Although multiple organizations have proposed guidelines for VTE prophylaxis, those suggested by the American Academy of Orthopaedic Surgeons (AAOS) and the American College of Chest Physicians (ACCP) are most frequently cited in the setting of hip and knee arthroplasty. Historically, substantial variability existed between these guidelines. These inconsistencies were largely attributable to the use of different end points (symptomatic PE vs. all VTE) while interpreting the data. Although differences in the recommendations remain, the most recent versions have the greatest degree of uniformity (13,14).

Both the AAOS and ACCP stratify their recommendations based on the level of recommendation and the level of evidence. The AAOS assigns an overall grade (strong, moderate, weak, inconclusive, or consensus). The ACCP assigns separate grades for the strength of the recommendation (1, strong; 2, weak) and the level of the evidence (A, high quality; B, moderate quality; C, low or very low quality) (15,16).

Dual therapy (pharmacologic with antithrombotic medications and mechanical with intermittent pneumatic compression devices [IPCD]) is generally recommended in patients undergoing hip and knee arthroplasty during hospitalization (AAOS moderate, ACCP Grade 2C). However, in terms of pharmacologic agent choice, the AAOS has found insufficient evidence to make recommendations for or against specific agents and regimens (moderate). The ACCP has recommended low-molecular-weight heparin (LMWH), fondaparinux, apixaban, dabigatran, rivaroxaban, low-dose unfractionated heparin (LDUH), warfarin (Grade 1B), or IPCD (Grade 1C) as acceptable treatments; however, LMWH was preferred over fondaparinux, apixaban, dabigatran, rivaroxaban, LDUH (Grade 2B), and warfarin (Grade 2C). In patients with active bleeding disorders that preclude them from receiving pharmacologic prophylaxis, the AAOS recommends IPCD monotherapy (consensus); in patients with an increased risk of bleeding, the ACCP suggests IPCD or no prophylaxis (Grade 2C) (17,18).

The timing and duration of therapy are other extremely important considerations with VTE prophylaxis. The timing of the initiation of pharmacologic agents is critical, and the risk of VTE versus bleeding must be analyzed on a case-by-case basis. It is critical that the surgeon is able to determine when initial hemostasis has been achieved, as it is not always at the completion of the procedure. The current ACCP guidelines recommend initiating LMWH either 12 hours before the start or after the completion of surgery (Grade 1B). Although the AAOS guideline found insufficient evidence to recommend a duration of prophylaxis (consensus), the ACCP recommends a minimum of 10 to 14 days with extension up to 35 days being preferred (Grade 2B) (17,18).

Thrombi form in the peripheral venous vasculature under conditions described by Virchow’s triad (stasis, endothelial damage, hypercoagulability). The lower extremities are the most common location of DVT. Lower extremity thrombi are typically classified either proximal (pelvic and thigh) or distal (calf). Proximal thrombi are at higher risk of embolization to the pulmonary vasculature in general. They are also larger and so produce higher risk of developing into symptomatic PE. Distal thrombi are smaller, at lower risk of embolization to PE, and (although rare) more likely to lead to paradoxical arterial embolization through a patent foramen ovale or atrial septal defect than the larger, proximal thrombi. Upper extremity thrombi are less common and the least likely to embolize (19).

DVT alone can damage the venous valvular system and cause postphlebitic syndrome, which is characterized by chronic pain and edema. PE leads to hypoxemia, increased pulmonary vascular resistance, impaired gas exchange, alveolar hyperventilation, increased airway resistance, and decreased pulmonary compliance. The alveolar–arterial O₂ tension gradient becomes markedly elevated. Progressive right ventricular failure can lead to myocardial ischemia, circulatory collapse, and death (20).

It is important to note that both the AAOS and the ACCP recommend against duplex screening before discharge (strong recommendation and Grade 1B, respectively) (17,18). Therefore, the first layer of detection includes the patient’s symptoms and the clinical examination. A recent systematic review found the rates of symptomatic VTE in the setting of appropriate prophylaxis to be 1.09% and 0.53% for total knee arthroplasty (TKA) and THA, respectively (21).

DVT typically presents as persistent and progressive lower extremity cramping. Swelling, erythema, and fever may also be present. The differential diagnoses include cellulitis, venous insufficiency, and a ruptured Baker cyst. PE commonly presents as shortness of breath. Other signs include tachycardia, fever, syncope, hypotension, cyanosis, and coughing. The differential diagnosis includes pneumonia, costochondritis, pneumothorax, acute coronary syndrome, anxiety, and exacerbations of medical comorbidities like asthma, COPD, or congestive heart failure (CHF) (20).

A variety of nonimaging tests for the detection of VTE exist but have minimal utility. D-dimer ELISA is typically elevated in the setting of VTE. This test is relatively sensitive but with low specificity. In addition, the time required to receive a result minimizes its usefulness. Similarly, although PO₂ and PCO₂ typically decrease in the setting of PE, blood gas results lack specificity. Electrocardiogram signs, such as S1Q3T3 sign or V1–V4 T-wave inversion, are specific but not sensitive (20).

When clinical suspicion warrants further investigation, imaging modalities are the studies of choice. Although operator dependent, ultrasonography is the primary study for the diagnosis of DVT. The diagnosis is made by alternations in venous compressibility and flow dynamics. If ultrasound is not available, unable to be performed, or nondiagnostic,
computed tomography (CT) or magnetic resonance venography may be considered (20).

For the vast majority of patients, pulmonary CT with intravenous contrast is the primary imaging modality for PE. Although the previous generation of CT had limitations, current CT technology is capable of detecting even small peripheral emboli. Pulmonary ventilation–perfusion scanning is typically reserved for patients with contraindications to intravenous contrast. Unfortunately, with this modality there is a high rate of nondiagnostic or “intermediate-probability” examinations. Although pulmonary angiography is considered the “gold standard” for the diagnosis of PE, it has been replaced by pulmonary CT in most clinical settings. The use of pulmonary angiography is limited to cases with high clinical suspicion but nondiagnostic CT scan, or when an interventional treatment procedure is planned. Magnetic resonance pulmonary angiography is useful for the detection of large emboli (20).

Treatment following VTE is divided into primary (thrombolysis or embolectomy) or secondary (prevention of recurrent VTE); therefore, it is critical to stratify patients based upon clinical manifestations and risk of recurrence. Primary therapy is indicated in patients who develop hemodynamic instability following PE. Patients without discrete hemodynamic instability but some component of right ventricular failure should be analyzed on an individual basis. All other patients are best treated with a regimen of secondary prevention (20).

Secondary prevention regimens include the variables of agent and therapy duration. Unfractionated heparin, LMWHs, factor Xa pentasaccharide, warfarin, factor Xa inhibitors, and direct thrombin inhibitors are typical agents (or classes of agents) utilized in secondary prevention programs. Characteristics such as half-life, side effects, metabolism, and convenience should be considered when selecting an agent for a particular patient. Risk of recurrence ultimately determines the duration of therapy. VTE following hip arthroplasty is considered provoked, with these patients less likely to have long-term recurrence. It is generally recommended that patients with upper extremity and distal lower extremity DVT be treated for 3 months, and those with proximal lower extremity DVT or any PE be treated for 3 to 6 months. Indefinite anticoagulation is considered in patients with unprovoked or recurrent VTE (20).