Joshua S. Broder
Abdominal aortic aneurysm (AAA) is defined by an abdominal aortic diameter greater than or equal to 3 cm. Aortic aneurysms occur as the elastic connective tissue of the aortic wall weakens, resulting in aortic dilatation. Risk factors include male gender, hypertension, smoking, advancing age, and family history. As the aortic diameter increases, the risk of rupture rises. Current recommendations call for elective repair of AAA ≥ 5.5 cm. Rupture of an aortic aneurysm can lead to immediate and catastrophic hemorrhagic shock. Clinical signs and symptoms of AAA rupture can include syncope or cardiac arrest, abdominal and/or back pain, lightheadedness, and hypotension. Classically, a pulsatile mass is present on exam, but the absence of this finding does not rule out the disease. More subtle presentations can include extremity or groin pain as well as neurologic symptoms related to spinal cord hypoperfusion.
In the United States, AAA rupture is among the top 15 causes of death in patients older than 60 years of age. Early mortality in AAA rupture is around 90% (including out of hospital deaths), and 20% to 30% with operative repair. Without repair, one in eight patients dies within 2 hours of arrival to the hospital.
When AAA rupture is suspected, immediate resuscitative steps should include large bore intravenous (IV) access, preoperative laboratory studies including type and cross-match for massive blood transfusion, and surgical consultation based on suspicion alone. Unstable patients should be considered for operative care before definitive diagnosis.
Bedside ultrasound can be used to assess the presence of AAA. Because ultrasound is relatively insensitive for rupture, the presence of AAA in a symptomatic patient should be considered a strong surrogate for rupture. When ultrasound is used, the entire abdominal aorta (from xiphoid process to the iliac bifurcation at the level of the umbilicus) and the proximal iliac arteries should be screened. The majority of AAAs are infrarenal. Care should be taken to identify intravascular mural thrombus, which should be included in the measurement of aortic diameter. If mural thrombus is not recognized in the lumen and the thrombus is mistaken as part of the aortic wall, aortic size may be underestimated and the diagnosis missed.
Hemodynamically stable patients can be considered for rapid computer tomographic (CT) assessment. CT without contrast media can detect the presence of AAA and AAA rupture. IV contrast can assist in delineating a subtle AAA leak and intravascular complications such as aortic dissection. Oral contrast is not needed for the diagnosis and introduces potentially fatal diagnostic delay.
FIGURE 6.3
A CT without contrast reveals a ruptured AAA. In this axial image, the aorta itself is hardly visible, but calcifications in the aortic wall (a common feature of AAA) are seen in the expected location of the aorta, anterior to a lumbar vertebral body. Blood within the aortic lumen appears dark gray in the absence of IV contrast. Blood that had already leaked from the aorta before the CT is partially clotted and appears lighter gray.
FIGURE 6.4
A ruptured AAA is seen in the axial (A), coronal (B), and sagittal (C) reconstructions of this enhanced CT. In the axial image, blood within the aortic lumen appears bright white. Blood leaking from the aorta appears white because of active contrast extravasation. Mural thrombus within the aorta appears gray. Blood that had already leaked from the aorta before the administration of IV contrast appears gray.
Due to similarities in the location and severity of pain, care should be taken not to mistake pain from a rupturing AAA for renal colic.
Consult a surgeon immediately when AAA rupture is suspected, without delay for diagnostic confirmation.
Prepare for immediate operative care with large bore IV access and massive blood transfusion.
Assess the entire abdominal aorta with ultrasound, from xiphoid process to umbilicus, and include mural thrombus in diameter measurements to avoid underestimation of aortic size.
David James Story
Aortic dissection is a rare disease process that carries a high rate of morbidity and mortality (27.7%). It occurs more commonly in males, African Americans, and individuals 50 to 65 years of age. Dissection occurs when an injury to the intima layer of the vessel allows for blood to tunnel into the wall of the artery, creating a false lumen.
Dissection may include the ascending aorta, aortic arch (Stanford Type A), and/or the descending aorta (Stanford Type B) with presenting complaints that vary based on the location. Typically, it is described as a sudden, severe, midsternal, tearing pain that radiates to the back and is often accompanied by nausea, vomiting, and syncope. If the injury extends into aortic tributaries or abdominal aorta, pain may be reported in the neck, jaw, arms, and/or abdomen. Neurological findings are present in up to 20% of patients and may include cerebral vascular accident, Horner syndrome, peripheral weakness or paresthesias, and altered mental status. Pericardial effusion and hypotension from tamponade can occur if the dissection originates near the aortic valve. Myocardial infarction can result concurrently if the dissection extends into the coronary arteries. Physical exam may reveal hypertension, hypotension, widened pulse pressures, asymmetric extremity blood pressures, diastolic murmurs, pulmonary crackles, muffled heart sounds, carotid bruits, and neurological abnormalities.
Diagnosis of aortic dissection is confirmed with radiographic imaging. Laboratory evaluation and electrocardiograms (ECG) typically rule out only alternative diagnoses that present similarly. Chest radiographs are abnormal in the majority of cases but consist of nondiagnostic findings, such as widening of the mediastinum. In the stable patient, CT angiography and magnetic resonance imaging (MRI) are highly sensitive and specific in identifying this vascular catastrophe. In an unstable patient, bedside transesophageal echocardiography (TEE) is the modality of choice for diagnosing aortic dissection.
Emergency care is centered on decreasing the shear stress present by controlling the blood pressure. The beta-blockers esmolol and labetalol are first-line treatments for blood pressure control in aortic dissection. Esmolol is a pure beta antagonist administered via infusion allowing titration to effect, and often requires sequential administration of a vasodilator (ie, sodium nitroprusside) to achieve blood pressure goals. Labetalol is a mixed alpha/beta antagonist that can be used as a monotherapy, and is administered in bolus dosing or as an IV drip. The goal is the lowest systolic blood pressure that permits normal organ perfusion. Cardiothoracic surgery consultation is advised for all thoracic aortic dissections. Dissections involving the ascending aorta are treated surgically. Descending aortic dissections may be managed medically (most cases) or surgically in selected cases with aggressive blood pressure control in otherwise stable patients.
FIGURE 6.8
A coronal view of a chest CT scan that catches two sections of the descending aorta with acute dissection. As is typical, the true lumen (arrowheads) is smaller than the false lumen (arrows), and as can be seen in the distal portion of the aorta, the true lumen is often crescent shaped, and the false lumen is oval or round.
Nifedipine, a calcium channel blocker, is not recommended for blood pressure treatment in aortic dissection because it can increase sympathetic outflow and shear stress on the vessel walls.
Extremity exam should include evaluation of pulses and/or four extremity blood pressures to look for significant differences in arterial blood flow.
A high index of suspicion is needed to diagnose aortic dissection as the presentation can vary greatly in location of pain and associated symptoms.
David James Story
Acute arterial occlusion is a condition that carries high morbidity (13% amputation rate) and mortality (10%). It occurs when the blood supply to a distal part of the body (generally an extremity) is interrupted suddenly. This vascular compromise can be the result of thrombosis (50%) or an embolic event (50%). It most often affects the femoral (28%), brachial (20%), aortoiliac (18%), and popliteal artery (17%). Risk factors include peripheral arterial disease, atrial fibrillation, patent foramen ovale, hypercoagulable states, exogenous estrogen use, IV drug use, and smoking.
The diagnosis is primarily clinical. A typical patient will present with pain, pallor, and pulselessness (or diminished pulses) distal to the occlusion site, and may have paresthesia, paralysis, and poikilothermia (in this setting, cool extremity); “the 6 P’s” of acute limb ischemia.
A Doppler ultrasound should be used to evaluate for any distal blood flow of an extremity where no pulse is palpated. Paresthesias and paralysis are late signs in the disease and correlate with prolonged occlusion and increased morbidity. The ability to salvage the extremity decreases after 4 to 6 hours. The ankle-brachial index (ABI) is a sensitive bedside test. Using a blood pressure cuff, place a Doppler ultrasound at the brachial artery and record the pressure of occlusion. Repeat the procedure on the leg, measuring the occlusion pressure of the posterior tibial and dorsalis pedis arteries. The ABI is the highest leg occlusion pressure divided by the arm occlusion pressure; normal ABI is >0.9. A ratio lower than 0.41 is usually found in limbs with critical ischemia.
FIGURE 6.10
Arterial embolus. Note the pallor of this patient’s right foot, consistent with an acute arterial embolus, in this case is secondary to femoral artery occlusion. Photo contributor: Lawrence B. Stack, MD. Reproduced, with permission, from Chapter 12. Tubbs RJ, Savitt DL, Suner S. Extremity conditions. In: Knoop KJ, Stack LB, Storrow AB, Thurman R, eds. The Atlas of Emergency Medicine. 3rd ed. New York, NY: McGraw-Hill; 2010.
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