Aortic Abdominal Aneurysm - Nursing Case Study
Pathophysiology
• Primary mechanism: Degeneration of the aortic wall, primarily due to atherosclerosis, leads to weakening of the vessel structure. This results from chronic inflammation and infiltration of macrophages, which degrade elastin and collagen, essential for vessel integrity.
• Secondary mechanism: Hemodynamic stress, such as hypertension, exacerbates wall tension, promoting further dilation. The aorta's position and constant exposure to high-pressure blood flow contribute to progressive enlargement.
• Key complication: Aortic rupture is the most severe outcome, where the aneurysm bursts, causing massive internal bleeding. This is life-threatening and requires immediate medical intervention, highlighting the importance of early detection and management.
Patient Profile
Demographics:
67-year-old male, retired construction worker
History:
• Key past medical history: Hypertension, hyperlipidemia, and history of smoking (40 pack-years)
• Current medications: Lisinopril, atorvastatin, aspirin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Persistent abdominal pain and pulsating mass in the abdomen
• Key symptoms: Lower back pain, intermittent claudication, mild nausea
• Vital signs: Blood pressure 160/95 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 37.8°C (100°F)
Section 1
As the medical team conducts an initial assessment of the patient, several findings emerge that suggest an escalation of the situation. The abdominal pain has intensified, now described as sharp and radiating to the back, which raises suspicion of an impending rupture. The pulsating abdominal mass is more pronounced upon palpation, and there is a noticeable increase in the patient's anxiety level. His blood pressure remains elevated at 165/100 mmHg despite medication, and his heart rate has risen to 112 beats per minute, indicating a sympathetic response to pain or stress. Laboratory results reveal a hemoglobin level of 11 g/dL, lower than previous readings, suggesting possible microleakage or slow blood loss.
Simultaneously, the patient's renal function appears compromised, with creatinine levels elevated to 1.9 mg/dL from a baseline of 1.2 mg/dL. This may be due to decreased renal perfusion secondary to the hemodynamic instability or pressure effects from the expanding aneurysm. Additionally, a CT angiogram confirms the presence of a large infrarenal abdominal aortic aneurysm measuring 6.5 cm, with signs of impending rupture, including a crescent sign indicating mural thrombus compression of the aortic wall.
These findings necessitate urgent surgical consultation for potential endovascular repair or open surgical intervention. The healthcare team must prioritize stabilization, focusing on blood pressure management and fluid resuscitation to maintain adequate organ perfusion. The patient's status underscores the need for vigilant monitoring for signs of rupture, such as sudden hypotension or loss of consciousness, which would require immediate life-saving measures. This progression highlights the importance of prompt intervention in preventing catastrophic outcomes and reinforces the critical role of ongoing assessment and timely decision-making in managing complex vascular pathologies.
Section 2
As the medical team continues to monitor the patient, new complications begin to emerge, signaling a further escalation in his condition. Despite ongoing antihypertensive therapy, the patient's blood pressure has fluctuated erratically, with readings now dropping to 90/60 mmHg, indicating potential instability and raising concerns about hypovolemic shock. The patient experiences a sudden episode of altered mental status, characterized by confusion and disorientation, which prompts a rapid reassessment of his neurological state. Concurrently, his heart rate has climbed to 128 beats per minute, suggesting a compensatory response to decreased perfusion.
Laboratory results reveal a further drop in hemoglobin to 9 g/dL, supporting the clinical suspicion of ongoing blood loss, possibly due to an expanding microleak or a contained rupture. The lactate level has increased to 3.2 mmol/L, further indicating tissue hypoperfusion and anaerobic metabolism. Meanwhile, the patient's skin has become cool and clammy, and his urine output has decreased significantly to less than 20 mL/hr, reinforcing the likelihood of acute kidney injury secondary to poor perfusion.
The healthcare team initiates aggressive fluid resuscitation with crystalloid solutions to restore hemodynamic stability and improve organ perfusion. Continuous monitoring is established, focusing on vital signs, urine output, and mental status, while preparations for emergent surgical intervention are expedited. The situation demands careful clinical reasoning to balance fluid administration with the risk of exacerbating the aneurysm's pressure. These developments underscore the urgency for surgical correction and highlight the critical need for a multidisciplinary approach to mitigate the risk of catastrophic rupture and ensure the best possible outcome for the patient.
Section 3
As the medical team presses forward with their plan, they observe the patient's response to the aggressive fluid resuscitation. After administration of 1.5 liters of crystalloid solution, there is a moderate improvement in the patient's hemodynamic status; his blood pressure stabilizes slightly to 105/65 mmHg, and his heart rate decreases to 115 beats per minute. Despite these changes, the patient's mental status remains altered, with fluctuating periods of confusion. His skin continues to be cool and clammy, and urine output remains critically low at 15 mL/hr, indicating the kidneys have not yet responded to fluid therapy.
New diagnostic results return, showing a serum creatinine level that has increased to 2.1 mg/dL, confirming the presence of acute kidney injury. Furthermore, a repeat abdominal CT scan with contrast reveals an increase in the size of the aneurysm, now measuring 6.5 cm, with evidence of a thin, irregular mural thrombus, suggesting potential for a more significant rupture. The findings introduce the additional complexity of managing renal perfusion against the backdrop of possible aneurysmal expansion.
The healthcare team faces a challenging situation that requires careful consideration of the risks and benefits of further fluid administration and the timing of surgical intervention. They must balance the need to prevent further hypovolemic shock and renal damage against the danger of increasing aneurysmal pressure. The multidisciplinary team, including vascular surgery, nephrology, and critical care, convenes to reassess the patient's condition and adjust the management plan accordingly, prioritizing rapid surgical correction while addressing the ongoing renal compromise. The case emphasizes the importance of coordinated care and dynamic clinical reasoning to navigate the complexities of this unfolding scenario.
Section 4
As the healthcare team continues to monitor the patient closely, they notice a significant change in his status. Despite the initial stabilization of his blood pressure and heart rate, the patient's condition begins to deteriorate. His blood pressure drops again to 90/50 mmHg, and his heart rate increases to 125 beats per minute, signaling worsening hemodynamic instability. The patient's mental status also declines further; he becomes increasingly lethargic and difficult to arouse, indicating a potential decrease in cerebral perfusion.
In response to these alarming changes, the team promptly initiates additional diagnostic evaluations. An urgent bedside ultrasound is performed, revealing free fluid in the abdominal cavity, strongly suggestive of aneurysmal rupture. Simultaneously, laboratory results show a further decline in renal function, with serum creatinine rising to 3.0 mg/dL, while blood urea nitrogen (BUN) levels climb to 45 mg/dL. These findings confirm the progression of acute kidney injury, exacerbated by the ongoing hemodynamic instability.
Faced with these developments, the multidisciplinary team urgently revises the management plan. They decide to proceed with immediate surgical intervention to address the impending rupture, recognizing the high risk of a life-threatening bleed. Nephrology is consulted to optimize renal support, potentially considering renal replacement therapy post-operatively. The critical care team focuses on maintaining hemodynamic support with vasopressors while minimizing fluid overload, which could further compromise the aneurysm. This coordinated approach underscores the necessity of swift and decisive action to manage the complex interplay of complications and stabilize the patient.
Section 5
As the surgical team prepares for an emergency repair of the suspected ruptured abdominal aortic aneurysm, the patient is rapidly transferred to the operating room. During the brief preoperative period, the critical care team continues to monitor the patient's vital signs closely. His blood pressure remains precariously low at 85/45 mmHg despite aggressive vasopressor support with norepinephrine, and his heart rate continues to climb, reaching 130 beats per minute. These findings reflect ongoing hemodynamic instability and the urgent need for surgical intervention. The patient’s respiratory status also becomes a concern; his oxygen saturation drops to 88% on a non-rebreather mask, prompting the team to secure his airway through endotracheal intubation and mechanical ventilation to ensure adequate oxygen delivery to vital organs.
In the operating room, the surgical team encounters significant challenges due to the extent of the aneurysm rupture. They find a large retroperitoneal hematoma, confirming the source of the free fluid seen on ultrasound. As they work to control the bleeding, the anesthesiology team manages the patient's hemodynamics, administering additional blood products to counteract the massive blood loss and maintain tissue perfusion. Meanwhile, nephrologists stand by, anticipating the potential need for intraoperative renal replacement therapy given the patient's rising creatinine and BUN levels, which now indicate a critical acute kidney injury with creatinine at 3.5 mg/dL and BUN at 55 mg/dL.
The complex interplay of ongoing hemorrhage, acute kidney injury, and compromised respiratory function exemplifies the intricate challenges faced by the multidisciplinary team. Their coordinated efforts highlight the importance of each specialty's expertise in addressing the life-threatening complications that have arisen. As the surgeons work meticulously to repair the aneurysm and restore stability, the critical care and nephrology teams prepare for the intensive postoperative management that will be crucial to the patient's recovery. This stage of the patient's journey underscores the critical need for precise clinical reasoning and prompt intervention to navigate the multifaceted complications of a ruptured abdominal aortic aneurysm.