Bleeding and Bruising History OSCE, Haematology Station Guide

Why Bleeding and Bruising History Is Tested

Haematology history stations require you to distinguish between defects in primary haemostasis (platelets and vascular integrity) and secondary haemostasis (coagulation factors), identify whether the cause is congenital or acquired, and know which investigations to request. Many students struggle because they do not have a structured approach.

Primary vs Secondary Haemostasis: The Core Distinction

Understanding where in the haemostatic process the defect lies directs your whole history:

Core Symptom Questions

Go through each site of bleeding systematically:

Skin and Soft Tissue

• "Have you noticed easy bruising? How large are the bruises and do they appear without obvious injury?"
• "Do you get any small pinpoint spots of red under the skin?" (petechiae: platelet disorder)
• "Do you have any purple patches on your skin?" (purpura)

Nose and Mouth

• "Do you get nosebleeds? How often? How long do they last? Have they ever needed hospital treatment?"
• "Does your gum bleed when you brush your teeth?"
• "Have you ever had bleeding after dental treatment that was difficult to stop?"

Menstrual

• "How heavy are your periods? Do you soak through pads or tampons? Do you pass clots?"
• Heavy menstrual bleeding is a key presenting feature of von Willebrand disease in women

Gastrointestinal

• "Any blood when you open your bowels? Any black tarry stools?"
• "Have you vomited blood?"

Urinary

• "Any blood in your urine?"

Joints and Muscles

• "Have you ever had pain, swelling, or stiffness in a joint that wasn't caused by an injury?" (haemarthrosis: classic for haemophilia)
• "Any unusual swelling in your muscles after minor injury?"

Past History: Surgical and Dental Bleeding

• "Have you had any operations? Was there any unusual bleeding during or after?"
• "Any dental extractions? Did the bleeding stop normally?"
• Abnormal surgical or dental bleeding strongly suggests a coagulopathy
• Haemophilia often presents after circumcision or dental extraction

Family History

• "Is there anyone in your family with a bleeding or clotting disorder?"
• "Any male relatives who had unusual bleeding problems?"

Drug and Medication History

Always ask specifically:

• Anticoagulants: warfarin, apixaban, rivaroxaban, dabigatran, edoxaban
• Antiplatelet drugs: aspirin, clopidogrel, ticagrelor
• NSAIDs: ibuprofen, naproxen (reversibly inhibit platelet COX-1)
• Alcohol: causes thrombocytopenia and impairs coagulation factor synthesis
• Herbal supplements: ginkgo, fish oil, garlic (antiplatelet effects)
• Chemotherapy: bone marrow suppression reducing platelet production

Social History

• Alcohol use (quantify in units per week)
• Occupation (cuts and injuries in high-risk occupations)
• Domestic violence (bruising from unexplained injuries)

Specific Conditions to Know

Immune Thrombocytopenic Purpura (ITP)

• Autoimmune platelet destruction
• Petechiae, purpura, mucosal bleeding
• Normal coagulation, low platelets, normal PT and APTT
• Primary or secondary to SLE, HIV, lymphoma

Von Willebrand Disease

• Most common inherited bleeding disorder
• Mucosal bleeding: nosebleeds, menorrhagia, gum bleeding
• Prolonged bleeding time, low VWF antigen and activity
• Autosomal dominant (family history in both sexes)

Haemophilia A (Factor VIII deficiency) and B (Factor IX deficiency)

• X-linked recessive: almost exclusively affects males
• Deep bleeding: haemarthrosis, muscle haematomas
• Prolonged APTT, normal PT

Investigations to Mention

Frequently Asked Questions

"How do you distinguish a platelet disorder from a coagulation factor deficiency on history?"

The pattern of bleeding distinguishes the two. Platelet disorders and vascular defects cause superficial mucocutaneous bleeding: petechiae (small pinpoint bleeds under the skin), purpura, nosebleeds that are prolonged and recurrent, gum bleeding, and heavy menstrual periods. Bleeding from cuts is often prolonged but stops with pressure. Coagulation factor deficiencies cause deep tissue bleeding: haemarthrosis (blood in joints), muscle haematomas, and prolonged bleeding after surgery or dental extraction, sometimes hours later when the platelet plug has formed but the fibrin clot fails to stabilise. Petechiae are absent in factor deficiencies. On investigation, platelet disorders show a normal PT and APTT but abnormal platelet count or function. Factor deficiencies prolong PT (extrinsic pathway factors) or APTT (intrinsic pathway factors) in isolation or together.

"What is von Willebrand disease and how does it present?"

Von Willebrand disease (VWD) is the most common inherited bleeding disorder, affecting approximately 1 in 100 people. It is caused by a deficiency or dysfunction of von Willebrand factor (VWF), a glycoprotein that mediates platelet adhesion to damaged vessel walls and acts as a carrier protein for factor VIII. It is autosomal dominant in type 1 (most common, partial quantitative deficiency) and can affect both sexes equally. Presentation is mucocutaneous: recurrent epistaxis, gum bleeding, easy bruising, and menorrhagia in women. Unlike haemophilia, deep bleeding into joints is unusual. Diagnosis: low VWF antigen, low VWF ristocetin cofactor activity, and in type 1 disease often a mildly prolonged APTT due to secondary factor VIII deficiency. Treatment includes desmopressin (DDAVP) which releases VWF from endothelium, and VWF concentrate for severe cases.

"What is the difference between haemophilia A and B and how do they present?"

Haemophilia A is caused by deficiency of factor VIII and haemophilia B by deficiency of factor IX. Both are X-linked recessive, meaning they almost exclusively affect males, with females being carriers (who may have mildly reduced factor levels and some bleeding symptoms). Clinically they are indistinguishable: deep tissue bleeding including haemarthrosis (the knee, elbow, and ankle are most commonly affected), muscle haematomas, and prolonged bleeding after injury or surgery. Spontaneous bleeding occurs with severe disease (factor level below 1%). The APTT is prolonged in both; PT is normal. Haemophilia A is more common (1 in 5000 males) than B (1 in 30000). Treatment: haemophilia A with factor VIII concentrate or emicizumab (a bispecific antibody), haemophilia B with factor IX concentrate.

"Which drugs cause bleeding and how do they work?"

Multiple drug classes cause bleeding through different mechanisms. Anticoagulants: warfarin inhibits vitamin K-dependent factor synthesis (II, VII, IX, X, protein C and S), prolonging the PT/INR; direct oral anticoagulants (DOACs: apixaban, rivaroxaban, edoxaban) inhibit factor Xa; dabigatran inhibits thrombin directly; heparin and LMWH enhance antithrombin III activity, prolonging the APTT. Antiplatelet drugs: aspirin irreversibly inhibits COX-1, reducing thromboxane A2 production and platelet aggregation, for the platelet's 10-day lifespan; clopidogrel, ticagrelor, and prasugrel block the P2Y12 ADP receptor. NSAIDs reversibly inhibit COX-1. Alcohol impairs hepatic synthesis of all coagulation factors and causes thrombocytopenia through direct marrow suppression and hypersplenism. Always take a full drug history including over-the-counter drugs, herbal remedies, and alcohol.