A nurse is caring for a client who experienced an acute ischemic stroke 24 hours ago and has received tissue plasminogen activator (tPA). The client suddenly develops severe headache, nausea, vomiting, and altered level of consciousness. What is the nurse's priority action?

The symptoms suggest hemorrhagic transformation, a life-threatening complication of tPA. The priority is to stop anticoagulants and notify the physician immediately to prevent further bleeding.

Understanding the Clinical Scenario
The client is 24 hours post-tPA administration for an acute ischemic stroke and now presents with a sudden severe headache, nausea, vomiting, and an altered level of consciousness. This clinical picture is a classic and critical red flag. The administration of tissue plasminogen activator (tPA) carries the most feared risk of symptomatic intracranial hemorrhage (sICH), a serious complication that can substantially worsen patient outcomes and increase mortality ^[1]. The sudden onset of these neurological symptoms strongly suggests the client is developing this life-threatening complication.

Priority Action and Rationale
The nurse's priority action is to stop all anticoagulant therapy and notify the physician immediately. In the context of a suspected hemorrhagic conversion after thrombolysis, any ongoing or newly initiated anticoagulant or antiplatelet therapy will exacerbate the bleeding. The immediate cessation of these agents is a critical first step to prevent further expansion of the hemorrhage. Simultaneously, the physician must be notified emergently to obtain orders for a STAT head CT scan to confirm the diagnosis and to initiate medical or surgical interventions to manage the intracranial pressure and reverse the coagulopathy.

Analysis of Incorrect Options
Option 1: Administer prescribed antihypertensive medication immediately. While blood pressure management is a cornerstone of post-tPA care to prevent hemorrhagic transformation, aggressively lowering blood pressure in the setting of an active, evolving* intracranial hemorrhage can be detrimental. It may reduce cerebral perfusion pressure, worsening secondary brain injury. The immediate priority is to stop the bleeding, not to treat a blood pressure that may be a reactive physiological response to the hemorrhage. The physician will guide specific blood pressure parameters after the diagnosis is confirmed.
Option 3: Elevate the head of the bed to 45 degrees and provide oxygen. These are supportive interventions to reduce intracranial pressure and maintain oxygenation. However, they are not the first* or most critical action. The underlying cause—a potential active bleed exacerbated by thrombolytics—must be addressed first. Stopping the offending agent takes precedence over supportive measures.
Option 4: Perform a complete neurological assessment and document findings. A focused neurological assessment is vital to identify changes, but a complete* assessment delays definitive action. The nurse has already identified the cardinal signs of a serious complication (severe headache, altered consciousness). At this point, immediate intervention and notification are required, not a comprehensive assessment and documentation. A brief, focused assessment to confirm the Glasgow Coma Scale and pupil reactivity can be done concurrently with calling for help, but stopping the anticoagulant is the independent nursing action that directly impacts the pathophysiology.

Deep Dive into sICH Pathophysiology and Risk
The clinical benefit of tPA is counterbalanced by the risk of sICH ^[1]. tPA works by converting plasminogen to plasmin, which dissolves the fibrin mesh of the clot. However, this systemic fibrinolytic state also impairs the body’s ability to maintain hemostasis at the site of the initial ischemic injury, where the blood-brain barrier is already compromised. Reperfusion into a damaged vascular bed can lead to vessel rupture and hemorrhage into the brain parenchyma. This explains why the complication can occur hours after the infusion, as seen in this scenario at 24 hours post-treatment. The development of sICH dramatically alters the prognosis, making its rapid recognition and management a high-stakes nursing responsibility directly linked to the client's 3-month functional outcome ^[1].