A patient presents with a decreased Glasgow Coma Scale (GCS) score, right-sided hemiplegia, expressive aphasia, anisocoria, and a history of atrial fibrillation. Which immediate nursing intervention is priority to prevent further neurological deterioration?

D) Initiate high-flow oxygen therapy to improve oxygen saturation.

A) Administer intravenous mannitol to reduce intracranial pressure.

B) Prepare the patient for immediate neuroimaging.

C) Administer intravenous antihypertensive medication to rapidly lower blood pressure.

D) Initiate high-flow oxygen therapy to improve oxygen saturation.

A 65-year-old female with a history of poorly controlled atrial fibrillation and diabetes mellitus presents to the emergency department with a suspected cardioembolic stroke. Her Glasgow Coma Scale (GCS) score is 10, and she exhibits right-sided hemiplegia and expressive aphasia. Vital signs include a blood pressure of 210/120 mmHg, an irregular heart rate, and oxygen saturation of 85%. Which nursing intervention should be prioritized to address her immediate needs?

C) Prepare the patient for intubation to secure the airway and improve oxygenation.

A) Administer IV labetalol to rapidly reduce her blood pressure.

B) Initiate continuous cardiac monitoring to manage atrial fibrillation.

C) Prepare the patient for intubation to secure the airway and improve oxygenation.

D) Administer an insulin drip to control her elevated blood glucose level.

A patient with a suspected ischemic stroke and a critically elevated INR of 4.5 is under evaluation. The CT scan indicates a large left MCA thrombotic occlusion with ischemia and early cerebral edema, but no hemorrhagic transformation. Considering the patient's condition and the need for immediate intervention, which nursing action is most appropriate to prioritize?

C) Initiate blood pressure management protocols to reduce the risk of hemorrhagic transformation.

A) Prepare the patient for immediate administration of intravenous thrombolytics despite the high INR.

B) Contact the healthcare provider to discuss the feasibility of mechanical thrombectomy given the thrombus location and renal impairment.

C) Initiate blood pressure management protocols to reduce the risk of hemorrhagic transformation.

D) Arrange for the administration of vitamin K to reverse the elevated INR prior to any interventional treatment.

A patient with a large left middle cerebral artery (MCA) thrombotic occlusion and elevated INR due to anticoagulation therapy for atrial fibrillation presents with acute ischemic stroke symptoms. Given the elevated INR, renal impairment, and risk for hemorrhagic transformation, what is the nurse's priority intervention to prepare for the patient's potential treatment plan?

C) Collaborate with the multidisciplinary team to evaluate the risks of endovascular thrombectomy.

A) Administer fresh frozen plasma to reverse anticoagulation effects.

B) Prepare the patient for immediate thrombolytic therapy administration.

C) Collaborate with the multidisciplinary team to evaluate the risks of endovascular thrombectomy.

D) Monitor vital signs closely and implement seizure precautions.

A patient with acute neurological deterioration presents with right-sided hemiplegia, aphasia, and a GCS score drop from 12 to 8. The clinical team is administering intravenous labetalol to manage her blood pressure of 210/110 mmHg. Given her rising creatinine level and declining respiratory status, what should the nurse prioritize in the immediate management of this patient?

B) Prepare for potential intubation to secure the airway and improve oxygenation.

A) Monitor neurological status every 30 minutes to detect any further decline.

B) Prepare for potential intubation to secure the airway and improve oxygenation.

C) Increase the labetalol infusion rate to rapidly lower blood pressure to target levels.

D) Initiate renal-protective measures such as hydration to prevent further renal damage.

A patient with acute neurological deterioration presents with a Glasgow Coma Scale (GCS) score drop from 12 to 8, right-sided hemiplegia, aphasia, and elevated blood pressure. After initiating intravenous labetalol, what is the next most critical nursing intervention to prioritize?

B) Prepare for potential intubation to secure the airway given the patient's declining respiratory status.

A) Monitor the patient's blood pressure continuously to ensure it does not drop too rapidly.

B) Prepare for potential intubation to secure the airway given the patient's declining respiratory status.

C) Administer diuretics to manage cerebral edema and prevent further neurological damage.

D) Initiate tPA therapy to address the potential ischemic stroke despite the elevated INR.

A patient in the intensive care unit is being treated for a hypertensive crisis with intravenous labetalol. Despite blood pressure stabilization, the patient exhibits signs of substantial cerebral edema and declining neurological status. What is the nurse's priority intervention to prevent further neurological deterioration?

B) Elevate the head of the bed to 30 degrees to promote venous drainage from the brain.

A) Increase the rate of intravenous labetalol to further reduce blood pressure.

B) Elevate the head of the bed to 30 degrees to promote venous drainage from the brain.

C) Administer mannitol as prescribed to reduce cerebral edema.

D) Prepare for immediate intubation to secure the airway.

A 65-year-old female patient in the ICU is experiencing cerebral edema, acute kidney injury, and hypoxemia following a hypertensive crisis. Her blood pressure is stabilized at 180/95 mmHg with intravenous labetalol, but her neurological and renal status is deteriorating. As the patient's nurse, which intervention should be prioritized to prevent further complications?

C) Prepare for intubation to secure the airway and improve oxygenation.

A) Administer mannitol to reduce cerebral edema and prevent herniation.

B) Initiate dialysis immediately to address acute kidney injury and improve renal function.

C) Prepare for intubation to secure the airway and improve oxygenation.

D) Increase the dosage of labetalol to achieve a target blood pressure of 140/90 mmHg.

A patient with severe traumatic brain injury is experiencing a drop in Glasgow Coma Scale (GCS) score and signs of increased intracranial pressure. The critical care team has administered mannitol and hypertonic saline, and the patient has been intubated. Despite these interventions, metabolic acidosis is noted with a pH of 7.28. What is the priority nursing intervention at this time to address the complex needs of this patient?

C) Coordinate with the nephrologist to initiate dialysis to manage the acidosis and fluid overload.

A) Increase the rate of the ventilator to blow off more CO2 and correct the acidosis.

B) Administer a bolus of sodium bicarbonate to rapidly correct the metabolic acidosis.

C) Coordinate with the nephrologist to initiate dialysis to manage the acidosis and fluid overload.

D) Elevate the head of the bed to 30 degrees to promote venous drainage and reduce intracranial pressure.

A patient in the ICU exhibits neurological deterioration with a Glasgow Coma Scale score dropping from 12 to 8, unequal pupils, and Cheyne-Stokes respiration. The intensivist has initiated rapid-sequence intubation, and the neurosurgery team is considering a decompressive craniectomy. Despite treatment with mannitol and hypertonic saline, the patient develops metabolic acidosis with an ABG showing a pH of 7.28, bicarbonate of 15 mEq/L, and PaCO2 of 34 mmHg, indicating likely acute kidney injury and lactic acidosis. As the primary nurse, what is the most critical assessment to perform before initiating dialysis as recommended by the nephrologist?

C) Assess the patient's hemodynamic stability, focusing on blood pressure and heart rate.

A) Monitor the patient's urine output and assess for signs of fluid overload.

B) Evaluate the patient's neurological status for any changes post-intubation.

C) Assess the patient's hemodynamic stability, focusing on blood pressure and heart rate.

D) Review the patient's current medication regimen for potential nephrotoxic agents.

thrombotic stroke - Nursing Case Study

Pathophysiology

• Primary mechanism: Atherosclerosis leads to endothelial injury and plaque formation in cerebral arteries, causing turbulent blood flow and promoting platelet aggregation and thrombus formation, which narrows or occludes the vessel lumen, reducing cerebral blood flow.

• Secondary mechanism: Inflammatory processes within the arterial wall exacerbate plaque instability, increasing the risk of plaque rupture. This rupture exposes thrombogenic material to the bloodstream, accelerating thrombus formation and potentially leading to abrupt vessel occlusion.

• Key complication: Resultant ischemia causes neuronal injury and cell death in the affected brain region, leading to varying degrees of neurological deficits depending on the severity and location of the occlusion. This can escalate into severe complications like brain edema, hemorrhagic transformation, and long-term disability.

Patient Profile

Demographics:

67-year-old female, retired school teacher

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Atrial Fibrillation, Previous TIA (Transient Ischemic Attack)

• Current medications: Metformin, Lisinopril, Metoprolol, Warfarin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of right-sided weakness and difficulty speaking

• Key symptoms: Right hemiparesis, slurred speech, facial droop on the right side, severe headache, confusion

• Vital signs: Blood pressure 210/115 mmHg, heart rate 130 bpm and irregular, respiratory rate 24 breaths per minute, temperature 37.8°C, oxygen saturation 88% on room air

Section 1

Initial Assessment Findings:

Upon the patient's arrival to the emergency department, the initial assessment reveals a rapidly deteriorating neurological status. Her Glasgow Coma Scale (GCS) score has decreased to 10, indicating a decline in consciousness. Physical examination confirms pronounced right-sided hemiplegia, with a complete loss of motor function on the right side and an inability to follow simple commands. Her speech is severely dysarthric, and she exhibits expressive aphasia, struggling to articulate words or comprehend verbal instructions. Pupillary examination reveals anisocoria, with the right pupil dilated and sluggish in response to light, suggesting possible increased intracranial pressure.

The patient's vital signs are concerning, with persistent hypertension at 210/120 mmHg, tachycardia with an irregular rhythm indicative of poorly controlled atrial fibrillation, and oxygen saturation remaining critically low at 85% despite supplemental oxygen via nasal cannula. Auscultation of the lungs reveals basal crackles bilaterally, suggestive of fluid overload or aspiration. Given the history of atrial fibrillation and the current presentation, there is a high index of suspicion for a cardioembolic stroke, warranting urgent neuroimaging to confirm the diagnosis and assess the extent of cerebral involvement.

Laboratory results are pending, but initial bedside glucose testing shows a markedly elevated level of 340 mg/dL, indicating inadequate glycemic control, which may exacerbate the risk of further neurological injury. The clinical team is faced with the challenge of managing the patient's critical hemodynamics, optimizing cerebral perfusion while mitigating the risk of hemorrhagic transformation, and preventing further complications such as aspiration pneumonia due to compromised airway protection. These findings necessitate immediate multidisciplinary intervention to stabilize the patient and initiate appropriate stroke management protocols.

Section 2

New Diagnostic Results:

As the clinical team swiftly initiates a stroke protocol, the patient is transported for an emergent CT scan of the head. The imaging reveals a large left middle cerebral artery (MCA) thrombotic occlusion with significant areas of ischemia and early signs of cerebral edema. There is no evidence of hemorrhagic transformation at this point, but the risk remains high given her severely elevated blood pressure and the potential for reperfusion injury. Further imaging with CT angiography shows that the thrombus extends into the internal carotid artery, complicating potential interventional options such as thrombectomy.

Concurrently, laboratory results return, revealing a critically elevated INR of 4.5, which is concerning for an increased risk of bleeding. Her elevated INR is likely a result of anticoagulation for atrial fibrillation, which in the context of her thrombotic stroke, presents a significant therapeutic dilemma. Additionally, her creatinine level is elevated at 2.1 mg/dL, indicating possible acute kidney injury, which complicates the use of contrast in imaging and limits certain treatment modalities. The complete blood count indicates mild leukocytosis, possibly suggestive of an underlying infection or inflammatory response.

The clinical team must now weigh the risks and benefits of thrombolytic therapy given the elevated INR, potential for hemorrhage, and the pressing need to restore cerebral perfusion. Simultaneously, they must address the acute renal impairment, which could be exacerbated by ongoing hypertension and potential sepsis. In light of these findings, a multidisciplinary strategy involving neurology, nephrology, cardiology, and critical care is crucial to optimize the patient's management and mitigate the risk of further complications. The team faces a complex decision-making process, prioritizing interventions to stabilize the patient's hemodynamics and protect against secondary brain injury.

Section 3

As the clinical team deliberates on the best course of action, the patient experiences a sudden change in status, marked by a rapid decline in neurological function. Her Glasgow Coma Scale (GCS) score drops from 12 to 8, indicating a significant deterioration in her level of consciousness. Neurological assessment reveals new onset right-sided hemiplegia and aphasia, suggesting worsening cerebral ischemia or potential herniation due to increasing cerebral edema. Vital signs show a blood pressure of 210/110 mmHg, heart rate of 120 bpm, respiratory rate of 24 breaths per minute, and an oxygen saturation of 90% on room air, prompting immediate concern for respiratory compromise and further cerebral insult.

In response, the team urgently reevaluates the treatment strategy, considering the critical need to manage her elevated blood pressure while balancing the risk of exacerbating cerebral edema. The decision is made to initiate intravenous labetalol, titrating carefully to lower her blood pressure without jeopardizing cerebral perfusion. Concurrently, due to the worsening renal function with a rising creatinine level now at 2.5 mg/dL, nephrology is consulted to assess the risk of further renal compromise and to recommend potential renal-protective strategies.

The deterioration in the patient's condition necessitates a swift interdisciplinary approach. Neurology advises against the use of tissue plasminogen activator (tPA) due to the elevated INR and heightened risk of hemorrhage, while interventional radiology remains on standby should the patient's status allow for potential thrombectomy. The critical care team focuses on stabilizing the patient's hemodynamics and airway, preparing for potential intubation given her declining respiratory status. The complexity of the case underscores the need for continuous monitoring and dynamic decision-making to prevent further complications such as herniation, hemorrhagic transformation, or multi-organ failure.

Section 4

As the medical team implements the management plan, the patient is closely monitored in the intensive care unit. Over the next several hours, her response to intravenous labetalol shows a gradual reduction in blood pressure, now stabilizing around 180/95 mmHg. However, her neurological status remains precarious. A new computed tomography (CT) scan of the head is urgently performed, revealing substantial cerebral edema with signs of midline shift, raising concern for impending herniation. Additionally, there is evidence of a larger area of infarction than initially suspected, encompassing the left middle cerebral artery territory.

Concurrently, laboratory results indicate further deterioration in renal function, with a creatinine level now at 3.0 mg/dL and a blood urea nitrogen (BUN) of 40 mg/dL, suggesting acute kidney injury possibly secondary to sustained hypertension and reduced perfusion. The nephrology team recommends cautious fluid management and the potential initiation of renal replacement therapy if the trend continues. Despite the hemodynamic adjustments, the patient’s oxygen saturation drops to 85% on room air, necessitating supplemental oxygen and prompting the critical care team to prepare for probable intubation.

These developments highlight the growing complexity of the patient's condition, demanding an integrated and nuanced approach. The team must weigh the risks of further interventions against the potential for worsening cerebral and systemic complications. The interdisciplinary collaboration is vital as each specialty provides insights to mitigate the risk of brain herniation, control the hypertensive crisis, and manage the burgeoning renal failure. This precarious balance underscores the need for continuous re-evaluation and prompt adjustment of therapeutic strategies to navigate the potential for rapid and severe decompensation.

Section 5

As the critical care team prepares for intubation, the patient's neurological status deteriorates further. She becomes increasingly somnolent, with a Glasgow Coma Scale (GCS) score dropping from 12 to 8, indicating a significant decline in her level of consciousness. Her pupils are unequal, with the left pupil now 5 mm and sluggishly reactive, suggesting increased intracranial pressure. The urgency for neurosurgical intervention becomes apparent as her respiratory pattern shifts to irregular Cheyne-Stokes breathing, a forewarning of impending brainstem involvement due to the midline shift.

Given the precarious neurological signs and the CT findings of significant edema and midline shift, the neurosurgery team is consulted for potential decompressive craniectomy to alleviate pressure and prevent further herniation. Meanwhile, the intensivist manages the patient's airway with rapid-sequence intubation to secure ventilation and ensure adequate oxygenation. The team administers mannitol and hypertonic saline in an attempt to reduce cerebral edema, while continuous EEG monitoring is initiated to detect any subclinical seizure activity that might contribute to neurological deterioration.

Despite these aggressive measures, new complications arise as the patient develops metabolic acidosis, with an arterial blood gas (ABG) revealing a pH of 7.28, a bicarbonate level of 15 mEq/L, and a PaCO2 of 34 mmHg. The metabolic derangement adds another layer of complexity to her case, likely exacerbated by acute kidney injury and potential lactic acidosis from systemic hypoperfusion. The nephrologist recommends initiating dialysis to address the acidosis and manage fluid overload, while the critical care team adjusts the ventilation settings to optimize oxygenation and acid-base balance. This intricate web of complications necessitates seamless communication and swift decision-making to stabilize the patient and prevent further decline.