Pick Your Assessment Vessel Carefully

Contributed by readers. Edited by Sheldon Jacobson, MD

A 66-year-old man presents to the emergency department (ED) with retrosternal chest pain of six hours' duration. Just before his arrival, the patient noticed numbness in the left leg and foot and a dull aching pain in the left hip and flank and has had difficulty bearing weight on that side. The chest pain, which has been moderate since its onset, is poorly defined, in the general vicinity of the midsternum, and unaffected by activity, position, respiration, or swallowing.

Except for hypertension, which he is controlling with amlodipine, the patient's medical history is unremarkable. He smokes about half a pack of cigarettes a day and claims no significant alcohol use and no history of recreational drug use. His father died of a "heart attack" at age 46.

On examination, the patient appears to be in pain and is tachypneic and slightly diaphoretic. His blood pressure is 188/110 mm Hg; pulse, 88 and regular; and respirations, 20. Room-air oxygen saturation of arterial blood is 98%. Except for evidence of an S4 gallop, the results of a cardiopulmonary examination show clear lungs and a normal heart. The remaining examination findings are within normal limits.

The initial ECG shows left ventricular hypertrophy with T-wave flattening, compatible with a left ventricular strain pattern. A comparison with a previous ECG reveals no acute changes. Routine laboratory tests include a CBC and an SMA12, both of which reveal normal findings. The patient is given oxycodone for pain, metoprolol intravenously, and nitroglycerine ointment but is not given heparin.

The emergency physician believes the patient has atypical chest pain, but the family history and history of tobacco use and hypertension indicate that an acute coronary syndrome must be considered as the leading diagnosis. The patient is transferred to the adjacent chest pain unit, which is staffed by another group of providers, and the "rapid rule out" protocol is instituted.

After eight hours, the results of CPK-MB and troponin I tests are negative, and a second ECG shows no changes. Exercise stress testing is then considered, but although the patient's chest pain has diminished, he still has pain, weakness, and numbness in the left leg. The physician then arranges an appointment for a chemical stress for the following day and discharges the patient.

After leaving the hospital, the patient, who notices increasing pain with each step, is unable to walk to his car. He stops in the vicinity of the hospital's fast track unit, where the physician on duty examines the patient and finds the left lower extremity to be pulseless. The skin on that limb is slightly cooler than that on the other; the pedal pulses in the right foot are normal. The patient is transferred to the ED, where a chest film suggests a widened mediastinum but shows no other abnormalities. The patient is then rushed to the radiology suite where CT scans of the chest, abdomen, and lower extremities reveal an aortic dissection that begins in the distal aortic arch and extends through the abdominal aorta into the left iliac artery; distally, the dissection extends as far as the vessels in the mid thigh.

Within the hour, a graft is surgically inserted from the aortic arch to the iliac vessels. Except for mild paraparesis--most likely due to ischemia in the spinal cord that occurred during surgery or after the placement of the graft--the short-term recovery is unremarkable.

COMMENT

In this case, a patient with a type III aortic dissection extending into the leg presented with chest and leg pain. The patient began to undergo a fairly extensive work-up for a possible acute coronary syndrome, but the preparation was stopped prematurely when this leading diagnosis was considered to be unlikely. Other omitted procedures included initial chest radiography and a measurement of blood pressure in the right arm only.

Moreover, the patient's leg pain and weakness were never adequately evaluated or considered in the differential diagnosis. Most important, though, is that the femoral and pedal pulses were not evaluated during the first ED visit. When a patient presents with a potential cardiovascular emergency, the initial physical examination should include blood pressure measurements in both arms as well as the assessment of femoral and pedal pulses.

In this case, the pressure measurements would have been equal, because the dissection began just below the left subclavian artery. The pain that occurred at rest in the left leg could have been caused by ischemia or by the dissection progressing down the thigh, or both.

The decision to discharge the patient can also be faulted, albeit retrospectively. Patients who suddenly lose the ability to walk cannot be discharged from the ED. Such symptoms are a red flag that signifies some serious underlying process.

Aortic dissection can appear with a host of signs and symptoms. The most common presentation is the abrupt onset of tearing, searing pain that extends or radiates through the upper and mid back to the retrosternal area. The location of pain is believed to move as the dissection progresses down the aorta. In approximately 10% of cases, however, the dissection is actually silent and self-limited and is detected on a chest film that is obtained for another reason.

Because the process can obstruct any vessel, one would expect to see patients presenting with stroke syndromes, myocardial infarction and ischemia, intestinal infarction, spinal cord ischemia, and renal infarction. In type I and II dissections that involve the aortic arch and root, the aortic valve can be disrupted, thereby leading to acute aortic insufficiency. In these latter cases, the dissection can rupture into the pericardium and left pleural space. A rare presentation is the so-called pseudocoarctation syndrome, in which the aorta is obstructed below the subclavian arteries and hypoperfusion appears in the lower extremities.

In this case, the patient never underwent anticoagulation, which was fortunate, because it would have enhanced the rate of dissection. The procedure would also be catastrophic in cases of rupture into the pericardium or pleural space.

The causes of dissection are, most often, hypertension and, less often, underlying cystic medial necrosis of the aortic wall. The treatment of dissection types I and II consists of prompt aortic grafting. The best treatment for type III dissection is a regimen of antihypertensive agents and therapy that reduces the contractile force of cardiac ejection--a combination of beta-blocker and nitroprusside therapy is the current recommendation. Reducing the contractile force and blood pressure is believed to reduce the shearing forces that propel the dissection down the aortic wall.

Percutaneous aortic stents are also now used to treat type III aortic dissections. Although this therapy is still experimental, it shows significant promise as a minimally invasive method for improving a potentially grave prognosis.