Aortic dissection is a life-threatening condition in which a tear in the aortic intima allows blood to enter and separate the layers of the aortic wall, creating a false lumen.

Exam domain	One-glance essentials
Definition / diagnosis	Intimal tear permits blood to dissect through the media, creating a false lumen ^[1] Acute aortic syndrome includes classical dissection, intramural haematoma and penetrating atherosclerotic ulcer ^[1] Stanford type A involves the ascending aorta; type B spares it and guides definitive management ^[1]
Epidemiology / risks	Hypertension is the major modifiable risk factor ^[1] Marfan, Ehlers-Danlos, Loeys-Dietz, bicuspid aortic valve and familial aortopathy predispose ^[1] Consider cocaine, pregnancy, heavy isometric exercise, trauma, vasculitis and prior aortic disease ^[1]
Core mechanism	High-pressure blood propagates longitudinally within the media and may extend proximally or distally ^[1] False-lumen expansion compresses the true lumen, causing branch-vessel malperfusion ^[1] Proximal root involvement causes acute aortic regurgitation; rupture causes tamponade or haemothorax ^[1]
Clinical picture	Sudden severe chest or back pain, maximal at onset, often tearing and migratory ^[1] Pulse deficit or inter-arm BP difference >20 mmHg strongly raises suspicion ^[1] Look for new early diastolic murmur, syncope, neurological deficit, acute limb ischaemia, pulmonary oedema or shock ^[1]
Investigations	Use ADD-RS to structure pre-test probability; D-dimer <500 ng/mL is a rule-out option only in low probability ^[1] Stable patient: urgent CT aortogram to define flap, extent, branch involvement and complications ^[1] Unstable or CT-contraindicated: TEE; MRI is mainly for chronic follow-up ^[1] CXR may show widened mediastinum, but a normal film does not exclude dissection ^[1]
Management	Immediate ICU care, analgesia and anti-impulse therapy: target SBP 100–120 mmHg and HR <60/min ^[1] IV beta-blocker first; add vasodilator only after rate control; avoid hydralazine and thrombolysis ^[1] Type A: emergency open repair; uncomplicated type B: medical therapy ^[1] Complicated type B with rupture or malperfusion: intervention, usually TEVAR where anatomy permits ^[1]
Complications	Rupture may cause tamponade, left haemothorax, mediastinal haematoma or exsanguination ^[1] Malperfusion causes MI, stroke, paraplegia, mesenteric ischaemia, AKI or acute limb ischaemia ^[1] Root involvement causes acute AR and pulmonary oedema ^[1] Late risks include false-lumen aneurysmal degeneration, recurrent dissection and rupture ^[1]
Prevention / follow-up	Lifelong strict BP control and beta-blockade-based antihypertensive therapy reduce wall stress ^[1] Avoid smoking, cocaine and heavy isometric exertion; address inherited aortopathy and vasculitis ^[1] Serial CTA or MRA at 3, 6 and 12 months, then annually, detects enlargement, recurrence and endoleak ^[1]
Exam traps	Inferior STEMI with back pain, pulse deficit or BP asymmetry may be coronary malperfusion: exclude dissection before thrombolysis ^[1] Normal ECG or CXR does not exclude dissection ^[1] Do not treat BP with vasodilator monotherapy: reflex tachycardia increases aortic impulse ^[1] Hypotension is ominous: consider tamponade, rupture, severe AR or pseudo-hypotension from branch malperfusion ^[1]

References

^[1] Senior notes: Maksim Medicine Notes.pdf (p15, Cardiology section 1.4)

Aortic Dissection

Aortic dissection is a tear in the tunica intima (innermost layer) of the aorta that allows blood under systemic arterial pressure to enter and propagate within the tunica media, creating a false lumen that separates the intimal-medial layers longitudinally ^[1]^[2]^[3].

The term literally breaks down as:

"Aortic" = pertaining to the aorta (Greek aortē, from aeirein "to lift/carry" — the great vessel that carries blood from the heart)
"Dissection" = Latin dissectio, "to cut apart" — the wall is being split apart by blood tracking within it

Acute Aortic Syndrome (AAS)

Aortic dissection sits within the broader umbrella of acute aortic syndrome (AAS) — a term coined in 2001 to describe a spectrum of acute, life-threatening aortic conditions that share overlapping presentations and are all initially managed as aortic dissection until proven otherwise ^[2]^[3]:

Entity	Pathology
Classical aortic dissection	Intimal tear → blood enters media → creates a true and false lumen separated by an intimal flap
Limited dissection	Limited intimal tear with eccentric bulge at the tear site but no propagating haematoma
Intramural haematoma (IMH)	Haemorrhage within the medial layer without a demonstrable intimal tear or flap — due to rupture of the vasa vasorum (the tiny nutrient vessels within the aortic wall itself)
Penetrating atherosclerotic ulcer (PAU)	An atherosclerotic plaque ulcerates deeply enough to penetrate through the internal elastic lamina into the media, allowing haematoma formation

Clinical Pearl

All acute aortic syndromes are managed as aortic dissection until definitive imaging says otherwise. IMH and PAU can progress to classical dissection.

Incidence: approximately 2.6–3.5 per 100,000 per year — roughly equivalent to about 1 case per day across the whole of Hong Kong ^[3]
Incidence is notably higher in mainland China due to the enormous burden of uncontrolled hypertension ^[3]
Demographics: typically affects ages 60–80 years, but can occur much younger in the presence of connective tissue disease or other risk factors ^[3]
Sex: Male : Female ≈ 2 : 1 ^[3]
Stanford Type A accounts for approximately ~2/3 (66%) of cases; Type B accounts for the remaining ~1/3 ^[1]^[3]
DeBakey type I is the most common and the worst type ^[4]

High Yield – Epidemiology

In Hong Kong, roughly one aortic dissection presents per day across all hospitals. Uncontrolled hypertension is the single most important risk factor — present in ~77% of cases.

3. Anatomy and Function

To understand aortic dissection, you need to understand aortic wall structure and the functional segments of the aorta.

The aortic wall has three layers (from lumen outwards):

Tunica intima: a single layer of endothelial cells resting on a basement membrane and thin subendothelial connective tissue. The internal elastic lamina forms its outer boundary.
Tunica media: the thickest layer — composed of concentrically arranged elastic lamellae (40–60 layers in the thoracic aorta) interspersed with smooth muscle cells (SMCs) and an extracellular matrix (ECM) rich in collagen and elastin. This is the layer that bears most of the haemodynamic stress. It is also where the vasa vasorum (literally "vessels of the vessels") penetrate to supply the outer two-thirds of the wall.
Tunica adventitia: the outermost layer of collagenous connective tissue containing the vasa vasorum, nerves (including nociceptive fibres — this is why dissection hurts so intensely), and lymphatics.

The reason aortic dissection is so painful is that the dissecting haematoma stretches and tears through the media and stimulates adventitial nerve fibres. The reason it is so dangerous is that the media is the structural layer — once it is split, the thin adventitia is the only barrier between aortic pressure and catastrophic rupture.

Segment	Boundaries	Key Branches
Aortic root	Aortic valve annulus → sinotubular junction	Coronary arteries (RCA, LCA)
Ascending aorta	Sinotubular junction → brachiocephalic artery origin	—
Aortic arch	Brachiocephalic → left subclavian artery	Brachiocephalic trunk, left CCA, left subclavian
Descending thoracic aorta	Distal to left subclavian → diaphragm	Intercostal arteries, bronchial arteries, artery of Adamkiewicz (spinal cord supply, typically T9–T12)
Abdominal aorta	Diaphragm → aortic bifurcation (L4)	Coeliac trunk, SMA, renal arteries, IMA, gonadal arteries

The aortic isthmus (just distal to the left subclavian artery origin) is a crucial anatomical landmark — it is where the mobile aortic arch transitions to the relatively fixed descending thoracic aorta. This is the most common site of traumatic aortic injury (acceleration-deceleration) ^[5] and is also the boundary used in the Stanford classification.

The vasa vasorum ("vessels of the vessels") are small arteries that supply the outer two-thirds of the media and the adventitia. In the thoracic aorta, they are more prominent because the wall is thicker. Rupture of the vasa vasorum is the proposed mechanism for intramural haematoma — haemorrhage occurs within the media without a primary intimal tear ^[2]^[3].

4. Risk Factors

Coexisting HTN is present in 76.6% of cases — it is by far the most important modifiable risk factor ^[3].

Risk Factor	Mechanism
Hypertension (76.6%)	Chronic ↑ wall stress → accelerated medial degeneration; acute ↑ BP can be the trigger event
Cocaine use	Causes acute severe hypertension via sympathomimetic effects → abrupt ↑ aortic wall stress ^[1]^[3]
Phaeochromocytoma	Catecholamine surges → episodic severe hypertension ^[1]
Smoking	Accelerates atherosclerosis and medial degeneration
Atherosclerosis	Weakens the intima; PAU is a direct consequence
Heavy weight lifting / isometric exercise	Acute ↑ intrathoracic and aortic pressure → can trigger intimal tear in a susceptible aorta ^[3]^[6]
Pregnancy and delivery	Hormonal changes (↑ progesterone/oestrogen) → ↑ elastin fragmentation in the media; haemodynamic stress of pregnancy (↑ CO, ↑ blood volume); highest risk in 3rd trimester and peripartum ^[1]^[3]
Trauma (catheter-related, acceleration-deceleration)	Direct mechanical injury to the intima ^[3]

Risk Factor	Mechanism
Marfan syndrome	Fibrillin-1 (FBN1) mutation → defective elastic fibre assembly → cystic medial necrosis (loss of elastic lamellae, smooth muscle, and accumulation of basophilic ground substance). This makes the media intrinsically weak. These patients often dissect at a younger age and at smaller aortic diameters. ^[1]^[3]
Ehlers-Danlos syndrome (EDS type IV)	Mutations in type III collagen (COL3A1) → fragile arteries prone to spontaneous dissection/rupture ^[3]
Loeys-Dietz syndrome	Mutations in TGF-β receptor genes (TGFBR1/2) → abnormal vascular remodelling → aneurysm and dissection at young ages ^[3]
Bicuspid aortic valve (BAV)	Associated with aortopathy — the ascending aorta has intrinsic medial abnormalities independent of haemodynamic effects; ↑ risk of ascending aortic aneurysm and Type A dissection ^[3]
Turner syndrome	45,X karyotype → associated BAV and aortic coarctation → ↑ risk of dissection
Familial thoracic aortic aneurysm/dissection (FTAAD)	Mutations in ACTA2, MYH11, SMAD3, etc. — various genes encoding smooth muscle contractile proteins
Coarctation of the aorta	Chronic proximal hypertension + turbulent flow at the coarctation site → medial degeneration

Risk Factor	Mechanism
Takayasu arteritis	Granulomatous large-vessel vasculitis → mural inflammation and weakening → aneurysm/dissection ^[1]^[7]
Giant cell arteritis (GCA)	Granulomatous arteritis of the aorta and major branches → large-vessel involvement → aneurysm/dissection ^[7]
Syphilitic aortitis	Treponema pallidum causes obliterative endarteritis of the vasa vasorum → ischaemic necrosis of the media → weakening (historically more important, now rare)
Prior aortic diseases (aortic aneurysm, prior aortic surgery)	A pre-existing aneurysm stretches and thins the wall → lower threshold for dissection ^[3]

Hong Kong Focus

In Hong Kong, the dominant risk factor profile is: elderly Chinese male with poorly controlled hypertension (often non-adherent to medications). Connective tissue disease is a smaller but important subset — particularly Marfan syndrome presenting at younger ages. Cocaine-related dissection is less common in HK than in Western populations, but does occur.

5. Pathophysiology

The exact initiating event is debated, but two main theories exist ^[3]:

Primary intimal tear hypothesis (most widely accepted): Chronic medial degeneration (from hypertension, connective tissue disease, etc.) weakens the wall → a tear develops in the intima → high-pressure aortic blood enters the media → the blood propagates along the plane of least resistance within the media, creating a false lumen.
Primary vasa vasorum haemorrhage hypothesis: Rupture of the vasa vasorum within the media → intramural haematoma → the haematoma may then rupture inwards through the intima into the true lumen (creating a secondary intimal tear and classical dissection) or outwards through the adventitia (rupture).

Both pathways converge: once blood is within the media, it dissects along the vessel.

The false lumen can extend both proximally and distally from the initial tear
It can re-enter the true lumen at another point downstream → creating a "double-barrelled aorta" ^[3]
The false lumen typically compresses the true lumen → this can cause malperfusion of any branch vessel arising from the compressed segment
The false lumen may thrombose (partially or completely), which paradoxically can be stabilising (if the false lumen thromboses completely in Type B, the prognosis is generally better)

5.3 Consequences of Dissection

The consequences arise from two fundamental mechanisms: malperfusion and rupture.

When the dissection flap or false lumen compromises flow to branch arteries:

Branch Involved	Clinical Consequence	Mechanism
Coronary arteries (especially RCA — more commonly involved because the dissection flap often extends into the right coronary ostium)	MI	False lumen compresses coronary ostium or dissection extends into coronary artery
Brachiocephalic / Carotid	Ischaemic stroke, syncope, LOC	↓ Cerebral perfusion; may be transient if flap oscillates
Subclavian	Arm ischaemia, asymmetric BP/pulses	Compression of subclavian → ↓ flow to one arm
Intercostal / Artery of Adamkiewicz	Paraplegia	Spinal cord ischaemia — devastating and often irreversible
Coeliac trunk / SMA	Mesenteric infarction (acute abdomen)	Gut ischaemia → ↑ lactate, peritonitis
Renal arteries	AKI	Renal malperfusion → oliguria, ↑ creatinine
Iliac arteries	Acute limb ischaemia	Lower extremity malperfusion

Into the pericardial sac → cardiac tamponade (most common cause of death in acute Type A dissection) — because the ascending aorta is intrapericardial; the pericardium is relatively inelastic, so even a small amount of blood causes rapid ↑ intrapericardial pressure → ↓ ventricular filling → cardiogenic shock
Into the left pleural space → haemothorax (left side because the descending aorta is a left-sided structure)
Free rupture into the mediastinum or peritoneal cavity → rapid exsanguination

When the dissection involves the aortic root, the dissection flap can:

Dilate the aortic root → the aortic valve leaflets are pulled apart → incomplete coaptation
Prolapse through the aortic valve orifice → direct leaflet malcoaptation
Result: acute aortic regurgitation → acute pulmonary oedema (APO) ^[1]^[3]

In chronic AR, the LV has time to dilate and compensate. In acute AR from dissection, the LV is of normal size and cannot accommodate the sudden volume overload → LV end-diastolic pressure rises acutely → acute pulmonary oedema. This is a surgical emergency.

6. Classification

The Stanford classification is the one that drives management decisions:

Type	Definition	Frequency	Management
Type A	Involves the ascending aorta (regardless of where the tear originates — even if the tear is in the descending aorta but the dissection extends retrograde to involve the ascending aorta, it is Type A)	~2/3 (~66-80%)	Surgical treatment
Type B	Spares the ascending aorta (dissection begins distal to the left subclavian artery and does not extend proximally to involve the ascending aorta)	~1/3 (~20-34%)	Medical treatment, unless complicated

Why Does Type A Require Surgery?

Because the ascending aorta is intrapericardial — Type A dissection carries imminent risk of: (1) rupture into pericardium → tamponade, (2) coronary malperfusion → MI, (3) aortic root involvement → acute AR with APO. Without surgery, mortality is ~1-2% per hour in the first 48 hours. Medical therapy alone carries ~50% mortality at 48h.

Type	Origin of Tear	Extent	Corresponding Stanford
Type I	Ascending aorta	Extends to both ascending and descending aorta (beyond the arch)	Type A
Type II	Ascending aorta	Confined to the ascending aorta	Type A
Type IIIa	Descending aorta (distal to L subclavian)	Confined to thoracic descending aorta	Type B
Type IIIb	Descending aorta (distal to L subclavian)	Extends into abdominal aorta	Type B

DeBakey type I is the most common and the worst type — it involves the entire aorta, has the highest complication rate, and carries the worst prognosis ^[4].

Timeframe	Definition
Hyperacute	< 24 hours
Acute	< 14 days
Subacute	15–90 days
Chronic	> 90 days

The 14-day cutoff for "acute" is based on the observation that most deaths from untreated dissection occur within the first 2 weeks. After this period, the false lumen wall has typically organised enough to reduce (but not eliminate) the risk of rupture.

7. Clinical Features

7.1 Symptoms

Sudden onset, severe, "tearing" or "ripping" chest pain that is maximal at onset ^[1]^[2]^[3]^[6]

Why sudden and maximal at onset? Because the intimal tear is an instantaneous mechanical event — unlike MI where pain builds gradually as ischaemia worsens, dissection pain is immediate and at its worst right from the start. This "maximal at onset" character is a key distinguishing feature from ACS.
Why "tearing"? Because the media is literally being torn apart by the dissecting haematoma. Pain fibres in the adventitia are being activated by the acute stretching and disruption.
Radiation depends on the location and propagation of the dissection:
- Ascending aorta → anterior chest pain (may mimic MI) ± radiating to the back ^[3]
- Descending aorta → interscapular region, radiating to the abdomen ^[3]^[6]
- As the dissection propagates, the pain may migrate — e.g., starting in the chest and then moving to the back, then to the abdomen. This migratory quality is highly suggestive of dissection.

Classic Teaching Point

Do NOT confuse aortic dissection pain with MI pain. MI pain is typically described as "crushing/pressure", builds over minutes, and is often associated with diaphoresis and nausea. Dissection pain is "tearing/ripping", is maximal at onset, and often radiates to the back. The danger is that dissection can cause MI (coronary malperfusion), creating a diagnostic trap — always think of dissection before giving thrombolytics for an "inferior STEMI" in a hypertensive patient with back pain.

Syncope / loss of consciousness → from carotid involvement → cerebral hypoperfusion; or from tamponade → ↓ CO ^[3]^[8]
Focal neurological deficits (stroke) → carotid or vertebral artery malperfusion ^[3]
Angina / chest tightness → coronary malperfusion → MI ^[3]
Dyspnoea → acute AR → acute pulmonary oedema; or haemothorax
Abdominal pain → mesenteric ischaemia (coeliac/SMA involvement) ^[3]
Oliguria / anuria → renal malperfusion → AKI ^[3]
Lower limb pain / weakness → iliac artery malperfusion → acute limb ischaemia ^[3]; or spinal cord ischaemia → paraplegia ^[3]
Hoarseness → left recurrent laryngeal nerve compression by expanding aorta/haematoma (rare)
Dysphagia → oesophageal compression (rare)
Congestive heart failure → due to acute AR ^[3]

Chronic dissections can be asymptomatic — found incidentally on imaging ^[3]

7.2 Signs

Hypertension → present in the majority (reflects the underlying predisposing HTN) ^[3]
Hypotension → ominous sign, indicates: ^[3]
- Cardiac tamponade (rupture into pericardium)
- Free rupture (haemothorax, mediastinal haematoma)
- Dissection involving the brachiocephalic arteries → the "measured" BP is falsely low because the arm being measured is malperfused
- Severe acute AR → cardiogenic shock
Asymmetric BP between arms (inter-arm BP difference > 20 mmHg) → highly suggestive of dissection — occurs when the dissection flap compromises one subclavian artery ^[1]

Clinical Pearl – Pseudo-hypotension

A patient with Type A dissection may appear hypotensive because the dissection extends into the innominate artery (right subclavian) and/or left subclavian → both arm BPs are falsely low. Always check leg BP as well. True hypotension from tamponade/rupture vs. pseudo-hypotension from branch vessel compromise must be distinguished urgently.

Pulse deficits: the palpable radial pulse rate is less than the auscultated heart rate — because the dissection flap intermittently occludes the subclavian → some cardiac beats do not produce a palpable pulse ^[3]
Asymmetric pulses between limbs ^[1]:
- Radial-radial delay / asymmetry → suggests involvement of one subclavian artery (Type A — especially if the brachiocephalic is involved) ^[1]
- Radial-femoral delay / asymmetry → suggests involvement of the descending aorta/iliac arteries (Type B) ^[1]
- Absent femoral pulse → iliac involvement

Early diastolic murmur (EDM) → indicates acute aortic regurgitation → the dissection has distorted the aortic root ^[3]
Muffled heart sounds, raised JVP, hypotension → Beck's triad of cardiac tamponade (if rupture into pericardium)
Pulsus paradoxus → exaggerated ↓ in SBP (> 10 mmHg) during inspiration → another sign of tamponade

Hemiplegia / hemisensory loss → stroke from carotid malperfusion
Paraplegia → spinal cord ischaemia from intercostal/Adamkiewicz artery involvement ^[3]
Horner syndrome → compression of the superior cervical sympathetic ganglion by the expanding aortic arch or descending aorta (rare)

Signs of acute limb ischaemia → pale, pulseless, cold limb (the 6 Ps — Pain, Pallor, Pulseless, Perishingly cold, Paraesthesia, Paralysis) ^[9]
Signs of pleural effusion (usually left-sided) → dull percussion, ↓ breath sounds, ↓ vocal resonance → haemothorax from descending aortic rupture ^[3]
Abdominal tenderness / peritonism → mesenteric ischaemia

Feature	Type A (Ascending)	Type B (Descending)
Pain location	Anterior chest ± back	Interscapular ± abdomen
Coronary malperfusion (MI)	Yes (especially RCA → inferior STEMI)	No
Acute AR	Yes	No
Tamponade	Yes	No
Carotid involvement (stroke)	Yes	Rare
Subclavian (arm ischaemia)	Yes (especially right)	Yes (left)
Spinal cord ischaemia	Possible but less common	More common
Mesenteric/renal ischaemia	Possible (if Type I / extending distally)	More common
Limb ischaemia	Possible	More common
Mortality without surgery	~1–2% per hour in first 48h	~10% at 30 days with medical therapy

Clinical Feature	Pathophysiological Basis
Sudden tearing chest pain, maximal at onset	Instantaneous mechanical intimal tear → haematoma stretches adventitial nociceptors
Pain radiates to back	Dissection propagates into descending aorta → posterior mediastinal structures
Migratory pain	Progressive propagation of the dissection flap along the aorta
Inter-arm BP difference > 20 mmHg	Dissection flap compresses one subclavian artery
Pulse deficits	Intermittent or fixed occlusion of branch vessels by the flap
EDM of acute AR	Root dilatation → leaflet malcoaptation; or flap prolapses through valve
Acute pulmonary oedema	Acute AR → sudden volume overload on a non-dilated LV → ↑ LVEDP → pulmonary venous congestion
Tamponade (hypotension, muffled sounds, raised JVP)	Rupture into pericardium → rapid accumulation of blood → ↓ ventricular filling
Stroke / syncope	Carotid artery malperfusion → cerebral ischaemia
Paraplegia	Intercostal artery / artery of Adamkiewicz malperfusion → anterior spinal cord ischaemia
Acute limb ischaemia	Iliac artery compression by false lumen
AKI	Renal artery malperfusion
Mesenteric ischaemia (↑ lactate, acute abdomen)	SMA/coeliac malperfusion → gut ischaemia
Left pleural effusion	Rupture into left pleural space (descending aorta is left-sided)

High Yield Summary

Definition: Tear in aortic intima → blood dissects into media → false lumen. Part of the acute aortic syndrome spectrum (classical dissection, IMH, PAU, limited dissection).

Epidemiology: ~3/100k/year; ~1/day in HK; M:F = 2:1; age 60-80y; HTN in ~77%.

Stanford Classification (drives management):

Type A = involves ascending aorta → SURGICAL
Type B = spares ascending aorta → MEDICAL (unless complicated)
DeBakey I = most common and worst

Risk Factors: HTN (#1), connective tissue diseases (Marfan, EDS, Loeys-Dietz), BAV, cocaine, pregnancy, vasculitis, trauma, prior aortic disease.

Pathophysiology: Intimal tear → false lumen → (1) malperfusion of branch vessels (MI, stroke, paraplegia, mesenteric ischaemia, AKI, limb ischaemia) and (2) rupture (tamponade, haemothorax, exsanguination) and (3) acute AR (root distortion → APO).

Clinical Features:

Pain: Sudden, maximal at onset, tearing, radiates to back (ascending → anterior chest; descending → interscapular)
BP: HTN or pseudo-hypotension; inter-arm difference > 20 mmHg
Pulses: Deficits, radial-radial delay (Type A), radial-femoral delay (Type B)
Cardiac: EDM of acute AR, tamponade (Beck's triad)
Neurological: Stroke, syncope, paraplegia
Malperfusion: MI, mesenteric ischaemia, AKI, limb ischaemia
Rupture: Left haemothorax, tamponade

Mortality: ~1-2% per hour untreated (Type A); 90% survival if prompt Dx and Mx.

Active Recall - Aortic Dissection (Definition to Clinical Features)

^[1] Senior notes: Maksim Medicine Notes.pdf (p15, Cardiology section 1.4) ^[2] Senior notes: Maksim Surgery Notes.pdf (p168, Acute limb ischaemia — aortic dissection as a cause) ^[3] Senior notes: Ryan Ho Cardiology.pdf (p219–221, section 4.5.1 Aortic Dissection) ^[4] Lecture slides: Cardiac Surgery Tutorial_Prof. D Chan.pdf (p72, Acute Aortic Dissection) ^[5] Senior notes: Ryan Ho Radiology.pdf (p4, Acute traumatic aortic injury) ^[6] Senior notes: Ryan Ho Fundamentals.pdf (p201, Aortic dissection — chest pain differential) ^[7] Senior notes: Ryan Ho Rheumatology.pdf (p95–96, GCA and Takayasu arteritis) ^[8] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf ^[9] Senior notes: Maksim Surgery Notes.pdf (p168, 6P of acute limb ischaemia)

Differential Diagnosis of Aortic Dissection

The reason differential diagnosis matters so much here is straightforward: aortic dissection is a time-critical emergency (~1–2% mortality per hour for Type A if untreated), and its presentation — acute severe chest/back pain ± haemodynamic compromise — overlaps significantly with several other life-threatening conditions. Getting the diagnosis wrong in either direction is dangerous: missing a dissection and giving thrombolytics for a "STEMI" can be fatal, and treating every chest pain as dissection delays management of other emergencies.

The differentials are best organised by the dominant presenting feature because dissection is a great mimic — it can present as chest pain, back pain, abdominal pain, stroke, syncope, acute limb ischaemia, or shock.

1. Differential Diagnosis Organised by Presenting Feature

This is the most common presentation. The key differentials are the other "Big 5" causes of acute life-threatening chest pain ^[3]^[10]^[11]:

Condition	Why It Mimics Dissection	Key Distinguishing Features
Acute coronary syndrome (ACS)	Severe central chest pain ± diaphoresis; dissection itself can cause MI via coronary malperfusion, creating a double-mimicry trap	ACS pain is dull/crushing, builds over minutes, rarely maximal at onset. ECG shows ST changes. Troponin rises serially. No pulse deficits, no inter-arm BP difference. Danger: dissection causing RCA occlusion → inferior STEMI pattern → if you give thrombolytics → catastrophic haemorrhage. Always consider dissection before thrombolysis in inferior STEMI with back pain or inter-arm BP difference
Acute pulmonary embolism (PE)	Sudden onset pleuritic chest pain ± dyspnoea ± haemodynamic collapse (massive PE)	PE pain is typically pleuritic (↑ with inspiration), associated with tachypnoea, tachycardia, and DVT signs. ECG may show S1Q3T3 / RV strain. CTPA shows filling defects in pulmonary arteries. D-dimer elevated. No pulse deficits or BP asymmetry
Tension / massive pneumothorax	Sudden onset unilateral chest pain ± dyspnoea ± hypotension (tension)	Unilateral absent breath sounds, hyper-resonant percussion, tracheal deviation (tension). CXR diagnostic. No pulse deficits
Myopericarditis ± cardiac tamponade	Chest pain ± pericardial effusion → tamponade (which dissection can also cause)	Pericarditis pain is sharp, positional (↑ sitting forward), pleuritic. ECG shows diffuse ST elevation with PR depression. Tamponade from pericarditis is usually subacute with gradual accumulation vs. dissection tamponade which is acute and fulminant
Pneumonia	Pleuritic chest pain ± fever ± dyspnoea	Productive cough, fever, consolidation signs (bronchial breathing, crackles). CXR shows consolidation. No BP/pulse asymmetry

The Deadly Diagnostic Trap

Aortic dissection can cause MI (coronary malperfusion). If the ECG shows an inferior STEMI and you reflexively give thrombolytics or load dual antiplatelets without considering dissection, the patient can exsanguinate. Always think of dissection first in any patient with acute chest pain PLUS: back pain, tearing quality, maximal at onset, pulse deficits, BP asymmetry, new AR murmur, or widened mediastinum on CXR. The mnemonic is: before you open the coronaries, make sure the aorta is intact.

When dissection presents predominantly as back or abdominal pain (especially Type B extending into the abdominal aorta):

Condition	Why It Mimics Dissection	Key Distinguishing Features
Ruptured abdominal aortic aneurysm (AAA)	Severe abdominal/back pain + shock + pulsatile mass — overlaps with the abdominal extension of dissection	Ruptured AAA: triad of severe abdominal/back pain, pulsatile mass, hypotension ^[12]. Pulsatile expansile mass on examination. CT aortogram distinguishes: AAA shows aneurysmal dilatation ± retroperitoneal haematoma; dissection shows intimal flap and false lumen
Acute pancreatitis	Epigastric/back pain, can be severe and sudden	Relieved by leaning forward, associated with vomiting. ↑ Amylase/lipase. No pulse deficits
Peptic ulcer perforation (PPU)	Sudden severe epigastric pain radiating to back	Board-like rigidity, free air under diaphragm on erect CXR. No pulse deficits or BP asymmetry
Renal colic	Severe flank/back pain, can be sudden	Colicky nature, radiates to groin, haematuria. Non-contrast CT KUB shows stone
Aortic dissection presenting as acute abdomen	Tearing pain at epigastrium radiates to the back ± shock ^[13]	Must be distinguished from surgical causes of acute abdomen

When dissection presents with neurological symptoms (carotid malperfusion → stroke; or hypotension → syncope):

Condition	Why It Mimics Dissection	Key Distinguishing Features
Primary ischaemic stroke	Acute focal neurological deficits — dissection causing carotid occlusion produces the same deficits	Primary stroke: no chest/back pain, no pulse deficits, no BP asymmetry. CTA/MRA of head and neck can identify the dissection flap extending into the carotid
Cervical arterial dissection (carotid or vertebral)	Spontaneous or traumatic — ICA: retroorbital pain + Horner's syndrome; VA: occipital pain + vertebrobasilar symptoms. Ischaemia from arterial occlusion or embolism. Dissecting aneurysm can rupture intracranially causing SAH ^[14]	This is actually a form of dissection but confined to extracranial/intracranial cervical arteries rather than the aorta. Connective tissue disorders overlap. CTA/MRA of the neck differentiates
Subarachnoid haemorrhage (SAH)	"Thunderclap" headache — sudden and severe like dissection pain; cervical dissection can even cause SAH	SAH: headache is characteristically occipital/nuchal with meningism. CT brain shows blood in subarachnoid space. No chest pain or BP asymmetry (unless there is concurrent aortic dissection)
Vasovagal / other syncope	Syncope can be the presenting feature of dissection (via carotid malperfusion or tamponade)	Vasovagal: prodrome of nausea, diaphoresis, tunnel vision; triggered by prolonged standing. No focal neurology, no pain, no pulse deficits post-recovery

When dissection presents as an acutely ischaemic limb (iliac/subclavian malperfusion):

Condition	Why It Mimics Dissection	Key Distinguishing Features
Arterial embolism (cardiac source)	Sudden onset 6Ps — identical clinical picture to limb malperfusion from dissection	Look for embolic source (AF, recent MI, valvular disease). Contralateral pulses present. No back/chest pain. CTA shows sharp arterial cut-off without intimal flap ^[2]^[3]
Acute arterial thrombosis (in-situ)	Acute limb ischaemia over hours-days	Previous claudication history, PVD in contralateral limb, present bruits. CTA shows irregular cut-off with collaterals ^[2]
Phlegmasia cerulea dolens	Massively swollen, cyanotic, painful limb — can be mistaken for arterial ischaemia	This is actually massive ilio-femoral DVT → venous congestion → secondary arterial compromise. Limb is swollen and blue (not pale and white). Duplex USG shows DVT ^[2]

When dissection presents as undifferentiated shock:

Condition	Why It Mimics Dissection	Key Distinguishing Features
Cardiogenic shock (massive MI)	Hypotension + pulmonary oedema — dissection can cause this via acute AR or coronary malperfusion	ECG: regional ST changes. Echo: RWMA with normal aortic root (vs. dissection: aortic root dilatation ± flap ± pericardial effusion)
Cardiac tamponade (other causes)	Beck's triad — dissection is one cause, but malignant pericardial effusion, uraemic pericarditis, post-cardiac surgery can also cause tamponade	Dissection tamponade: acute + associated with chest/back pain + widened mediastinum. Other tamponade: usually more insidious onset
Massive PE	Obstructive shock with ↑ JVP, hypotension	RV dilation on echo, CTPA shows filling defects. No intimal flap
Haemorrhagic shock (GI bleed, ruptured ectopic, ruptured HCC)	Hypotension + tachycardia	Usually identifiable bleeding source, no BP/pulse asymmetry ^[15]

These are not so much "differentials" as they are part of the same clinical spectrum — but they are managed somewhat differently and should be distinguished on imaging ^[1]^[3]:

Entity	Key Imaging Distinction	Clinical Significance
Intramural haematoma (IMH)	Crescentic or circumferential thickening of the aortic wall (> 5 mm) on CT, no intimal flap, no false lumen with flow	Can progress to classical dissection (especially Type A IMH). Type A IMH → surgery; Type B IMH → medical ± surveillance
Penetrating atherosclerotic ulcer (PAU)	Focal contrast outpouching beyond the expected aortic lumen contour, associated with extensive atherosclerotic calcification, often in the descending aorta	Typically elderly patients with heavy atherosclerotic burden. Can progress to IMH, dissection, or pseudoaneurysm
Limited dissection	Limited intimal tear with eccentric bulge but no propagating haematoma	Can be managed conservatively with close surveillance

The key clinical features that should raise suspicion for aortic dissection over its mimics are:

Feature	Sensitivity	Specificity	Why It Points to Dissection
Pain maximal at onset	High	High	Mechanical tear is instantaneous — ACS pain builds, dissection pain starts maximal
Tearing / ripping quality	Moderate	Moderate–High	Medial layer being physically torn
Radiation to back	Moderate	Moderate	Descending aorta is a posterior mediastinal structure
Migratory pain	Moderate	High	Propagation of the dissection flap
Inter-arm BP difference > 20 mmHg	Moderate (~30%)	High	Unilateral subclavian compromise
Pulse deficits	Low–Moderate (~30%)	High	Branch vessel compromise by the flap
New diastolic murmur (AR)	Low–Moderate (~30–45%)	High	Root involvement → leaflet malcoaptation
Widened mediastinum on CXR	Moderate (60–90%)	Moderate	Expanding aorta / mediastinal haematoma
Neurological deficits + chest pain	Low	Very High	Stroke from carotid malperfusion + aortic pain — unusual combination in primary stroke
Known Marfan / CTD	Low	Very High in context	Intrinsic medial weakness → low threshold for dissection

Clinical Decision Point

Before thrombolysis or primary PCI for any STEMI — especially inferior STEMI — actively exclude aortic dissection. Check for: tearing pain, maximal at onset, back radiation, inter-arm BP difference, pulse deficits, widened mediastinum on CXR. If ANY of these are present, get a CT aortogram first. Thrombolysing a dissection can be fatal ^[3]^[10].

Feature	Aortic Dissection	ACS	PE	Pneumothorax	Pericarditis	Ruptured AAA
Pain onset	Sudden, maximal at onset	Gradual, builds	Sudden, pleuritic	Sudden	Gradual or sudden	Sudden
Pain quality	Tearing / ripping	Crushing / pressure	Sharp, pleuritic	Sharp, pleuritic	Sharp, positional	Tearing / severe
Radiation	Back, interscapular	Jaw, L arm	None specific	Shoulder tip	Shoulder, trapezius	Back, flank
BP asymmetry / pulse deficit	Yes (~30%)	No	No	No	No	No
New AR murmur	Yes (Type A)	No	No	No	Pericardial rub	No
Widened mediastinum	Yes (60-90%)	No	No	No	± cardiomegaly	No
Pulsatile mass	No	No	No	No	No	Yes
ECG	Non-specific (may show MI)	ST changes	S1Q3T3, RV strain	Normal	Diffuse ST↑, PR↓	Usually normal
Key Ix	CT aortogram	ECG + Troponin	CTPA	CXR	Echo	CT aortogram

This deserves special mention because it is a form of dissection but involving the cervical arteries (internal carotid artery or vertebral artery) rather than the aorta, and it is a key differential for young stroke ^[14]:

Spontaneous — often in patients with connective tissue disorders (Marfan, EDS, fibromuscular dysplasia)
Traumatic — fall, sports, chiropractic manipulation ^[14]
ICA dissection: retroorbital pain + Horner's syndrome (disruption of sympathetic fibres running along the ICA) ± ipsilateral stroke from occlusion/embolism ^[14]
Vertebral artery dissection: occipital pain + vertebrobasilar symptoms (dizziness, diplopia, ataxia, dysarthria) ^[14]
Dissecting aneurysm can rupture intracranially and cause SAH ^[14]
Management: anticoagulation if no intracranial bleeding; endovascular or bypass surgery in selected cases ^[14]

The mechanism of ischaemia in cervical dissection is twofold: (1) the false lumen expanding to occlude the true lumen (haemodynamic compromise), and (2) thrombus forming at the intimal tear site → embolism to distal cerebral vessels. The latter is actually more common than the former.

High Yield Summary

Differential Diagnosis of Aortic Dissection — organised by presentation:

Chest pain: ACS (most important — beware dissection causing MI), PE, pneumothorax, pericarditis, pneumonia
Back/abdominal pain: Ruptured AAA (triad: pain + pulsatile mass + hypotension), pancreatitis, PPU, renal colic
Neurological (stroke/syncope): Primary ischaemic stroke, cervical arterial dissection (ICA → retroorbital pain + Horner; VA → occipital pain + vertebrobasilar symptoms), SAH
Acute limb ischaemia: Arterial embolism, in-situ thrombosis, phlegmasia cerulea dolens
Shock: Massive MI, massive PE, tamponade from other causes, haemorrhagic shock

Within-spectrum differentials: IMH (no flap, wall thickening), PAU (focal ulcer, heavy atherosclerosis), limited dissection

Critical safety point: ALWAYS exclude dissection before giving thrombolytics for STEMI — especially inferior STEMI with back pain, pulse deficit, or BP asymmetry.

Cervical arterial dissection: ICA (retroorbital pain + Horner's ± stroke) vs VA (occipital pain + posterior circulation symptoms). Can be spontaneous or traumatic. Anticoagulation if no bleeding; surgery in selected cases.

Key features pointing TO dissection over mimics: Pain maximal at onset, tearing quality, back radiation, migratory pain, inter-arm BP difference > 20 mmHg, pulse deficits, new AR murmur, widened mediastinum.

Active Recall - Differential Diagnosis of Aortic Dissection

References

^[1] Senior notes: Maksim Medicine Notes.pdf (p5, p15, p119 — chest pain DDx, aortic dissection, abdominal pain DDx) ^[2] Senior notes: Maksim Surgery Notes.pdf (p168 — acute limb ischaemia, embolism vs thrombosis) ^[3] Senior notes: Ryan Ho Cardiology.pdf (p54, p58, p210, p219-220 — chest pain approach, acute limb ischaemia DDx, aortic dissection DDx) ^[10] Senior notes: Ryan Ho Fundamentals.pdf (p199-203 — chest pain approach and DDx) ^[11] Senior notes: Ryan Ho Critical Care.pdf (p16-17 — shock differentials, CXR widened mediastinum) ^[12] Lecture slides: GC 199. Pulsating abdominal mass aortic aneurysm.pdf (p20 — ruptured AAA triad) ^[13] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p44 — ruptured AAA/aortic dissection in acute abdomen DDx) ^[14] Lecture slides: GC 109. Headache and loss of consciousness Acute stroke, subarachnoid haemorrhage and vascular malformation.pdf (p25 — cervical arterial dissection) ^[15] Senior notes: Maksim Surgery Notes.pdf (p45, p163 — acute abdomen DDx, ruptured AAA DDx)

Diagnosis of Aortic Dissection

There is no single "diagnostic criterion" for aortic dissection in the way that, say, the Jones criteria exist for rheumatic fever. Instead, diagnosis relies on a clinical pre-test probability assessment (using the Aortic Dissection Detection Risk Score — ADD-RS) combined with biomarkers (D-dimer) and definitive imaging (CT aortogram). The philosophy is: use clinical features to decide how urgently and directly you go to imaging, then let imaging make the definitive diagnosis.

The ADD-RS was developed by the AHA/ACC (2010) and refined in subsequent ESC and Society for Vascular Surgery guidelines. It is the recommended structured tool to stratify clinical suspicion before deciding on the next step. It works by scoring three domains — each domain scores 0 or 1, giving a total of 0–3 ^[3].

Domain	Features (Score 1 if ANY feature present in that domain)
A. High-risk conditions	Marfan syndrome or other connective tissue disease; family history of aortic disease; known aortic valve disease (including BAV); known thoracic aortic aneurysm; previous aortic manipulation/surgery
B. High-risk pain features	Chest, back, or abdominal pain described as: (1) abrupt onset, (2) severe intensity, (3) tearing or ripping quality
C. High-risk examination features	Pulse deficit or systolic BP difference > 20 mmHg between limbs; focal neurological deficit + pain; new aortic regurgitation murmur (with pain); hypotension/shock

Interpretation:

ADD-RS 0: Low probability → proceed to D-dimer
ADD-RS 1: Intermediate probability → D-dimer may still help stratify
ADD-RS ≥ 2–3: High probability → proceed directly to urgent CT aortogram (do not wait for D-dimer)

The logic here is straightforward: if a patient has high-risk conditions, high-risk pain features, AND high-risk exam findings, the pre-test probability is so high that waiting for a blood test wastes precious time. Go straight to imaging.

Exam-Critical: ADD-RS in 30 Seconds

Think of it as 3 buckets: (1) Who is this patient? (predisposing conditions), (2) What does the pain sound like? (abrupt, severe, tearing), (3) What do I find on examination? (pulse deficit, BP asymmetry, AR murmur, neuro deficit). One point per bucket. Score ≥ 2 → straight to CT aortogram.

D-dimer is a fibrin degradation product. In aortic dissection, the expanding false lumen activates the coagulation cascade within it → fibrin is laid down → plasmin degrades the fibrin → D-dimer is released into the circulation.
Role: primarily a rule-out test in patients with low pre-test probability (ADD-RS 0–1).
Threshold: D-dimer < 500 ng/mL within the first 24 hours of symptom onset has a sensitivity ~96–97% and negative predictive value ~95% for excluding acute aortic dissection.
Limitation: D-dimer is not specific — elevated in PE, DVT, DIC, sepsis, malignancy, post-operative states, pregnancy. So a positive D-dimer does not confirm dissection; it merely means you cannot rule it out and must proceed to imaging.
Time-dependency: D-dimer sensitivity drops if the patient presents > 24 hours after symptom onset (chronic dissections may have normal D-dimer).

Think of D-dimer in aortic dissection the same way you think of D-dimer in PE: a negative D-dimer in a low-probability patient effectively rules it out; a positive D-dimer in anyone just tells you to image.

D-dimer in AAS

D-dimer is useful to RULE OUT dissection, not to rule it in. Never rely on a negative D-dimer if clinical suspicion is high (ADD-RS ≥ 2). And remember: D-dimer loses sensitivity after 24 hours from onset — it is a test for the acute phase.

This algorithm integrates the ADD-RS, D-dimer, and imaging into a stepwise approach based on current (2022 ACC/AHA, 2024 ESC) guidelines ^[1]^[3]^[10]:

4. Investigation Modalities — Detailed Breakdown

4A. Bedside Investigations (Done Immediately, Before Definitive Imaging)

Purpose: Not to diagnose dissection but to (1) assess for concurrent MI from coronary malperfusion, (2) rule out other causes of chest pain (PE, pericarditis), (3) baseline before surgery.
Common findings in aortic dissection:
- Normal ECG (~30%) — a normal ECG does NOT exclude dissection
- Non-specific ST-T changes (~40%) — due to LV hypertrophy from longstanding HTN
- ST elevation (especially inferior leads — II, III, aVF) → suggests RCA malperfusion → dissection-induced MI. This is the classic diagnostic trap — if you see an inferior STEMI with back pain, check for dissection before giving thrombolytics ^[1]^[3]
- Low voltage / electrical alternans → suggests pericardial effusion/tamponade (fluid around the heart attenuates electrical signals)
- LVH pattern → reflects chronic hypertension (the most common risk factor)

ECG in Dissection

~30% of patients with aortic dissection have a completely normal ECG. A normal ECG does NOT rule out dissection. Conversely, ST elevation (especially inferior) may be present because the dissection involves the RCA — do NOT reflexively thrombolyse without excluding dissection first.

Test	Rationale	Expected Findings in Dissection	Interpretation
Troponin T / I (or hs-TnT)	Rule out MI — dissection can cause MI via coronary malperfusion ^[1]	↑ if coronary malperfusion → MI	Elevated troponin in a patient with tearing chest pain + back radiation → think dissection causing MI, not primary ACS
Lactate	Elevated in ischaemic gut / shock ^[1]	↑ if mesenteric ischaemia or shock	Rising lactate = tissue hypoperfusion — may indicate mesenteric malperfusion (SMA compromise) or generalised shock from rupture/tamponade
D-dimer	Rule-out biomarker (see above)	↑ in acute dissection (> 500 ng/mL in ~97%)	Negative D-dimer in low pre-test probability → rules out; positive is non-specific
FBC (CBC)	Baseline; anaemia assessment	May show ↓ Hb if ongoing haemorrhage (rupture), ↑ WCC (stress response)	Falling Hb → ongoing bleeding (rupture into pleural/pericardial space)
Renal function (U&E/Cr)	Assess for renal malperfusion → AKI ^[17]	↑ creatinine, ↑ urea if renal artery involvement	Rising creatinine → renal malperfusion (a marker of complicated dissection)
LFT	Baseline	Usually normal; ↑ ALT/AST in shock liver
Clotting (PT/aPTT/INR)	Pre-operative baseline; DIC screening	May be deranged in DIC from massive haemorrhage
Group & Save / Crossmatch	Pre-operative preparation	—	Always crossmatch at least 4–6 units of packed red cells for Type A
ABG	Assess oxygenation, ventilation, acid-base, lactate	Metabolic acidosis (↑ lactate) in malperfusion/shock	Lactic acidosis = tissue hypoperfusion → urgent intervention needed

CXR is abnormal in > 80% of cases ^[3] but is not diagnostic — it raises suspicion and should prompt definitive imaging.

Key CXR Findings:

Finding	Frequency	Pathophysiology
Broadening/widening of the upper mediastinum	60–90% ^[3]	The expanding false lumen and/or mediastinal haematoma pushes the mediastinal pleura laterally. The normal superior mediastinum is < 8 cm on a PA film. A widened mediastinum (> 8 cm on PA, or > 6 cm on AP supine) is suggestive but not diagnostic
Distorted aortic knuckle	Moderate	The aortic arch contour becomes irregular or blurred as the dissection distorts the normal anatomy
Left pleural effusion	~19% ^[3]	Rupture of the descending aorta through the adventitia into the left pleural space → haemothorax. Left-sided because the descending aorta is a left-sided structure
Displacement of intimal calcification	Low–Moderate	In a normal aorta, intimal calcification sits at the outer edge of the aortic shadow. If there is a false lumen beyond it, the calcification is displaced inward (> 6 mm from the outer aortic wall → "calcium sign")
Tracheal/oesophageal deviation to the right	Low	Expanding arch/descending aorta pushes the trachea and oesophagus (seen as NG tube deviation) to the right
Normal CXR	~10–20%	A normal CXR does NOT exclude dissection

The CXR is a rapid, bedside screening tool. Its main value is in increasing your clinical suspicion and prompting a CT aortogram. A normal CXR does not rule out dissection, and a widened mediastinum has many other causes (eg. lymphoma, mediastinal mass, poor AP film technique). Always interpret in clinical context.

4B. Definitive Imaging

CT aortogram is the preferred method of imaging ^[3] for suspected aortic dissection.

Why CT aortogram is first-line:

CT is usually quicker to perform and thus is preferred (over MRI) as aortic dissection is an acute situation ^[3]
Widely available 24/7 in most EDs
Very high sensitivity (~95–100%) and specificity (~98–100%) for aortic dissection
Can assess the entire aorta from root to bifurcation in a single scan
Provides information for surgical planning (anatomy, branch involvement, entry/re-entry tears)
MRI is unsuitable for pacing wiring and life support equipment → ICU patients often cannot undergo MRI ^[3]

Technique:

ECG-gated CT of the entire aorta with IV contrast (arterial phase)
ECG-gating reduces motion artefact from the beating heart, which is crucial for imaging the ascending aorta and root

Key CT Aortogram Findings:

Finding	Description	Clinical Significance
Intimal flap	A thin, linear hypodensity within the aortic lumen separating the true lumen from the false lumen	Hallmark finding — pathognomonic of classical aortic dissection
Demonstration of false lumen ^[3]	A second channel parallel to the true lumen, separated by the intimal flap	Confirms dissection; allows classification (Stanford A vs B)
True lumen identification	True lumen can be traced from normal aorta (it is continuous with the undissected segment) and is compressed by the false lumen ^[1]	The true lumen is typically smaller, smoothly marginated, and sits anteriorly and to the right in Type A
Contrast density differences	True lumen is more hyperdense (new blood) [because contrast arrives here first via direct arterial flow]; false lumen is more hypodense (slower flow / old blood / partial thrombosis) ^[1]	Helps distinguish true from false lumen — the "beak sign" (acute angle of the false lumen) and "cobweb sign" (residual medial strands in false lumen) are ancillary signs
Extent of dissection	Site of entry and re-entry tears, proximal and distal extent ^[3]	Essential for surgical planning — determines Stanford type and extent of repair needed
Branch involvement	Involvement of brachiocephalic, carotid, subclavian, coeliac, SMA, renal, iliac arteries ^[3]	Identifies malperfusion syndromes — determines if Type B is "complicated"
Thrombus in false lumen	Partial or complete thrombosis of the false lumen ^[3]	Complete false lumen thrombosis in Type B is prognostically favourable; partial thrombosis is worse (because there is still flow but impaired drainage → progressive expansion)
Pericardial effusion	Hyperdense fluid around the heart ^[3]	Indicates haemopericardium → impending/existing tamponade → emergent surgery
Pleural effusion	Hyperdense fluid in pleural space (usually left)	Haemothorax from descending aortic rupture
Mediastinal haematoma	Hyperdense collection in mediastinum surrounding the aorta	Indicates rupture through adventitia contained by mediastinal tissues

For IMH on CT:

Crescentic or circumferential hyperdense (on non-contrast phase) thickening of the aortic wall > 5 mm
No intimal flap or false lumen with flow on contrast phase
May have focal enhancement suggesting a small intimal tear

For PAU on CT:

Focal contrast-filled outpouching extending beyond the expected aortic lumen contour
Surrounded by extensive mural thrombus and atherosclerotic calcification
Usually in the descending thoracic aorta

TEE is indicated if CTA is contraindicated or if the patient is haemodynamically unstable ^[3] — i.e., too unstable to transport to the CT scanner.

Why TEE and not TTE?

Transthoracic echo (TTE) can only provide images of the first 3–4 cm of the ascending aorta ^[3] — it cannot visualise the arch or descending aorta reliably
TEE provides much better views because the oesophagus sits immediately posterior to the heart and descending aorta, allowing high-frequency imaging without lung or chest wall interference
However, TEE cannot visualise the entire distal aorta ^[3] — there is a "blind spot" in the distal ascending aorta/proximal arch where the trachea/left main bronchus interposes between the oesophagus and aorta

TEE Findings:

Finding	Description
Dilated aortic root ± intimal flap ^[3]	Directly visualises the flap oscillating in real-time
Aortic regurgitation on Doppler ^[3]	Colour-flow Doppler shows diastolic flow from aorta back into LV
Pericardial effusion	Anechoic/echoic fluid surrounding the heart
RWMA (regional wall motion abnormalities)	If coronary malperfusion → MI → the affected myocardial segments will be hypokinetic/akinetic ^[1]
True vs false lumen	Real-time assessment of flow dynamics — the true lumen typically expands in systole (when aortic pressure is highest) and the false lumen expands in diastole

Advantages:

Can be performed at the bedside / in the operating theatre
Real-time assessment of AR severity
Does not require contrast or radiation

Disadvantages:

Semi-invasive (requires sedation, oesophageal intubation)
Operator-dependent
Blind spot in distal ascending aorta/proximal arch
Cannot assess abdominal aorta or iliac arteries

TTE role:

Useful as an initial rapid bedside assessment to look for pericardial effusion, AR, LV function, and RWMA
If TTE shows pericardial effusion + dilated aortic root in a patient with acute chest pain → very high suspicion for Type A dissection → can expedite surgical decision even before CT

MRI is usually reserved for serial follow-up of chronic dissections ^[3].

MRI characteristics:

Feature	Detail
Sensitivity and specificity	Highly sensitive and specific — almost 100% ^[3]
Identification	Intimal flaps, great vessel anatomy, type of dissection and degree of AR ^[3]
Advantages	No radiation, no iodinated contrast (gadolinium instead), excellent soft tissue contrast, multiplanar imaging
Disadvantages	Time consuming ^[3]; need disconnecting from monitoring devices and IV pumps ^[3]; CI in patients with pacemakers/metallic implants; limited availability for emergencies

When MRI is used:

Serial follow-up (at 3, 6, 12 months and then annually) to monitor: false lumen size, residual dissection, aneurysmal degeneration, endoleak after TEVAR ^[3]
When CT is contraindicated (severe contrast allergy, renal impairment)
Chronic dissection where time is not as critical

DSA was historically considered the gold standard but is now rarely used for diagnosis alone ^[5]^[16]
It is an invasive procedure: catheter inserted (usually via femoral artery) → contrast injected → real-time fluoroscopic images
Almost never done except if endovascular intervention is required ^[5]
Advantages: real-time dynamic imaging, allows simultaneous endovascular intervention (TEVAR)
Disadvantages: catheter- and contrast-related complications (arterial injury, dissection extension, embolism, contrast nephropathy, stroke risk ~2-3% for cerebral vessels) ^[5]^[16]
Current role: primarily intra-operative — used to guide stent-graft placement during TEVAR

Investigation	Purpose	Key Findings
Coronary angiography	Assess coronary involvement (if planning surgery and time allows)	Coronary ostial occlusion by the dissection flap; may identify pre-existing CAD for concomitant CABG
CT brain	If neurological deficits present → assess for stroke	Acute ischaemic infarct or haemorrhage
Duplex USG of carotids	Assess carotid involvement if neurological symptoms	Dissection flap extending into carotid; abnormal flow patterns
Duplex USG of lower limbs	If limb ischaemia suspected	Absent flow distal to occlusion
Renal function monitoring	Ongoing assessment of renal malperfusion	Rising creatinine → worsening renal ischaemia
Serial lactate	Monitor for mesenteric ischaemia progression	Persistently rising lactate → ongoing gut ischaemia
Serial imaging (MRA/CTA at 3, 6, 12 months)	Detect recurrence, aneurysm formation, leakage post-intervention ^[3]	False lumen expansion, new dissection, endoleak after TEVAR

This is a commonly tested concept and worth understanding from first principles:

Feature	True Lumen	False Lumen
Continuity	Can be traced from normal undissected aorta ^[1]	Cannot be traced from normal aorta
Size	Usually smaller (compressed by false lumen) ^[1]	Usually larger (blood under pressure expands it)
Shape	Smoothly marginated	Irregular margins, may have "cobweb sign" (residual medial strands)
Contrast enhancement	More hyperdense (contrast arrives first) ^[1]	More hypodense (delayed filling, partial thrombosis) ^[1]
Position (ascending aorta)	Typically anteriorly and to the right	Typically posteriorly and to the left
Beak sign	Absent	Present — the acute angle where the intimal flap meets the aortic wall
Systolic expansion	Expands in systole (receives direct aortic flow)	Expands in diastole (recoil from compressed true lumen)

Why is the false lumen usually larger? Because the blood in the false lumen is under systemic pressure but the false lumen wall (just the outer media + thin adventitia) is weaker than the intact aortic wall → it expands more easily. The true lumen is sandwiched and compressed.

Scenario	First-Line Imaging	Rationale
Haemodynamically stable, suspected AAS	Urgent CT aortogram	Fast, widely available, high sensitivity/specificity, provides complete anatomical information ^[3]
Haemodynamically unstable, cannot transport to CT	Bedside TEE	Can be done at bedside/OR; identifies flap, AR, pericardial effusion ^[3]
CT contraindicated (contrast allergy, renal failure)	TEE or MRI (if stable enough)	MRI has near-100% sensitivity but is time-consuming and requires stable patient
Chronic dissection follow-up	MRA or CTA at 3, 6, 12 months	Monitor false lumen, aneurysm formation, endoleak ^[3]
Planned endovascular intervention	DSA (intra-operative)	Real-time guidance for stent-graft deployment ^[5]
Traumatic aortic injury	CT aortogram (fast with high sensitivity) ^[5]	Most ATAI patients are polytrauma → CT is part of trauma workup

High Yield Summary

Diagnostic Approach:

Pre-test probability — ADD-RS (3 domains: conditions, pain, exam) → 0 = low, ≥ 2 = high
D-dimer — rule-out test in low probability (ADD-RS 0-1); < 500 ng/mL within 24h effectively excludes AAS (sensitivity ~97%). Not useful if high probability or > 24h from onset
CT aortogram — gold-standard imaging for stable patients; identifies intimal flap, true/false lumen, extent, branch involvement, complications
TEE — for unstable patients or CT contraindicated; sees flap, AR, pericardial effusion at bedside
MRI — near-100% sensitivity but reserved for follow-up or when CT is contraindicated

Key CT findings: intimal flap (pathognomonic), true lumen traced from normal aorta and compressed by larger false lumen, true lumen more hyperdense (contrast arrives first), false lumen more hypodense

Key CXR findings: widened mediastinum (60-90%), distorted aortic knuckle, left pleural effusion (19%), displaced intimal calcification. Normal CXR does NOT exclude dissection (10-20% normal)

ECG: often normal or non-specific; ST elevation (especially inferior) may indicate coronary malperfusion → DO NOT thrombolyse without excluding dissection

Bloods: Troponin (rule out MI), lactate (mesenteric ischaemia/shock), D-dimer (rule-out), CBC, RFT, clotting, crossmatch

Active Recall - Diagnosis of Aortic Dissection

References

^[1] Senior notes: Maksim Medicine Notes.pdf (p15 — aortic dissection investigations, true vs false lumen on CT) ^[3] Senior notes: Ryan Ho Cardiology.pdf (p219–221 — investigations: CXR, CT aortogram, TEE, MRI findings and rationale; serial follow-up; prognosis) ^[5] Senior notes: Ryan Ho Radiology.pdf (p4 — CT aortogram for traumatic aortic injury, DSA as gold standard, TEE) ^[10] Senior notes: Ryan Ho Fundamentals.pdf (p199–203 — approach to acute chest pain, ECG and initial workup) ^[16] Senior notes: Maksim Surgery Notes.pdf (p165 — DSA as gold standard for vascular imaging, advantages and disadvantages) ^[17] Senior notes: Ryan Ho Urogenital.pdf (p96 — aortic dissection as cause of pre-renal AKI via renal artery malperfusion) ^[18] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p36, p43 — CT applications including aortic dissection, CT angiography) ^[19] Senior notes: Ryan Ho Critical Care.pdf (p17 — early investigations in shock including CXR widened mediastinum, ECG, bloods)

Management of Aortic Dissection

The management of aortic dissection is a race against time — untreated Type A dissection carries ~1% mortality per hour in the first 48 hours ^[3]. The overarching principles are simple: (1) stabilise the patient immediately, (2) reduce aortic wall stress to prevent propagation and rupture, and (3) determine the definitive treatment based on Stanford classification and complication status.

To understand management, think about what is physically happening to the aorta:

The intimal flap is being driven apart by the force of each heartbeat (dP/dt — the rate of rise of aortic pressure)
This force is determined by two factors: blood pressure (how much pressure) and heart rate (how fast the pressure cycles)
Therefore, the fundamental medical goal is to reduce dP/dt — literally reduce the "impulse" of each heartbeat on the aortic wall. This is called anti-impulse therapy ^[3]
The reason we target both BP and HR is that dropping BP alone without controlling HR can trigger reflex tachycardia → actually increases dP/dt → makes dissection worse

Think of it like a hammer hitting a wall: you need to reduce both how hard the hammer hits (BP) and how often it hits (HR). Reducing only the force but increasing the frequency doesn't help — the wall still gets destroyed.

3. Immediate Stabilisation (All Patients)

Every patient with suspected aortic dissection receives these measures immediately, regardless of Stanford type. The goal is to buy time while awaiting imaging and definitive treatment ^[1]^[3].

Measure	Rationale
NPO (nil by mouth)	Patient may need emergency surgery; general anaesthesia requires fasting to reduce aspiration risk ^[1]
Complete bed rest	Any physical activity ↑ sympathetic tone → ↑ HR and BP → ↑ dP/dt → propagation of dissection ^[1]
O₂ supplementation	Maintain SpO₂ > 94%; may be hypoxic from haemothorax, pulmonary oedema (acute AR), or shock
Cardiac monitor	Continuous ECG for arrhythmia detection (coronary malperfusion → MI → VT/VF); continuous BP monitoring ^[1]
IV access + arterial line	Arterial line for continuous BP monitoring (non-invasive cuff BP is intermittent and may be inaccurate with BP asymmetry) ^[3]; large-bore IV for fluid/drug/blood administration
Foley catheter	Monitor urine output — a key indicator of renal perfusion (renal malperfusion → oliguria) ^[3]
IV opioid analgesia	IV opioids (morphine or fentanyl) for pain control ^[3]. Pain itself causes sympathetic activation → ↑ HR and BP → worsens dissection. Adequate analgesia is therapeutic, not just humane
Book CCU / ICU bed	Intensive monitoring of BP/P, ECG, I/O is essential ^[1]

Why Analgesia is Not Optional

Pain drives the sympathetic nervous system → catecholamine surge → ↑ HR + ↑ BP → ↑ aortic wall stress → dissection propagation. Controlling pain with IV opioids is one of the most important early interventions — it directly reduces the force tearing the aorta apart.

3B. Anti-Impulse Therapy (Medical BP/HR Control)

This is the cornerstone of acute medical management for ALL aortic dissections.

Target goals: SBP 100–120 mmHg (MAP 60–75 mmHg) and HR < 60 bpm ^[1]^[3]

Agent	Class	Mechanism	Dose / Route	Why First-Line
Labetalol	Combined α₁-blocker + non-selective β-blocker ^[3]	β-blockade: ↓ HR + ↓ contractility → ↓ dP/dt. α₁-blockade: ↓ SVR → ↓ SBP. The combination gives both heart rate control AND vasodilation without reflex tachycardia	IV 10–20 mg bolus, then infusion 1–2 mg/min, titrate to target ^[1]	Labetalol is a combined α- and β-blocker, and therefore confers extra vasodilating effect ^[3]. Ideal because it addresses both components (HR + BP) in one drug
Esmolol	Cardioselective β₁-blocker (ultra-short acting)	Pure β₁-blockade → ↓ HR + ↓ contractility → ↓ dP/dt. Short half-life (~9 min) allows precise titration	IV 500 μg/kg bolus over 1 min, then 50–200 μg/kg/min infusion	Preferred when you want tight control and rapid on/off (e.g., unstable patients where you might need to quickly stop the drug if BP drops too much)
Non-dihydropyridine CCBs: Diltiazem / Verapamil	Non-DHP calcium channel blockers	Block L-type Ca²⁺ channels in cardiac myocytes and SA/AV nodes → ↓ HR + ↓ contractility + some vasodilation	Diltiazem IV 0.25 mg/kg bolus then 5–15 mg/h infusion; Verapamil IV 2.5–5 mg bolus	Used if β-blocker is contraindicated ^[1]^[3] (e.g., severe asthma/COPD, decompensated HF with bradycardia). Remember these are the "non-dipine" CCBs — the amlodipine/nifedipine type CCBs cause reflex tachycardia and are NOT used

Why β-blockers first? Because they directly ↓ dP/dt (the rate of aortic pressure rise), which is the primary physical force driving dissection propagation. Other antihypertensives lower BP but may cause reflex tachycardia (↑ HR → ↑ dP/dt → worse). β-blockers prevent this.

Agent	Class	Mechanism	Dose / Route	Important Caveats
Sodium nitroprusside (SNP)	Direct arterial and venous vasodilator	Releases nitric oxide → smooth muscle relaxation → ↓ SVR → ↓ BP	IV 0.25–10 μg/kg/min infusion	Nitroprusside alone may trigger reflex tachycardia and thus ↑ dP/dt → must be pre-treated with a β-blocker ^[3]. Caution if renal failure (accumulation of cyanide metabolite) ^[1]. Contraindicated in pregnancy ^[1]
IV GTN (glyceryl trinitrate)	Predominantly venodilator at low dose, arterial at high dose	Releases NO → ↓ preload (low dose) and ↓ afterload (high dose)	IV 5–200 μg/min	Alternative to SNP; less cyanide risk but also can cause reflex tachycardia if used without β-blocker
Nicardipine	DHP CCB (IV formulation)	Arterial vasodilation → ↓ SVR → ↓ BP; minimal reflex tachycardia at controlled infusion rates	IV 5–15 mg/h	Unlike oral nifedipine, IV nicardipine can be titrated carefully; used in some centres

Agent	Why Contraindicated
Hydralazine	Contraindicated in aortic dissection ^[1] — it is a direct arterial vasodilator that causes marked reflex tachycardia → ↑ dP/dt → propagation of dissection
Oral nifedipine (sublingual)	Same reason — causes reflex tachycardia. Never use sublingual nifedipine for BP control in dissection
Thrombolytics / fibrinolytics	Suspected aortic dissection is an absolute contraindication to thrombolysis ^[20]. If given to a dissection patient, it prevents haemostasis at the tear site → uncontrolled haemorrhage → death

Drug Selection Logic

Step 1: Start IV β-blocker (labetalol or esmolol) → get HR < 60. Step 2: If SBP still > 120 despite HR < 60, add sodium nitroprusside (or nicardipine). Never give a vasodilator without β-blocker cover first — the reflex tachycardia is dangerous. If β-blocker CI → use diltiazem/verapamil instead, then add vasodilator if needed.

4. Definitive Treatment by Stanford Type

The Stanford classification directly determines management:

Type A = surgical treatment ^[4] Type B = medical treatment, unless complicated ^[4]

4A. Stanford Type A — Emergency Surgery

ALL Type A dissections require emergency surgery ^[3]^[4]

Type A dissections are treated more aggressively because further proximal extension will lead to cardiac tamponade, MI, and acute aortic regurgitation ^[3]. The ascending aorta is intrapericardial — any rupture goes directly into the pericardial sac → tamponade → death within minutes. Without surgery, mortality approaches 50% at 48 hours and 80% at 2 weeks.

Procedure	Description	When Used
Open aortic repair (standard)	Excise the intimal tear, obliterate the entry site, place an interposition synthetic aortic graft (Dacron tube graft) ^[3]	Standard procedure for most Type A dissections involving the ascending aorta alone (DeBakey II)
Bentall procedure	Composite replacement of the aortic valve, aortic root, and ascending aorta with a valved conduit + reimplantation of coronary ostia ^[3]	When the aortic valve, root, and ascending aorta are all involved ^[3] — e.g., significant AR from root dilatation, annuloaortic ectasia (Marfan), or irreparable valve damage
Valve-sparing root replacement (David or Yacoub procedure)	Replace the aortic root and ascending aorta but preserve the native aortic valve leaflets by reimplanting them inside the graft	Used when the aortic valve leaflets are structurally normal but the root is dilated — avoids lifelong anticoagulation of a mechanical valve. Increasingly favoured in younger patients and Marfan patients
Hemiarch or total arch replacement	Extension of the graft to replace part or all of the aortic arch	When dissection extends into the arch; total arch replacement may use the "frozen elephant trunk" technique (hybrid open + endovascular)
Aortic valve repair/replacement	± repair or replacement of the aortic valve ^[3]	If acute AR is present — may use mechanical valve (requires lifelong warfarin), bioprosthetic valve, or repair

Operative Principles:

Performed under deep hypothermic circulatory arrest (DHCA) at 18–22°C — the body is cooled to reduce metabolic demand during the period when the heart and brain receive no blood flow (while the arch is being repaired)
Cardiopulmonary bypass (CPB) is essential — the heart must be arrested and circulation maintained by a heart-lung machine
The surgeon opens the ascending aorta, identifies the entry tear, and resects the affected segment
The false lumen is obliterated and the graft is sewn in place
Coronary ostia are reimplanted if the root is replaced

Emergency pericardiocentesis if cardiac tamponade ^[3] — this is a temporising measure to relieve tamponade physiology while awaiting definitive surgery. However, there is a risk: removing too much pericardial blood may "release the tamponade effect" that was paradoxically limiting further bleeding → sudden increase in bleeding rate. Therefore, pericardiocentesis should only drain enough to restore haemodynamic stability, and surgery should follow immediately.

Uncomplicated Type B dissection is managed medically ^[4].

"Uncomplicated" means:

No malperfusion syndrome (no end-organ ischaemia)
No rupture or impending rupture
No uncontrolled pain despite maximal medical therapy
No rapid false lumen expansion
No retrograde extension into the ascending aorta

Medical management consists of:

Anti-impulse therapy (as described above) — continued until stable
Transition to oral antihypertensives once stabilised:
- Oral β-blocker (e.g., atenolol, bisoprolol, carvedilol)
- ± CCB, ACE inhibitor/ARB as needed to achieve target
Lifelong antihypertensive therapy to aim target BP < 120/80 mmHg ^[3]
ICU monitoring for at least 48–72 hours to detect complications early
Serial imaging (MRA/CTA at 3, 6, 12 months) to detect recurrence, aneurysm, leakage ^[3]

Why is medical management sufficient for uncomplicated Type B? Because the descending aorta is outside the pericardium — there is no immediate risk of tamponade or coronary/cerebral malperfusion. The natural history is much better: with medical therapy alone, in-hospital mortality for uncomplicated Type B is ~10%, and many patients do well long-term with aggressive BP control and surveillance.

4C. Stanford Type B — Complicated

Complicated Type B dissection requires intervention (surgical or endovascular) ^[1]^[3]

Complication	Why It Mandates Intervention
Malperfusion of distal organs (renal, mesenteric, limb ischaemia) ^[1]^[3]	Ongoing end-organ damage is irreversible if not restored. Mesenteric ischaemia in particular has very high mortality if untreated
Associated aneurysm formation ^[3]	Progressive dilatation of the false lumen → ↑ risk of rupture
Rupture (haemothorax, haemomediastinum) ^[3]	Active haemorrhage → imminent death
Retrograde dissection into ascending aorta ^[3]	Effectively becomes a Type A dissection → emergent surgery
Marfan syndrome ^[3]	Intrinsic connective tissue weakness → higher risk of progression even if initially uncomplicated
Refractory pain	Ongoing pain despite maximal medical therapy suggests ongoing dissection propagation
Refractory hypertension	Cannot achieve target SBP despite maximal IV anti-impulse therapy → ongoing wall stress
Rapid false lumen expansion	Progressive ↑ in false lumen diameter on serial imaging → impending rupture

Procedure	Description	When Used
TEVAR (Thoracic Endovascular Aortic Repair)	A covered stent-graft is deployed via femoral artery access under fluoroscopic guidance. The stent covers the primary entry tear in the descending aorta → seals off flow into the false lumen → promotes false lumen thrombosis and aortic remodelling	Endovascular stent-grafting is the preferred approach for most complicated Type B dissections ^[3]. Less invasive than open surgery, lower perioperative mortality
Open surgical repair	Thoracotomy → resection of affected descending aorta → interposition graft	If anatomy is complex (e.g., involvement of visceral branches not amenable to TEVAR, connective tissue disease where stent durability is questioned, or failed TEVAR) ^[3]
Fenestration procedures	Endovascular creation of a tear in the intimal flap to allow communication between true and false lumens → equalises pressure → restores flow to malperfused branches	Used specifically for malperfusion syndromes where the intimal flap is compressing true lumen. Can be percutaneous (balloon fenestration) or surgical
Branch vessel stenting	Stenting of specific malperfused branch arteries (renal, SMA, iliac)	Adjunct to TEVAR or fenestration when individual branches are compromised

TEVAR — How It Works (From First Principles):

"TEVAR" = Thoracic Endovascular Aortic Repair
A sheathed stent-graft is advanced retrogradely via the femoral artery into the descending thoracic aorta
Under fluoroscopic guidance, it is positioned to cover the primary intimal entry tear
When deployed, the stent-graft expands against the true lumen wall, sealing the entry point
With the entry tear sealed, flow into the false lumen is eliminated → the false lumen gradually thromboses and may eventually remodel
This restores flow through the true lumen and relieves malperfusion

Complications of TEVAR:

Endoleak (persistent flow into false lumen despite stent)
Stent migration
Access site injury (femoral artery)
Spinal cord ischaemia (coverage of intercostal arteries including the artery of Adamkiewicz → paraplegia — risk ~3–5%)
Retrograde Type A dissection (rare but catastrophic — the stent deployment can create a new tear in the ascending aorta)
Stroke

Complication	Management
Cardiac tamponade	Emergency pericardiocentesis ^[3] as bridge to surgery; definitive treatment is emergent open repair (Type A)
Acute aortic regurgitation	Emergent surgery — aortic valve repair or replacement (often as part of Bentall procedure)
Coronary malperfusion → MI	Emergent surgery with coronary revascularisation (reimplantation of coronary ostia or CABG); do NOT give thrombolytics
Stroke (carotid malperfusion)	Emergent aortic repair is the priority — restoring true lumen flow may restore cerebral perfusion; thrombolysis is absolutely contraindicated
Mesenteric ischaemia	TEVAR + fenestration/branch stenting; if bowel necrosis → laparotomy and resection
Renal malperfusion → AKI	TEVAR/fenestration to restore renal perfusion; may need temporary renal replacement therapy
Acute limb ischaemia	TEVAR + iliac stenting or surgical bypass; femoral embolectomy if embolic component

After surviving the acute phase (whether treated medically or surgically), every patient needs lifelong follow-up:

Measure	Rationale
Lifelong antihypertensive therapy aiming for BP < 120/80 mmHg ^[3]	Uncontrolled HTN is the #1 driver of recurrent dissection, false lumen expansion, and aneurysm formation. Oral β-blockers are the backbone of long-term therapy
Serial imaging: CTA or MRA at 3, 6, 12 months, then annually ^[3]	Monitor for: (1) false lumen expansion, (2) new/recurrent dissection, (3) aneurysmal degeneration, (4) endoleak after TEVAR
Cardiovascular risk factor modification	Smoking cessation (absolute), lipid control (statins), diabetes management, weight management
Genetic counselling	If connective tissue disease suspected (Marfan, EDS, Loeys-Dietz) → refer for genetic testing; screen first-degree relatives
Activity restriction	Avoid isometric exercise (heavy weightlifting), competitive sports, and stimulant drugs (cocaine). Moderate aerobic exercise is generally permitted
Anticoagulation	Generally NOT used chronically in dissection (increases bleeding risk from the false lumen). Exception: if concurrent AF or mechanical valve post-Bentall

	Type A	Type B — Uncomplicated	Type B — Complicated
Acute medical Mx	Anti-impulse therapy (bridge to surgery)	Anti-impulse therapy (definitive)	Anti-impulse therapy + plan intervention
Definitive Mx	Emergency open surgery (ALL patients)	Medical management	TEVAR (preferred) or open repair
Surgical procedure	Open aortic repair ± valve (Bentall if root involved)	—	TEVAR ± fenestration ± branch stenting
BP target	SBP 100–120, HR < 60 (acute); < 120/80 (chronic)	Same	Same
Long-term	Lifelong antihypertensives + serial imaging	Same	Same

Entity	Type A (involves ascending)	Type B (spares ascending)
Intramural Haematoma (IMH)	Emergency surgery (same as Type A dissection — IMH has similar risk of progression to tamponade/rupture)	Medical management with close surveillance; some progress to dissection/rupture (20–30%) → intervene if progression
Penetrating Atherosclerotic Ulcer (PAU)	Rare in ascending aorta; surgery if present	Medical management if stable; TEVAR if symptomatic, expanding, or complicated

High Yield Summary

Immediate stabilisation (ALL patients):

NPO, bed rest, O₂, cardiac monitor, arterial line, Foley, IV opioids, ICU bed

Anti-impulse therapy targets: SBP 100–120 mmHg, HR < 60 bpm

1st line: IV β-blocker (labetalol or esmolol) or non-DHP CCB (diltiazem/verapamil if BB CI)
2nd line: add sodium nitroprusside (ONLY after β-blocker cover — never alone due to reflex tachycardia)
Hydralazine is CONTRAINDICATED (reflex tachycardia)
Thrombolytics are ABSOLUTELY CONTRAINDICATED

Definitive treatment:

Type A: ALL → Emergency open surgery (excise tear, interposition graft ± Bentall if root/valve involved)
Type B uncomplicated: Medical management (anti-impulse therapy → oral antihypertensives)
Type B complicated (malperfusion, rupture, retrograde extension, aneurysm, Marfan): TEVAR preferred, open if complex anatomy
Emergency pericardiocentesis if tamponade

Long-term: Lifelong BP < 120/80, serial CTA/MRA at 3, 6, 12 months then annually

Active Recall - Management of Aortic Dissection

References

^[1] Senior notes: Maksim Medicine Notes.pdf (p15 — management: supportive measures, anti-impulse therapy targets, labetalol, nitroprusside caveats, hydralazine CI, surgical indications) ^[3] Senior notes: Ryan Ho Cardiology.pdf (p221 — management: supportive, anti-impulse therapy, first-line and second-line agents, surgical indications Type A and B, Bentall procedure, TEVAR, pericardiocentesis, lifelong antihypertensives, serial imaging; p220 footnotes on labetalol MOA, nitroprusside reflex tachycardia, Type A rationale) ^[4] Lecture slides: Cardiac Surgery Tutorial_Prof. D Chan.pdf (p72 — Type A = surgical, Type B = medical unless complicated, DeBakey I most common and worst) ^[5] Senior notes: Ryan Ho Radiology.pdf (p4 — endovascular intervention for traumatic aortic injury) ^[19] Senior notes: Ryan Ho Critical Care.pdf (p17 — initial investigations and monitoring in shock) ^[20] Senior notes: Ryan Ho Cardiology.pdf (p138 — suspected aortic dissection as absolute contraindication to thrombolysis) ^[21] Senior notes: Ryan Ho Cardiology.pdf (p182 — hypertensive emergency management, SBP target < 120 in aortic dissection) ^[22] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p84-85 — endovascular stenting principles, stent graft for aneurysm repair)

Complications of Aortic Dissection

Complications of aortic dissection fall into two broad temporal categories: acute complications (arising from the dissection itself) and chronic/late complications (arising from the residual diseased aorta or from treatment). Mechanistically, acute complications derive from two fundamental processes we have discussed — malperfusion (the false lumen compresses branch vessels) and rupture (the weakened outer wall gives way). Post-treatment complications relate to the specific surgical or endovascular procedure performed.

1. Acute Complications of the Dissection Itself

These complications often co-present — a patient with Type A dissection may simultaneously have tamponade, MI, AR, and stroke. The mortality is cumulative: each additional complication worsens prognosis dramatically.

Complication	Mechanism (First Principles)	Clinical Features	Management
Cardiac tamponade	Aortic dissection can extend proximally leading to rupturing into pericardium giving rise to tamponade ^[3]. The ascending aorta is intrapericardial — the dissecting haematoma erodes through the adventitia into the pericardial sac. The pericardium is relatively inelastic (in the acute setting it cannot stretch to accommodate the blood) → even 150–200 mL of rapid accumulation → ↑ intrapericardial pressure → impedes ventricular filling → ↓ CO → obstructive shock	Beck's triad: hypotension, muffled heart sounds, raised JVP. Pulsus paradoxus (↓ SBP > 10 mmHg on inspiration). Electrical alternans on ECG	Emergency pericardiocentesis ^[3] as a bridge — drain just enough to restore haemodynamics. Definitive treatment: emergency open surgery (Type A repair). Caution: aggressive drainage may release the tamponade effect that was limiting further bleeding → accelerate haemorrhage
Haemothorax (left-sided)	The descending thoracic aorta is a left-sided posterior mediastinal structure. Rupture through the adventitia into the left pleural space → haemothorax ^[3]	Dull percussion, ↓ breath sounds, ↓ vocal resonance over the left hemithorax. Haemodynamic instability. CXR: left-sided opacification	Chest drain for decompression + volume resuscitation + emergent TEVAR or open repair
Mediastinal haematoma	Rupture contained by mediastinal tissues (parietal pleura, connective tissue) → contained haematoma	May present as widened mediastinum on CXR without frank haemodynamic collapse. The contained haematoma can "buy time" — but it can decompress at any moment → sudden cardiovascular collapse	Emergent surgical repair. This is a tenuous, unstable situation — treat as impending free rupture
Free aortic rupture (exsanguination)	Complete transmural rupture through all three layers → uncontained haemorrhage into the mediastinum, pleural cavity, or (rarely) peritoneal cavity	Sudden cardiovascular collapse. Most patients do not survive to reach hospital. Those who do arrive alive are in profound haemorrhagic shock	Immediate emergency surgery (Type A: open repair; Type B: TEVAR or open). Massive transfusion protocol. Death usually results from progression of dissection ^[3] — many die before any intervention is possible

Why Is Tamponade the #1 Killer in Type A?

The ascending aorta lies within the pericardial sac. When the false lumen ruptures outward, blood accumulates in a closed, non-compliant space. Unlike pleural haemorrhage where the large pleural space can accommodate several litres before shock, the pericardium can only tolerate ~150-200 mL acutely before it critically impedes diastolic filling. This is why Type A dissection demands emergency surgery — the ascending aorta is essentially a ticking bomb sitting inside a rigid container.

These complications arise when the dissection flap or expanding false lumen compresses or occludes branch arteries. The specific malperfusion syndrome depends on which branch is involved.

Complication	Branch Involved	Mechanism	Clinical Features	Prognosis / Management
Myocardial infarction (MI)	Coronary arteries (RCA more commonly — because the dissection flap in the ascending aorta tends to involve the right coronary ostium, which is anteriorly positioned) ^[1]^[3]	False lumen compresses the coronary ostium, or dissection extends into the coronary artery itself → coronary malperfusion → myocardial ischaemia/infarction	Chest pain (may be masked by the dissection pain itself), ST elevation on ECG (classically inferior leads — II, III, aVF for RCA; anterior leads for LCA), rising troponin	Emergency surgery with coronary reimplantation or CABG. Thrombolytics are absolutely contraindicated — will cause fatal haemorrhage from the dissected aorta. This is the single most dangerous diagnostic trap in acute medicine
Ischaemic stroke	Carotid arteries (brachiocephalic → right CCA; or left CCA directly from the arch) ^[3]	Dissection flap extends into or compresses the carotid artery → cerebral ischaemia	Acute focal neurological deficit: hemiplegia, hemisensory loss, aphasia (if dominant hemisphere), facial droop. May present with syncope/LOC	Emergent aortic repair is priority — restoring true lumen flow may restore cerebral perfusion. Thrombolysis for the stroke is absolutely contraindicated. Prognosis depends on stroke territory and duration of ischaemia
Syncope / loss of consciousness	Carotid arteries or due to tamponade/shock ^[3]	Transient or sustained ↓ cerebral perfusion from either carotid malperfusion (may be transient as the flap oscillates) or from ↓ CO (tamponade, AR, haemorrhage)	Transient or sustained LOC ± focal neurological deficit if carotid involved	Assess for tamponade (echo), stroke (CT brain), and haemorrhage. Emergent surgical repair for Type A
Paraplegia	Intercostal arteries / artery of Adamkiewicz (typically arises T9–T12) ^[3]	Malperfusion of the anterior spinal artery supply → anterior spinal cord syndrome (motor loss + pain/temperature loss, preserved proprioception/vibration). The spinal cord is particularly vulnerable because it has limited collateral circulation	Bilateral lower limb weakness/paralysis, sensory level, urinary retention, loss of bowel control	Often irreversible. Emergent restoration of true lumen flow (TEVAR for Type B, open repair for Type A) may help if very early. CSF drainage (lumbar drain) can ↓ spinal cord pressure and improve perfusion. Devastating complication with poor prognosis
Mesenteric infarction	Coeliac trunk and/or SMA ^[3]	Compression or occlusion of mesenteric arteries → gut ischaemia → if prolonged → bowel necrosis and perforation	Severe abdominal pain out of proportion to examination (initially), then peritonism as bowel becomes necrotic. ↑ Lactate ^[1], metabolic acidosis, bloody diarrhoea (late)	TEVAR + fenestration/branch stenting to restore flow. If bowel necrosis already established → laparotomy with resection of non-viable bowel. Carries very high mortality (> 60–80%)
Acute kidney injury (AKI)	Renal arteries ^[1]^[3]^[23]	Compression of one or both renal arteries → renal ischaemia → ↓ GFR → ↑ creatinine, oliguria	Rising creatinine, oliguria/anuria. May present as a pre-renal cause of AKI (aortic dissection is listed as a cause of pre-renal AKI from renal vascular disease) ^[23]	TEVAR/fenestration/renal artery stenting. Temporary RRT (renal replacement therapy) may be needed. Recovery depends on duration and severity of ischaemia
Acute limb ischaemia	External iliac / common iliac arteries ^[1]^[3]	False lumen compresses the iliac artery → ↓ lower limb perfusion → 6Ps (Pain, Pallor, Pulseless, Perishingly cold, Paraesthesia, Paralysis) ^[2]	Cool, pale, pulseless lower limb. Late: fixed mottling, sensory/motor loss → non-viable limb	TEVAR with iliac extension or surgical bypass to restore flow. May need fasciotomy if ischaemia > 6 hours (reperfusion injury risk). Amputation if limb is non-viable
Upper limb ischaemia	Subclavian artery	Dissection flap extends into or compresses the subclavian → ↓ upper limb perfusion	Asymmetric BP, pulse deficits, cool pale arm	Usually resolves with aortic repair. May need additional subclavian stenting/bypass in refractory cases

Complication	Mechanism	Clinical Features	Management
Acute aortic regurgitation (AR) → acute pulmonary oedema (APO)	Dissection involving the aortic root can: (1) dilate the root → the leaflets are pulled apart → incomplete coaptation, (2) the dissection flap prolapses through the valve orifice → direct obstruction of leaflet closure ^[1]^[3]. In acute AR the LV is normal-sized and cannot accommodate the sudden volume overload → ↑↑ LVEDP → acute pulmonary venous congestion → APO	New early diastolic murmur (EDM), signs of acute pulmonary oedema (tachypnoea, crackles, pink frothy sputum), cardiogenic shock	Emergency aortic valve repair or replacement during open surgery. May be part of Bentall procedure ^[3]. Medical temporisation with IV nitroprusside (↓ afterload → ↓ regurgitant fraction) but only as bridge

Even after surviving the acute phase (whether with medical or surgical management), the residual dissected aorta remains a source of long-term complications.

Complication	Mechanism	Timeframe	Detection	Management
Aneurysmal degeneration of the false lumen	The false lumen wall (outer media + thin adventitia) is structurally weak. Over time, persistent flow in a patent false lumen → progressive dilatation → aneurysm formation. This is the most common late complication	Months to years	Serial imaging (CTA/MRA at 3, 6, 12 months then annually) ^[3] → monitor for ↑ aortic diameter	Elective TEVAR or open repair when the aneurysm reaches > 5.5 cm or is rapidly expanding (same principles as degenerative aortic aneurysm)
Recurrent / new dissection	The remaining aorta still has the underlying risk factors (HTN, connective tissue disease) → new dissections can occur at sites remote from the original tear	Months to years	Serial imaging + clinical vigilance for new symptoms	Treat as a new dissection episode; reinforce BP control
Aortic rupture (late)	Aneurysmal degeneration → ↑ wall tension (La Place's law: T = P × r / wall thickness) → eventual rupture	Months to years	Serial imaging. Acute symptoms: sudden chest/back pain + haemodynamic collapse	Emergency repair
Chronic aortic regurgitation	If the aortic valve was not addressed during the initial surgery, or if the repair degenerates, chronic AR may develop. In chronic AR the LV has time to dilate and compensate initially, but eventually decompensates → heart failure	Months to years	Echocardiographic surveillance; symptoms of HF (dyspnoea, orthopnoea, PND)	Aortic valve replacement when symptomatic or when LV function deteriorates (LVEF < 50% or LV dilation: ESD > 55 mm or EDD > 75 mm)
Redissection at graft anastomosis	The suture line between the native aorta and the synthetic graft is a stress point. New intimal tears can occur at the proximal or distal anastomotic sites	Months to years	Serial imaging	Redo surgery or TEVAR
Chronic malperfusion syndromes	A partially thrombosed false lumen may cause chronic ischaemia of branch vessels (renal → CKD, mesenteric → chronic mesenteric ischaemia with postprandial pain and weight loss)	Ongoing	Duplex USS of relevant arteries, serial RFT, clinical symptoms	Endovascular stenting or surgical bypass of affected branches

3. Complications of Surgical Treatment

These are largely analogous to the complications of any major cardiothoracic surgery performed under deep hypothermic circulatory arrest (DHCA) and cardiopulmonary bypass (CPB):

Complication	Mechanism	Comments
Bleeding / haemorrhage	Complex suture lines on a fragile dissected aortic wall; coagulopathy from CPB and DHCA; massive transfusion requirements	Often requires re-exploration; transfusion-related complications (TRALI, TACO, citrate toxicity)
Stroke	Air embolism during CPB, atheromatous embolism from aortic manipulation, prolonged cerebral ischaemia during DHCA	Improved by subclavian cannulation and antegrade cerebral perfusion ^[4] — modern techniques maintain cerebral perfusion during arch repair
Myocardial dysfunction	Perioperative MI (ischaemia during aortic cross-clamping), myocardial stunning from CPB, coronary malperfusion	Managed with inotropes, IABP; may need coronary revascularisation
Paraplegia	Ligation/occlusion of intercostal arteries or artery of Adamkiewicz during repair	More common in thoracic/thoracoabdominal aortic surgery ^[24]^[25]. CSF drainage via lumbar drain can ↓ risk
Renal failure	Renal ischaemia during aortic clamping + perioperative hypotension + contrast nephropathy	More common in suprarenal repair ^[24]. May need RRT
Respiratory failure / ARDS	CPB-induced systemic inflammatory response, prolonged ventilation, atelectasis	Lung-protective ventilation strategies in ICU
Graft infection (late)	Bacterial seeding of prosthetic material (haematogenous or at time of surgery)	Rare but devastating; usually requires graft excision + extra-anatomical bypass
Pseudoaneurysm at anastomosis (late)	Suture line weakening or degeneration → contained rupture at graft-aorta junction ^[24]	Serial imaging; surgical revision if expanding
Bowel ischaemia	IMA ligation, SMA hypoperfusion during clamping, low-flow state	Specific to aortic surgery ^[24]^[25] — may present as bloody diarrhoea, ↑ lactate post-operatively. Colonoscopy to assess viability
Sexual dysfunction	Damage to retroperitoneal autonomic nerves (hypogastric plexus) ^[24]	More relevant in abdominal/thoracoabdominal aortic surgery

Improving Surgical Outcomes

Early surgical results for acute dissection have improved over the years ^[4]. Key advances include: early diagnosis, subclavian cannulation (provides antegrade cerebral perfusion during circulatory arrest), cerebral oximetry monitoring, and growing surgical experience ^[4]. At QMH, mortality for acute dissection surgery decreased from 15.6% to 5.4% over the 2012–2019 period ^[4].

Complication	Mechanism	Incidence / Comments
Endoleak	Persistent flow into the false lumen/aneurysm sac despite the stent-graft ^[24]	~30% overall for endovascular aortic repair ^[24]. Type I (inadequate seal at attachment zones — proximal or distal) and Type III (graft component separation or fabric tear) are high-pressure leaks → require re-intervention. Type II (backflow from branch vessels, e.g., intercostal arteries) is usually benign and monitored. Type IV (graft porosity) is self-limiting
Retrograde Type A dissection	The stent deployment force can create a new intimal tear in the ascending aorta → catastrophic retrograde dissection	Rare (~1–4%) but highly lethal; requires emergency open surgery
Spinal cord ischaemia → paraplegia	Extensive coverage of intercostal arteries by the stent-graft → loss of spinal cord perfusion	Risk ~3–5%, higher with longer coverage segments. CSF drainage (lumbar drain) to ↓ spinal cord oedema and improve perfusion pressure
Access site complications	Femoral artery injury, pseudoaneurysm, AV fistula, bleeding/haematoma ^[24]	9–16% ^[24]. Managed with surgical repair or thrombin injection
Graft migration	Proximal aortic neck dilatation over time → stent graft slips distally → proximal endoleak ^[24]	Detected on serial imaging; may need proximal extension cuff
Limb kinking and occlusion	Graft limbs may kink at angulation points → thrombosis → distal ischaemia ^[24]	May require additional stenting or surgical bypass
Post-implantation syndrome	Transient flu-like inflammatory syndrome following endograft placement in first 7–10 days ^[24]. Mechanism unknown (possibly immune response to the graft material). Fever, ↑ WCC, malaise	13–60% ^[24]. Self-limiting — no specific management required ^[24]. Important to distinguish from graft infection (which would present later and with more severe/persistent symptoms)
Contrast nephropathy	IV iodinated contrast used during fluoroscopy → nephrotoxic effect on renal tubules	0.7–2% ^[24]. Risk ↑ with pre-existing CKD, diabetes, volume depletion. Prevention: hydration, avoid nephrotoxins

After successful revascularisation (whether from aortic repair restoring true lumen flow, or from branch vessel stenting), reperfusion injury can occur in the previously ischaemic tissues:

Complication	Mechanism	Clinical Features	Management
Compartment syndrome (limbs)	Prolonged ischaemia → cell death → ↑ capillary permeability → on reperfusion, fluid leaks into interstitial space → intracompartmental pressure > 30 mmHg → compresses arteries/veins/nerves within the compartment → further ischaemia ^[2]	Pain out of proportion worsening despite analgesia; tense compartment on palpation; pain on passive stretch of muscles in the compartment. Pulses may still be present (SBP is >> intracompartmental pressure) ^[2]	Urgent fasciotomy (medial + lateral incisions) ^[2]. Delay → muscle necrosis → irreversible damage
Rhabdomyolysis	Reperfusion of ischaemic muscle → release of intracellular contents: K⁺ (→ hyperkalaemia → arrhythmia), H⁺ (→ metabolic acidosis), myoglobin (→ precipitation in renal tubules → myoglobinuric AKI), phosphate (→ hypocalcaemia), CK ^[2]	Dark brown "tea-coloured" urine, rising CK (often > 10,000 U/L), hyperkalaemia, metabolic acidosis, AKI (rising creatinine)	Aggressive IV hydration (aim UO > 200 mL/h), IV bicarbonate (alkalinise urine to prevent myoglobin precipitation), diuresis with mannitol, cardiac monitoring for arrhythmia, treat hyperkalaemia ^[2]. May need RRT if severe AKI
Reperfusion gut injury	Restoration of mesenteric flow to ischaemic bowel → release of reactive oxygen species, inflammatory mediators → mucosal injury → potentially worsening gut necrosis despite restored flow	Worsening abdominal pain, ↑ lactate, bloody diarrhoea after initially "successful" revascularisation	Re-assess bowel viability (laparotomy/second-look laparotomy at 24–48 hours); resect non-viable segments

Scenario	Mortality
Type A — untreated	~1% per hour in the first 48h ^[3]; ~50% at 48 hours; ~80% at 2 weeks
Type A — with prompt surgery	90% survival if prompt diagnosis and management ^[3]; in-hospital surgical mortality ~15–25% (improving — 5.4% at QMH in recent years ^[4])
Type B — uncomplicated, medically managed	~10% in-hospital mortality; ~80–90% 5-year survival with good BP control
Type B — complicated	Higher mortality (20–50% depending on complications); TEVAR has improved outcomes

Death usually results from progression of dissection (instead of vascular compromise/rupture) ^[3] — meaning that the ongoing propagation of the flap leading to new complications (extending into new branches, causing new rupture sites) is more lethal than a single static ischaemic event.

Acute Complications of Aortic Dissection
├── RUPTURE
│   ├── Cardiac tamponade (most common cause of death in Type A)
│   ├── Haemothorax (usually left-sided)
│   ├── Mediastinal haematoma
│   └── Free rupture / exsanguination
├── MALPERFUSION
│   ├── Coronary → MI (especially RCA → inferior STEMI)
│   ├── Carotid → Stroke / Syncope
│   ├── Subclavian → Arm ischaemia / BP asymmetry
│   ├── Intercostal / Adamkiewicz → Paraplegia
│   ├── Coeliac / SMA → Mesenteric infarction
│   ├── Renal → AKI
│   └── Iliac → Acute limb ischaemia
└── VALVE / ROOT
    └── Acute AR → APO

Chronic / Late Complications
├── Aneurysmal degeneration of false lumen
├── Recurrent dissection
├── Late rupture
├── Chronic AR → HF
├── Redissection at anastomosis
└── Chronic malperfusion (CKD, chronic mesenteric ischaemia)

Treatment Complications
├── Open repair: bleeding, stroke, paraplegia, renal failure, graft infection, bowel ischaemia
├── TEVAR: endoleak, retrograde Type A dissection, spinal ischaemia, access complications, post-implantation syndrome
└── Reperfusion injury: compartment syndrome, rhabdomyolysis, reperfusion gut injury

High Yield Summary

Acute complications — 3 mechanisms:

Rupture: tamponade (most common cause of death in Type A), haemothorax (usually left), free rupture
Malperfusion: MI (coronary), stroke (carotid), paraplegia (spinal), mesenteric infarction (SMA/coeliac), AKI (renal), limb ischaemia (iliac)
Acute AR: root involvement → leaflet malcoaptation → APO (LV cannot compensate acutely)

Key exam trap: Dissection causing inferior STEMI (RCA malperfusion) → do NOT thrombolyse → fatal

Chronic complications: Aneurysmal degeneration of false lumen (most common), recurrent dissection, late rupture, chronic AR → HF

Surgical complications: Open → stroke, paraplegia, bleeding, renal failure, bowel ischaemia, graft infection. TEVAR → endoleak (~30%), retrograde Type A dissection (~1-4%), spinal ischaemia (~3-5%), post-implantation syndrome (13-60%, self-limiting)

Reperfusion injury: Compartment syndrome (fasciotomy), rhabdomyolysis (hydration + bicarb + mannitol), reperfusion gut injury (second-look laparotomy)

Prognosis: Type A untreated = ~1%/h mortality; treated = ~90% survival. QMH surgical mortality improved from 15.6% to 5.4% over 2012-2019. Death usually from progression of dissection rather than a single static event.

Active Recall - Complications of Aortic Dissection

References

^[1] Senior notes: Maksim Medicine Notes.pdf (p15 — complications: ischaemia and rupture list, troponin and lactate as markers) ^[2] Senior notes: Maksim Surgery Notes.pdf (p168-169 — acute limb ischaemia 6Ps, reperfusion injury: compartment syndrome, rhabdomyolysis management) ^[3] Senior notes: Ryan Ho Cardiology.pdf (p219-221 — malperfusion syndromes, tamponade, AR, prognosis, serial imaging; p225-226 — open repair and EVAR complications) ^[4] Lecture slides: Cardiac Surgery Tutorial_Prof. D Chan.pdf (p72 — high mortality and morbidity; p74 — improving surgical results at QMH, subclavian cannulation, antegrade cerebral perfusion, mortality 15.6% to 5.4%) ^[23] Senior notes: Ryan Ho Critical Care.pdf (p25 — aortic dissection as cause of pre-renal AKI via renovascular disease) ^[24] Senior notes: Ryan Ho Cardiology.pdf (p225-226 — open repair complications: paraplegia, renal failure, bowel ischaemia, sexual dysfunction, graft infection, pseudoaneurysm; EVAR complications: endoleak types and management, access site complications, post-implantation syndrome) ^[25] Lecture slides: GC 199. Pulsating abdominal mass aortic aneurysm.pdf (p15, p22 — operative complications: haemorrhage, bowel ischaemia, impotence, renal failure, distal embolism, paraplegia, trash foot; late: graft infection, anastomotic aneurysm, graft-duodenal fistula; ruptured AAA specific complications)

High Yield Summary

Definition: Tear in aortic intima → blood dissects into media → false lumen. Part of the acute aortic syndrome spectrum (classical dissection, IMH, PAU, limited dissection).

Epidemiology: ~3/100k/year; ~1/day in HK; M:F = 2:1; age 60–80y; HTN in ~77%.

Stanford Classification (drives management):

Type A = involves ascending aorta → SURGICAL
Type B = spares ascending aorta → MEDICAL (unless complicated)
DeBakey I = most common and worst

Risk Factors: HTN (#1), connective tissue diseases (Marfan, EDS, Loeys-Dietz), BAV, cocaine, pregnancy, vasculitis, trauma, prior aortic disease.

Clinical Features:

Pain: Sudden, maximal at onset, tearing, radiates to back (ascending → anterior chest; descending → interscapular)
BP: HTN or pseudo-hypotension; inter-arm difference > 20 mmHg
Pulses: Deficits, radial-radial delay (Type A), radial-femoral delay (Type B)
Cardiac: EDM of acute AR, tamponade (Beck's triad)
Neurological: Stroke, syncope, paraplegia
Malperfusion: MI, mesenteric ischaemia, AKI, limb ischaemia
Rupture: Left haemothorax, tamponade

Mortality: ~1–2% per hour untreated (Type A); 90% survival if prompt Dx and Mx.

High Yield Summary — Differential Diagnosis

Differential Diagnosis of Aortic Dissection — organised by presentation:

Chest pain: ACS (most important — beware dissection causing MI), PE, pneumothorax, pericarditis, pneumonia
Back/abdominal pain: Ruptured AAA (triad: pain + pulsatile mass + hypotension), pancreatitis, PPU, renal colic
Neurological (stroke/syncope): Primary ischaemic stroke, cervical arterial dissection (ICA → retroorbital pain + Horner; VA → occipital pain + vertebrobasilar symptoms), SAH
Acute limb ischaemia: Arterial embolism, in-situ thrombosis, phlegmasia cerulea dolens
Shock: Massive MI, massive PE, tamponade from other causes, haemorrhagic shock

Within-spectrum differentials: IMH (no flap, wall thickening), PAU (focal ulcer, heavy atherosclerosis), limited dissection

Critical safety point: ALWAYS exclude dissection before giving thrombolytics for STEMI — especially inferior STEMI with back pain, pulse deficit, or BP asymmetry.

High Yield Summary — Diagnosis

Diagnostic Approach:

Pre-test probability — ADD-RS (3 domains: conditions, pain, exam) → 0 = low, ≥ 2 = high
D-dimer — rule-out test in low probability (ADD-RS 0–1); < 500 ng/mL within 24h effectively excludes AAS (sensitivity ~97%). Not useful if high probability or > 24h from onset
CT aortogram — gold-standard imaging for stable patients; identifies intimal flap, true/false lumen, extent, branch involvement, complications
TEE — for unstable patients or CT contraindicated; sees flap, AR, pericardial effusion at bedside
MRI — near-100% sensitivity but reserved for follow-up or when CT is contraindicated

Key CXR findings: widened mediastinum (60–90%), distorted aortic knuckle, left pleural effusion (19%), displaced intimal calcification. Normal CXR does NOT exclude dissection (10–20% normal)

ECG: often normal or non-specific; ST elevation (especially inferior) may indicate coronary malperfusion → DO NOT thrombolyse without excluding dissection

Bloods: Troponin (rule out MI), lactate (mesenteric ischaemia/shock), D-dimer (rule-out), CBC, RFT, clotting, crossmatch

High Yield Summary — Management

Immediate stabilisation (ALL patients):

NPO, bed rest, O₂, cardiac monitor, arterial line, Foley, IV opioids, ICU bed

Anti-impulse therapy targets: SBP 100–120 mmHg, HR < 60 bpm

1st line: IV β-blocker (labetalol or esmolol) or non-DHP CCB (diltiazem/verapamil if BB CI)
2nd line: add sodium nitroprusside (ONLY after β-blocker cover — never alone due to reflex tachycardia)
Hydralazine is CONTRAINDICATED (reflex tachycardia)
Thrombolytics are ABSOLUTELY CONTRAINDICATED

Definitive treatment:

Type A: ALL → Emergency open surgery (excise tear, interposition graft ± Bentall if root/valve involved)
Type B uncomplicated: Medical management (anti-impulse therapy → oral antihypertensives)
Type B complicated (malperfusion, rupture, retrograde extension, aneurysm, Marfan): TEVAR preferred, open if complex anatomy
Emergency pericardiocentesis if tamponade

Long-term: Lifelong BP < 120/80, serial CTA/MRA at 3, 6, 12 months then annually

High Yield Summary — Complications

Acute complications — 3 mechanisms:

Rupture: tamponade (most common cause of death in Type A), haemothorax (usually left), free rupture
Malperfusion: MI (coronary), stroke (carotid), paraplegia (spinal), mesenteric infarction (SMA/coeliac), AKI (renal), limb ischaemia (iliac)
Acute AR: root involvement → leaflet malcoaptation → APO (LV cannot compensate acutely)

Key exam trap: Dissection causing inferior STEMI (RCA malperfusion) → do NOT thrombolyse → fatal

Chronic complications: Aneurysmal degeneration of false lumen (most common), recurrent dissection, late rupture, chronic AR → HF

Surgical complications: Open → stroke, paraplegia, bleeding, renal failure, bowel ischaemia, graft infection. TEVAR → endoleak (~30%), retrograde Type A dissection (~1–4%), spinal ischaemia (~3–5%), post-implantation syndrome (13–60%, self-limiting)

Reperfusion injury: Compartment syndrome (fasciotomy), rhabdomyolysis (hydration + bicarb + mannitol), reperfusion gut injury (second-look laparotomy)

Prognosis: Type A untreated = ~1%/h mortality; treated = ~90% survival. QMH surgical mortality improved from 15.6% to 5.4% over 2012–2019. Death usually from progression of dissection rather than a single static event.

Aortic Dissection

1. Definition

2. Epidemiology

3. Anatomy and Function

3.1 Aortic Wall Layers

3.2 Segments of the Aorta

3.3 Vasa Vasorum

4. Risk Factors

4.1 Acquired Risk Factors

4.2 Congenital / Inherited Risk Factors

4.3 Inflammatory / Vasculitic Risk Factors

5. Pathophysiology

5.1 Initiating Event

5.2 Propagation

5.3 Consequences of Dissection

5.3.1 Malperfusion Syndromes

5.3.2 Rupture

5.3.3 Aortic Regurgitation (AR)

6. Classification

6.1 Stanford Classification (Most Clinically Used)

6.2 DeBakey Classification

6.3 Temporal Classification

7. Clinical Features

7.1 Symptoms

7.1.1 Pain (Present in > 90% of acute dissections)

7.1.2 Symptoms from Malperfusion

7.1.3 Asymptomatic / Chronic

7.2 Signs

7.2.1 Blood Pressure

7.2.2 Pulse Abnormalities

7.2.3 Cardiac Signs

7.2.4 Neurological Signs

7.2.5 Other Signs

8. Summary of Clinical Features by Dissection Type

9. Pathophysiological Basis of Key Clinical Features — Summary Table

Active Recall - Aortic Dissection (Definition to Clinical Features)

References

1. Differential Diagnosis Organised by Presenting Feature

1A. Chest Pain Differentials

1B. Back / Abdominal Pain Differentials

1C. Neurological Differentials (Syncope / Stroke)

1D. Acute Limb Ischaemia Differentials

1E. Shock Differentials

2. Other Acute Aortic Syndromes (Within-Spectrum Differentials)

3. Systematic Approach: Distinguishing Dissection from Its Mimics

4. Diagnostic Algorithm for Differentiating Aortic Dissection from Key Mimics

5. Summary Table: "At a Glance" Differentiation

6. Special Consideration: Cervical Arterial Dissection

Active Recall - Differential Diagnosis of Aortic Dissection

1. Pre-Test Probability: The Aortic Dissection Detection Risk Score (ADD-RS)

2. Biomarker: D-Dimer

3. Overall Diagnostic Algorithm

4. Investigation Modalities — Detailed Breakdown

4A. Bedside Investigations (Done Immediately, Before Definitive Imaging)

4A-i. ECG

4A-ii. Bloods

4A-iii. CXR (Chest X-ray)

4B. Definitive Imaging

4B-i. CT Aortogram (CTA) — The Preferred First-Line Imaging

4B-ii. Transoesophageal Echocardiography (TEE)

4B-iii. MRI / MRA (Magnetic Resonance Imaging / Angiography)

4B-iv. Digital Subtraction Angiography (DSA) — Formerly the Gold Standard

5. Additional Investigations to Assess Complications / Plan Surgery

6. Interpretation Pearls: True Lumen vs False Lumen on CT

7. Summary: Which Imaging When?

Active Recall - Diagnosis of Aortic Dissection

1. Principles of Management — First Principles

2. Management Algorithm — Overview

3. Immediate Stabilisation (All Patients)

3A. Supportive Measures

3B. Anti-Impulse Therapy (Medical BP/HR Control)

First-Line Agents

Second-Line Agents (Add If First-Line Fails to Achieve Target)

Contraindicated Agents

4. Definitive Treatment by Stanford Type

4A. Stanford Type A — Emergency Surgery

Why Is Surgery Mandatory for Type A?

Surgical Options

Emergency Pericardiocentesis

4B. Stanford Type B — Uncomplicated