Acute Aortic Syndrome (AAS) - MCh Cardiac Surgery Level

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1. DEFINITION AND SPECTRUM

• Grainger & Allison's Diagnostic Radiology, p. 2061

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2. THE THREE ENTITIES - ANATOMY AND PATHOPHYSIOLOGY

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2.1 Aortic Dissection

1. Primary intimal tear (caused by shear stresses on aortic wall) - most common. Tear is usually transverse/oblique, 1-5 cm long, with jagged edges, situated within 10 cm of the aortic valve in ascending dissections.
2. Intramural hemorrhage from vasa vasorum rupturing and weakening the intima at the tear site.

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2.2 Intramural Hematoma (IMH)

• No visible intimal flap delineating true and false lumens
• Hematoma is located circumferentially around the aortic lumen (not obliquely)
• No identifiable entry/exit tear on imaging

• Persist unchanged
• Resorb (aorta returns to normal appearance)
• Leave an aneurysm (risk of rupture)
• Transform into frank dissection (the most dangerous evolution)

• Fuster & Hurst's The Heart, p. 769

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2.3 Penetrating Aortic Ulcer (PAU)

• Local medial penetration
• Can mimic or result in aortic dissection
• Can cause pseudoaneurysm formation, IMH, or rupture

• Accounts for 2-7% of AAS
• Descending aorta in 90% of cases (below the left subclavian artery)
• Often asymptomatic - detected incidentally (87% in one Mayo Clinic series)
• Defined on contrast CT as a focal outpouching through intimal calcification in a region of diffuse atherosclerosis

• Sabiston Textbook of Surgery

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3. EPIDEMIOLOGY AND RISK FACTORS

• Braunwald's Heart Disease, Chapter 42

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4. CLASSIFICATION

4.1 Anatomical Classification

• Acute: <14 days (much higher mortality)
• Subacute: 14 days - 2 months
• Chronic: >2 months (in 20-40%, significant aneurysmal dilatation of the descending/thoracoabdominal aorta develops)

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5. CLINICAL PRESENTATION

5.1 Cardinal Symptoms

• Pain is the most common presenting symptom:
  • Abrupt onset, maximum intensity at outset (distinguishes from MI where pain builds)
  • "Tearing," "ripping," or "knife-like" quality
  • Anterior chest pain - suggests ascending aorta involvement (Type A)
  • Interscapular/back pain - suggests descending aorta (Type B)
  • Abdominal or migratory pain - dissection extending distally
• Silent dissection exists in a small proportion

5.2 Anatomical Complications and Their Presentation

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6. DIAGNOSTIC WORKUP

6.1 Risk Stratification - "High Suspicion" Features

1. Predisposing condition (Marfan, bicuspid AV, prior aortic surgery, hypertension)
2. Abrupt-onset severe pain
3. "Tearing" chest pain descriptor
4. Evidence of distal compromise - pulse deficit, neurologic symptoms, R-L arm BP differential

6.2 Chest X-Ray

• Widened mediastinum (>8 cm) - classic but non-specific
• Pleural effusion (left hemothorax - blood tracking into pleural space)
• A normal CXR does NOT exclude AAS - 12-15% of dissections have a normal CXR

6.3 Cross-Sectional Imaging - The Diagnostic Standard

• Available 24/7, rapid acquisition, full aortic visualization
• Sensitivity and specificity >95%
• Identifies: entry tear, flap extent, true/false lumen, branch vessel involvement, pericardial effusion
• Limitations: contrast load (renal impairment), radiation, no real-time assessment of AR or coronary involvement

• TTE: Limited sensitivity for dissection (poor windows for ascending aorta); if definite undulating intimal flap seen, specificity is high. A negative TTE does NOT exclude dissection.
• TEE: High sensitivity and specificity; particularly useful:
  • Intraoperatively to confirm dissection and assess AR before/after repair
  • Identifies fenestrated dissection flap, AR severity, pericardial effusion, wall motion abnormalities (RCA involvement)
  • Cannot image the distal ascending aorta ("blind spot" between left main bronchus and aorta)

• Dilated aortic lumen
• Linear, mobile echogenic intimal flap with motion different from aortic wall
• Differential color Doppler flow patterns in true vs false lumen (true lumen: pulsatile flow; false lumen: sluggish or absent flow)
• Pericardial effusion / tamponade
• Regional wall motion abnormalities (coronary involvement)

• Highest accuracy; ideal for chronic dissections and follow-up
• No radiation, no contrast required for basic sequences
• Limitations: time-consuming, limited access in emergencies, contraindicated with many pacemakers

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7. INITIAL MEDICAL MANAGEMENT (ALL AAS)

1. Eliminate pain - IV opioids (morphine 2-4 mg IV)
2. Reduce systolic BP - target SBP 100-120 mmHg
3. Reduce dP/dt (rate of pressure rise) - target HR <60 bpm

• IV beta-blocker: Labetalol (20 mg IV bolus, then 2 mg/min infusion) or esmolol (500 mcg/kg bolus, then 50-200 mcg/kg/min infusion) - reduces both HR and BP
• If beta-blocker insufficient: Add IV vasodilator (sodium nitroprusside 0.3-10 mcg/kg/min)
• Do NOT use vasodilators alone without beta-blockade - reflex tachycardia increases dP/dt and worsens dissection

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8. SURGICAL MANAGEMENT - TYPE A DISSECTION

8.1 Indications

8.2 Operative Strategy

• Femoral artery - traditional; risk of retrograde malperfusion if cannulating false lumen
• Right axillary/subclavian artery - preferred when femoral access is compromised or in Marfan syndrome; provides antegrade flow and safe cerebral perfusion
• Direct aortic cannulation - only when clearly in true lumen

• Venous cannulation via right atrium or bicaval
• Cooling to moderate hypothermia (24-27°C nasopharyngeal) before circulatory arrest
• Hypothermic Circulatory Arrest (HCA) is essential for open distal anastomosis without aortic cross-clamp

• Antegrade Cerebral Perfusion (ACP) via right axillary/direct carotid cannulation - 10 mL/kg/min to right carotid, maintain R cerebral O2 sat ≥60%
• Retrograde Cerebral Perfusion (RCP) via superior vena cava - simpler but less effective
• ACP is associated with improved neurological outcomes and allows longer safe arrest times

• Resect entire ascending aorta from sinotubular junction to innominate artery with a bevel at the lesser curve of the arch
• Inspect arch for complex intimal disruptions under direct vision
• Confirm brachiocephalic branches arise from true lumen
• Obliterate the false lumen: Two main techniques:
  • Teflon felt sandwich: Two strips of felt sandwiching the dissected aortic wall → anastomose Dacron graft to felt-reinforced aorta
  • Felt plug into false lumen: Author-preferred technique to avoid late pseudoaneurysm from glue (biological glues are avoided as they can be destructive and promote pseudoaneurysm)

• Aortic valve preservation (commissure resuspension) - when no root aneurysm (<5 cm) and valve is structurally sound
• Composite aortic root replacement (Bentall procedure) - when:
  • Root aneurysm >5 cm
  • Complex aortic valve pathology
  • Dissection extending to coronary ostia
  • Genetically triggered disease (Marfan, Loeys-Dietz)
• Valve-sparing root replacement (David / Yacoub procedure) - only in experienced centers with appropriate anatomy

• Routine arch replacement is not necessary for most Type A dissections (increases complexity and risk)
• Arch replacement is indicated when:
  • Complex intimal disruptions in the arch
  • Arch aneurysm >5 cm
  • Genetically triggered thoracic aortic disease

• For large intimal disruptions in the distal arch or proximal descending aorta
• Antegrade stent-graft deployment under direct vision through the open arch
• Stabilizes the distal aorta, reduces need for early reintervention, addresses distal malperfusion
• Bridges toward second-stage descending aorta treatment

• In cases with AI + coronary malperfusion: LV venting on bypass before cross-clamp
• Retrograde coronary sinus cardioplegia + direct antegrade coronary ostial cardioplegia

8.3 Surgical Results (IRAD Data)

• Coagulopathic bleeding (massive transfusion - use thromboelastography-guided protocol)
• Transient neurologic dysfunction / stroke
• Renal insufficiency
• Acute lung injury
• New malperfusion syndromes - persistent false lumen flow
• Refractory hypertension
• Multiorgan failure

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9. MANAGEMENT OF TYPE B DISSECTION

9.1 Uncomplicated Type B - Medical Management

• HR <60 bpm
• SBP 100-120 mmHg

9.2 Complicated Type B - Indications for Intervention

9.3 TEVAR for Type B - Technique

• Zone 3 to Zone 5 (caudal left subclavian to just proximal to celiac axis) is standard
• Zone 2 coverage may be needed if entry tear involves the left subclavian artery
• If Zone 2 coverage is planned non-emergently: left subclavian revascularization first (carotid-subclavian bypass or subclavian-carotid transposition) to reduce risk of vertebrobasilar stroke, left arm ischemia, and paraplegia

1. Iliofemoral access (open or percutaneous under US/fluoroscopy guidance)
2. Systemic heparin (ACT >250 sec)
3. J-wire advanced into ascending aorta
4. IVUS confirmation of true lumen access along entire wire length - critical step
5. IVUS delineates LSA origin, celiac axis, compressed true lumen, and branch vessel involvement
6. Exchange for stiff Lunderquist wire
7. Sequential stent-graft deployment with controlled BP lowering (SBP ~80 mmHg during deployment)
8. Post-deployment IVUS + fluoroscopy to confirm coverage and true lumen expansion

• Uncovered fenestrations
• Retrograde flow from abdominal aortic fenestrations
• Back-bleeding from branch vessels

9.4 Prognostic Factors Favoring Intervention in "Uncomplicated" Type B

9.5 Open Surgery for Type B

• Unsuitable anatomy for TEVAR (extensive branch vessel involvement, aortic tortuosity, inadequate landing zones)
• Genetically triggered aortic disease (Marfan - risk of late stent-graft failure)
• Failed TEVAR

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10. INTRAMURAL HEMATOMA - SPECIFIC MANAGEMENT

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11. PENETRATING AORTIC ULCER - SPECIFIC MANAGEMENT

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12. CHRONIC DISSECTION AND ANEURYSMAL DEVELOPMENT

• Late aneurysm formation occurs in up to 50% of patients with chronic Type B dissection
• Management requires exclusion of false lumen flow by closing all fenestrations between true and false lumens
• Complex (fenestrated or branched) endografts or surgical bypass of major aortic branches may be needed
• Surveillance: CT/MRI at 1, 3, 6, 12 months then annually for all AAS survivors
• Strict BP control (SBP <130 mmHg) is essential for all chronic dissection patients

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13. SPECIAL SITUATIONS AT MCh LEVEL

13.1 Coronary Malperfusion with Type A Dissection

• Dissection can shear coronary ostia (usually RCA) causing acute MI presentation
• Do not give thrombolytics if there is any possibility of aortic dissection - can be fatal
• In the OR: direct coronary ostial cardioplegia; if RCA involvement recognized pre-bypass, prepare for coronary artery bypass or ostial reconstruction

13.2 Tamponade with Type A Dissection

• Do NOT drain pericardial tamponade percutaneously pre-operatively (raises BP → worsens dissection; can cause sudden decompression → death)
• Go directly to OR; open pericardium on CPB under controlled conditions

13.3 Marfan Syndrome

• Valve-sparing root replacement preferred when possible (David procedure)
• TEVAR is relatively contraindicated for Type B - late stent-graft failure and aortic dilation distal to the graft
• Open surgery preferred for Type B in young Marfan patients

13.4 Iatrogenic Dissection During Catheterization/CPB

• Type A iatrogenic dissections often have better outcomes than spontaneous (less medial fragility)
• Same surgical principles apply

13.5 Malperfusion Syndrome Strategy

• True lumen collapse (dynamic obstruction) - TEVAR or fenestration restores flow
• Static obstruction from dissection flap occluding branch vessel orifice - may need stenting of the branch vessel in addition to TEVAR
• Visceral malperfusion with established bowel ischemia (rising lactate, peritonism) - consider laparotomy + TEVAR hybrid approach

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14. PARAPLEGIA PREVENTION IN AORTIC SURGERY

• Distal aortic perfusion (partial CPB or centrifugal pump) during thoracoabdominal repair
• CSF drainage (lumbar drain) - target CSF pressure <10 mmHg
• Motor evoked potential (MEP) / somatosensory evoked potential (SSEP) monitoring
• Moderate hypothermia (32-34°C)
• Steroid administration
• Re-implantation of intercostal arteries (T8-L2 segment)
• Maintain MAP >90 mmHg post-operatively

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15. KEY NUMBERS TO KNOW (MCh Examinations)

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16. CURRENT GUIDELINES (2024 ESC)

• Type A AAS: Emergency surgery remains standard of care
• Type B complicated AAS: TEVAR preferred over open surgery
• Type B uncomplicated AAS: Medical management as first-line; TEVAR may be considered in high-risk uncomplicated cases
• IMH Type B: Initial medical management + surveillance (Class I); TEVAR for progression (Class IIa)
• PAU symptomatic: Intervention recommended; TEVAR preferred for descending lesions

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SUMMARY FRAMEWORK FOR MCh LEVEL

AAS
├── Type A (ascending involved)
│   ├── ALL → Emergency Surgery
│   ├── Root: resuspend valve vs Bentall vs David
│   ├── Arch: routine replacement only if disrupted/aneurysmal/genetic
│   ├── Distal: HCA + ACP, felt obliteration of FL, Dacron graft
│   └── FET if distal arch/proximal descending involvement
│
├── Type B (descending only)
│   ├── Uncomplicated → Medical (anti-impulse) + surveillance
│   ├── Complicated (rupture/malperfusion/expansion) → TEVAR
│   └── TEVAR unsuitable/genetic → Open surgery
│
├── IMH
│   ├── Type A → Surgical (same as Type A AD)
│   └── Type B → Medical; TEVAR if progressing
│
└── PAU
    ├── Asymptomatic, small → Medical + surveillance
    ├── Large (>20mm / neck >10mm) or symptomatic → Intervention
    └── TEVAR preferred for descending PAU

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• Braunwald's Heart Disease (2 Vol Set), Chapters 42 & 84
• Fuster & Hurst's The Heart, 15e, Chapter 23
• Robbins & Kumar Basic Pathology, Chapter 8
• Grainger & Allison's Diagnostic Radiology, Chapters 17 & 79
• Textbook of Clinical Echocardiography, Chapters 16 & 18
• Miller's Anesthesia 10e, Chapter 52
• Current Surgical Therapy 14e, Chapter on Aortic Dissection
• Schwartz's Principles of Surgery 11e, Chapter 22
• Sabiston Textbook of Surgery
• 2024 ESC Guidelines [PMID: 39210722]That is a complete MCh Cardiac Surgery-level teaching document on Acute Aortic Syndrome. Here is a summary of what was covered and the sources used:

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What was covered (16 sections):

1. Definition and spectrum - AAS as a triad: Dissection (75%), IMH (10-20%), PAU (2-7%)
2. Pathophysiology of all three entities with gross pathology and histology images from Robbins
3. Epidemiology and risk factors including IRAD demographics, Marfan, cocaine, pregnancy
4. DeBakey + Stanford classification with the classic diagram from Miller's Anesthesia
5. Clinical presentation - pain characteristics, the full malperfusion syndrome table (Schwartz)
6. Diagnostic workup - CXR limitations, CTA protocol, TEE features (intraoperative image included), MRI
7. Medical management / anti-impulse therapy - targets, drug choices, monitoring
8. Type A surgical strategy - cannulation options, HCA + cerebral perfusion, felt technique, root management decision-making, arch/FET indications, IRAD mortality data
9. Type B management - uncomplicated vs complicated, malperfusion indications, TEVAR technique step-by-step including IVUS
10. IMH management - Japanese vs Western controversy for Type A; Type B algorithm
11. PAU management - size thresholds, TEVAR challenges
12. Chronic dissection - surveillance, aneurysmal evolution in 50%
13. Special situations - coronary malperfusion (no thrombolytics!), tamponade (no percutaneous drainage!), Marfan, malperfusion strategies
14. Paraplegia prevention - CSF drainage, MEP monitoring, intercostal reimplantation
15. Key numbers for MCh examinations
16. 2024 ESC Guidelines summary

Blunt Traumatic Aortic Injury (BTAI) - MCh Cardiac Surgery Level

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1. EPIDEMIOLOGY AND MORTALITY PROFILE

• Fischer's Mastery of Surgery, p. 7029; Miller's Anesthesia, p. 7775

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2. MECHANISMS OF INJURY

2.1 Three Biomechanical Mechanisms

• The mobile aortic arch continues forward while the relatively fixed descending thoracic aorta (fixed by ligamentum arteriosum, intercostal arteries, and paravertebral tissues) is anchored
• The transition zone - the aortic isthmus (just distal to the left subclavian artery) - receives the maximal shear force
• This accounts for 50-70% of all BTAI
• Mechanism: high-speed MVA (especially >30 mph / 48 km/h), motorcycle crashes, pedestrian vs automobile

• Anteroposterior compression of the chest causes the heart and aorta to be crushed between the sternum and vertebral column
• Results in direct full-thickness compression injury
• Involves the ascending aorta close to the innominate artery or just above the aortic valve
• Mechanism: falls from large heights (>10 ft / LD50 = 4 stories), crush injuries

• Sudden displacement of the heart to the left during AP compression creates torque at the arch-isthmus junction
• Rapid increase in intraluminal aortic pressure (transient hypertension exceeding tensile strength of aortic wall)
• Can cause injury at any aortic segment

• Aortic isthmus (distal to L. subclavian artery): 50-90%
• Ascending aorta / aortic arch: 18%
• Distal thoracic / diaphragmatic aorta: 14%
• Abdominal aorta: rare (infrarenal; usually "osseous pinch" mechanism)
• Grainger & Allison's, p. 430; Miller's Anesthesia, p. 7775

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3. SPECTRUM OF INJURY (PATHOLOGICAL)

1. Simple subintimal hemorrhage - intimal disruption only, no hemodynamic consequence
2. Intimal flap / tear - intima disrupted, media intact
3. Intramural hematoma - media involved, adventitia intact
4. Pseudoaneurysm - all layers except adventitia disrupted; adventitia + periaortic tissues provide containment (the "false aneurysm")
5. Frank transection/rupture - complete transmural disruption → exsanguination (80-90% die at scene)

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4. CLASSIFICATION - SVS GRADING SYSTEM (Azizzadeh/ATF)

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5. CLINICAL PRESENTATION AND INITIAL ASSESSMENT

5.1 The "High Index of Suspicion" Principle

• High-speed MVA (>30 mph / 48 km/h), especially frontal or lateral impact
• Motorcycle collision
• Pedestrian struck by vehicle
• Fall from >10 feet
• Airplane crash
• Crush injury

• Chest wall ecchymosis / "seat belt sign"
• Sternal fracture (associated with ascending aortic injury)
• Crepitus, flail chest
• Unequal bilateral blood pressure (subclavian involvement or pseudocoarctation)
• Absent or reduced distal pulses
• Hoarseness (recurrent laryngeal nerve compression by periaortic hematoma)
• Paraplegia or paraparesis (spinal cord ischemia)
• Harsh systolic murmur (turbulent flow across pseudoaneurysm)

5.2 ATLS Primary Survey in BTAI Context

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6. DIAGNOSTIC IMAGING

6.1 Plain Chest X-Ray - Screening Tool, Not Diagnostic

6.2 CT Angiography (CTA) - Gold Standard

• Rapid acquisition (seconds for entire thorax + abdomen)
• Available 24/7 adjacent to ICU/trauma bay
• Simultaneously evaluates brain, thorax, abdomen, and pelvis (mandatory in polytrauma)
• Provides preoperative planning data: aortic diameters, landing zone lengths, access vessel anatomy, relationship to arch vessels

• Intimal flap
• Focal calibre change (pseudocoarctation) at the isthmus
• Contrast extravasation (pseudoaneurysm / frank rupture)
• Intramural hematoma (hyperdense crescent on non-contrast)
• Aortic contour abnormality

• Mediastinal/periaortic hematoma
• Left hemothorax (without other explanation)

• Ductus diverticulum - normal anatomical variation at the isthmus (smooth, well-defined concavity on the inferior aspect of the isthmus)
• Prominent superior intercostal vein ("aortic nipple")
• Bronchial artery or intercostal artery infundibulum
• Aberrant subclavian artery
• Streak artefacts (non-elevated arms, left arm IV contrast injection, monitoring lines)
• Severe aortic atherosclerosis

6.3 Conventional Aortography

• Lower accuracy than CTA (sensitivity 84-96%)
• False positives: ductus diverticulum, atheroma, overlapping vessel densities
• False negatives: poor aortic opacification, small intimal defects
• Does not show indirect signs (mediastinal hematoma, other injuries)
• Now reserved for: equivocal CTA findings + IVUS, or as part of endovascular intervention planning

6.4 Transesophageal Echocardiography (TEE)

• Sensitivity 91%, specificity 98% for isthmic injuries
• Performed at bedside in 15-20 minutes, even in unstable patients
• Not available in the ICU in all centers; operator-dependent

• Mural flap at the intimal disruption site
• Aortic wall deformity from contained rupture
• Gap >7 mm between probe and aortic wall at the proximal descending aorta level (with blood between aortic wall and pleura) - strongly suggests aortic disruption
• Can also detect: cardiac tamponade, left pleural effusion, myocardial contusion (wall motion abnormalities), hypovolemia (small, hyperdynamic LV)

• Contraindicated in severe facial injuries, unstable cervical spine fractures, or esophageal injury
• Full circumference visualization not achieved in ~30% (aortic arch especially limited - the classic "blind spot")
• Cannot assess for other organ injuries simultaneously

6.5 MRI

• Fastest modern sequences: oblique sagittal black-blood fast spin-echo (BFBSE) - full thoracic aorta in minutes
• Can characterize partial vs circumferential injury
• Can identify and date IMH without contrast
• Limited by: restricted urgent access, patient monitoring challenges, incompatible equipment
• Role: useful for chronic traumatic pseudoaneurysms and serial follow-up

6.6 IVUS (Intravascular Ultrasound)

• Used when CTA is equivocal (especially for Grade 1 intimal tears)
• Performed during angiography/endovascular procedure
• Confirms true lumen access, aortic diameters, branch vessel origins
• Identifies extent of injury not visible on conventional angiography

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7. INITIAL RESUSCITATION AND ANTI-IMPULSE THERAPY

7.1 ATLS-Guided Resuscitation

1. Airway + C-spine control
2. Hemorrhage control - massive transfusion protocol (MTP) if hemorrhagic shock
3. FAST examination - pericardial blood, hemothorax
4. CTA chest/abdomen/pelvis once sufficiently stable

7.2 Anti-Impulse Therapy

• SBP <120 mmHg (most centers, ATF consensus)
• HR <60 bpm
• Note: In concurrent TBI (common in BTAI), aggressive BP lowering may worsen cerebral perfusion pressure - modified targets of SBP 100-140 mmHg are used based on neurosurgical guidance; this requires multidisciplinary discussion.

• Esmolol infusion (500 mcg/kg bolus → 50-200 mcg/kg/min) - short-acting, easily titratable
• Labetalol (alpha + beta blockade) - 20 mg IV bolus, then infusion
• If BP not controlled with beta-blocker alone: add sodium nitroprusside or nicardipine (avoid without beta blockade - reflex tachycardia worsens dP/dt)

7.3 Damage Control Resuscitation Priorities

1. Active intracranial hemorrhage (neurosurgery first)
2. Unstable pelvic fracture (external fixation/IR embolization)
3. Solid organ injury with hemorrhagic shock
4. BTAI repair - typically urgent but can be delayed 24 hours in stable patients while managing other injuries

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8. MANAGEMENT BY GRADE

8.1 Grade 1 (Intimal Tear) - Expectant Management

• Anti-impulse medical therapy alone
• Serial CTA at 24-72 hours, then weekly for 4 weeks, then monthly
• Most resolve spontaneously
• SVS and ATF data support definitive non-operative management with low risk of progression
• Close monitoring for signs of injury progression: increasing mediastinal hematoma, new pseudoaneurysm, hemodynamic instability

8.2 Grade 2 (IMH) - Medical vs Interventional

• Anti-impulse medical therapy first-line
• Serial CTA monitoring
• Intervene if: progression to pseudoaneurysm, expansion of hematoma, uncontrolled pain, hemodynamic instability
• Emerging evidence (ATF registry): MAI (grades 1+2) can be safely managed non-operatively in the majority

8.3 Grade 3 (Pseudoaneurysm) - Urgent TEVAR <24 Hours

• Standard of care: TEVAR
• Timing: urgent within 24 hours; delayed repair (24-72 hours) acceptable if managing higher-priority injuries
• SVS guidelines: TEVAR preferred over OSR if anatomically suitable (regardless of age)

8.4 Grade 4 (Free Rupture) - Emergent Intervention

• Emergent TEVAR or open surgical repair
• Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) Zone 1 may be used as a bridge to definitive repair in extremis
• In proximal aortic or arch injuries not suitable for TEVAR: emergent surgical repair via median sternotomy + CPB + DHCA

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9. ENDOVASCULAR REPAIR (TEVAR) - DETAILED TECHNIQUE

• Avoids general anesthesia induction in unstable polytrauma patients
• No thoracotomy - avoids one-lung ventilation, positional injuries, lateral decubitus positioning
• No aortic cross-clamp (eliminates cross-clamp related paraplegia risk for short-duration cases)
• Lower blood loss, shorter operative time
• Reduced risk of spinal cord ischemia compared to clamp-and-sew
• Equivalent or better mortality compared with historical open repair

9.1 Preoperative Planning (CTA Assessment)

1. Injury location: confirm aortic isthmus; note distance from left subclavian artery (LSA) to injury
2. Proximal landing zone: need ≥2 cm (15-20 mm minimum) of normal aorta proximal to injury for adequate seal
   • LSA coverage in 40% of BTAI cases required because the injury is very close to the LSA origin
3. Distal landing zone: ≥2 cm of normal aorta distal to injury
4. Aortic diameters: at planned landing zones (oversizing 10-20% for TEVAR devices)
5. Access vessels: bilateral common femoral and iliac arteries - minimum 7 mm diameter, assess for calcification/tortuosity
6. Cerebrovascular anatomy: size and origin of vertebral arteries; dominant left vertebral or left vertebral terminating in PICA requires LSA revascularization before coverage
7. Associated injuries: pneumothorax, hemothorax, pulmonary contusion, solid organ injury

9.2 Left Subclavian Artery (LSA) Coverage

• Dominant left vertebral artery (right VA diminutive or absent)
• Left VA terminating in the PICA (posterior inferior cerebellar artery) - stroke risk
• Existing LIMA-based CABG (left internal mammary artery graft - will be devascularized)
• Functional left arm AV fistula or graft (dialysis access)
• Planned long-segment coverage (≥20 cm, especially T8-L1)

• Urgent/emergent TEVAR required (life takes precedence)
• Normal right vertebral artery (good circle of Willis)
• No prior CABG using LIMA

9.3 Spinal Cord Ischemia (SCI) Risk

• Prior lumbar/intercostal artery coverage (previous aortic surgery)
• Hypogastric artery occlusions
• Long-segment (≥20 cm) coverage T8-L1 (Adamkiewicz artery territory)
• Concurrent injury to intercostal supply

• Lumbar drain (CSF pressure target <10 mmHg) - for long segment coverage
• Maintain MAP >90 mmHg post-operatively
• Selective LSA revascularization

9.4 TEVAR Operative Steps (Step-by-Step)

• Patient supine, prep nipples to knees
• Percutaneous common femoral artery access via ultrasound guidance + micropuncture kit
• Serial dilation of arteriotomy (5 Fr → 8 Fr)
• "Pre-close technique": Two Perclose ProGlide devices deployed before upsizing sheath, for suture-mediated arteriotomy closure at case completion
• Place 8 Fr sheath

• Advance marker pigtail catheter over soft angled glidewire to ascending aorta
• Arch aortogram at steep left anterior oblique (LAO) angulation to "open up" the arch and great vessels
• Confirm injury location; evaluate cerebrovascular anatomy (vertebral artery size, origin, and termination)

• Confirms sizing of aorta at landing zones
• Determines adequate length of coverage
• Identifies precise locations of LSA and celiac origins
• Can identify injury extent not visible on angiography

• Systemic heparin 100 IU/kg IV (standard weight-based dosing)
• Can be modified/withheld if multiple concurrent injuries with active hemorrhage (increased thrombosis risk without heparin)

• Soft glidewire → stiff double-curved wire (e.g., Lunderquist)
• Use guide catheter or IVUS catheter as conduit to protect aorta from stiff wire trauma
• Maintain forward tension on wire to facilitate device tracking on the outer curve of the arch

• Large access sheath placed over wire (or device delivered directly without sheath depending on device)
• Device advanced to target position
• Pre-deployment angiogram to confirm precise positioning relative to LSA
• Two-person technique during deployment: one fixes the device in position while the other deploys - prevents device migration
• During deployment: maintain forward tension on the stiff wire to keep device on outer curve of aortic arch

• Aortic molding balloon (selective use) - only if Type Ia endoleak suspected
• Completion aortogram to confirm: adequate landing, proximal and distal sealing, no endoleak, patency of arch vessels

• Retrieve devices
• Suture-mediated closure via pre-placed ProGlide devices
• Assess for hemostasis; open cut-down if percutaneous closure fails

9.5 Special Scenarios in TEVAR for BTAI

• TEVAR is usually not anatomically feasible
• Requires open surgical repair via median sternotomy + CPB + DHCA
• Zone 0 or Zone 1 injuries need open repair; hybrid approaches with debranching + TEVAR occasionally possible

• Iliac conduit via retroperitoneal approach to the common iliac artery
• Alternative: axillary artery access (rare)

• Severe narrowing of the true lumen at the injury site creating a pressure gradient
• Can cause upper limb hypertension and distal ischemia
• TEVAR restores lumen diameter and abolishes gradient

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10. OPEN SURGICAL REPAIR

• Ascending aortic or arch injury (not anatomically suitable for TEVAR)
• Access vessel anatomy unsuitable for TEVAR (calcified aortoiliac occlusive disease, small iliac arteries)
• Failed TEVAR (endoleak requiring conversion)
• Younger patients with genetic aortopathy (Marfan) in elective setting
• Concurrent cardiac injury requiring sternotomy (coronary laceration, aortic valve injury)

10.1 Descending Aortic Open Repair (Left Thoracotomy Approach)

• Left heart bypass (centrifugal pump): Left inferior pulmonary vein → left femoral artery (or descending aorta distal to repair). Provides distal aortic perfusion maintaining spinal cord, renal, and visceral blood flow during cross-clamp. Does NOT require systemic heparinization (heparin-bonded circuit; important in polytrauma with coagulopathy).
• Femoral-femoral (femorofemoral) CPB: Also used; does require heparin.
• "Clamp-and-sew" technique: Aortic cross-clamp only, no bypass. Acceptable if cross-clamp time <30 minutes and adequate collateral supply. Associated with higher paraplegia risk (3.8-40% depending on duration). Rarely used in modern practice.

1. Left thoracotomy; enter pleural space; evacuate hemothorax
2. Identify proximal (zone between LSCA and injury) and distal aorta for clamping
3. Initiate left heart bypass
4. Apply proximal clamp (ideally between LSCA and injury; sometimes distal arch clamp required)
5. Apply distal clamp to descending aorta distal to injury
6. Transect aorta at injury; inspect ends - confirm healthy aortic wall for anastomosis
7. Interposition Dacron graft with end-to-end anastomoses (running polypropylene suture)
8. Remove clamps in sequence; de-air; check for hemostasis
9. Wean from left heart bypass; close thoracotomy with drains

• Historical mortality: >15-20% (emergency context + polytrauma)
• Paraplegia: 3-8% with distal perfusion techniques; up to 40% with clamp-and-sew
• Modern TEVAR has largely supplanted open repair due to significantly lower morbidity

10.2 Ascending Aorta / Arch Open Repair

• Femoral or axillary artery cannulation (avoid ascending aorta due to injury)
• Venous return via right atrium
• Cooling to DHCA temperatures (18-20°C)
• Antegrade cerebral perfusion (ACP) via right axillary artery for arch work
• Open distal anastomosis technique under circulatory arrest
• Dacron interposition graft for aortic transection
• Aortic root preservation where possible (rarely involved in traumatic BTAI)

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11. ANESTHETIC MANAGEMENT (MCh Level - Key Points)

• Full stomach: All trauma patients treated as having a full stomach - rapid sequence induction
• Induction agents: Ketamine (1-2 mg/kg) ± etomidate - preserve hemodynamic stability; avoid propofol bolus in hypotensive patients
• Two large-bore IV lines + arterial line before induction
• Right radial arterial line preferred (left subclavian may be compressed or covered by TEVAR)
• One-lung ventilation is required for left thoracotomy open repair - use double-lumen ETT or bronchial blocker
• TEE is mandatory intraoperatively for TEVAR guidance and for open repair to assess cardiac function, guide volume resuscitation, detect tamponade
• Temperature management: Active warming (hypothermia worsens coagulopathy)
• Coagulation management: TEG/ROTEM-guided MTP; avoid aggressive crystalloid (dilutional coagulopathy)
• Post-op: ICU with controlled ventilation; vasopressors to maintain MAP >90 mmHg (spinal cord protection)

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12. COMPLICATIONS AND THEIR MANAGEMENT

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13. TIMING STRATEGY AND DAMAGE CONTROL PRINCIPLES

• Allows stabilization of hemodynamics and coagulopathy
• Allows management of higher-priority injuries
• Reduces overall procedural risk
• Recent ATF evidence: timing of TEVAR does not significantly impact overall outcome; individualized approach is favored

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14. FOLLOW-UP SURVEILLANCE

• CTA at 24-72 hours, 1 week, 1 month, 3 months - looking for: progression to pseudoaneurysm, hematoma expansion, hemodynamic changes

• Endoleak (late type Ia especially as aortic anatomy changes with remodeling)
• Device fatigue / fracture
• Late aneurysmal degeneration (descending aorta distal to graft)
• Stent-graft collapse in hypoplastic aorta (young trauma patients - smaller native aortic diameter)

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15. SPECIAL SITUATIONS AT MCh LEVEL

15.1 Young Patients (Pediatric / Adolescent)

• Aortic diameter often <20 mm - most commercial TEVAR devices have lower limit of ~17-18 mm
• Risk of stent-graft collapse in very angulated aortic arch (acute angle between arch and descending)
• Open repair may be preferable in children; can use homograft
• Long-term device surveillance is critical - the stent-graft will need re-intervention as the child grows

15.2 BTAI with Concurrent TBI

• The most challenging management dilemma: anti-impulse therapy (low BP) vs cerebral perfusion pressure maintenance (adequate BP)
• Multidisciplinary approach (neurosurgery + cardiac surgery/vascular surgery + critical care)
• Modified BP targets: SBP 100-140 mmHg (not <100 mmHg)
• Grade 1-2 BTAI with concurrent moderate TBI: usually managed medically (anti-impulse therapy at modified targets)
• Grade 3-4 BTAI with concurrent TBI: TEVAR preferred (shorter, less invasive; allows earlier ICP management)

15.3 BTAI with Concurrent Solid Organ Injury

• If splenectomy or hepatorrhaphy required: perform laparotomy first (usually faster to control bleeding)
• TEVAR second (semi-urgent within 24 hours)
• Avoid full-dose heparin during TEVAR if recent hepatic or splenic repair - consider heparin-free or reduced-dose TEVAR

15.4 Ascending Aortic BTAI

• Rare (18%) but requires sternotomy + CPB + DHCA
• Associated with massive pericardial hematoma, tamponade, acute AR, and coronary ostial avulsion
• Higher mortality than isthmic injury

15.5 Chronic Traumatic Pseudoaneurysm

• Occasionally diagnosed incidentally weeks to months after trauma
• False aneurysm contains the injury; adventitia and fibrotic reaction maintain integrity
• Still requires treatment (risk of late rupture is significant)
• TEVAR is preferred; open repair has higher risk than acute injury (fibrotic adhesions)

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16. KEY NUMBERS FOR MCh EXAMINATIONS

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17. CURRENT GUIDELINES SUMMARY

• TEVAR is the preferred approach for BTAI of the descending thoracic aorta when anatomically suitable (Class I)
• Anti-impulse therapy (HR <60, SBP <120 mmHg) is mandated for all BTAI during the perioperative period
• Grade 1-2 injuries can be managed with anti-impulse therapy and serial imaging
• Open repair reserved for ascending/arch injuries or when TEVAR not feasible

• Supports TEVAR over open surgical repair for descending BTAI
• Emerging evidence for definitive medical management of MAI (grades 1-2)
• Timing of TEVAR (immediate vs delayed) does not significantly impact overall outcomes

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MANAGEMENT ALGORITHM

BTAI confirmed on CTA
│
├── Grade 4 (Free Rupture) → EMERGENT TEVAR or Open Surgery
│   └── Ascending/Arch → Sternotomy + CPB + DHCA
│
├── Grade 3 (Pseudoaneurysm) → URGENT TEVAR within 24 hrs
│   ├── Anti-impulse therapy NOW
│   ├── Manage higher-priority injuries first
│   ├── Assess: landing zones, access vessels, LSA, cerebrovascular anatomy
│   └── TEVAR (preferred) vs Open (if unsuitable anatomy)
│
├── Grade 2 (IMH) → Anti-impulse therapy + Serial CTA
│   ├── Consider TEVAR if: hematoma expansion, pain, hemodynamic instability
│   └── Most can be managed medically
│
└── Grade 1 (Intimal tear) → Anti-impulse therapy + Serial CTA
    ├── Expectant management
    └── Intervene only if: progression on imaging, instability

All patients:
→ ICU admission with invasive monitoring
→ Beta-blocker infusion (esmolol preferred)
→ SBP target <120 mmHg, HR target <60 bpm
→ Polytrauma co-management (TBI, ortho, abdo)
→ CTA at 24-72 hrs, 1 week, 1 month, 3 months, 6 months, then annually

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• Fischer's Mastery of Surgery, 8e, Chapter 261
• Grainger & Allison's Diagnostic Radiology, Chapters 17 & 79
• Miller's Anesthesia, 10e, Chapter 52
• Sabiston Textbook of Surgery, Chapter 36
• Schwartz's Principles of Surgery, 11e, Chapter 22
• Textbook of Clinical Echocardiography, Chapter 16
• 2022 ACC/AHA Guideline for Aortic Disease [PMID: 36322642]
• SVS Systematic Review for BTAI guidelines 2026 [PMID: 40482894]That is a complete MCh Cardiac Surgery-level note on Blunt Traumatic Aortic Injury. Here is what was covered across 17 sections:

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What Was Covered:

1. Epidemiology - 80% prehospital mortality; 20% of all MVA deaths; only adventitially contained injuries survive to hospital
2. Mechanisms (3 biomechanical forces with diagram) - Deceleration/shear at isthmus (50-90%), osseous pinch (ascending), torsional/hydraulic. Site frequency by mechanism.
3. Spectrum of pathology - Subintimal tear → IMH → pseudoaneurysm → frank transection, with cross-sectional diagram
4. Classification - SVS/Azizzadeh Grades 1-4 (ATF registry frequencies) + Presley Trauma Center CT system (full table)
5. Clinical presentation - High index of suspicion; physical signs; ATLS primary survey relevance; "normal BP does not rule out BTAI"
6. Diagnostic imaging with real images:
   • CXR - all signs with widened mediastinum photo
   • CTA (gold standard) - direct + indirect signs, false positive pitfalls, pseudocoarctation
   • Conventional aortography - why abandoned
   • TEE - bedside value, contraindications, 7 mm probe gap sign
   • MRI and IVUS roles
7. Initial resuscitation - ATLS priorities, anti-impulse therapy targets, drug choices, TBI conflict resolution
8. Management by grade - Grade 1 (expectant) → Grade 4 (emergent)
9. TEVAR - detailed step-by-step technique - access, pre-close technique, arch aortogram, IVUS, anticoagulation, stiff wire exchange, two-person deployment, completion angiogram
10. LSA coverage - 40% incidence; when to revascularize first (LIMA CABG, dominant left VA, PICA termination); when safe to cover without revascularization
11. Spinal cord ischemia - risk factors, prevention strategies, Adamkiewicz territory
12. Open surgical repair - left thoracotomy, left heart bypass vs clamp-and-sew, paraplegia rates; ascending injury via sternotomy/CPB/DHCA
13. Anesthetic management - RSI, ketamine, one-lung ventilation, TEE, coagulopathy management
14. Complications - Type Ia endoleak, SCI, stroke, stent collapse, access injury, device migration
15. Timing strategy - damage control principles, injury priority hierarchy, evidence for delayed TEVAR
16. Follow-up surveillance - detailed CTA schedule post-TEVAR and for medically managed cases
17. Special situations - young patients, concurrent TBI (the hardest management dilemma), solid organ injury, ascending BTAI, chronic pseudoaneurysm