From the Research
Aspirin (acetylsalicylic acid) is not the standard medication for deep vein thrombosis (DVT) prophylaxis in patients with ankle septic arthritis. Low molecular weight heparins (LMWHs) such as enoxaparin (40mg subcutaneously once daily) or fondaparinux (2.5mg subcutaneously once daily) are the preferred agents for DVT prophylaxis in these patients. For patients with contraindications to anticoagulants, mechanical prophylaxis with intermittent pneumatic compression devices should be used. The duration of prophylaxis typically continues until the patient regains full mobility. Septic arthritis patients are at increased risk for DVT due to inflammation, immobility, and potential surgical interventions. While aspirin does have antiplatelet properties, it is not potent enough for DVT prevention in this high-risk scenario. LMWHs directly inhibit factor Xa in the coagulation cascade, providing more effective prevention of clot formation in the setting of infection-related hypercoagulability and reduced mobility associated with ankle septic arthritis. Some studies, such as 1, have investigated the use of aspirin for VTE prophylaxis after total hip and knee replacement, but the evidence does not support its use in patients with ankle septic arthritis. In fact, a study published in 2 found that the incidence of VTE following foot and ankle surgery is very low and routine use of chemoprophylaxis does not appear necessary for patients who are not in the high risk group for VTE. However, patients with septic arthritis are considered high-risk, and therefore, require more effective prophylaxis, such as LMWHs. Other studies, such as 3 and 4, have compared the effectiveness of low-dose and standard-dose aspirin for VTE prophylaxis after total hip arthroplasty and total knee arthroplasty, but these findings are not directly applicable to patients with ankle septic arthritis. In summary, LMWHs are the preferred agents for DVT prophylaxis in patients with ankle septic arthritis, due to their ability to effectively prevent clot formation in the setting of infection-related hypercoagulability and reduced mobility.