A patient who has suffered an ischemic stroke is being closely monitored in the stroke unit. The patient exhibits increasing drowsiness and a decline in consciousness, with vital signs showing elevated blood pressure and heart rate. Which nursing intervention is most appropriate to address the suspected complication of cerebral edema?

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

A) Administer an additional dose of antihypertensive medication to lower blood pressure immediately.

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

C) Encourage the patient to perform deep breathing exercises to increase oxygenation.

D) Provide oral glucose to address potential hypoglycemia.

A patient with a recent ischemic stroke in the left middle cerebral artery territory is experiencing increasing drowsiness and a slight decline in consciousness. Which nursing intervention is most appropriate to prioritize based on these changes?

B) Conduct a Glasgow Coma Scale assessment to monitor neurological status

A) Administer supplemental oxygen to enhance cerebral oxygenation

B) Conduct a Glasgow Coma Scale assessment to monitor neurological status

C) Increase the administration of intravenous fluids to maintain blood pressure

D) Notify the healthcare provider and prepare for potential intubation

A patient in the stroke unit is showing signs of increased intracranial pressure (ICP) after initial improvement with mannitol. The healthcare team is considering further interventions. Which nursing intervention is most appropriate to support cerebral perfusion while avoiding exacerbation of cerebral edema?

C) Elevate the head of the bed to 30 degrees to enhance venous outflow and cerebral perfusion.

A) Position the patient flat to promote venous drainage.

B) Administer a hypotonic saline solution to decrease ICP.

C) Elevate the head of the bed to 30 degrees to enhance venous outflow and cerebral perfusion.

D) Increase fluid intake to maintain adequate blood volume.

A patient with a recent ischemic stroke is showing signs of increased intracranial pressure (ICP) despite initial treatment with mannitol. The CT scan reveals a significant midline shift. What is the priority nursing intervention to address the patient's current condition?

B) Prepare the patient for a potential decompressive craniectomy.

A) Administer an additional dose of mannitol immediately.

B) Prepare the patient for a potential decompressive craniectomy.

C) Elevate the head of the bed to 30 degrees to facilitate venous drainage.

D) Initiate hypertonic saline infusion to reduce cerebral edema.

In managing the patient's fluctuating blood pressure and neurological decline, which nursing intervention is most critical to prioritize to prevent further cerebral complications?

D) Adjust intravenous fluid rate to optimize cerebral perfusion.

A) Administer antihypertensive medication to stabilize blood pressure.

B) Prepare the patient for immediate decompressive craniectomy.

C) Monitor and document neurological status every hour.

D) Adjust intravenous fluid rate to optimize cerebral perfusion.

A patient with known autonomic instability and fluctuating blood pressure is experiencing unequal pupil size and deteriorating motor function. Which nursing intervention is the priority to address the current clinical signs and prevent further neurological decline?

B) Administer prescribed mannitol to reduce intracranial pressure.

A) Increase the rate of intravenous fluids to ensure adequate cerebral perfusion.

B) Administer prescribed mannitol to reduce intracranial pressure.

C) Encourage the patient to perform deep breathing exercises to improve oxygenation.

D) Prepare for immediate intubation to secure the airway.

A postoperative neurosurgical patient in the ICU exhibits tachycardia, tachypnea, and hyponatremia. As the nurse responsible for her care, which intervention should be prioritized to address her current condition?

A) Administer hypertonic saline cautiously to correct hyponatremia.

B) Increase fluid intake to promote renal clearance of excess electrolytes.

C) Initiate a cooling blanket to manage potential hyperthermia.

D) Prepare for immediate intubation due to increased respiratory rate.

A postoperative neurosurgical patient in the ICU is displaying increased heart rate and respiratory rate, with lab results indicating hyponatremia and an elevated white blood cell count. What is the nurse's priority intervention to address the potential complications in this scenario?

A) Administer ordered antibiotics to address the suspected infection.

B) Initiate seizure precautions due to the risk of hyponatremia-induced seizures.

C) Prepare for intubation due to the increased respiratory rate.

D) Administer hypertonic saline to correct hyponatremia.

A patient in the ICU has developed a fever and has blood cultures positive for a multi-drug resistant organism. After a change in the antibiotic regimen, her Glasgow Coma Scale score decreased from 10 to 8. What is the most appropriate nursing intervention at this time?

C) Elevate the head of the bed to 30 degrees and administer hypertonic saline as ordered.

A) Administer antipyretics to reduce the fever.

B) Prepare for immediate intubation to protect the airway.

C) Elevate the head of the bed to 30 degrees and administer hypertonic saline as ordered.

D) Increase the frequency of neurological assessments to every 2 hours.

A patient in the ICU is experiencing a decline in neurological status with a Glasgow Coma Scale score dropping from 10 to 8 and an increase in cerebral edema. Which of the following interventions should the nurse prioritize to help manage the patient's intracranial pressure?

B) Elevate the head of the bed to 30 degrees.

A) Administer broad-spectrum antibiotics immediately.

B) Elevate the head of the bed to 30 degrees.

C) Increase IV fluid rate to maintain adequate hydration.

D) Encourage frequent turning and repositioning to prevent skin breakdown.

CVA - Nursing Case Study

Pathophysiology

• Primary mechanism: Ischemic stroke occurs when a blood clot obstructs a cerebral artery, leading to reduced blood flow and oxygen delivery to brain tissues, causing cell death and neurological deficits.

• Secondary mechanism: Hemorrhagic stroke results from the rupture of a blood vessel in the brain, leading to bleeding, increased intracranial pressure, and potential damage to surrounding brain tissue.

• Key complication: Both mechanisms can lead to cerebral edema, which exacerbates brain tissue damage and can result in significant and potentially irreversible impairment of neurological function.

Patient Profile

Demographics:

65-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 right side of the body

• Key symptoms: Slurred speech, difficulty walking, facial droop on the right side, headache

• Vital signs: Blood pressure 160/100 mmHg, heart rate 98 bpm, respiratory rate 22 breaths per minute, temperature 99.2°F, SpO2 94% on room air

Section 1

Following the initial presentation, the patient was swiftly transported to the hospital for further evaluation and management. Upon arrival, the medical team conducted a comprehensive neurological assessment. The patient exhibited right-sided hemiparesis, with a notable decrease in grip strength and inability to lift her right arm against gravity. Her speech was characterized by expressive aphasia, with the patient struggling to articulate words but appearing to comprehend simple commands. The National Institutes of Health Stroke Scale (NIHSS) score was calculated to be 14, indicating a moderate stroke severity.

Immediate diagnostic imaging with a CT scan of the brain was performed, which revealed an ischemic infarct in the left middle cerebral artery territory, consistent with the clinical presentation. No evidence of hemorrhage was noted. Blood tests showed elevated blood glucose levels at 230 mg/dL, likely exacerbated by stress hyperglycemia, and a cholesterol panel revealed LDL at 150 mg/dL. Given her history of hypertension and hyperlipidemia, these findings underscore the need for aggressive management of risk factors to prevent future cerebrovascular events.

As the patient remained under observation in the stroke unit, there was a notable change in her status. She developed increasing drowsiness and a slight decline in her level of consciousness. Repeat vital signs showed a blood pressure of 180/105 mmHg and a heart rate of 104 bpm. These changes raised concerns about the development of cerebral edema, a common complication following an ischemic stroke. The healthcare team initiated measures to manage intracranial pressure, including elevating the head of the bed and administering intravenous mannitol. The situation required close monitoring and reevaluation to prevent further neurological deterioration and guide ongoing therapeutic interventions.

Section 2

As the patient continued to be monitored in the stroke unit, her response to the interventions for managing intracranial pressure was closely evaluated. Initially, there was a mild improvement in her level of consciousness after the administration of mannitol, as she became slightly more responsive to verbal stimuli. However, this improvement was transient. Within hours, the healthcare team noticed that her drowsiness had returned, and she exhibited further decline in responsiveness, now opening her eyes only to painful stimuli. Her pupils were equal but sluggishly reactive to light, raising concerns about increasing cerebral edema or potential herniation.

Repeat imaging with a CT scan was performed, revealing progression of the ischemic infarct with evidence of significant midline shift, indicative of worsening cerebral edema. The clinical team recognized the urgent need for escalation in management to prevent irreversible brain damage. Neurosurgical consultation was promptly obtained to evaluate the possibility of decompressive craniectomy as a last-resort intervention. Meanwhile, the medical team optimized her blood pressure management, aiming to maintain a delicate balance to ensure adequate cerebral perfusion without exacerbating the edema.

Concurrently, her blood glucose levels remained elevated despite initial attempts at control, with a repeat measurement showing a level of 210 mg/dL. This prompted the initiation of an insulin infusion protocol to achieve tighter glycemic control, as hyperglycemia can further contribute to poor neurological outcomes. The team also reviewed her medication regimen, making adjustments to her antihypertensive therapy, and continued to emphasize the importance of controlling modifiable risk factors. The evolving situation required vigilant monitoring and frequent reassessments to guide ongoing treatment decisions and prepare for potential surgical intervention.

Section 3

As the medical team continued to monitor the patient's condition, her clinical status exhibited concerning changes, signaling the emergence of new complications. Her vital signs revealed a fluctuating pattern, with her blood pressure becoming increasingly labile. Initially stabilized at 140/85 mmHg, it began to vary widely, spiking to 160/100 mmHg and then dropping to 110/70 mmHg, complicating the efforts to maintain adequate cerebral perfusion pressure. These fluctuations suggested possible autonomic instability and further exacerbated the risk of cerebral edema worsening. Despite the insulin infusion, her blood glucose levels remained erratic, with readings oscillating between 180 mg/dL and 220 mg/dL, underscoring the challenges in achieving metabolic control.

Concurrently, the patient's neurological status continued to decline. Repeat neurological assessments showed that her pupils were now unequal, with the right pupil notably larger and slower to react to light, heightening the concern for transtentorial herniation. Her motor responses regressed, with only weak withdrawal noted in her left limbs and no response in the right, indicating a deterioration in her motor function and potential hemispheric asymmetry. These findings prompted the clinical team to expedite the neurosurgical intervention, as the risk of irreversible brain injury loomed larger.

The healthcare team gathered for a multidisciplinary discussion to reassess the treatment strategy, weighing the risks and benefits of proceeding with decompressive craniectomy. The decision was made to move forward with the surgical intervention, recognizing it as the most viable option to alleviate the intracranial pressure and prevent further neurological compromise. Meanwhile, supportive measures were intensified, including careful titration of intravenous fluids to manage her hydration status without contributing to cerebral swelling, and the administration of medications to mitigate potential complications such as seizures, which can be precipitated by the evolving cerebral pathology. The evolving complexity of her situation underscored the necessity for continuous, dynamic clinical reasoning and rapid adaptation to the patient's shifting needs.

Section 4

As the neurosurgical intervention proceeded, the team remained vigilant for any signs of improvement or deterioration. In the immediate postoperative period, the patient was carefully monitored in the intensive care unit. Despite the hopes of alleviating intracranial pressure, her clinical status took an unexpected turn. The vital signs revealed an alarming trend: her heart rate, previously stable, began to climb, reaching 120 beats per minute. Simultaneously, her respiratory rate increased to 28 breaths per minute, indicating a potential shift in her physiological status. These changes raised suspicion for a developing complication, possibly related to systemic inflammation or an evolving infection.

Laboratory results soon confirmed these concerns. A complete blood count showed a white blood cell count of 14,000/mm³, up from 8,000/mm³ preoperatively, suggesting a possible infectious process. Blood cultures were obtained, and broad-spectrum antibiotics were initiated empirically to cover potential pathogens. Additionally, her electrolyte panel revealed a sodium level of 128 mEq/L, indicative of hyponatremia, which could exacerbate cerebral edema and alter mental status. This prompted the team to adjust her fluid management strategy and consider the use of hypertonic saline to correct the electrolyte imbalance cautiously.

The patient's neurological assessment showed no significant improvement, with persistent unequal pupils and diminished motor responses. As the team evaluated these findings, the importance of integrating clinical reasoning became evident. They needed to balance the aggressive management of potential infection while ensuring that cerebral perfusion and oxygenation were optimized. The multidisciplinary team, including infectious disease specialists, neurologists, and intensivists, reconvened to refine the treatment plan. The focus shifted towards stabilizing her systemic condition while maintaining vigilance for any further neurological changes. This phase of her care highlighted the complexity of managing multiple intersecting complications in a patient with a critical neurological event.

Section 5

As the hours passed in the intensive care unit, the patient's condition continued to evolve, presenting new challenges for the healthcare team. Her vital signs remained unstable, with heart rate oscillating between 115 and 130 beats per minute and respiratory rate persistently elevated at 30 breaths per minute. Despite the initiation of broad-spectrum antibiotics, her fever spiked to 102.5°F, suggesting that the infection may be more resistant or virulent than initially anticipated. The blood cultures returned positive for a multi-drug resistant organism, necessitating a change in the antibiotic regimen under the guidance of infectious disease specialists. This prompted the team to escalate to a more targeted antibiotic therapy, emphasizing the need for precise antimicrobial stewardship in the face of resistant pathogens.

Concurrently, her neurological status showed subtle yet concerning changes. The patient's level of consciousness decreased, with her Glasgow Coma Scale score dropping from 10 to 8, indicating a decline in her neurological function. This raised the possibility of worsening cerebral edema or an extension of the original cerebrovascular accident. The team decided to obtain a repeat CT scan of the brain to assess for any new or worsening intracranial pathology. The scan revealed an increase in midline shift and signs of evolving cerebral edema, corroborating the clinical suspicion of deteriorating intracranial dynamics. In response, the intensivists and neurologists collaborated to adjust her treatment plan, incorporating measures to reduce intracranial pressure, including the cautious use of hypertonic saline and the optimization of her head positioning to facilitate venous drainage.

Throughout this phase, the team remained committed to a holistic approach, integrating infection control measures with rigorous neurological management. The complexity of her condition underscored the necessity of a dynamic and adaptive treatment strategy, where ongoing assessment and timely intervention were critical. The focus was not only on addressing the current complications but also on preempting further deterioration by closely monitoring her fluid balance, electrolyte levels, and neurological status. As the patient journeyed through this critical period, the healthcare team remained poised to navigate the intricate web of challenges presented by her multi-faceted clinical picture, demonstrating the profound need for interdisciplinary collaboration and astute clinical reasoning.