A 70-year-old client has been receiving UFH IV continuous in… | MyMerci
Adverse Effects/Contraindications/Interactions PA
Question

A 70-year-old client has been receiving UFH IV continuous infusion for 7 days for a deep vein thrombosis. The morning labs and assessment show: platelets dropped from a baseline 240 K to 95 K (60% reduction), unilateral swollen and painful right calf with new positive Homans sign, no obvious bleeding. Which action by the nurse is most important?

Explanation
Heparin-Induced Thrombocytopenia (HIT) — recognition and management
HIT is an immune-mediated reaction. IgG antibodies form against platelet factor 4 (PF4)–heparin complexes, activating platelets, causing simultaneous thrombocytopenia AND paradoxical thrombosis. Hallmarks:

Timing: typical onset Day 5–10 of heparin exposure (rapid-onset HIT can occur within 24 hours if previously exposed).
Thrombocytopenia: drop ≥50% from baseline OR absolute platelet count generally 30–100 K (rarely < 15 K — different from other thrombocytopenias).
Thrombosis: arterial or venous, including limb DVT, PE, MI, stroke, skin necrosis at injection sites.
Other causes ruled out.

The 4T score (each item 0–2 points; total 0–8) stratifies clinical probability. Score ≥6 = high probability. Confirmation requires anti-PF4 ELISA plus a functional assay (serotonin release SRA — gold standard).

Management:
(1) Stop ALL heparin immediately — UFH, LMWH, heparin flushes (incl. line locks), heparin-coated catheters.
(2) Start a non-heparin anticoagulant: argatroban (direct thrombin inhibitor, hepatic clearance — preferred in renal impairment), bivalirudin, or fondaparinux (Xa inhibitor; off-label but commonly used).
(3) Send anti-PF4 antibody and confirmatory test.
(4) Do NOT give platelets (would feed thrombosis); transfuse only for major bleed.
(5) Avoid warfarin until platelets recover (>150 K) — early warfarin can cause venous limb gangrene.
(6) Document HIT diagnosis prominently — lifetime heparin avoidance, allergy band.

Continuing or increasing heparin (options 1, 3) feeds the disease; switching UFH to LMWH (option 3) does NOT help — HIT is a class effect (cross-reactivity ~85%).

In-depth explanation

Clinical reasoning summary
Heparin-Induced Thrombocytopenia (HIT) — recognition and management
HIT is an immune-mediated reaction. IgG antibodies form against platelet factor 4 (PF4)–heparin complexes, activating platelets, causing simultaneous thrombocytopenia AND paradoxical thrombosis. Hallmarks:

Timing: typical onset Day 5–10 of heparin exposure (rapid-onset HIT can occur within 24 hours if previously exposed).
Thrombocytopenia: drop ≥50% from baseline OR absolute platelet count generally 30–100 K (rarely < 15 K — different from other thrombocytopenias).
Thrombosis: arterial or venous, including limb DVT, PE, MI, stroke, skin necrosis at injection sites.
Other causes ruled out.

The 4T score (each item 0–2 points; total 0–8) stratifies clinical probability. Score ≥6 = high probability. Confirmation requires anti-PF4 ELISA plus a functional assay (serotonin release SRA — gold standard).

Management:
(1) Stop ALL heparin immediately — UFH, LMWH, heparin flushes (incl. line locks), heparin-coated catheters.
(2) Start a non-heparin anticoagulant: argatroban (direct thrombin inhibitor, hepatic clearance — preferred in renal impairment), bivalirudin, or fondaparinux (Xa inhibitor; off-label but commonly used).
(3) Send anti-PF4 antibody and confirmatory test.
(4) Do NOT give platelets (would feed thrombosis); transfuse only for major bleed.
(5) Avoid warfarin until platelets recover (>150 K) — early warfarin can cause venous limb gangrene.
(6) Document HIT diagnosis prominently — lifetime heparin avoidance, allergy band.

Continuing or increasing heparin (options 1, 3) feeds the disease; switching UFH to LMWH (option 4) does NOT help — HIT is a class effect (cross-reactivity ~85%).
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