The Clinical Challenges of Acute Thoracic Aortic Dissection
Part II: Definitive Diagnosis, Patient Evaluation, and Outcome Optimizing Management in the Emergency Department
Author: Gary Hals, MD, PhD, Attending Physician, Department of Emergency Medicine, Palmetto Richland Memorial Hospital, Columbia, SC.
Peer Reviewer: Laurence J. Gavin, MD, Chief, Department of Emergency Medicine, Presbyterian Medical Center and Pennsylvania Hospital; Clinical Associate Professor, Department of Emergency Medicine, University of Pennsylvania Health System, Philadelphia, PA.
Diagnostically challenging, deceptive in its presentation, and potentially deadly in its clinical outcome. Put simply, these are the well-documented pitfalls of evaluating and managing patients with acute dissection of the thoracic aorta.
There are other problems. The propensity for misdiagnosis is high, and while outcome-enhancing strategies are available, they cannot be pressed into service until the diagnosis is established. It is well-known that such risk factors as heart disease, age, and, especially, uncontrolled hypertension place individuals at greater risk for acute thoracic aortic dissection. Moreover, recent autopsy data suggest that the correct diagnosis rate for type A dissections is no better than 35%. Diagnoses that may be confused with thoracic dissection include myocardial infarction (MI), abdominal disease, stroke, and lower extremity ischemic thrombosis.
Although such diagnostic modalities as transesophageal echocardiography (TEE) and computed tomography (CT) can provide definitive confirmation of the diagnosis and such techniques are available at most institutions, establishing the diagnosis requires a high degree of clinical suspicion, especially in a high-risk subset of patients, i.e., those with a history of hypertension who present to the emergency department with complaints of sudden onset of "tearing" back pain that is migratory in nature, and who have other findings consistent with acute thoracic dissection. A systematic approach to using these modalities, and a thorough understanding of their advantages and pitfalls, is essential for decreasing morbidity and mortality.
Once the diagnosis is established—or is judged to be extremely likely—prompt medical intervention with beta-blockers and nitroprusside is required to reduce sheer stress and minimize the risk of progression. Surgical consultation is always required early in the patient’s course, at which point more invasive evaluation of the anatomy may be required. Finally, it should be stressed that newer techniques—among them intravascular ultrasound and intra-aortic stenting—are slowly changing the diagnostic and interventional landscape of this condition.
The purpose of this review is to present a systematic and practical approach to the evaluation of patients suspected of having acute thoracic aortic dissection. Using evidence-based trials, the author identifies current diagnostic modalities and their role in patient evaluation, and present a sequential approach to patient management, with an emphasis on both medical and surgical interventions.
— The Editor
Diagnostic Evaluation
At present, there are no laboratory studies which are considered useful for confirming or excluding the diagnosis of aortic dissection, although a recent report identifies a biochemical marker for smooth muscle injury (creatinine kinase subtype bb).1 While sensitivity and specificity for this isoenzyme are 90% and 97%, respectively, these levels are not reached until 12 hours after symptom onset. However, further study in this area may prove fruitful in the future.
Changes in other blood tests will depend on end-organ ischemic changes (i.e., hematuria with renal involvement). ECG changes are often present (10-40% of cases),2 but these are non-specific. Most commonly, signs of left ventricle (LV) hypertrophy are noted and reflect long-standing hypertension. Ischemic changes can also be present, and historical features of the quality of chest pain ("ripping" or "tearing") or presence of a migratory component may provide the only clues to suggest dissection. As these features have a high degree of correlation with the diagnosis of aortic dissection, they should always be taken seriously and should initiate prompt work-up for this condition. Heart block also may be seen due to AV node compression, but is a non-specific finding. Currently, four imaging studies (transesophageal echocardiography, angiography, computed tomography, and magnetic resonance imaging [MRI]), are the only tools available to the emergency department (ED) physician for making the diagnosis. A recent article used a statistical decision analysis based on an exhaustive literature review to help suggest which of the four modalities should be used in the ED.3 These authors confirm recommendations of the American College of Emergency Physicians, that even in a patient with low clinical suspicion for dissection, one of these four diagnostic tests should be ordered.4 In patients with a low clinical probability of dissection, any of the four tests was felt to be accurate enough to exclude the diagnosis, and TEE (or, if unavailable, CT) was the test of choice (based on safety, convenience, and cost). For high clinical probability, the time delay in obtaining a particular test was equally important as the accuracy of the test. Furthermore, their model confirmed the practice of ordering a second diagnostic test when suspicion is high and the first test is negative for dissection.
The ideal test would quickly and safely identify aortic dissection, discern between type A and B dissections, locate the presence and site of an intimal tear, assess LV function, and detect aortic valve insufficiency, pericardial effusion, and coronary artery and great vessel patency. Unfortunately, among the four tests that can establish the definitive diagnosis of aortic dissection, none meets all of the objectives. However, TEE does fulfill many of these criteria, and when available, it is considered the initial test of choice in most ED patients.
If the diagnosis of dissection is suspected with any degree of certainty, and definitive tests such as TEE or CT scan cannot be completed within the time it takes for transportation to be arranged, then the patient should be urgently transferred to a facility where proper testing and intervention can be done. When the diagnosis is highly suspected, treatment of the patient should be initiated as soon as possible. Valuable time and irreversible damage may occur while the physician pursues the diagnosis. Thus, no patient should be transferred or made to wait during testing without the ED physician beginning treatment for the suspected condition. Frequent re-examination of patients for their responses to treatment is vital while they remain in the ED.
Chest Films. The screening upright chest x-ray will be abnormal in 80-90% of cases of aortic dissection,5 and in most cases, the findings will be new compared to a previous x-ray.6 It is important to note at the outset that a normal chest film does not exclude the diagnosis. ED physicians should be concerned about the possibility of inappropriate administration of thrombolytics to a patient for treatment of myocardial infarction, only to later discover aortic dissection as the cause of the patient’s symptoms. With this in mind, it is surprising to find one article suggesting that if the chest film has signs of dissection the patient should still be given "immediate thrombolysis" if "clinical features suggest MI."7 However, most authors recommend rapid rule out of aortic dissection with TEE or CT before tPA use in patients with high suspicion of aortic dissection.8
The myriad of findings (see Table 1) correlated with aortic dissection on chest films include: widened mediastinum (> 8 cm or the length of an average beeper); extension of aortic shadow greater than 5 mm beyond its calcified wall ("eggshell" or "calcium" sign); blurred aortic knob or localized bulge; aortic enlargement; loss of space between the aorta and pulmonary artery; and a double density appearance suggesting presence of true and false channels (false lumen is less radiopaque). Findings more often seen on the right side of the film are deviation of the trachea or nasogastric tube to the right (away from developing hematoma); shift and elevation of the right main stem bronchus; and deviation of the right paraspinous line. Signs on the left side of the film include a depressed left mainstem bronchus; with rupture into the left chest; a new pleural effusion (free hemothorax); or apical cap (localized apical hemothorax).
| Table 1. Chest X-ray Findings Suggestive of Aortic Dissection |
| Mediastinal Findings |
| • Widened mediastinum (most common) |
| • Extension of aortic shadow beyond calcified wall (most specific) |
| • Blurred aortic knob or localized bulge |
| • Aortic enlargement |
| • Double density of the aorta (false lumen less radiopaque) |
| • Loss of space between aorta and pulmonary artery |
| Right Side of Film |
| • Deviation of trachea/NG tube to the right |
| • Shift and elevation of right mainstem bronchus |
| • Deviation of right paraspinal line |
| Left Side of Film |
| • Depressed left mainstem bronchus |
| • New pleural effusion |
| • Apical cap (localized apical hemothorax) |
Inasmuch as the screening upright chest film may be the only routine study ordered on most patients with chest pain that may provide clues to the diagnosis, the findings consistent with aortic dissection are summarized in Table 2. Of the signs on chest x-ray, mediastinal widening is the most common and is reported in 75% of films.9 The widening can occur in the ascending, transverse, or descending aorta. It may also be difficult to discern widening from a torturous aorta associated with chronic hypertension. In the setting of trauma, the mediastinum may be widened as a result of upper thoracic spine fractures,10 and mediastinal tumors may also give misleading x-ray findings. The most diagnostic sign is the "eggshell" or "calcium" sign, an indication that the acute dissection has created expansion of the adventitia away from the calcified intima. This is not seen on most films, but is considered pathognomonic for dissection when present.11
| Table 2. Summary of ED Management of Acute Aortic Dissection |
| A. Medical Therapy for Aortic Dissection |
| Combination Therapy: |
| • Beta-blocker—Goal of heart rate between 60 bpm and 80 bpm |
| • Propranolol 1 mg IV slow push every 5 minutes, or |
| • Metoprolol 5 mg IV push every 5 minutes up to 15 mg, or |
| • Esmolol 500 mcg/kg bolus over 12 minutes followed by 50 mcg/kg/min to 200 mcg/kg/min infusion, with |
| • Nitroprusside—Goal of systolic blood pressure between 100 mmHg and 120 mmHg or BP sufficient to maintain mentation and urine output |
| • Begin 0.5 mcg/kg/min and titrate up to reach target blood pressure |
| Monotherapy: |
| • Labetalol 20 mg IV bolus initially followed by 20-80 mg every 5-10 minutes until target heart rate reached, and then start infusion at 1-2 mg per hour |
| B. Indications for Surgical repair of Aortic Dissection |
| • All Type A dissections |
| • Type B dissections with complications of (rupture, severe distal ischemia, intractable pain, progression, uncontrolled hypertension) |
| • Aortic rupture |
| • Severe distal ischemia |
| • Intractable pain |
| • Uncontrolled hypertension |
| • Progression of dissection |
| c. Key Points to Remember |
| • All patients receive medical therapy initially, regardless of dissection type |
| • Start beta-blocker therapy before or simultaneously with nitroprusside to avoid reflex tachycardia |
| • Lifelong medical therapy is required |
A retrospective review of chest x-rays in 75 patients with aortic dissections found that 48% of films had sufficient findings to suggest the diagnosis of dissection.12 Interestingly, however, only 25% of these films were identified prospectively as suggesting dissection. The conclusion here is that although the films were being read by experienced radiologists, x-ray findings may be easily missed. Consequently, regardless of findings on chest x-ray, a definitive test (TEE, CT, or MRI) will be required. Nevertheless, the chest film may identify other diagnoses, or if it is very suggestive of dissection, it may provide justification to mobilize consultants early or transport to a definitive treatment facility.
Computed Tomography. Newer helical CT scans have almost 100% specificity and sensitivity.13 In most cases, CT scan with intravenous (IV) contrast (dynamic CT scan) can accurately discern type A and B dissections, which greatly aids in guiding treatment. Dynamic CT scanning is performed by rapidly scanning after a bolus injection of IV contrast. Other advantages of the CT scan include its wide availability and its ability to identify thrombosed false lumens (an advantage over angiography), as seen in Figure 1. The procedure is less invasive than angiography, and can often identify pathology other than aortic dissection (i.e., pulmonary embolus or a mediastinal mass).14
A disadvantage of the CT scan is that it may miss a dissection flap if it is moving rapidly. High speed cine CT scans improve sensitivity, but are still not 100% accurate. Furthermore, motion artifacts of the ascending aorta may simulate dissection on CT when not actually present.15 While dye may not be able to be used in patients with significant renal disease, fatal dye reactions occur in fewer than 1 in 10,000 patients overall.3 Finally, the CT scan may not provide information about extension into branches of the aorta, cannot locate the intimal tear, or evaluate for aortic insufficiency. Consequently, operative candidates may require a pre-operative angiogram before surgery. In general, the helical CT scan is a good initial choice for EDs without access to TEE.
Transesophageal Echocardiography. TEE using Doppler color flow mapping has had a major impact on evaluation of aortic dissection.16 In Japan and Europe, TEE is the initial and frequently the only test used for work-up of dissection.17 Recent studies combining transthoracic and TEE demonstrate sensitivities and specificities greater than 95%.18 Furthermore, the data with first-generation probes (no Doppler color flow) were better than with CT or angiography,19 and results with multi-plane probes and color flow imaging should be even better.16 TEE has the unique advantage of being very rapid (about 10 minutes for each exam), and it can be done at the patient’s bedside with minimal risk; it is safe in critical patients.20 It is less invasive and expensive than other modalities, and no contrast exposure is required. Intimal tears can often be detected and evaluation of aortic regurgitation also can be performed. Although intimal flaps over coronary ostia can be seen, the remainder of the coronary anatomy will not be defined. Figure 2 shows TEE images of an acute dissection. Given the proximity of the probe in the descending thoracic aorta, type A and B dissections can easily be differentiated. Multi-plane probes have eliminated a previous "blind spot" in the proximal aortic arch (from air in the trachea that blocked the ultrasound waves).16 Color flow mapping can define flow in both true and false lumens, as well as extrinsic compression of the true lumen by thrombus in the false lumen. One disadvantage is the limited visualization of the distal aorta; therefore, TEE provides no data on the perfusion status of renal and visceral arteries. Another disadvantage is that false-positive results are possible, leading several authors to suggest that, in some cases, a second confirmatory test may be required before surgery.21,22 Unfortunately, the biggest problem with TEE is its limited availability in some institutions. Hopefully, this will be corrected with time, as TEE is now recognized as the primary diagnostic test for aortic dissection in most hospitals.22,23
Angiography. Historically, this was the gold standard24 because it delineates the anatomy of the entire aortic tree, which most surgeons require preoperatively. The sensitivity (81%) and specificity (96%)17 are acceptable, but the primary problem is the frequency of false-negative tests. This occurs when the false lumen is completely thrombosed, blocking contrast material from entering the dissection, or when the true and false lumens have equal flow rates and may not be differentiated. One recent review reported a 23% false-negative rate in 65 patients examined by angiography using TEE as a confirmatory test.25 They used TEE to determine the cause of the false-negative angiography result, and found that 87% of the false negatives were due to a clotted false lumen or intramural hematoma with no intimal tear.25 The remaining patients had dissections with equal flow in true and false lumens.
These studies illustrate that angiography may be misleading in patients with acute dissections. Digital subtraction angiography has been used to reduce these problems, but is not available in most centers.26 Advantages of angiography include its ability to locate the intimal flap; that coronary anatomy can be articulated; type A and B dissections are detectable; and aortic insufficiency can be evaluated. The risk of the procedure is low, with an average mortality of less than 0.3%.27 Disadvantages, other than the potential for false negatives, include that it is invasive and takes time to perform. It also removes the patient from the ED and is the most expensive of the four diagnostic tests.
Magnetic Resonance Imaging. MRI is one of the most accurate tests for aortic dissection, with sensitivity and specificity of almost 100%.28 It can define the various anatomic abnormalities associated with aortic dissection well, identifying intimal flaps, great vessel anatomy, type A and B dissections, and degree of aortic insufficiency. It is also non-invasive and safe. However, most authors agree that MRI does not play a major role today in diagnosis, especially in critically ill patients.17 Even though one study considers it the "gold standard" for diagnosis of aortic dissection, only 3% of patients in this study used MRI as a diagnostic test, with the authors citing logistical considerations as the principal limiting factor.29 Because patients need to be disconnected from monitoring devices, IV pumps, and respirators, and because the test is time consuming (around 60 minutes), it is not ideal for many ED patients with acute disease.
As newer generation machines reduce capture time, MRI may become more valuable in the acute setting, but patients with implanted devices will always be excluded from MRI scanning. MRI, however, is a useful test for serial follow-up of patients with chronic dissections and evaluating patients postoperatively.
Intravascular Ultrasound. The "new kid on the block" is intravascular ultrasound (IVUS), a technological improvement in the ultrasound arena. In this modality, the ultrasound probe is small enough to fit inside the vessels. It is inserted percutaneously into the femoral artery and guided up the aorta. It has been used as an aide for treatment of coronary artery disease since 1997.30 The latest application for IVUS is to identify plaques that may be more prone to rupture and cause acute MI.31 Although preliminary reports appeared as early as 1991,32-34 it is currently used in conjunction with other conventional modalities (CT, TEE, or angiography), after the diagnosis of dissection has been made, to further define the pathoanatomy of the dissection. The most recent reports use three-dimensional IVUS, which provides anatomic detail of the aorta and surrounding vascular structures.35
Remarkably, some centers already are using the probe to perform initial diagnosis and treatment. In some cases, the procedure has eliminated the need for conventional corrective surgery. In addition to using IVUS to guide endovascular stent placement (See Treatment section, page 6), the IVUS probe can be used to fenestrate the intimal flap, and thereby restore flow to the true lumen of the aorta or its major vessels (i.e., the renal or iliac arteries). Some disadvantages of this new procedure are: it is not available in most centers at this time and long-term (> 12 months) follow-up has not yet been performed. It has several advantages: it makes accurate diagnosis of all the associated complications of dissection; it is minimally invasive; and it can potentially be used for definitive treatment. Patients who were clearly not candidates for classical surgical intervention have already benefited from use of IVUS and stent placement as a life-saving procedure. Without question, aortic stenting through IVUS will find a place in the diagnosis and treatment of aortic dissection in the near future.
Diagnostic Pitfalls
Acute aortic dissection is difficult to diagnose in a timely fashion. Recent autopsy data estimate that the correct diagnosis rate is between 11% and 35% in patients with Stanford type A dissections.36,37 The fact that this entity can present in so many forms, from sudden, ripping chest pain with hypertension to painless ischemia (up to 15% of cases are painless)38 in one limb, certainly contributes to the high misdiagnosis rate. The wide range of presentations associated with aortic dissection is linked to a complex differential diagnosis, including cardiac, pulmonary, gastrointestinal, neurologic, renal, and musculoskeletal etiologies. One recent review of initially misdiagnosed dissections found 33% mislabeled as abdominal disease, 27% as lower extremity thrombosis, 11% as MI, 11% as acute stroke, and 5% each as pneumonia or pericardial disease.39 Few entities are the potential cause of so many varied conditions and carry such a high mortality rate in the ED.
Pain History. With so many possible presentations, it is difficult to suggest foolproof guidelines, but there are a few consistent features of aortic dissection that should be emphasized. Chest pain is the most common complaint in aortic dissection. Sudden onset of "ripping" or "tearing" pain, with maximal intensity noted at time of onset and that migrates over time, is highly suggestive of aortic dissection. History of pain moving from chest to back or back to chest should always raise a high suspicion for dissection. As a rule, the pain of acute MI is not migratory, and when the two occur together, the dissection typically begins first and leads to the MI. However, in the case of painless dissection, the patient’s history may not provide any clues to the true nature of his disease.
Hypoxia and pleuritic chest pain are more suggestive of pulmonary embolus, and when using chest CT to evaluate for pulmonary embolism, the scan can also rule out dissection. Such physical findings as new onset murmurs and pulse deficits are also highly correlated with aortic dissection. Perhaps the most challenging presentation is when aortic dissection manifests as peripheral vascular complications. The presence of unusual neurologic deficits, including isolated extremity numbness or weakness or unusual transient ischemic attack patterns, also suggest dissection. These presentations should prompt a thorough investigation for signs consistent with dissection (i.e., pulse deficits, presence of risk factors, and historical features of chest pain).
Screening Modalities. Screening chest x-rays taken in the ED should be examined closely for signs consistent with aortic dissection (wide mediastinum or "calcium" sign, see Table 1), especially when a patient with risk factors presents to the ED with any findings suggestive of dissection. In the case of painless dissection, the chest x-ray may be the only test that contains evidence to suggest a unifying diagnosis. Finally, the patient’s complaints of abdominal and back pain may raise the suspicion of symptomatic acute aortic aneurysm (AAA). Use of transabdominal ultrasound in the ED to screen for AAAs may be of use in cases of aortic dissection as well. In type B dissections, the intimal flap may be apparent on ultrasound as a mobile structure inside the aorta. (See Figure 3.) Similarly, on CT scan, type B dissections may be apparent with use of intravascular dye typically given for abdominal CTs; if no contrast is given, the scan may not show the dissection.
Misdiagnosis. It is helpful to know what conditions may initially suggest aortic dissection only to yield negative studies for dissection. Figure 4 shows data summarized from two papers on such cases;40-41 one is a 20-year review.40 While the ultimate diagnosis was unknown in 19% of cases, the most common condition confused with aortic dissection was acute MI or unstable angina (23%). If one includes patients with aortic regurgitation, thoracic aneurysm, and pericarditis, almost 60% had a cardiac source for their complaints. The authors compared the clinical presentation of all these patients with 125 patients who presented with true dissection. They found that patients who had dissection were more likely to have hypertension, migratory pain, and acute onset (< 24 hours) of symptoms. Those who did not have dissections were younger, had fewer complications (i.e., congestive heart failure [CHF], aortic regurgitation, or pulse deficits), and were more likely to have pain for more than 24 hours before presentation. Ultimately, one should strive for a relatively high negative work-up record when evaluating patients for acute dissection (similar to the negative laparotomy rate in appendicitis). In other words, because the disease is difficult to diagnose, one should look for it more often than one finds it, or it can be assumed that cases are being missed.
When a patient is initially evaluated for aortic dissection and the entity is not found, remember the following points. In some cases, multiple tests (i.e., TEE followed by CT, etc.) are needed to find the dissection; the next most likely cause of the patient’s complaints could be another type of serious cardiac disease. Therefore, if a patient needs to be evaluated for aortic dissection, it usually should be done with admission as the ultimate disposition, regardless of the results of the diagnostic tests. It should be stressed that patients with a negative evaluation for aortic dissection have a high rate (23%) of acute MI or unstable angina, both of which should not be overlooked if dissection is excluded.
Initial Management and Definitive Therapy
The goal of treatment for patients with acute aortic dissection is to prevent death and irreversible end-organ damage. All patients should be aggressively treated initially with IV antihypertensives and negative ionotropic agents; oral medication alone is inadequate. IV narcotics are also indicated for the severe pain of dissection. These agents should be started as soon as the diagnosis is strongly suspected, and should never be delayed for results of definitive diagnostic tests.
The risk of death for untreated acute dissection is reported at 1-2% per hour.42 The aim of medical therapy is to lower the rate of rise of blood pressure (dP/dT) by lowering blood pressure and decreasing force of contraction of the left ventricle (the two primary determinants of dP/dT). By doing so, the sheer stress and driving force for continued propagation of the dissecting column of blood is reduced and progression of the dissection may be halted. The indication for definitive surgery depends on the type of dissection present: type A dissections are referred for emergency repair of the aorta, while type B dissections usually are treated conservatively with medical management, with exceptions for significant complications. The next section will review current recommendations for medical and surgical intervention in patients with acute aortic dissection.
Initial Medical Treatment. Most patients with acute aortic dissection present with significant hypertension. In fact, the dissection may be a result of an uncontrolled acute rise in arterial blood pressure. A small percentage of critical patients will present with hypotension from aortic rupture into the pleural space or into the pericardium with subsequent tamponade. As with any critically ill and unstable patient, aggressive resuscitation with IV fluids and adherence to the ABCs are essential. Treatment for cardiac tamponade not responding to fluid resuscitation is immediate pericardiocentesis. In acute tamponade, removal of as little as 10 cc may make a dramatic difference in the patient’s condition, but pericardial fluid should continue to be removed until the patient responds. All patients should have appropriate cardiac monitoring, two large bore IVs, and preoperative baseline blood tests, including type and cross for at least four units of packed red blood cells.
For several decades, the mainstay of medical treatment has been use of nitroprusside to lower blood pressure in conjunction with a beta-adrenergic blocker to lower the heart rate. As nitroprusside may produce reflex tachycardia, treatment with an IV beta-blocker should be started before or simultaneously with nitroprusside. Propranolol has been the drug of choice in the past, and is given in doses of 1 mg IV push every 5 minutes until a target heart rate of 60-80 beats per minute is achieved. Newer, more selective beta-blockers such as esmolol may also be used, and may avoid some of the side effects of propranolol. Mix 5 g esmolol in 500 cc dextrose in water (D5W) (10 mg/1 cc), give an initial bolus of 500 mcg/kg, and follow with an infusion from 50 mcg/kg/min up to 200 mcg/kg/min. In some EDs these agents may not be stored for rapid use in the ED, and consequently may have a significant time delay associated with their use. Metoprolol is another alternative for beta blockade, but like the other pure beta-blockers, it must be used in combination with nitroprusside.
IV labetalol may be more readily accessible, and is a good alternative as it produces both alpha- and beta-adrenergic block. Thus, IV bolus of labetalol will act alone to decrease blood pressure as well as heart rate, achieving the goal of lowering dP/dT. Doses for labetalol are 20 mg IV push every 5-10 minutes, with subsequent doses increased up to 80 mg IV push until a total of 300 mg is given. Continuous infusion is then started at 1-2 mg per hour.
Contraindications for beta-blocker use include patients with history of CHF, heart block, asthma, or chronic obstructive pulmonary disease (COPD). One possible alternative is the calcium channel blocker diltiazem, which is often used to control heart rate in atrial fibrillation. Mix 125 mg in 100 cc of D5W (1 mg/1 cc), and give as 20 mg IV bolus followed by rebolus in 15 minutes or start infusion at 5-15 mg/hr.
Sodium nitroprusside should be started immediately after control of heart rate has been initiated. It is mixed 50 mg in 500 cc of 5% D5W, and infused at an initial rate of 0.5 mcg/kg/min or 10 mL/hr. The rate of infusion may be titrated rapidly over several minutes to maintain a target range of systolic pressures between 100 mmHg and 120 mmHg, or the lowest level compatible with adequate renal and cerebral perfusion. As some patients may have a much higher baseline blood pressure, systolic blood pressures of 100 mmHg may be too low, and they should be monitored closely for signs of inadequate end-organ function (mentation and urine output). As nitroprusside is sensitive to light, the IV bag and all tubing should be protected with aluminum foil. It is essential to stress that patients with documented aortic dissection who are normotensive or have no pain should still be treated with a medical regimen. Further decreases of their blood pressure and heart rate to the aforementioned ranges are unlikely to cause harm and will help stop progression of the dissection in the same manner as in hypertensive patients. Medical management of aortic dissection is summarized in Table 2.
Surgical Candidates. Urgent consultation with cardiothoracic and/or vascular surgeons should be initiated as soon as the diagnosis is suspected and while medical therapy is being instituted. Although not all patients will be taken to surgery, it is not the role of the emergency physician to make this determination, and early involvement of consultants will speed the process for those patients who are ultimately taken for surgical repair.
The standard treatment for all patients with type A dissections is emergent surgical correction.17 These patients are treated surgically to avoid aortic rupture or extension of their dissection into the pericardium and death by tamponade. Tamponade and rupture were the causes of death in 79% of patients with type A dissections who had surgical intervention in a 1998 autopsy series.43 Therefore, the ascending aorta and proximal arch, or the segment with the intimal tear, are excised and replaced with a Dacron graft. The aortic valve is replaced (or repaired) if aortic regurgitation is present. In the Stanford series, no difference in mortality or reoperation was found if the primary intimal tear was not resected,44 and two recent studies confirm this.45,46 Overall, the quoted surgical mortality for type A dissection repair ranges from 7-12%47,48 and has changed little in the past 20 years.
A new aspect to repair of the aorta is use of a wound "glue" (gleatin-resorcin-formalin or GFR) to help maintain closure of the intima and media at anastomosis sites. In other words, the glue is used to ensure attachment of the layers of the aorta at the surgical incision to the graft. One group even compared use of glue as a local repair without typical replacement of the damaged aortic segment.49 They found that although satisfactory initial results were obtained, an increased incidence of reoperations due to breakdown of the glue repair site was required. When looking at repair of type A dissections, another group found similar results with significant risk for proximal aortic redissection when glue was used in repair.50 The formalin component of the glue is suspected as a cause of these late complications.
Contraindications to surgical repair of type A dissections include comorbid conditions (i.e., metastatic cancer) which prevent realistic recovery. Some authors also recommend that patients with large acute strokes not be taken to the OR,47 due to their higher operative mortality rates.48 Factors associated with higher risk of death in one recent study were liver failure, sepsis, and reoperation;51 another review found preoperative shock, increased blood loss in surgery, and prolonged aorta cross-clamp time were factors as well.52 Interestingly, the Stanford series found that of the possible peripheral vascular complications (renal, cerebral, spinal, mesenteric, or limb ischemia), only renal involvement (operative mortality of 50%) was statistically shown to be an independent predictor of operative mortality.42 This may be due to a small sample size, as the mortality rates for patients with mesenteric or spinal ischemia were as high as 43%.42 In their study, however, stroke had a markedly lower mortality rate (14%) than in previously reported data, but sample size was still a concern.42
In contrast to type A dissections, the recommended treatment for type B dissections is still a subject of debate in the surgical literature.24,17,53,54 The basis of this controversy centers on the relatively good prognosis of type B patients treated with medical management (20% mortality),55 lack of improvement with surgery, and the higher operative mortality for these patients. Type B surgical repair carried an overall mortality of 38% as late as the 1970s,56 but has improved to as little as 10-15% using more strict selection of surgical candidates.44 However, the mortality for acute cases complicated by end-organ ischemia rises to 50%.57 Moreover, recent studies still quote the risk of new paraplegia at 3.5-36%42,58 depending on the extent of resection and cross clamp time for type B repair. Currently, patients with uncomplicated type B dissections are still treated medically at most centers worldwide,53 with surgery being reserved for patients who have aortic rupture, severe distal ischemia, intractable pain, progression of the dissection, or uncontrollable hypertension.17 Exceptions are made for younger, low-risk patients (usually suffering from Marfan’s syndrome), or those with large (> 5 cm) descending false aneurysms. As can be expected, mortality is near 100% for those patients who are initially medically treated and then develop a complication necessitating emergency surgery (usually aortic rupture or renal/mesenteric infarction).17
Unfortunately, these complications are not rare. During the five years after dissection, up to 20% of patients with type B dissections treated with medical therapy alone will develop an aortic aneurysm from dilation of the false lumen.59 Chronic dissections (> 2 weeks duration) of either type A or B are treated surgically much less often, and are only referred for surgery when significant complications of their dissection arise (CHF from aortic insufficiency, end organ ischemia, or expansion of the aortic diameter > 5-6 cm).
Management of Peripheral Complications. Five major categories of peripheral vascular complication are associated with acute aortic dissection: cerebral, renal, mesenteric, spinal, or limb ischemia. Aortic dissection is complicated by major symptoms of peripheral vascular ischemia in up to 50% of patients.42 Although treatment of these complications is beyond the purview of the ED physician, it is useful to understand how these complications are managed. More importantly, it is helpful to know which complications carry higher risk for the patient, so the ED physician can appropriately evaluate patients and make outcome-sensitive management decisions.
Although not life-threatening initially, limb ischemia deserves the most attention as it is the most common complication seen in both types of aortic dissection (40% in type B and 60% in type A. See Figure 5). In addition, along with stroke and paraplegia, it is one of the easiest to recognize. But unlike stroke and paraplegia, where recovery after surgery is rare, repair of aortic dissection frequently will restore limb function. The fact that central nervous system tissue can only withstand brief periods of hypoxia, compared to the several hour tolerance of limbs, contributes to this outcome. The current recommendations for patients with significant ischemic limb complications are for surgery of both type A and B dissections. High-risk patients with limb-threatening ischemia may benefit from local revascularization if primary repair of the dissection is not attempted. Newer treatment options, however, may soon change the approach to limb revascularization (See New Advances section, page 9).
Finally, renal involvement is especially challenging; detection is difficult as back pain is often thought to come from the aorta itself; oliguria can be seen for many other reasons in these patients; hematuria may not be present in the early stages; and it carries a high mortality rate of 50%.42 Debate exists currently as to whether primary repair of the dissection should take precedence over local renal revascularization. Likewise, visceral ischemia is difficult to diagnosis, even when not combined with aortic dissection, and is associated with a high mortality rate.60-61
Prognosis Survival. The five-year survival rates for patients undergoing surgery is almost 78% for type A dissections and 88% for type B,42 and only 50% overall at 10 years after repair.24 Again, end organ problems, including stroke, MI, and renal failure, were the cause of most deaths. It is important to stress that 15-18%62 of the patients died from rupture of the graft site or a remote portion of the aorta—a potentially preventable complication with adequate follow-up and surveillance. Risk factors for rupture of chronic type B dissections include older age, associated COPD, and continued hypertension.62 Interestingly, these are similar to risk factors noted for AAA rupture.63 This suggests that no matter what the cause of aneurysm formation, factors determining the risk for rupture are very similar, and perhaps a more aggressive approach to surgical intervention for type B dissections should be followed (i.e., surgery for patients based on aneurysm size, etc., as with classic AAAs). A striking 23% of patients underwent reoperation in 10 years following the original dissection repair.42 In the majority of patients, this was to correct new problems arising in the remaining diseased aorta.
These data underscore the following objectives: Lifelong blood pressure control and surveillance studies are mandatory, especially for type B dissections, as medical treatment is often the only therapy. A recent study confirmed this idea. The authors followed two groups of patients: one with good hypertension control and another with poor control.64 While the difference in average blood pressure and heart rate (measured as in-home levels) was not dramatic (166 ± 10 mmHg and 58 ± 7 beats/min in the good group vs 177 ± 7 mmHg and 80 ± 8 beats/min in the poor control group, respectively), the differences in survival were significant. During the follow-up period (mean of 34 months), only one patient died in the good control group, whereas four patients (40%) experienced sudden death in the poor control group.64 All of these patients had type A dissections and most likely died from cardiac involvement, although autopsy support of this was lacking. Regardless of the cause of death, the difference in mortality in the two groups still exists, again stressing the importance of medical compliance for these patients.
Since many patients are not compliant with follow-up with their primary physicians, the ED physician may become their primary source of medical care. It is essential, therefore, that ED physicians be aware of the importance of anti-hypertensive treatment in these patients. Hypertension in this subset of ED patients deserves more close attention than a recommendation of a "repeat blood pressure reading in the next 30 days" and "call your doctor for an appointment soon." When possible, their physicians should be contacted, and unless their surgeon or internist disagrees, they should not leave the ED without a dose of and a prescription for anti-hypertensive medication. If overdue for surveillance studies (typically recommended at 6-12 month intervals), an outpatient test should be scheduled if possible or written instructions for the patient to schedule one the next day should be given.
New Advances: Endovascular Repair
Angioplasty and stenting of coronary vessels are now common and performed with excellent success rates. It is natural to extend these same concepts to other vessels. In the early 1990s, researchers began experimenting with these techniques in cases of aortic dissection. Balloon angioplasty per se has little to offer in aortic dissection, except in cases of chronic dissection where a localized stenosis of a major aortic branch becomes symptomatic. On the other hand, good results have been achieved with percutaneous placement of intravascular stents, which can provide definitive, non-surgical treatment for aortic stenosis and coarctation,65 thoracic,66 and abdominal aneurysms.67 This approach has been quite successful; complications of stent migration or persistent leakage around the stent in AAA repair using this technique are seen in only 3-4% of cases.67 Most recently, intravascular stents have been used successfully to cover the intimal flap and reduce flow to the false lumen, thus "repairing" the aorta.68,69 This technique has been used in type A and B dissections, both acute and chronic.
In these cases, 100% clotting of the false lumen (false lumen clot is associated with increased survival rates) and significant shrinkage of the false lumen diameter are noted if performed on acute dissections.70 One study found that blood flow to end-organs was restored in 76% of patients.69 Combined with intravascular ultrasound, some investigators are using the probe to fenestrate aortic flaps and thereby restore blood flow in the true lumen without resorting to conventional surgery.71 Fenestration of aortic flaps not only serves to restore blood flow to the true lumen directly, but by diverting blood from the false lumen, decreases its size and compression on nearby vessels. Reports of using catheter fenestration of intimal flaps in type B dissections show complete relief of ischemia to the spinal cord, kidneys, or intestines has been achieved.72-74
Currently, the clinical experience with these catheter-based techniques is limited, and additional study is necessary to fully evaluate their limits and potential.75 These methods show great promise, however, with no neurological complications reported in two studies.68,69 Moreover, the time for the procedure was an average of 1.6 hours compared to 8.0 hours for conventional surgery.68 However, there are technical limitations in performing this procedure. The authors recommend using a femoral site not involved with the dissection, and they do not recommend attempting this approach in torturous aortas. Finally, they recommend that an additional imaging technique such as MRI, TEE, or digital angiography be used in conjunction for optimal results. The future of this approach will provide additional options and, perhaps, improve morbidity and mortality figures for aortic dissection.
Summary
The problems associated with making a timely diagnosis of acute aortic dissection do not result from a lack of accurate diagnostic tests. TEE, CT scan, angiography, and MRI (in order of ED utility) are all accurate, and in most cases, will make the diagnosis clear. The difficulty usually arises from lack of suspicion on the part of the ED physician. Recognition that a patient may have an acute dissection is essential. When a patient is initially diagnosed with MI, unstable angina, intestinal ischemia, ischemic stoke, CHF with a pleural effusion, or pulseless extremities, the ED physician also should consider aortic dissection. If it is a significant possibility, dissection should be ruled out.
Chest pain migrating to the back is the key historical feature to recognize, and chest x-ray findings (see Table 1) suggestive of the diagnosis should be kept in mind. It is important to remember that acute aortic dissection is 2-3 times as common as ruptured abdominal aortic aneurysm,47 and the misdiagnosis rate of dissection is as high as 90%36,37 compared to 30-60% for AAA rupture.76,77 Furthermore, the mortality of untreated type A dissections is 1% per hour in the first 48 hours.42
Appropriate management consists of nitroprusside and beta-blockers (when not contraindicated) for all patients, followed by surgical intervention for type A dissections and for those with complicated type B dissections. Optimal management of uncomplicated type B dissections is controversial, with most centers opting for surgery only in carefully selected patients. Medical therapy and surveillance studies for survivors of dissection are lifelong and mandatory. By looking for these cases, the ED physician is fully evaluating the patients before their disposition and increasing the chances that this diagnosis will not slip through their fingers. Thus, when the patient is found to have aortic dissection, it will be due to the physician’s skill and not through the infamous question all ED physicians dread: "Do you remember the patient you saw last night . . . ?"
References
1. Suzuki T, Datoh H, Kurabayashi M, et al. Biochemical diagnosis of aortic dissection by raised concentrations of creatine kinase BB-isozyme. Lancet 1997;350:784-785.
2. Griffith GL, Todd EP. Acute aortic dissection. South Med J 1985;78:1487-1493.
3. Sarasin FP, Louis-Simonet M, Gaspoz, J-M, et al. Detecting acute thoracic aortic dissection in the emergency department: Time constraints and choice of the optimal diagnostic test. Ann Emerg Med 1996;28:278-288.
4. American College of Emergency Physicians: Clinical policy for the initial approach to adults presenting with a chief complaint of chest pain, with no history of trauma. Ann Emerg Med 1995;25:274-299.
5. Slater EE, DeSanctis RW. The clinical recognition of dissecting aortic aneurysm. Am J Med 1976;60:625-651.
6. Fuster V, Halperin JL. Aortic dissection: A medical perspective. J Card Surg 1994;9:713-728.
7. Hartnell GG, Wakeley CJ, Tottle A, et al. Limitations of chest radiography in discriminating between aortic dissection and myocardial infarction: Implications for thrombolysis. J Thorac Imaging 1993;8:152-155.
8. Kamp TJ, Goldschmidt-Clermont PJ, Brinker JA, et al. Myocardial infarction, aortic dissection, and thrombolytic therapy. Am Heart J 1994;128:1234-1237.
9. Zappa MJ. Recognition and management of acute aortic dissection and thoracic aortic aneurysm. Emerg Med Reports 1993;14:1-8.
10. Dennis LN, Rogers LF. Superior mediastinal widening from spine fractures mimicking aortic rupture on chest radiographs. AJR Am J Roentgenol 1989;152:27-30.
11. Godwin JD, Korobkin M. Acute diseases of the aorta: Diagnosis by computed tomography and ultrasound. Radiol Clin North Am 1983;21:551-574.
12. Luker GD, Galzer HS, Eager G, et al. Aortic dissection: Effect of prospective chest radiographic diagnosis on delay to definitive diagnosis. Radiology 1994;193:813-819.
13. Sebastia C, Pallisa E, Quiroga S, et al. Aortic dissection: Diagnosis and follow-up with helical CT. Radiographics 1999;19:45-60.
14. Oliver TB, Murchison JT, Reid JH. Spiral CT in acute non-cardiac chest pain. Clin Radiol 1999;54:38-45.
15. Quanadli SD, El Hajjam M, Mesurolle B, et al. Motion artifacts of the aorta simulating aortic dissection on spiral CT. J Comput Assist Tomogr 1999;23:1-6.
16. Adachi H, Kyo S, Takamoto S, et al. Early diagnosis and surgical intervention of acute aortic dissection by transesophageal color flow mapping. Circulation 1990;82(Suppl IV):IV-19.
17. Walker PJ, Sarris, GE, Miller DC. Peripheral vascular manifestations of acute aortic dissection. In: Rutherford RB, ed. Vascular Surgery, 4th Ed. Philadelphia: WB Saunders; 1995:1087-1102.
18. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1-9.
19. Erbel R, Engberding R, Daniel W, et al. Echocardiography in diagnosis of aortic dissection. Lancet 1989;1:457-461.
20. Pearson AC, Castello R, Labovitz AJ. Safety and utility of transesophageal echocardiography in the critically ill patient. Am Heart J 1990;119:1083-1089.
21. Chu VF, Chow CM, Stewart J, et al. Transesophageal echocardiography for ascending aortic dissection: Is it enough for surgical intervention? J Card Surg 1998;13:260 - 265.
22. Wiet SP, Pearce WH, McCarthy WJ, et al. Utility of transesophageal echocardiography in the diagnosis of disease of the thoracic aorta. J Vasc Surg 1994;20:613-620.
23. Nienaber Ca, Daolitsch Y, Nicolasa V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993;328:1-9.
24. Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990;264:2537-2541.
25. Bansal RC, Chandrasekaran K, Ayala K, et al. Frequency and explanation of false negative diagnosis of aortic dissection by aortography and transesophageal echocardiography. J Am Coll Cardiol 1995;25:1393-1401.
26. Guthaner DR, Miller DC. Digital subtraction angiography of aortic dissection. AJR 1983;141:157-161.
27. Sanders C. Current role of conventional and digital aortography in the diagnosis of aortic dissection. J Thorac Imaging 1990;5:48-59.
28. Nienaber CA, Spielmann RP, von Kodolitsch Y, et al. Diagnosis of thoracic aortic dissection: Magnetic resonance imaging versus transesophageal echocardiography. Circulation 1992;85:434-447.
29. Torossov M, Singh A, Fein SA. Clinical presentation, diagnosis, and hospital outcome of patients with documented aortic dissection: The Albany Medical Center experience, 1986 to 1996. Am Heart J 1999;137:154-161.
30. Eberle MJ. The latest in electronic imaging. Semin Interv Cardiol 1997;2:19-13.
31. Ge J, Chirillo F, Schwedtmann J, et al. Screening of ruptured plaques in patients with coronary artery disease by intravascular ultrasound. Heart 1999;81:621-627.
32. Pande A, Meier B, Fleisch M, et al. Intravascular ultrasound for diagnosis of aortic dissection. Am J Cardiol 1991;67:662-663.
33. Weintraub AR, Schwartz SL, Pandian NG, et al. Evaluation of acute aortic dissection by intravascular ultrasound. N Engl J Med 1990;323:1566-1567.
34. Cavaye DM, French WJ, White RA, et al. Intravascular ultrasound imaging of an acute dissecting aortic aneurysm: A case report. J Vasc Surg 1991;13:510-512.
35. Liu JB, Bonn J, Needleman L, et al. Feasibility of three-dimensional intravascular ultrasonography: Preliminary clinical studies. J Ultrasound Med 1999;18:489-495.
36. Jamieson WR, Munro AI, Miyagishima RT, et al. Aortic dissections: Early diagnosis and surgical management are the keys to survival. Can J Surg 1982;25:145-149.
37. Doroghazi RM, Slater EE, DeSanctis RW, et al. Long-term survival of patients with treated aortic dissections. J Am Coll Cardiol 1984;3:1026-1034.
38. Spittal PC, Spittal JA Jr, Joyce JW, et al. Clinical features and differential diagnosis of aortic dissection: Experience with 236 cases (1980 through 1990). May Clin Proc 1993;68:642-651.
39. Hashimoto S, Kumada T, Kubo S, et al. The pitfalls in the clinical diagnosis of dissecting aortic aneurysm. J Cardiol 1992;22: 467-474.
40. Eagle KA, Quertermous T, Kritzer GA, et al. Spectrum of conditions initially suggesting acute aortic dissection but with negative aortograms. Am J Cardiol 1986;57:322-326.
41. Chan KL. Usefulness of transesophageal echocardiography in the diagnosis of conditions mimicking aortic dissection. Am Heart J 1991;122:495-504.
42. Fann JI, Sarris GE, Mitchell RS, et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990; 212:705-713.
43. Van Arsdell GS, David TE, Butany J. Autopsies in acute Type A aortic dissection. Surgical implications. Circulation 1998;10(19 Suppl):II 299-II 302.
44. Miller DC, Mitchell RS, Oyer PE, et al. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984;70(Suppl I):II 53-II 64.
45. Lansman SL, McCullough JN, Nguyen KH, et al. Subtypes of acute aortic dissection. Ann Thorac Surg 1999;67:1975-1978.
46. David TE, Armstrong, Ivanov J, et al. Surgery for acute type A aortic dissection. Ann Thorac Surg 1999;67:1999-2001.
47. Bourland MD. Aortic Dissection. In: Rosen P, et al, eds. Emergency Medicine: Concepts and Clinical Practice, 4th edition. Mosby-Year Book, Inc; 1998:1819-1825.
48. Safi HJ, Miller CC, Reardon MJ, et al. Operation for acute and chronic aortic dissection: Recent outcome with regard to neurologic deficit and early death. Ann Thorac Surg 1998;66:402-411.
49. Niederhouser U, Kaplan Z, Kunzli A, et al. Disadvantages of local repair in acute type A aortic dissection. Ann Thorac Surg 1998;66:1592-1599.
50. Fukunaga S, Karck M, Harringer W, et al. The use of gelatin- resorcin-formalin glue in acute aortic dissection type A. Eur J Cardiothorac Surg 1999;15:564-569.
51. Ehrlich M, Fang WC, Grabenwoger M, et al. Perioperative risk factors for mortality in patients with acute type A aortic dissection. Circulation 1998;98(19 Suppl):II 294-II 298.
52. Pansini S, Gagliardotto PV, Pompei F, et al. Early and late risk factors in surgical treatment of acute type A aortic dissection. Ann Thorac Surg 1998;66:779-784.
53. Glower DD, Fann JI, Speier RH, et al. Comparison of medical and surgical therapy for uncomplicated descending aortic dissection. Circulation 1990;82(Suppl IV):IV 39-IV 46.
54. Miller DC. The continuing dilemma concerning medical versus surgical management of patients with acute type B dissections. Semin Thorac Cardiovasc Surg 1993;5:33-46.
55. Delfteriades JA, Hartleroad J,, Gusberg RJ, et al. Long-term experience with descending aortic dissection: The complication-specific approach. Ann Thorac Surg 1992;53:11-21.
56. Miller DC, Stinson EB, Oyer PE, et al. Operative treatment of aortic dissections: Experience with 125 patients over a 16-year period. J Thorac Cardiovasc Surg 1979;78:365-382.
57. Cambria RP, Brewster DC, Gertler J, et al. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988;7:199-209.
58. Borst GH, Jurmann M, Buehner B, et al. Risk of replacement of descending aorta with a standardized left heart bypass technique. J Thorac Cardiovasc Surg 1994;107:126-133.
59. Wheat MW. Current status of medical therapy of acute dissecting aneurysms of the aorta. World J Surg 1980;4:563-569.
60. Lass J, Heinemann M, Schaefers H-J, et al. Management of thoracoabdominal malperfusion in aortic dissection. Circulation 1991;84Supp III):III 20-III 24.
61. Pinet F, Froment JC, Guillot M, et al. Prognostic factors and indications for surgical treatment of acute aortic dissections: A report based on 191 observations. Cardiovasc Intervent Radiol 1984;7:257-266.
62. Juvonen T, Ergin MA, Galla JD, et al. Risk factors for rupture of chronic type B dissections. J Thorac Cardiovasc Surg 1999;117:776-786.
63. Nicholls SC, Gardner JB, Meissner MH, et al. Rupture in small abdominal aortic aneurysms. J Vasc Surg 1998;28:884-888.
64. Grajek S, Cieslinski A, Mitkowski P, et al. Results of long-term medical treatment of patients with arterial hypertension complicated by aortic dissection. J Hum Hypertens 1995;9:987-992.
65. Dake MD, Miller DC, Semba CP, et al. Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 1994;331:1729-1734.
66. Mitchell RS, Dake MD, Semba CP, et al. Endovascular stent-graft repair of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 1996;111:1054-1062.
67. Jacobowitz GR, Lee AM, Riles TS. Immediate and late explantation of endovascular aortic grafts: The endovascular technologies experience. J Vasc Surg 1999;29:309-316.
68. Nienaber CA, Fattori R, Lund G, et al. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med 1999;340:1539-1545.
69. Dake MD, Kato N, Mitchell S, et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999;340:1546-1552.
70. Kato M, Matsuda T, Kaneko M, et al. Outcomes of stent-graft treatment of false lumen in aortic dissection. Circulation 1998;10(19 Suppl):II 305-II 311.
71. Slonim SM, Miller DC, Mitchell RS, et al. Percutaneous balloon fenestration and stenting for life-threatening ischemic complications in patients with acute aortic dissection. J Thorac Cardiovasc Surg 1999;117:1118-1126.
72. Reber D, Aebert H, Manke M, et al. Percutaneous fenestration of the aortic dissection membrane in malperfusion syndrome. Eur J Cardiothroac Surg 1999;15:91-94.
73. Chavan A, Hausmann D, Dressler C, et al. Intravascular ultrasound-guided percutaneous fenestration of the intimal flap in the dissected aorta. Circulation 1997;7:2124-2127.
74. Williams DM, Lee DY, Hamilton BH, et al. The dissected aorta: Percutaneous treatment of ischemic complications—Principles and results. J Vasc Interv Radiol 1997;8:605-625.
75. Walker PJ, Dake MD, Mitchell RS, et al. The use of endovascular techniques for the treatment of complications of aortic dissection. J Vasc Surg 1993;18:1042-1051.
76. Akkersdijk GJ, Hajo van Bockel J. Ruptured abdominal aortic aneurysm: Initial misdiagnosis and effect on treatment. Eur J Surg 1988;164:29-34.
77. Banerjee A. Atypical manifestations of ruptured abdominal aortic aneurysms. Postgrad Med 1993;69:6-11.
Physician CME Questions
9. Which chest x-ray indication is most accurate for aortic dissection?
A. Widened mediastinum
B. Left pleural effusion
C. "Calcium" sign (extension of aortic shadow > 5 mm beyond aortic calcification)
D. Depressed left mainstem bronchus
E. Shift of nasogastric tube to the right
10. Concerning diagnostic tests for acute aortic dissection, which is true?
A. CT scan is never the initial diagnostic procedure of choice.
B. TEE is considered by most the gold standard to diagnosis acute dissection.
C. Chest x-ray alone may be enough for diagnosis.
D. Angiography does not give a significant number of false negative readings.
11. Which patients are typically taken to the OR for their dissections?
A. Type A
B. Type B with complications of severe end-organ ischemia
C. Type B in younger, good surgical candidates
D. All of the above
12. The upright chest film will be abnormal in about what percentage of cases of aortic dissection?
A. 50% of cases
B. 50-60% of cases
C. 60-70% of cases
D. 70-80% of cases
E. 80-90% of cases
13. Of signs suggesting acute thoracic aortic dissection on chest x-ray, the most common finding is:
A. left ventricular enlargement.
B. enlarged aortic knob.
C. mediastinal widening.
D. clacified aortia.
14. Newer helical CT scans have a sensitivity and specificity rate for acute aortic dissection of:
A. almost 100%.
B. about 95%.
C. about 90%.
D. about 80%.
15. The most common physical complaint in acute thoracic aortic dissection is:
A. shortness of breath.
B. back pain.
C. chest pain.
D. difficulty swallowing.
E. headache.
16. Medical intervention for acute thoracic dissection is primarily based upon use of:
A. beta-blockers and calcium blockers.
B. nitroglycerine and calcium blockers.
C. beta-blockers and nitroprusside.
D. beta-agonists and nitroprusside.
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