Aortic dissection
Aortic dissection is the most common catastrophe of the aorta, 2-3 times more common than rupture of the abdominal aorta. When left untreated, about 33% of patients die within the first 24 hours, and 50% die within 48 hours. The 2-week mortality rate approaches 75% in patients with undiagnosed ascending aortic dissection.
The establishment of the International Registry of Acute Aortic Dissection in 1996, which gathers information from 24 centers in 11 countries, has helped in the development of an understanding of the complexity of aortic dissection.
Dissections of the thoracic aorta have been classified anatomically by 2 different methods. The more commonly used system is the Stanford classification, which is based on involvement of the ascending aorta and simplifies the DeBakey classification.
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The Stanford classification divides dissections into 2 types, type A and type B. Type A involves the ascending aorta (DeBakey types I and II); type B does not (DeBakey type III).
This system helps to delineate treatment. Usually, type A dissections require surgery, while type B dissections may be managed medically under most conditions.
The DeBakey classification divides dissections into 3 types, as follows:
Type III dissections are further divided into IIIa and IIIb. Type IIIa refers to dissections that originate distal to the left subclavian artery but extend proximally and distally, mostly above the diaphragm.
Type IIIb refers to dissections that originate distal to the left subclavian artery, extend only distally, and may extend below the diaphragm.
Thoracic aortic dissections should be distinguished from aneurysms (ie, localized abnormal dilation of the aorta) and transections, which are caused most commonly by high-energy trauma.
Aortic dissection essentially features a tear in the intimal layer, followed by the formation and propagation of a subintimal hematoma. The dissecting hematoma commonly occupies up to 50% and, occasionally, 100% of the aortic circumference, leading to the development of a false lumen or double-barreled aorta. This can reduce the flow of blood to any of the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade can result.
The normal aorta contains collagen, elastin, and smooth muscle cells, which help contribute to the layers of the aorta, the intima, the media, and the adventitia. Degenerative changes associated with aging lead to the breakdown of the collagen, elastin, and smooth muscle, as well as to an increase in basophilic ground substance. This is termed cystic medial necrosis, the hallmark histologic change associated with dissection and with Marfan syndrome.
Any disease that weakens the strength of the aortic wall will predispose one to aortic dissection. Shearing forces give rise to the separation of the layers in the media of the aorta. Intimal rupture occurs at points of fixation along the aorta where the hydraulic stress is maximal. The most common site is the first few centimeters of the ascending aorta, with 90% found within 10 cm of the aortic valve. The second most common site is just distal to the left subclavian artery.
Risk factors for aortic dissection include the following:
Assure adequate breathing, maintain oxygenation, treat shock, and obtain useful historical information.
Establishing the diagnosis in the field is usually difficult or impossible, but certain salient features of aortic dissection may be observed. It is life threatening if not quickly recognized and treated.
Radio communication with the receiving hospital permits the medical control physician to direct care and select a capable destination hospital, while permitting the emergency department (ED) to mobilize appropriate resources.
In the rare event that the diagnosis can be made based on prehospital information, the physician directing prehospital care should request transport to a facility capable of operative treatment of an aortic dissection.
The mortality rate of patients with aortic dissection is 1-2% per hour for the first 24-48 hours. Initial therapy should begin when the diagnosis is suspected. This includes 2 large-bore intravenous lines (IVs), oxygen, respiratory monitoring, and monitoring of cardiac rhythm, blood pressure, and urine output.
Clinically, the patient must be assessed frequently for hemodynamic compromise, mental status changes, neurologic or peripheral vascular changes, and development or progression of carotid, brachial, and femoral bruits.
Note the following:
End organ perfusion should be evaluated. Balancing the risks of dP/dt on the aortic wall versus the benefits of acceptable end organ perfusion may be a difficult clinical decision.
Aortic dissection associated with cocaine ingestion is challenging. It has been argued that using beta blockers alone without any simultaneous alpha blockers may allow unopposed alpha aderenergic vasoconstriction, potentially worsening myocardial ischemia. Therefore, it is recommended labetalol be used as it has both alpha- and beta-blocking properties.
Retrograde cerebral perfusion may increase the protection of the central nervous system during the arrest period.
Up to one third of patients with acute aortic dissection may have their diagnosis missed.[3] Factors that contribute to an initial missed diagnosis of aortic dissection include female sex, the absence of back pain, and/or the presence of extracardiac atherosclerosis. Patients whose aortic dissection was initially missed also tend to have more imaging studies and longer time to surgery; however, these do not appear to affect adjusted long-term all-cause mortality.[3]
Magnetic resonance angiography (MRA) may help in the evaluation of, and guide management of, suspected acute aortic dissection in patients with contraindications to compute tomography angiography (CTA) in the emergency department.[4]
The mortality rate from aortic arch dissections is about 10-15%, with significant neurologic complications occurring in another 10% of patients. The mortality rate is influenced by the patient's clinical condition.
The American College of Radiology has established ACR Appropriateness Criteria for the diagnosis and treatment of suspected aortic dissection.[5]
Urgent surgical intervention is required in type A dissections. The area of the aorta with the intimal tear usually is resected and replaced with a Dacron graft. The operative mortality rate is usually less than 10%, and serious complications are rare with ascending aortic dissections.
The development of more impermeable grafts, such as woven Dacron, collagen-impregnated Hemashield (Meadox Medicals, Oakland, NJ), aortic grafts, and gel-coated Carbo-Seal Ascending Aortic Prothesis (Sulzer CarboMedics, Austin, Tex), has greatly enhanced the surgical repair of thoracic aortic dissections.
With the introduction of profound hypothermic circulatory arrest and retrograde cerebral perfusion, the morbidity and mortality rates associated with this highly invasive surgery have decreased.
Dissections involving the arch are more complicated than those involving only the ascending aorta, because the innominate, carotid, and subclavian vessels branch from the arch. Deep hypothermic arrest usually is required. If the arrest time is less than 45 minutes, the incidence of central nervous system complications is less than 10%.
Aortic stent grafting is a challenging technique. It may prove feasible and has offered good results in a small series of patients. It may be a reasonable alternative in high-risk patients in the near future.
The definitive treatment for type B dissections is less clear. Uncomplicated distal dissections may be treated medically to control blood pressure. Distal dissections treated medically have a mortality rate that is the same as or lower than the mortality rate in patients who are treated surgically.
Surgery is reserved for distal dissections that are leaking, ruptured, or compromising blood flow to a vital organ.
Acute distal dissections in patients with Marfan syndrome usually are treated surgically.
Inability to control hypertension with medication is also an indication for surgery in patients with a distal thoracic aortic dissection.
Patients with a distal dissection are usually hypertensive, emphysematous, or older.
Long-term medical therapy involves a beta-adrenergic blocker combined with other antihypertensive medications. Avoid antihypertensives (eg, hydralazine, minoxidil) that produce a hyperdynamic response that would increase dP/dt (ie, alter the duration of P or T waves).
Survivors of surgical therapy also should receive beta-adrenergic blockers.
A series of patients with type B dissections demonstrated that aggressive use of distal perfusion, CSF drainage, and hypothermia with circulatory arrest improves early mortality and long-term survival rates.
Endovascular stenting remains an option for treatment of some type B dissections. Some studies recommend that patients with complicated acute type B dissections undergo endovascular stenting with the goal of covering the primary intimal tear.[6] More recent studies suggest that a combination medical therapy with endovascular aortic repair may inprove outcomes in acute and chronic uncomplicated type B dissections.[7]
Definitive treatment involves segmental resection of the dissection, with interposition of a synthetic graft.
When thoracic dissections are associated with aortic valvular disease, replace the defective valve. With combined reconstruction–valve replacement, the operative mortality rate is approximately 5%, with a late mortality rate of less than 10%.
Operative repair of the transverse aortic arch is technically difficult, with an operative mortality rate of 10% despite induction of hypothermic cardiocirculatory arrest.
Repair of the descending aorta is associated with a higher incidence of paraplegia than repair of other types of dissections because of interruption of segmental blood supply to the spinal cord.
The operative mortality rate is approximately 5%.
In a study by Mimoun et al of patients with Marfan syndrome who had acute aortic dissection, the patients were found to have a better event-free survival when there were no dissected portions of the aorta remaining after surgery.[8]
A study by Rylski et al indicated that in patients with type A aortic dissection, aggressive hemiarch replacement is associated with a low mortality rate and a low incidence of reintervention. The study involved 534 patients with acute type A dissection who underwent hemiarch replacement. The investigators found that at 1-, 5-, and 10-year follow-up, the patient survival rate was 80%, 68%, and 51%, respectively. During the same follow-up period, no distal reintervention was required in 97%, 90%, and 85% of patients, respectively.[9]
Patients with symptomatic dissection should undergo immediate repair, especially if it is leaking or expanding.
Symptomatic patients require admission to a center experienced in cardiopulmonary bypass and operative care.
Completely asymptomatic patients may have their repair performed electively but may require admission to expedite their evaluation or for preoperative stabilization of their condition.
Patients with chest pain should undergo serial echocardiograms (ECGs) and creatine kinase (CK) determinations if acute myocardial infarction (AMI) is indicated.
Follow-up examinations with radiologic studies are recommended at 3-month intervals for the first year and every 6 months for the next 2 years. After this, patient follow-up should occur annually.
Once a thoracic dissection is suspected, consult a thoracic surgeon. Because many patients with this disorder have concomitant medical illness, consult the patient's primary care provider to expedite preoperative preparation. Early consultation is encouraged when ordering further imaging studies if the patient requires rapid operative intervention.
Consult a radiologist prior to obtaining aortography.
Symptomatic patients require care at a facility equipped to perform cardiopulmonary bypass with aortic and/or valvular repair.
Contact the receiving physician as soon as possible to transfer patients before their condition deteriorates.
Early airway management is indicated in the presence of hemoptysis or stridor.
If coronary insufficiency is suspected, nitrates may be used, but therapy with thrombolytic agents and aspirin should be avoided.
Patients should be monitored and accompanied by personnel capable of resuscitation.
If a prolonged ground transport time is anticipated, consider air transport.
Initial therapeutic goals include elimination of pain and reduction of systolic blood pressure to 100-120 mm Hg or to the lowest level commensurate with adequate vital organ (ie, cardiac, cerebral, renal) perfusion.
Whether systolic hypertension or pain is present, beta blockers are used to reduce arterial dP/dt.
To prevent exacerbations of tachycardia and hypertension, treat patients with IV morphine sulfate. This reduces the force of cardiac contraction and the rate of rise of the aortic pressure (dP/dt). It then retards the propagation of the dissection and delays rupture.
These agents are used to reduce arterial dP/dt. For acute reduction of arterial pressure, the potent vasodilator sodium nitroprusside is effective. To reduce dP/dt acutely, administer an IV beta blocker in incremental doses until a heart rate of 60-80 beats/min is attained.
When beta blockers are contraindicated, such as in second- or third-degree atrioventricular block, consider using calcium channel blockers. Sublingual nifedipine successfully treats refractory hypertension associated with aortic dissection.
Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and prevents exacerbations of tachycardia and hypertension.
Checking for dissection prior to the administration of thrombolytics in the patient presenting with chest pain and ECG changes
Multiple case reports describe patients who received thrombolytics and were found later to have a dissection. The diagnosis of aortic dissection can be subtle.
The diagnosis depends on clinical suspicion, with contributory findings on history, physical examination, and imaging studies.
Obtaining a chest radiograph prior to administering thrombolytics is considered prudent.
Checking blood pressures in both arms and listening for carotid bruits also can help to diagnose aortic dissection prior to administering thrombolytics. The entire clinical picture must be taken into account.
Aortic dissection
Chest radiograph of a patient with aortic dissection. Image courtesy of Dr. K. London, University of California at Davis Medical Center.
Chest radiograph of a patient with aortic dissection presenting with hemothorax.
Chest radiograph demonstrating widened mediastinum in a patient with aortic dissection.
Angiogram demonstrating dissection of the aorta in a patient with aortic dissection presenting with hemothorax.
Electrocardiogram of a patient presenting to the ED with chest pain; this patient was diagnosed with aortic dissection.
Patient with an ascending type A aortic dissection showing the intimal flap. Image courtesy of Kaiser-Permanente.
Patient with an ascending type A aortic dissection showing the intimal flap. Image courtesy of Kaiser-Permanente.
Patient with an ascending type A aortic dissection showing the intimal flap. Image courtesy of Kaiser-Permanente.
Patient with an ascending type A aortic dissection showing the intimal flap. Image courtesy of Kaiser-Permanente.
Patient with a type A aortic dissection involving the ascending and descending aorta. Image courtesy of Kaiser-Permanente.
Patient with a type A aortic dissection involving the ascending and descending aorta. Image courtesy of Kaiser-Permanente.
Patient with a type A aortic dissection involving the ascending and descending aorta. Image courtesy of Kaiser-Permanente.
Patient with a type A aortic dissection involving the ascending and descending aorta. Image courtesy of Kaiser-Permanente.
Patient showing a type B aortic dissection with extravasation of blood into the pleural cavity. Image courtesy of Kaiser-Permanente.
Patient showing a type B aortic dissection with extravasation of blood into the pleural cavity. Image courtesy of Kaiser-Permanente.
Patient showing a type B aortic dissection with extravasation of blood into the pleural cavity. Image courtesy of Kaiser-Permanente.
Patient showing a type B aortic dissection with extravasation of blood into the pleural cavity. Image courtesy of Kaiser-Permanente.
