Don’t Be Fooled by the Great Masquerader
Jennifer Nofar Boukouris, M.D.
Co-Chief Resident, St John Hospital and Medical Center


You are in the middle of a busy shift when you pick up a chart that lists a chief complaint of chest pain. As you enter the patient room, you observe a middle age African American female in mild distress. She appears tachypneic. A quick look at the other triage vital signs reveals that she is tachycardic, hypertensive, and has a low grade temperature. The nursing staff has already put her on the cardiac monitor and performed the ECG which was remarkable only for sinus tachycardia. During the patient interview you discover that she has had a dry cough and pluertic chest pain over the past 2 days. Review of systems is positive for dyspnea on exertion and orthopnea. She denies any past medical history, drug use, or sick contacts. You decide to pursue a cardiac workup and check a chest x-ray. The x-ray revealed a left lower lobe infiltrate. So, you attribute her chest pain to pleurisy from the pneumonia and start IV antibiotics and give her a bolus for the tachycardia and morphine for the pain. After the therapies have been instituted you reassess the patient and notice she is still tachycardic, hypertensive, and uncomfortable. Things just are not adding up in your mind. You wonder how pneumonia could cause so much discomfort and such a systemic response in a previously healthy woman...

Aortic dissection is a rare but life-threatening emergency that often goes undiagnosed to even the sharpest clinician. Some studies have quoted a near 50% miss rate. Each hour that an aortic dissection goes undiagnosed, the mortality rate increases 1-2%. Therefore, it should always be part of the differential diagnosis for patients complaining of chest pain. Incidence of aortic dissection is estimated to range from 2.6 to 3.5 per 100,000 person-years. This may be an underestimate because of the underreporting of the condition. The International Registry of Acute Aortic Dissection (IRAD) reviewed 464 patients who were diagnosed with aortic dissection, and found that65% were men and the mean age was 63 years.

Two mechanisms exist for creating an aortic dissection. First, increasing hydrodynamic stress tears the intimal wall of the aorta and a column of blood slips in between the intimal and medial layers creating a false lumen.The other less common type of aortic dissections are intramural hematomas. They develop without tearing the intimal wall. They are proposed to be instigated by hydrodynamic forces damaging the vaso vasorum which eventually ruptures and bleeds into the medial wall. The Stanford classification has become the more popular way to describe aortic dissections. Type A dissections involve the ascending aorta while Type B includes all others. Ascending aortic dissections are twice
as common as descending dissections.

Keeping the following risk factors and scenarios in mind will help aid in the diagnosis. The most predisposing factor for aortic dissection is uncontrolled hypertension. In the IRAD study 72% for patients had a history of hypertension. Another important risk factor is previous history or aortic dissection. One third of those patients will re-dissect, rupture, or extend their dissection in the next 5 years. Other risk factors include: atherosclerosis, connective tissues diseases such as Marfan Syndrome and Ehler’s Danlos, vascullitis such as giant cell arteritis, cocaine use, pregnancy, sleep apnea, Turner’s syndrome, bicuspid aortic valve, polycystic kidney disease, trauma, cardiac catheterization, and a family history of aortic dissection. We should document lack of the above risk factors in the medical record.

Patients with aortic dissection classically present with severe, sharp, or tearing chest pain that is worst at onset, radiating to their back (73% of cases according to the IRAD study). Signs and symptoms of an aortic dissection are related to the location and extent of the dissection. Clues to an ascending aortic aneurysm are new aortic insufficiency murmur, inferior ST elevation MI secondary to extension into the right coronary ostia, cardiac tamponade, hemothorax, asymmetrical radial or carotid pulses, and difference in systolic blood pressure between the two arms of 20mm of mercury or more. Patients with Type B dissections are more likely to be hypertensive than Type A dissections. They may present with migrating pain, back pain, and asymmetrical pulses. Think of this disease if you have complaints above and below the diaphragm such as chest pain and abdominal pain.

Atypical presentations make the diagnosis more challenging. One study quoted that 15% of dissections present pain free. A good rule is to consider aortic dissection if you have chest pain and another complaint. Rare and interesting presentations include chest pain and voice hoarseness secondary to left recurrent laryngeal nerve palsy, chest pain and dysphagia secondary to compression of the esophagus. There have been case reports of aortic dissection leading to neurologic deficits including altered mental status, seizures, and strokes. These deficits can be due to direct extension of the dissection into the carotid arteries or diminished carotid blood flow. Moreover, if a patient presents with sudden lower extremity paralysis and mentions that they had some chest and back pain as well, they could have had an aortic dissection that occluded the spinal artery. Another way that aortic dissection can present is with syncope. The IRAD study found that 13% of the patients with aortic dissection had syncope as their only complaint, and no pain. Needless to say, always approach each patient with a high clinical index of suspicion and wide differential.

Chest x-ray is indicated if an aortic dissection is suspected. Abnormal CXR findings related to aortic dissection are numerous and include mediastinal widening, “calcium sign” which is a calcium deposit 5mm or more from the wall of the aorta, and a left sided pleural effusion. However, up to 12% of patients with aortic dissection have a normal chest x-ray. Multiple advanced imaging modalities are available to confirm the diagnosis, but most physicians chose helical CT if the patient is stable because it is readily available. Transesophageal echocardiograms are useful in Type A dissections when the patient is not stable enough to leave the emergency department.

It is imperative that patients suspected of having an aortic dissection be treated while diagnostic tests are performed. Medical management is necessary to reduce heart rate and blood pressure. A beta blocker should be used in conjunction with vasodilator therapy. Target heart rate should be between 60 and 80, and target systolic blood pressure should be between 100 and 120. Labetalol is recommended in cocaine associated aortic dissection. Type A aortic dissections require prompt surgical treatment. Type B dissections only require surgery in certain instances: if a major vessel is blocked and oftentimes this is corrected by interventional radiology, uncontrolled hypertension, frank aortic leaking or rupture, or development of a localized aneurysm. Therefore, surgery should be consulted for all aortic dissections.

Reviewing the chest x-ray again, you notice that the mediastium could be widened. As you finish telling the patient and her spouse that you plan on checking a CT scan to rule out other causes for her pain, her husband follows you to the desk and asks you if his wife is going to die. In your astonishment to his question you ask “Why do you say that?” He responds by telling you that her sister and niece were both diagnosed with pneumonia and then died suddenly after. You reassure the man and call CT to take the lady next. So although you almost fell into the trap of “tunnel vision” your gestalt was correct, the lady had an aortic dissection.

References:

Eagle KA, Isselbacher EM, DeSanctis RW: International Registry for Aortic Dissection (IRAD) Investigators: Cocaine-related aortic dissection in perspective. Circulation 105:1529, 2002.

Hagan PG, et al: The International Registry for Aortic Dissection (IRAD): New insights into an old disease. JAMA 283:897, 2000

Ankel, F Chapter 84 Aortic Dissection. Rosen’s Emergency Medicine Concepts and Clinical practice 6th edition1324-1329, 2006

Soddeck G, et al: D-Dimer in ruling out acute aortic dissection: a systematic review and prospective cohort study. European Heart Journal 2007 28(24):3067-3075

Swahney N, et al: Aortic Intramural Hematoma – An increasingly recognized and potentially fatal entity. Chest. 2001;120:1340-1346.

Manning, W: Clinical Manifestations and diagnosis of aortic dissection. UptoDate.2008

Elefteriades, J, et al: Management of descending aortic dissections. Ann Thorac Surg 1999;67:2002-2005

Rogers, R. “Aortic Dissection”. Audio Lecture from EMRAP April 2008.

 



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Posted: Sunday, October 26, 2008