A patient with a history of hypertension and a recent subarachnoid hemorrhage is showing signs of vasospasm, including new-onset weakness in the left arm and leg, increased confusion, and difficulty speaking. Which nursing intervention is most appropriate to prioritize in this situation to address the vasospasm?

A) Administering calcium channel blockers as prescribed

B) Increasing oxygen therapy to maintain saturation above 98%

C) Elevating the head of the bed to 45 degrees to reduce intracranial pressure

D) Encouraging the patient to perform range of motion exercises to prevent muscle atrophy

A patient with a subarachnoid hemorrhage is exhibiting signs of vasospasm, including left-sided weakness and increased confusion. The nurse should prioritize which of the following interventions to address the patient's vasospasm?

B) Administer prescribed calcium channel blockers as ordered

A) Encourage the patient to perform active range of motion exercises

B) Administer prescribed calcium channel blockers as ordered

C) Increase the patient's fluid intake to promote hydration

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

A patient with a recent subarachnoid hemorrhage is experiencing significant vasospasm and hyponatremia due to SIADH. Nimodipine has been initiated, and hypertonic saline is being administered. Which nursing intervention is most critical to prevent further neurological deterioration in this patient?

A) Monitoring the patient's fluid intake and output closely

B) Administering analgesics as needed for headache management

C) Encouraging the patient to perform range-of-motion exercises

D) Educating the patient about the importance of bed rest

A nurse is caring for a patient with significant vasospasm following a subarachnoid hemorrhage. The patient has been started on nimodipine and hypertonic saline to manage vasospasm and hyponatremia. Which nursing intervention is most critical to monitor the effectiveness of these treatments and prevent complications?

D) Monitor serum electrolyte levels and neurological status

A) Monitor urine output and daily weights

B) Assess for signs of increased intracranial pressure

C) Check peripheral pulses and capillary refill

D) Monitor serum electrolyte levels and neurological status

A nurse is caring for a patient with increasing intracranial pressure (ICP) and recent placement of an external ventricular drain (EVD). Which intervention should the nurse prioritize to effectively manage the patient's condition?

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

B) Administer a sedative to decrease metabolic demands.

C) Increase intravenous fluid rate to improve cerebral perfusion.

D) Position the patient flat to facilitate CSF drainage.

A patient with a complex aneurysm and signs of increasing intracranial pressure is being managed with an external ventricular drain (EVD) and hypertonic saline for hyponatremia due to SIADH. Which assessment finding should the nurse prioritize and report immediately to the healthcare provider?

C) New onset of bradycardia and widening pulse pressure.

A) Serum sodium level increased from 130 mEq/L to 135 mEq/L.

B) The patient's Glasgow Coma Scale (GCS) score improved from 9 to 12.

C) New onset of bradycardia and widening pulse pressure.

D) The patient's urine output increased to 50 mL/hour.

A patient with a recent diagnosis of cerebral vasospasm following a CT angiography showing involvement of the left middle cerebral artery is being managed with nimodipine and fluid optimization. During your assessment, the patient presents with new-onset slurred speech and right-sided weakness. What is the priority nursing action?

B) Notify the healthcare provider immediately.

A) Reassess the patient's blood pressure and heart rate.

B) Notify the healthcare provider immediately.

C) Increase the rate of intravenous fluids.

D) Administer an additional dose of nimodipine.

A patient with a new cerebral vasospasm in the left middle cerebral artery is being treated with nimodipine and fluid management to promote cerebral perfusion. The nurse is monitoring for potential complications. Which finding should prompt the nurse to immediately contact the healthcare provider?

C) Onset of focal neurological deficits

A) Serum sodium level of 134 mEq/L

C) Onset of focal neurological deficits

D) Blood pressure of 150/80 mmHg

A patient undergoing nimodipine therapy for vasospasm has developed hyponatremia and cerebral edema. Which nursing intervention is most appropriate to address the patient's current condition?

B) Administer hypertonic saline while monitoring neurological status.

A) Increase oral fluid intake to improve serum sodium levels.

B) Administer hypertonic saline while monitoring neurological status.

C) Discontinue nimodipine to reduce the risk of further hyponatremia.

D) Implement a fluid restriction to prevent further cerebral edema.

A patient on nimodipine therapy for subarachnoid hemorrhage begins to exhibit increasing confusion, lethargy, and hyponatremia. Which nursing intervention is most appropriate to address the patient's electrolyte imbalance while maintaining cerebral perfusion?

B) Initiate hypertonic saline infusion and monitor neurological status closely.

A) Administer hypotonic saline to quickly correct hyponatremia.

B) Initiate hypertonic saline infusion and monitor neurological status closely.

C) Increase oral fluid intake to dilute serum sodium levels.

D) Discontinue nimodipine to reduce the risk of further hyponatremia.

Aneurysm - Nursing Case Study

Pathophysiology

• Primary mechanism: Aneurysms primarily arise from the weakening of the vessel wall due to factors like hypertension, atherosclerosis, or genetic connective tissue disorders. This weakening leads to a localized dilation of the artery, as the structural integrity of the vessel is compromised.

• Secondary mechanism: Chronic inflammation contributes to aneurysm formation by degrading the elastin and collagen in the arterial wall. Inflammatory cells release enzymes that further weaken the vessel structure, promoting expansion and risk of rupture.

• Key complication: The most critical complication of an aneurysm is rupture, which can lead to life-threatening hemorrhage. This risk escalates with increased aneurysm size and continued wall stress, necessitating timely monitoring and intervention to prevent catastrophic outcomes.

Patient Profile

Demographics:

54-year-old female, office manager

History:

• Key past medical history: Hypertension, type 2 diabetes, hyperlipidemia

• Current medications: Lisinopril, Metformin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe headache and dizziness

• Key symptoms: Blurred vision, nausea, neck stiffness, intermittent confusion

• Vital signs: Blood pressure 150/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 99.1°F, oxygen saturation 94% on room air

Section 1

During the initial assessment, the healthcare team noted that the patient exhibited increasing confusion and a decline in her level of consciousness, which prompted an urgent further evaluation. A CT scan of the brain was ordered, revealing a subarachnoid hemorrhage, indicating that the aneurysm had likely ruptured. This finding was consistent with her presenting symptoms of severe headache, neck stiffness, and blurred vision. Blood tests showed elevated white blood cell count and C-reactive protein levels, suggesting an inflammatory process. Her blood pressure remained elevated at 160/100 mmHg, despite being on Lisinopril, pointing to poorly controlled hypertension, which might have contributed to the aneurysm's rupture.

Given these findings, the medical team initiated several interventions. The patient was started on intravenous labetalol to manage her blood pressure more effectively and prevent further bleeding. Neurosurgery was consulted for potential surgical intervention, and the patient was placed on strict bed rest in a quiet, low-stimulation environment to prevent increased intracranial pressure. Oxygen therapy was provided to maintain an oxygen saturation above 95%, stabilizing her respiratory status. The nursing staff closely monitored her neurological status, noting any changes that might indicate worsening of her condition.

Despite these interventions, the patient began to exhibit signs of vasospasm, a common complication after a subarachnoid hemorrhage. She developed new-onset weakness in her left arm and leg, along with increased confusion and difficulty speaking. This change in status necessitated further diagnostic imaging and consideration of calcium channel blockers to alleviate the vasospasm and improve cerebral blood flow. The healthcare team prepared for possible endovascular treatment to address both the aneurysm and associated complications, ensuring that all steps were taken to optimize the patient's outcome and prevent further deterioration.

Section 2

In response to the patient's worsening condition, repeat imaging studies, including a cerebral angiogram, were performed, confirming the presence of significant vasospasm in the middle cerebral artery territory. This finding correlated with the new-onset left-sided weakness and speech difficulties. The angiogram also revealed that the previously identified aneurysm had a complex morphology, necessitating endovascular coiling to prevent further bleeding. Concurrently, the patient's laboratory results indicated worsening electrolyte imbalances, with a serum sodium level dropping to 128 mEq/L, suggestive of syndrome of inappropriate antidiuretic hormone secretion (SIADH), a potential complication of subarachnoid hemorrhage.

Given the patient's critical condition, the medical team prioritized interventions to address both the vasospasm and the electrolyte imbalance. Nimodipine, a calcium channel blocker, was initiated to mitigate the vasospasm and improve cerebral perfusion. Additionally, hypertonic saline was administered to correct the hyponatremia and prevent cerebral edema. The patient's fluid balance was carefully monitored to avoid aggravating the SIADH. Her vital signs were closely observed, with particular attention to maintaining systolic blood pressure within target range to optimize cerebral perfusion without exacerbating the risk of re-bleeding.

Despite these measures, the patient's neurological status remained tenuous, with fluctuating levels of consciousness and persistent left-sided weakness. The healthcare team engaged in ongoing clinical reasoning, weighing the risks and benefits of proceeding with endovascular intervention versus continued medical management. The decision-making process involved collaboration among neurology, neurosurgery, and critical care teams, reflecting the complexity of managing such a multifaceted case. As the medical team evaluated the evolving situation, they remained vigilant for further complications, such as rebleeding or hydrocephalus, and prepared to adapt their management plan accordingly.

Section 3

As the medical team continued to monitor the patient's condition, a new complication emerged. The patient developed signs of increasing intracranial pressure (ICP), evidenced by a sudden deterioration in her level of consciousness. She became increasingly lethargic, with a GCS score dropping from 14 to 9. Her pupils were unequal, with the right pupil dilated and sluggishly reactive to light, indicating potential herniation. These alarming changes prompted the immediate repeat of imaging studies, including a CT scan, which revealed worsening hydrocephalus due to impaired cerebrospinal fluid (CSF) drainage, likely exacerbated by the vasospasm and complex aneurysm morphology.

In response, the clinical team swiftly initiated measures to alleviate the rising ICP. An external ventricular drain (EVD) was urgently placed to facilitate CSF drainage and relieve pressure. Concurrently, the patient's blood pressure was meticulously managed to maintain adequate cerebral perfusion pressure, aiming to stabilize her neurological status. Despite these interventions, the patient's serum sodium remained low at 130 mEq/L, requiring continued administration of hypertonic saline and careful fluid management to address the persistent SIADH. The team also remained vigilant for potential signs of rebleeding, given the complex nature of the aneurysm, and prepared for possible surgical intervention if necessary.

The unfolding situation required the healthcare providers to engage in dynamic clinical reasoning, balancing the need to control the ICP with the ongoing risk of aneurysm rupture. The multidisciplinary team continued to assess the patient's response to the interventions, ready to adapt their management plan based on her evolving condition. The focus remained on stabilizing her neurological status while preventing further complications, underscoring the intricate interplay of factors influencing her recovery trajectory.

Section 4

As the clinical team continued to closely monitor the patient's condition, a new complication arose, further challenging the management strategy. During a routine assessment, the patient's vital signs revealed a mildly elevated heart rate of 102 bpm, coupled with an increase in systolic blood pressure to 160 mmHg. These subtle but significant changes prompted further investigation into her cardiovascular status. A repeat CT angiography was performed, revealing a new area of cerebral vasospasm in the left middle cerebral artery, which posed an increased risk of ischemic stroke. This finding necessitated immediate adjustments to the patient's management plan, highlighting the interconnectedness of her symptoms and underlying conditions.

In response, the team initiated targeted therapies to address the vasospasm, including the administration of nimodipine and the optimization of her hydration status to promote cerebral perfusion. Meanwhile, vigilant monitoring for neurological deficits became paramount, as any new signs of focal weakness or speech difficulties could signal an acute ischemic event. The patient's sodium levels remained a concern, with serum sodium stabilizing at 132 mEq/L, necessitating a delicate balance in fluid management to prevent exacerbating the SIADH while ensuring effective hemodynamic support.

This new development prompted the team to reevaluate the overall treatment strategy, emphasizing the need for continued interdisciplinary collaboration. The patient's evolving clinical picture required dynamic adjustments to therapy, underscoring the critical role of real-time clinical reasoning. The focus remained on mitigating the risk of further complications while enhancing her recovery trajectory, with the team prepared to escalate care should her condition further deteriorate. This multifaceted approach highlighted the complexities of managing a patient with an intricate interplay of neurological and systemic challenges.

Section 5

As the clinical team continued to monitor the patient's response to the implemented interventions, a new complication emerged. Approximately 24 hours after initiating nimodipine therapy and optimizing hydration status, the patient began to exhibit signs of increasing confusion and lethargy. Her vital signs indicated a further elevation in heart rate to 108 bpm, while her blood pressure remained stable at 158/90 mmHg. Neurological assessment revealed subtle changes: the patient was oriented only to person, and her pupils were sluggishly reactive, raising concerns about potential cerebral edema or worsening vasospasm.

A repeat CT scan of the head was promptly ordered, revealing mild cerebral edema with no acute hemorrhagic changes. Concurrently, serum sodium levels were reassessed and found to have decreased to 129 mEq/L, suggesting a recurrence of hyponatremia likely linked to worsening SIADH. These findings necessitated an urgent reassessment of her fluid management strategy to address the sodium imbalance without compromising cerebral perfusion. The team decided to cautiously initiate hypertonic saline and re-evaluate fluid restrictions, while also considering the potential need for further pharmacological intervention to address the SIADH.

This turn of events highlighted the ongoing complexity of her case, requiring careful integration of neurological, cardiovascular, and electrolyte management principles. The team's focus shifted to preventing further neurological decline while maintaining systemic stability. The collaborative effort underscored the necessity of adaptive clinical reasoning, as each intervention carried the potential to influence multiple aspects of the patient's condition. Anticipating possible further complications, the team remained vigilant, ready to escalate care as needed to navigate the nuanced challenges of this intricate clinical scenario.