Acute Aortic Occlusion



Acute Aortic Occlusion



Salvatore T. Scali and Thomas S. Huber


Acute aortic occlusion is a true vascular emergency associated with significant morbidity and mortality secondary to the underlying etiology, the related comorbidities, and the ischemia–reperfusion injury resulting from revascularization. Indeed, the morbidity and mortality rates are comparable to those associated with a ruptured abdominal aortic aneurysm (AAA). The optimal management requires early recognition and definitive treatment, similar to most vascular surgical emergencies. Despite the evolution of various percutaneous therapies, open surgical reconstruction remains the cornerstone of treatment. Fortunately, acute aortic occlusion is a relatively uncommon problem and, not surprisingly, the published experience with it is quite limited.



Etiology


The leading causes of an acute aortic occlusion are an embolus originating from the heart and in-situ thrombosis in the setting of severe aortoiliac occlusive disease. Review of the largest published series (Table 1) suggests that the incidence of these two events are comparable and somewhat series dependent. Emboli usually occlude the aortic bifurcation as a saddle embolus with retrograde propagation of thrombus to the next patent vessel, usually the lowest renal artery. A variety of cardiac conditions and pathologies can result in peripheral emboli, including atrial fibrillation, acute myocardial infarction, valve diseases, prosthetic valves, dilated cardiomyopathy, congestive heart failure, and ventricular aneurysms. Massive or saddle emboli can also originate from aortic aneurysms, although this is distinctly less common.



In-situ thrombosis in the setting of severe aortoiliac occlusive disease is often precipitated by an exacerbating event such as dehydration or diminished cardiac output from a myocardial infarction. Similar to the scenario with saddle emboli, the thrombotic process usually extends to the level of the renal arteries, with rare suprarenal extension of the thrombus. A number of other mechanisms have been implicated and should be considered in the differential diagnosis of an acute aortic occlusion given the appropriate clinical setting (Table 2). These include acute aortic dissections, thrombosis secondary to a hypercoaguable state, trauma, and postoperative complications after aortic reconstruction. Among the hypercoagulable states, heparin-induced thrombocytopenia merits consideration given the high prevalence of exogenous heparin use in the hospital setting. A small number of interesting collections of case reports have described several additional rare etiologies.




Clinical Presentation and Diagnosis


Patients with an acute aortic occlusion usually present with sudden lower torso and extremity ischemia as reflected by some or all of the classic six Ps of acute limb ischemia (pulseless, pallor, poikilothermia, pain, paresthesia, paralysis). The severity and extent of the ischemia ranges over a wide spectrum and is contingent upon the thrombus burden, presence of distal embolization, and adequacy of the collateral network. Indeed, patients without peripheral vascular disease might recall the exact moment when their symptoms began, whereas the presentation may be more subtle in patients with long-standing occlusive disease. Pain is usually the predominant complaint, although the skin pallor and/or mottling may be quite impressive, extending to the level of the umbilicus in up to 30% of patients. The spectrum of neurologic deficits can range from mild numbness to paresthesia and frank paralysis. Notably, these clinical findings are likely secondary to peripheral nerve or lumbar plexus ischemic injury rather than frank spinal cord ischemia. Inappropriate focus on the neurologic complaints during the initial presentation can lead to inadvertent delays in diagnosis and definitive treatment. Indeed, several reports have documented initial referral to various specialists for evaluation of the neurologic deficit in patients with classic symptoms of their aortic occlusion. Patients with visceral and/or renal artery involvement can experience anuria, hypertensive crisis, and/or abdominal pain.


The diagnosis of an acute aortic occlusion can usually be made by history and physical examination and confirmed with the appropriate imaging study if there is any question about the diagnosis or the initial treatment approach. Computed tomography (CT) arteriography has emerged as the definitive diagnostic test for acute aortic occlusion (Figure 1). CT arteriography image acquisition times are rapid, and the quality of the images with the newer-generation multi-slice technology is excellent. Furthermore, it overcomes many of the limitations of catheter-based arteriography in the setting of an acute aortic occlusion, including the need to cannulate the brachial artery and the potential limited contrast delivery for vessel visualization below the aortic occlusion. Admittedly, the decision to obtain a confirmatory imaging study must be balanced by the additional risk in terms of the potential delay of the definitive treatment and the associated contrast nephrotoxicity. Given the relative ease of obtaining a CT arteriogram in our center, we have a low threshold for obtaining such a study in the setting of a presumed aortic occlusion, particularly if there is any concern about visceral and/or renal involvement. The slight risk or delay appears justified by the additional anatomic information provided by the study.


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FIGURE 1 A, Preoperative three-dimensional (3-D) computed tomography (CT) arteriogram and intraoperative CT arteriogram with 3-D reconstructions in a patient with a 5-hour history of bilateral leg pain and mottling of his lower torso demonstrated an acute aortic occlusion at the level of the renal arteries, with reconstitution of the iliac and femoral system. Note the large epigastric vessels that suggest presence of a significant amount of preexisting underlying arterial occlusive disease. B, A catheter-based arteriogram performed in the operating room confirmed the findings on the CT. An aortobifemoral bypass with bilateral fasciotomies was performed. The patient’s postoperative course was complicated by an acute lung and renal injury, which required prolonged mechanical ventilation and hemodialysis, respectively.

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Aug 25, 2016 | Posted by in CARDIOLOGY | Comments Off on Acute Aortic Occlusion

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