stroke - Nursing Case Study
Pathophysiology
• Primary mechanism: Ischemic stroke occurs when a blood clot obstructs a cerebral artery, leading to reduced blood flow and oxygen supply to brain tissue, resulting in cell death and loss of neurological function.
• Secondary mechanism: Hemorrhagic stroke is caused by the rupture of a blood vessel in the brain, leading to bleeding and increased intracranial pressure, which damages brain cells and disrupts normal brain activity.
• Key complication: Both types of stroke can lead to significant neurological deficits, such as paralysis, speech difficulties, and cognitive impairments, due to the loss of brain function in the affected areas. Prompt medical intervention is crucial to minimize damage and improve recovery outcomes.
Patient Profile
Demographics:
62-year-old male, retired construction worker
History:
• Key past medical history: Hypertension, Type 2 Diabetes, Hyperlipidemia
• Current medications: Lisinopril, Metformin, Atorvastatin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Sudden onset of weakness on the right side of the body
• Key symptoms: Slurred speech, difficulty walking, facial droop on the right side, headache, mild confusion
• Vital signs: Blood pressure 185/110 mmHg, heart rate 92 bpm, respiratory rate 18 breaths per minute, temperature 98.6°F, oxygen saturation 92% on room air
Section 1
As the healthcare team proceeds with the initial assessment, further examination reveals that the patient's neurological status is deteriorating. The Glasgow Coma Scale (GCS) score has decreased to 12, indicating a decrease in his level of consciousness, and there is an increase in the severity of his right-sided weakness. The patient is now unable to lift his right arm or leg against gravity, and his speech has become more garbled. Repeat vital signs show a blood pressure of 190/115 mmHg, heart rate of 98 bpm, and oxygen saturation has dropped to 89% on room air, indicating a potential compromise in his respiratory status.
A CT scan of the brain is promptly performed to differentiate between ischemic and hemorrhagic stroke. The results confirm an acute ischemic stroke in the left middle cerebral artery territory, with no evidence of hemorrhage. However, the imaging also reveals a concerning sign of cerebral edema, which is likely contributing to the patient's worsening neurological status. This edema could lead to increased intracranial pressure, necessitating immediate intervention to prevent further brain tissue damage.
Based on these findings, the medical team decides to initiate treatment with intravenous tissue plasminogen activator (tPA) to dissolve the clot, given that the patient is within the therapeutic window for thrombolysis. Concurrently, measures to manage his hypertension aggressively are initiated, including an intravenous infusion of labetalol to reduce the risk of further vascular injury. The patient's oxygen saturation is addressed by administering supplemental oxygen via nasal cannula to maintain adequate cerebral perfusion. Close monitoring is required to watch for any signs of improvement or potential complications, such as hemorrhagic transformation or worsening edema, as the patient's journey through stroke recovery continues.
Section 2
As the medical team continues to monitor the patient closely, several hours after the administration of intravenous tissue plasminogen activator (tPA) and antihypertensive therapy, a change in the patient’s status becomes evident. The patient begins to exhibit signs of increased restlessness and agitation, which could indicate a change in intracranial pressure or further neurological compromise. Despite the supplemental oxygen, his oxygen saturation fluctuates between 88% and 91%, and his respiratory rate has increased to 24 breaths per minute, suggesting possible respiratory distress or the need for advanced airway management.
During the reassessment, his GCS score has further declined to 10, raising concerns about potential cerebral herniation due to increasing cerebral edema. The patient's blood pressure remains elevated at 185/110 mmHg, despite the labetalol infusion, indicating a potential need for titration or additional antihypertensive agents. Urgent repeat imaging is considered to evaluate the progression of cerebral edema and to rule out any hemorrhagic transformation, which would necessitate a change in management strategy.
In addition to the neurological changes, laboratory results return showing an elevated white blood cell count, suggesting the potential onset of an infection, possibly pneumonia, given the patient's decreased respiratory effort and compromised state. This new development requires prompt initiation of broad-spectrum antibiotics and consideration of respiratory support, potentially necessitating mechanical ventilation. The healthcare team must now balance the management of the acute ischemic stroke with the emerging complications, ensuring a comprehensive approach to stabilize the patient and prevent further deterioration.
Section 3
As the healthcare team works diligently to manage the patient's complex condition, the decision is made to proceed with urgent repeat imaging, including a CT scan of the head. The imaging reveals an increase in cerebral edema with a midline shift, indicating significant intracranial pressure. Fortunately, there is no evidence of hemorrhagic transformation at this point. Given these findings, the medical team decides to initiate osmotic therapy with mannitol to attempt to reduce intracranial pressure and prevent further neurological decline. Alongside this, the team discusses the potential benefits and risks of initiating hypertonic saline therapy as an adjunctive measure.
In light of the patient's respiratory status, the healthcare team decides to intubate the patient to secure the airway and ensure adequate ventilation. This decision is further supported by the continued fluctuation in oxygen saturation and the growing concern for aspiration pneumonia, as evidenced by the patient's lab results and decreased respiratory effort. Broad-spectrum antibiotics, including vancomycin and piperacillin-tazobactam, are started promptly to address the suspected infection, and blood cultures are obtained to guide further antibiotic therapy based on sensitivity results.
As the team continues to monitor the patient, they adjust the labetalol infusion to better control his blood pressure, while closely monitoring for any adverse effects. The elevated blood pressure is a significant concern, as it can exacerbate cerebral edema and increase the risk of further neurological compromise. The medical team remains vigilant, balancing the management of the acute stroke with the emerging complications, recognizing that each decision has a critical impact on the patient's outcomes. The next steps include continuous monitoring in the intensive care unit, with a focus on maintaining neurological stability and preventing further complications.
Section 4
As the patient is transferred to the intensive care unit (ICU), the healthcare team conducts an initial assessment to establish a baseline for ongoing monitoring. Upon arrival, the patient remains intubated and on mechanical ventilation. Vital signs reveal a blood pressure of 160/95 mmHg, a heart rate of 92 beats per minute, a respiratory rate of 16 breaths per minute on ventilatory support, and an oxygen saturation of 94% on 40% FiO2. Neurological assessment shows a Glasgow Coma Scale (GCS) score of 6, with the patient exhibiting no verbal response, withdrawal to painful stimuli, and eye-opening to pain. Pupils are equal but sluggishly reactive to light, suggesting ongoing intracranial pressure concerns. The patient's temperature is slightly elevated at 38.2°C, consistent with the suspicion of infection.
Laboratory results return, revealing a white blood cell count of 15,000/mm³, indicating a possible infectious process, which aligns with the clinical picture of suspected aspiration pneumonia. Blood cultures are pending, but preliminary results show gram-positive cocci, potentially guiding further antibiotic adjustments. Electrolytes are monitored carefully due to the administration of hypertonic saline, showing sodium levels at the upper limit of normal at 146 mmol/L, necessitating meticulous balance to prevent hypernatremia.
Despite the ongoing interventions, the patient exhibits a new complication with the development of mild acute kidney injury, as evidenced by an increase in serum creatinine from 1.0 mg/dL to 1.5 mg/dL. This change prompts the team to reassess fluid management and medication dosing, particularly regarding nephrotoxic agents. The multidisciplinary team remains focused on optimizing renal function while continuing to address the critical aspects of cerebral edema and potential infection. Careful titration of medications, ongoing assessment for signs of cerebral herniation, and regular communication among healthcare providers become paramount as the patient’s condition remains precarious.
Section 5
As the healthcare team continues to monitor the patient in the ICU, they observe a change in the patient's status that necessitates immediate attention. Over the next 12 hours, the patient's blood pressure rises to 175/100 mmHg, and the heart rate increases to 105 beats per minute. The oxygen saturation remains stable at 94% on 40% FiO2, but the patient's respiratory rate increases to 20 breaths per minute, indicating possible respiratory distress or increased metabolic demand. The GCS remains at 6, with no improvement in the patient's neurological status. The pupils remain equal but continue to react sluggishly to light, raising concerns about worsening intracranial pressure.
New laboratory results reveal a further increase in serum creatinine to 1.8 mg/dL, confirming a progression of the acute kidney injury. Additionally, blood cultures return positive for Streptococcus pneumoniae, corroborating the suspicion of aspiration pneumonia. The team promptly adjusts the antibiotic regimen to target this pathogen effectively. Electrolyte re-evaluation shows a sodium level of 148 mmol/L, suggesting a need for careful recalibration of fluid therapy to avoid further complications from hypernatremia.
In response to these developments, the multidisciplinary team convenes to reassess the management plan. They decide to initiate a cautious reduction in fluid rates and review all nephrotoxic medications to minimize renal strain. The team also considers the introduction of a diuretic to manage fluid overload, balancing the risk of further kidney injury. Continuous monitoring of intracranial pressure is prioritized, and the team maintains close communication to detect any signs of cerebral herniation. As the patient's condition evolves, the team remains vigilant, prepared to adapt their approach as the situation demands.