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PA20.1-2 | Platelet & Vascular Bleeding Disorders — Part 3
Laboratory Approach to Platelet & Vascular Bleeding
Laboratory Approach to Platelet and Vascular Bleeding
A systematic lab approach prevents over-investigation and focuses on the right diagnosis.
Step 1 — Platelet count + peripheral blood film:
• Count quantifies severity of thrombocytopenia.
• Film: schistocytes (TTP/HUS/DIC), large platelets (ITP, Bernard-Soulier), giant platelets (MYH9 disorders), platelet clumping (EDTA pseudo-thrombocytopenia — always repeat in citrate).
Step 2 — Coagulation screen (PT, aPTT):
• Normal in pure platelet and vascular disorders.
• Abnormal → secondary haemostasis defect or DIC.
Step 3 — Bleeding time / PFA-100:
• Prolonged in thrombocytopenia AND qualitative platelet defects AND vascular purpuras.
• Normal PT + aPTT + prolonged BT = platelet or vascular aetiology confirmed.
Step 4 — Bone marrow biopsy (when needed):
• Megakaryocytes increased/normal → peripheral destruction (ITP, TTP, hypersplenism).
• Megakaryocytes absent/reduced → production failure (aplasia, infiltration, megaloblastic).
Step 5 — Targeted assays:
• Anti-platelet IgG: ITP.
• ADAMTS13 activity + inhibitor: TTP.
• Platelet aggregation studies: Glanzmann (no ADP/collagen response), Bernard-Soulier (no ristocetin response).
• VWF antigen + activity: von Willebrand disease (covered in SDL 3).
| Condition | Platelet count | BT/PFA | PT | aPTT | Key film finding |
|---|---|---|---|---|---|
| ITP | Very low | Prolonged | Normal | Normal | Large platelets |
| TTP | Low | Prolonged | Normal/↑ | Normal/↑ | Schistocytes |
| Glanzmann | Normal | Prolonged | Normal | Normal | Normal |
| Bernard-Soulier | Low-normal | Prolonged | Normal | Normal | Giant platelets |
| HSP | Normal | Normal/↑ | Normal | Normal | — |
| Haemophilia A | Normal | Normal | Normal | Prolonged | — |
SELF-CHECK
A bone marrow biopsy in a patient with isolated thrombocytopenia (platelet count 15,000/µL) shows markedly increased megakaryocytes. What does this indicate?
A. Marrow infiltration by malignant cells suppressing megakaryopoiesis
B. Ineffective thrombopoiesis due to megaloblastic change
C. Peripheral platelet destruction with reactive marrow compensation
D. Aplastic anaemia with selective megakaryocyte sparing
Reveal Answer
Answer: C. Peripheral platelet destruction with reactive marrow compensation
Increased marrow megakaryocytes mean the marrow is producing platelets normally — even at an accelerated rate. The thrombocytopenia is therefore caused by peripheral destruction (e.g., ITP, TTP, hypersplenism) not by a production defect. Aplastic anaemia and marrow infiltration would show absent or reduced megakaryocytes.
Putting It Together: A Diagnostic Approach Summary
Diagnostic Approach to Bleeding Disorders
When approaching any bleeding disorder:
- Pattern first: mucocutaneous + immediate → platelet/vascular. Deep + delayed → coagulation.
- Count the platelets: thrombocytopenia present? → classify by mechanism (production ↓ vs destruction ↑ vs dilutional).
- Film: schistocytes (microangiopathy → TTP/HUS/DIC), large/giant platelets (ITP/Bernard-Soulier).
- PT + aPTT: normal in pure platelet disorders; useful to exclude DIC.
- Marrow megakaryocytes: increased = peripheral problem; absent = central problem.
- Vascular purpura clues: palpable + post-infection + IgA → HSP; family history + telangiectasias → HHT; elderly + sun-exposed + minor trauma → senile; C deficiency context + perifollicular → scurvy.
This stepwise framework reduces a wide differential to a short, actionable list within a few clinical and laboratory steps.