Ischemic stroke - Nursing Case Study
Pathophysiology
• Primary mechanism: Ischemic stroke primarily occurs due to blockages or clots (ischemia) in arteries supplying the brain. This reduces or stops blood flow, depriving brain cells of oxygen and nutrients, leading to cell death. This is often due to atherosclerosis, a condition where fatty deposits build up on the inner walls of the arteries.
• Secondary mechanism: A secondary trigger is embolism, where a clot forms elsewhere in the body, travels and lodges in brain arteries. This can be due to conditions such as atrial fibrillation, which cause abnormal blood clot formation.
• Key complication: Post-stroke complications include cerebral edema, where swelling from excess fluid causes increased intracranial pressure, potentially leading to further brain damage.
Patient Profile
Demographics:
67 years old, male, retired construction worker
History:
• Key past medical history: Hypertension, type II diabetes, smoker
• Current medications: Metformin, Lisinopril, Nicotine patches
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Sudden onset of weakness on the right side of the body, difficulty speaking
• Key symptoms: Right-sided weakness, slurred speech, confusion, difficulty swallowing, dizziness
• Vital signs: Blood pressure 165/95 mmHg, pulse 100 bpm, respiratory rate 22 breaths per minute, oxygen saturation 92% on room air, temperature 37.2°C (98.96°F)
Section 1
Change in Patient Status:
Within 24 hours of admission, the patient's condition worsened. His right-sided weakness progressed to a complete inability to move his right arm and leg. His speech became more slurred and unintelligible, and he was unable to follow simple commands. His level of consciousness declined, and he became lethargic and less responsive. His vital signs were as follows: blood pressure 175/100 mmHg, pulse 110 bpm, respiratory rate 28 breaths per minute, and oxygen saturation dropped to 88% on room air.
New Complications:
Neurological examination and repeat imaging revealed cerebral edema, a feared complication of ischemic stroke. The cerebral edema was causing increased intracranial pressure, leading to further neurological deterioration. In addition, the patient developed difficulty in swallowing, with a high risk of aspiration. He also developed new-onset atrial fibrillation (irregular and rapid heart rate), which was confirmed on a 12-lead ECG. This likely exacerbated the cerebral ischemia, as the atrial fibrillation could have led to the formation of more clots. The patient's worsening neurological status and new complications highlighted the need for aggressive medical management and close monitoring.
Section 2
New Diagnostic Results:
The healthcare team carried out an urgent repeat CT scan in light of the patient's declining status. The scan showed a significant increase in cerebral edema and the ischemic area had extended. His lab results returned with an elevated D-dimer at 1.5 mg/L (normal range is less than 0.5 mg/L) and an elevated troponin I level at 1.4 ng/mL (normal range is 0.00-0.03 ng/mL), indicating possible clot formation and cardiac damage respectively. His white blood cell count was also elevated at 15,000 cells/mcL, suggesting a possible infection.
Change in Patient Status:
The patient's condition continued to deteriorate. He became non-responsive, his blood pressure rose to 185/110 mmHg, and his oxygen saturation dropped further to 82% despite supplemental oxygen. His pulse became irregular with episodes of rapid beats, reflecting his new-onset atrial fibrillation. The patient also developed a fever of 38.5°C, raising concerns of a possible infection. His respiratory rate increased to 32 breaths per minute and his breathing became labored, suggesting possible aspiration or pneumonia. The team recognized the escalating situation and decided to intubate the patient to secure his airway and provide mechanical ventilation.
These new findings underscored the urgency to address the cerebral edema and possible infection while managing his atrial fibrillation and elevated blood pressure. The complexity of his condition required careful clinical reasoning to prioritize interventions and treatments. His case also highlighted the need for vigilance in monitoring the progression of stroke and its complications.
Section 3
New Complications:
Despite the ongoing interventions, the patient's condition continued to worsen. His Glasgow Coma Scale (GCS) deteriorated from 11 to 7, indicating a significant decrease in his level of consciousness. His blood pressure remained in hypertensive crisis levels and his atrial fibrillation became resistant to rate control with medications. Furthermore, his temperature continued to rise to 39.1°C, despite antipyretic medications, suggesting that the possible infection was not yet under control.
Laboratory results also indicated further complications. His D-dimer increased to 2.0 mg/L, suggesting an ongoing clot formation or thrombotic activity. His troponin I level also increased to 2.0 ng/mL, indicating ongoing cardiac damage or myocardial infarction. His white blood cell count continued to rise to 20,000 cells/mcL, further supporting the suspicion of infection. The patient's arterial blood gas (ABG) showed severe hypoxemia with a PaO2 of 54 mmHg and hypercapnia with a PaCO2 of 55 mmHg, indicating respiratory failure.
These new developments highlighted the need for immediate reassessment of the current interventions and consideration of more aggressive strategies to manage his condition. The team might need to consider thrombolytic therapy for the possible clot and broader-spectrum antibiotics for the suspected infection. They may also need to intensify his cardiovascular support, given the ongoing cardiac damage and uncontrolled hypertension. The drastic change in his condition emphasized the importance of constant monitoring and rapid response to prevent further deterioration.
Section 4
Change in Patient Status:
Despite the aggressive interventions, the patient's condition did not seem to stabilize. His GCS further dropped to 5, and his blood pressure spiked to 220/120 mmHg. His heart rate also became irregular, fluctuating between 110 and 160 beats per minute. His oxygen saturation levels continued to drop, reaching a low of 84% on room air.
The patient's respiratory status also took a turn for the worse. He became increasingly dyspneic, with a respiratory rate of 30 breaths per minute, and his use of accessory muscles became more pronounced. His ABG results further deteriorated, with a PaO2 of 48 mmHg and a PaCO2 of 60 mmHg. Clinically, the patient appeared pale, diaphoretic, and lethargic. His pupils were dilated and slow to react to light, suggesting an increase in intracranial pressure. These developments signaled a critical turn in the patient's condition, necessitating a rapid response and a potential reconsideration of the plan of care.
Section 5
New Diagnostic Results:
The neurologist ordered an emergency CT scan to evaluate the extent of the patient’s ischemic stroke, particularly given the signs of increased intracranial pressure. The scan showed that the patient had developed cerebral edema, a dangerous complication where fluid accumulates in the brain resulting in increased pressure. This finding was consistent with his symptoms of deteriorating consciousness, high blood pressure, and irregular heart rate.
In light of these findings, the medical team also ordered a complete blood count and coagulation profile. The lab results showed a significant increase in the patient's white blood cell count, indicating a possible infection. His platelet count was also elevated, suggestive of hypercoagulability. The PT and INR values were elevated, indicating a prolonged clotting time. These results prompted the need for immediate intervention and further investigation to manage the cerebral edema, potential infection, and the patient's hypercoagulable state. The medical team was also alerted to closely monitor the patient for signs of a possible hemorrhagic transformation of the ischemic stroke, given his elevated blood pressure and coagulation abnormalities.