Fractures are common and most of us will experience at least one during a lifetime. In modern times, with medical and surgical assistance, the majority heal without problems or significant loss of function. However, complications when they arise can pose a risk to life and limb.
This article will consider complications from all fractures. It is important to emphasise that the risk of complications varies with the particular fracture and factors particular to the affected patient. For example, age and comorbid conditions will clearly affect the risk of complications.
Complications of fractures tend to be classified according to whether they are local or systemic and when they occur - early or late.  Early complications occur at the time of the fracture (immediate) or soon after. Early local complications tend to affect mainly the soft tissues.
- Vascular injury causing haemorrhage, internal or external
- Visceral injury causing damage to structures such as the brain, lung or bladder
- Damage to surrounding tissue, nerves or skin
- Compartment syndrome (or Volkmann's ischaemia)
- Wound Infection - more common for open fractures
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Fractures of the limbs can cause severe ischaemia, even without damage to a major blood vessel. Bleeding or oedema in an osteofascial compartment increases pressure within the compartment, reducing capillary flow and causing muscle ischaemia. A vicious circle develops of further oedema and pressure build-up, leading swiftly to muscle and nerve necrosis. Limb amputation may be required if untreated. Compartment syndromes can also result from:
- Crush injuries caused by falling debris or from a patient's unconscious compression of their own limb.
- Swelling of a limb inside an over-tight cast.
Compartment syndrome can occur in any compartment, eg the hand, forearm, upper arm, abdomen, buttock, thigh, and leg. 40% occur following fracture of the shaft of the tibia (with an incidence of 1-10%) and about 14% following fracture of a forearm bone. Risk is highest in those under 35 years.
- Signs of ischaemia (5 P's: Pain, Paraesthesia, Pallor, Paralysis, Pulselessness) - but diagnosis should be made before all these features are present. Note: the presence of a pulse does not exclude the diagnosis.
- Signs of raised intracompartmental pressure:
- Swollen arm or leg
- Tender muscle - calf or forearm pain on passive extension of digits
- Pain out of proportion to injury
- Redness, mottling and blisters
- Watch for signs of renal failure (low-output uraemia with acidosis)
Where the diagnosis is uncertain, measure intracompartmental pressure directly. The pressure at which fasciotomy becomes mandatory is controversial.
- Remove/relieve external pressures
- Prompt decompression of threatened compartments by open fasciotomy
- Debride any muscle necrosis
- Treat hypovolaemic shock and oliguria urgently
- Renal dialysis may be necessary
- Acute renal failure secondary to rhabdomyolysis
- Disseminated intravascular coagulation (DIC)
- Volkmann's contracture (where infarcted muscle is replaced by inelastic fibrous tissue)
See seperate Fat Embolism article.
Late complications of fractures
- Delayed union
- Joint stiffness
- Myositis ossificans
- Avascular necrosis
- Algodystrophy (or Sudeck's atrophy)
- Growth disturbance or deformity
Problems with bone healing (nonunion, delayed union and malunion)
Nonunion is where there are no signs of healing after >3-6 months (depending upon the site of fracture). Nonunion is one endpoint of delayed union. Malunion occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction. Causes of delayed union include:
- Severe soft tissue damage
- Inadequate blood supply
- Insufficient splintage
- Excessive traction
Causes of nonunion are similar but also include:
- Too large a space for bony remodelling to bridge
- Interposition of periosteum, muscle or cartilage
Nonunion occurs in approximately 1% of all fractures but is more common in lower leg fractures (19% nonunion) or where there is motion at the fracture site.
- Pain at fracture site
- Nonuse of extremity
- Tenderness and swelling
- Joint stiffness (prolonged >3 months)
- Movement around the fracture site (pseudarthrosis)
- Absence of callus (remodelled bone) or lack of progressive change in the callus suggests delayed union.
- Closed medullary cavities suggest nonunion.
- Radiologically, bone can look inactive, suggesting the area is avascular (known as atrophic nonunion) or there can be excessive bone formation on either side of the gap (known as hypertrophic nonunion).
Nonsurgical approaches such as early weight bearing and casting may be helpful for delayed union and nonunion. Surgical treatments include:
- Debridement to establish a healthy infection-free vascularity at the fracture site
- Internal fixation to reduce and stabilise the fracture.
- Bone grafting to stimulate new callus formation.
Myositis ossificans is where calcifications and bony masses develop within muscle and can occur as a complication of fractures, especially in supracondylar fractures of the humerus. It tends to present with pain, tenderness, focal swelling, and joint/muscle contractions. Avoid excessive physiotherapy, rest the joint until pain subsides, non-steroidal anti-inflammatory drugs (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.
Sudeck's atrophy is a form of reflex sympathetic dystrophy (or complex regional pain syndrome type 1), usually found in the hand or foot. 89% of reflex sympathetic dystrophies follow trauma, notably fractures. A continuous, burning pain develops, accompanied at first by local swelling, warmth and redness which progresses 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, IV bisphosphonates and regional blocks.
- Pressure ulcers
- Thermal burns during plaster hardening
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 should avoid these problems.
Traction prevents patients mobilising, causing additional muscle wasting and weakness. Other complications include:
- Pressure ulcers
- Pneumonia/urinary tract infections
- Permanent footdrop contractures
- Peroneal nerve palsy
- Pin tract infection
- 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
Further reading & references
- Non Union, Wheeless' Textbook of Orthopaedics
- Apley AG & Solomon L, Concise system of orthopaedics and fractures, 2nd edition (1994), Butterworth Heinemann ISBN 0750617675
- Elliott KG, Johnstone AJ; Diagnosing acute compartment syndrome. J Bone Joint Surg Br. 2003 Jul;85(5):625-32.
- Gourgiotis S, Villias C, Germanos S, et al; Acute limb compartment syndrome: a review. J Surg Educ. 2007 May-Jun;64(3):178-86.
- Hartigan BJ, Benson LS; Myositis ossificans after a supracondylar fracture of the humerus in a child. Am J Orthop. 2001 Feb;30(2):152-4.
- Gould CF, Ly JQ, Lattin GE Jr, et al; Bone tumor mimics: avoiding misdiagnosis. Curr Probl Diagn Radiol. 2007 May-Jun;36(3):124-41.
- Duman I, Dincer U, Taskaynatan MA, et al; Reflex sympathetic dystrophy: a retrospective epidemiological study of 168 patients. Clin Rheumatol. 2007 Sep;26(9):1433-7. Epub 2007 Jan 13.
- Quisel A, Gill JM, Witherell P; Complex regional pain syndrome: which treatments show promise? J Fam Pract. 2005 Jul;54(7):599-603.
- Buckley R, Panaro C; General principles of fracture care, eMedicine, Jan 2010.
|Original Author: Dr Chloe Borton||Current Version: Dr Richard Draper|
|Last Checked: 01/06/2010||Document ID: 1986 Version: 22||© EMIS|
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