Management of Unexplained Bruising in Adults

Structured Clinical History

Use a validated bleeding assessment tool to systematically record mucocutaneous bleeding (e.g., epistaxis, heavy menstrual bleeding, gingival bleeding, easy bruising). 3
A positive family history of bleeding problems strongly suggests an inherited coagulation defect. 4
Review all current medications, including non‑steroidal anti‑inflammatory drugs, anticoagulants, antiplatelet agents, and herbal supplements. 2

Inspect the skin for bruises, hematomas, petechiae, and sites of active bleeding. 4
Look for signs of chronic liver disease, joint hyper‑laxity (suggesting connective‑tissue disorders), telangiectasias, and anemia. 4
In female patients, perform a gynecologic examination to exclude genital lesions that could mimic bruising. 4

Order a complete blood count with platelet count and peripheral smear to detect thrombocytopenia or thrombocytosis. 4
Measure prothrombin time (PT) to assess the extrinsic coagulation pathway. 4
Measure activated partial thromboplastin time (aPTT) to assess the intrinsic coagulation pathway. 4
Perform simultaneous von Willebrand factor (VWF) testing: VWF antigen, VWF ristocetin cofactor activity (VWF:RCo), and factor VIII activity. 3

Obtain blood atraumatically, avoid testing during acute illness or pregnancy, and minimize patient stress. 3
Transport samples at room temperature; separate plasma promptly, and if processing is delayed > 2 h, freeze plasma at ≤ ‑40 °C. 3
Recognize that VWF is an acute‑phase reactant and may be falsely elevated during stress or illness; repeat testing when indicated. 1

Normal PT and aPTT do not exclude a bleeding disorder because standard coagulation tests often miss von Willebrand disease (VWD). 1
A VWF:RCo level < 30 IU/dL confirms the diagnosis of VWD. 3
A VWF:RCo / VWF:Ag ratio < 0.5–0.7 indicates type 2 (qualitative) VWD rather than type 1 (quantitative). 3

Acquired VWD should be strongly considered in adults with new‑onset bleeding without personal or family history of hemorrhagic disorders. 3
Acquired VWD is associated with conditions such as aortic stenosis, lymphoproliferative disorders, and monoclonal gammopathies. 3
In patients with anogenital bruising, include lichen sclerosus in the differential diagnosis; it presents with porcelain‑white plaques and may be mistaken for abuse in children. 5

Refer promptly when initial VWF studies are abnormal and require sub‑typing. 3
Refer when a history of severe bleeding persists despite repeatedly normal routine tests. 3
Refer if acquired VWD is suspected. 3
Refer for specialized assays (VWF multimers, VWF‑collagen binding, ristocetin‑induced platelet aggregation) when indicated. 3
Refer when bleeding symptoms continue despite normal initial laboratory evaluation. 1

Do not rely solely on PT/aPTT, as these miss VWD and mild platelet function disorders. 1
Do not overlook the impact of ABO blood type; individuals with blood type O have lower baseline VWF levels, affecting result interpretation. 3
Ensure proper sample handling; mishandling can produce false‑negative or false‑positive results. 3
Recognize the high analytical variability of VWF:RCo (10–30 % CV); repeat testing may be necessary for accurate diagnosis. 3
Do not dismiss VWD when VWF:RCo is 30–50 IU/dL if clinical or familial evidence supports the diagnosis. 3