Ischemic stroke - Nursing Case Study

Pathophysiology

• Primary mechanism: Ischemic stroke occurs when a blood clot obstructs a blood vessel supplying the brain, leading to a lack of blood supply which deprives brain tissue of oxygen and nutrients. This can be due to a thrombotic stroke (clot forms directly in an artery) or an embolic stroke (clot forms elsewhere and travels to the brain).

• Secondary mechanism: The lack of blood flow leads to an energy failure, causing ion pump dysfunction. This results in a build-up of glutamate causing excitotoxicity, and an influx of calcium ions, damaging cells and leading to cell death.

• Key complication: The area of the brain affected by the stroke can lead to different complications. For example, if the stroke occurs in the left side of the brain, this could result in paralysis on the right side of the body, speech/language problems, or slow, cautious behavior.

Patient Profile

Demographics:

67-year-old male, retired accountant

History:

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

• Current medications: Metformin, atorvastatin, lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden weakness on right side of body, difficulty in speaking

• Key symptoms: Right-sided weakness, slurred speech, drooping of right side of face, confusion, dizziness

• Vital signs: Blood pressure 170/95 mmHg, pulse 90 bpm, respiratory rate 18 breaths per minute, temperature 98.6 F, oxygen saturation 94% on room air

Section 1

New Diagnostic Results:

After an initial physical examination and assessment, the patient was immediately sent for a CT scan to confirm the diagnosis of an ischemic stroke. The results demonstrated a clear area of low attenuation in the left middle cerebral artery territory, confirming an ischemic stroke. Concurrently, blood tests were done which revealed a slightly elevated blood glucose level of 210 mg/dL, indicating poor control of his type 2 diabetes. His lipid profile was also abnormal with high total cholesterol at 240 mg/dL and LDL at 160 mg/dL, further suggesting that his hyperlipidemia was not optimally managed. His renal function was normal with a creatinine level of 0.9 mg/dL.

Change in Patient Status:

Overnight, the patient's right-sided weakness seemed to intensify, and he was now unable to move his right arm and leg completely. His speech became more slurred and incomprehensible. His Glasgow Coma Scale score dropped from 15 to 13. His blood pressure also increased to 180/110 mmHg, and his pulse rate escalated to 100 bpm. His oxygen saturation dropped slightly to 92% on room air. These changes signal a worsening of his stroke and potential expansion of the infarct area. His elevated blood pressure might reflect a physiological response to maintain cerebral perfusion, but it also poses a risk of transforming the ischemic stroke into a hemorrhagic one. His elevated pulse could be a response to stress or could indicate an undiagnosed cardiac issue, which is common in stroke patients.

Section 2

New Complications:

By the following morning, the patient began showing signs of acute confusion and restlessness. His Glasgow Coma Scale score had further decreased to 10, indicating a significant decline in his neurological status. In addition, he was now complaining of severe headache and nausea. His blood pressure had continued to rise and was now recorded at 200/120 mmHg, and the pulse rate had also increased to 110 bpm. His oxygen saturation had further decreased to 90%, despite receiving supplemental oxygen via nasal cannula at 2L/min. His blood glucose remained elevated at 220 mg/dL.

These new developments suggested a possible transformation of the ischemic stroke into a hemorrhagic one, a potentially life-threatening complication. The severe headache and nausea could be indicative of increased intracranial pressure, a common occurrence in hemorrhagic strokes. The persistent hypertension, despite antihypertensive therapy, could be due to the body's attempt to maintain cerebral perfusion, but it also increases the risk of further cerebral bleeding. The elevated pulse rate could be a response to the body's increased demand for oxygen due to the reduced cerebral perfusion. The ongoing hyperglycemia could be worsening the patient's neurological status, as high blood glucose levels have been associated with poorer outcomes in stroke patients.

Section 3

New Diagnostic Results:

In an effort to verify the suspicion of a hemorrhagic transformation, the medical team ordered an urgent CT scan which revealed a large intracranial hemorrhage in the right hemisphere. This finding was consistent with the patient's symptoms and explained the significant decline in his neurological status. The CT scan also showed signs of cerebral edema, a common complication following a hemorrhagic stroke, which can further increase intracranial pressure and worsen neurological outcomes.

This new diagnosis necessitated a change in the treatment plan. Anticoagulant therapy, which had been initiated to treat the initial ischemic stroke, was immediately discontinued to prevent further bleeding. The team also started the patient on an osmotic diuretic, mannitol, to help reduce cerebral edema and intracranial pressure. The patient's blood pressure and blood glucose levels were closely monitored, as both needed to be controlled meticulously to prevent further deterioration. The patient's family was informed about the new diagnosis and the changes in the treatment plan. The gravity of the situation was explained to them, including the increased risk of significant disability or death due to the hemorrhagic stroke.

Section 4

Change in Patient Status:

Over the next 24 hours, the patient's neurological status continued to deteriorate. He became less responsive, with a Glasgow Coma Score decreasing to 7 from 12 and his pupils became unequal and sluggish to light, indicating increasing intracranial pressure. Hypertension persisted despite antihypertensive therapy, with blood pressure readings consistently above 160/90 mmHg. His blood glucose levels were also elevated, ranging from 180 to 210 mg/dL, despite insulin therapy.

The patient's respiratory status also worsened. He became increasingly dyspneic with an oxygen saturation dropping to 88% on room air, and his respiratory rate increased to 24 breaths per minute. Auscultation of the lungs revealed bibasilar crackles, suggesting the possible development of pulmonary edema. His heart rate was also elevated at 110 beats per minute, and his rhythm was irregular, raising suspicion of atrial fibrillation, a common complication of acute stroke. These changes indicated a rapid decline in the patient's condition, necessitating further intervention and reassessment of the treatment plan.

Section 5

New Diagnostic Results:

An urgent non-contrast CT scan of the brain was performed, revealing a large left-sided middle cerebral artery (MCA) infarct, with signs of early cerebral edema and mass effect. The infarct size indicated that the patient was no longer a candidate for thrombolytic therapy. A 12-lead EKG also confirmed the suspicion of atrial fibrillation, with no signs of acute myocardial ischemia. Blood tests showed a high D-dimer level of 900 ng/mL (Normal < 500 ng/mL), suggesting the presence of a clot formation. His serum creatinine was also elevated at 1.5 mg/dL (Normal 0.6-1.2 mg/dL) indicating a possible impairment of his renal function.

The arterial blood gas (ABG) showed a pH of 7.29, PaCO2 of 50 mmHg, PaO2 of 60 mmHg and HCO3 of 24 mEq/L, suggestive of respiratory acidosis. The worsening respiratory status, combined with the ABG result, indicated that the patient might be retaining carbon dioxide due to hypoventilation, causing the acidosis. These new diagnostic results are concerning and require immediate action to prevent further deterioration of the patient's condition. Critical thinking and timely interventions are now necessary to manage these complications.