When aortic abnormalities are life-threatening
'Thoracic aortic dissection' and 'abdominal aortic aneurysm' are frequently interchanged but are actually very different in nature
By DeWayne Miller
A 76-year-old male calls 911 complaining of acute onset of severe back and abdominal pain. The medics find him in moderate distress, restless and reporting numbness in both legs. He denies chest pain or shortness of breath. Past medical history includes tobacco use, hypertension and COPD.
In discussion, the terms "thoracic aortic dissection" and "abdominal aortic aneurysm" (AAA) are frequently interchanged. These conditions involve the same vessel but are actually very different in nature.
Abdominal aortic aneurysm
Is this a life threat? When responding for a patient with this diagnosis, what should you consider?
A diagnosis of AAA is not an ominous condition. Most are diagnosed incidentally by radiographic studies ordered for other reasons, such as vague abdominal or flank pain.
But it is bad when rapid expansion occurs or its diameter is 5 cm or larger. These conditions can both quickly end in rupture.
A syncopal episode followed by severe abdominal or back pain that is described as "ripping" or "tearing" strongly suggests rupture in the patient with a known AAA2.
A true aneurysm involves all layers of the vessel wall and the vessel expanded to at least 1.5 times its normal diameter. Complications include thrombosis, which can cause ischemia to organs and extremities distal to the site, and rupture, which is life-threatening. The larger the aneurysm, the more likely it is to rupture.
Most AAA patients are asymptomatic and may simply visit a specialist yearly to monitor for any change in the size or symptoms. An average change of 0.25 to 0.5 cm per year can be expected. Once the size reaches 5 cm or greater, the risk for rupture is unacceptably high.
Bedside ultrasound has shown to be very useful for diagnosis, especially for unstable patients. It can be rapidly performed and does not require the patient to be removed from the resuscitation area1.
Rupture is rare, but when it occurs, it has a high mortality rate. When the rupture is posterior and into the retroperitoneum, there is typically a hypotensive period followed by temporary stabilization of vital signs. This occurs because the retroperitoneum fills with blood, then tamponades allowing vital signs to improve.
Treatment: All symptomatic AAA patients should have a surgical consult, preferably in a facility capable of performing emergency repair. Approximately half of patients with rupture who reach the operating room die4.
Along with oxygen therapy and cardiac monitoring, these patients should have two large-bore IVs. Volume resuscitation may be required, and blood products would then be essential.
The consensus is that a blood pressure of 100 to 120 mm Hg (MAP 60 to 65 mm Hg), or the lowest pressure compatible with good organ perfusion, and a heart rate of 60 to 80 is desirable. This target is the same in management of both hypotensive and hypertensive patients. To date, there is no conclusive evidence from studies to support or disprove this target range.
Thoracic aortic dissection
Aortic dissection typically occurs due to damage to the inner wall of the aorta, allowing blood to form a false lumen between the intimal and adventitial layers. A flap that can freely occlude branches of vital vessels may also form.
This condition is three times as prevalent as a ruptured AAA. Pregnancy, hypertension and connective tissue disease are all risk factors. One-fourth of patients with Marfan syndrome will develop dissection.
The Stanford and the DeBakey systems are two methods to describe the anatomy involved. The Stanford type A involves either the ascending aorta or the ascending and descending. The Stanford type B involves only the descending aorta.
Dissection can involve the aortic root, the coronaries, the pericardium and/or various branches such as the subclavian and carotid arteries.
A dissection can compromise coronary artery circulation, causing an ST elevation myocardial infarction (STEMI). Giving thrombolytics to this patient can prove fatal. Any patient with chest and back pain presenting with what appears to be a STEMI should have dissection ruled out.
Only 60 percent of confirmed dissections show as a widened mediastinum on a chest x-ray3, 5.
Most patients have an acute onset of chest or upper back pain. This often changes as the injury extends. Chest pain accompanied by neurologic symptoms (stroke symptoms, paraplegia) should raise strong suspicion of dissection.
Cardiac tamponade is a leading cause of death in patients with type A dissection. Typically a pericardiocentesis is indicated for this condition, but it is contraindicated in the case of dissection unless the patient is in cardiac arrest or near arrest. Rebleeding and increased mortality are associated with the procedure in dissection. Emergent operative intervention is the treatment of choice.
Treatment: The goal of treatment for both AAA and aortic dissection is decreasing the shear forces on the aortic wall, the "water hammer effect."
Oxygen therapy and cardiac monitoring are indicated. Pain control is also important and by increasing patient comfort vital signs may also improve.
If there are symptoms of hypoperfusion and shock with known or suspected AAA rupture, fluid therapy with crystalloids and blood is indicated. Optimal resuscitation strategy has not been established, but a reasonable target is to maintain a blood pressure range of 80 to 100 mmHg systolic and provide expeditious transport to the operative suite for repair. Vasopressors are also indicated; patients that present to the operative suite hypoperfused have very poor outcomes.
The treatment approach for the patient not presenting in a shock state starts with beta blockers.
Labetalol can be used as a monotherapy starting in small doses.
Another viable option is combination therapy, starting with either metoprolol or esmolol. If the target vital signs have not been reached after initiating beta blocker therapy, sodium nitroprusside (Nipride®) can be added and carefully titrated to a systolic pressure of 100 to 120 mmHg. Blood pressure monitoring with an arterial line is preferred when using Nipride. If arterial pressure monitoring is not available, noninvasive blood pressures every five minutes can be used.
- Definitive treatment for AAA ruptures or aortic dissections with complications is the operating suite. Rapid patient prep and fast efficient transport are essential.
- Hypoperfused patients have much worse outcomes, even with timely surgical repair attempts.
- Initial stabilization attempts with crystalloids should be augmented with packed red blood cells as soon as possible.
- Evangelista, A. Aortic intramural haematoma: remarks and conclusions. Heart 90(4): 379, 2004. [PMID: 15020508]
- Hagan P. G., C. A. Nienaber, E. M. Isselbacher, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 283(7): 897, 2000.[PMID: 10685714]
- Klompas, M. Does this patient have an acute aortic dissection? JAMA. 2002;287:2262-2272.
- Manghat, N. E., G. J. Morgan-Hughes, C. A. Roobottom. Multi-detector row computed tomography: imaging in acute aortic syndrome. Clin Radiol 60(12): 1256, 2005.[PMID: 16291307]
- von Kodolitsch, Y., C. Nienaber, C. Dieckmann, et al. Chest radiography for the diagnosis of acute aortic syndrome. Am J Med. 2004; 116:73-77.