Discuss the clinical approach to identify the diagnosis of bleeding in a patient. Give the relevant questions to ask during history taking in a chronological order, and also the physical examinations to do with its expected findings, also in a chronological order.
Clinical Approach to the Diagnosis of Bleeding Disorders
A structured clinical approach integrates history and physical examination to determine whether a bleeding disorder exists, whether it is inherited or acquired, and whether it arises from a defect in primary haemostasis (vessel wall/platelets) or secondary haemostasis (coagulation factors).
PART 1: HISTORY TAKING
1. Presenting Complaint
Begin with open-ended questions to characterise the bleeding:
- Where is the bleeding? Mucosal sites (nose, gums, GI tract, menorrhagia) versus deep sites (joints, muscles, retroperitoneum) point to very different diagnoses.
- When did it start? Lifelong bleeding since infancy suggests an inherited disorder; recent onset suggests an acquired cause.
- Was it spontaneous or provoked? Spontaneous haemarthroses are a hallmark of moderate-to-severe factor VIII/IX deficiency. Spontaneous mucosal bleeding suggests thrombocytopenia or von Willebrand disease (VWD).
2. Characterisation of Bleeding Episodes (in order of eliciting)
| Question | Clinical reasoning |
|---|---|
| Do you bleed or bruise easily without obvious injury? | General screen for haemostatic defect |
| Do your bruises have lumps (haematomas), or are they flat? | Flat/superficial bruising → platelet/vascular disorder; raised haematomas → coagulopathy |
| Do you bleed from multiple sites simultaneously? | Suggests a generalised haemostatic defect rather than local pathology |
| How long does bleeding last after a cut or scratch? | Prolonged capillary bleeding → platelet dysfunction or thrombocytopenia |
| Do you have nosebleeds (epistaxis)? How frequent, how long, do they require treatment or cautery? | Epistaxis not varying with season, requiring medical attention → likely VWD or HHT; seasonal epistaxis in children is usually benign |
| Do you have bleeding gums, or prolonged bleeding after dental extractions or tooth eruption? | Platelet/vWF disorders cause prolonged mucosal bleeding; haemophilia causes delayed bleeding after extractions |
| Have you had excessive bleeding after surgery, trauma, or procedures (including tonsillectomy, biopsy, or colonic polypectomy)? | Critical at-risk challenge; delayed post-tonsillectomy bleeding (~day 7) is characteristic of haemophilia and VWD. Bleeding only after major surgery → mild disorder |
| (For women) Do you have heavy menstrual bleeding? Do you pass clots >1 inch in diameter, change pads/tampons more than hourly, or have iron-deficiency anaemia? Did it start at menarche? | Heavy menstrual bleeding from menarche strongly suggests an underlying bleeding disorder (VWD, factor XI deficiency, platelet disorders, carrier haemophilia) |
| Have you experienced postpartum haemorrhage? | Common in VWD type 1/haemophilia A carriers; may be delayed because VWF/factor VIII normalise in pregnancy then drop postpartum |
| Do you bleed into your joints (haemarthroses) — pain, swelling, heat in a joint without discoloration? | Pathognomonic of moderate-to-severe haemophilia A or B; rarely seen in other disorders unless severe |
| Do you have muscle swellings or deep haematomas? | Characteristic of haemophilia; a psoas bleed can compress the femoral nerve; calf haematomas may cause compartment syndrome |
3. Temporal Relationship and Severity
- Onset in infancy/childhood (e.g., bleeding from umbilical cord stump, intracranial haemorrhage at birth, bleeding at circumcision) → severe inherited coagulopathy (factor XIII deficiency, severe haemophilia).
- Onset only after surgery or trauma in adulthood → mild inherited defect or acquired disorder.
- Acute onset in a previously well patient → acquired cause (ITP, acquired haemophilia A, DIC, anticoagulant effect, liver disease).
4. Drug and Dietary History
| Question | Clinical reasoning |
|---|---|
| Are you taking aspirin, NSAIDs, clopidogrel, ticagrelor, or dipyridamole? | Impair primary haemostasis by inhibiting platelet function |
| Are you on anticoagulants (warfarin, rivaroxaban, apixaban, dabigatran, heparin)? | Direct cause of acquired coagulopathy |
| Are you taking any herbal supplements? | Ginkgo, garlic, ginger, fish oil, vitamin E, willow bark, and coumarin-containing herbs impair platelet function or coagulation |
| What is your diet like? Do you eat fresh fruit and vegetables? | Vitamin C deficiency (scurvy) → perifollicular/petechial haemorrhage and bruising |
| Do you take broad-spectrum antibiotics or have malabsorption? | Reduce gut synthesis and absorption of vitamin K → prolonged PT |
5. Past Medical and Systemic Disease History
| Question | Clinical reasoning |
|---|---|
| Do you have liver disease (hepatitis, cirrhosis, alcohol excess)? | Reduced synthesis of factors V, VII, VIII, IX, X, XI, prothrombin, fibrinogen; thrombocytopenia from hypersplenism |
| Do you have kidney disease? | Uraemia impairs platelet function; severity proportional to plasma urea |
| Do you have any autoimmune conditions (SLE, connective tissue disease, thyroid disease)? | ITP, acquired VWD, acquired haemophilia A; antiphospholipid antibodies |
| Have you had a recent viral infection (including COVID-19, HIV, EBV)? | Post-viral ITP (more common in children); HIV-associated thrombocytopenia |
| Do you have a malignancy? | Bone marrow failure, DIC (especially acute promyelocytic leukaemia), acquired factor X deficiency (amyloid) |
| Have you been pregnant recently? | Post-partum acquired haemophilia A; gestational thrombocytopenia; TTP |
| Do you have jaundice or cholestasis? | Reduced vitamin K absorption → deficiency of factors II, VII, IX, X, protein C and S |
6. Family History
| Question | Clinical reasoning |
|---|---|
| Is there a family history of bleeding disorders? | Establishes inherited vs. acquired; determines pattern of inheritance |
| Does the bleeding affect males only, or males and females? | X-linked recessive → haemophilia A or B (only males affected; females are carriers) |
| Does it affect both sexes across generations? | Autosomal dominant → VWD type 1/2, HHT |
| Does it affect both sexes but skip generations? | Autosomal recessive → VWD type 3, Glanzmann's thrombasthenia, Bernard-Soulier syndrome, factor VII/X/XIII deficiency |
| Were there any infant or neonatal deaths from bleeding in the family? | Severe inherited coagulopathy |
7. Social History
- Alcohol use: contributes to liver disease and thrombocytopenia.
- Intravenous drug use: HIV infection → thrombocytopenia; femoral vein thrombosis risk.
- Nutritional status: malnutrition → vitamin K or C deficiency.
- Occupation/trauma exposure: to clarify whether bleeding is proportionate.
PART 2: PHYSICAL EXAMINATION
Perform in a head-to-toe, systematic order.
Step 1: General Observation
| Finding | Significance |
|---|---|
| Pallor (conjunctivae, palmar creases) | Chronic blood loss → iron-deficiency anaemia (e.g., from GI bleeding in HHT, VWD) |
| Jaundice (scleral icterus) | Liver disease → coagulopathy; cholestasis → vitamin K deficiency |
| Cushingoid features (moon face, buffalo hump, striae) | Chronic steroid use → senile-type purpura; impaired collagen support |
| Cachexia / weight loss | Malignancy → DIC, bone marrow failure, acquired factor deficiency |
| Ill-looking, shocked patient | Acute DIC, severe haemorrhage |
Step 2: Skin
| Finding | Significance |
|---|---|
| Petechiae (pinpoint, non-blanching, 1–3 mm) | Thrombocytopenia or platelet dysfunction (primary haemostatic defect) |
| Ecchymoses (flat, large, irregular bruising) | Platelet/vascular disorders if superficial; coagulopathy if deep |
| Haematomas (raised, palpable bruising with induration) | Coagulation factor deficiency (secondary haemostatic defect) |
| Distribution: perifollicular haemorrhage and corkscrew hairs | Scurvy (vitamin C deficiency) |
| Purpura on legs and buttocks in a child | Henoch-Schönlein purpura (vasculitis) |
| Senile purpura on dorsum of hands/forearms | Age-related atrophy of vascular supporting tissue; also steroid-induced |
| Excessive skin laxity, joint hyperextensibility | Ehlers-Danlos syndrome → fragile vessel walls; bleeding with normal coagulation tests |
| Spider naevi, palmar erythema, caput medusae | Chronic liver disease → coagulopathy, portal hypertension |
Step 3: Head and Face
| Finding | Significance |
|---|---|
| Telangiectasia on lips, tongue, face, fingertips (small red spots that blanch on pressure) | Hereditary haemorrhagic telangiectasia (HHT) — cause of recurrent epistaxis and occult GI bleeding |
| Scleral icterus | Liver disease or haemolysis |
| Pallor of conjunctivae | Anaemia from blood loss or bone marrow failure |
| Retinal haemorrhages (fundoscopy, if indicated) | Severe thrombocytopenia, DIC, hypertensive disease |
Step 4: Oral Cavity and Oropharynx
| Finding | Significance |
|---|---|
| Gingival bleeding or haematoma at tooth extraction site | Platelet/VWF disorders, coagulopathy |
| Telangiectasia on the tongue or buccal mucosa | HHT |
| Oropharyngeal haematoma | Life-threatening in haemophilia (can obstruct airway) |
| Pale mucous membranes | Anaemia |
Step 5: Abdomen
| Finding | Significance |
|---|---|
| Hepatomegaly | Liver disease → coagulopathy; haematological malignancy |
| Splenomegaly | Portal hypertension → thrombocytopenia (hypersplenism); haematological malignancy (leukaemia, lymphoma) causing bone marrow failure; myeloproliferative disorders |
| Tenderness / rigidity | Retroperitoneal haemorrhage (severe haemophilia); splenic rupture |
| Ascites | Portal hypertension, advanced liver disease |
Step 6: Musculoskeletal System
| Finding | Significance |
|---|---|
| Haemarthrosis — hot, swollen, tender joint (typically knees, elbows, ankles, hips) with restricted movement but without skin discoloration | Pathognomonic of moderate-to-severe haemophilia A or B |
| Chronic haemophilic arthropathy — joint deformity, loss of cartilage space, crepitus, limited range of motion | Recurrent haemarthroses in haemophilia |
| Muscle haematoma — tender, firm swelling (particularly calf and psoas) | Haemophilia; psoas bleed may extend to compress femoral nerve → hip flexion posture, loss of hip extension |
| Compartment syndrome signs — tense, painful limb with paraesthesia | Calf haematoma causing fascial compartment pressure in haemophilia |
| Joint hypermobility | Ehlers-Danlos syndrome |
Step 7: Neurological Assessment
| Finding | Significance |
|---|---|
| Focal neurological deficit, altered consciousness | Intracranial haemorrhage — most common bleeding-related cause of death in severe haemophilia |
| Femoral nerve palsy (weak hip flexion, loss of knee extension, reduced anterior thigh sensation) | Psoas muscle haematoma in haemophilia |
Step 8: Lymph Nodes
| Finding | Significance |
|---|---|
| Generalised lymphadenopathy | Haematological malignancy (lymphoma, CLL → immune thrombocytopenia); HIV |
| Localised lymphadenopathy | Less specific; requires further investigation |
SUMMARY: Distinguishing Primary vs. Secondary Haemostatic Defects
| Feature | Primary Haemostasis (Platelet/Vascular) | Secondary Haemostasis (Coagulation) |
|---|---|---|
| Bleeding type | Mucosal, petechial, superficial | Deep: joints, muscles, retroperitoneum |
| Bruising | Flat ecchymoses | Raised haematomas |
| Onset after injury | Immediate | Delayed (hours) |
| Spontaneous bleeding | Yes (especially if platelets <20 × 10⁹/L) | Yes (in severe factor deficiency <0.01 U/mL) |
| Sites | Skin, nose, gums, GI, menorrhagia | Joints, muscles, CNS |
| Examples | ITP, VWD, Glanzmann's, HHT, scurvy | Haemophilia A/B, liver disease, DIC, vitamin K deficiency |
Sources: Davidson's Principles and Practice of Medicine (Haematology, Ch. 38); Harrison's Principles of Internal Medicine (Ch. 65 – Bleeding and Thrombosis); Davidson's Haematology and Transfusion Medicine (Bleeding Disorders section)
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