American Journal of Emergency Medicine 36 (2018) 1497-1520

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Correspondence

The wider implications of AD-related AR and pulmonary oedema

When aortic dissection (AD) presents with aortic regurgitation (AR) and pulmonary edema the coexistence of chest pain should be sufficient to raise the index of suspicion for AD, as was the case in the recent report [1]. Even when chest pain is initially attributed to acute myocardial infarction(AMI) [2,3], and the electrocardiogram is supportive of that diag- nosis, the coexistence of AR and either pulmonary edema [2] or pulmonary congestion [3] should still raise awareness of AD, given the fact that AD could be an underlying cause of both AMI [4] and AR [1]. In the absence of chest pain the coexistence of AR and pulmonary oedema should still raise the index of suspicion for AD. This was the case when AR and radio- graphically validated pulmonary edema was documented In a 44 year old man who presented with a 4 weeks history of new onset breathlessness. Even though he had no chest pain further investigations revealed aortic dissection, which was managed surgically by aortic root and aortic valve replacement [5]. In this example the most plausible rationale for a high index of suspicion for AD was that AD-related AR is one of the few diagno- ses with high pretest probability of being positive in a patient with the as- sociation of AR and Rapid progression to pulmonary edema [6]. In the latter example, far from being deterred by a falsely negative contrast enhanced computed tomography scan, the clinical team selected trans esophageal echochardiography as the next diagnostic tool “due to high pretest proba- bility of aortic dissection”. That was the strategy that ultimately generated the correct diagnosis of Stanford type A dissection [6].

There should be a high index of suspicion for AD even when pulmo- nary edema is unilateral [7,8]. Unilateral pulmonary edema may occur when one of the pulmonary arteries is compressed by a dissecting aortic aneurysm. In that context pulmonary edema is contralateral to the oc- cluded pulmonary artery [8].

Crack cocaine is a risk factor both for pulmonary edema [9] and for AD itself [10]. Accordingly, especially in Young individuals with no known risk factors for AD, there should be a high index of suspicion for illicit drug use as the underlying cause for AD [10], and for its association with either AMI [9] or pulmonary edema [9]. In that context, as well, pre- test probability of AD is enhanced by documentation of coexistence of AR.

Acknowledgment

I have no conflict of interest and no funding.

Oscar M.P. Jolobe

Manchester Medical Society, Simon Building, Brunswick Street, Manchester

M13 9PL, United Kingdom E-mail address: [email protected].

6 May 2018

https://doi.org/10.1016/j.ajem.2018.06.012

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   Response to “The wider implications of AD-related AR and pulmonary edema”

   We really appreciate the response from the readers regarding the implications of acute aortic regurgitation (AR) and pulmonary edema in the diagnosis of aortic dissection. As mentioned by the authors, AR, whenever present, is an important clue to the diagnosis of aortic dissec- tion. This is most likely if the AR is new-onset. Even in patients without clear history or previous physical examination records of AR murmur (as is commonly encountered at the emergency room), the identification of AR murmur on auscultation should raise the suspicion of specific etiol- ogies such as aortic dissection. This is especially true in this era when rheumatic heart disease has been less prevalent and AR murmur less fre- quently heard. The AR can occur alone or in combination with pulmonary edema or congestion, depending on the severity of regurgitation. When pulmonary edema is noted in patients with chest pain, careful ausculta- tion becomes even more important since the AR murmur could be overwhelmed by the prominent pulmonary rales or wheezing.

   Another important point notified by the authors is that aortic dissec- tion can cause not only AR but also acute myocardial infarction [1-3]. If acute pulmonary edema occurs in a patient with acute myocardial infarc- tion, the pathogenic mechanism can usually be attributed to: (1) reduced left ventricular ejection fraction, (2) acute Mitral regurgitation (MR) resulting from papillary Muscle dysfunction or chordae tendinae rupture,

   (3) ruptured interventricular septum (VSD) leading to left to right shunt, etc. [4]. Under such circumstances, systolic MR or VSD murmur, instead

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