Prescribed: epoetin alfa 8,000 units SQ three times a week

Available: epoetin alfa 4, 000 units/mL

How many mL will the nurse administer?  Record the answer to the tenth.

A. Continue heparin therapy and monitor platelet counts: Heparin-induced thrombocytopenia (HIT) is an immune-mediated adverse reaction in which antibodies form against the heparin–platelet factor 4 complex, leading to platelet activation and thrombosis. Continuing heparin can worsen platelet consumption and increase the risk of life-threatening thromboembolic events.

B. Discontinue heparin immediately and start an alternative anticoagulant: The priority intervention in suspected HIT is the immediate cessation of all heparin products to prevent further antibody-mediated platelet activation. Because HIT creates a prothrombotic state, an alternative non-heparin anticoagulant is initiated to reduce the risk of DVT or PE.

C. Administer platelet transfusion to manage thrombocytopenia: In HIT, thrombocytopenia results from platelet activation and consumption, not from decreased production. Transfusing platelets may exacerbate thrombosis by providing additional substrate for clot formation. Platelet transfusions are generally avoided unless there is significant active bleeding.

D. Administer intravenous fluids to prevent dehydration: While maintaining adequate hydration is important for overall circulatory stability, IV fluids do not address the immune-mediated platelet activation or thrombotic risk associated with HIT. The immediate threat is thrombosis, which requires stopping heparin and initiating alternative anticoagulation.

A. Administer IV potassium to correct hypokalemia: During the failure stage of acute kidney injury (AKI), hyperkalemia is more common than hypokalemia due to impaired renal excretion. Administering IV potassium without careful monitoring can precipitate life-threatening cardiac arrhythmias. Electrolyte management must be guided by laboratory values.

B. Prepare for hemodialysis to manage fluid and electrolyte imbalances: The failure stage of AKI is characterized by severe reduction in glomerular filtration rate, oliguria or anuria, and accumulation of toxins, electrolytes, and fluid. Hemodialysis provides rapid removal of excess potassium, urea, and fluid, which is critical to preventing complications such as pulmonary edema, hyperkalemia-induced arrhythmias, and severe acidosis.

C. Begin fluid restriction to prevent overload: Fluid restriction may be indicated, especially in oliguric or anuric patients, but it is not sufficient as the primary intervention in the failure stage. Restricting fluid alone does not correct severe electrolyte disturbances or remove accumulated toxins. It is supportive, whereas renal replacement therapy addresses the derangements.

D. Encourage oral intake and high protein to support kidney function: High-protein intake may worsen azotemia in AKI because protein metabolism generates nitrogenous waste that the failing kidneys cannot excrete efficiently. Oral intake is encouraged only if not contraindicated, but promoting protein-heavy intake is not a priority in the failure stage.