A patient with an ischemic stroke in the left middle cerebral artery territory is being considered for tissue plasminogen activator (tPA) administration. Which nursing action is most critical prior to the administration of tPA?

C) Confirm the time of symptom onset

A) Assess the patient's blood pressure

B) Verify the patient's allergy history

C) Confirm the time of symptom onset

D) Review the patient's medication list for anticoagulants

A patient has received tissue plasminogen activator (tPA) for an ischemic stroke and later developed hemorrhagic transformation. What is the nurse's priority intervention in managing this complication?

B) Initiate hyperosmolar therapy to manage cerebral edema

A) Administer aspirin to prevent further clot formation

B) Initiate hyperosmolar therapy to manage cerebral edema

C) Increase IV fluids to maintain blood pressure

D) Prepare the patient for immediate surgical intervention

A patient who received tissue plasminogen activator (tPA) for acute ischemic stroke is now presenting with a sudden severe headache, lethargy, and increased blood pressure. A CT scan confirms a hemorrhagic transformation. What is the nurse's priority action in managing this complication?

C) Initiate hyperosmolar therapy with mannitol to reduce cerebral edema.

A) Administer anticoagulants to prevent further clot formation.

B) Prepare the patient for immediate neurosurgical intervention.

C) Initiate hyperosmolar therapy with mannitol to reduce cerebral edema.

D) Increase the patient's fluid intake to maintain adequate hydration.

A patient with a recent history of hemorrhagic transformation is receiving hyperosmolar therapy with mannitol and begins to exhibit episodes of agitation and confusion. Considering the clinical data and potential complications, what should be the nurse's priority action?

B) Assess the patient's electrolyte levels and correct any imbalances.

A) Administer a sedative to manage the patient's agitation and confusion.

B) Assess the patient's electrolyte levels and correct any imbalances.

C) Increase the rate of oxygen delivery to improve oxygenation.

D) Notify the healthcare provider to discuss potential changes in the patient's medication regimen.

A patient receiving hyperosmolar therapy with mannitol for elevated intracranial pressure begins to show signs of agitation and confusion. Considering the patient's laboratory results and ongoing treatment, what is the nurse's priority intervention?

C) Assess serum electrolyte levels and notify the healthcare provider

A) Increase the rate of mannitol infusion to enhance diuresis

B) Administer an anxiolytic to manage agitation

C) Assess serum electrolyte levels and notify the healthcare provider

D) Elevate the head of the bed to 30 degrees to reduce intracranial pressure

A patient with increased intracranial pressure is exhibiting irregular respiratory patterns and has been placed on a ventilator. Her sodium level is 130 mEq/L, and she is receiving hypertonic saline. What is the nurse's priority action in managing this patient?

B) Perform frequent neurological assessments to detect changes in patient status.

A) Monitor for signs of fluid overload and pulmonary edema.

B) Perform frequent neurological assessments to detect changes in patient status.

C) Adjust the ventilator settings to hyperventilate the patient and reduce CO2 levels.

D) Administer additional mannitol to further decrease intracranial pressure.

A patient with increased intracranial pressure and hyponatremia is showing signs of neurological deterioration. Which nursing intervention is most appropriate to prioritize in this scenario to prevent further neurological damage?

B) Increase the patient's head of bed to 45 degrees to promote venous drainage.

A) Administer a bolus of 0.9% normal saline to rapidly correct sodium levels.

B) Increase the patient's head of bed to 45 degrees to promote venous drainage.

C) Initiate a continuous infusion of mannitol to reduce intracranial pressure.

D) Encourage oral fluid intake to address fluid imbalances and support hydration.

A patient with elevated intracranial pressure (ICP) is receiving hypertonic saline to manage cerebral edema. Which of the following nursing interventions is the most appropriate to monitor for complications associated with this treatment?

B) Assess for signs of osmotic demyelination syndrome, such as confusion and muscle weakness.

A) Monitor for signs of fluid overload, such as peripheral edema and weight gain.

B) Assess for signs of osmotic demyelination syndrome, such as confusion and muscle weakness.

C) Check urine output hourly to detect any signs of acute kidney injury.

D) Evaluate for signs of infection, such as fever and increased white blood cell count.

A patient with increased intracranial pressure (ICP) and a midline shift is scheduled for an emergent decompressive craniectomy. The nurse notes a decrease in the Glasgow Coma Scale (GCS) score from 10 to 8 and unequal pupils. What is the priority nursing intervention before the surgical team arrives?

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

A) Administer mannitol as prescribed to reduce ICP.

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

C) Perform passive range of motion exercises to prevent contractures.

D) Prepare the patient for immediate transport to the operating room.

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, causing cell injury and death.

• Secondary mechanism: Hemorrhagic stroke results from a ruptured blood vessel, leading to bleeding in or around the brain, increasing intracranial pressure and damaging brain cells.

• Key complication: Both types can result in neurological deficits, such as weakness, speech difficulties, and cognitive impairments, depending on the brain area affected.

Patient Profile

Demographics:

67-year-old female, retired school teacher

History:

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

• Current medications: Lisinopril, Metformin, Aspirin

• Allergies: Penicillin

Current Presentation:

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

• Key symptoms: Slurred speech, facial droop on the right side, right arm and leg weakness, headache

• Vital signs: Blood pressure 190/105 mmHg, heart rate 98 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F, oxygen saturation 92% on room air

Section 1

New Diagnostic Results:

Following the initial assessment, the patient was swiftly transported to the imaging department for a CT scan of the head to differentiate between an ischemic and hemorrhagic stroke. The CT scan results revealed an ischemic stroke in the left middle cerebral artery territory, explaining the right-sided weakness and speech difficulties. An MRI was subsequently ordered to assess the extent of cerebral infarction and confirm the absence of hemorrhagic transformation, which could complicate treatment options. The MRI findings corroborated the CT results, showing significant ischemia in the left hemisphere with no evidence of bleeding.

Laboratory tests were also conducted to evaluate the patient's overall health and to rule out any underlying conditions that could affect treatment. Her blood glucose level was slightly elevated at 180 mg/dL, consistent with her history of Type 2 Diabetes Mellitus, necessitating careful management to prevent further neurological damage. Additionally, her lipid profile showed elevated LDL cholesterol at 160 mg/dL, indicating a need for more aggressive lipid-lowering therapy to reduce the risk of future cerebrovascular events. The patient's renal function tests were within normal limits, and coagulation studies showed no abnormalities, allowing for the consideration of thrombolytic therapy.

With the diagnostic results in hand, the healthcare team discussed the risks and benefits of administering tissue plasminogen activator (tPA) given the relatively recent onset of symptoms and the absence of contraindications. The decision was made to proceed with tPA administration to potentially reverse the effects of the stroke. Close monitoring was initiated to observe the patient's response to the intervention and to promptly address any emerging complications, such as bleeding or worsening neurological status. The team remained vigilant, knowing that the window for effective intervention was narrow and crucial for the patient's recovery.

Section 2

As the medical team closely monitored the patient following the administration of tissue plasminogen activator (tPA), they observed her vital signs and neurological status for any signs of improvement or potential complications. Approximately two hours post-administration, the patient displayed subtle improvements in motor function, with a slight increase in strength in her right arm and leg, suggesting a positive response to the thrombolytic therapy. Her speech, however, remained slurred, and she continued to struggle with word-finding difficulties. Vital signs were stable, with a blood pressure of 140/85 mmHg, heart rate of 78 beats per minute, respiratory rate of 18 breaths per minute, and oxygen saturation at 94% on room air. The team noted the need for ongoing monitoring and supportive care to maximize neurological recovery.

However, later that evening, the nursing staff observed a change in the patient's status. She began to experience a sudden onset of severe headache and became increasingly lethargic, raising concerns about a possible complication. Her blood pressure had risen to 162/95 mmHg, and her heart rate increased to 92 beats per minute. A repeat neurological assessment revealed decreased responsiveness and worsening right-sided weakness, prompting an immediate consultation with the on-call neurologist. The team suspected a hemorrhagic transformation despite earlier imaging results showing no initial bleeding, necessitating urgent repeat imaging to confirm the diagnosis and guide further management.

The repeat CT scan revealed a small area of bleeding within the ischemic region, confirming the complication of hemorrhagic transformation. This unexpected development required the immediate cessation of any further anticoagulant or antiplatelet therapy and the initiation of measures to control intracranial pressure and stabilize the patient. The healthcare team initiated a hyperosmolar therapy protocol, using mannitol to reduce cerebral edema, while preparing for potential neurosurgical intervention if the patient's condition continued to deteriorate. This new complication prompted a re-evaluation of the patient's overall management plan, highlighting the importance of interdisciplinary collaboration and vigilant clinical reasoning in adapting to evolving clinical scenarios.

Section 3

Following the initiation of hyperosmolar therapy with mannitol, the healthcare team observed the patient closely for signs of improvement or deterioration. Over the next several hours, her intracranial pressure began to stabilize, evidenced by a gradual decrease in her lethargy and a slight improvement in her level of consciousness. However, her neurological status remained compromised, with persistent right-sided weakness and continued difficulty with speech. Vital signs showed a blood pressure of 150/90 mmHg, heart rate of 88 beats per minute, respiratory rate of 20 breaths per minute, and oxygen saturation at 95% with supplemental oxygen via nasal cannula. Although the stabilization was a positive sign, the team remained vigilant for further complications.

In light of the patient's hemorrhagic transformation, the medical team ordered a series of laboratory tests to guide further management. Results indicated a slight elevation in her INR at 1.3, reflecting an increased risk of bleeding, while her platelet count was within normal limits. Electrolytes showed a mild hyponatremia, with sodium at 132 mEq/L, likely secondary to the mannitol administration, necessitating careful fluid and electrolyte management to prevent further complications. The team also noted a mild increase in her serum creatinine, suggesting a need for renal monitoring due to the osmotic diuresis effect of mannitol.

As the night progressed, the patient began to exhibit episodes of agitation and confusion, suggesting potential delirium or further neurological compromise. The healthcare team promptly assessed her for potential causes, including metabolic imbalances, medication effects, or worsening intracranial pressure. These new developments underscored the need for continuous interdisciplinary collaboration and adaptation of the management plan, emphasizing the importance of timely interventions and reassessment to optimize patient outcomes. The evolving clinical picture required not only a focus on immediate stabilization but also a long-term plan to address potential rehabilitation and recovery challenges.

Section 4

As the early morning light filtered into the room, the healthcare team observed a change in the patient's status that required immediate attention. Her respiratory pattern had become irregular, with episodes of shallow breathing followed by periods of tachypnea. This alteration in her breathing pattern raised concerns about further neurological deterioration, possibly indicating worsening intracranial pressure or brainstem involvement. A repeat CT scan was ordered to assess for any new or expanding lesions. Meanwhile, her blood pressure remained elevated at 160/95 mmHg, and her heart rate increased slightly to 92 beats per minute, suggesting a possible sympathetic response to increased intracranial pressure or discomfort.

The CT scan results revealed a slight expansion of the hemorrhagic area, with evidence of midline shift, indicating increased brain edema. This finding necessitated a reassessment of her current treatment regimen, including the potential need to adjust mannitol dosage or consider additional measures to control intracranial pressure, such as hyperventilation or surgical intervention. The possibility of surgical decompression was discussed with the neurosurgery team, weighing the risks and benefits given her current instability. In addition, her sodium level had further decreased to 130 mEq/L, prompting the team to carefully recalibrate her fluid management plan to address the hyponatremia while avoiding exacerbation of cerebral edema.

In response to these changes, the interdisciplinary team convened to adapt the management plan, with a focus on optimizing cerebral perfusion and mitigating further neurological damage. The patient was placed on a ventilator to stabilize her respiratory status, aiming to maintain normocapnia and prevent additional fluctuations in intracranial pressure. The team also initiated a continuous infusion of hypertonic saline to gradually correct her sodium imbalance while monitoring for any signs of osmotic demyelination syndrome. These interventions were part of a comprehensive strategy to address the immediate threats to her neurological integrity while laying the groundwork for potential recovery and rehabilitation efforts once her condition stabilized.

Section 5

As the day progressed, the healthcare team noted a change in the patient's neurological status, marked by a decrease in her Glasgow Coma Scale (GCS) score from 10 to 8, indicating a decline in her level of consciousness. Her pupils were unequal, with the left pupil reacting sluggishly to light, suggesting possible worsening of brainstem compression or herniation risk due to the midline shift observed on the CT scan. Her blood pressure had climbed further to 175/100 mmHg, and her heart rate had increased to 98 beats per minute, reinforcing concerns about sympathetic overdrive in response to elevated intracranial pressure. These changes prompted urgent communication with the neurosurgery team to reevaluate the need for surgical intervention.

In parallel, the laboratory results indicated a rising white blood cell count of 15,000/mm³, raising suspicion for an infectious process, possibly aspiration pneumonia, given her recent history of irregular respiratory patterns and her current ventilator dependency. The team initiated empirical antibiotic therapy while awaiting culture results to tailor treatment more precisely. Her sodium level rose to 132 mEq/L following the hypertonic saline infusion, showing a positive trend towards correction, but the team remained vigilant for any early signs of osmotic demyelination syndrome, which could complicate her recovery.

The neurosurgery team, after reviewing the patient's rapid neurological decline and imaging findings, decided to proceed with an emergent decompressive craniectomy to relieve intracranial pressure and prevent further herniation. This decision was communicated to the patient's family, who were counseled about the risks and benefits, including the potential for improved neurological outcomes versus the inherent surgical risks. The patient's care plan was adjusted to prepare for surgery, including optimizing her hemodynamic stability and ensuring adequate sedation and analgesia, as the team worked collaboratively to address these acute challenges and support her through this critical phase of her clinical journey.