Pulmonary Infarction Medication
- Author: Lennox H Huang, MD, FAAP; Chief Editor: Michael R Bye, MD more...
Anticoagulants are the treatment of choice in most children with pulmonary emboli. Thrombolytics are rarely used. To date, little data are available regarding the use of LMWH in children with thromboembolic disease; however, numerous studies have described the efficacy of LMWH in thromboembolic disease.
A review that compared the use of LMWH with standard unfractionated heparin (UFH) in the treatment of venous thromboembolic disease in adult patients concluded that therapy with LMWH is associated with a decreased risk of major hemorrhage and a decreased mortality rate. Benefits of using LMWH include a lower overall cost, the convenience of twice-daily subcutaneous injections, decreased requirement for laboratory monitoring, and a more favorable antithrombotic-to-hemorrhagic ratio.
Duration of therapy must be individualized. One review recommends that in adult patients with transient risk factors (ie, surgery, immobilization, estrogen administration), therapy less than 3 months may be sufficient; however, no studies are available to validate this statement. Patients with slowly resolving or persistent risk factors should be treated for at least 3 months.
Previous studies have confirmed that longer duration of therapy is associated with decreased risk of disease recurrence. Adult patients with idiopathic thrombosis benefit most, although the relevance of comparing these patients with children (most of whom have identifiable risk factors) is uncertain. Patients with genetic thrombophilic states (factor V Leiden) may benefit from longer courses of therapy. Individuals with recurrent embolic disease should be treated for at least 12 months and possibly longer.
Inhibition of thrombin prevents extension of the thrombus, thus allowing recanalization of the blood vessel over time, and reduces the risk of further embolization. Anticoagulation does not lyse the clot per se. It merely allows the body time to lyse the clot while reducing the risk of subsequent embolization.
Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.
Reduces production of vitamin K–dependent clotting factors. Allows anticoagulation on an outpatient basis. Generally should be commenced shortly after initiating heparin, and their use should overlap by 5-10 d; adjust dosage to maintain INR of 2-3.
Has become first-line therapy in many patients with thromboembolism. Prevents DVT, which may lead to PE in patients undergoing surgery who are at risk for thromboembolic complications. Enhances inhibition of factor Xa and thrombin by increasing antithrombin III activity. In addition, preferentially increases inhibition of factor Xa. Average duration of treatment is 7-14 d.
These convert plasminogen to plasmin, leading to clot lysis. Thrombolytic agents are rarely used in pediatric practice. Their use should be considered investigational and should be restricted to patients with severe pulmonary or cardiovascular compromise. If thrombolysis is being considered, the diagnosis of pulmonary embolism should first be confirmed by pulmonary angiography. Newborns may be relatively resistant to thrombolytics because of their lack of fibrinogen activity.
Streptokinase (Kabikinase, Streptase)
Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots, as well as fibrinogen and other plasma proteins. Increase in fibrinolytic activity that degrades fibrinogen levels for 24-36 h takes place with IV infusion of streptokinase.
Also called tissue plasminogen activator (TPA). Produced naturally by vascular endothelium; however, the therapeutic agent is derived using recombinant technology. Binds tightly to fibrin, thus activating plasminogen, which results in clot lysis. With ongoing shortage of urokinase, more studies are emerging for use in pediatrics.
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