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PA20.1-2 | Platelet & Vascular Bleeding Disorders — Part 3

Laboratory Approach to Platelet & Vascular Bleeding

A four-panel infographic shows the laboratory algorithm for platelet and vascular bleeding, including blood film clues, PT/aPTT and bleeding time patterns, and bone marrow megakaryocyte interpretation.

Laboratory Approach to Platelet and Vascular Bleeding

Panel A: Stepwise algorithm showing platelet count and peripheral blood film, PT/aPTT coagulation screen, bleeding time/PFA-100, and bone marrow biopsy when needed. Panel B: Peripheral blood film findings: thrombocytopenia, schistocytes, large platelets, giant platelets, and EDTA-related platelet clumping. Panel C: Screening test pattern comparing normal PT/aPTT with prolonged bleeding time in platelet or vascular disorders versus abnormal PT/aPTT in coagulation defects or DIC. Panel D: Bone marrow biopsy interpretation showing megakaryocytes increased or normal in peripheral destruction and reduced in marrow production failure.

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).

ConditionPlatelet countBT/PFAPTaPTTKey film finding
ITPVery lowProlongedNormalNormalLarge platelets
TTPLowProlongedNormal/↑Normal/↑Schistocytes
GlanzmannNormalProlongedNormalNormalNormal
Bernard-SoulierLow-normalProlongedNormalNormalGiant platelets
HSPNormalNormal/↑NormalNormal
Haemophilia ANormalNormalNormalProlonged

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

A four-panel diagnostic flow diagram summarizes how bleeding pattern, platelet count, blood film, PT/aPTT, marrow megakaryocytes, and vascular purpura clues narrow the differential diagnosis of bleeding disorders.

Diagnostic Approach to Bleeding Disorders

Panel A: Clinical bleeding pattern: mucocutaneous immediate bleeding with petechiae, purpura, epistaxis, gum bleeding, menorrhagia; deep delayed bleeding with hemarthrosis, muscle hematoma, delayed post-procedure bleeding.. Panel B: Platelet count classification and peripheral smear findings: thrombocytopenia, decreased production, increased destruction, dilutional loss, schistocytes, large platelets, giant platelets, TTP, HUS, DIC, ITP, Bernard-Soulier syndrome.. Panel C: Laboratory and marrow interpretation: PT, aPTT, normal coagulation screening in pure platelet disorders, abnormal PT/aPTT suggesting coagulation disorder or DIC, increased marrow megakaryocytes, absent marrow megakaryocytes.. Panel D: Vascular purpura clinical clues: palpable purpura with IgA and post-infection context for Henoch-Schonlein purpura, telangiectasias and family history for hereditary hemorrhagic telangiectasia, senile purpura on elderly sun-exposed skin, perifollicular hemorrhage in vitamin C deficiency scurvy..

When approaching any bleeding disorder:

  1. Pattern first: mucocutaneous + immediate → platelet/vascular. Deep + delayed → coagulation.
  2. Count the platelets: thrombocytopenia present? → classify by mechanism (production ↓ vs destruction ↑ vs dilutional).
  3. Film: schistocytes (microangiopathy → TTP/HUS/DIC), large/giant platelets (ITP/Bernard-Soulier).
  4. PT + aPTT: normal in pure platelet disorders; useful to exclude DIC.
  5. Marrow megakaryocytes: increased = peripheral problem; absent = central problem.
  6. 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.