A 45-year-old patient with a confirmed subarachnoid hemorrhage presents with a sudden decrease in responsiveness, a drop in GCS score from 15 to 10, a dilated right pupil, and new-onset left-sided weakness. Vital signs show blood pressure of 180/100 mmHg and heart rate of 60 bpm. What is the nurse's priority intervention to address the suspected complication?

C) Initiate intracranial pressure monitoring and administer hypertonic saline.

A) Administer nimodipine to manage cerebral vasospasm.

B) Prepare the patient for endovascular treatment to alleviate vasospasm.

C) Initiate intracranial pressure monitoring and administer hypertonic saline.

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

A 45-year-old patient with a subarachnoid hemorrhage (SAH) has developed a sudden decrease in responsiveness, left-sided weakness, and Cushing's triad. What is the most appropriate initial nursing intervention to address the suspected increased intracranial pressure and cerebral vasospasm?

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

A) Administer nimodipine as prescribed to manage vasospasm

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

C) Prepare the patient for immediate CT angiography to assess cerebral blood flow

D) Initiate hyperventilation to rapidly decrease intracranial pressure

A patient is being monitored for intracranial pressure following nimodipine therapy and presents with a Glasgow Coma Scale of 12, a sluggish right pupil, and left-sided weakness. The patient's serum sodium is 135 mEq/L. Which of the following nursing interventions is most appropriate to prioritize at this time?

A) Increase the frequency of neuromonitoring assessments to detect changes in neurological status.

B) Administer additional doses of nimodipine to further alleviate vasospasm.

C) Restrict fluid intake to prevent dilutional hyponatremia.

D) Prepare for an immediate CT angiography to assess cerebral vasospasm.

A patient with a history of subarachnoid hemorrhage is being monitored for intracranial pressure and cerebral edema. Her current management includes nimodipine therapy and fluid management. Given her recent lab results showing a serum sodium level of 135 mEq/L and persistent symptoms, which nursing intervention should be prioritized?

B) Monitor neurological status and prepare to administer hypertonic saline as prescribed.

A) Increase the administration of hypotonic fluids to address potential dehydration.

B) Monitor neurological status and prepare to administer hypertonic saline as prescribed.

C) Reduce nimodipine dosage to prevent further lowering of blood pressure.

D) Encourage oral fluid intake to improve electrolyte balance.

A patient with subarachnoid hemorrhage is experiencing significant vasospasm in the middle cerebral artery, contributing to neurological decline. The healthcare team is considering endovascular intervention. Which nursing action is most critical when preparing the patient for this procedure?

B) Ensuring the patient remains NPO for at least 6 hours before the procedure

A) Administering prescribed oral antihypertensive medication

B) Ensuring the patient remains NPO for at least 6 hours before the procedure

C) Educating the patient on the risks and benefits of the procedure

D) Monitoring the patient's electrolyte levels closely

A nurse is caring for a patient with subarachnoid hemorrhage who has exhibited a decrease in neurological status and has been diagnosed with significant vasospasm in the middle cerebral artery. Which of the following interventions should the nurse anticipate to effectively manage the patient's current condition?

A) Increasing the frequency of hypertonic saline administration to manage cerebral edema.

C) Administering diuretics to reduce intracranial pressure and improve neurological status.

D) Initiating a fluid restriction protocol to prevent further hyponatremia.

A patient in the ICU is being monitored for complications following subarachnoid hemorrhage (SAH). The patient has developed worsening cerebral edema with a midline shift, and her GCS score has fallen to 8. Her blood pressure is 190/110 mmHg, and her serum sodium level has dropped to 130 mEq/L. Given these findings, what is the most appropriate immediate nursing action to help manage the patient's condition?

C) Administer a bolus of mannitol to reduce cerebral edema.

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

B) Prepare the patient for possible surgical intervention to relieve intracranial pressure.

C) Administer a bolus of mannitol to reduce cerebral edema.

D) Implement seizure precautions to prevent further neurological deterioration.

A patient with subarachnoid hemorrhage (SAH) is exhibiting signs of increasing intracranial pressure (ICP), including a GCS score of 8 and worsening cerebral edema. The nurse notes a serum sodium level of 130 mEq/L and a urine output of less than 0.5 mL/kg/hr. Which nursing intervention should the nurse prioritize to address the current complications and prevent further deterioration?

A) Administer mannitol to decrease cerebral edema.

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

C) Restrict fluid intake to prevent fluid overload.

D) Prepare the patient for immediate decompressive craniectomy.

A patient with increased intracranial pressure (ICP) is being treated with hyperosmolar therapy using mannitol and hypertonic saline. Recent lab results show hyponatremia and signs of acute kidney injury. What is the nurse's priority intervention to address these findings while managing the patient's ICP?

B) Administer isotonic fluids cautiously and monitor electrolyte levels closely

A) Increase the rate of hypertonic saline infusion to correct hyponatremia more rapidly

B) Administer isotonic fluids cautiously and monitor electrolyte levels closely

C) Discontinue mannitol to prevent further renal impairment

D) Administer a diuretic to promote renal excretion and reduce cerebral edema

A patient with increased intracranial pressure is receiving hyperosmolar therapy with mannitol and hypertonic saline. The nurse notes the patient's serum sodium level has decreased to 127 mEq/L and creatinine has risen to 2.1 mg/dL. What is the nurse's priority action?

B) Notify the healthcare provider about the patient's electrolyte imbalance and renal status.

A) Administer additional hypertonic saline to correct the hyponatremia.

B) Notify the healthcare provider about the patient's electrolyte imbalance and renal status.

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

D) Hold the next dose of mannitol to prevent further renal compromise.

SAH - Nursing Case Study

Pathophysiology

• Primary mechanism: Subarachnoid hemorrhage (SAH) occurs when a cerebral aneurysm ruptures, leading to bleeding in the subarachnoid space. This sudden bleeding increases intracranial pressure, disrupting cerebral perfusion and oxygen delivery to the brain tissue.

• Secondary mechanism: The presence of blood in the cerebrospinal fluid triggers a cascade of inflammatory responses, causing cerebral vasospasm. This vasospasm can lead to delayed cerebral ischemia, further compromising blood flow and potentially resulting in brain tissue injury.

• Key complication: If not managed promptly, increased intracranial pressure and delayed cerebral ischemia can lead to significant neurological deficits, coma, or even death, highlighting the urgent need for rapid diagnosis and treatment in SAH cases.

Patient Profile

Demographics:

45-year-old female, school teacher

History:

• Hypertension, hyperlipidemia

• Amlodipine 10 mg daily, Atorvastatin 20 mg daily

• Allergic to penicillin

Current Presentation:

• Chief complaint: Sudden, severe headache described as the "worst headache of her life"

• Key symptoms: Nausea, vomiting, photophobia, neck stiffness

• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 bpm, respiratory rate 20 breaths per minute, temperature 37.8°C, oxygen saturation 95% on room air

Section 1

New Complications

As the medical team continued to manage the 45-year-old patient with a confirmed subarachnoid hemorrhage (SAH), she began to exhibit signs of worsening neurological status. Approximately 48 hours post-admission, the patient developed a sudden decrease in responsiveness. Her Glasgow Coma Scale (GCS) score dropped from 15 to 10, indicating a significant alteration in her level of consciousness. In addition, her right pupil became sluggishly reactive and slightly dilated, suggesting possible increased intracranial pressure or early cerebral herniation.

Concurrent with these observations, the patient's vital signs showed a concerning trend. Her blood pressure spiked to 180/100 mmHg, and her heart rate decreased to 60 bpm, suggesting Cushing's triad, a classic sign of increased intracranial pressure. The patient also exhibited new-onset left-sided weakness, further indicating potential ischemic insult due to cerebral vasospasm. A repeat CT angiography confirmed severe vasospasm in the right middle cerebral artery territory, correlating with her clinical deficits.

This deterioration necessitated immediate clinical reasoning and intervention. The healthcare team promptly initiated nimodipine to manage vasospasm and considered endovascular treatment options to alleviate the vasospasm and improve cerebral perfusion. Simultaneously, intracranial pressure monitoring was implemented, and hypertonic saline was administered to reduce cerebral edema. These developments underscore the importance of vigilance in monitoring for complications like vasospasm and the critical need for timely intervention to prevent further neurological injury. The unfolding situation sets the stage for evaluating the effectiveness of these interventions and determining the next steps in the patient's care.

Section 2

As the healthcare team closely monitored the patient following the initiation of nimodipine therapy and intracranial pressure management, they observed her response to these interventions over the next 24 hours. Initially, there was mild improvement in her neurological status; her GCS improved slightly to 12, indicating a partial recovery in consciousness. However, her right pupil remained sluggish, and her left-sided weakness persisted, suggesting that while some aspects of cerebral function were stabilizing, others continued to be compromised.

Despite these mixed results, the patient's vital signs began to reflect more positive trends. Her blood pressure decreased to 160/90 mmHg, and her heart rate increased slightly to 68 bpm, suggesting a partial alleviation of intracranial pressure. However, repeat intracranial pressure measurements showed only a modest reduction, indicating that cerebral edema was not fully resolved. These findings prompted the team to reassess the effectiveness of the current therapeutic strategy and consider additional measures, such as increasing the frequency of hypertonic saline administration or exploring alternative pharmacological options.

Concurrently, new laboratory results raised further concerns. The patient's serum sodium level was noted to be at the lower limit of normal at 135 mEq/L, raising the risk of hyponatremia, which could exacerbate cerebral edema. This finding prompted a reevaluation of her fluid management plan to ensure optimal electrolyte balance. Additionally, the team considered repeating the CT angiography to assess the current status of the vasospasm and guide further endovascular interventions. These developments highlighted the need for continued vigilance and adaptive clinical reasoning to navigate the complexities of the patient's evolving condition.

Section 3

The healthcare team decided to increase the frequency of hypertonic saline administration to address the persistent cerebral edema and potential hyponatremia. Over the next 12 hours, they closely monitored the patient's response to this adjustment. Unfortunately, her neurological status began to deteriorate. The GCS dropped back to 10, indicating a decrease in consciousness, and her right pupil became fixed and dilated. These changes suggested an increase in intracranial pressure, possibly due to evolving complications or insufficient response to current interventions.

New diagnostic results from a repeat CT angiography revealed significant vasospasm in the middle cerebral artery, which was likely contributing to her neurological decline. The vasospasm was more pronounced than previously observed, emphasizing the need for aggressive management. The team discussed the potential benefits of endovascular intervention, such as balloon angioplasty or intra-arterial vasodilator therapy, to alleviate the vasospasm and improve cerebral perfusion.

In light of these developments, the patient's care plan was adjusted to include a more comprehensive approach to vasospasm management. The team also re-evaluated her fluid and electrolyte management strategy, aiming to mitigate the risk of further hyponatremia while addressing the underlying causes of her symptoms. As they navigated these challenges, the importance of continual reassessment and adaptation of therapeutic strategies became clear, underscoring the dynamic nature of managing subarachnoid hemorrhage and its complications.

Section 4

As the healthcare team implemented the revised care plan, they closely monitored the patient's response to the aggressive vasospasm management and fluid-electrolyte adjustments. Over the next 24 hours, the patient was kept under continuous observation in the ICU. Despite the interventions, her condition took a concerning turn. The nursing staff noted an increase in her blood pressure to 190/110 mmHg, a heart rate that fluctuated between bradycardia and tachycardia, and a persistently low urine output of less than 0.5 mL/kg/hr, suggesting the possibility of acute kidney injury. Her serum sodium levels, previously managed with hypertonic saline, dropped to 130 mEq/L, raising concerns about the effectiveness of the current electrolyte management strategy.

In addition to these findings, a new neurological assessment revealed further deterioration. The patient exhibited increased hemiparesis on the left side, and her GCS score fell to 8, indicating severe impairment of consciousness. These changes prompted the team to conduct a follow-up CT scan, which unfortunately confirmed the presence of worsening cerebral edema and a slight midline shift, indicating escalating intracranial pressure. The team recognized the need for more aggressive measures to manage these complications, including the potential for surgical intervention to alleviate pressure and prevent additional neurological damage.

Faced with these developments, the team gathered to reassess their approach, considering both pharmacological and surgical options. They discussed the feasibility and timing of a decompressive craniectomy to address the increasing intracranial pressure. The patient's fluid management was further scrutinized to prevent worsening hyponatremia and support renal function, while ensuring optimal cerebral perfusion. This juncture emphasized the delicate balance required in managing SAH with evolving complications, underscoring the critical need for timely and precise clinical decisions to navigate the patient's complex and dynamic clinical trajectory.

Section 5

As the healthcare team focused on addressing the patient's increasing intracranial pressure, they prioritized the implementation of hyperosmolar therapy with mannitol and hypertonic saline, aimed at reducing cerebral edema. Over the next several hours, careful monitoring of her neurological status and vital signs was essential to assess the effectiveness of these interventions. However, the patient's condition remained precarious. Her blood pressure continued to be elevated, now reading 195/115 mmHg, while her heart rate oscillated between 55 and 120 beats per minute, complicating hemodynamic management.

A new set of laboratory results revealed further complications. Her serum sodium had decreased to 127 mEq/L, despite efforts to manage hyponatremia, indicating an inadequate response to the hypertonic saline. Additionally, renal function markers showed a rise in creatinine levels to 2.1 mg/dL and blood urea nitrogen to 38 mg/dL, confirming acute kidney injury. This necessitated a careful reevaluation of her fluid and electrolyte management strategy to stabilize her renal function while continuing to address the risk of cerebral edema and maintain cerebral perfusion pressure.

Given these developments, the interdisciplinary team convened once again to discuss the potential need for urgent surgical intervention. The neurosurgeon emphasized the risks and benefits of proceeding with a decompressive craniectomy, considering the persistent midline shift and deteriorating neurological status. The fluid management protocol was revised to include cautious administration of isotonic fluids, alongside continued monitoring of electrolytes and renal function. This challenging scenario underscored the importance of dynamic, evidence-based decision-making and close collaboration among the healthcare team to tailor interventions to the patient's rapidly evolving condition, setting the stage for the next critical phase in her care.