Chest pain is a common complaint in the ED that can be associated with serious and even lethal conditions. Two of these deadly entities, acute myocardial infarction (AMI) and aortic dissection (AD), are quite different and treated by different specialists. Both conditions are time-sensitive pathologies whose ultimate outcome depends on rapid identification and intervention.
AD is probably more difficult to diagnose because it can present with a broad spectrum of signs and symptoms. Acute MI, on the other hand, is usually relatively straightforward when the ECG signals its presence. In rare cases, however, a type A aortic dissection can actually dissect backwards and occlude the ostia of coronary arteries, producing signs, symptoms, and ECG changes of a classic AMI.
This month's column discusses such a case, in which an astute emergency physician made the diagnosis of aortic dissection in the ED in a patient, who by all signs, symptoms, and ECG findings, had an acute MI. This clinician was skilled in bedside ultrasound, a technique that is not always easy and is not in the clinical repertoire of many older emergency physicians.
Diagnosis of Acute Aortic Dissection Presenting as ST-Elevation Myocardial Infarction Using Point-of-Care Ultrasound
J Emerg Med
This report by a Canadian EP describes a 69-year-old man with chest pain who drove himself to the ED. The pain had started two hours before presentation while he was shoveling snow, and he described it as sharp and retrosternal, with no radiations, and as 8/10 on the pain scale. The peak severity occurred about 10 minutes after onset. He also described shortness of breath and diaphoresis, but had no nausea, vomiting, or dizziness. The patient had no medical history and no cardiac, pulmonary embolism, or aortic dissection risk factors. Most of his pain had resolved by the time he reached the ED.
The initial vital signs revealed a heart rate of 73 bpm, blood pressure of 185/101 mm Hg, a respiratory rate of 18 bpm, and oxygen saturation 98% on room air. The first ECG was normal. He appeared well and in no distress. The physical exam was unremarkable, but the chest pain returned during the ED stay. The patient became short of breath and diaphoretic. Another ECG was obtained, which showed ST segment elevation in V1 and V2, with diffuse ST depressions that were not present in the initial triage ECG. The ECG was characteristic of an acute myocardial infarction. An acute STEMI was diagnosed. The cardiac catheterization team was activated.
Because of the shortness of breath, the treating clinician performed a bedside ultrasound (POCUS; point-of-care ultrasound) to assess left ventricular function. A parasternal long access view of the heart revealed an echogenic flap of the ascending aorta, and color Doppler revealed significant aortic regurgitation. The examination of the abdominal aorta and right carotid artery also revealed intimal flaps. These findings were consistent with a type A aortic dissection, and a cardiac surgeon was consulted. A labetalol infusion was started, and all anticoagulants were held. CT angiography was performed and confirmed the diagnosis. The patient was transported to the operating room, but he had a cardiac arrest and could not be resuscitated.
Comment: This patient had a type A aortic dissection that progressed backwards and occluded the origin of the right coronary artery, producing AMI on the ECG. The diagnosis of type A dissections in an expeditious manner is essential because the mortality rate is about two percent per hour after the onset of symptoms. The overall mortality rate without treatment is about 60 percent, but the mortality rate can be reduced to about seven percent to 36 percent with surgery. About 20 percent of type A aortic dissection are not amenable to surgery because of comorbidities. Medical therapy has about a 50 percent mortality. Common underlying comorbidities and risk factors are found in the table.
AD, as noted by this author, can present with a variety of nonspecific symptoms, and it is referred to as the great masquerader. Ten percent of patients reported no chest pain. Other initial findings from obstruction of the aortic branches include stroke, paraplegia, visceral ischemia, and limb ischemia. The overall missed diagnosis rate is about 25 percent. Aortic dissection is rarely considered initially in a patient with a stroke. Delayed diagnosis is, of course, associated with a higher mortality rate.
An AMI is an uncommon presentation of aortic dissection, but it occurs in one to two percent of type A dissections. The dissection flap in the aorta extends into the ostia of the coronary arteries, causing acute occlusion and ST segment elevation or depression on the ECG. It most frequently affects the right coronary artery, but the left coronary artery can also be involved. Many cases of AD causing acute MI are not readily diagnosed, but can be ferreted out during cardiac catheterization. Some of the therapy used to treat presumed myocardial ischemia, such as prolonged observation and anticoagulants, can be lethal for patients with aortic dissection.
The bedside ultrasound in this case allowed the clinician to distinguish between a true STEMI and proximal aortic dissection. There was no suspicion for aortic dissection based on the history, and no other findings were suggestive of that diagnosis. This clinician used bedside US in a rather amazing way. He was able to diagnose AD within a few minutes and consult cardiac surgery. I doubt if many cardiac surgeons would take a patient to the operating room based on a bedside US in the ED. Subsequent tests, such as a CTA, is just one of the always-present delays in such a scenario.
It's instructive to note that an early type A dissection produces anterior chest pain like an AMI. This dissection does not usually produce back pain or posterior chest pain until it moves further distally in the aorta. Like an AMI, AD can occur after exertion, and shoveling snow is a classic precipitant of both conditions. The pain of a dissection, somewhat unlike an AMI, has an abrupt onset, peaks early, and is described not as pressure but as sharp, tearing, or ripping. Of course, one has to ask that specific question if this answer is to surface. Given the time constraints on getting an acute MI to the cath lab, it is nearly impossible to obtain a detailed history or examination when the history and ECG are so classic.
The notorious and often-described pulse deficit in the arms of greater than 20 mm Hg may be seen if looked for, but is found in only about 20 to 30 percent. A diastolic decrescendo heart murmur on the right sternal border, heard in about 50 to 60 percent, is caused by aortic valve involvement (acute insufficiency). Other nonspecific findings are a wide pulse pressure (from aortic insufficiency) or CHF from cardiac ischemia. One might consider US if the patient presents with shortness of breath and distended neck veins to look for pericardial tamponade, which can also occur.
The D-dimer in AD is usually elevated to some extent, but this is a difficult-to-interpret nonspecific test that is elevated by many conditions. For a D-dimer less than 500 ng/mL, the negative predictive value is about 96 percent. Patients with a D-dimer less than 500 ng/mL are not likely to benefit from further aortic imaging. Caution should be exercised, however, because some authors have reported that up to 18 percent of patients with confirmed aortic dissection may have levels under 400 ng/mL.
A chest x-ray can suggest aortic dissection if there is aortic root or mediastinal widening or calcium separation in the arch. It's not known if a D-dimer, murmur of aortic insufficiency, chest x-ray, or both side blood pressures were investigated in this report.
Clinicians who had more than two years of experience with cardiac US diagnosed aortic dissection with a sensitivity of 54 percent and a specificity of 94 percent. The US had a negative predictive value of 94 percent for ruling out aortic dissection when combined with other physical findings. (Intern Emerg Med 2014;9:665.) The use of bedside US by EPs in another study was associated with reduced time to diagnoses of AD by 146 minutes. (Am J Emerg Med 2016;34:486.)
Bedside US can be a useful tool to assess rapidly for signs of aortic dissection for a STEMI with an atypical presentation (not this case, in my opinion). This, of course, includes thinking of US in the first place as well as having the ability to find and interpret US findings in the aorta.
CT angiography is considered the best screening test for aortic dissection, but an ED transesophageal echocardiogram (TEE) is an alternative. Neither is easy or quick in most hospitals. A video clip of this ultrasound is available at https://goo.gl/9R3rzU.
My impression of this case report is that the vast majority of emergency clinicians would not make the correct diagnosis in the ED, and would go the aspirin/heparin and cardiac cath route. Most cardiac cath labs would accept this patient with open arms, and would likely make the correct diagnosis during their attempts to treat a STEMI. Whether the time required to make this final diagnosis would save many such patients is unclear, and the process of taking patients from the cath lab to the operating room is never easy. Best advice: Don't get an aortic dissection.
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Dear Dr. Roberts: I am an ED pharmacist and just read your article, “The Best Three Treatments for Migraine.” (EMN 2018;40:12; http://bit.ly/2DkSuLI.)
The article recommends a ketorolac regimen consistent with the package insert and FDA recommendations. I would argue that this dose is probably too high for most people based on the evidence.
Multiple studies now indicate the analgesic ceiling of ketorolac is 10 mg, regardless of the route of administration. Other studies suggest that rates of GI ulceration, platelet inhibition, and worsening post-operative hemorrhage are likely dose-related.
This information is not new, but the FDA has no particular reason to revisit the approved dosage information, and these high doses continue to be the published recommended dose despite the potential to optimize the risk/benefit ratio of adequate analgesia with less risks using lower doses of ketorolac as our routine doses.
We have removed all ketorolac doses above 15 mg (the injectable form comes as 15 mg) in our emergency department. This is the dose we recommend for most indications in adults. One major caveat to this is that the average weight of patients was not reported in any of the trials I know. Presumably, mg/kg may have some impact, but that question was not addressed. — Gabriel R. Golfus, PharmD, Mayo Clinic Hospital, Rochester
Dr. Roberts responds: Thanks for your letter concerning the best analgesic dose for ketorolac. Your references support your conclusions, but they do not note any complications from short-term, high-dose use, as would be the case in the ED for migraine. I totally agree with using a maximum of 15 mg per dose for treating migraine, and one to two doses would likely be the most used. I personally don't use much ketorolac at all except for biliary colic and kidney stones, preferring short-term opiates for significant pain.
Dear Dr. Roberts: I would like to suggest another treatment for migraine and headaches in general. (“The Best Three Treatments for Migraine,” EMN 2018;40:12; http://bit.ly/2DsFBQZ.) This is based on my 40-year ED practice and a 26-year longitudinal study I performed across several hospitals (unpublished but with an approximate efficacy rate of 40%). It consists of one minute of rhythmic squeezing of bilateral thenar eminences, once a second for 60 seconds. Yes, I know, it's alternative medicine, but it is free, quick, easy, and painless, and it has no apparent harmful effects. It was also approved as effective by two of the most cynical populations I know—ED nurses and my wife. — Michael H. LeWitt, MD, Berwyn, PA
Dr. Roberts responds: Interesting. I have actually heard of that intervention, but never used it myself.
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