Tran and Khoynezhad Type A Type B Figure 3B Stanford classiﬁcation of aortic dissection. Stanford type A includes dissections that involve the ascending aorta, arch, and descending thoracic aorta. Stanford type B includes dissections that originate in the descending (and thoracoab- dominal) aorta, regardless of any retrograde involvement of the arch. Diagnostic strategy and management Timely and accurate diagnosis of acute aortic dissection in the ED remains a clinical challenge. Of the approximately 4.4 million patients who present annually to the US ED’s for chest pain, only about 2,000 have AAD.9,10 Partly as a result, AAD is only correctly diagnosed in 15%–43% of patients in the initial presentation.11,12 A somewhat more humbling fact is that up to 53% of cases of AAD were diagnosed after patients have been in the hospital for more than 24 hours.13 History and physical examination alone are not sufﬁciently sensitive to rule out an AAD. Although deﬁni- tive imaging tools are available to rule out an acute aortic syndrome, indiscriminate use of invasive diagnostic tools in patients with low pre-test probabilities will inevitably lead to false positives, and in turn, higher health care costs, unnecessary anxiety, and potential complications for patients. AAD, however, carries a mortality rate of 1%–2% per hour if unrecognized or not treated promptly. The human toll and medical legal implications for failures to diagnose an acute aortic dissection promptly are well publicized.14 The strategy of deferring the workup to the consultants or the admitting service is unacceptable.15 In approaching patients with acute chest pain in the ED, physicians need to methodically rule 58 out the life threatening causes, ascertain the diagnosis, and initiate the stabilization measures. These life threatening causes include acute aortic syndrome, acute coronary syndrome, pulmonary embolus, tension pneumothorax, and esophageal rupture. The evaluation should begin with an immediate assessment of vital signs and hemodynamic status. If patients are critically unstable, ACLS protocol should immediately be started. Patients should be placed on a monitor, have two large bore ( 18 gauge) intravenous access, and oxygen administered. An electrocardiogram (EKG) should be performed within 10 minutes of patient’s arrival. A portable chest X-ray should also be done concurrently with other stabilization measures. In patients at high risks for aortic dissection, 10 units of red blood cells should be typed and crossed. In the setting of chest or back pain, the presence of a pulse differential between carotid, radial, or femoral arteries strongly suggests the diagnosis of acute aortic dissection (LR 5.7).9 The presence of focal neurological deﬁcits such as transient ischemic attack or hemiplegia even more strongly suggests the possibility of an aortic dissection. The likelihood ratio for aortic dissection among patients presenting with focal neurological deﬁcits range from 6.6 to 33.9 Chest X-rays ﬁndings classically associated with aortic dissection include abnormal aortic contour, pleural effusion, displaced intimal calciﬁcation, and wide mediastinum. Although these classic radiographic ﬁndings are not always present, collectively, up to 90% of patients with aortic dissection proved to have some abnormal ﬁndings on chest X-rays. Absence of wide mediastinum and abnormal aortic contour on chest X-ray lowers the likelihood of aortic dissection (LR 0.3).9 Biochemical markers The Holy Grail in the workup of acute aortic dissection is an inexpensive bedside blood test with sufﬁcient sensitivity (good negative predictive value) that physicians can use to rapidly rule out an acute dissection. Of the several biochemi- cal markers that were evaluated in the last decade, the fol- lowing three assays deserve further discussion. Smooth muscle myosin heavy chain, a major component of the smooth muscle in the aortic medial layer, is released to the circulation shortly after the onset of dissection. In a pilot study, the assay ( 2.5 microgram/L) had a sensitivity of 90.9% and speciﬁcity of 98% in detecting acute aortic dissec- tion as compared to healthy volunteers.16 These test numbers are, however, limited to patients with proximal dissection who present within 3 hours of onset of symptoms. Vascular Health and Risk Management 2009:5