A patient with a suspected acute ischemic stroke presents with a GCS score of 9, right-sided hemiparesis, and expressive aphasia. The CT scan indicates a dense MCA sign, suggesting a large vessel occlusion. Considering the patient's elevated blood pressure and INR of 1.3, which is the most appropriate initial nursing action to prioritize while awaiting further orders from the stroke team?

B) Initiate advanced airway management due to declining oxygen saturation.

A) Administer thrombolytic therapy immediately.

B) Initiate advanced airway management due to declining oxygen saturation.

C) Prepare for mechanical thrombectomy by ensuring the patient remains NPO.

D) Implement aggressive blood pressure management with IV antihypertensives.

A 68-year-old patient presents to the emergency department with symptoms indicative of an acute ischemic stroke, including a Glasgow Coma Scale (GCS) score of 9 and right-sided hemiparesis. The stroke team is considering thrombolytic therapy but is concerned about the elevated INR of 1.3 and potential for hemorrhagic transformation. The patient's blood pressure is critically high, and there is evidence of atrial fibrillation and pulmonary congestion. What is the most appropriate nursing intervention to prioritize while waiting for the stroke team's decision on thrombolytic therapy?

C) Monitor and document neurological status every 15 minutes to detect any changes in the patient's condition.

A) Administer IV labetalol to rapidly control the patient's blood pressure to reduce the risk of hemorrhagic transformation.

B) Assist in preparing the patient for a mechanical thrombectomy by ensuring consent and pre-procedure checklist are completed.

C) Monitor and document neurological status every 15 minutes to detect any changes in the patient's condition.

D) Initiate an immediate infusion of IV heparin to address the subtherapeutic INR and prevent further thromboembolic events.

After a patient undergoes a mechanical thrombectomy with a subsequent small hemorrhagic transformation, which nursing intervention is most critical to prioritize in the first 24 hours post-procedure to prevent further neurological deterioration?

B) Closely monitor and control blood pressure using prescribed antihypertensives to prevent further bleeding.

A) Administer anticoagulation therapy as prescribed to prevent re-occlusion.

B) Closely monitor and control blood pressure using prescribed antihypertensives to prevent further bleeding.

C) Initiate early mobilization and physical therapy to enhance neurological recovery.

D) Provide continuous glucose monitoring and adjust insulin therapy to maintain normoglycemia.

A patient post-mechanical thrombectomy for middle cerebral artery occlusion is being managed in the ICU. The interventional team successfully restored partial blood flow, but a small hemorrhagic transformation was detected. Given the patient's history of atrial fibrillation and the need to prevent further clot formation, which nursing intervention is most critical at this time to optimize neurological recovery and prevent complications?

B) Monitor for signs of increased intracranial pressure and adjust antihypertensive therapy accordingly.

A) Administer anticoagulation therapy immediately to prevent further clot formation.

B) Monitor for signs of increased intracranial pressure and adjust antihypertensive therapy accordingly.

C) Initiate aggressive physical therapy to promote neuroplasticity and motor recovery.

D) Increase the frequency of neurological assessments to every 15 minutes to detect changes early.

A patient in the ICU with cerebral edema shows signs of Cushing's triad and a decreasing Glasgow Coma Scale (GCS) score. Which nursing intervention is the highest priority to prevent further neurological deterioration?

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

A) Administer a hypertonic saline bolus to rapidly correct hyponatremia.

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

C) Prepare the patient for an immediate decompressive craniectomy.

D) Initiate continuous EEG monitoring to assess for seizure activity.

A patient in the ICU with signs of cerebral edema and potential SIADH has been started on mannitol and placed on fluid restriction. The nurse observes that the patient’s serum sodium is 128 mmol/L and serum osmolality is low. Which nursing intervention is the priority to address these findings?

A) Administer 3% hypertonic saline as prescribed to correct hyponatremia.

B) Increase the patient's fluid restriction to further manage SIADH.

C) Monitor the patient for signs of fluid overload and pulmonary edema.

D) Educate the patient and family about the importance of adhering to fluid restrictions.

A patient in the critical care unit is experiencing increased intracranial pressure (ICP) that is unresponsive to osmotic therapy. The patient's neurological status is deteriorating with a Glasgow Coma Scale (GCS) score of 6, anisocoria, and signs of Cushing's triad. What is the most appropriate nursing intervention to prioritize while awaiting decompressive craniectomy?

C) Initiating hyperventilation to decrease carbon dioxide levels and reduce ICP

A) Administering additional doses of mannitol to further reduce ICP

B) Preparing the patient for immediate transfer to the operating room

C) Initiating hyperventilation to decrease carbon dioxide levels and reduce ICP

D) Increasing sedation and analgesia to manage pain and agitation

In the context of the patient's deteriorating neurological and cardiovascular status, which nursing intervention is most critical to implement immediately?

B) Prepare the patient and necessary equipment for immediate decompressive craniectomy.

A) Initiate a continuous infusion of hypotonic saline to reduce cerebral edema.

B) Prepare the patient and necessary equipment for immediate decompressive craniectomy.

C) Administer an increased dose of mannitol to further reduce intracranial pressure.

D) Adjust the ventilator settings to increase the respiratory rate and depth to manage Cheyne-Stokes respirations.

A patient in the critical care unit has undergone a decompressive craniectomy and now presents with significant hyponatremia, elevated INR, and a deteriorating neurological status, including a GCS score of 4 and decerebrate posturing. The latest CT scan shows a midline shift of 12 mm. In prioritizing the patient's care, which intervention should the nurse anticipate as the most crucial to stabilize the patient's condition?

A) Initiate hypertonic saline therapy to correct hyponatremia and reduce cerebral edema.

B) Administer fresh frozen plasma to address the elevated INR and prevent bleeding complications.

C) Begin continuous renal replacement therapy to manage oliguria and potential acute kidney injury.

D) Increase the dose of mannitol to further reduce intracranial pressure.

A patient with a significant midline shift and elevated intracranial pressure post-decompressive craniectomy has developed critical hyponatremia and coagulation abnormalities. As the nursing team prepares for potential interventions, which action should be prioritized to optimize the patient's neurological status and minimize complications?

A) Administer a bolus of hypertonic saline to address hyponatremia immediately.

B) Initiate fresh frozen plasma transfusion to correct coagulation abnormalities before any other intervention.

C) Increase the dosage of mannitol to further reduce intracranial pressure.

D) Collaborate with the healthcare team to initiate continuous renal replacement therapy (CRRT) to manage oliguria.

thrombotic stroke - Nursing Case Study

Pathophysiology

• Primary mechanism: Atherosclerosis leads to endothelial injury and plaque formation in cerebral arteries, triggering local thrombus formation as platelets adhere to the exposed collagen and release pro-thrombotic factors.

• Secondary mechanism: The coagulation cascade is activated, resulting in fibrin deposition and stabilization of the thrombus, which can occlude the cerebral blood vessel and reduce blood flow to brain tissue.

• Key complication: Ischemia ensues, causing neuronal injury and death due to lack of oxygen and nutrients, potentially leading to severe neurological deficits or death if not rapidly addressed.

Patient Profile

Demographics:

68-year-old male, retired construction worker

History:

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

• Current medications: Metformin, Lisinopril, Atorvastatin, Warfarin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of right-sided weakness and slurred speech

• Key symptoms: Hemiparesis on the right side, aphasia, severe headache, dizziness, altered level of consciousness

• Vital signs: Blood pressure 210/110 mmHg, heart rate 130 bpm (irregular), respiratory rate 24 breaths per minute, temperature 37.8°C, oxygen saturation 88% on room air

Section 1

Initial Assessment Findings:

Upon arrival at the emergency department, the patient was immediately assessed by the stroke team. A focused neurological examination revealed a Glasgow Coma Scale (GCS) score of 9, indicating a moderate level of impaired consciousness. The right-sided hemiparesis was confirmed, with an inability to lift the right arm or leg against gravity, and expressive aphasia was evident, with the patient struggling to find words and form coherent speech. The pupils were equal and reactive to light, but the right-sided facial droop was pronounced. Auscultation of the chest revealed irregular heart sounds consistent with atrial fibrillation, and crackles were noted bilaterally at the lung bases, suggesting potential pulmonary congestion.

Given the critical nature of the presentation, immediate imaging studies were prioritized. A non-contrast CT scan of the head was obtained, revealing a dense middle cerebral artery (MCA) sign, indicative of a large vessel occlusion. This finding, coupled with the elevated blood pressure and irregular heart rate, highlighted a high-risk scenario for both intracerebral hemorrhage and further thromboembolic events. Initial laboratory results showed an INR of 1.3, suggesting subtherapeutic anticoagulation levels, while blood glucose was elevated at 250 mg/dL, complicating the metabolic picture. The patient's oxygen saturation further declined to 85% despite supplemental oxygen, necessitating consideration of advanced airway management.

These findings underscore the critical need for swift intervention, with the stroke team's consideration of thrombolytic therapy tempered by the elevated risk of hemorrhagic transformation given the hypertensive crisis and recent INR results. The team is prompted to deliberate on the urgency of mechanical thrombectomy and aggressive blood pressure management strategies, recognizing the delicate balance required to mitigate ischemic damage while preventing catastrophic bleeding.

Section 2

After deliberating on the potential interventions, the decision was made to proceed with mechanical thrombectomy due to the high risk of hemorrhagic conversion with thrombolytic therapy. The interventional radiology team was alerted, and the patient was quickly prepped for the procedure. Despite aggressive oxygen therapy, the patient's oxygen saturation continued to fluctuate between 82% and 88%, prompting the anesthesia team to secure the airway through endotracheal intubation to ensure adequate ventilation and oxygenation during the procedure. The blood pressure remained precariously high at 210/110 mmHg, necessitating the initiation of an intravenous labetalol infusion to achieve controlled reduction of blood pressure without compromising cerebral perfusion.

During the thrombectomy, the interventional team successfully removed a large clot from the middle cerebral artery, restoring partial blood flow to the affected region. However, post-procedure imaging revealed a new complication: a small area of hemorrhagic transformation had developed at the core of the ischemic region. This bleed, while concerning, was not large enough to cause immediate neurological deterioration, but it necessitated an even more cautious approach to blood pressure management and anticoagulation therapy moving forward. The neurology team was tasked with balancing the complexities of preventing further clot formation due to the underlying atrial fibrillation, while closely monitoring for signs of increased intracranial pressure or expanding hemorrhage.

Post-procedural monitoring showed a slight improvement in the patient's neurological status; the GCS score increased to 10 with the patient exhibiting some regained movement in the right leg. However, expressive aphasia persisted, and the facial droop showed minimal improvement. Vital signs remained a critical focus, with blood pressure stabilizing to 170/95 mmHg under careful titration of antihypertensive medications. The patient’s glucose level was managed with an insulin drip, aiming to maintain levels within a target range to optimize neurological recovery. This phase of care demanded vigilant assessment for signs of further complications, including cerebral edema and re-occlusion, as the team developed a comprehensive plan for ongoing management and rehabilitation.

Section 3

As the critical care team continued to monitor the patient in the ICU, a new complication emerged: signs of cerebral edema. This was evidenced by a sudden increase in intracranial pressure (ICP), with readings escalating from 15 mmHg to 25 mmHg within a span of two hours. The patient began to exhibit a decreased level of consciousness, with the GCS score dropping back to 8. Anisocoria was noted, with the left pupil becoming slightly dilated and sluggish to respond to light, indicating potential pressure effects on the cranial nerves. Vital signs showed a concerning trend with bradycardia developing, heart rate dropping to 52 bpm, and blood pressure fluctuating unpredictably, suggesting the onset of Cushing's triad.

In response to these alarming developments, the neurosurgical team was consulted for the potential necessity of a decompressive craniectomy to relieve pressure and prevent further brain injury. Meanwhile, osmotic therapy with mannitol was initiated to aggressively manage cerebral edema, and the patient was placed in a semi-Fowler position to facilitate venous drainage. Serial imaging and continuous neurological assessments were scheduled to closely monitor progression. The team was tasked with the delicate balance of managing the patient's anticoagulation therapy to prevent further thrombotic events while mitigating the risk of exacerbating the hemorrhagic transformation.

Amidst these developments, the patient's lab values revealed metabolic derangements, with serum sodium dropping to 128 mmol/L and serum osmolality decreasing, pointing towards possible syndrome of inappropriate antidiuretic hormone secretion (SIADH) secondary to neurological insult. Fluid restriction and careful electrolyte management were implemented to address this issue, closely monitored by the nephrology team. This multifaceted situation required the healthcare team to exercise advanced clinical judgment, integrating complex clinical data to prioritize interventions that would stabilize the patient while preparing for potential surgical intervention.

Section 4

As the critical care team continued to monitor the patient, a change in status was observed, necessitating immediate reassessment of the treatment plan. Despite the initiation of osmotic therapy with mannitol, the patient's intracranial pressure remained elevated, fluctuating between 22 mmHg and 28 mmHg, indicating that the cerebral edema was not responding adequately to medical management. Furthermore, the patient's level of consciousness deteriorated further, with the Glasgow Coma Scale (GCS) score dropping to 6, as they became unresponsive to verbal stimuli and only exhibited a localized response to pain. The anisocoria persisted, with the left pupil now fully dilated and non-reactive, suggesting increased pressure on the oculomotor nerve.

Concurrent with these neurological changes, the patient's cardiovascular status became increasingly unstable. Cushing's triad was fully manifest, with the heart rate decreasing further to 48 bpm and blood pressure readings showing a widening pulse pressure, with systolic values peaking at 180 mmHg and diastolic values dropping to 60 mmHg. The respiratory pattern shifted to irregular Cheyne-Stokes respirations, complicating the patient's ventilatory support needs and raising concerns about impending brainstem herniation.

The urgent nature of the patient's deteriorating condition prompted the neurosurgical team to expedite the decision for decompressive craniectomy to alleviate intracranial pressure. Simultaneously, the critical care team was tasked with fine-tuning the delicate balance of anticoagulation therapy. Given the significant risk of hemorrhagic transformation, a temporary pause in anticoagulation was considered, with close monitoring for any thrombotic complications. This complex scenario demanded precise coordination among the multidisciplinary team, emphasizing the critical importance of rapid decision-making and clinical reasoning to navigate the patient's evolving needs and stabilize their precarious status.

Section 5

As the critical care team proceeded with the decompressive craniectomy, new diagnostic results emerged, adding another layer of complexity to the patient's condition. A repeat CT scan of the brain revealed an increase in midline shift to 12 mm, confirming significant mass effect despite surgical intervention. Laboratory results indicated a marked derangement in coagulation parameters, with an international normalized ratio (INR) elevated at 1.8 and a partial thromboplastin time (PTT) extending to 65 seconds, suggesting a heightened risk of bleeding complications. Concurrently, serum sodium levels were critically low at 126 mEq/L, raising concerns about potential hyponatremia-induced cerebral edema.

The patient's neurological and hemodynamic status further deteriorated post-operatively. Despite aggressive management, the GCS score dropped to 4, with the patient exhibiting decerebrate posturing in response to noxious stimuli, indicative of severe brain injury. The cardiovascular instability persisted as the heart rate fluctuated between 42-50 bpm, and systolic blood pressure soared to 190 mmHg, with diastolic pressure remaining at 58 mmHg. The nursing team noted a progressive decline in urine output to 15 mL/hr, signaling possible acute kidney injury secondary to compromised perfusion and the effects of mannitol.

In response to these developments, the multidisciplinary team was faced with critical decisions regarding the management of the patient's evolving complications. The priority was to address the electrolyte imbalance and optimize intracranial pressure management while minimizing the risk of hemorrhagic transformation. Discussions regarding the potential initiation of hypertonic saline therapy to correct hyponatremia were underway, alongside considerations for temporary renal support if oliguria persisted. The team recognized the urgency of recalibrating the treatment strategy to stabilize the patient's condition and prevent further neurological decline, underscoring the necessity for vigilant monitoring and swift, evidence-based interventions.