2.1 Deep vein thrombosis

Venous thrombosis is thought to initiate at or shortly after traumatic injury. Venous thromboembolism most often occurs as DVT in the lower limbs, although it can occur in any vein of the body. Thrombosis isolated to the calf veins may remain asymptomatic with little risk of clot embolization but without prophylaxis these clots can extend into the popliteal veins or above in 15–25% of patients [8]. Deep vein thrombosis above the popliteal veins is clinically important because more than 50% are associated with PE [1, 2].

2.2 Pulmonary embolism

Pulmonary embolism involves obstruction of a pulmonary artery by a dislodged DVT that has traveled through the right ventricle, although fatal PE has been found without apparent DVT on postmortem examinations. Pulmonary embolism is a serious and potentially life-threatening complication that is associated with a mortality risk of approximately 10% [8].

2.3 Recurrent deep vein thrombosis and postthrombotic syndrome

Inadequately treated VTE can lead to recurrent DVT with the highest risk during the first year, although the risk persists for several years after acute DVT [8]. Risk factors for recurrent DVT include proximal location of prior DVT, obesity, old age, malignancy, and male gender [9]. Thrombophilia may also play a role [9, 10].

Postthrombotic syndrome is the most common long-term complication of VTE with an incidence of 20–50% after proximal DVT, with severe manifestations that have a profound impact on patient quality of life in 5–10% of cases [10, 11]. It is believed to be caused by persistent venous obstruction or valvular damage resulting in venous hypertension. Inflammation and vein wall fibrosis after DVT are involved in the development of PTS, but the pathophysiology is incompletely understood. Symptoms and signs of PTS vary from minor leg swelling to intractable pain, chronic edema and skin changes (lipodermatosclerosis), discoloration, and leg ulceration.

3.1 Deep vein thrombosis

A clinical diagnosis of DVT cannot be relied upon because most orthopedic trauma patients have signs and symptoms consistent with DVT, such as leg swelling and pain. The risk of DVT is highest in the first 3 months after trauma and then returns to the baseline population risk between 12 and 15 months [12].

Routine screening of trauma patients for the presence of DVT cannot be supported based on the available evidence [13]. However, venous duplex ultrasonography is highly accurate for the detection of proximal DVT in symptomatic patients. Other imaging modalities, such as magnetic resonance venography and contrast-enhanced computed tomography (CT) venography are being explored but continue to have a high false-positive rate [13].

D-dimer is a product of fibrin degradation and levels are typically high in patients with VTE but are also elevated in other conditions. Thus elevated D-dimer levels are not specific for the presence of VTE, but a negative D-dimer test is highly sensitive for ruling out VTE, depending on the type of assay performed. In patients with a suspicion of DVT, a negative D-dimer test performed using a sensitive assay can effectively rule out the presence of clinically significant VTE that would require treatment.

3.2 Pulmonary embolism

The diagnosis of PE can be challenging in trauma patients with chest wall injuries, lung contusions, fat embolism, pneumonia, and systemic inflammatory response syndrome [14].

Routine screening for PE is not recommended for trauma patients receiving prophylaxis [14, 15]). For patients with a suspected PE, a duplex CT pulmonary angiography is definitive, but there are significant associated costs and potential morbidity [5].

3.3 Postthrombotic syndrome

Postthrombotic syndrome is primarily a clinical diagnosis in someone with a previous DVT [11]. One should wait at least 3–6 months following an acute DVT episode before considering the diagnosis of PTS [11]. A number of clinical scoring systems exist and can be used for making the diagnosis and for grading severity. The Villalta-Prandoni scale, Ginsberg measure, and Brandjes scale [11] are specific to PTS.

Risk factors for the development of PTS include [11]:

• 
  

  Body mass index/obesity

  
  
• 
  

  Older age

  
  
• 
  

  Smoking

  
  
• 
  

  Extent of original DVT (femoral and iliac versus popliteal)

  
  
• 
  

  Recurrent DVT [10]

  
  
• 
  

  Underlying thrombophilia [10]

  
  
• 
  

  Residual thrombosis after DVT treatment and subtherapeutic treatment

4.1 Patient risk factors

Numerous potential patient risk factors have been proposed over many years, with conflicting evidence for some of them [7, 16, 17]. A recent attempt to develop a validated risk model to predict VTE within 90 days of surgery identified seven risk factors, including the following patient-related factors:

• 
  

  Increasing age

  
  
• 
  

  Obesity

  
  
• 
  

  Male gender

  
  
• 
  

  Current cancer

  
  
• 
  

  History of VTE

  
  
• 
  

  Family history of VTE

Others have noted a consistent increase in risk for women using oral contraceptive medication, with variable risk depending on the specific formulation used. It is also accepted that various genetic factors increase the risk of VTE [18]. The inherited thrombophilia risk factors have been summarized by Westrichin in a recent instructional course lecture ( Table 4.6-1 ).

Testing for these factors is not routinely required but should be considered in anyone with a strong family history or a history of VTE, especially if the episode occurred in people younger than 40 years [18].

4.2 Injury and surgery risk factors

Patients with polytrauma, hip fractures, spinal cord injury, pelvic or acetabular fractures, and lower extremity injuries are at high risk of VTE [2, 5, 13]. The risk may be higher for high thoracic spinal cord injuries versus other spinal cord injury levels. Traumatic brain injury in the context of polytrauma does not appear to increase the risk of VTE.

Longer duration of surgery is associated with increased VTE risk for all surgical specialty procedures, including orthopedic surgery [5]. Prolonged cardiothoracic, neurological, and gynecological operations are associated with an especially high risk.

Prolonged immobility, including prolonged extrication time after injury [19] increases the risk of VTE, even in the absence of injury.