Acute coronary syndrome is 100 to 200 times more common than aortic dissection, and of all the patients we work up for dissection, only about 0.3% actually have one. That low prior probability is exactly why it gets missed: the index of suspicion has to come from you, because the numbers are quietly telling you it’s something else. And the cost of getting it wrong is steep — in-hospital mortality runs at around 27%, and for an untreated Stanford Type A the mortality climbs by roughly 1 to 2% for every hour that passes in the first 48 hours.

Two things decide the mark, and neither is recall: the clues planted in the stem and the exact wording of the question. The exam hides the dissection behind a mimic or an unusual presentation, so first you pick up the features that point to the aorta. Then read precisely what is being asked — the immediate next step in a suspected case (the CT to confirm) is not the same as the definitive management. Common ways it appears:

• Sudden, maximal-at-onset chest pain that the patient can time precisely → CT aortogram, not a troponin-and-wait.
• A blood pressure differential between the arms recorded in the obs and then ignored → you are meant to act on it.
• An inferior STEMI in a patient with abrupt tearing pain and a pulse deficit → think aorta before you thrombolyse.
• A raised D-dimer assumed to be a PE → the CTPA has the wrong contrast timing and can miss the dissection.
• Stroke, limb ischaemia or paraplegia with chest or back pain → dissection presenting through a complication.

It sits across SLO1 and SLO3 (the acutely unwell, undifferentiated patient), and it pairs naturally with the cardiac and resuscitation curriculum. The discriminating detail is almost always in the history of the pain and the examination — the things that should raise suspicion before any test comes back.

It is missed because it is rare and it hides. With ACS 100 to 200 times more common and only about 0.3% of those worked up actually having a dissection, the diagnosis is easy to talk yourself out of. On top of the low base rate, the presentation actively works against you:

• Often no specific signs. The examination can be entirely normal.
• The pain may have migrated or resolved by the time you see the patient — a settling pain is falsely reassuring.
• It can be young or atypical. A connective-tissue disorder can put it in a 30-year-old.
• Around 5 to 15% are painless, presenting instead with syncope or stroke.

Crucially, it can present via a complication rather than as chest pain at all. The branch the false lumen compromises decides how the patient walks in:

The single most discriminating feature is the onset, not the quality. The pain is sudden and maximal at the very start — it does not build up the way ischaemic pain tends to. Patients can usually pinpoint the exact moment it began, often to the minute and the activity they were doing. That precise, instantaneous onset is what should make you think aorta.

The textbook description — tearing or ripping interscapular pain — is real but unreliable:

• The classic tearing interscapular pain is present in only about half of cases, so its absence proves nothing.
• The pain migrates as the dissection propagates, typically chest → back → abdomen. Be especially wary of the patient who arrived with chest pain and now has abdominal pain — that is the dissection extending down the aorta.

Let the clinical risk drive the imaging, and let the emergency department own that decision. The RCEM/RCR 2025 guideline stratifies by how strongly the picture suggests dissection, using the Aortic Dissection Detection Risk Score (ADD-RS) for the in-between cases. ADD-RS scores one point per category (maximum 3) across three groups:

The pathway then runs on the level of suspicion. A useful way to hold it:

The CT aortogram is the test that both confirms the diagnosis and shows the location (Type A versus B), which is what then drives management. Request an urgent whole-aorta CT angiogram and let radiology choose the technique — an ECG-gated arterial phase gives a motion-free aortic root, and a non-contrast phase first catches an intramural haematoma. Two things the ED must not do: do not wait for a creatinine before scanning (it is time-critical), and do not hand the request to another team — the ED requests the scan and acts on it.

D-dimer is a rule-out adjunct, never a stand-alone test, and never a reason to wait in a classical presentation. At a 500 cut-off it is about 96.5% sensitive but only 56.5% specific, so it catches most dissections but produces a lot of false positives. Its evidence base for this use is the ADvISED pathway, which showed that an ADD-RS of 1 or less combined with a D-dimer below 500 is 98.8% sensitive for excluding dissection. That is why the score and the D-dimer are read together.

• Know your units. A positive result is > 500 ng/mL if the lab reports in FEU (fibrinogen equivalent units). Some labs report in DDU (D-dimer units) with a different upper limit, around 250 — check which yours uses before you interpret the number.
• Never use it alone. A low D-dimer in a higher-risk patient does not exclude dissection — the high-risk pathway still mandates the CT.
• Never wait for it in a classical presentation. That patient goes straight to CT aortogram.

Almost nothing reassuring at the bedside excludes it — this is the most heavily tested idea in the topic. Only a CT aortogram confirms or excludes dissection. Each of the following is a normal finding that does not let you off the hook:

Both can support the suspicion and both can mislead, but neither confirms nor excludes — an abnormal film or tracing still needs the CT, and a normal one cannot rule it out. Take the chest X-ray first:

Remember that a normal film cannot exclude dissection, and even an abnormal one still needs a CT to define the location.

The ECG is normal in about 30% of cases, and when abnormal it tends to mimic ACS, which is precisely the trap:

• Inferior STEMI if the dissection extends into the right coronary ostium — the dissection is the cause of the infarct.
• LVH and non-specific ST/T changes from the underlying hypertension.

Two systems matter, and they map onto each other. The one that drives the decision is Stanford, because it sorts straight into surgical versus medical:

The quick translation: DeBakey I and II are Stanford A; DeBakey III is Stanford B. If the ascending aorta is involved at all, it is a surgical emergency.

Dissection also sits within the broader umbrella of the acute aortic syndrome — three related conditions that present the same way and follow the same diagnostic pathway:

• Classic aortic dissection — a true and false lumen separated by an intimal flap.
• Intramural haematoma (IMH) — bleeding within the wall, no entry tear seen.
• Penetrating aortic ulcer (PAU) — an ulcerated atherosclerotic plaque eroding into the wall.

The medical cornerstone is anti-impulse therapy — reducing the heart rate, the force of each contraction (dP/dt, the rate of rise of aortic pressure) and the blood pressure, so as to cut the shear stress that propagates the flap. The order of drugs is the point the exam tests:

• Beta-blocker first — esmolol or labetalol — to bring down rate and contractility, plus an opioid for pain (pain itself drives up the BP).
• Add a vasodilator only if the BP is still high — GTN or sodium nitroprusside — and never a vasodilator alone, because the reflex tachycardia it triggers propagates the dissection.
• Targets: systolic 100–120 mmHg, heart rate < 60. Measure both arms and treat to the higher reading.

The definitive treatment is decided by the Stanford type:

A Type B is “complicated” — and so needs TEVAR rather than medical management — when there is malperfusion, rapid expansion, refractory pain, refractory hypertension, rupture or impending rupture, or periaortic haematoma. If a patient is too unstable for CT, the route is a bedside transoesophageal echo (TOE) then straight to theatre.

The “don’ts” are as important as the “dos”:

• No thrombolysis, anticoagulation or antiplatelets — even with ischaemic ECG changes. This is the trap behind the inferior-STEMI presentation.
• Do not blindly drain a tamponade from a Type A — uncontrolled pericardiocentesis can precipitate fatal re-bleeding. The answer is controlled surgical drainage / straight to theatre.

Aortic dissection rewards a low threshold and a clear next step. The recurring pitfalls are predictable: a BP differential recorded and then ignored; a raised D-dimer blamed on a PE, sending the patient for a CTPA that misses the aorta; abrupt chest pain labelled musculoskeletal or gastritis; and an inferior STEMI that is actually a dissection, where thrombolysis would be catastrophic — the ADD features and the onset of the pain should make you think aorta.

The cleanest way to handle the “next step” SBA is to separate immediate from definitive. If dissection is only suspected — ADD criteria present, no CT yet — you cannot organise definitive treatment, because you do not yet have a diagnosis. The next step is the CT aortogram to confirm it. Surgery, TEVAR or medical management all come after the scan tells you the type. Hold that order and the algorithm questions become straightforward.

Go to the primary source — the RCEM/RCR 2025 guideline — and the RCEM Learning reference on aortic dissection alongside it. For how this fits the wider blueprint, see our FRCEM Final high-yield topics for 2026.

Sources: RCEM/RCR, Diagnosis of Thoracic Aortic Dissection in the Emergency Department (2025); ESC guidance on aortic diseases; RCEMLearning. Drug doses are for reference only — confirm against the BNF.