stroke - Nursing Case Study
Pathophysiology
• Primary mechanism: Reduced Blood Flow - Stroke occurs when blood supply to the brain is disrupted. This is mainly due to either a blockage (ischemic stroke) or rupture (hemorrhagic stroke) of a blood vessel. The affected brain tissue is deprived of oxygen and nutrients, causing neuronal death.
• Secondary mechanism: Excitotoxicity - Following the primary injury, excessive release of glutamate, a neurotransmitter, leads to overactivation of its receptors on neurons. This triggers an influx of calcium into cells, initiating processes that damage cell structures and lead to cell death.
• Key complication: Brain Edema - Post-stroke, the brain often swells due to the accumulation of fluids, causing intracranial pressure to rise. This can lead to further neuronal damage, functional losses and could be life-threatening.
Patient Profile
Demographics:
62-year-old male, retired construction worker
History:
• Key past medical history: Hypertension, type II diabetes, smoker for 40 years
• Current medications: Lisinopril for hypertension, Metformin for diabetes, nicotine patch for smoking cessation
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Sudden slurred speech, weakness on left side of body
• Key symptoms: Difficulty speaking and understanding, paralysis or numbness of the face, arm or leg, particularly on one side of the body, blurred or blackened vision in one or both eyes, sudden severe headache, trouble walking, dizziness, loss of balance or coordination
• Vital signs: Blood pressure 172/98 mmHg, pulse 110 bpm, respiratory rate 22 breaths per minute, oxygen saturation 92% on room air, temperature 98.7 degrees Fahrenheit
Section 1
New Diagnostic Results:
The CT scan of the brain revealed an occlusion in the right middle cerebral artery, confirming an ischemic stroke. This finding is consistent with his symptoms of left-sided weakness and difficulty with speech. His blood glucose level was found to be elevated at 240mg/dL, likely due to stress response, but could also indicate poor control of his diabetes. His hemoglobin A1c was also elevated at 8.5%, further suggesting suboptimal diabetes management. His lipid profile showed elevated cholesterol levels with LDL at 160mg/dL, which is a risk factor for atherosclerosis and subsequently ischemic stroke. His EKG showed sinus tachycardia, likely a response to the stress of the stroke and elevated blood pressure.
Change in Patient Status:
Over the course of the next couple of hours, the patient's speech became more garbled and he had increasing difficulty swallowing. His left-sided weakness remained, now with a noted facial droop. His blood pressure remained elevated at 180/100 mmHg, pulse at 112 bpm, and respiratory rate increased to 24 breaths per minute. He now required 2 liters of supplemental oxygen via nasal cannula to maintain an oxygen saturation above 94%. These findings suggest progressive neurological deterioration, likely due to increasing brain edema and potentially expanding area of ischemia. This has implications for his safety, particularly risk of aspiration due to dysphagia, and indicates the need for urgent medical and nursing intervention.
Section 2
New Complications:
Following the escalation in his symptoms, the patient was found unresponsive and had a significant decrease in his Glasgow Coma Scale score from 15 to 7, indicating severe neurological impairment. He was also noted to have irregular respirations with periods of apnea, suggestive of Cheyne-Stokes respiration, which is often seen in severe stroke or brain injury. His blood pressure spiked further to 190/110 mmHg and his pulse rate was irregular at 120 bpm. His oxygen saturation dropped to 88% on 2 liters of supplemental oxygen. Arterial blood gas analysis showed a PaO2 of 60 mmHg, PaCO2 of 50 mmHg, and a pH of 7.30, indicating hypoxemia and hypercapnia with respiratory acidosis.
These alarming changes in his clinical status suggest the patient may be developing malignant middle cerebral artery syndrome, a lethal complication of large middle cerebral artery infarction characterized by rapid neurological deterioration, increasing brain edema, and raised intracranial pressure. This could potentially lead to brain herniation if not urgently managed. The respiratory changes could be secondary to brainstem involvement or a consequence of aspiration due to previously noted dysphagia. Additionally, his uncontrolled hypertension could be contributing to the worsening cerebral edema by disrupting the blood-brain barrier. The irregular pulse might suggest a new onset atrial fibrillation, a frequent complication of stroke, and this could further increase his risk of additional embolic events.
Section 3
Change in Patient Status:
Despite the aggressive medical management, the patient's condition continued to decline. His Glasgow Coma Scale score further decreased to 4, indicating profound neurological impairment. His respiratory pattern deteriorated further, with periods of prolonged apnea, and oxygen saturation dropped to 84% on 4 liters of supplemental oxygen. Repeat arterial blood gas analysis revealed a PaO2 of 55 mmHg, PaCO2 of 55 mmHg, and a pH of 7.25, suggestive of worsening hypoxemia, hypercapnia, and respiratory acidosis.
The patient also developed new neurological findings, including a dilated and nonreactive right pupil, indicative of impending uncal herniation due to increasing intracranial pressure. His blood pressure remained persistently high at 200/115 mmHg, despite antihypertensive treatment, and his pulse rate was irregular at 130 bpm. His ECG now showed signs of atrial fibrillation, consistent with the irregular pulse. This new development, coupled with the patient's severe neurological and respiratory deterioration, necessitates immediate escalation of care and potentially invasive interventions to prevent further brain injury and maintain adequate oxygenation and circulation. The team must also consider the likelihood of further stroke events given the new onset atrial fibrillation.
Section 4
New Complications:
In the early hours of the morning, the patient had a sudden drop in his blood pressure to 90/60 mmHg, which was accompanied by increasing lethargy and a further decrease in Glasgow Coma Scale to 3. His temperature began to rise, peaking at 38.5 degrees Celsius, indicating a possible infection. His white blood cell count was elevated at 15,000 cells/mcL, with a left shift, and C-reactive protein was raised at 20 mg/dL, also suggestive of an inflammatory response. Blood cultures were ordered to identify the probable source of infection.
Meanwhile, a CT scan of his brain showed an increase in the size of the ischemic stroke, confirming the suspicion of a progressive cerebral edema. A new area of low attenuation was also observed in the left temporal lobe, suggestive of a new ischemic event. This raises concerns of a recurrent stroke, potentially secondary to his new onset atrial fibrillation. These new complications add another layer of complexity to the patient's condition, requiring the healthcare team to reassess their strategy and further intensify their interventions to prevent further neurological damage and manage the suspected infection effectively.
Section 5
New Diagnostic Results:
The patient's blood cultures returned positive for Streptococcus pneumoniae, a common cause of pneumonia. This was consistent with the patient's elevated temperature, leukocytosis, and elevated C-reactive protein. Chest X-ray further confirmed the diagnosis, showing consolidation in the right lower lobe of the lung. Concurrently, a cerebral angiogram revealed occlusion of the left middle cerebral artery, confirming the source of the patient's recurrent stroke.
In the midst of these findings, the patient's EKG monitoring showed new-onset frequent ventricular ectopics and couplets, raising concerns about potential ventricular tachycardia. The patient's blood pressure continued to remain low at 88/58 mmHg, and his pulse rate was elevated to 110 bpm. These findings are indicative of possible hemodynamic instability and may be related to the new cardiac arrhythmia. The healthcare team now needs to consider the broader picture of potential sepsis secondary to pneumonia, recurrent stroke, and possible cardiac complications, making the course of this patient's care increasingly complex.