A patient with an ischemic stroke in the left middle cerebral artery territory is receiving thrombolytic therapy and intravenous labetalol for blood pressure management. Several hours into treatment, the patient becomes increasingly drowsy, less responsive, and exhibits a drop in oxygen saturation to 88% on room air. What is the nurse's priority intervention?

A) Administer supplemental oxygen and reassess the patient's respiratory status.

B) Increase the rate of the labetalol drip to further manage blood pressure.

C) Prepare the patient for immediate intubation and mechanical ventilation.

D) Request an immediate neurology consult for further evaluation.

A patient with a left middle cerebral artery ischemic stroke is receiving intravenous tPA and labetalol. Several hours into treatment, the patient exhibits increased drowsiness and a decrease in responsiveness. A repeat CT scan is ordered. Which of the following nursing assessments is most critical at this time?

B) Checking pupil size and reactivity to assess for neurological changes

A) Monitoring urine output to assess for renal function

B) Checking pupil size and reactivity to assess for neurological changes

C) Measuring blood glucose levels to monitor for hyperglycemia

D) Observing for signs of bleeding from intravenous sites

A patient with a recent ischemic stroke in the left middle cerebral artery has developed a small hemorrhagic transformation. The patient also shows signs of respiratory acidosis with hypoxemia and is on non-invasive positive pressure ventilation (NIPPV). Which nursing intervention is most critical to prioritize at this time?

B) Frequently assess the patient's neurological status and Glasgow Coma Scale (GCS) score.

A) Continuously monitor the patient's blood glucose levels and administer insulin per sliding scale.

B) Frequently assess the patient's neurological status and Glasgow Coma Scale (GCS) score.

C) Regularly check the patient's pupils for size and reactivity.

D) Monitor the effectiveness of NIPPV and adjust settings as needed.

A patient with a history of ischemic stroke has developed a hemorrhagic transformation and is now experiencing respiratory acidosis with hypoxemia. Which of the following nursing interventions should be prioritized to address the patient's current respiratory status?

B) Initiate non-invasive positive pressure ventilation (NIPPV) to improve oxygenation.

A) Administer intravenous diuretics to reduce cerebral edema.

B) Initiate non-invasive positive pressure ventilation (NIPPV) to improve oxygenation.

C) Increase the frequency of neurological assessments to monitor for changes.

D) Implement a fluid restriction to prevent fluid overload.

A patient with acute respiratory failure and declining neurological status shows a Glasgow Coma Scale score of 9, right-sided weakness, and sluggish pupillary reaction on the left. The patient's arterial blood gas indicates respiratory acidosis. Which nursing intervention is the most appropriate to prioritize at this time?

B) Prepare for immediate intubation and mechanical ventilation

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

B) Prepare for immediate intubation and mechanical ventilation

C) Administer antihypertensive medications to lower blood pressure rapidly

D) Increase the frequency of neurological assessments to monitor for changes

A patient with declining neurological status and inadequate respiratory function is placed on mechanical ventilation. The arterial blood gas analysis indicates respiratory acidosis with hypoxemia. Given the patient's current clinical status, which of the following interventions should the nurse prioritize to address the patient's compromised condition?

A) Increase the oxygen concentration on the ventilator to improve oxygenation.

B) Administer a bolus of mannitol to decrease intracranial pressure.

C) Prepare the patient for an immediate CT scan to assess for cerebral hemorrhage.

D) Titrate antihypertensive medication to maintain cerebral perfusion.

A patient on mechanical ventilation is experiencing refractory hypertension and increased intracranial pressure with cerebral edema. Which of the following nursing interventions is most appropriate to address both the hypertension and intracranial pressure effectively?

B) Administer a diuretic to reduce fluid overload and intracranial pressure.

A) Increase sedative medication to reduce blood pressure.

B) Administer a diuretic to reduce fluid overload and intracranial pressure.

C) Adjust ventilator settings to improve oxygenation and cerebral perfusion.

D) Initiate beta-blocker therapy to directly lower blood pressure.

A patient on mechanical ventilation is being treated with hypertonic saline for cerebral edema. The nurse notes a serum sodium level of 150 mEq/L. What is the most appropriate nursing intervention at this time?

B) Notify the healthcare provider to discuss possible adjustment of the hypertonic saline therapy.

A) Increase the rate of hypertonic saline infusion to reduce intracranial pressure more quickly.

B) Notify the healthcare provider to discuss possible adjustment of the hypertonic saline therapy.

C) Restrict the patient's fluid intake to prevent further increase in serum sodium levels.

D) Continue the current treatment plan and recheck serum sodium levels in 12 hours.

A patient with acute kidney injury (AKI) is experiencing decreased urine output and elevated serum creatinine levels following the administration of hypertonic saline. Which nursing intervention is most appropriate to help improve renal perfusion while monitoring the patient’s fluid balance?

B) Administer a low-dose diuretic to enhance renal perfusion.

A) Increase the rate of IV fluids to promote diuresis.

B) Administer a low-dose diuretic to enhance renal perfusion.

C) Encourage oral fluid intake to restore hydration levels.

D) Discontinue all antihypertensive medications to prevent further renal damage.

A patient with acute kidney injury (AKI) secondary to recent administration of hypertonic saline is being monitored for fluid balance and renal function. Which nursing intervention is most important to prioritize to prevent further renal compromise?

B) Monitor serum creatinine and urine output closely.

A) Encourage oral fluid intake to promote diuresis.

B) Monitor serum creatinine and urine output closely.

C) Administer nephrotoxic medications at reduced doses.

D) Increase the dose of diuretics to ensure adequate urine output.

Stroke - Nursing Case Study

Pathophysiology

• Primary mechanism: Ischemic stroke results from the obstruction of blood flow to brain tissue due to a thrombus or embolus, leading to reduced oxygen and nutrient delivery, causing cell death and neurological deficits.

• Secondary mechanism: Hemorrhagic stroke occurs when a blood vessel in the brain ruptures, leading to bleeding, increased intracranial pressure, and subsequent compression of brain structures, further impairing neurological function.

• Key complication: Both types can result in cerebral edema, causing additional pressure on brain tissues, which may worsen neurological outcomes and increase the risk of further damage if not managed promptly.

Patient Profile

Demographics:

67-year-old male, 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 walking, headache

• Vital signs: Blood pressure 180/100 mmHg, heart rate 98 bpm, respiratory rate 20 breaths per minute, temperature 98.6°F, oxygen saturation 92% on room air

Section 1

Following the initial assessment, the patient was promptly transferred to the emergency department for further evaluation and management. A CT scan of the head was performed, which revealed an ischemic stroke in the left middle cerebral artery territory. This finding was consistent with the patient's presenting symptoms of right-sided weakness and facial droop. Laboratory results indicated elevated blood glucose levels at 280 mg/dL, suggestive of suboptimal diabetes control, and a slightly elevated LDL cholesterol level at 150 mg/dL, despite ongoing atorvastatin therapy.

The patient was started on a thrombolytic therapy protocol with intravenous tPA (tissue plasminogen activator) within the allowed time window for ischemic stroke. Additionally, his blood pressure was managed with a titrated intravenous labetalol drip to gradually lower his systolic blood pressure to target levels, reducing the risk of hemorrhagic transformation. Continuous cardiac monitoring was initiated to detect any potential arrhythmias, given his age and cardiovascular risk factors.

Several hours into treatment, the patient began to exhibit increased drowsiness and a decrease in responsiveness, prompting immediate concern for potential complications. A repeat CT scan was ordered to evaluate for hemorrhagic transformation or significant cerebral edema. The nursing staff also noted a slight increase in the patient's respiratory rate and a drop in oxygen saturation to 88% on room air, indicating possible deteriorating respiratory function. These new findings necessitated a swift reassessment of the treatment plan, emphasizing the need for vigilant monitoring and possible escalation of care, including potential intubation and mechanical ventilation to support the patient's compromised neurological and respiratory status.

Section 2

The repeat CT scan revealed a small area of hemorrhagic transformation in the region of the initial ischemic stroke in the left middle cerebral artery. This finding was concerning and necessitated an immediate halt to the thrombolytic therapy. The neurology team was consulted, and they recommended close monitoring of the patient's neurological status and blood pressure management to minimize further bleeding risk. Additionally, the patient's elevated blood glucose level was addressed with a sliding scale insulin protocol to optimize glycemic control, aiming to prevent hyperglycemia-induced exacerbation of the cerebral edema.

Simultaneously, the patient's respiratory status was deteriorating. Arterial blood gas analysis showed a pH of 7.32, PaCO2 of 50 mmHg, and PaO2 of 60 mmHg, indicating respiratory acidosis with hypoxemia. The decision was made to initiate non-invasive positive pressure ventilation (NIPPV) to support the patient's breathing and improve oxygenation. This intervention aimed to alleviate the increased work of breathing and stabilize the patient's respiratory function. Over the next hour, close observation was maintained to assess the effectiveness of NIPPV and determine if intubation would be necessary.

As the team worked collaboratively, the patient's neurological status was frequently reassessed. The patient's Glasgow Coma Scale score fluctuated, reflecting intermittent periods of increased somnolence. The healthcare team emphasized the importance of regular neuro-checks, evaluating pupils for size and reactivity, and continuous monitoring of vital signs. This vigilant approach was crucial to detect any further deterioration promptly and to guide subsequent interventions. This evolving situation underscored the necessity for ongoing interdisciplinary communication and coordination to address the complex interplay of the patient's neurological and respiratory complications.

Section 3

As the patient continued under close observation, a change in status became evident. Approximately two hours after initiating non-invasive positive pressure ventilation, the patient's respiratory rate began to decrease, dropping to 10 breaths per minute, and the oxygen saturation fell to 85%. Despite the NIPPV, the patient's work of breathing had not significantly improved, and there was a notable decrease in tidal volume. In response to these developments, the healthcare team decided to initiate intubation and mechanical ventilation to ensure adequate ventilation and oxygenation. This decision was supported by the patient's arterial blood gas analysis, which showed a pH of 7.28, PaCO2 of 55 mmHg, and PaO2 of 58 mmHg, indicating worsening respiratory acidosis and hypoxemia.

Simultaneously, the patient's neurological status showed further decline. The Glasgow Coma Scale score dropped from 12 to 9, with increased difficulty in arousing the patient and a new onset of right-sided weakness. Pupillary assessment revealed a sluggish reaction to light in the left eye, suggesting possible increased intracranial pressure or further hemorrhagic transformation. Blood pressure readings were elevated, averaging 180/95 mmHg, prompting the team to adjust antihypertensive therapy to better manage cerebral perfusion and minimize the risk of additional intracranial bleeding. The interdisciplinary team, including neurology, pulmonology, and critical care specialists, convened to reevaluate the treatment plan, ensuring that all potential complications were addressed systematically.

These developments necessitated an urgent review of the patient's management plan, emphasizing the need for frequent neurological assessments, titration of ventilatory support, and careful monitoring of hemodynamic parameters. The collaborative approach and timely adjustments in therapy aimed to address the patient's deteriorating condition, highlighting the critical balance between managing respiratory compromise and preventing further neurological damage. The unfolding scenario presented new challenges and required ongoing clinical reasoning to navigate the complex interplay of the patient's evolving complications. As the team anticipated possible additional interventions, maintaining clear communication and coordination remained paramount in the patient's care trajectory.

Section 4

As the healthcare team embarked on managing the patient's evolving complications, they observed a new set of challenges within hours of initiating mechanical ventilation. The patient's blood pressure remained persistently elevated despite adjustments in antihypertensive therapy, with readings now reaching 190/100 mmHg. This prompted further investigation into possible causes of refractory hypertension, including a review of the patient's fluid status and medication regimen. Concurrently, a repeat CT scan of the head was ordered to assess for any progression of cerebral edema or hemorrhagic transformation, given the changes in the patient's neurological examination.

The CT scan revealed a slight increase in midline shift and subtle signs of increased cerebral edema, but no new hemorrhagic areas. In response to these findings, the clinical team decided to implement hypertonic saline therapy to manage the cerebral swelling, aiming to reduce intracranial pressure while closely monitoring electrolyte levels to prevent complications such as hypernatremia. Laboratory results showed a serum sodium level of 150 mEq/L, necessitating cautious titration of the hypertonic solution.

While addressing the neurological issues, the team also focused on optimizing respiratory function. A follow-up arterial blood gas analysis showed some improvement, with a pH of 7.32, PaCO2 of 50 mmHg, and PaO2 of 65 mmHg. This indicated a partial correction of the respiratory acidosis and hypoxemia, although the patient's ventilatory settings required further adjustment to maintain adequate gas exchange. The interdisciplinary team continued to prioritize frequent assessments and dynamic alterations to the treatment plan, emphasizing the need for balance between controlling intracranial pressure and ensuring effective ventilation. As the patient's condition remained precarious, the team prepared for potential escalation of care, maintaining vigilant monitoring and open communication to navigate the complexities of the situation.

Section 5

As the clinical team continued to manage the patient's complex condition, a new complication emerged. Over the next few hours, the patient developed signs of acute kidney injury, as evidenced by a sharp rise in serum creatinine to 2.3 mg/dL from a baseline of 1.0 mg/dL, and a decrease in urine output to less than 20 mL/hr. This development raised concerns about the patient's fluid balance, particularly in light of the recent administration of hypertonic saline. The nephrology team was consulted to assist in evaluating the potential causes of the renal impairment, considering factors such as the patient's current medications, hemodynamic status, and the possibility of contrast-induced nephropathy from recent imaging studies.

In response to these findings, the healthcare team made several adjustments to the treatment plan. They decided to temporarily hold nephrotoxic medications and carefully monitor the patient's fluid intake and output, as well as electrolyte levels, to prevent further renal compromise. Additionally, they initiated a low-dose diuretic therapy to support renal perfusion and enhance diuresis, while ensuring close monitoring of blood pressure and volume status. The team also reviewed the patient's antihypertensive regimen, considering potential adjustments to better control the refractory hypertension without exacerbating the renal injury.

As the team implemented these interventions, they noted a slight improvement in the patient's neurological status, with subtle increases in responsiveness and motor function. However, the ongoing challenges highlighted the need for continuous reassessment and collaboration among the multidisciplinary team. The focus remained on balancing the management of cerebral edema, hypertension, and renal function, while preparing for any further complications that might arise. The team remained committed to optimizing patient outcomes through vigilant monitoring and timely interventions, emphasizing the importance of comprehensive clinical reasoning in navigating the complexities of the patient's condition.