Anticoagulant therapy in patients with thrombocytopenia

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Anticoagulant therapy is used in a number of cardiovascular conditions including atrial fibrillation (AF) and prosthetic heart valves. Excess bleeding is the most common serious adverse effect of anticoagulant therapy, whether this be with direct oral anticoagulants (DOACs), unfractionated/low molecular weight heparins or warfarin.


Multiple scoring systems (e.g. HEMORR2HAGES and HAS-BLED) aid in estimation of bleeding risk. They vary in complexity, but both named systems consider all-cause impairment of platelet function as a risk factor. Such impairment is commonly qualitative (e.g. due to anti-platelet agents) though quantitative defects, independent of platelet function, are also a risk factor for bleeding.

Dr Simon Kavanagh
MBBS FRACP FRCPA
Dr Kavanagh is a clinical and laboratory haematologist in Perth, WA.
Following admission to the RACP and RCPA in 2015, he completed a two-year fellowship, specialising in the research and management of acute leukaemias and myelodysplastic syndromes. He maintains an active interest in the targeted treatment of these conditions in addition to various aspects of general haematology. Simon currently sees patients privately at St John of God Hospital Subiaco and works as a laboratory haematologist for Australian Clinical Labs.

Thrombocytopenia is a common problem and, when defined as a platelet count of <150×109/L, has been reported in 11.4% of patients with AF in the Italian START registry. The bleeding risk attributable to thrombocytopenia depends on factors including tempo of onset, severity, duration and platelet function.

Bleeding risk is generally proportional to degree of thrombocytopenia though the platelet count, in isolation, is a poor predictor for spontaneous haemorrhage. Bleeding risk is compounded by concurrent anticoagulation/anti-platelet therapy and presence of anaemia. 

When thrombocytopenia is identified in a patient on anticoagulant therapy, consideration must be given to whether treatment may be safely continued. The presence of bleeding typically warrants anticoagulant cessation (+/- reversal) and concurrent investigation and treatment of thrombocytopenia. This is particularly true when bleeding is present at a critical site. 

In the absence of bleeding, mild thrombocytopenia (platelet count ≥100×109/L) generally does not warrant interruption of anticoagulant therapy. Where thromobcytopenia is severe but anticipated to be of short duration (e.g. following cytotoxic chemotherapy) platelet transfusion support may allow ongoing anticoagulant therapy when thrombotic risks are deemed unacceptably high. Chronic transfusion is generally not feasible in those with persistent severe thromobcytopenia.

Formal data for moderate/severe thrombocytopenia in anticoagulation for cardiovascular indications is lacking. Guidance, in the form of expert consensus, exists for patients with venous thromboembolism and thrombocytopenia due to malignant haematological disease. Anticoagulation with low molecular weight heparins is considered safe for platelet counts ≥50×109/L. A dose reduction of 50% is recommended when the platelet count lies between 30-49×109/L. Anticoagulation cessation is generally advised with a platelet count <30×109/L.

This balance is particularly challenging in those with a mechanical valve prosthesis, particularly in the mitral position, as valve thrombosis has a high short-term morbidity and mortality. A cautious reduction in anticoagulant intensity is appropriate but anticoagulation may need to be continued well below the thresholds stated above. 

Ultimately, the decision to continue, temporarily interrupt or cease anticoagulation in the context of thrombocytopenia hinges on the clinical context, presence of additional risk factors for thrombosis and bleeding and the potential consequences of either outcome. 

Any decision represents a trade-off – anticoagulation increases the risk of bleeding while omission increases the risk of thrombotic complications. The balance of risk needs regular re-evaluation with updated platelet counts and clinical review. Wherever possible, the cause for thrombocytopenia should be identified and treated. Patient involvement in the discussion-making process is important.

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