Interesting case from recently I thought I’d share… a 71 year old female brought by EMS with an unusual report (never happens, right?). Initial call went out for hip pain for the past couple days and well as shortness of breath and not acting right today. Was initially awake, alert, and speaking normally on EMS arrival but developed acute respiratory distress en route and required intubation. On arrival was tachycardic to 130s-140s and had SBP of 100s. Skin was cool and mottled appearing. No obvious external signs of trauma. Pupils equal and reactive. No reported fall but family was unsure. Pretty broad differential at this point, anywhere from PE to intracranial injury to sepsis to MI to …, especially difficult due to lack of context and inconsistent reports.

Chest xray in room 9 showed what appeared to be a widened mediastinum. To fully evaluate for PE vs dissection, we proceeded from room 9 with CTA of chest and abdomen, to also cover for intra-abdominal injury. CT head and cspine were also done and negative. Lactic was elevated at 5, WBC was 32, and troponin was 0.5. Blood pressure began to trend downward, so we continued fluids. CTAs were quickly viewed and demonstrated ascending aortic pseudoaneurysm with rupture due to penetrating ulcer, resulting in mediastinal hematoma and hemopericardium. Blood pressure continued to trend downward into the 70s systolic. We continued fluids, and started blood. Bedside US demonstrated the aforementioned hemopericardium but no signs of tamponade, so we could hold off on pericardiocentesis.. Also placed central line and started pressors. Transferred to Jewish for OR and had definitive repair.

So that went pretty quickly but had some interesting findings. Penetrating aortic ulcer is something I hadn’t seen before but usually occurs secondary to atherosclerosis. Basically the intima of the aorta becomes denuded due to atherosclerotic plaque formation and can progress through the aortic wall, leading to intramural hematoma and eventually dissection and/or perforation. Interestingly, this is not a common cause of dissection, being the initiating lesion in less than 5% of dissection.

Dissection is something we’ve all learned about and something we always have to be concerned for, as they can go pretty badly pretty quickly. Classically, these patients have “tearing chest pain radiating to the back” and are hypertensive, but as this case demonstrates that is not always the case. They can nonspecific complaints or nonspecific exams. CT is the gold standard for diagnosis, chest xray can show the widened mediastinum or obscuration of aortic knob but these are unreliable. If you have a suspicion, best to order CT and act quickly. D-dimer is also emerging as a possible screening modality, as it has demonstrated 97% sensitivity, but has poor specificity (56%). We all know the classic teaching on how to treat these as well, with rate control first (esmolol or labetalol) and BP control if needed (nitroprusside or nicardipine). However, this presumes that they are hypertensive, so what about the hypotensive patient, like we saw? Definitely something to act on quickly and correct. A 2005 study showed that hypotension is not a common characteristic of dissection (29% of patients studied), but had significantly higher mortality than patients without hypotension.

So what can cause hypotension in the dissecting patient? First off, it’s much more common in type A dissections than type B. The most common reasons for these patients to become hypotensive are acute cardiogenic failure and tamponade. The cardiogenic failure can result from involvement of the coronary arteries causing a STEMI, or from aortic valve involvement causing aortic regurgitation. If blood collects in the pericardium, it can cause tamponade, and pretty quickly at that. Tamponade is relatively rare, but has a very high early mortality. Other possible reasons for hypotension can include hypovolemia from blood loss into the chest, or spinal ischemia that can lead to a neurogenic shock.

Awesome, right? So many reasons for hypotension in an already really sick patient. Having these in mind though is very important as it guides management and can be crucial for rapid intervention. Bedside US is quick and can identify a tamponade, and quick pericardiocentesis can stabilize for surgical intervention. Early pressor use can be beneficial in acute cardiogenic or neurologic shock. Of course all of these are stabilizing measures until you can get the patient to a surgeon, but it’s always important to preserve perfusion to those vital organs. Fluids and blood can help with the possibility of volume loss, although that’s a much less common reason. Also be judicious in the patient that is in acute cardiogenic failure.

Thanks for sticking with me on that one. I’ve also included links to video for pericardiocentesis, as it is a procedure we don’t get a ton of practice with. Enjoy!

• Resources:
• Tintinalli’s Emergency Medicine 8th Edition, Chapter 59, pages 412-415
• Uptodate: Overview of acute aortic dissection and other acute aortic syndromes
• Tsai, T, et al. Clinical Characteristics of Hypotension in Patients with Acute Aortic Dissection. The American Journal of Cardiology Vol 95. January 2005
• Isselbacher, E., Cigarroa, J., Eagle, K. Cardiac Tamponade Complicating Proximal Aortic Dissection. Circulation. American Heart Association Journals. Volume 90, No 5. Novemnber 1994