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Acute Aortic Occlusion
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.
TABLE 1
Series of Acute Aortic Occlusions
Babu SC, Shah PM, Nitahara J: Acute aortic occlusion—factors that influence outcome, J Vasc Surg 21:567–572, 1995; Dossa CD, Shepard AD, Reddy DJ, et al: Acute aortic occlusion. A 40-year experience, Arch Surg 129:603–607, 1994; Littooy FN, Baker WH: Acute aortic occlusion—a multifaceted catastrophe, J Vasc Surg 4:211–216, 1986; Surowiec SM, Isiklar H, Sreeram S, et al: Acute occlusion of the abdominal aorta, Am J Surg 176:193–197, 1998; Tapper SS, Jenkins JM, Edwards WH, et al: Juxtarenal aortic occlusion, Ann Surg 215:443–449, 1992.
| ETIOLOGY | |||||||
|---|---|---|---|---|---|---|---|
| Author | Patients | Embolus (%) | Thrombus (%) | Mortality (%) | Morbidity (%) | Limb Salvage (%) | 5-Year Survival (%) ∗ |
| Littooy & Baker 1986 | 18 | 56 | 44 | 50 | 67 | 100 | NA |
| Tapper et al. 1992 | 26 | 50 | 50 | 31 | 37 | NA | 56 |
| Dossa et al. 1994 | 46 | 65 | 35 | 34 | 74 | 95 | 70 |
| Babu et al. 1995 | 48 | 8 | 92 | 52 | NA | NA | NA |
| Surowiec et al. 1998 | 33 | 16 | 17 | 21 | 63 | 88 | NA |
NA , Not available.
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.
TABLE 2
Reported Causes of Acute Aortic Occlusions
| Category | Example |
|---|---|
| Embolic | Cardiogenic (e.g., Afib, valve disease) |
| In-situ thrombosis | PAD, plaque rupture, AAA |
| Dissection | Type B aortic dissection |
| Postsurgical | Bypass graft thrombosis (e.g., ABF), endograft collapse (i.e., TEVAR/EVAR, iliac stents) |
| Metabolic | Diabetic ketoacidosis |
| Infectious | Aspergillus spp, Candida spp |
| Inflammatory | Arteritis |
| Low-flow state | Dehydration, CHF, diarrhea, vomiting |
| Hypercoagulable state | HIT, thrombophilic state (e.g., cancer) |
| Trauma | Aortic transection (e.g., lap belt injury) |
| Miscellaneous | Umbilical artery catheterization, tension pneumoperitoneum, lymphoma, SBO |
AAA , Abdominal aortic aneurysm; ABF , aortobifemoral bypass; Afib , atrial fibrillation or other cardiac arrhythmia; CHF , congestive heart failure; HIT , heparin-induced thrombocytopenia; PAD , peripheral artery disease; SBO , small bowel obstruction; TEVAR/EVAR , thoracic or abdominal aortic stent graft.
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 P s 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.
Principles of Management
The treatment goals for patients with acute aortic occlusions are to stop the thrombotic process and restore blood flow to the lower torso and extremities, while limiting the ischemia–reperfusion injury. Unfortunately, the variable presentations and common failure to make the appropriate initial diagnosis often lead to significant delays before definitive treatment can be provided. There is no true golden period for limb or life salvage. However, the duration, extent, and severity of the ischemia needs to be factored into the treatment algorithm.
All patients should be anticoagulated once the diagnosis of acute limb ischemia is made, provided that there are no contraindications. We typically use unfractionated heparin with a bolus of 80 units/kg followed by infusion of 18 units/kg unless there is a concern about heparin-induced thrombocytopenia. The restoration of blood flow to the ischemic tissues has traditionally required open operative intervention. However, several reports have described successful outcomes with percutaneous endovascular approaches. The role of the complete endovascular approach remains to be determined given the inherent delays to complete revascularization, and it is likely only appropriate for high-risk patients with minimal ischemic symptoms.
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