Introduction: A well-documented complication of administering tissue plasminogen activator (tPA) in stroke patients is acute intracranial bleeding. A lesser known but still significant complication is angioedema secondary to tPA administration, which can develop in certain individuals with risk factors such as angiotensin converting enzyme (ACE) inhibitor use and location of the stroke. Knowing the potential for this life-threatening complication and being prepared for its proper management is vital for emergency physicians.
Case Report: We report a 53-year-old Black female who presented to the emergency department with sudden onset of slurred speech and a facial droop. She was found to have an acute ischemic stroke and tPA was administered. She subsequently developed angioedema. Retrospectively, the patient was found to have risk factors that are thought to predispose patients to tPA-induced angioedema.
Conclusion: Risk factors associated with angioedema secondary to tPA administration have been documented in patients taking ACE inhibitors, as well as patients who develop strokes in the frontal lobe. While many cases may be mild, some patients may develop life-threatening angioedema. Although this complication does not necessarily contraindicate tPA use, it is prudent for the emergency physician to be vigilant for its development, prepared for its treatment, and to be diligent in assessing the need for control of the patient’s airway.
Case Presentation: A 64-year-old man with a history of a 5.5-centimeter (cm) abdominal aortic aneurysm (AAA) presented to the emergency department (ED) complaining of severe back pain after climbing over a fence and falling a distance of eight feet. Prior to arrival, the prehospital paramedics reported that the patient did not have palpable pulses in either lower extremity. The initial physical examination in the ED was significant for absent dorsalis pedis pulses bilaterally as well as absent posterior tibialis pulses bilaterally and cold, insensate lower extremities. Point-of-care ultrasound identified an approximate 7-cm infrarenal AAA with a mural thrombus present. After receiving several computed tomography (CT) studies including CT head without contrast and CT angiography of the chest, abdomen and pelvis, the patient was diagnosed with acute thrombosis of AAA and associated thromboembolic occlusion of both his right and left distal iliac vessels causing bilateral acute limb ischemia. He immediately received unfractionated heparin and was admitted to the hospital for embolectomy and intra-arterial tissue plasminogen activator.
Discussion: Acute thrombosis of AAA and subsequent thromboembolic events are a rare but significant complication that can occur in patients with a history of AAA. Thromboembolic events may occur spontaneously or in the setting of blunt abdominal trauma. Common presenting signs and symptoms include distal limb ischemia and absent femoral pulses. Timely management and recognition of this rare complication is vital as this condition can ultimately result in limb loss or death if not treated in a timely manner. Heparinization after confirmation of non-ruptured AAA as well as vascular surgery, and therapeutic and vascular interventional radiology consultations are key steps that should be taken to decrease patient morbidity and mortality.
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