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Successful anticoagulation is a fine balance between clotting and bleeding, which can easily go wrong. The good news is that basic principles can help manage this scenario effectively. The author provides background information on low molecular weight heparins, their use in the treatment and prevention of deep vein thrombosis and pulmonary embolism, its monitoring and reversal, and dose adjustment for body weight and renal function.
The recent guidelines on management of aneurysmal subarachnoid hemorrhage (aSAH) advise pharmacological thromboprophylaxis (PTP) after aneurysm obliteration. However, no study has addressed the safety of PTP in the aSAH population. Therefore, the aim of this study was to assess the safety of early PTP after aSAH.
Retrospective cohort of aSAH patients admitted between January 2012 and June 2013 in a single high-volume aSAH center. Traumatic SAH and perimesencephalic hemorrhage patients were excluded. Patients were grouped according to PTP timing: early PTP group (PTP within 24 hours of aneurysm treatment), and delayed PTP group (PTP started > 24 hours).
A total of 174 SAH patients (mean age 56.3±12.5 years) were admitted during the study period. Thirty-nine patients (22%) did not receive PTP, whereas 135 patients (78%) received PTP after aneurysm treatment or negative angiography. Among the patients who received PTP, 65 (48%) had an external ventricular drain. Twenty-eight patients (21%) received early PTP, and 107 (79%) received delayed PTP. No patient in the early treatment group and three patients in the delayed PTP group developed an intracerebral hemorrhagic complication. Two required neurosurgical intervention and one died. These three patients were on concomitant PTP and dual antiplatelet therapy.
The initiation of PTP within 24 hours may be safe after the treatment of a ruptured aneurysm or in angiogram-negative SAH patients with diffuse aneurysmal hemorrhage pattern. We suggest caution with concomitant use of PTP and dual antiplatelet agents, because it possibly increases the risk for intracerebral hemorrhage.
The most important risk factor for thrombosis in pregnancy is a history of thrombosis. Although both heparin and warfarin are satisfactory for use postpartum, including in women who are breastfeeding, many women prefer to use low-molecular-weight heparin (LMWH) (with once-daily dosing postpartum) because they have become accustomed to its administration and because they can avoid the monitoring associated with coumarin therapy. With massive life-threatening pulmonary thromboembolism (PE), the pregnant woman needs emergency assessment by a multidisciplinary team of obstetricians, surgeons, and radiologists, who should decide rapidly on appropriate treatment ranging from intravenous unfractionated heparin (UFH) to systemic thrombolysis, catheter thrombolysis or embolectomy, or surgical embolectomy. Women are at an increased risk of venous thromboembolism (VTE), during pregnancy. In anticipation of delivery, surgery, or other invasive procedures, anticoagulation should be manipulated to reduce the risk of bleeding complications while minimizing the risk of thrombosis.
This chapter describes the coagulation pathway, the pharmacology of heparin, monitoring of anticoagulation status, problems associated with heparin usage, alternatives to heparin, the reversal of anticoagulation following termination of cardiopulmonary bypass (CPB) and the prevention and management of bleeding. Unfractionated heparin (UFH) remains the standard anticoagulant for CBP for several reasons. Activated clotting time (ACT) is a functional assay of heparin anticoagulation and is the most widely employed test. Thrombocytopenia can occur after CPB due to dilution of blood volume with the extracorporeal circuit volume and platelet consumption or sequestration. Platelet function impairment is considered to be the main hemostatic defect during CPB. The synthetic antifibrinolytic agents ε-aminocaparoic acid (EACA) and tranexamic acid (TA) bind to lysine binding sites in both plasminogen and plasmin and produce a structural change. This prevents the conversion of plasminogen to plasmin and also prevents the activation of plasmin.
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