be cadaveric.

• Bone graft substitutes/osteobiologics.

• Internal fixation to reduce and stabilise the fracture. (Bone grafting provides no stability.)

• Depending on the type of non-union, any combination of the above.⁶

Myositis ossificans

Myositis ossificans occurs when calcifications and bony masses develop within muscle and can occur as a complication of fractures, especially in supracondylar fractures of the humerus.⁵

The condition tends to present with pain, tenderness, focal swelling, and joint/muscle contractures. Avoid excessive physiotherapy; rest the joint until pain subsides; NSAIDs may be helpful; and consider excision after the lesion has stabilised (usually 6-24 months). It may be difficult to distinguish from osteogenic sarcoma.⁵

Algodystrophy

Algodystrophy, also known as complex regional pain syndrome (CRPS) or Sudeck's atrophy, is a form of reflex sympathetic dystrophy (or complex regional pain syndrome type 1), usually found in the hand or foot. More than 40% of reflex sympathetic dystrophies follow trauma, notably fractures.⁸ A continuous, burning pain develops, accompanied at first by local swelling, warmth and redness, progressing to pallor and atrophy. Movement of the afflicted limb is very restricted. Treatment is usually multi-pronged:

• Rehabilitation - physiotherapy and occupational therapy to decrease sensitivity and gradually increase exercise tolerance.

• Psychological therapy.

• Pain management - often difficult and with a disputed evidence base. Approaches used are neuropathic pain medications (eg, amitriptyline, gabapentin, opioids), steroids, calcitonin, intravenous bisphosphonates and regional blocks.

Iatrogenic complications of fracture treatment

Casts
Poor cast placement may lead to problems of malunion, either because the bones are not accurately aligned or because the fracture is not sufficiently immobilised.

Prolonged cast immobilisation, or 'cast disease', can create circulatory disturbances, inflammation, and bone disease resulting in osteoporosis, chronic oedema, soft tissue atrophy, and joint stiffness. Good physiotherapy will help avoid these problems. Casts may also cause:

• Pressure ulcers.

• Thermal burns during plaster hardening.

• Thrombophlebitis.

Patients need clear information on managing a cast - for example, on keeping it dry, on reporting increased pain or tingling/numbness. Sharp edges rubbing on the skin may need to be trimmed or filed. Poor cast management leading to wetness of the skin beneath the cast can affect skin integrity, which increases the risk of infection.

Casts lead to some loss of bone density in the affected limb, a phenomenon which is seen regardless of the type of casting or skill involved.⁹

Traction
Traction prevents patients mobilising, causing additional muscle wasting and weakness. Other complications of traction include:

• Pressure ulcers.

• Pneumonia/urinary tract infections.

• Permanent footdrop contractures.

• Peroneal nerve palsy.

• Pin tract infection.

• Thromboembolism.

External fixation
Problems caused by external fixation include:

• Pin tract infection.

• Pin loosening or breakage.

• Interference with movement of the joint.

• Neurovascular damage due to pin placement.

• Misalignment due to poor placement of the fixator.

• Psychological complications: external fixation can have a massive psychological impact on the patient. Altered body image and a sense of visible disability, deformity or mutilation can occur. Some patients have to adjust their device and assist with pin site care, and this may also be frightening. Provision of adequate information before fixation, where possible, and support and information after the procedure are an essential part of care.

Dr Mary Lowth is an author or the original author of this leaflet.