A patient with a NIH Stroke Scale score of 15 is receiving tenecteplase for an acute ischemic stroke and has an INR of 2.5 due to therapeutic anticoagulation with warfarin. After the initiation of thrombolytic therapy, the patient's blood pressure drops to 85/55 mmHg during a mechanical thrombectomy. Which of the following actions should the nurse prioritize to address this situation?

C) Reassess the patient's neurological status and notify the physician immediately.

A) Increase the rate of intravenous fluids to rapidly restore blood pressure.

B) Administer a vasopressor to address the patient's hypotension.

C) Reassess the patient's neurological status and notify the physician immediately.

D) Stop the thrombolytic infusion and prepare for an emergency CT scan.

A patient with a moderate to severe stroke is undergoing mechanical thrombectomy after receiving tenecteplase. During the procedure, the patient experiences a sudden drop in blood pressure. Which nursing intervention is most critical to prioritize in this scenario to prevent further complications?

B) Initiate vasopressor support while closely monitoring for signs of reperfusion injury.

A) Increase the rate of intravenous fluids to rapidly elevate blood pressure.

B) Initiate vasopressor support while closely monitoring for signs of reperfusion injury.

C) Administer an additional dose of antihypertensive medication to control blood pressure.

D) Prepare for immediate intubation to secure the airway due to risk of respiratory failure.

A patient in the neurocritical care unit following a thrombectomy develops a hemorrhagic transformation at the site of the previously occluded vessel, labile blood pressure, and acute kidney injury. The INR is elevated at 2.7, and hemoglobin has decreased significantly. Which nursing intervention is the most critical to prioritize in this situation?

C) Implement strict blood pressure control to maintain cerebral perfusion pressure.

A) Administer Vitamin K to reverse anticoagulation and prevent further bleeding.

B) Initiate renal replacement therapy to manage acute kidney injury.

C) Implement strict blood pressure control to maintain cerebral perfusion pressure.

D) Prepare for an urgent surgical intervention to evacuate the hemorrhage.

A patient in the neurocritical care unit post-thrombectomy exhibits hemorrhagic transformation at the site of occlusion, labile blood pressure, and acute kidney injury. The team must decide on the next step in management to minimize complications. What is the most appropriate nursing action to address the current clinical situation?

C) Adjust antihypertensive medications to maintain systolic blood pressure below 140 mmHg while monitoring renal function.

A) Administer fresh frozen plasma to reverse anticoagulation and prevent further bleeding.

B) Initiate fluid resuscitation aggressively to improve renal perfusion and stabilize blood pressure.

C) Adjust antihypertensive medications to maintain systolic blood pressure below 140 mmHg while monitoring renal function.

D) Withhold anticoagulation and increase frequency of neurological assessments to monitor for changes.

A 72-year-old patient, six hours post-thrombectomy, is exhibiting increased confusion, a drop in Glasgow Coma Scale from 13 to 9, and a re-emergence of right upper extremity weakness with decreased sensation. Vital signs show hypertension, tachycardia, and tachypnea. Lab results indicate a drop in hemoglobin and elevated INR. Which nursing intervention should be prioritized to prevent further neurological deterioration?

B) Prepare for an immediate CT scan to assess for hemorrhagic expansion or new ischemic events.

A) Administer a bolus of intravenous fluids to address potential hypovolemia.

B) Prepare for an immediate CT scan to assess for hemorrhagic expansion or new ischemic events.

C) Increase the antihypertensive medication dose to manage elevated blood pressure.

D) Monitor respiratory status and prepare for potential intubation due to tachypnea.

A 65-year-old patient, six hours post-thrombectomy, exhibits increased confusion, decreased consciousness with a Glasgow Coma Scale drop from 13 to 9, and right upper extremity weakness with decreased sensation. Vital signs indicate hypertension and tachycardia, while lab results show declining renal function and elevated INR. Which of the following nursing interventions is most critical to prioritize in this situation?

B) Prepare the patient for an urgent CT scan to assess for possible hemorrhagic transformation.

A) Administer a bolus of intravenous fluids to address potential hypovolemia.

B) Prepare the patient for an urgent CT scan to assess for possible hemorrhagic transformation.

C) Adjust the antihypertensive medication to achieve immediate blood pressure control.

D) Initiate renal replacement therapy to address worsening creatinine levels.

A patient with a recent ischemic stroke has developed a hemorrhagic transformation with increased intracranial pressure (ICP). The neurocritical care team is considering a decompressive craniectomy but is concerned about the elevated INR. As the nurse, what is the priority action to prepare the patient for potential surgical intervention?

B) Prepare fresh frozen plasma and vitamin K to correct the elevated INR.

A) Administer mannitol to reduce cerebral edema before surgery.

B) Prepare fresh frozen plasma and vitamin K to correct the elevated INR.

C) Increase the patient's intravenous antihypertensive medication to control blood pressure.

The nurse is caring for a patient with a hemorrhagic transformation following an ischemic stroke, who is at risk of increased intracranial pressure (ICP) and herniation. Considering the multidisciplinary team's plan and current patient condition, what is the most critical nursing intervention to prioritize?

C) Intensify blood pressure control with a titratable intravenous antihypertensive agent.

A) Administer vitamin K and fresh frozen plasma immediately to reverse elevated INR.

B) Initiate continuous renal replacement therapy (CRRT) to manage rising creatinine levels.

C) Intensify blood pressure control with a titratable intravenous antihypertensive agent.

D) Prepare the patient for an emergency decompressive craniectomy.

A patient with increased intracranial pressure is showing signs of potential uncal herniation, and their Glasgow Coma Scale (GCS) score has decreased to 7. The patient's blood pressure remains high despite treatment, and their lab results indicate an elevated INR and worsening renal function. Which nursing intervention should be prioritized to prevent further neurological deterioration?

A) Administer mannitol to decrease intracranial pressure and monitor fluid balance closely.

B) Increase the dosage of antihypertensive medication to further lower blood pressure.

C) Prepare the patient for immediate surgical intervention to address potential herniation.

D) Initiate continuous renal replacement therapy (CRRT) to manage fluid overload and improve renal function.

A patient with worsening neurological function and increased intracranial pressure is being managed by a multidisciplinary team. Despite aggressive management, the patient's condition is deteriorating. Which nursing action should be prioritized to address the patient's current clinical status?

C) Prepare the patient for an immediate decompressive craniectomy as advised by neurosurgery.

A) Administer an osmotic diuretic as prescribed to reduce cerebral edema.

C) Prepare the patient for an immediate decompressive craniectomy as advised by neurosurgery.

D) Collaborate with the healthcare team to reverse anticoagulation therapy to prevent further bleeding complications.

Thrombolytic Stroke with LVO - patient receiving tenecteplase and a thrombectomy in the neuroendovascular lab - Nursing Case Study

Pathophysiology

• Primary mechanism: Large vessel occlusion (LVO) in a thrombolytic stroke occurs when a blood clot obstructs a major cerebral artery, leading to ischemia and potential infarction of brain tissue due to impaired cerebral blood flow. This significantly increases the risk of severe neurological deficits and brain damage.

• Secondary mechanism: Tenecteplase, a thrombolytic agent, is administered to dissolve the clot by enhancing fibrinolysis. It converts plasminogen to plasmin, breaking down fibrin and restoring partial blood flow, which is crucial for minimizing tissue damage before mechanical intervention.

• Key complication: If pharmacological thrombolysis is insufficient, a thrombectomy is performed in the neuroendovascular lab. This mechanical removal of the clot restores blood flow, reducing the risk of extensive brain injury but carries risks such as vessel injury or hemorrhagic transformation.

Patient Profile

Demographics:

67-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Atrial Fibrillation, Prior Ischemic Stroke (5 years ago)

• Current medications: Metformin, Lisinopril, Warfarin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of right-sided weakness and slurred speech

• Key symptoms: Severe headache, difficulty speaking, right arm and leg paralysis, facial droop on the right side, confusion, nausea

• Vital signs: Blood pressure 210/110 mmHg, heart rate 130 bpm (irregular), respiratory rate 24 breaths per minute, oxygen saturation 88% on room air, temperature 37.8°C (100.0°F)

Section 1

Initial assessment findings reveal critical details that guide the clinical team in their approach. Upon arrival at the emergency department, the patient exhibits a NIH Stroke Scale score of 15, indicating a moderate to severe stroke. Neurological examination confirms complete right-sided hemiparesis and expressive aphasia. The patient's blood glucose level is elevated at 220 mg/dL, complicating metabolic control and potentially exacerbating cerebral injury. An urgent CT scan of the head without contrast shows no evidence of intracerebral hemorrhage, permitting the administration of tenecteplase. Continuous cardiac monitoring reveals persistent atrial fibrillation with rapid ventricular response, which further contributes to cerebral hypoperfusion and complicates blood pressure management.

As the tenecteplase infusion begins, the patient's blood pressure remains critically high despite administration of intravenous antihypertensive medications, necessitating careful titration to avoid precipitating intracranial hemorrhage. Oxygen supplementation is initiated to address hypoxia, and the patient's oxygen saturation improves to 94% on 2L nasal cannula. Blood tests reveal an INR of 2.5, indicating therapeutic anticoagulation from warfarin, which poses an additional bleeding risk following thrombolytic therapy and during the mechanical thrombectomy.

The decision to proceed with an emergent thrombectomy is made as the patient's condition remains dire despite initial pharmacological intervention. In the neuroendovascular lab, the interventional radiology team faces a challenging procedure due to tortuous vascular anatomy and calcified plaque, complicating catheter navigation. During the intervention, the patient experiences a sudden drop in blood pressure to 85/55 mmHg, requiring vasopressor support. This hemodynamic instability raises concerns of possible reperfusion injury or hemorrhagic conversion, necessitating immediate post-procedural imaging and vigilant monitoring in the neurocritical care unit.

Section 2

Following the thrombectomy, the patient is transferred to the neurocritical care unit for close monitoring. Initially, there is a transient improvement in neurological status; the patient exhibits some return of movement in the right upper extremity and partial improvement in expressive aphasia. However, this progress is soon overshadowed by a new complication. Repeat imaging, including a CT angiogram, reveals a small area of hemorrhagic transformation at the site of the previously occluded vessel, raising immediate concerns about the optimal balance between anticoagulation and risk of further bleeding.

The patient's blood pressure remains labile, fluctuating between 90/60 mmHg and 150/95 mmHg, despite careful titration of vasopressors and antihypertensives. Laboratory tests show a drop in hemoglobin to 9.5 g/dL from an initial 13.2 g/dL, suggestive of bleeding complications. The INR remains elevated at 2.7, complicating management decisions regarding reversing anticoagulation. Additionally, the patient develops acute kidney injury, with serum creatinine rising from 1.0 mg/dL to 2.3 mg/dL, likely secondary to contrast-induced nephropathy and hemodynamic instability.

In light of these developments, the multidisciplinary team must engage in advanced critical thinking and clinical judgment to navigate the complex interplay of anticoagulation management, blood pressure control, and renal support. The focus shifts to stabilizing the patient’s hemodynamics, monitoring for further neurological changes, and reassessing the anticoagulation strategy to prevent additional thromboembolic events while minimizing bleeding risk. This scenario demands a nuanced approach to ensure both cerebral protection and systemic stability, underscoring the delicate balance of interventions in the setting of severe stroke with complications.

Section 3

As the neurocritical care team continues to monitor the patient, a change in status becomes apparent. Approximately six hours post-thrombectomy, the patient begins to exhibit increased confusion and disorientation, deviating from the initial partial recovery of expressive aphasia. Neurological assessments reveal a decrease in consciousness, with the Glasgow Coma Scale dropping from 13 to 9, indicating a significant decline in cognitive responsiveness. Pupillary response remains sluggish but equal bilaterally, and there is a re-emergence of weakness in the right upper extremity, now accompanied by decreased sensation, suggesting potential expansion of the hemorrhagic area or new ischemic insult.

Concurrent with the neurological decline, vital signs show persistent instability. The patient's blood pressure spikes to 170/105 mmHg despite ongoing antihypertensive management. Heart rate has increased to 115 beats per minute, and there is a noted tachypnea with a respiratory rate of 24 breaths per minute. The oxygen saturation remains stable at 96% on 2L of nasal cannula. Repeat laboratory investigations reveal a further drop in hemoglobin to 8.7 g/dL, while INR remains elevated at 2.5, complicating the anticoagulation strategy. Creatinine continues to rise, now at 2.8 mg/dL, signaling worsening renal function and necessitating consideration of renal replacement therapy.

In response to these developments, the team faces critical decisions regarding the management of anticoagulation and blood pressure, balancing the risk of further hemorrhagic transformation against the potential for new thromboembolic events. An urgent neurology consult is requested to assess the need for surgical intervention or additional imaging, while nephrology is consulted for early initiation of renal support. The evolving clinical picture underscores the need for meticulous reassessment and adaptation of the care plan to stabilize the patient's systemic and cerebral status, illustrating the complexity and precision required in managing such multifaceted cases.

Section 4

As the neurocritical care team continues to navigate the complexities of the patient's condition, new diagnostic imaging is expedited to elucidate the cause of the neurological deterioration. A stat CT scan of the head reveals the presence of a large hemorrhagic transformation at the site of the initial ischemic stroke, raising concerns about increased intracranial pressure (ICP) and the risk of herniation. The hemorrhage appears to have expanded into the frontal and temporal lobes, correlating with the patient's declining neurological status and re-emergence of motor deficits. Additionally, a CT angiography is performed to assess for any new vascular occlusions or reperfusion injury, which could further complicate the patient's fragile cerebral state.

The imaging results prompt an immediate multidisciplinary discussion among the neurocritical care team, neurology, and neurosurgery specialists. The team deliberates on the potential need for surgical intervention, such as decompressive craniectomy, to alleviate the pressure caused by the expanding hematoma. However, the elevated INR poses a significant surgical risk, necessitating careful consideration of the timing and approach to any invasive procedures. Concurrently, nephrology evaluates the patient's renal function, suggesting a cautious initiation of continuous renal replacement therapy (CRRT) to manage the rising creatinine levels and potential fluid overload, which could exacerbate cerebral edema.

In light of these findings, the team decides to adjust the management plan with a dual focus on stabilizing the patient's systemic status and preventing further neurological compromise. Blood pressure control is intensified using a titratable intravenous antihypertensive agent to reduce the risk of further hemorrhagic expansion while closely monitoring the patient's hemodynamic response. The anticoagulation strategy is re-evaluated; vitamin K and fresh frozen plasma are considered to reverse the elevated INR if surgical intervention becomes necessary. The evolving scenario highlights the critical need for precise clinical judgment and rapid adaptation of therapeutic strategies in response to the dynamic and interconnected challenges presented by this complex case.

Section 5

As the team implements the revised management plan, the patient's status continues to evolve, presenting new challenges that test the limits of clinical acumen. Despite aggressive blood pressure control, the patient exhibits signs of worsening neurological function. The neurologic exam reveals anisocoria, with the right pupil significantly larger than the left and sluggish to light, indicative of increased intracranial pressure and possible uncal herniation. The patient's Glasgow Coma Scale (GCS) score has decreased to 7, reflecting a decline in motor response and verbal output. Vital signs are concerning: blood pressure is 180/90 mmHg despite titration of antihypertensives, heart rate is tachycardic at 115 bpm, and respiratory rate is irregular at 10 breaths per minute, suggesting brainstem involvement.

Lab results compound the complexity of the situation. The INR remains elevated at 2.5, complicating the potential for surgical intervention. Additionally, the patient's renal function continues to deteriorate, with creatinine levels rising to 3.2 mg/dL, indicative of acute kidney injury possibly exacerbated by contrast-induced nephropathy from recent imaging. Fluid balance is precarious; despite cautious diuresis, the patient remains edematous, with a positive fluid balance of 2 liters over the past 24 hours, raising the risk of exacerbating cerebral edema.

In response to these critical developments, the team must quickly reassess the intervention priorities. The neurosurgery team is contacted for an urgent re-evaluation of the need for decompressive craniectomy, while nephrology expedites the initiation of CRRT to manage fluid overload and support renal function. The potential reversal of anticoagulation is revisited, balancing the imminent surgical risk against the possibility of further embolic events. This juncture demands precise decision-making and swift coordination across specialties to stabilize the patient and prevent irreversible neurological damage. The next hours are critical, with the team's interventions holding the potential to alter the course of this complex case.