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DIAGNOSIS AND
MANAGEMENT OF
AORTIC DISSECTION
Overview
 Classification
 Diagnostic modalities
 Diagnostic strategy
 Management strategy
 Surgical principles
 Complications
 Follow up
 Results
DeBakey’s Classification
(1965)
 Type I – Involvement of ascending aorta, arch
and variable length of DTA and
abdo aorta.
 Type II – Involvement of ascending aorta
only.
 Type III – Involvement of descending aorta ,
distal to left subclavian artery.
 III-A:- Limited to Thoracic aorta
 III-B:- Involvement of Thoracic and abdominal aorta.
Stanford Classification
 Type A- Involvement of ascending
aorta +/- arch or DTA inv
 Type B- No involvement of ascending
aorta (arch may be
involved)
Site of Tear- Type A Dissection
Site of Tear- Type B Dissection
Type A Aortic Dissection
Aims of Investigations
 Confirm Diagnosis.
 Ascending aorta involved or not (Type A or Type B)
 Site of proximal intimal tear (PIT).
 Extent of dissection.
 Diameter of aorta.
 Involvement of coronary ostia, arch vessels, visceral arteries.
 Pericardial effusion.
 Left ventricular function.
 Valve function (esp aortic valve regurgitation)
Diagnosis
Chest Radiography
 Low Sensitivity (67%) and Specificity.
 Normal Chest X- Ray 12-20%
 Suggestive findings:
1. Mediastinal widening.
2. Calcium sign – intimal calcification displacement.
3. Pleural effusion
4. Tracheal deviation.
5. Widening of the aortic knob.
Mediastinal Widening
Calcium Sign
Pleural Effusion: Hemothorax
Electrocardiogram
 Normal ECG with Severe chest pain- ?? Dissection.
 MI: 1 - 2% aortic dissections. (ST segment elevation)
 Involvement of coronary artery (RCA > LCA).
 Thrombolytic therapy – 70% mortality.
 Non-specific ST-T changes most common
40% of patients (associated LVH 30%).
Aortic Dissection Acute Myocardial
Infarction
History Connective tissue
disorder
Marfans Syndrome.
Angina pectoris.
Pain: Character Sharp, excruciating. Heaviness, crushing
Pain: localization /
radiation
Well localized
Typical propagation
pattern
Vague chest pain-
radiating Left upper limb
Examination:
BP differential (arms) Present Absent
Pulse differential (limbs,
carotids)
Present Absent
AR Wide pulse pressure
Murmur
Absent
Pericardial Effusion Muffled heart sounds Absent
Malperfusion Pain / Paresthesia limbs
Pain abdomen
Absent
Transthoracic Echocardiography: Findings
 Presence of dissection flap.
 Site of entry point.
 Aortic arch vessel occlusion.
 Dilatation of aorta.
 Aortic valve regurgitation, other valve status.
 Pleural / Pericardial Effusion
 LV function / RWMA
Transthoracic Echocardiography:
Disadvantages
 Low sensitivity and specificity (59% & 83%).
(N. Eng. J. Med. 1993;328:1-9)
 Difficulty due to technical problems, narrow
intercostal spaces, Obesity, emphysematous chest.
Trans Esophageal
Echocardiography
 Performed rapidly, relatively non invasive.
 Pericardial effusion
 Pericardial tamponade
 Aortic regurgitation / other valve status
 Involvement of proximal coronary artery.
 LV function / RWMA
TEE Sensitivity Specificity
Type A dissection 96% - 100% 86% - 100%
Type B dissection 98% - 100% 96% - 100%
Trans Esophageal Echocardiography- Disadvantages
 Investigator dependent.
 Poor visualization of arch vessels.
 Difficulty in detecting fresh thrombus.
 Frequent retching causes tachycardia and hypertension.
 Can’t detect distal extent of dissection – below celiac axis.
 Can’t be used in patients with esophageal varices and
stenosis.
Type A Dissection Circumferential Dissection
Computed Tomography
 Rapid / minimally invasive / less operator dependant.
 3 D reconstruction can visualize course of dissection.
 Identify dissection membrane , TL , FL.
 Extent of Dissection / Arch involvement / Perfusion of
major aortic branches.
 Proximal coronary artery.
 Sensitivity- 82 - 100%; Specificity- 90 – 100%.
 Can be useful as follow-up study
Computed Tomography:
Disadvantages
 Dissection obscured by complete thrombosis of false
lumen.
 Cannot identify proximal intimal tear, aortic regurgitation.
 Use of contrast
 Movement of patient creates inferior quality of the scan.
 Contraindication: contrast allergy
Dissection : PIT
MRI: Advantages
 Localize PIT, extent of dissection.
 Identifies arch vessels involvement.
 Severity of Aortic regurgitation / flow patterns in TL, FL
 Can evaluate LV functions.
 No contrast material / No radiation hazard.
 Sensitivity and specificity in the range of 95 – 100%.
(Better than TEE,circulation,1992).
MRI: Disadvantages
 Lack of immediate availability.
 Long examination time.
(Unsuitable for sick patients)
 Restricts monitoring of vitals.
 Patients with PPI, Aneurysm clips and
defibrillators and metallic implants are not
favorable candidates.
Aortography: Historical Interest
Findings (sensitivity 88% , specificity 75-94 % )
 Double lumen or Intimal flap.
 Compressed true aortic lumen
 AR
 Occlusion of branch vessels.
Disadvantages
 Invasive procedure
 Harmful effect of contrast material
 Iatrogenic propagation of dissection.
Coronary Angiography
 Indications-
Hemodynamically stable patient with
H/o Angina pectoris / MI / CAD
H/o CABG
Diagnostic Strategy
 High index of suspicion.
 Chest pain:
Cardiac cause- AMI.
Pericarditis
Myocarditis.
Valvular heart disease.
Aortic dissection.
Pulmonary causes: Acute pulmonary embolism.
Pneumonitis.
GI causes: GERD
Chest wall pain
Neurogenic
 Suspect Aortic Dissection if —
Young patient with Connective tissue disorder
(Marfans)
Old patient >60 yrs with h/o hypertension
Unexplained syncope
Pain: Severity / Character / Radiation
Unexplained stroke
Acute CHF
Pulse : differential
E/O malperfusion- lower limb ischemia
mesenteric ischemia
renal ischemia
Algorithm for management of Type A Dissection
Clinical suspicion
Secure i.v. access / send cross match blood inv.
Shift for CT Angiography
Confirm Diagnosis
Shift to Operation theatre
TEE under Anesthesia
Exceptions
 Irreversible stroke.
 Advanced debilitating systemic illness.
 > 80 yrs with multiple major complications.
 New onset hemiplegia – not an absolute
contraindication.
 Paraplegia – chances of spinal cord deficit
improvement is low.
Pre-operative management
 Comprehensive monitoring:
Neurological status
Arterial blood pressure
Electrocardiogram
Urine output
Peripheral pulses
 Arterial line – in limb with better pulse
 Central venous catheter.
 Urinary catheter
Anti-Impulsive Therapy
 Wheat and associates 1965.
 Factors for progression of aortic dissection-
Change in pressure over time (dP/dT)
Neither high pressure nor high blood flow alone.
 Combination of vasodilator therapy with the
sympathetic control of β-blockade constitutes
effective “anti-impulse therapy” for acute aortic
dissection.
Anti impulsive therapy
 Target: Mean arterial pressure = 60 – 75mmhg
Systolic presure = 100 – 110mm hg
Heart rate = 60 – 80bpm
 Eliminate Pain: Morphine.
 Beta blockade:
Esmolol- 500mcg/kg iv bolus
50 mcg/kg/min infusion (max 200mcg/kg/min)
Propranolol – 1mg every 5 min to achieve target HR
(max 10 mg)
 SNP – 20 mcg/min (max 800mcg/min)
 Refractory hypertension: ACEI - Enalapril
Hemodynamic instability
 Free aortic rupture.
 Intrapericardial rupture with tamponade.
 Acute LVF – Severe AR / Coronary
compromise.
 Management- immediate surgical intervention.
Brief Surgical History
 Gurin et al (1935) – surgical iliac artery fenestration
for dissection related lower extremity ischemia.
 DeBakey 1955: Graft replacement of dissected aorta.
 Spancer and Black (1962) – Chronic Type A
Dissection with AR– Used valve resuspension
technique.
 Griepp (1975) used Hypothermic circulatory arrest.
 Livesay (1982) – Open distal anastamosis.
Surgical Principles
 Complete resection of aortic segment containing
proximal intimal tear: convert Type A to Type B
Dissection
Surgical Principles
 Reconstitution of dissected aortic layers proximally and
distally.
Surgical Principles
 Addressing Aortic valve regurgitation
aortic valve resuspension
aortic root replacement
 Addressing coronary malperfusion
repair of dissected coronary ostia
saphanous vein bypass grafting.
General anesthesia and monitoring
 Induction:
Midazolam
Fentanyl
Pancuronium.
 Maintainance:
Inhaled isoflurane
Fentanyl / Short acting narcotics.
 Antifibrinolytics:
Alpha aminocaproic acid
General anesthesia and monitoring
 ECG
 Pulse Oxymetry
 Right Radial and
Femoral artery pressure.
 Central venous
pressure.
 Nasopharyngeal/rectal/
bladder temperature
 Jugular bulb oxymetry.
CPB Circuit J. Coselli, Scott LeMaire, Jon Cecil Walkes
CPB Circuit Tirone E. David
CPB Circuit
Operating Technique
 Median sternotomy.
 CPB established.
 TEE flow monitoring: organ malperfusion.
 Vent LV via Rt Superior pulmonary vein.
 Core cooling ( temp gradient <10o C) to 24o C.
Cerebral – renal protection
 Cerebral protection:
Dexamethasone (8 – 12 mg).
Thiopental (7 – 15 mg/kg).
Ice packing on head.
CO2 flooding (5 - 10 l/m) in operative field.
 Renal protection:
Mannitol (0.3 – 0.4 g/kg)
Furosemide (40 – 80mg).
Myocardial protection
 Direct ostial cold blood cardioplegia.
 Retrograde cold blood cardioplegia.
 Topical cooling
Management of the distal aorta
 Proximal Intimal Tear (PIT) location:
Ascending Aorta.
Lesser curvature of Arch.
Greater curvature of Arch
PIT in Ascending aorta / Lesser curve of arch
Hemiarch Replacement
PIT in Transverse Arch
Management of Aortic Root
Predissection Diseased sinuses Diseased sinuses and
normal sinuses normal cusps cusps
and valve
Aortic cusps Valve sparing Composite valve graft
Resuspension root replacement root replacement
Predissection normal sinus and valve cusps:
Mechanism of Aortic Regurgitation
Management Of Aortic Root
Predissection normal sinus and valve cusps:
Aortic valve resuspension
Valve sparing root replacement
 David procedure and its modifications.
 Yacoub
Valve sparing root replacement: David procedure
and its modifications
Valve sparing root replacement: Yacoub’s
David V
Composite Valve Graft Root Replacement
Bentall and DeBono 1968. Kouchoukos modification.
Cabrol procedure
Management of coronary artery dissection
 Dissection just at the ostia:
 Repair with obliteration of false lumen.
 Reimplantation of reconstituted coronary ostia as
Carrel buttons into graft.
 Cabrol II “moustache coronary resconstruction”
 Suture ligation of coronary artery with bypass grafting
Role of Frozen Elephant Trunk
 Dilated distal Aorta with predisposig factors eg
Marfans.
Post – operative management
 Control hypertension.
beta blockers
calcium channel blockers
ACE inhibitors.
 Monitor for malperfusion syndrome.
- Compression of true lumen by false lumen
- Extension of dissection into branch artery with
compression of true lumen.
- Intussusception of inner wall of aorta into branch artery.
- Occlusion of branch vessel by dissection flap
Malperfusion syndrome
 Extremities: pain / paresthesia / cold
 Kidneys: uncontrolled hypertension.
 Mesenteric malperfusion: unexplained acidosis /
volume loss / tachycardia.
 Diagnosis: CT Angiography
 Management: fenestration of dissecting membrane.
Follow up
Time of study Study Indication
Before hospital
discharge
CT or MRI
TTE
Arteriography
All patients
Valve reconstruction
Suspected
malperfusion
After hospital discharge
3 months CT or MRI
TTE
Residual dissection.
Valve reconstruction
9 months CT or MRI
TTE
Residual dissection.
Valve reconstruction
Subsequent
examination
Every 6 months CT or MRI
TTE
Progression of aortic
dis
Aortic Regurgitation
Every 12 months CT or MRI Aortic dia >5cm
Every 24 months CT or MRI Aortic diameter <5cm.
Type B Aortic Dissection
Management strategy
 Aim of therapy-
Prevent death
Prevent irreversible end organ damage.
 Optimal treatment strategy- debated ????
Optimal treatment strategy ???
Optimal treatment strategy???
Approach to type B Dissection
Arguments in favour of medical treatment
 Medical treatment prevents death in majority.
 Operative mortality type B dissection high.
 Similar long term outcome of surgically and medically
managed patients.
 “Complication Specific” approach for Type B Dissection
Indications for Intervention
 Persistent pain.
 Refractory arterial hypertension.
 Progression / expansion of dissection.
 Aortic rupture / impending rupture.
 Impaired distal organ perfusion.
 Sizable localized false aneurysm.
 Young with CTD- Marfan syndrome without complications.
Management Strategy for IMH
 Uncomplicated Type B IMH: Medical.
 Type B IMH with persistent pain / associated large –
deep PAU: high incidence of aortic rupture.
 Intervention for complicated Type B IMH
Initial Medical Treatment
 Goal of medical treatment:
Relieve pain.
Control blood pressure.
Limit extension of dissection.
 Extensive monitoring:
 ECG / Radial – Femoral arterial line / CVP /
Pulse Oxymeter / Foley catheter.
Anti impulsive therapy
 Target: Mean arterial pressure = 60 – 75mmhg
Systolic presure = 100 – 110mm hg
Heart rate = 60 – 80bpm
 Eliminate Pain: Morphine.
 Beta blockade:
Esmolol- 500mcg/kg iv bolus
50 mcg/kg/min infusion (max
200mcg/kg/min)
Propranolol – 1mg every 5 min to achieve target HR
(max 10 mg)
 SNP – 20 mcg/min (max 800mcg/min)
 Refractory hypertension: ACEI - Enalapril
Definitive long term medical management
 Oral beta blockers-
Labetalol, Metoprolol, Atenolol.
 Calcium channel antagonists.
 Oral ACEI / ARB
Lisinopril.
 Hydralizine avoided-
Incorporated into mucopolysaccharides of media and
weaken aortic wall.
Aims Of Intervention
(Surgical / Endovascular)
 Seal the entry Point.
 Seal area of leak (if any).
 Establish perfusion to branch arteries.
 Expansion of true lumen and obliteration of false
lumen.
Surgical Principles
Acute Type B Dissection
No visceral malperfusion Visceral malperfusion
Replace the tear point Fenestation
Graft replacement
with visceral
artery reconstruction
Surgical Approach
 Full CPB
 Venous Cannulation- Right Femoral Vein.
 Arterial Cannulation- Left subclavian artery.
Undissected ascending aorta
Descending aortic true lumen
 Moderate hypothermia 25 – 28oC.
 Open Proximal Anastamosis (OPA) in distal arch under
HCA.
Management of visceral malperfusion
Aortic dissection + Visceral malperfusion
Dynamic Obstruction Static Obstruction
Visceral artery Visceral artery
from true lumen from false lumen
Central aortic repair Central aortic repair
visceral artery revascularisation
Surgical fenestration
Mortality according to indication for surgery
Endovascular treatment
 JACC 2008
Endovascular therapy
 Medical management
70% patients- persistent patent false lumen
20 – 30% eventually aneurysmal
 Surgical replacement:
High mortality – 20 – 30%
Visceral ischemia – 30 – 50%
Endovascular treatment
 Balloon Fenestration.
 Stenting
 Stent grafting
Endovascular Balloon Fenestration
Endovascular Balloon Fenestration
Visceral malperfusion- Stenting
Stent Graft
Stent Grafting
Penetrating Atherosclerotic Ulcer
Future developments in
endovascular repair
Future developments in
endovascular repair
Future developments in
endovascular repair
THANK YOU

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Diagnosis and management of aortic dissection

  • 2. Overview  Classification  Diagnostic modalities  Diagnostic strategy  Management strategy  Surgical principles  Complications  Follow up  Results
  • 3. DeBakey’s Classification (1965)  Type I – Involvement of ascending aorta, arch and variable length of DTA and abdo aorta.  Type II – Involvement of ascending aorta only.  Type III – Involvement of descending aorta , distal to left subclavian artery.  III-A:- Limited to Thoracic aorta  III-B:- Involvement of Thoracic and abdominal aorta.
  • 4.
  • 5. Stanford Classification  Type A- Involvement of ascending aorta +/- arch or DTA inv  Type B- No involvement of ascending aorta (arch may be involved)
  • 6. Site of Tear- Type A Dissection
  • 7. Site of Tear- Type B Dissection
  • 8. Type A Aortic Dissection
  • 9. Aims of Investigations  Confirm Diagnosis.  Ascending aorta involved or not (Type A or Type B)  Site of proximal intimal tear (PIT).  Extent of dissection.  Diameter of aorta.  Involvement of coronary ostia, arch vessels, visceral arteries.  Pericardial effusion.  Left ventricular function.  Valve function (esp aortic valve regurgitation)
  • 11. Chest Radiography  Low Sensitivity (67%) and Specificity.  Normal Chest X- Ray 12-20%  Suggestive findings: 1. Mediastinal widening. 2. Calcium sign – intimal calcification displacement. 3. Pleural effusion 4. Tracheal deviation. 5. Widening of the aortic knob.
  • 15. Electrocardiogram  Normal ECG with Severe chest pain- ?? Dissection.  MI: 1 - 2% aortic dissections. (ST segment elevation)  Involvement of coronary artery (RCA > LCA).  Thrombolytic therapy – 70% mortality.  Non-specific ST-T changes most common 40% of patients (associated LVH 30%).
  • 16.
  • 17. Aortic Dissection Acute Myocardial Infarction History Connective tissue disorder Marfans Syndrome. Angina pectoris. Pain: Character Sharp, excruciating. Heaviness, crushing Pain: localization / radiation Well localized Typical propagation pattern Vague chest pain- radiating Left upper limb Examination: BP differential (arms) Present Absent Pulse differential (limbs, carotids) Present Absent AR Wide pulse pressure Murmur Absent Pericardial Effusion Muffled heart sounds Absent Malperfusion Pain / Paresthesia limbs Pain abdomen Absent
  • 18. Transthoracic Echocardiography: Findings  Presence of dissection flap.  Site of entry point.  Aortic arch vessel occlusion.  Dilatation of aorta.  Aortic valve regurgitation, other valve status.  Pleural / Pericardial Effusion  LV function / RWMA
  • 19. Transthoracic Echocardiography: Disadvantages  Low sensitivity and specificity (59% & 83%). (N. Eng. J. Med. 1993;328:1-9)  Difficulty due to technical problems, narrow intercostal spaces, Obesity, emphysematous chest.
  • 20. Trans Esophageal Echocardiography  Performed rapidly, relatively non invasive.  Pericardial effusion  Pericardial tamponade  Aortic regurgitation / other valve status  Involvement of proximal coronary artery.  LV function / RWMA TEE Sensitivity Specificity Type A dissection 96% - 100% 86% - 100% Type B dissection 98% - 100% 96% - 100%
  • 21. Trans Esophageal Echocardiography- Disadvantages  Investigator dependent.  Poor visualization of arch vessels.  Difficulty in detecting fresh thrombus.  Frequent retching causes tachycardia and hypertension.  Can’t detect distal extent of dissection – below celiac axis.  Can’t be used in patients with esophageal varices and stenosis.
  • 22. Type A Dissection Circumferential Dissection
  • 23. Computed Tomography  Rapid / minimally invasive / less operator dependant.  3 D reconstruction can visualize course of dissection.  Identify dissection membrane , TL , FL.  Extent of Dissection / Arch involvement / Perfusion of major aortic branches.  Proximal coronary artery.  Sensitivity- 82 - 100%; Specificity- 90 – 100%.  Can be useful as follow-up study
  • 24. Computed Tomography: Disadvantages  Dissection obscured by complete thrombosis of false lumen.  Cannot identify proximal intimal tear, aortic regurgitation.  Use of contrast  Movement of patient creates inferior quality of the scan.  Contraindication: contrast allergy
  • 26. MRI: Advantages  Localize PIT, extent of dissection.  Identifies arch vessels involvement.  Severity of Aortic regurgitation / flow patterns in TL, FL  Can evaluate LV functions.  No contrast material / No radiation hazard.  Sensitivity and specificity in the range of 95 – 100%. (Better than TEE,circulation,1992).
  • 27. MRI: Disadvantages  Lack of immediate availability.  Long examination time. (Unsuitable for sick patients)  Restricts monitoring of vitals.  Patients with PPI, Aneurysm clips and defibrillators and metallic implants are not favorable candidates.
  • 28.
  • 29. Aortography: Historical Interest Findings (sensitivity 88% , specificity 75-94 % )  Double lumen or Intimal flap.  Compressed true aortic lumen  AR  Occlusion of branch vessels. Disadvantages  Invasive procedure  Harmful effect of contrast material  Iatrogenic propagation of dissection.
  • 30.
  • 31. Coronary Angiography  Indications- Hemodynamically stable patient with H/o Angina pectoris / MI / CAD H/o CABG
  • 32. Diagnostic Strategy  High index of suspicion.  Chest pain: Cardiac cause- AMI. Pericarditis Myocarditis. Valvular heart disease. Aortic dissection. Pulmonary causes: Acute pulmonary embolism. Pneumonitis. GI causes: GERD Chest wall pain Neurogenic
  • 33.  Suspect Aortic Dissection if — Young patient with Connective tissue disorder (Marfans) Old patient >60 yrs with h/o hypertension Unexplained syncope Pain: Severity / Character / Radiation Unexplained stroke Acute CHF Pulse : differential E/O malperfusion- lower limb ischemia mesenteric ischemia renal ischemia
  • 34. Algorithm for management of Type A Dissection Clinical suspicion Secure i.v. access / send cross match blood inv. Shift for CT Angiography Confirm Diagnosis Shift to Operation theatre TEE under Anesthesia
  • 35. Exceptions  Irreversible stroke.  Advanced debilitating systemic illness.  > 80 yrs with multiple major complications.  New onset hemiplegia – not an absolute contraindication.  Paraplegia – chances of spinal cord deficit improvement is low.
  • 36. Pre-operative management  Comprehensive monitoring: Neurological status Arterial blood pressure Electrocardiogram Urine output Peripheral pulses  Arterial line – in limb with better pulse  Central venous catheter.  Urinary catheter
  • 37. Anti-Impulsive Therapy  Wheat and associates 1965.  Factors for progression of aortic dissection- Change in pressure over time (dP/dT) Neither high pressure nor high blood flow alone.  Combination of vasodilator therapy with the sympathetic control of β-blockade constitutes effective “anti-impulse therapy” for acute aortic dissection.
  • 38.
  • 39. Anti impulsive therapy  Target: Mean arterial pressure = 60 – 75mmhg Systolic presure = 100 – 110mm hg Heart rate = 60 – 80bpm  Eliminate Pain: Morphine.  Beta blockade: Esmolol- 500mcg/kg iv bolus 50 mcg/kg/min infusion (max 200mcg/kg/min) Propranolol – 1mg every 5 min to achieve target HR (max 10 mg)  SNP – 20 mcg/min (max 800mcg/min)  Refractory hypertension: ACEI - Enalapril
  • 40. Hemodynamic instability  Free aortic rupture.  Intrapericardial rupture with tamponade.  Acute LVF – Severe AR / Coronary compromise.  Management- immediate surgical intervention.
  • 41. Brief Surgical History  Gurin et al (1935) – surgical iliac artery fenestration for dissection related lower extremity ischemia.  DeBakey 1955: Graft replacement of dissected aorta.  Spancer and Black (1962) – Chronic Type A Dissection with AR– Used valve resuspension technique.  Griepp (1975) used Hypothermic circulatory arrest.  Livesay (1982) – Open distal anastamosis.
  • 42. Surgical Principles  Complete resection of aortic segment containing proximal intimal tear: convert Type A to Type B Dissection
  • 43. Surgical Principles  Reconstitution of dissected aortic layers proximally and distally.
  • 44. Surgical Principles  Addressing Aortic valve regurgitation aortic valve resuspension aortic root replacement  Addressing coronary malperfusion repair of dissected coronary ostia saphanous vein bypass grafting.
  • 45. General anesthesia and monitoring  Induction: Midazolam Fentanyl Pancuronium.  Maintainance: Inhaled isoflurane Fentanyl / Short acting narcotics.  Antifibrinolytics: Alpha aminocaproic acid
  • 46. General anesthesia and monitoring  ECG  Pulse Oxymetry  Right Radial and Femoral artery pressure.  Central venous pressure.  Nasopharyngeal/rectal/ bladder temperature  Jugular bulb oxymetry.
  • 47. CPB Circuit J. Coselli, Scott LeMaire, Jon Cecil Walkes
  • 48. CPB Circuit Tirone E. David
  • 50. Operating Technique  Median sternotomy.  CPB established.  TEE flow monitoring: organ malperfusion.  Vent LV via Rt Superior pulmonary vein.  Core cooling ( temp gradient <10o C) to 24o C.
  • 51. Cerebral – renal protection  Cerebral protection: Dexamethasone (8 – 12 mg). Thiopental (7 – 15 mg/kg). Ice packing on head. CO2 flooding (5 - 10 l/m) in operative field.  Renal protection: Mannitol (0.3 – 0.4 g/kg) Furosemide (40 – 80mg).
  • 52. Myocardial protection  Direct ostial cold blood cardioplegia.  Retrograde cold blood cardioplegia.  Topical cooling
  • 53. Management of the distal aorta  Proximal Intimal Tear (PIT) location: Ascending Aorta. Lesser curvature of Arch. Greater curvature of Arch
  • 54. PIT in Ascending aorta / Lesser curve of arch Hemiarch Replacement
  • 55.
  • 57.
  • 58.
  • 59.
  • 60. Management of Aortic Root Predissection Diseased sinuses Diseased sinuses and normal sinuses normal cusps cusps and valve Aortic cusps Valve sparing Composite valve graft Resuspension root replacement root replacement
  • 61. Predissection normal sinus and valve cusps: Mechanism of Aortic Regurgitation
  • 62. Management Of Aortic Root Predissection normal sinus and valve cusps: Aortic valve resuspension
  • 63.
  • 64. Valve sparing root replacement  David procedure and its modifications.  Yacoub
  • 65. Valve sparing root replacement: David procedure and its modifications
  • 66.
  • 67. Valve sparing root replacement: Yacoub’s
  • 69. Composite Valve Graft Root Replacement Bentall and DeBono 1968. Kouchoukos modification. Cabrol procedure
  • 70. Management of coronary artery dissection  Dissection just at the ostia:  Repair with obliteration of false lumen.  Reimplantation of reconstituted coronary ostia as Carrel buttons into graft.  Cabrol II “moustache coronary resconstruction”  Suture ligation of coronary artery with bypass grafting
  • 71. Role of Frozen Elephant Trunk  Dilated distal Aorta with predisposig factors eg Marfans.
  • 72. Post – operative management  Control hypertension. beta blockers calcium channel blockers ACE inhibitors.  Monitor for malperfusion syndrome. - Compression of true lumen by false lumen - Extension of dissection into branch artery with compression of true lumen. - Intussusception of inner wall of aorta into branch artery. - Occlusion of branch vessel by dissection flap
  • 73. Malperfusion syndrome  Extremities: pain / paresthesia / cold  Kidneys: uncontrolled hypertension.  Mesenteric malperfusion: unexplained acidosis / volume loss / tachycardia.  Diagnosis: CT Angiography  Management: fenestration of dissecting membrane.
  • 74. Follow up Time of study Study Indication Before hospital discharge CT or MRI TTE Arteriography All patients Valve reconstruction Suspected malperfusion After hospital discharge 3 months CT or MRI TTE Residual dissection. Valve reconstruction 9 months CT or MRI TTE Residual dissection. Valve reconstruction Subsequent examination Every 6 months CT or MRI TTE Progression of aortic dis Aortic Regurgitation Every 12 months CT or MRI Aortic dia >5cm Every 24 months CT or MRI Aortic diameter <5cm.
  • 75.
  • 76.
  • 77. Type B Aortic Dissection
  • 78. Management strategy  Aim of therapy- Prevent death Prevent irreversible end organ damage.  Optimal treatment strategy- debated ????
  • 81. Approach to type B Dissection Arguments in favour of medical treatment  Medical treatment prevents death in majority.  Operative mortality type B dissection high.  Similar long term outcome of surgically and medically managed patients.  “Complication Specific” approach for Type B Dissection
  • 82. Indications for Intervention  Persistent pain.  Refractory arterial hypertension.  Progression / expansion of dissection.  Aortic rupture / impending rupture.  Impaired distal organ perfusion.  Sizable localized false aneurysm.  Young with CTD- Marfan syndrome without complications.
  • 83. Management Strategy for IMH  Uncomplicated Type B IMH: Medical.  Type B IMH with persistent pain / associated large – deep PAU: high incidence of aortic rupture.  Intervention for complicated Type B IMH
  • 84. Initial Medical Treatment  Goal of medical treatment: Relieve pain. Control blood pressure. Limit extension of dissection.  Extensive monitoring:  ECG / Radial – Femoral arterial line / CVP / Pulse Oxymeter / Foley catheter.
  • 85. Anti impulsive therapy  Target: Mean arterial pressure = 60 – 75mmhg Systolic presure = 100 – 110mm hg Heart rate = 60 – 80bpm  Eliminate Pain: Morphine.  Beta blockade: Esmolol- 500mcg/kg iv bolus 50 mcg/kg/min infusion (max 200mcg/kg/min) Propranolol – 1mg every 5 min to achieve target HR (max 10 mg)  SNP – 20 mcg/min (max 800mcg/min)  Refractory hypertension: ACEI - Enalapril
  • 86. Definitive long term medical management  Oral beta blockers- Labetalol, Metoprolol, Atenolol.  Calcium channel antagonists.  Oral ACEI / ARB Lisinopril.  Hydralizine avoided- Incorporated into mucopolysaccharides of media and weaken aortic wall.
  • 87. Aims Of Intervention (Surgical / Endovascular)  Seal the entry Point.  Seal area of leak (if any).  Establish perfusion to branch arteries.  Expansion of true lumen and obliteration of false lumen.
  • 88. Surgical Principles Acute Type B Dissection No visceral malperfusion Visceral malperfusion Replace the tear point Fenestation Graft replacement with visceral artery reconstruction
  • 89. Surgical Approach  Full CPB  Venous Cannulation- Right Femoral Vein.  Arterial Cannulation- Left subclavian artery. Undissected ascending aorta Descending aortic true lumen  Moderate hypothermia 25 – 28oC.  Open Proximal Anastamosis (OPA) in distal arch under HCA.
  • 90.
  • 91.
  • 92.
  • 93.
  • 94. Management of visceral malperfusion Aortic dissection + Visceral malperfusion Dynamic Obstruction Static Obstruction Visceral artery Visceral artery from true lumen from false lumen Central aortic repair Central aortic repair visceral artery revascularisation
  • 96. Mortality according to indication for surgery
  • 98. Endovascular therapy  Medical management 70% patients- persistent patent false lumen 20 – 30% eventually aneurysmal  Surgical replacement: High mortality – 20 – 30% Visceral ischemia – 30 – 50%
  • 99. Endovascular treatment  Balloon Fenestration.  Stenting  Stent grafting
  • 105.