Complications
Factors associated with bleeding during anticoagulant therapy include older age (>65 years and particularly >75 years), previous bleeding, cancer, metastatic cancer, renal failure, liver failure, thrombocytopenia, previous stroke, diabetes, anemia, antiplatelet therapy, poor anticoagulant control, reduced functional capacity, recent surgery, frequent falls, alcohol abuse, and nonsteroidal anti-inflammatory drugs.[21] Unrecognized pathologic lesions, such as duodenal ulcer, angiodysplasia in the colon, microvascular disease (e.g., a striatal intracerebral bleed in a patient with hypertension), or (rarely) amyloid angiopathy in the central nervous system, contribute to increased risk of major bleeding.[218][219]
Localized necrosis of lung tissue, due to obstruction of the arterial blood supply.
Pulmonary infarction is uncommon when emboli obstruct central arteries, but is frequent when distal arteries are occluded.[220]
HIT is an adverse immune-mediated drug reaction that leads to the formation of immunoglobulin G antibodies against heparin-platelet factor IV complexes.[225]
The incidence of HIT (following a minimum of 4 days heparin exposure) is believed to be between 0.1% and 1% in medical patients receiving prophylactic or therapeutic doses of heparin.[225] In patients with cancer, the incidence may be 1%.[225]
Risk factors include (but are not limited to) duration and type of heparin exposure, patient population, severity of trauma, and gender.[225] Women have approximately twice the risk of developing HIT as men.[226] The incidence can be minimized by use of a low molecular weight heparin or fondaparinux.[227]
Clinical prediction rules to assist physicians with determining the probability that a patient has HIT have been developed.[225]
Recurrent venous thromboembolism is unusual among patients receiving therapeutic-dose anticoagulant therapy, with the exception of cancer (7% to 9% on-therapy recurrence with low molecular weight heparin).[4][21][211]
Available evidence shows there is probably little or no difference between the efficacy and safety of DOACs and conventional anticoagulation in the prevention of recurrent venous thromboembolism.[208]
[ 
]
[Evidence B]
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