We had an awesome lecture by Dr. K Gore this past week–this blog is a quick review of her lecture on aortic dissection.


An aortic dissection (AD) is a tear into the intimal layer of the aortic wall. It is commonly described as a “tearing” chest pain that radiates to the back–which is convenient that a tearing phenomenon presents as a tearing pain. Allegedly, the first case to describe AD was on the post-mortem of King George II of Britain in 1760–not to be confused with King George III from Hamilton and Revolution fame.

It is a rare diagnosis with an incidence of around 3-4 per 100,000 person-years. It is more common in men than women with a ratio of ~2:1. Due to it’s rare incidence, there isn’t a tremendous amount of data or randomized controlled trials on the syndrome.

Risk Factors

Risk factors for AD include anything that can damage the integrity of the vessel wall. HTN is by far the most common cause of AD, however, we commonly associate connective tissue diseases such as Marfan Syndrome with the disorder. The average age of diagnosis is in the 60s (although patients with connective tissue disorder have a much lower age of presentation often in their 30s).

  • Risk Factors
    • Congenital Disease: Marfans, Ehlers-Danlos (type IV), Turners, annulo-aortic ectasia, Familial Aortic Dissection
    • Aortic Wall Stress: HTN, previous CV surgery, infection (syphilis), arteritis (Takayasu/Giant Cell), cocaine
    • Reduced Resistance: older age, pregnancy

Signs and Symptoms

As Dr. Gore pointed out, the big issue with diagnosing AD is that it is rare, and from the above chart, it doesn’t have a classic presentation. We get drilled into us that AD presents as a “tearing/ripping pain,” but this in fact is only present 51% of the time. We also get told to suspect AD in patients with Chest Pain + Neurologic symptoms, but again a focal neurologic deficit is only present 14% of the time. I think it would be easy to get discouraged about the above data, but my big takeaway is that AD presents as pain and “something weird.” More than likely, it’ll be a severe/worst pain ever with something else that makes you raise your eyebrows, and makes you think this isn’t your typical chest pain work-up with a few troponins and a dispo.

Also fun fact, although cardiac tamponade is a relatively rare presentation of AD (~4%), it is the most common cause of death in AD.


In addition to the imaging options below, it is important to get all of your basic labs including CBC, CMP (check for end organ damage), troponin, BNP, INR/PTT, and T+S (possible surgery and need for blood products).

  • EKG: 15% may show signs of ischemia (most commonly inferior lead ischemia). 40% will show non-specific ST-T wave changes.
  • CXR: ~60% will have a wide mediastinum on CXR, while only ~16% will have a completely normal CXR.
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  • Pulse Deficit: defined as >20 SBP point difference between arms
  • CT Angio: this is typically the quickest and best modality of diagnosis available in the ED. However, it’s important to note that surprisingly (or at least I was surprised) to learn it only has a sensitivity 94% and specificity 77%. I think we’ve all heard of 1-2 cases online or in-person of an initial CTA that missed a dissection that was later diagnosed on the return trip to the ED.
    • Also may want to consider getting CTA of Chest/Abdomen/Pelvis in patients with high suspicion as will need to address the entire length of dissection
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  • Suprasternal Notch US
  • TEE: this is great to have in your back pocket in patients with CKD or where CTA may not be an option. It has a great sensitivity 98% but may have a few more false positive with specificity 83%.
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  • MRA: this is the best imaging study for AD but is definitely limited by availability and time. Also may have some fear of sending suspected AD to MRI scanner early in their work-up before labs and HR/BP control have started. Sensitivity and specificity 98%.
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  • D-Dimer: First10EM D-Dimer Review does a great job of the studies on use of D-dimer in AD. Essentially, there is some good evidence that D-dimer can help rule out aortic dissection when used with ADD risk score However, it is a tremendously tough thing to study as the incidence of AD is so low, therefore, almost any study will find a relatively good sensitivity on AD.
    • D-Dimer with ADD Tool
      • Source: RebelEM
    • ADD Score
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Treatment depends on the type dissection that is diagnosed: Type A vs. Type B.

This is one of the favorite test questions: what is the management of Type A vs. Type B? Essentially Type A involves the aortic arch and the branching vessels from the arch (innominate, left common carotid, left subclavian arteries) and this requires emergent surgery. However, in the emergency department, the initial treatment is the same for both including a stepwise fashion of treating pain, then HR, then BP, with consult to CT surgery or vascular surgery depending on the institution.

  1. Treat Pain: one of the best ways to treat BP in these patients is to aggressively treat pain. This pain is severe, and to effectively treat BP, we first need to control this. Nausea can also be an issue and we want to treat anything that can increase BP or cause valsalva
  2. Treat HR: we treat HR first to avoid the shear force caused by the stroke volume of each beat. Furthermore, we start with rate control because if start with BP agent, then may cause reflex tachycardia which can worsen shear force. Esmolol is the go-to agent for this with a goal HR<60. Typically, esmolol is given as a 500 mcg/kg bolus over 1 min and start at 50 mcg/kg/min infusion. If no response in HR in 4 minutes (since onset of action is 1-4 minutes), then can give additional bolus of 500 mcg/kg and increase infusion to 100 mcg/kg/min. Typically, the max infusion for esmolol is 200 mcg/kg/min.
    1. Labetalol IV 10 or 20 mg is also an option if esmolol infusion is not readily available and need HR control fast. Also may consider Labetalol in cases with cocaine as provides both alpha- and beta-blockade. Labetalol is also available as an infusion.
  3. Treat BP: the goal SBP is <110. If you are not at your goal SBP after maxing esmolol to goal HR<60, then can add either nicardipine or nitroprusside.
    1. Nicardipine is typically started as an infusion of 5 mg/hr and titrated by 2.5 mg/hr every 10 minutes until at goal. Max of 30 mg/hr.
    2. Nitroprusside: is a pure vasodilator. Infusion rate is 0.3-0.5 mcg/kg/min to start. Can be increased in 0.3-0.5 mcg/kg/min q5 minutes. Typical dose for BP control is 3-4 mcg/kg/min infusion. Fun board question is to watch out for cyanide toxicity in these patients as possible side effect
  4. Consult your surgeons
    1. Type A: immediately to OR
    2. Type B: surgery will be needed as consult. Depending on institution and surgery recommendations, either admit to CICU or SICU.

Fun History

Dr. Michael Debakey

While working on this blog, I started reading up on Dr. Michael Debakey of Debakey Classification fame. This guy was a boss. He was born in 1908 and graduated from Tulane University . He served in WW2 in one of the surgical MASH units. In 1953, he performed the first successful carotid endarterectomy. He also pioneered the first aortic repairs of aortic dissection which bears his name. He practiced medicine until his death at age 99. At age 97, he actually suffered from an aortic dissection himself. Initially, he opted for medical management, but after becoming unresponsive, it was decided to proceed with surgical intervention. At the time of the operation in 2005, he was the oldest person to have ever undergone surgical correction of aortic dissection at 97 yoa. After a complicated post-op course and 8 months in the hospital, he returned to good health and continued to practice medicine until his death at age 99.

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