Complications
Factors associated with bleeding during anticoagulant therapy include older age (>65 years and particularly >75 years), previous bleeding, cancer, metastatic cancer, kidney failure, liver failure, thrombocytopenia, previous stroke, diabetes, anaemia, antiplatelet therapy, poor anticoagulant control, reduced functional capacity, recent surgery, frequent falls, alcohol abuse, and non-steroidal anti-inflammatory drugs.[166] Unrecognised pathological 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.[253][254]
Localised 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.[255]
Incidence of approximately 1.5% to 3.8% following an acute episode of PE.[257][258][259]
CTEPH should be ruled out in patients with persistent dyspnoea and poor physical performance 3-6 months after acute PE. Consider transthoracic echocardiogram to assess for (chronic) pulmonary hypertension and consequently possible CTEPH.[67]
HIT is an adverse immune-mediated drug reaction that leads to the formation of immunoglobulin G antibodies against heparin-platelet factor IV complexes.[260]
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.[260] In patients with cancer, the incidence may be 1%.[260]
Risk factors include (but are not limited to) duration and type of heparin exposure, patient population, severity of trauma, and sex.[260] Women have approximately twice the risk of developing HIT as men.[261] The incidence can be minimised by use of a low molecular weight heparin or fondaparinux.[262]
Clinical prediction rules to assist physicians with determining the probability that a patient has HIT have been developed.[260]
In a meta-analysis of randomised controlled trials in which patients with confirmed PE were allocated to receive a direct-acting oral anticoagulant for a minimum of 3 months, risk of recurrent PE did not appear to differ between: dabigatran and warfarin (20 per 1000 people vs. 20 per 1000 people, respectively; odds ratio [OR] 1.02, 95% CI 0.50 to 2.04); oral factor Xa inhibitors (rivaroxaban, apixaban, edoxaban, betrixaban) and warfarin (24 per 1000 people vs. 22 per 1000 people, respectively; OR 1.08, 95% CI 0.46 to 2.56).[179]
[ 
]
[Evidence B]
Risk of recurrent venous thromboembolism did not appear to differ between: dabigatran and warfarin (29 per 1000 people vs. 31 per 1000 people, respectively; OR 0.93, 95% CI 0.52 to 1.66); oral factor Xa inhibitors (rivaroxaban, apixaban, edoxaban, betrixaban) and warfarin (20 per 1000 people vs. 24 per 1000 people, respectively; OR 0.85, 95% CI 0.63 to 1.15).[179]
[ ]
[Evidence B]
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