A patient with an acute ischemic stroke in the left middle cerebral artery territory is being treated with tissue plasminogen activator (tPA). Which assessment finding should the nurse prioritize to report immediately to the healthcare provider?

B) New onset of severe headache

A) Blood glucose level of 230 mg/dL

B) New onset of severe headache

D) Blood pressure of 150/90 mmHg

A patient with an acute ischemic stroke in the left middle cerebral artery territory has been administered tissue plasminogen activator (tPA). Which nursing action is most critical to perform immediately following the administration of tPA?

B) Assess the patient's neurological status every 15 minutes.

A) Monitor the patient's blood glucose levels hourly.

B) Assess the patient's neurological status every 15 minutes.

C) Obtain a lipid panel to evaluate hyperlipidemia control.

D) Initiate dietary modifications to manage hyperglycemia.

A patient who received tissue plasminogen activator (tPA) for an ischemic stroke shows a decrease in the Glasgow Coma Scale (GCS) score and a CT scan reveals a small hemorrhagic transformation. What is the most appropriate nursing action to prioritize at this time?

B) Elevate the head of the bed to 30 degrees to manage intracranial pressure.

A) Administer a bolus of intravenous fluids to improve cerebral perfusion.

B) Elevate the head of the bed to 30 degrees to manage intracranial pressure.

C) Increase the rate of anticoagulation therapy to prevent further ischemic events.

D) Initiate seizure precautions as the first intervention.

A patient in a stroke unit who received tissue plasminogen activator (tPA) therapy is now showing signs of neurological decline with a decreased Glasgow Coma Scale (GCS) score and a repeat CT scan indicating a small hemorrhagic transformation. What is the nurse's priority action in response to these findings?

B) Elevate the head of the bed and monitor vital signs closely to manage increased intracranial pressure.

A) Administer an additional dose of thrombolytic therapy to improve cerebral perfusion.

B) Elevate the head of the bed and monitor vital signs closely to manage increased intracranial pressure.

C) Increase the intravenous fluid rate to ensure adequate hydration and cerebral perfusion.

D) Arrange for urgent surgical consultation for decompressive craniectomy.

A patient with a declining GCS score and signs of increased intracranial pressure is being managed in the ICU. Her lab results show metabolic acidosis and hyponatremia. Which nursing intervention is most critical to prioritize in this situation?

C) Administer hypertonic saline to address hyponatremia and cerebral edema

A) Increase the rate of IV fluids to improve perfusion

B) Position the patient in Trendelenburg to improve cerebral circulation

C) Administer hypertonic saline to address hyponatremia and cerebral edema

D) Increase sedation to prevent further neurological decline

A patient with increased intracranial pressure is showing signs consistent with Cushing's triad and worsening metabolic acidosis. Which nursing intervention should be prioritized to address these findings and stabilize the patient?

A) Administer a hypertonic saline infusion to address hyponatremia and cerebral edema.

B) Increase the rate of the patient's intravenous fluids to manage hypotension.

C) Prepare the patient for immediate intubation to secure the airway and manage irregular respirations.

D) Administer sodium bicarbonate to correct the metabolic acidosis.

A nurse is caring for a patient with a decreased Glasgow Coma Scale (GCS) score, Cheyne-Stokes respirations, and signs of uncal herniation. The patient also presents with metabolic acidosis and hyponatremia. What is the nurse's priority intervention at this time?

C) Initiate mechanical ventilation to support the patient's respiratory function.

A) Administer additional doses of hypertonic saline to correct hyponatremia.

B) Prepare the patient for immediate decompressive craniectomy as ordered by the physician.

C) Initiate mechanical ventilation to support the patient's respiratory function.

D) Reassess the patient's neurological status every 15 minutes.

A patient with a decreased Glasgow Coma Scale (GCS) score, Cheyne-Stokes respirations, and uncal herniation is being evaluated by the healthcare team. What is the priority nursing intervention to prevent further neurological deterioration?

D) Initiate mechanical ventilation to manage respiratory insufficiency.

A) Administer mannitol to reduce intracranial pressure.

B) Increase the rate of hypertonic saline infusion to correct hyponatremia.

C) Prepare the patient for an immediate decompressive craniectomy.

D) Initiate mechanical ventilation to manage respiratory insufficiency.

A patient in the ICU with suspected increased intracranial pressure exhibits bradycardia, hypotension, and unequal pupils. Which nursing intervention should be prioritized to address these clinical findings?

D) Prepare for emergent decompressive craniectomy to relieve pressure.

A) Administer a hypertonic saline solution to address hyponatremia.

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

C) Initiate mechanical ventilation to ensure adequate oxygenation.

D) Prepare for emergent decompressive craniectomy to relieve pressure.

A patient in the ICU is undergoing mechanical ventilation and shows signs of Cushing's triad. The healthcare team is planning an emergent decompressive craniectomy. As the nurse, what is your priority intervention to optimize the patient's pre-surgical condition?

C) Initiate vasopressor support as ordered.

A) Administer a fluid bolus to correct hypotension.

B) Prepare equipment for endotracheal intubation.

C) Initiate vasopressor support as ordered.

D) Apply warming blankets to prevent hypothermia.

stroke - Nursing Case Study

Pathophysiology

• Primary mechanism: Ischemic stroke occurs when a blood clot obstructs a cerebral artery, leading to reduced blood flow and oxygen deprivation in brain tissue. This results in neuronal injury and death, primarily due to energy failure and excitotoxicity.

• Secondary mechanism: Hemorrhagic stroke arises from the rupture of a blood vessel in the brain, causing bleeding and increased intracranial pressure. This disrupts normal brain function and can lead to further neuronal damage from mechanical pressure and toxic blood components.

• Key complication: Both types of stroke can lead to significant neurological deficits, such as paralysis or speech difficulties, due to the loss of brain tissue function depending on the affected area. Prompt recognition and treatment are crucial to minimize brain damage and improve outcomes.

Patient Profile

Demographics:

67-year-old female, retired school teacher

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Hyperlipidemia

• Current medications: Lisinopril, Metformin, Atorvastatin, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden weakness on the right side of the body

• Key symptoms: Slurred speech, facial droop on the right side, difficulty in coordination, mild headache

• Vital signs: Blood pressure 180/95 mmHg, heart rate 102 bpm, respiratory rate 20 breaths per minute, temperature 37.2°C, oxygen saturation 92% on room air

Section 1

New Diagnostic Results

Following the initial assessment, the patient was promptly transferred to the hospital's stroke unit for further evaluation and management. A CT scan of the brain was performed, revealing evidence of an acute ischemic stroke in the left middle cerebral artery territory. This finding correlates with the patient's right-sided weakness and facial droop. Laboratory tests showed that the patient's blood glucose level was elevated at 230 mg/dL, likely exacerbating the ischemic process by promoting a pro-inflammatory state and increasing blood viscosity. Her lipid panel further showed elevated LDL levels at 150 mg/dL, despite ongoing atorvastatin therapy, indicating suboptimal control of her hyperlipidemia, which may have contributed to the development of atherosclerosis and subsequent cerebrovascular event.

Given these results, the healthcare team initiated treatment with tissue plasminogen activator (tPA) to dissolve the clot and restore cerebral perfusion, as the patient presented within the therapeutic window. Additionally, her antihypertensive and diabetic medications were reviewed and optimized to prevent further vascular complications. The multidisciplinary team, including a neurologist, endocrinologist, and a dietitian, collaborated to adjust her treatment plan, aiming to achieve better management of her chronic conditions and reduce the risk of future strokes.

These diagnostic insights highlight the importance of comprehensive management of underlying risk factors in stroke patients. The findings necessitate close monitoring of the patient's neurological status and vital signs, especially during the critical period following thrombolysis, to detect any signs of hemorrhagic transformation or other complications. The integration of clinical reasoning in interpreting these results and adjusting the treatment plan is essential in guiding the next steps in the patient's care journey, focusing on stabilizing her current condition and preventing recurrent strokes.

Section 2

As the patient settled into the stroke unit, the initial response to the tissue plasminogen activator (tPA) appeared promising, with slight improvement in her right-sided weakness. However, within 24 hours, the patient began to exhibit new complications. Her neurological status showed subtle but concerning changes; she became increasingly lethargic and less responsive to verbal stimuli. A repeat neurological examination revealed a decrease in the Glasgow Coma Scale (GCS) score from 14 to 11, indicating a decline in her level of consciousness. The healthcare team promptly arranged for a repeat CT scan of the brain to assess for potential hemorrhagic transformation or other complications such as cerebral edema.

The repeat CT scan revealed the development of a small hemorrhagic transformation at the site of the initial ischemic stroke, a recognized complication following thrombolytic therapy. Vital signs indicated a slight increase in blood pressure to 160/95 mmHg, which may have contributed to the bleeding risk. The patient's blood glucose remained elevated at 200 mg/dL, despite insulin therapy, suggesting a need for more aggressive glycemic control. These findings prompted the team to adjust her anticoagulation therapy and initiate measures to manage the increased intracranial pressure, including head elevation and cautious fluid management.

This new development required the healthcare team to reassess and modify the patient's treatment strategy. The neurologist and intensivist collaborated to balance the risk of further hemorrhagic complications while maintaining cerebral perfusion. The team emphasized the importance of continuous monitoring for any neurological deterioration or further bleeding. The patient's family was informed about the change in her condition and involved in discussions regarding the plan of care, highlighting the complex interplay between therapeutic interventions and their potential risks. This situation underscores the need for vigilant clinical reasoning and prompt intervention to navigate the challenges of stroke management.

Section 3

Following the adjustments to her treatment plan, the healthcare team observed the patient's condition closely over the next 12 hours. Despite the interventions to manage intracranial pressure and modify anticoagulation therapy, the patient began to develop new complications. Her neurological status continued to decline, with her GCS score dropping further to 9, characterized by a reduction in her verbal response and eye-opening. The patient also began exhibiting signs of increased intracranial pressure, such as bradycardia with a heart rate decreasing to 58 beats per minute and irregular respirations, indicative of Cushing's triad.

Concurrent with these developments, the patient’s laboratory results showed worsening metabolic acidosis, with an arterial blood gas (ABG) revealing a pH of 7.31, PaCO2 of 50 mmHg, and HCO3- of 22 mEq/L. Her serum sodium levels were slightly hyponatremic at 133 mEq/L, which, along with her elevated blood pressure now at 165/100 mmHg, suggested worsening cerebral edema. The team recognized the need for aggressive management to prevent further deterioration. They initiated hypertonic saline therapy to address the hyponatremia and potential cerebral edema, while carefully titrating medications to manage her blood pressure without compromising cerebral perfusion.

The family was updated about the patient's critical status and the new complications. They were informed of the need for possible escalation of care, including the potential for mechanical ventilation due to her declining respiratory function. The situation emphasized the importance of ongoing clinical reasoning to adjust the treatment plan in response to the dynamic changes in the patient's condition. The healthcare team prepared for the next steps in her care, which would require close monitoring of her neurological status and vital signs to swiftly address any further complications that might arise.

Section 4

As the healthcare team continued to monitor the patient closely, they noted a change in her respiratory pattern, characterized by increasing periods of apnea and Cheyne-Stokes respirations. Her Glasgow Coma Scale (GCS) score further decreased to 7, indicating a significant decline in her level of consciousness. This was compounded by a further drop in her heart rate to 52 beats per minute, despite ongoing treatment for intracranial pressure and hypertonic saline therapy. The team recognized these signs as potential indicators of further brainstem involvement and were concerned about the progression towards brain herniation.

In response to these alarming changes, an urgent repeat CT scan of the brain was ordered. The imaging revealed increased midline shift and signs of uncal herniation, confirming the team's suspicions of worsening cerebral edema and increased intracranial pressure. Blood tests showed a further decline in her serum sodium levels to 130 mEq/L, despite hypertonic saline therapy, and a continued metabolic acidosis with a pH of 7.28. These findings pointed towards a systemic decompensation that required immediate intervention.

The healthcare team quickly convened to reassess the treatment strategy, considering the possibility of surgical intervention such as decompressive craniectomy to relieve pressure on the brain. Simultaneously, they prepared for the initiation of mechanical ventilation to support her deteriorating respiratory function. The family was informed of these developments, and the potential need for life-saving surgical intervention was discussed. The team emphasized the critical nature of the situation, underscoring the importance of ongoing assessment and rapid response to changes in the patient's status to prevent irreversible damage.

Section 5

The healthcare team proceeded with the initiation of mechanical ventilation, aiming to stabilize the patient's respiratory status and manage her deteriorating condition. Despite these efforts, the patient's condition continued to decline. Her blood pressure, previously stable, began to drop, with readings now at 90/60 mmHg, indicating the onset of hypotension. Given her bradycardia and hypotension, the team suspected the development of Cushing's triad, a classic sign of increased intracranial pressure.

Further laboratory tests revealed a worsening electrolyte imbalance, with serum sodium levels dropping to 128 mEq/L and a rising lactate level of 4.5 mmol/L, suggesting ongoing tissue hypoperfusion and possible lactic acidosis. The patient's neurological status remained critical, with a GCS score persisting at 6, and her pupils became unequal, with one becoming fixed and dilated, indicating potential further brainstem compression and injury.

In light of these findings, the team decided to proceed with an emergent decompressive craniectomy to relieve the intracranial pressure. The surgical team was rapidly assembled, and preparations were made for the operating room. Concurrently, vasopressor support was initiated to stabilize her blood pressure and improve cerebral perfusion. The family was updated on the urgency of the situation and gave consent for the surgery, understanding the high-risk nature but potential life-saving benefit of the intervention. As the patient was transported to the operating room, the healthcare team remained vigilant, ready to address any further complications that might arise.