Stroke - Nursing Case Study
Pathophysiology
• Primary mechanism: Ischemic Stroke - This is the most common type of stroke, occurring when a blood vessel supplying blood to the brain is obstructed. It's often caused by the formation of a thrombus or embolus. The blockage deprives a part of the brain of oxygen and nutrients, causing neuronal cells to die, impairing the functions controlled by the affected area.
• Secondary mechanism: Hemorrhagic Stroke - This occurs when a weakened blood vessel ruptures and bleeds into the surrounding brain tissue. The blood accumulates and compresses the surrounding brain tissue. The two types of hemorrhagic strokes are intracerebral (within the brain) and subarachnoid (between the brain and the membranes covering it).
• Key complication: Brain Edema - Following a stroke, inflammation and fluid build-up can cause brain edema. This increases intracranial pressure, potentially leading to brain injury, herniation, and death. Management of edema is crucial in the acute phase of stroke treatment.
Patient Profile
Demographics:
68 years old, Male, Retired Construction Worker
History:
• Key past medical history: Hypertension, Type 2 Diabetes, Smoking for 30 years until 5 years ago
• Current medications: Lisinopril, Metformin, Aspirin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Sudden weakness on the right side of the body, difficulty speaking
• Key symptoms: Right-sided weakness, slurred speech, trouble walking, headache, dizziness, loss of balance and coordination
• Vital signs: Blood Pressure 170/95 mmHg, Pulse 88 bpm, Respiratory rate 20 breaths per minute, Temperature 98.6 F, Oxygen saturation 94% on room air
Section 1
Change in Patient Status:
In the following hours, the patient's condition began to deteriorate. His blood pressure spiked to 180/105 mmHg, pulse increased to 95 bpm, and his respiratory rate raised to 24 breaths per minute. His oxygen saturation fell to 90% on room air. This deterioration was accompanied by an increase in his right-sided weakness, now unable to move his right arm and leg at all. His speech became more slurred and he was increasingly disoriented.
On neurological reevaluation, his Glasgow Coma Scale (GCS) score was 12, decreased from initial 15, with a decrease in motor response and verbal output. His pupils were unequal and sluggish to respond to light, indicating increased intracranial pressure. Sensory examination revealed a loss of sensation on the right side of the body. This sudden change in status indicated that the patient might be experiencing a secondary hemorrhagic stroke or increasing brain edema, significantly increasing the risk of severe brain injury or herniation. Immediate intervention was necessary to prevent further neurological damage.
Section 2
New Diagnostic Results:
The patient was immediately sent for a repeat CT scan which revealed an expanding hemorrhagic area in the left cerebral hemisphere, confirming the suspicion of a secondary hemorrhagic stroke. The lab results showed a significant increase in his prothrombin time (PT) to 21 seconds and international normalized ratio (INR) to 2.3, both indicating a possible coagulation disorder and increased risk of bleeding. His platelets were low at 90,000 per microliter, further compounding the risk.
The patient's blood electrolytes were also out of balance with a potassium level of 3.2 mEq/L, sodium at 152 mEq/L and calcium at 8.0 mg/dL, all contributing to the patient's neurological status and potentially influencing his blood pressure. His blood glucose was high at 190 mg/dL, which may have contributed to the stroke and could further exacerbate the brain injury. The patient's renal function was also impaired with a creatinine level of 1.8 mg/dL and blood urea nitrogen (BUN) of 28 mg/dL, indicating potential dehydration, a condition that could have been aggravated by his high sodium levels.
These new findings provided a clear understanding of the patient’s deteriorating condition and the need for immediate, targeted interventions. The medical team needed to address his coagulation disorder, electrolyte imbalance, high blood pressure, and impaired renal function to prevent further neurological damage and potential systemic complications. This would require careful monitoring and clinical reasoning to balance the need for aggressive treatment with the risk of exacerbating the patient's coagulopathy and hemorrhagic stroke.
Section 3
Change in Patient Status:
Over the next few hours, the patient's neurological status worsened. He became increasingly disoriented and lethargic, and his left-sided weakness progressed to complete paralysis. His speech became slurred and he was unable to follow simple commands, suggesting that the hemorrhagic stroke was expanding and affecting more regions of his brain. His blood pressure also continued to rise, reaching 185/95 mmHg, despite administration of antihypertensive medication.
When re-assessed, his Glasgow Coma Scale (GCS) score had dropped to 9 (E2V2M5), indicating a severe decrease in his level of consciousness. His pulse was slightly tachycardic at 102 beats per minute, potentially indicating a compensatory response to his elevated blood pressure and decreased cerebral perfusion. His respiratory rate was 22 breaths per minute, and his oxygen saturation was 94% on room air. His urinary output had also decreased to less than 30 mL per hour, potentially indicating worsening renal function or dehydration.
These developments indicated a rapid progression of the patient's condition, necessitating immediate re-evaluation of the current treatment plan and consideration of more aggressive interventions. This could include measures to control his intracranial pressure, manage his coagulopathy, correct his electrolyte imbalance, and ensure adequate hydration and renal function. The team would need to use clinical reasoning to balance the potential benefits and risks of these interventions, considering the patient's complex medical situation and the potential for further complications.
Section 4
New Diagnostic Results:
The patient's blood work revealed a significant elevation in his potassium levels at 6.2 mEq/L, implying hyperkalemia. His BUN and creatinine levels were also increased at 30 mg/dL and 2.1 mg/dL, respectively, indicating a worsening renal function. An urgent CT scan of his head was ordered which confirmed an increased size of the hemorrhage and localized brain edema. The radiologist also noted a midline shift, raising concerns about increased intracranial pressure and potential herniation.
These new diagnostic results were alarming, pointing towards a rapid deterioration of the patient's condition. The hyperkalemia posed a risk of severe cardiac dysrhythmias, while the increased BUN and creatinine levels suggested acute kidney injury, possibly secondary to dehydration or hypoperfusion. The findings on the CT scan were indicative of a significant increase in intracranial pressure which could lead to life-threatening brain herniation if not managed promptly.
The medical team needed to act swiftly to address these issues. The correction of the patient's hyperkalemia, measures to improve renal function, and management of his increased intracranial pressure became the immediate priorities. They also had to keep in mind the connectedness of these issues - the need to hydrate the patient for renal protection, for instance, could worsen cerebral edema, adding another layer of complexity to the clinical decision-making process.
Section 5
Change in Patient Status:
Over the next few hours, the patient's condition further deteriorated. His pulse became irregular, and his heart rate fluctuated between 50 and 110 beats per minute, likely due to the hyperkalemia. His blood pressure also escalated to 170/95 mmHg. Furthermore, he was becoming increasingly lethargic and confused, and his pupils were noted to be uneven, with the left pupil slightly larger than the right, a sign of potential uncal herniation due to the increased intracranial pressure.
Simultaneously, the patient's renal function continued to decline, as evidenced by decreased urine output (less than 30 mL/hr) and a further increase in his BUN and creatinine levels to 36 mg/dL and 2.5 mg/dL, respectively. He also complained of muscle weakness and numbness, likely secondary to his elevated potassium levels and potential nerve compression due to the increased intracranial pressure. These changes indicated a pressing need for immediate interventions to manage his hyperkalemia, acute kidney injury, and increased intracranial pressure to prevent further complications.