Aneurysm - Nursing Case Study

Pathophysiology

• Primary mechanism: Aneurysms are bulges that form in the wall of an artery due to weakening. The primary mechanism involves continuous stress on the arterial wall from high blood pressure. This results in stretching and thinning of the arterial lining, leading to bulge formation.

• Secondary mechanism: Atherosclerosis, or hardening of the arteries, can also contribute to aneurysm development. Atherosclerotic plaques erode the arterial wall, leading to its weakening and subsequent bulging.

• Key complication: The most serious complication is rupture of the aneurysm. This can lead to internal bleeding and can be life-threatening, especially when it occurs in the brain (brain aneurysm) or the aorta (aortic aneurysm). Rapid intervention is vital to prevent mortality.

Patient Profile

Demographics:

62-year-old male, retired engineer

History:

• Key past medical history: Hypertension, high cholesterol, family history of aneurysms

• Current medications: Lisinopril, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden severe headache, often described as "the worst headache of my life"

• Key symptoms: Double vision, neck pain, sensitivity to light, fainting, vomiting

• Vital signs: Blood pressure 180/100 mmHg, pulse 92 bpm, respiratory rate 18 breaths per minute, temperature 98.6°F, oxygen saturation 95%

Section 1

Change in Patient Status:

The patient's condition deteriorated rapidly. His blood pressure spiked to 200/110 mmHg, pulse went up to 105 bpm, and his oxygen saturation dropped to 90%. He became increasingly restless and disoriented, exhibiting signs of neurological deficit such as slurred speech and left-sided weakness. The patient's headache intensified and he reported a scale of 9 on the pain scale. He also complained of worsening double vision and started having difficulty swallowing.

New Complications:

During this period, the patient experienced a seizure, characterized by tonic-clonic movements of all his limbs, upward gaze, and loss of consciousness. Post-seizure, the patient was extremely drowsy and his Glasgow Coma Scale score dropped to 9 (E2V2M5). His pupils were unequal, with the right pupil measuring 4 mm and the left pupil measuring 2 mm, and the right pupil was sluggish in response to light, indicating possible compression of the cranial nerves. An urgent CT scan was ordered to evaluate the cause of the seizure and the sudden neurological decline. The situation suggested a likely rupture of the aneurysm leading to subarachnoid hemorrhage, a life-threatening complication. Prompt neurosurgical consultation was sought as the clinical scenario pointed towards the need for potential surgical intervention.

Section 2

New Diagnostic Results:

The CT scan confirmed the suspicion of a ruptured aneurysm, with a large subarachnoid hemorrhage observed. The bleed was causing a significant mass effect, leading to midline shift and compression of the ventricles, which was likely the cause of the patient's new onset of neurological symptoms and seizure. Additionally, a complete blood count revealed a drop in hemoglobin levels to 8.6 g/dL, suggesting internal bleeding. The patient's coagulation profile showed prolonged PT and PTT times, indicating a coagulation disorder, perhaps due to the consumption of clotting factors in response to the hemorrhage.

Change in Patient Status:

Post-diagnosis, the patient's condition became critical. His blood pressure continued to fluctuate, and despite supplemental oxygen, his SpO2 remained at 90%. He developed respiratory distress with an increased respiratory rate of 26 breaths per minute. His level of consciousness continued to decrease with a GCS score now at 7 (E1V2M4). Pupillary size and reaction continued to worsen, with the right pupil now at 6 mm and non-reactive. The patient's left-sided weakness became more profound, and he was unable to move his left arm or leg against gravity. An emergent neurosurgical intervention was deemed necessary to control the hemorrhage and prevent further neurological damage.

Section 3

New Complications:

While preparing for the neurosurgical intervention, the patient experienced a sudden drop in blood pressure to 85/50 mmHg and his heart rate spiked to 130 bpm. His SpO2 dropped further to 88%, despite the supplemental oxygen. Concurrently, his ECG started to show signs of tachycardia with ST segment elevation, suggesting possible myocardial ischemia or infarction. His skin became clammy, and his level of consciousness further decreased with a GCS score dropping to 5 (E1V1M3).

Response to Interventions:

The medical team immediately responded to the sudden change in his condition. They increased the oxygen flow rate and started him on IV fluids to target his hypotension. Nitroglycerin was administered sublingually for the suspected myocardial ischemia. The patient was given a bolus dose of mannitol to decrease his intracranial pressure and reduce the midline shift. The medical team also prepared to intubate the patient due to his decreasing level of consciousness and worsening respiratory distress. Despite these interventions, the patient's condition remained critical, and he was rushed into the operation room for an emergency craniotomy to prevent further neurological deterioration. The team also prepared for possible cardiac catheterization due to the changes in his ECG. The rapid shift in the patient's status necessitated swift and comprehensive clinical reasoning to address the multiple organ systems involved.

Section 4

New Complications:

In the operating room, the patient's condition took another downturn. His blood pressure plummeted further to 70/40 mmHg, and his heart rate climbed to 140 bpm. His SpO2 levels remained below 90% despite the increased oxygen flow rate. The patient also began to exhibit signs of respiratory distress, with a respiratory rate of 28 breaths per minute and shallow breathing. His skin became increasingly pale and clammy, and his level of consciousness decreased further with a GCS score of 3 (E1V1M1). Moreover, his pupils became dilated and non-reactive, indicative of increasing pressure on the brainstem.

Response to Interventions:

The medical team responded to these new symptoms with heightened urgency. They initiated vasopressor support to manage his hypotension and increased the oxygen supply. The patient was immediately intubated to improve his oxygenation and ventilation. The neurosurgeon expedited the craniotomy procedure to relieve the increasing intracranial pressure. In parallel, the cardiology team on standby was alerted for possible cardiac catheterization in response to his worsening tachycardia and the ongoing ST segment elevation in his ECG. The patient's rapidly deteriorating condition demanded swift, critical decisions and interventions from the multidisciplinary team to prevent irreversible damage to his brain and heart.

Section 5

Change in Patient Status:

Despite the expedited craniotomy and the initiation of vasopressor support, the patient's vital signs continued to fluctuate. His blood pressure remained critically low at 65/35 mmHg, and his heart rate continued to surge at 145 bpm. Following intubation, his SpO2 levels showed minor improvement to 92%, but his respiratory rate remained worryingly high at 30 breaths per minute. Furthermore, the patient's level of consciousness remained alarmingly low, with a GCS score of 3, and his pupils remained dilated and non-reactive.

New Diagnostic Results:

A repeat CT scan post-craniotomy showed a decrease in the size of the aneurysm but revealed a new complication - cerebral edema, suggestive of a possible rebleeding or vasospasm. His ECG continued to show ST elevation, raising concerns for a concomitant myocardial infarction. Lab results showed elevated troponin levels at 0.5 ng/mL (normal range 0.0 - 0.4 ng/mL), confirming the suspicion of a cardiac event. His hemoglobin level had also dropped to 7.3 g/dL (normal range 13.5 - 17.5 g/dL for men), indicating significant blood loss. These findings further complicated the clinical picture and required careful consideration in the management plan to prevent further deterioration of the patient's condition.