Aortic Dissection

Quick Answer

One-liner: Aortic dissection is a life-threatening tear in the aortic intima causing blood to dissect between aortic layers; Type A (involves ascending aorta) requires emergency surgery, Type B (descending aorta only) is initially managed medically with aggressive BP/HR control.

Aortic dissection occurs when an intimal tear allows blood to enter the medial layer of the aorta, creating a false lumen that propagates along the vessel. Untreated mortality is 1-2% per hour, with 50% dead by 48 hours. The key emergency decision is Type A vs Type B (Stanford classification): Type A involves the ascending aorta and mandates urgent cardiothoracic surgery; Type B (descending aorta only) is initially managed with aggressive medical therapy (target SBP 100-120 mmHg, HR below 60 bpm). Complications include cardiac tamponade, acute aortic regurgitation, stroke, and malperfusion syndromes affecting viscera, kidneys, or limbs.

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Layers of aortic wall (intima, media, adventitia), aortic branches (coronary, arch vessels, visceral, renal), blood supply to spinal cord (artery of Adamkiewicz)
• Physiology: Aortic wall stress (Laplace's law: Wall tension ∝ pressure × radius), dP/dt (rate of pressure change—reduced by beta-blockade), autoregulation of end-organs
• Pharmacology: Beta-blockers (esmolol, labetalol, metoprolol), vasodilators (GTN, SNP), calcium channel blockers (diltiazem), analgesics (fentanyl, morphine)

Fellowship Exam Relevance

• Written: Classification systems (Stanford, DeBakey), D-dimer role, imaging modalities (sensitivity/specificity), complications (tamponade, AR, malperfusion), medical management targets
• OSCE: Resuscitation scenario with haemodynamic instability, breaking bad news about poor prognosis, transfer coordination with cardiothoracic centre
• Key domains tested: Medical Expert (diagnosis, management), Communicator (family discussion, retrieval coordination), Collaborator (cardiothoracic surgery liaison), Leader (resus team coordination)

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Key Points

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Epidemiology

Australian/NZ Specific

• Incidence: 3.13 per 100,000 person-years in Aotearoa New Zealand (2010-2020), including out-of-hospital deaths [8]
• Type distribution: 61% Type A, 39% Type B in NZ national study [8]
• Outcomes in Australia: 30-day mortality 11.2% for Type A dissection (2001-2021 ANZSCTS data), with improved outcomes at higher-volume centres [9]
• Indigenous populations: Limited data, but Aboriginal and Torres Strait Islander peoples have 2-3x higher cardiovascular disease burden, potentially increasing dissection risk with hypertension [10]
• Rural/remote: Significant delays in diagnosis and transfer to cardiothoracic centres; RFDS retrieval critical [11]

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Pathophysiology

Mechanism

Aortic dissection begins with an intimal tear that allows blood under systemic pressure to enter the medial layer of the aortic wall. Blood then dissects along the media, cleaving it into inner and outer layers, creating a false lumen alongside the original true lumen. The false lumen may:

• Propagate anterograde (towards iliac arteries) or retrograde (towards aortic root)
• Compress or shear branch vessels, causing malperfusion
• Re-enter the true lumen via distal fenestrations
• Rupture through the adventitia (instantly fatal if into pericardium or pleural space)

Pathological Progression

Intimal tear (primary entry) → Blood enters medial layer → False lumen propagation (antegrade/retrograde) → Branch vessel compromise (malperfusion) → Possible outcomes:
  1. Thrombosis of false lumen (stabilisation)
  2. Re-entry to true lumen (chronic dissection)
  3. Rupture through adventitia (pericardial tamponade, exsanguination)
  4. Progressive aneurysmal dilatation

Predisposing Factors

• Cystic medial degeneration: Degradation of elastic fibres and smooth muscle in aortic media (seen in Marfan, Ehlers-Danlos, Loeys-Dietz syndromes)
• Hypertension: Chronic elevated wall stress (Laplace's law: Wall tension = Pressure × Radius / (2 × Wall thickness))
• Inflammatory aortitis: Giant cell arteritis, Takayasu arteritis, syphilitic aortitis
• Iatrogenic: Cardiac surgery, catheterisation, IABP insertion
• Trauma: Deceleration injury causing intimal tear

Why It Matters Clinically

• dP/dt (shear stress): Rate of change of pressure during systole determines propagation—hence beta-blockade to reduce HR and contractility is first-line
• Malperfusion: False lumen can compress or dissect into branch vessels (coronaries → MI; carotids → stroke; visceral → mesenteric ischaemia; renal → AKI; iliacs → limb ischaemia)
• Aortic regurgitation: Retrograde dissection disrupts aortic valve annulus or cusp support → acute severe AR → cardiogenic shock
• Tamponade: Rupture into pericardium → obstructive shock

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Clinical Approach

Recognition

High-risk triggers:

• Pain: Sudden-onset, severe, "tearing/ripping", maximal at onset (vs crescendo in ACS)
• Location: Anterior chest pain (Type A), interscapular back pain (Type B)
• Risk factors: Known hypertension, connective tissue disorder, bicuspid aortic valve, cocaine/amphetamine use
• Associated features: Syncope, stroke symptoms, pulse deficit, new AR murmur

Initial Assessment

Primary Survey

• A: Patent, protect if GCS below 8 (esp. if stroke from carotid dissection extension)
• B: RR, SpO₂, asymmetric breath sounds (haemothorax if rupture into pleura), pulmonary oedema (if acute AR)
• C: Pulse deficit (compare radial pulses, palpate femorals), BP differential (greater than 20 mmHg between arms in 30-40%), JVP elevated (tamponade), muffled heart sounds (tamponade), new diastolic murmur (AR)
• D: GCS, focal neurology (stroke from carotid/vertebral involvement, spinal cord ischaemia if artery of Adamkiewicz compromised)
• E: Abdominal tenderness (mesenteric ischaemia), cool/pulseless limbs (iliac dissection)

ECG changes:

• Usually non-specific ST/T changes
• If coronary ostia involved: STEMI pattern (RCA more common) [12]
• Always obtain 12-lead ECG to assess for concurrent ACS vs coronary malperfusion

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Distress level: Extreme distress despite opioids
• Marfanoid features: Tall, arm span > height, pectus deformity, arachnodactyly, lens dislocation
• Haemodynamic state: Hypertensive (70-80% of Type B), hypotensive or shocked (tamponade, rupture, severe AR)

Specific Findings

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Investigations

Immediate (Resus Bay)

Standard ED Workup

Advanced/Specialist

ADD-RS (Aortic Dissection Detection Risk Score)

Purpose: Identify low-risk patients in whom dissection can be ruled out (used with D-dimer)

Interpretation:

• ADD-RS = 0 AND D-dimer below 500 ng/mL: Negative predictive value 99.7% [21]
• ADD-RS ≥1 OR D-dimer ≥500 ng/mL: Proceed to CT aorta (cannot rule out)

Point-of-Care Ultrasound

TTE (Transthoracic Echo):

• Pericardial effusion: Suggests Type A with pericardial rupture (tamponade)
• Aortic regurgitation: Colour Doppler shows regurgitant jet
• Dilated aortic root: greater than 4 cm suggests aneurysm or dissection
• Intimal flap: May be visible in proximal ascending aorta or arch (sensitivity 60-80%) [13]

Limitations: Cannot reliably exclude dissection; cannot assess descending aorta; operator-dependent

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Management

Immediate Management (First 10 minutes)

1. Resuscitation position: Head-up 30° if possible to reduce cerebral oedema
2. High-flow oxygen if SpO₂ below 94% (target 94-98%)
3. IV access: Two large-bore cannulae (14-16G)
4. Monitoring: Continuous ECG, SpO₂, NIBP q5min (right arm), urine output
5. Analgesia: Fentanyl 50-100 mcg IV or morphine 5-10 mg IV (reduces sympathetic surge)
6. Beta-blockade: Esmolol 500 mcg/kg IV over 1 min, then 50-200 mcg/kg/min infusion (or metoprolol 5 mg IV q5min to max 15 mg) — TARGET HR below 60 bpm
7. Blood pressure control: If SBP greater than 120 mmHg despite beta-blocker, add GTN infusion 10-200 mcg/min or sodium nitroprusside 0.3-10 mcg/kg/min — TARGET SBP 100-120 mmHg
8. Urgent CT aorta if haemodynamically stable
9. Activate cardiothoracic surgery if Type A suspected
10. Nil by mouth (NBM) in case of emergency surgery

CRITICAL: Always beta-block (or rate-control with diltiazem) BEFORE vasodilator. Vasodilator alone causes reflex tachycardia → increased dP/dt → dissection propagation.

Resuscitation (if applicable)

Airway

• Intubation indications: GCS below 8, loss of airway reflexes, respiratory failure, severe pulmonary oedema (acute AR)
• Caution: Intubation causes sympathetic surge → hypertensive crisis → dissection propagation. Pre-treat with beta-blocker and/or opioid. Avoid ketamine (increases BP/HR).
• Agent choice: Fentanyl 2-3 mcg/kg + propofol 1-2 mg/kg (blunts response). Rocuronium 1 mg/kg for paralysis.

Breathing

• Targets: SpO₂ 94-98%, avoid hyperoxia (no benefit, potential harm)
• If intubated: Lung-protective ventilation (Vt 6-8 mL/kg IBW, PEEP 5-8 cmH₂O), avoid excessive PEEP (reduces venous return, may worsen tamponade)

Circulation

• Haemodynamic targets: SBP 100-120 mmHg, HR below 60 bpm, MAP 60-75 mmHg
• Tamponade: If suspected (Beck's triad: hypotension, elevated JVP, muffled heart sounds + pulsus paradoxus), urgent pericardiocentesis (echo-guided if time permits). This is a bridge to surgery, NOT definitive treatment.
• Hypotension management:
  • "If tamponade: pericardiocentesis + surgery"
  • "If rupture/exsanguination: permissive hypotension (SBP ~90 mmHg), activate massive transfusion protocol, emergency surgery"
  • "If cardiogenic shock (acute severe AR): inotropes (dobutamine 2.5-20 mcg/kg/min), avoid excessive afterload reduction, urgent surgery"
• Avoid excessive fluid resuscitation: Increases BP/shear stress → propagation/rupture

Disability

• Stroke management: If carotid dissection extension, maintain MAP 80-100 mmHg (cerebral perfusion), urgent neurology consult
• Spinal cord ischaemia: Maintain MAP greater than 80 mmHg to optimise spinal cord perfusion, urgent surgery (Type A) or TEVAR (Type B)

Medications

Beta-Blockers (FIRST-LINE)

Contraindications: Severe bradycardia (HR below 50), high-grade AV block, decompensated heart failure (pulmonary oedema), severe asthma/COPD

Alternative if beta-blocker contraindicated: Diltiazem 0.25 mg/kg IV over 2 min (usually 15-25 mg), then 5-15 mg/h infusion

Vasodilators (SECOND-LINE—only after beta-blockade)

Analgesia

Avoid NSAIDs: May worsen platelet function (pre-operative concern)

Paediatric Dosing

Definitive Care

Type A Dissection (Stanford Type A, DeBakey I/II)

URGENT CARDIOTHORACIC SURGERY (within 6 hours if possible) [22]

• Procedure: Replacement of ascending aorta ± aortic valve ± aortic arch (depending on extent)
• Goals: Resect intimal tear, obliterate false lumen, restore true lumen flow, repair/replace aortic valve if AR
• Pre-operative optimisation: Maintain SBP 100-120 mmHg, HR below 60 bpm, adequate analgesia
• Transfer: If not at cardiothoracic centre, arrange urgent retrieval with medical escort maintaining BP/HR control

Type B Dissection (Stanford Type B, DeBakey III)

MEDICAL MANAGEMENT (initial approach) [23]

• Goals: Control BP/HR (as above), monitor for complications
• Duration: ICU/HDU admission for 48-72h
• Follow-up imaging: CT at discharge, 3 months, 6 months, then annually

Indications for intervention (TEVAR or open surgery):

• Complicated Type B:
  • Rupture or impending rupture (periaortic haematoma)
  • Malperfusion syndrome (visceral, renal, limb)
  • Refractory hypertension despite maximal medical therapy
  • Severe pain despite analgesia
  • Rapid aneurysmal expansion (greater than 1 cm in 6 months)

TEVAR (Thoracic Endovascular Aortic Repair): Stent-graft deployed via femoral access to cover primary entry tear, promoting false lumen thrombosis

Intramural Haematoma (IMH) & Penetrating Atherosclerotic Ulcer (PAU)

• Type A IMH: Treat as Type A dissection (surgery)
• Type B IMH: Medical management initially; 30-40% progress to classic dissection or rupture [24]
• PAU: Usually descending aorta; medical management unless rupture/expansion

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Disposition

Admission Criteria (ALL patients with confirmed dissection)

• Type A: Urgent cardiothoracic surgery (transfer if not at tertiary centre)
• Type B uncomplicated: ICU/HDU admission for BP/HR control, serial monitoring
• Type B complicated: ICU admission, interventional radiology or cardiothoracic surgery consult

ICU/HDU Criteria

• All Type A dissections (pre- and post-operative)
• All Type B dissections (first 48-72h for BP/HR control)
• Malperfusion syndromes: Require intensive monitoring, may need urgent intervention
• Haemodynamic instability: Hypotension, tamponade, severe AR
• Neurological compromise: Stroke, spinal cord ischaemia

Discharge Criteria

No patient with acute dissection is discharged from ED.

If diagnosis excluded (CT aorta negative):

• Identify alternative cause of symptoms (ACS, PE, MSK)
• Ensure safe discharge diagnosis and follow-up
• Red flags: "Return if sudden severe tearing chest/back pain, syncope, limb weakness"

Follow-up (Post-Discharge after Surgical/Medical Management)

• Cardiothoracic surgery clinic (Type A post-op): 2-4 weeks
• Vascular surgery or cardiology (Type B): 2 weeks
• Serial imaging: CT aorta at 3 months, 6 months, 12 months, then annually for life
• Lifelong beta-blocker therapy: Target SBP below 120 mmHg, HR below 60 bpm [25]
• Genetic counselling: If connective tissue disorder suspected (Marfan, Ehlers-Danlos, Loeys-Dietz)

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Classification

Stanford Classification (MOST COMMONLY USED)

Key point: Even if the primary tear is in the descending aorta, if dissection propagates retrograde into the ascending aorta, it is Type A.

DeBakey Classification (ANATOMICALLY DETAILED)

Acute Aortic Syndrome (Broader Category)

Acute aortic syndrome encompasses:

1. Classic aortic dissection (intimal tear + false lumen)
2. Intramural haematoma (IMH): Haemorrhage within aortic media without intimal tear (10-20% of AAS) [26]
3. Penetrating atherosclerotic ulcer (PAU): Atherosclerotic plaque ulcerates through intima into media (5-10% of AAS) [27]
4. Traumatic aortic injury: Blunt deceleration injury (usually at aortic isthmus)

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Complications

Acute Complications (Emergency Department)

Malperfusion Syndromes

Definition: Inadequate end-organ perfusion due to branch vessel involvement (compression by false lumen, dissection flap extension, thrombosis)

Key point: Any malperfusion increases operative mortality 2-4 fold. Early recognition and expedited surgery (or percutaneous intervention for Type B) is critical [36].

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Special Populations

Paediatric Considerations

• Rare: below 5% of all dissections occur in patients below 40 years
• Causes: Connective tissue disorders (Marfan, Loeys-Dietz, Turner syndrome), bicuspid aortic valve, coarctation of aorta, iatrogenic (cardiac surgery, catheterisation)
• Presentation: May be atypical; high index of suspicion needed in patients with predisposing conditions
• Management: Same principles (beta-blockade, BP control), paediatric cardiothoracic surgery centre

Pregnancy

• Incidence: 40% of dissections in women below 40 occur during pregnancy (especially third trimester or peripartum) [41]
• Risk factors: Marfan syndrome (risk up to 10% per pregnancy), pre-eclampsia, bicuspid aortic valve
• Management:
  • "Haemodynamics: Target SBP 100-120 mmHg, HR below 70 bpm"
  • "Beta-blocker: Labetalol preferred (combined alpha/beta-blocker; safe in pregnancy)"
  • "Type A: Urgent surgery regardless of gestational age. Caesarean section if viable fetus (≥24-28 weeks)"
  • "Type B: Medical management; delivery timing depends on gestational age and maternal stability"
• Avoid: ACE inhibitors, ARBs (teratogenic); sodium nitroprusside (fetal cyanide toxicity risk)

Elderly (greater than 75 years)

• Increased incidence: Age-related aortic degeneration, atherosclerosis
• Higher operative mortality: 25-35% vs 15-20% in younger patients [42]
• Atypical presentations: May present with confusion, syncope, "collapse" rather than pain
• Comorbidities: Balance surgical risk vs certain death without surgery; shared decision-making critical

Connective Tissue Disorders

• Marfan syndrome: 40% of Type A dissections in patients below 40 years; lifetime risk 40% [43]
• Ehlers-Danlos (vascular type, type IV): Risk of rupture often exceeds dissection; extremely fragile tissues complicate surgery
• Loeys-Dietz syndrome: Similar to Marfan; aggressive aortic root dilatation and dissection at younger age
• Turner syndrome: Associated with coarctation, bicuspid valve, aortic dilatation

Screening: First-degree relatives of patients with dissection and connective tissue disorder should undergo echocardiography and genetic counselling [44]

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori considerations:

• Cardiovascular disease burden: Aboriginal and Torres Strait Islander Australians have 2-3 times higher rates of hypertension, coronary disease, and stroke compared to non-Indigenous Australians [10]—key risk factors for aortic dissection
• Delayed presentation: Barriers to healthcare access (geographic isolation, socioeconomic factors, cultural factors) may result in delayed diagnosis with higher mortality
• Cultural safety: Involve Aboriginal Liaison Officers or Māori health workers early; family/whānau involvement in decision-making (especially around high-risk surgery, end-of-life planning)
• Communication: Use professional interpreters if language barrier (not family members for medical discussions). Explain procedures clearly; avoid medical jargon.
• Remote/rural health: Many Indigenous communities are remote; RFDS retrieval critical. Early discussion with retrieval coordination centre.

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Pitfalls & Pearls

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Imaging Interpretation

CT Aorta Findings

Definitive Signs (Diagnostic)

Secondary Signs (Supportive)

True Lumen vs False Lumen Differentiation

Why it matters: True lumen perfuses branch vessels; false lumen may thrombose or rupture

TOE (Transoesophageal Echocardiography) Findings

Indications: Haemodynamically unstable patient (cannot go to CT), intra-operative assessment (pre-cardiothoracic surgery)

Sensitivity/Specificity: 98%/97% for ascending aorta and arch [18]

Key views:

• Mid-oesophageal aortic valve long-axis: Assess aortic root, proximal ascending aorta, AR
• Mid-oesophageal aortic valve short-axis: Circumferential view of aortic valve, identify coronary ostia
• Descending aortic long-axis and short-axis: Assess descending thoracic aorta (best visualised structure on TOE)
• Upper oesophageal aortic arch: Limited by trachea interposition (blind spot)

Findings:

• Intimal flap: Mobile, thin (1-3 mm), oscillates with cardiac cycle
• True vs false lumen: Colour Doppler shows flow direction (true lumen: systolic flow towards transducer; false lumen: systolic flow away)
• Aortic regurgitation: Colour Doppler regurgitant jet, jet width/LVOT ratio greater than 65% = severe AR
• Pericardial effusion: Anechoic space around heart; RV diastolic collapse = tamponade
• LV function: Global hypokinesis (cardiogenic shock from severe AR or coronary malperfusion)

Limitations:

• Blind spot: Distal ascending aorta/proximal arch (obscured by trachea with air artifact)
• Intramural haematoma: May be missed (no flap, only wall thickening)
• Operator-dependent: Requires skilled echocardiographer
• Semi-invasive: Requires sedation, risk of oesophageal perforation (rare)

CXR Findings (Low Sensitivity—Cannot Exclude)

Widened mediastinum (greater than 8 cm at level of T4):

• Seen in 60-80% of dissections
• Measured from right paratracheal stripe to left paraspinal line
• May be normal in 12-20% of cases—cannot rely on CXR to exclude dissection

Other findings (less specific):

• Abnormal aortic contour (loss of aortic knob definition)
• Pleural effusion (left > right): haemothorax from rupture
• Apical capping (mediastinal haematoma tracking superiorly)
• Deviation of trachea to right (by enlarged aorta)
• Depression of left main bronchus
• Displacement of nasogastric tube to right (by enlarged aorta)

Key point: Normal CXR does NOT exclude aortic dissection. If clinical suspicion is moderate-high, proceed to CT aorta regardless of CXR findings.

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Risk Stratification and Prognostication

IRAD (International Registry of Acute Aortic Dissection) Risk Factors

High-risk features predicting mortality [3,6]:

Protective factors (better outcomes):

• Younger age (below 50 years): 10-15% mortality
• No complications: Uncomplicated Type A has 15-20% mortality vs 30-50% with complications
• Early surgery (below 6h from symptom onset): Each hour delay increases mortality 1-2%

Penn Classification (Malperfusion-Based)

Purpose: Guide surgical strategy based on malperfusion pattern

Key concept: Class Ab (localised malperfusion) often resolves with aortic repair alone (restores true lumen flow). Class Ac (generalised) may require additional intervention (fenestration, stenting, bypass).

German Registry Acute Aortic Dissection Type A (GERAADA) Score

Purpose: Pre-operative risk stratification for Type A dissection

Variables (each 1 point):

• Age greater than 70 years
• Female sex
• Previous cardiac surgery
• Preoperative malperfusion
• Cardiac tamponade
• Cardiogenic shock (SBP below 90 mmHg)
• Resuscitation before surgery

Score interpretation:

• 0-1 points: Low risk (mortality 10-15%)
• 2-3 points: Moderate risk (mortality 20-30%)
• ≥4 points: High risk (mortality greater than 40%)

Use: Informs family discussions ("Your father has 4 risk factors; his chance of survival is around 50-60%")

Type B Dissection Risk Stratification

Uncomplicated Type B (good prognosis with medical management):

• No rupture, malperfusion, refractory pain, or uncontrolled hypertension
• 30-day mortality: 5-10%
• Management: Medical (beta-blocker + vasodilator), ICU 48-72h, serial imaging

Complicated Type B (requires intervention):

• Rupture, malperfusion, refractory pain/hypertension, rapid expansion
• 30-day mortality: 20-30% (with TEVAR/surgery); 50-70% (without)
• Management: TEVAR (preferred) or open surgery

Chronic Type B (greater than 14 days):

• False lumen thrombosis: Good prognosis (low risk of complications)
• False lumen patent: Higher risk of aneurysmal degeneration (30-40% over 5 years)
• Surveillance: CT at 3, 6, 12 months, then annually; TEVAR if diameter greater than 5.5 cm or growth greater than 1 cm/year

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Differential Diagnosis

The "Big 5" Causes of Sudden Severe Chest Pain

Mimics of Aortic Dissection

When to Suspect Aortic Dissection (High Pretest Probability)

Use ADD-RS (Aortic Dissection Detection Risk Score) ≥1:

• Predisposing condition: Marfan, Ehlers-Danlos, Loeys-Dietz, bicuspid aortic valve, family history of aortic disease, previous aortic valve surgery, known thoracic aortic aneurysm
• High-risk pain features: Sudden onset, severe intensity (worst pain ever), tearing/ripping/sharp quality
• High-risk exam features: Pulse deficit, BP differential greater than 20 mmHg, focal neurological deficit + pain, new AR murmur, hypotension/shock

Clinical gestalt: If you are thinking "Could this be dissection?", it probably warrants CT aorta. Missed dissection has catastrophic outcomes—low threshold for imaging.

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Viva Practice

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OSCE Scenarios

Station 1: Acute Aortic Dissection Resuscitation

Format: Resuscitation Time: 11 minutes Setting: Emergency Department resuscitation bay

Candidate Instructions:

You are the emergency registrar. A 62-year-old man has presented with sudden-onset severe chest and back pain. He is in extremis. You have 11 minutes to assess and manage this patient. A nurse and senior registrar are available to assist. The examiner will provide clinical information as you request it.

Examiner Instructions: Scenario: The patient has a Stanford Type A aortic dissection. Initial vital signs: HR 115, BP 185/100 (right arm), RR 24, SpO₂ 96% on air, GCS 15. The patient is in severe distress. As the candidate progresses, provide information based on their actions:

• If they examine pulses: "Right radial pulse present, left radial pulse weak. Both femoral pulses present."
• If they auscultate: "You hear a soft early diastolic murmur at the left sternal edge."
• If they request bedside echo: "There is a dilated aortic root, a small pericardial effusion, and trace aortic regurgitation."
• If they order CT: "CT confirms Type A aortic dissection from aortic root to descending aorta, with a small pericardial effusion."
• If they give beta-blocker: HR decreases to 85, BP 160/90.
• If they give vasodilator WITHOUT beta-blocker first: HR increases to 130, BP 170/95 (worse).
• If they activate cardiothoracic surgery: "The CT surgeon will accept the patient for urgent transfer to theatre."

Actor/Patient Brief: You are a 62-year-old man with sudden severe chest pain that started while lifting a heavy box 2 hours ago. The pain is in the front of your chest and between your shoulder blades. It was worst at the very beginning (10/10), now 8/10 despite paracetamol. You describe it as "sharp, tearing". You have a history of high blood pressure (on amlodipine). You are very distressed and frightened. You can answer questions but are in obvious pain.

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Systematic approach, recognises dissection, beta-blocks before vasodilator, activates cardiothoracic surgery
• Key discriminators:
  • Giving vasodilator BEFORE beta-blocker (major error—fail station)
  • Failing to activate cardiothoracic surgery (fail station)
  • Missing pulse examination or AR murmur (loses marks but may still pass)

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Station 2: Breaking Bad News—Type A Dissection Poor Prognosis

Format: Communication Time: 11 minutes Setting: Relatives' room

Candidate Instructions:

You are the emergency consultant. You have diagnosed a 68-year-old man with Type A aortic dissection. He has been transferred to theatre for emergency surgery, but the cardiothoracic surgeon has advised that his chance of survival is only 30-40% due to extensive dissection and cardiac tamponade. The patient's wife and daughter are waiting in the relatives' room. Please explain the diagnosis, treatment, and prognosis.

Examiner Instructions: Observe the candidate's communication skills. The wife and daughter are distressed but want to understand what is happening. They ask:

• "What is an aortic dissection?"
• "Will he survive the surgery?"
• "What happens if he doesn't survive?"
• "Should we call other family members?"

Assess: introduction, explanation in plain language, empathy, responding to questions, realistic expectations, offering support.

Actor/Patient Brief: You are the patient's wife (or daughter). You are very worried. The patient is your husband of 40 years (or your father). He has always been healthy apart from high blood pressure. This is a huge shock. You are tearful but composed. You want honest information. You ask: "Is he going to die?" and "What are his chances?"

Marking Criteria:

Expected Standard:

• Pass (≥6/11): Clear explanation, realistic prognosis, empathic approach, offers support
• Key discriminators:
  • Giving false hope ("He'll be fine") or excessive pessimism ("There's no hope") → fail
  • Explaining in medical jargon without checking understanding → loses marks
  • Showing empathy and offering ongoing support → key to passing

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Station 3: Transfer Coordination for Type A Dissection

Format: Communication / Clinical Judgement Time: 11 minutes Setting: ED resus bay (simulated phone call)

Candidate Instructions:

You are the emergency registrar at a metropolitan hospital WITHOUT cardiothoracic surgery. You have diagnosed a 55-year-old woman with Type A aortic dissection on CT. She is currently stable (BP 115/70, HR 68 on esmolol and GTN infusions). You need to call the on-call cardiothoracic surgeon at the tertiary centre (10 km away) to arrange urgent transfer. The examiner will play the role of the CT surgeon. You have 11 minutes to make the call and arrange transfer.

Examiner Instructions: You are the on-call cardiothoracic surgery registrar. You will accept the patient but need appropriate information to prepare. Ask:

• "What type of dissection? What's the extent?"
• "Any complications—tamponade, AR, malperfusion?"
• "What are the current vital signs and what infusions are running?"
• "When can you send the patient? Do you need retrieval or can you send via ambulance?" If the candidate provides clear, structured information, you say: "That's great, I'll accept the patient for urgent surgery. Theatre 5 will be ready in 30 minutes. Send her via ambulance with the infusions running and a medical escort. I'll see her in theatre."

If the candidate is disorganised or missing key info, prompt: "I need to know [missing information] before I can accept."

Actor/Patient Brief: N/A (phone call scenario)

Marking Criteria:

Expected Standard:

• Pass (≥6/11): ISBAR structure, key clinical info (type, extent, complications, vital signs, infusions), clear transfer plan
• Key discriminators:
  • Using ISBAR structure → passes; disorganised rambling → fails
  • Mentioning all infusions and doses → key to safe transfer
  • Confirming plan at the end → professionalism mark

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SAQ Practice

Question 1: Classification and Immediate Management (8 marks)

Stem: A 60-year-old man presents with sudden-onset severe interscapular pain. CT aorta shows a dissection originating in the descending thoracic aorta distal to the left subclavian artery and extending to the abdominal aorta. There is no pericardial effusion. BP 170/95, HR 102.

Question: a) What is the Stanford classification of this dissection? (1 mark) b) List FOUR immediate management priorities. (4 marks) c) What are the blood pressure and heart rate targets? (2 marks) d) When would this patient require surgical or endovascular intervention? Give THREE indications. (3 marks, maximum 3)

Model Answer: a) Stanford Type B (1 mark)

• (Dissection originates distal to left subclavian artery, does not involve ascending aorta)

b) Immediate management priorities (4 marks, 1 mark each, maximum 4):

• Analgesia: Fentanyl 50-100 mcg IV or morphine 5-10 mg IV (reduces sympathetic response)
• Beta-blockade: Esmolol 500 mcg/kg loading + 50-200 mcg/kg/min infusion OR metoprolol 5 mg IV q5min (reduce heart rate and dP/dt)
• Blood pressure control: GTN 10-200 mcg/min IV infusion (AFTER beta-blocker) to reduce shear stress
• Monitoring: Continuous ECG, NIBP q5min, SpO₂, urine output (IDC), serial neuro observations (for malperfusion)
• (Accept: IV access, bloods (UEC, lactate, FBC, coag, G&H), ICU/HDU admission, nil by mouth)

c) Targets (2 marks):

• SBP 100-120 mmHg (1 mark)
• HR below 60 bpm (1 mark)

d) Indications for intervention (complicated Type B dissection) (3 marks, 1 mark each, maximum 3):

• Rupture or impending rupture (periaortic haematoma, expanding aneurysm)
• Malperfusion syndrome (visceral, renal, limb ischaemia)
• Refractory hypertension despite maximal medical therapy
• Refractory pain despite adequate analgesia
• Rapid aneurysmal expansion (greater than 1 cm in 6 months)
• (Accept any 3 of the above)

Examiner Notes:

• Accept: "Type B" or "DeBakey III" for (a)
• For (b), must include both beta-blocker AND vasodilator; analgesia alone insufficient (must have 2/3 of these for full marks)
• For (c), accept SBP 100-120 or "SBP below 120"; accept HR below 60 or "HR 50-60"
• Do not accept: "Type A" (incorrect classification—fail entire question if this is the answer), "immediate surgery" for Type B (incorrect unless complications present)

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Question 2: D-Dimer and ADD-RS Score (6 marks)

Stem: A 45-year-old woman presents with sudden-onset central chest pain radiating to the back. She has no past medical history. On examination: HR 88, BP 135/80 (equal in both arms), all pulses present and equal, no murmurs. ECG shows non-specific T-wave changes. You are considering aortic dissection.

Question: a) Calculate her ADD-RS (Aortic Dissection Detection Risk Score). Show your working. (3 marks) b) Her D-dimer is 320 ng/mL. Can you rule out aortic dissection based on ADD-RS and D-dimer? Explain. (2 marks) c) What is the sensitivity of D-dimer for intramural haematoma compared to classic dissection? (1 mark)

Model Answer: a) ADD-RS = 1 (3 marks: 1 mark for correct total, 1 mark for correctly identifying high-risk pain, 1 mark for correctly identifying no other features)

• Predisposing condition: 0 (no Marfan, family history, bicuspid valve, prior aortic disease mentioned)
• High-risk pain features: 1 (sudden-onset, severe, radiating to back—tearing quality not specified but sudden + severe + back pain = 1 point)
• High-risk exam features: 0 (BP equal both arms, all pulses equal, no focal neuro deficit, no AR murmur, no hypotension)
• Total: 1

b) No, cannot rule out (2 marks: 1 mark for "no", 1 mark for explanation)

• To rule out aortic dissection, need ADD-RS = 0 AND D-dimer below 500 ng/mL
• This patient has ADD-RS = 1 (high-risk pain), so cannot rule out even though D-dimer is below 500
• Must proceed to CT aorta

c) Sensitivity for IMH: 67-87% (1 mark)

• (Compared to 97% sensitivity for classic dissection)

Examiner Notes:

• Accept ADD-RS 0-1 depending on interpretation of "high-risk pain" (if candidate argues pain is not "ripping/tearing" and therefore scores 0, accept this if they justify it—but then answer to (b) changes to "yes, can rule out" if ADD-RS=0 and D-dimer below 500)
• Most likely intended answer: ADD-RS = 1 (pain is sudden + severe + back = high-risk), so cannot rule out
• For (c), accept range "67-87%" or "approximately 70-80%" or "lower than 97%"
• Do not accept: "D-dimer negative rules out dissection" (WRONG—this is a key misconception)

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Question 3: Malperfusion Syndromes (8 marks)

Stem: A 58-year-old man with Type A aortic dissection is awaiting urgent surgery. He suddenly develops right arm weakness and dysphasia.

Question: a) What complication has occurred? (1 mark) b) What is the pathophysiological mechanism? (2 marks) c) List FOUR other types of malperfusion syndrome that can occur in aortic dissection. (4 marks) d) How does the presence of malperfusion affect operative mortality? (1 mark)

Model Answer: a) Cerebral malperfusion / Stroke (1 mark)

• (Right arm weakness + dysphasia suggests left hemisphere stroke—carotid involvement)

b) Mechanism (2 marks):

• Dissection flap extension into the carotid artery OR compression of carotid artery by false lumen (1 mark)
• Causes reduced blood flow to the brain → ischaemic stroke (1 mark)
• (Accept: Thromboembolism from false lumen)

c) Other malperfusion syndromes (4 marks, 1 mark each, maximum 4):

• Cardiac (coronary ostia involvement → myocardial infarction)
• Spinal cord (artery of Adamkiewicz occlusion → paraplegia)
• Visceral (SMA/coeliac involvement → mesenteric ischaemia, bowel necrosis)
• Renal (renal artery involvement → acute kidney injury, oliguria/anuria)
• Limb (iliac/femoral involvement → acute limb ischaemia, cool pulseless leg)

d) Impact on mortality (1 mark):

• Increases operative mortality 2-4 fold (from ~15% to 30-50%)
• (Accept: "significantly increases mortality" or "doubles/triples mortality")

Examiner Notes:

• For (b), must mention BOTH the mechanism (dissection into vessel or compression) AND the outcome (reduced flow → ischaemia) for full 2 marks
• For (c), need 4 distinct organ systems; do not accept "cardiac malperfusion" and "myocardial infarction" as separate (same thing)
• For (d), accept any phrasing indicating malperfusion worsens outcomes (exact numbers not required but help)

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Question 4: Pharmacological Management (8 marks)

Stem: You are managing a patient with confirmed Type A aortic dissection. Current BP 180/100, HR 110.

Question: a) Why must beta-blocker be given BEFORE vasodilator? (2 marks) b) Name TWO intravenous beta-blockers suitable for this scenario and give their doses. (4 marks) c) If beta-blockers are contraindicated (severe asthma), what alternative can be used for heart rate control? Give the drug and dose. (2 marks)

Model Answer: a) Rationale for beta-blocker first (2 marks):

• Vasodilator alone causes reflex tachycardia (baroreceptor response to BP drop) (1 mark)
• Increased heart rate increases dP/dt (shear stress) → propagates dissection → worsens outcome (1 mark)
• Beta-blocker given first prevents this reflex tachycardia and also reduces dP/dt (rate of pressure change during systole), which is the primary driver of dissection propagation

b) Beta-blockers (4 marks: 2 marks per drug = 1 for name, 1 for dose):

• Esmolol: Loading 500 mcg/kg IV over 1 min, then infusion 50-200 mcg/kg/min (2 marks)
• Metoprolol: 5 mg IV q5min, maximum 15 mg total (2 marks)
• (Also accept: Labetalol 10-20 mg IV bolus, then 0.5-2 mg/min infusion; Propranolol 0.5-1 mg IV q5min, max 0.15 mg/kg)

c) Alternative if beta-blocker contraindicated (2 marks):

• Diltiazem (calcium channel blocker) (1 mark)
• Dose: 0.25 mg/kg IV over 2 min (usually 15-25 mg), then 5-15 mg/h infusion (1 mark)

Examiner Notes:

• For (a), must explain reflex tachycardia AND propagation risk for full 2 marks; just saying "reflex tachycardia" without explaining consequence is 1 mark
• For (b), accept any TWO of the beta-blockers listed; must give BOTH drug name AND dose for each (1+1=2 marks per drug)
• For (c), accept diltiazem (most common alternative); also accept verapamil (but less commonly used in ED)
• Do not accept: "give vasodilator alone" (WRONG), "labetalol is not a beta-blocker" (WRONG—it is a combined alpha/beta-blocker)

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Australian Guidelines

ARC/ANZCOR

• Not directly applicable: Aortic dissection is not a primary focus of ARC/ANZCOR resuscitation guidelines
• Cardiac arrest: If patient with aortic dissection arrests, follow standard ALS algorithms, but prognosis is extremely poor (survival below 5%) [45]

Therapeutic Guidelines

• Cardiovascular Guidelines: Recommend beta-blockers (esmolol, labetalol, metoprolol) as first-line for BP/HR control in acute aortic syndromes
• Blood pressure targets: SBP 100-120 mmHg, HR below 60 bpm
• Type A dissection: Urgent cardiothoracic surgery referral
• Type B dissection: Initial medical management; TEVAR for complicated cases

Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS)

• National audit data: 30-day mortality for Type A dissection 11.2% (2001-2021) [9]
• Volume-outcome relationship: Higher-volume centres (greater than 10 cases/year) have lower mortality (9.8% vs 13.5% at low-volume centres) [9]
• Recommendation: Type A dissection patients should be transferred to high-volume cardiothoracic surgery centres when possible

State-Specific

• NSW: Cardiothoracic surgery available at Royal Prince Alfred, St Vincent's, Westmead, John Hunter (Newcastle), Liverpool
• VIC: Alfred, Austin, Monash, St Vincent's, Royal Melbourne
• QLD: Prince Charles, Royal Brisbane, Townsville
• SA: Flinders, Royal Adelaide
• WA: Fiona Stanley, Royal Perth
• TAS: Royal Hobart (limited; complex cases may transfer to mainland)

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Remote/Rural Considerations

Pre-Hospital

• High index of suspicion: "Sudden severe chest/back pain" in older patient with hypertension → consider dissection, not just ACS
• Avoid thrombolysis: Paramedics should NOT administer pre-hospital thrombolysis if dissection possible (check for back pain, pulse deficit, syncope)
• Analgesia: Fentanyl or methoxyflurane for pain control (reduces sympathetic surge)
• Avoid excessive IV fluids: Risk of increasing BP → propagation
• Notify receiving hospital: "Possible aortic dissection" so ED can prepare (CT aorta, cardiothoracic consult)

Resource-Limited Setting

Rural hospital without CT:

• Clinical diagnosis: High suspicion based on history (sudden tearing chest/back pain, risk factors) + exam (pulse deficit, BP differential, AR murmur)
• Bedside echo: May show dilated aortic root, pericardial effusion, AR (but sensitivity only 60-80% [13])
• Stabilise and transfer: Do NOT wait for CT if high suspicion—start beta-blocker + vasodilator, arrange urgent transfer to centre with CT and cardiothoracic surgery
• Use available agents: If esmolol unavailable, use metoprolol IV or oral; if GTN unavailable, use oral nifedipine (10 mg sublingually—though less ideal due to unpredictable absorption)

Rural hospital with CT but no cardiothoracic surgery:

• Confirm diagnosis: Urgent CT aorta (non-contrast + arterial phase)
• Medical stabilisation: Beta-blocker + vasodilator to target SBP 100-120, HR below 60
• Arrange transfer:
  • "Type A: Urgent retrieval via RFDS (if available) or road ambulance with medical escort (doctor or advanced care paramedic). Continue infusions during transfer."
  • "Type B: Discuss with tertiary centre; may be managed locally in ICU if uncomplicated (with remote support from vascular surgeon or intensivist via telemedicine), or transfer if complicated"

Retrieval

RFDS (Royal Flying Doctor Service):

• Indications: Type A dissection requiring transfer greater than 200 km, or Type B with complications
• Preparation:
  • Medical escort (retrieval doctor/nurse) with experience in critical care
  • Portable infusion pumps (esmolol, GTN, fentanyl)
  • Blood products if available (risk of rupture in transit)
  • Intubation kit (if patient deteriorates)
• Communication: Detailed handover to RFDS team (diagnosis, extent, complications, vital signs, infusions, anticipated complications)
• Flight time: Factor in weather, distance, landing site availability. Typical 400-500 km retrieval = 90-120 min flight time + 30 min loading/unloading.
• Destination: Nearest cardiothoracic surgery centre (may not be nearest hospital—bypass smaller centres without CT surgery)

Ground ambulance transfer:

• Use if: Distance below 100-200 km, RFDS unavailable, weather precludes flight
• Risks: Longer transit time (3-4 hours for 200 km by road vs 60 min by air), limited space for equipment, road vibrations (may worsen haemodynamics)
• Advantages: May be faster for short distances, weather-independent

Telemedicine

• Use case: Rural ED consultant discusses management with cardiothoracic surgeon or intensivist at tertiary centre
• Platforms: HealthDirect Video Call, Emergency Telehealth, state-based systems (NSW Virtual Rural Generalist Service, VIC NURSE-ON-CALL)
• Benefits: Real-time advice on BP/HR targets, medication doses, transfer timing
• Limitations: Cannot replace definitive CT or surgery; temporary support only

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References

Guidelines

1. Erbel R, Aboyans V, Boileau C, et al. 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. Eur Heart J. 2014;35(41):2873-2926. PMID: 25173340
2. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. Circulation. 2010;121(13):e266-369. PMID: 20233780

Key Epidemiology

3. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903. PMID: 10685714
4. Howard DP, Banerjee A, Fairhead JF, et al. Population-based study of incidence and outcome of acute aortic dissection and premorbid risk factor control: 10-year results from the Oxford Vascular Study. Circulation. 2013;127(20):2031-2037. PMID: 23599348
5. Olsson C, Thelin S, Ståhle E, et al. Thoracic aortic aneurysm and dissection: increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002. Circulation. 2006;114(24):2611-2618. PMID: 17145990

Mortality and Outcomes

6. Pape LA, Awais M, Woznicka EM, et al. Presentation, diagnosis, and outcomes of acute aortic dissection: 17-year trends from the International Registry of Acute Aortic Dissection. J Am Coll Cardiol. 2015;66(4):350-358. PMID: 26205591
7. Nienaber CA, Clough RE, Sakalihasan N, et al. Aortic dissection. Nat Rev Dis Primers. 2016;2:16071. PMID: 27711124

Australian/NZ Data

8. Lim ETA, Khanafer A, Baskaran D, et al. Acute aortic syndrome: nationwide study of epidemiology, management, and outcomes in Aotearoa New Zealand. BJS Open. 2023;7(4):zrad078. PMID: 37494189
9. Knox A, Yii M, Beltrame J, et al. Outcomes of type A aortic dissection in Australia. ANZ J Surg. 2025;95(6):1122-1128. PMID: 39907174
10. Australian Institute of Health and Welfare. Cardiovascular disease in Aboriginal and Torres Strait Islander people. Canberra: AIHW; 2023.
11. Royal Flying Doctor Service. Annual Report 2022-23. Sydney: RFDS; 2023.

Pathophysiology

12. Nienaber CA, von Kodolitsch Y, Petersen B, et al. Intramural hemorrhage of the thoracic aorta. Diagnostic and therapeutic implications. Circulation. 1995;92(6):1465-1472. PMID: 7664428
13. Evangelista A, Flachskampf FA, Erbel R, et al. Echocardiography in aortic diseases: EAE recommendations for clinical practice. Eur J Echocardiogr. 2010;11(8):645-658. PMID: 20823280

Clinical Features

14. von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinical prediction of acute aortic dissection. Arch Intern Med. 2000;160(19):2977-2982. PMID: 11041906
15. Shiga T, Wajima Z, Apfel CC, et al. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection: systematic review and meta-analysis. Arch Intern Med. 2006;166(13):1350-1356. PMID: 16831999

D-dimer and ADD-RS

16. Asha SE, Miers JW. A systematic review and meta-analysis of D-dimer as a rule-out test for suspected acute aortic dissection. Ann Emerg Med. 2015;66(4):368-378. PMID: 25805111
17. Goodacre S, Horspool K, Nelson-Piercy C, et al. Diagnostic accuracy of D-dimer for acute aortic syndromes: systematic review and meta-analysis. Ann Emerg Med. 2024;84(3):284-297. PMID: 38795020
18. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med. 1993;328(1):1-9. PMID: 8416265
19. Sommer T, Fehske W, Holzknecht N, et al. Aortic dissection: a comparative study of diagnosis with spiral CT, multiplanar transesophageal echocardiography, and MR imaging. Radiology. 1996;199(2):347-352. PMID: 8668776
20. Cigarroa JE, Isselbacher EM, DeSanctis RW, et al. Diagnostic imaging in the evaluation of suspected aortic dissection. Old standards and new directions. N Engl J Med. 1993;328(1):35-43. PMID: 8416268
21. Nazerian P, Mueller C, Soeiro AM, et al. Diagnostic accuracy of the aortic dissection detection risk score plus D-dimer for acute aortic syndromes: the ADvISED prospective multicenter study. Circulation. 2018;137(3):250-258. PMID: 29030346

Management

22. Czerny M, Schmidli J, Adler S, et al. Current options and recommendations for the treatment of thoracic aortic pathologies involving the aortic arch: an expert consensus document of the European Association for Cardio-Thoracic Surgery (EACTS) & the European Society for Vascular Surgery (ESVS). Eur J Cardiothorac Surg. 2019;55(1):133-162. PMID: 30312382
23. Lombardi JV, Hughes GC, Appoo JJ, et al. Society for Vascular Surgery (SVS) and Society of Thoracic Surgeons (STS) reporting standards for type B aortic dissections. J Vasc Surg. 2020;71(3):723-747. PMID: 31668497
24. Harris KM, Strauss CE, Eagle KA, et al. Correlates of delayed recognition and treatment of acute type A aortic dissection: the International Registry of Acute Aortic Dissection (IRAD). Circulation. 2011;124(18):1911-1918. PMID: 21969019
25. Liisberg M, Larsen KL, Diederichsen ACP, et al. Beta blockers as primary and secondary prevention for aortic dissections. J Am Heart Assoc. 2025;14(12):e040149. PMID: 40500875
26. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer: a clinical and radiological analysis. Circulation. 2002;106(3):342-348. PMID: 12119251
27. Vilacosta I, San Román JA, Ferreirós J, et al. Natural history and serial morphology of aortic intramural hematoma: a novel variant of aortic dissection. Am Heart J. 1997;134(3):495-507. PMID: 9327708

Complications

28. Isselbacher EM, Preventza O, Hamilton Black J 3rd, et al. 2022 ACC/AHA guideline for the diagnosis and management of aortic disease. J Am Coll Cardiol. 2022;80(24):e223-e393. PMID: 36334595
29. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients with valvular heart disease. Circulation. 2017;135(25):e1159-e1195. PMID: 28298458
30. Gaul C, Dietrich W, Friedrich I, et al. Neurological symptoms in type A aortic dissections. Stroke. 2007;38(2):292-297. PMID: 17204686

Malperfusion

31. Estrera AL, Garami Z, Miller CC, et al. Acute spinal cord ischemia in thoracic and thoracoabdominal aortic surgery: incidence, risk factors, and outcome. Ann Thorac Surg. 2001;72(2):425-432. PMID: 11515878
32. Cambria RP, Brewster DC, Gertler J, et al. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg. 1988;7(2):199-209. PMID: 3276930
33. Geirsson A, Szeto WY, Pochettino A, et al. Significance of malperfusion syndromes prior to contemporary surgical repair for acute type A dissection: outcomes and need for additional revascularizations. Eur J Cardiothorac Surg. 2007;32(2):255-262. PMID: 17576068
34. Fann JI, Sarris GE, Mitchell RS, et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg. 1990;212(6):705-713. PMID: 2256761
35. Hirst AE Jr, Johns VJ Jr, Kime SW Jr. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine (Baltimore). 1958;37(3):217-279. PMID: 13577293
36. Chandiramani A, Al-Tawil M, Elleithy A, et al. Organ-specific malperfusion in acute type A aortic dissection: epidemiological meta-analysis of incidence rates. BJS Open. 2025;9(1):zrae146. PMID: 39792052
37. Penn MS, Smedira N, Lytle B, et al. Does coronary angiography before emergency aortic surgery affect in-hospital mortality? J Am Coll Cardiol. 2000;35(4):889-894. PMID: 10732885
38. Tsagakis K, Dohle DS, Benedik J, et al. Visceral malperfusion in aortic dissection: still a lethal event? Eur J Cardiothorac Surg. 2016;49(5):1381-1387. PMID: 26272901
39. Deeb GM, Williams DM, Bolling SF, et al. Surgical delay for acute type A dissection with malperfusion. Ann Thorac Surg. 1997;64(6):1669-1675. PMID: 9436553
40. Williams DM, Lee DY, Hamilton BH, et al. The dissected aorta: percutaneous treatment of ischemic complications--principles and results. J Vasc Interv Radiol. 1997;8(4):605-625. PMID: 9232575

Special Populations

41. Immer FF, Bansi AG, Immer-Bansi AS, et al. Aortic dissection in pregnancy: analysis of risk factors and outcome. Ann Thorac Surg. 2003;76(1):309-314. PMID: 12842582
42. Piccardo A, Regesta T, Zannis K, et al. Outcomes after surgical treatment of type A aortic dissection in octogenarians: a multicenter study. Ann Thorac Surg. 2009;88(5):1433-1440. PMID: 19853089
43. Judge DP, Dietz HC. Marfan's syndrome. Lancet. 2005;366(9501):1965-1976. PMID: 16325700
44. Elefteriades JA, Farkas EA. Thoracic aortic aneurysm clinically pertinent controversies and uncertainties. J Am Coll Cardiol. 2010;55(9):841-857. PMID: 20185035
45. Kühn S, Fichtlscherer S, Nienaber CA, et al. Out-of-hospital cardiac arrest due to aortic dissection: a systematic review. Resuscitation. 2021;169:28-37. PMID: 34634407