On day 8 of unfractionated heparin after surgery, a client's platelets fall from 284,000 to 108,000/mm3 (reference 150,000-400,000). Ultrasound confirms a new leg-vein thrombosis. The clinician documents a high-probability 4Ts score; there is no bleeding or competing strong cause of thrombocytopenia. A non-heparin anticoagulant is prescribed while confirmatory testing is pending. Its drug-specific laboratory titration is already assigned to the anticoagulation service. Select the most likely complication, TWO actions now, and TWO additional trends that assess platelet recovery and progression of the affected limb's disease.

Correct answer
Choose immune HIT with thrombosis; stop all heparin and administer the prescribed non-heparin anticoagulant. Follow platelet count and affected-limb clinical findings.

Why this is correct
The timing, greater-than-half platelet decline, objectively confirmed thrombosis and high clinical probability fit immune HIT. Thrombocytopenia does not mean the client is protected from clotting. High-probability disease requires action while confirmatory testing proceeds.

Clinical picture
Platelet recovery and the limb examination follow the disease course. Continue the ordered anticoagulant-specific monitoring and routine bleeding surveillance as well; the question explicitly asks for additional disease-response trends.

Memory hook
A falling platelet count can accompany increasing thrombosis. In HIT, remove the trigger while preserving anticoagulation through a suitable alternative.

NCLEX decision rule
For high-probability HIT, do not wait for the antibody result to stop heparin and begin the prescribed alternative. Include small heparin exposures such as flushes when reviewing the medication list.

Why the alternatives are wrong
Early nonimmune thrombocytopenia usually occurs earlier and does not explain this thrombotic pattern. Sepsis-related DIC needs a supporting systemic illness/coagulation pattern absent here. Excess anticoagulation does not explain new thrombosis with this characteristic platelet fall. Continuing heparin or substituting low-molecular-weight heparin maintains exposure to the trigger. Starting warfarin before recovery creates additional thrombotic risk. INR is not the selected disease-response marker before warfarin; stool blood testing and hemoglobin are relevant to bleeding surveillance rather than platelet recovery or limb progression. The selected limb assessment supplements rather than replaces diagnostic imaging when deterioration occurs.