Complications
VTE prophylaxis diminishes the risk of developing a VTE, but it does not nullify it. Therefore, the treating physicians and nurses should routinely look for signs and symptoms of DVT when patients are admitted to hospital. If DVT is suspected, proper diagnostic testing must be performed rapidly to rule out this potentially deadly complication. Early mobilisation facilitated by attending staff on the wards is strongly encouraged to diminish the likelihood of developing a clot. Moreover, thromboprophylaxis should not be interrupted unless there is a valid reason (e.g., active bleeding). Mechanical thromboprophylaxis should then be implemented.
Due to high mortality in the early stages of PE, aggressive treatment is necessary in the case of high-risk patients (modified Wells' score >4, systolic BP <90 mmHg).[148] Hypoxaemia with systolic blood pressure <90 mmHg suggests massive PE, which has a high mortality.
O2/ALS protocol, haemodynamic support (including judicious use of inotropics), and anticoagulation with low molecular weight or unfractionated heparin should be instituted without delay in all patients who present with these high-risk features.
Deciding whether to initiate thrombolysis or anticoagulation should be made on a case-by-case basis according to clinical presentation, risk of PE, and pre-existing morbidity. This tends to vary according to local expertise and centre provision.
Inferior vena cava filter placement and surgical embolectomy may be appropriate when anticoagulation and/or thrombolytics are contraindicated. Risk/benefit decisions need to be made on an individual basis according to local provision and clinical presentation.
Following the acute phase, long-term anticoagulation with warfarin should be tailored to the underlying condition (e.g., thrombophilia) and risk factors.[149]
The risk of anticoagulant bleeding varies according to type of anticoagulant (mode of administration, half-life, and reversibility) and patient risk factors (medical/surgical, coagulopathy). Prophylactic doses obviously cause less bleeding than therapeutic doses. In addition, the definition of major and minor bleeding is not standard across studies, and the reported incidence of bleeding in the literature varies.
Risk factors for bleeding (e.g., active peptic ulcer disease, liver disease, thrombocytopenia, post-surgical haemostasis, neuraxial anaesthesia) must be thoroughly assessed before any decision to prescribe prophylactic anticoagulants. Daily clinical assessments of bleeding as well as monitoring of haemoglobin help to identify any source of bleeding early.
Managing anticoagulation-associated bleeding depends on the location and severity of bleeding.[150] It usually necessitates promptly removing the anticoagulant, giving an antidote if available (for unfractionated heparin [UFH], low molecular weight heparin [LMWH], and warfarin), and giving supportive treatment using transfusions. For example, Kcentra®, a prothrombin complex concentrate that contains 4 vitamin K-dependent factors, including factor II, factor VII, factor IX, and factor X, as well as protein C and S, is approved for the reversal of vitamin-K antagonist mediated bleeding.[150]
Prothrombin complex concentrates can be administered following the manufacturer's recommendations, but no large published studies support the efficacy of this approach. Recombinant coagulation factor Xa (andexanet alfa) is a bio-engineered analogue of factor Xa with no direct effect on the coagulation cascade, which acts as a decoy target for factor Xa inhibitors. It is approved in the US and Europe for patients treated with rivaroxaban and apixaban when reversal of anticoagulation is needed due to life-threatening or uncontrolled bleeding. Idarucizumab, a monoclonal antibody binding dabigatran, was found to be effective at normalising coagulation tests in the REVERSE-AD trial.[151] It is now approved for reversal of dabigatran's anticoagulation effects in emergency situations. Although data are limited, dabigatran (but not rivaroxaban or apixaban) seems to be removed by dialysis.
Heparin-induced thrombocytopenia (HIT) is a rare but serious complication in patients who are receiving or who have recently received heparin. It is usually manifested by a 50% or greater platelet count drop 5 to 14 days after starting a course of heparin. It is more commonly associated with unfractionated heparin (UFH) than with low molecular weight heparin (LMWH). HIT can therefore be prevented by using LMWH rather than UFH as a prophylactic agent. Thrombosis is an important complication of HIT.
To detect HIT, measuring platelet count is recommended at least every other day for the highest-risk patients (post-surgical patients receiving prophylactic UFH). For surgical patients receiving prophylactic LMWH or UFH catheter flushes, as well as for medical patients receiving prophylactic UFH, measuring platelet counts at least every 2 to 3 days is recommended for 4 to 14 days. No routine platelet count is recommended for medical patients receiving prophylactic LMWH (low risk).[3] However, any patient developing thrombosis or a necrotic reaction at the injection site while receiving UFH or LMWH should have a full blood count to measure platelets. If HIT is suspected, referral to a haematologist or thrombosis specialist is recommended.
Reactions can include severe, life-threatening symptoms such as breathing difficulties, wheezing, and angio-oedema with swelling of the face, lips, tongue, or throat. These reactions require immediate medical assistance. Less severe reactions include an allergic rash or injection site reactions. For all these reactions, discontinuing the offending agent is recommended and a physician should be consulted.
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