acute arterial occlusion - Nursing Case Study

Pathophysiology

• Primary mechanism: Acute arterial occlusion is primarily caused by an embolus or thrombus obstructing blood flow, leading to ischemia. This blockage halts oxygen and nutrient delivery to tissues, initiating cellular hypoxia and metabolic waste accumulation.

• Secondary mechanism: The resulting ischemic cascade triggers endothelial dysfunction and inflammatory responses, exacerbating vascular injury. This further compromises blood flow and enhances coagulation, risking further clot propagation.

• Key complication: Rapid progression to tissue necrosis can occur if blood flow is not promptly restored, leading to severe complications such as limb loss, systemic inflammatory response syndrome (SIRS), and multi-organ failure.

Patient Profile

Demographics:

67-year-old male, retired construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes Mellitus, Chronic Kidney Disease Stage 3, Coronary Artery Disease with previous stent placement, Peripheral Artery Disease

• Current medications: Lisinopril, Metformin, Aspirin, Atorvastatin, Clopidogrel

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of severe pain in the right leg

• Key symptoms: Coldness and pallor in the right leg, numbness and tingling, difficulty moving the right foot, absent pulse in the right dorsalis pedis artery

• Vital signs: Blood pressure 190/110 mmHg, heart rate 120 bpm, respiratory rate 24 breaths per minute, temperature 100.2°F, oxygen saturation 88% on room air

Section 1

As the healthcare team initiated a comprehensive assessment, the patient's condition continued to evolve, revealing further complexities. On examination, the right leg was markedly cooler to touch compared to the left, with a pronounced bluish discoloration extending from the mid-calf to the toes. The absence of a palpable pulse extended from the dorsalis pedis to the popliteal artery, despite Doppler ultrasound attempts to detect flow. Capillary refill time in the right toes was prolonged, exceeding 5 seconds, indicating severe vascular compromise. The patient reported intensifying pain, now described as a constant, burning sensation, and increased difficulty in attempting any movement of the affected limb.

The patient's vital signs further deteriorated; blood pressure dropped to 85/60 mmHg, indicating potential hypovolemic shock, while heart rate rose to 132 bpm. Oxygen saturation remained critically low at 84% despite supplemental oxygen via a non-rebreather mask, suggesting compromised systemic perfusion. Laboratory results returned showing a rapidly rising lactate level of 5.8 mmol/L, consistent with acute metabolic acidosis and tissue hypoperfusion. Serum creatinine had increased to 3.1 mg/dL from a baseline of 2.2 mg/dL, signaling worsening renal function, possibly exacerbated by the ongoing ischemia and systemic stress response.

Concurrently, an emergent CT angiography of the lower extremities confirmed a large thrombus occluding the right femoral artery, while also revealing smaller embolic events in the renal arteries, suggesting systemic embolization. This finding raised concerns about potential sources of emboli, such as cardiac arrhythmias or a dislodged plaque. The interdisciplinary team deliberated the urgency of revascularization strategies, balancing the risks of surgical thrombectomy against the patient's complex medical background. The potential for reperfusion injury and the heightened risk of systemic inflammatory response syndrome (SIRS) intensified the need for vigilant monitoring and strategic intervention planning.

Section 2

The healthcare team, recognizing the critical nature of the patient's condition, swiftly initiated advanced interventions to address the acute arterial occlusion and systemic complications. An urgent decision was made to proceed with endovascular intervention to attempt revascularization of the right leg. The patient was transferred to the interventional radiology suite where a catheter-directed thrombolysis procedure was undertaken. During the procedure, the interventional radiologist successfully administered a thrombolytic agent directly into the occluded femoral artery, aiming to dissolve the thrombus and restore perfusion. Concurrently, a heparin infusion was initiated to prevent further thromboembolic events.

Despite the procedural efforts, the patient’s status continued to evolve, reflecting the complex interplay of systemic responses. Post-procedure, the patient's vital signs remained unstable; blood pressure fluctuated, and the heart rate persisted at elevated levels around 130 bpm, indicating ongoing hemodynamic compromise. Additionally, the patient's respiratory status deteriorated, with oxygen saturation dropping further to 80%, necessitating the escalation to mechanical ventilation. Arterial blood gases revealed a worsening metabolic acidosis with a pH of 7.25, confirming inadequate tissue perfusion and oxygenation despite aggressive measures.

As the team monitored the patient closely in the intensive care unit, new complications emerged. The nursing team noted signs of compartment syndrome in the right leg, characterized by increasing tension and swelling, accompanied by severe, unrelenting pain unresponsive to analgesics. This development necessitated emergent surgical intervention to prevent irreversible muscle and nerve damage. Meanwhile, renal function continued to decline, with serum creatinine rising to 4.0 mg/dL, raising concerns of acute kidney injury secondary to both systemic embolization and contrast-induced nephropathy from the imaging studies. The complex clinical picture demanded meticulous coordination among the multidisciplinary team to address the evolving challenges while optimizing the patient's chances of recovery.

Section 3

As the multidisciplinary team continued to manage the patient in the ICU, new diagnostic results provided further insight into the patient’s deteriorating condition. A Doppler ultrasound of the right leg confirmed the presence of significantly decreased blood flow distal to the occlusion site, corroborating the clinical suspicion of compartment syndrome. Additionally, a repeat CT angiography of the abdomen and pelvis revealed multiple small emboli in the mesenteric vessels, potentially compromising intestinal perfusion, which raised the concern for ischemic bowel.

Laboratory results painted a grim picture of the patient’s systemic status. The lactate level had risen to 7 mmol/L, indicating severe tissue hypoxia and ongoing anaerobic metabolism. The complete blood count showed leukocytosis with a white blood cell count of 18,000/mm³, suggestive of a systemic inflammatory response. The patient’s coagulation profile revealed an elevated prothrombin time and activated partial thromboplastin time, highlighting the risk of disseminated intravascular coagulation as a consequence of both the thrombolytic therapy and the underlying ischemic insult.

These findings necessitated a reevaluation of the treatment strategy. The surgical team prepared for an urgent fasciotomy to relieve the compartment syndrome, while nephrology was consulted to discuss renal support options, including possible initiation of continuous renal replacement therapy. The ongoing hemodynamic instability and new evidence of potential intestinal ischemia required the critical care team to intensify monitoring and consider parenteral nutrition to mitigate the risk of bowel necrosis. As the patient’s condition remained precarious, the healthcare team faced the formidable task of balancing aggressive interventions with the need to prevent further systemic deterioration, underscoring the complexity and gravity of the clinical scenario.

Section 4

As the team proceeded with the urgent fasciotomy to address the compartment syndrome, the patient's clinical status abruptly changed, presenting a new set of complications. Post-procedure, the patient's vital signs revealed persistent hypotension, with blood pressure readings fluctuating around 85/50 mmHg, despite aggressive fluid resuscitation and vasopressor support. Tachycardia intensified, with the heart rate escalating to 130 beats per minute, indicating heightened sympathetic response to systemic stress. The patient's respiratory rate increased to 28 breaths per minute, with an oxygen saturation dropping to 88% on 50% high-flow oxygen, suggesting worsening respiratory compromise potentially linked to metabolic acidosis and fluid shifts.

Concurrent with these developments, the patient's neurological status deteriorated. Previously alert and oriented, the patient now presented with confusion and a Glasgow Coma Scale score reduction to 11, raising concerns about possible cerebral hypoperfusion and the need for neuroprotective strategies. Arterial blood gas analysis confirmed a mixed metabolic and respiratory acidosis, with a pH of 7.25, pCO2 of 32 mmHg, HCO3- of 15 mmol/L, and base excess of -10 mmol/L, underscoring the severity of the metabolic derangement and the need for comprehensive metabolic correction.

Amidst these escalating challenges, the critical care team initiated discussions on the potential for emergent exploratory laparotomy to assess and possibly resect ischemic bowel segments, given the ongoing risk of bowel necrosis indicated by worsening abdominal distension and guarding. Meanwhile, nephrology recommended starting continuous renal replacement therapy promptly to manage the acute renal failure and electrolyte imbalances. As the team coordinated these multifaceted interventions, they remained vigilant for signs of further systemic deterioration, weighing the benefits and risks of each clinical decision in this highly complex and rapidly evolving scenario.

Section 5

As the critical care team continued to monitor the patient closely, attention was directed towards the response to interventions, particularly the initiation of continuous renal replacement therapy (CRRT). Initially, the therapy appeared to stabilize the patient's renal function, with a slight improvement in urine output and gradual correction of electrolyte imbalances. However, within hours, the patient's condition took a concerning turn. An acute drop in urine output was observed, prompting a repeat renal ultrasound that revealed worsening renal perfusion. Serum creatinine levels continued to rise, reaching 4.5 mg/dL, and potassium levels spiked to 6.2 mmol/L, raising immediate concerns for hyperkalemia-induced cardiac complications.

Simultaneously, despite the aggressive management of metabolic acidosis, with bicarbonate infusions and optimization of ventilatory settings, the patient's acid-base status showed little improvement. Repeat arterial blood gas analysis revealed a persistent mixed acidosis with a pH of 7.22, pCO2 of 30 mmHg, and HCO3- of 14 mmol/L, indicating ongoing systemic metabolic disturbance. The patient's respiratory status remained tenuous, with oxygen saturation barely maintained at 90% on increased respiratory support, necessitating further consideration of advanced airway management and mechanical ventilation.

Compounding these issues, the patient's neurological status continued to decline. A repeat neurological assessment indicated a further reduction in Glasgow Coma Scale score to 9, with diminished pupillary response suggesting potential cerebral edema or ischemic insult. In light of these developments, the team faced critical decisions regarding the prioritization of interventions, weighing the need for exploratory laparotomy against the risks posed by the patient's hemodynamic instability and deteriorating systemic condition. The situation demanded urgent reevaluation of the current management strategy, necessitating a multidisciplinary approach to address the complex interplay of cardiovascular, renal, respiratory, and neurological challenges, each threatening to precipitate further systemic collapse.