Complications
Venous thromboembolism (VTE) occurs in 20% to 90% of trauma patients.[102] VTE after major orthopaedic surgery is a significant concern, and warrants appropriate prophylaxis and monitoring. VTE also occurs after long bone fractures that are treated non-operatively.
VTE has been reported in 1.3% to 1.6% of patients undergoing open surgical treatment for hip fracture, despite postoperative prophylaxis measures.[103]
In patients undergoing surgery for proximal humerus fracture, deep vein thrombosis was reported in 0.19% of patients and pulmonary embolism in 0.4% of patients in one study.[104]
Guidelines exist for VTE prophylaxis in patients undergoing major orthopaedic surgery.[73] However, there is no universal consensus on how to approach anticoagulation in patients who have sustained fractures but are not necessarily undergoing surgical repair of the fracture. In these situations, it is especially important to consider the potential risks and benefits of instituting VTE prophylaxis. Patients deemed to be at higher risk of VTE complications may be more likely to benefit from more intense, multimodal prophylaxis; whereas those who are at lower risk of VTE disease or a higher risk of bleeding complications may benefit more from a less intensive regimen based on early mobilisation. The most critical period for VTE development is within the first month after orthopaedic surgery, but the risk of VTE may persist for longer.[105]
Mainly occurs with open fractures and/or after surgery. Symptoms include increasing pain, redness, swelling, discharge from wound or operative site, fever.
Patients are managed with debridement and appropriate antibiotic therapy.
The key clinical findings are pain out of proportion to the associated injury and pain on passive movement of the muscles of the involved compartments. Although the classic signs of acute compartment syndrome are loss of distal pulses, pallor, increased pain with passive stretch of tissues distal to the fracture site, paraesthesias, and poikilothermia, these signs are more often indicative of arterial ischaemia than acute extremity compartment syndrome.[48][51] A high index of suspicion is therefore needed. Palpable pulses distal to the involved compartment do not rule out compartment syndrome.[48] Absent pulses are usually due to systemic hypotension, arterial occlusion, or vascular injury.[48] To recognise extremity compartment syndrome in a timely fashion, it is important to maintain a high index of suspicion and serially examine patients at risk to document changes over time. If the examination is equivocal or diagnosis is unclear, then there is a role for pressure measurement.[46][69] However, a 'normal' compartment pressure alone should not be relied on to rule out acute compartment syndrome if the clinical picture is consistent with a compartment syndrome.
Should be suspected in any patient who suddenly develops respiratory distress or mental status changes after the initial injury or after surgery. Classically develops within 1-2 days after injury, and is more common after long bone fracture and in patients with polytrauma.
Major criteria for diagnosis include hypoxaemia, pulmonary oedema, mental status changes, and a petechial rash. Minor criteria include fever, tachycardia, retinal emboli, fat in sputum or urine, thrombocytopenia, and decreased haematocrit.[107]
Treatment is generally supportive, but early recognition is crucial. Proper immobilisation, rapid (within 24 hours) open reduction and internal fixation, and use of prophylactic corticosteroids potentially decrease risk.[108][109][110] However, there are no convincing data that corticosteroids ameliorate the clinical course of established fat embolism syndrome.
In malunion, the fracture has healed in an abnormal position, which can lead to impaired function, deformity, and/or discomfort.
Radiographic healing often lags behind clinical progress. Consider patient factors such as pain and ability to function as well as the imaging when deciding any further treatment; the patient, not just the x-rays, should be treated.
A complication of shoulder fracture or other upper extremity injury.
Typically occurs with protracted immobilisation and/or disuse, and manifests within weeks.
The process may persist for approximately 6 months to 2 years.
Increased risk in those with prolonged immobilisation, older people, women, and those with diabetes, thyroid disease, lower body mass index, or stroke.[118][119]
Non-healing of a fracture is often due to inadequate immobilisation, impaired blood supply, improper alignment, significant soft-tissue damage, or infection.
Fractures may be complicated by complex regional pain syndrome, often also called reflex sympathetic dystrophy.[106]
Manifestations often begin within weeks of injury but may not be diagnosed until later.
Characterised by pain, swelling, hyperaesthesia, allodynia, and colour and temperature changes around the site of injury. Impaired function may result. Local autonomic dysfunction and localised osteopenia may develop.
Early recognition of this condition allows prompt treatment, which may improve long-term outcome.
Death of bone tissue resulting from a lack of adequate blood supply.
Most commonly reported in the femoral head, but has also been reported at the humeral head and distal femur (especially the medial femoral condyle).
Most cases are associated with trauma, especially fracture and/or dislocation.
Presentation is variable. In some cases, no clinical symptoms or signs are noted, and it may only be discovered incidentally (i.e., during imaging for another indication). Pain, often described as deep and aching, is the most common presenting complaint. It is worse with weight-bearing and/or increased activity, although pain at rest and at night may also occur. In avascular necrosis (AVN) of the femoral head, the pain may be felt mainly in the groin or buttock.[111][112] The exact nature and severity of the symptoms depends on the bone involved, and the size, extent, and stage of the process.
Different staging systems have been proposed for classifying AVN of the femoral head. The most commonly used are the Ficat classification and the University of Pennsylvania classification.[113][114]
Treatment varies depending upon many factors, including the location of the damage, the severity and extent of involvement, and the age, medical condition, and functional status of the patient. In mild cases that are detected early, non-weight bearing and rest may be sufficient to allow healing; in more advanced cases, surgical treatment (ranging from core decompression, with or without bone grafting, to total joint replacement) may be necessary.[115]
Extracorporeal shock wave therapy has been proposed as being superior to core decompression, and bisphosphonates have been shown to possibly delay AVN progression in the femoral head (which is especially interesting in light of their association with osteonecrosis of the jaw).[116][117] However, the data supporting these therapies are limited, and no medical therapy has been conclusively proven to stop or reverse AVN.
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