Heparin-Induced Thrombocytopenia

Correct answer: C — High probability (6–8 points).

4Ts scoring:
— Thrombocytopenia: 60% fall, nadir ≥20,000 → 2 points
— Timing: POD#1 looks too early for de novo HIT (classic window day 5–10). But prior UFH within 30 days means antibodies may already be present — rapid-onset HIT. Scores 2 points.
— Thrombosis: none → 0 points
— oTher causes: none → 2 points
Total: 6/8 — High probability.

Stop all heparin sources immediately (including flushes and heparin-bonded catheters). Send anti-PF4 ELISA and SRA. Start bivalirudin if ELISA is positive and patient is not bleeding. Avoid platelet transfusion unless there is significant bleeding — HIT is prothrombotic and transfusing platelets risks accelerating clot formation.

Correct answer: B — IgG-mediated platelet FcγRIIa activation with massive thrombin generation.

HIT type 2 is immune-mediated: heparin binds PF4, forming an immunogenic complex. IgG antibodies bind the platelet FcγRIIa receptor, triggering platelet activation and massive thrombin generation. Activated platelets are cleared — hence the falling count — but thrombin generation far outpaces platelet consumption, so thrombosis dominates.

HIT type 1 vs type 2:
— Type 1: non-immune, direct effect on platelet membranes. Occurs days 1–2, mild (rarely <100,000/µL), self-limiting, no thrombotic risk. No treatment required.
— Type 2: immune-mediated, as above. Thrombotic risk 30–50% if untreated.

Correct answer: E — Stop all heparin sources; hold anticoagulation briefly while awaiting ELISA; start bivalirudin promptly once confirmed.

In post-cardiac surgery HIT, the prothrombotic risk of withholding anticoagulation — amplified here by a mechanical valve — must be weighed against hemorrhagic risk in a patient who required re-exploration days ago.

Heparin elimination is immediate and non-negotiable:
— Stop IV UFH infusion
— Replace heparin flushes with normal saline
— Replace heparin-bonded PA catheter as clinically indicated
— Switch CRRT circuit to citrate anticoagulation

On anticoagulation timing: ASH guidelines recommend starting a non-heparin anticoagulant empirically at high 4Ts probability. In a patient with recent re-exploration, briefly awaiting ELISA confirmation is clinically reasonable — provided the result is expected within hours and the patient is monitored closely. Once confirmed, start bivalirudin promptly. This decision should be made jointly with surgery.

Why bivalirudin over argatroban? Argatroban is exclusively hepatically cleared. With shock liver (ALT 640, bilirubin 4.1), it will accumulate unpredictably. Bivalirudin is cleared ~80% by proteolytic degradation — preferred when hepatic dysfunction is present.

Correct answer: B — Bivalirudin for CPB.

Management depends on the phase of HIT.

The five phases of HIT and their implications for cardiac surgery:

Phase	Platelets	Functional Assay	Immunoassay	CPB Anticoagulation
Suspected HIT	↓	?	?	Alternative agent
Acute HIT	↓	+	+	Alternative agent
Subacute HIT A	Normal	+	+	Alternative agent
Subacute HIT B	Normal	−	+	UFH intraop acceptable
Remote HIT	Normal	−	−	UFH intraop acceptable

If surgery can be delayed, wait until subacute HIT B or remote HIT, when intraoperative UFH is acceptable. Antibodies typically clear within 50–85 days.

This patient is in subacute HIT A — platelets recovered but SRA is 15%, not fully negative. UFH re-exposure requires both ELISA (OD <0.4) and SRA (<20%) to be fully undetectable. Re-exposure risks acute anaphylactoid reaction, rapid platelet consumption, and catastrophic intraoperative thrombosis.

Bivalirudin for CPB:
— Direct thrombin inhibitor; does not require antithrombin
— Dosing: bolus 1–1.5 mg/kg + circuit prime 50 mg + infusion 2.5 mg/kg/hr; target ACT >400 sec
— Short half-life (~25 min); degraded by thrombin — stasis causes clot. Minimize vent suction, avoid cardiotomy recirculation, keep pump running
— No reversal agent — plan controlled discontinuation 15–30 min before separation

If bivalirudin unavailable:
— Plasmapheresis + UFH: reduces antibody titers, allowing safer heparin exposure; IgG rebound can occur
— Platelet anesthesia + UFH: cangrelor, iloprost, or abciximab prevent activation in the presence of heparin; iloprost causes vasodilation
— Argatroban or danaparoid: additional alternatives with more limited CPB data

Correct answer: C — Stop all heparin; transition to bivalirudin with cautious titration given hepatic dysfunction.

1. Anticoagulation discontinuation on ECMO carries high risk. Even at flows >3 L/min, circuit surfaces generate thrombin continuously. Stopping anticoagulation risks oxygenator thrombosis and systemic embolism — particularly dangerous on VA-ECMO where arterial emboli reach the brain and coronaries.

2. Why bivalirudin over argatroban? Argatroban is exclusively hepatically cleared. With congestive hepatopathy (ALT 420, bilirubin 3.2), it will accumulate and make titration unreliable. Bivalirudin is cleared ~80% by proteolytic degradation — preferred with hepatic dysfunction.

3. Bivalirudin monitoring on ECMO:
— Target aPTT 40–60 sec initially in post-surgical patients; advance to standard ECMO targets (60–100 sec) once early bleeding risk has passed
— Ecarin clotting time (ECT) is the most accurate monitor for direct thrombin inhibitors — less affected by circuit-induced factor consumption than aPTT
— Anti-Xa assay does not measure bivalirudin effect — it measures heparin and LMWH activity only
— ECMO consumes bivalirudin via thrombin-mediated degradation at circuit surfaces — dose requirements are often higher than in non-ECMO patients

4. Why not fondaparinux? Fondaparinux has very limited data for ECMO anticoagulation, cannot be monitored by standard ECMO assays, and has no antidote.