Thrombocytopenia

A low platelet count from reduced production, increased destruction, dilution or sequestration. The count alone does not tell you what to do; the mechanism does. Two situations make transfusing platelets actively harmful — heparin-induced…

Find the mechanism — and the two times NOT to transfuse

The pathway

1 · Is it real?

EDTA-induced clumping gives a spuriously low count in a well patient with no bleeding
Repeat in a citrate tube to confirm
Always ask for a blood film — it is the single most informative test and it is free

2 · Is there bleeding, and how bad?

Petechiae, purpura, mucosal or gum bleeding, epistaxis — wet purpura (mucosal) is more concerning than dry
Count under 20 raises spontaneous bleeding risk; generally under 10 is the prophylactic threshold in reversible marrow failure, risk-adjusted within 10-20
Major bleeding at any count means resuscitate first

3 · Work out the mechanism

Drugs — heparin, antibiotics, anticonvulsants, quinine, chemotherapy
Sepsis and DIC — check clotting and fibrinogen
Liver disease and hypersplenism
Marrow failure — other lineages down, blasts on the film
Immune (ITP) — isolated low count, otherwise well
Microangiopathy — fragments on the film

4 · ⚠ HIT — do not transfuse, stop the heparin

Platelets fall 5 to 14 days after first heparin exposure, typically by more than 50%
Rapid-onset HIT can occur within hours where there has been heparin in the preceding weeks
Thrombosis, not bleeding, is the problem — a new DVT, PE or line clot with a falling count
Score it with the 4Ts
STOP all heparin, including flushes and LMWH, and start appropriate non-heparin anticoagulation urgently — this is a haematology conversation, not a wait-and-see
Avoid routine platelet transfusion; the problem is thrombosis, not bleeding
Do not start warfarin until the platelet count recovers — early warfarin risks venous limb gangrene

5 · ⚠ TTP — do not transfuse, call haematology

Thrombocytopenia with microangiopathic haemolysis — fragments on the film, raised LDH, low haptoglobin
With fever, renal impairment and fluctuating neurology, though the full pentad is uncommon
Urgent haematology and the plasma exchange pathway — the delay costs lives
Platelet transfusion is contraindicated UNLESS there is life-threatening haemorrhage — outside that exception it fuels the microthrombi

6 · When platelets ARE the answer

Major bleeding at any count
Prophylaxis in reversible marrow failure generally below 10, risk-adjusted upward within 10-20 with added bleeding risks such as sepsis, per local policy
Before a procedure to the threshold local policy specifies
Avoid routine transfusion in HIT, and in TTP unless there is life-threatening haemorrhage. Of little value in ITP, where they are destroyed as fast as they are given

Drugs

Drug	Dose	Route	Notes
Platelets	One adult therapeutic dose	IV	Avoid routinely in HIT. Contraindicated in TTP unless there is life-threatening haemorrhage. Of limited value in ITP.
Non-heparin anticoagulant	Per haematology — e.g. argatroban, fondaparinux	IV / SC	HIT needs urgent alternative anticoagulation, not simply heparin withdrawal. Do not start warfarin until the platelets recover.
Prednisolone / IVIG	Per haematology	PO / IV	ITP with bleeding or a very low count. A haematology decision.
Plasma exchange	Urgent	Procedure	TTP. The treatment, and the delay is what kills.

When to escalate

Fragments on the film — TTP until excluded. Urgent haematology and the plasma exchange pathway,Count falling on heparin with a new thrombosis — HIT. Stop all heparin, score the 4Ts, and ring haematology for urgent non-heparin anticoagulation,Major bleeding at any count — major haemorrhage protocol,Pancytopenia or blasts on the film — urgent haematology, this is marrow failure until proven otherwise

Reference: British Society for Haematology guidelines on the investigation and management of thrombocytopenia, ITP, HIT and TTP. Local transfusion policy and haematology advice take precedence.

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