FRCPath Haem Part 1 EMQs-Haemostasis 44 and 45

Theme: Diagnosis and Management of HIT

Options

A. Stop heparin and start argatroban

B. Stop heparin and start fondaparinux

C. Start warfarin immediately

D. Perform PF4 IgG ELISA only

E. Perform platelet activation assay with high-dose heparin inhibition and Fc receptor blockade

F. Give IVIG 1 g/kg for 2 days

G. Continue LMWH and repeat platelet count

H. Therapeutic anticoagulation for 3 months

I. Therapeutic anticoagulation for 4 weeks

J. Provide HIT alert card and clearly document diagnosis

K. Use DOAC once clinically stable

L. Plasma exchange (PEx)

M. Suspect spontaneous HIT

N. Test for anti-PF4 antibodies using ELISA in suspected VITT-like syndrome

O. Delay treatment until confirmatory testing completed

Scenarios

1.

A 67-year-old man undergoes total hip replacement. Five days later he develops painful swelling of the left leg and acute dyspnoea. CTPA confirms pulmonary embolism and Doppler shows proximal DVT. Platelet count has fallen from 310 ×10⁹/L pre-operatively to 92 ×10⁹/L. He has been receiving prophylactic LMWH since surgery.

There is no bleeding. Renal function is normal. The clinical team asks for the immediate next step in management.

2.

A 58-year-old woman with NSTEMI receives unfractionated heparin during PCI. Seven days later she develops digital ischaemia and platelet count falls from 280 to 74 ×10⁹/L. HIT ELISA is strongly positive.

The medical registrar wishes to commence warfarin immediately because the patient will require long-term anticoagulation.

What is the most appropriate immediate management?

3.

A 45-year-old woman presents 10 days after laparoscopic cholecystectomy with abdominal pain and headache. CT demonstrates portal vein thrombosis and cerebral venous sinus thrombosis. Platelet count is 38 ×10⁹/L.

She has had no exposure to heparin before or after surgery. D-dimer is markedly elevated. Fibrinogen is mildly reduced.

The haematologist suspects spontaneous HIT.

What is the most appropriate investigation?

4.

A 39-year-old man develops severe thrombocytopenia (platelets 22 ×10⁹/L) and extensive lower limb DVT following a severe adenovirus respiratory infection 2 weeks earlier. No heparin exposure is documented.

The consultant suspects a VITT-like syndrome associated with anti-PF4 antibodies.

Which test is most appropriate initially?

5.

A 71-year-old woman with confirmed HIT develops progressive thrombosis despite therapeutic argatroban. Platelet count remains 18 ×10⁹/L and functional assay shows strong heparin-independent platelet activation.

She has extensive iliofemoral thrombosis and new adrenal haemorrhage.

What additional treatment is most appropriate?

6.

A 62-year-old dialysis patient develops thrombocytopenia 8 days after repeated heparin exposure during haemodialysis. Platelet count falls from 240 to 95 ×10⁹/L. There is no thrombosis.

HIT is confirmed and heparin is stopped.

How long should therapeutic anticoagulation continue?

7.

A 54-year-old man with orthopaedic trauma develops HIT-associated PE after therapeutic UFH. Platelets recover after treatment with danaparoid. He is now clinically stable and wishes to avoid INR monitoring.

Which longer-term anticoagulant strategy is most appropriate?

8.

A 60-year-old woman with severe sepsis develops thrombocytopenia and bilateral adrenal vein thrombosis. She has not received heparin during this admission. Previous admission 3 months ago included LMWH prophylaxis only.

Platelet count is 44 ×10⁹/L. The team suspects spontaneous HIT triggered by infection.

What should be suspected first?

9.

A patient with classical HIT-associated DVT has completed inpatient treatment and platelet count has normalised. He is ready for discharge.

Apart from anticoagulation, what additional important step should be taken to reduce future risk?

10.

A 50-year-old woman with severe autoimmune HIT presents with limb-threatening thrombosis and active gastrointestinal bleeding from peptic ulcer disease. Platelets are 15 ×10⁹/L.

Therapeutic anticoagulation is considered unsafe because of major bleeding risk. Functional testing confirms strong platelet activation independent of heparin.

What additional therapy is most appropriate?