Complications
Venous thromboembolism (VTE) occurs in 20% to 90% of trauma patients.[120] VTE after major orthopedic surgery is a significant concern, and warrants appropriate prophylaxis and monitoring.[75] VTE also occurs after long bone fractures that are treated nonoperatively.
VTE has been reported in 1.3% to 1.6% of patients undergoing open surgical treatment for hip fracture, despite postoperative prophylaxis measures.[121]
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.[122] Data from a Canadian prospective cohort study (n=1200) showed that the risk of symptomatic VTE in nonoperative distal leg fracture was 0.6%.[123][124] A Danish registry study of 57,619 patients reported that within 6 months of operative distal leg fracture, 1.0% experienced a VTE event.[124][125] Guidelines exist for VTE prophylaxis in patients undergoing major orthopedic surgery.[75][76][115][126] 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 mobilization. The most critical period for VTE development is within the first month after orthopedic surgery, but the risk of VTE may persist for longer.[75]
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.
Progressively worsening pain, increased pain with passive range of motion, paresthesiae, and significant edema/tense soft tissues are common indicators. Pulselessness, pallor, and poikilothermia, the other classic findings of acute compartment syndrome, are not usually present until much later, unless serious vascular injury has already occurred. Symptoms usually develop within hours after injury.
If acute compartment syndrome is suspected, emergent orthopedic consultation and fasciotomy is required.[128]
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 hypoxemia, pulmonary edema, mental status changes, and a petechial rash. Minor criteria include fever, tachycardia, retinal emboli, fat in sputum or urine, thrombocytopenia, and decreased hematocrit.[129]
Treatment is generally supportive, but early recognition is crucial. Proper immobilization, rapid (within 24 hours) open reduction and internal fixation, and use of prophylactic corticosteroids potentially decrease risk.[130][131][132] 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; the patient, not just the x-rays, should be treated.
A complication of shoulder fracture or other upper extremity injury.
Typically occurs with protracted immobilization and/or disuse, and manifests within weeks.
The process may persist for approximately 6 months to 2 years.
Increased risk in those with prolonged immobilization, older people, women, and those with diabetes, thyroid disease, lower BMI, or stroke.[140][141]
Nonhealing of a fracture is often due to inadequate immobilization, 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.[127]
Manifestations often begin within weeks of injury but may not be diagnosed until later.
Characterized by pain, swelling, hyperesthesia, allodynia, and color and temperature changes around the site of injury. Impaired function may result. Local autonomic dysfunction and localized 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.[133][134] 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.[135][136]
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, nonweight 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.[137]
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).[138][139] However, the data supporting these therapies are limited, and no medical therapy has been conclusively proven to stop or reverse AVN.
Use of this content is subject to our disclaimer