Aortic Dissection
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  • 1. Aortic Dissection Zahir Rahman MD 10/14/02
  • 2. ED History – 9:55 A.M.
    • 46 y.o AA male with with no pmhx cc: of weakness lower extremities and inability to walk. Pt said 6 to 7 hours prior to arrival, he had sudden onset interscapular and abdominal pain which progressed to weakness.
    • Neurosurgery called by ED staff for acute onset paraplegia.
  • 3. Neurosurgery PE – 10:30 AM
    • VS: 122/70 P: 72 RR: 14
    • Muscle Strength: 2/5 L foot, all other LE muscle strength 0/5
    • Sensory level below T5, diminished but can feel light touch
    • Rectal Sphincter Tone:
  • 4. Neurosurgery A/P
    • W/u for aortic aneurysm/ dissection
    • R/o Spinal Cord compression
    • Continue Solumedrol, send for MRA.
  • 5. MRA
    • Pt. had MRA done at 11:30 A.M.
    • CICU resident called with result at 12:30 A.M.
    • Patient was found to have a Type 1 Aortic Dissection. No Pericardial effusion. No Aortic Regurgitation
    • Dissection from Proximal Aorta to below the Renal arteries.
    • False Lumen was communicating with the Left Renal Artery.
  • 6. RCA RSC LCA INTIMA TRUE LUMEN FALSE LUMEN PULMONARY TRUNK RSC
  • 7. THROMBUS IN FALSE LUMEN TRUE LUMEN
  • 8. FALSE LUMEN LRA TRUE LUMEN
  • 9.  
  • 10. CV Fellow Called: 12:30 P.M.
    • 46 y.o AA male from Liberia – No PMHx woke up at 3 AM with sudden onset 10/10 Anterior Chest Pain (Pressure like) and interscapular pain with radiation down both arms. Over the course of the next 6-7 hours, he developed diffuse abdominal pain, followed by numbness from chest to feet which progressed to bilateral weakness at which point he called for an Ambulance.
  • 11.
    • 12:40 P.M. – pt complaining of CP 5/10 and abdominal pain, but no longer has sensory or motor weakness of lower extremities.
    • PMHx: Pt says he has seen a doctor here and there and his bp was always fine.
    • SHx: denies cocaine/drug use
    • Exsmoker – quit 1 year ago. 10 pack year history
    • FHx: No h/o sudden cardiac deaths. Mother and Father with HTN.
  • 12. PE
    • Vs: BP: R arm: 150/90 L arm: 154/90
    • Neck: No JVD, No Bruits
    • Lungs: CTA b/l
    • CV: RRR, S1,S2 nl, + S4, no murmurs
    • ABD: Diffuse tenderness, no rebound, normal BS.
    • EXT: Pulses equal and symmetric B/L
    • NEURO: No defecits, DTRs’ normal b/l
  • 13. Labs: 7/30/02 9:35 AM
    • Bun/Cr: 29/2
    • AST: 41
    • ALT: 39
    • AP: 70
    • CK: 257
    • MB: 2.4
    • Trop: 0.3
  • 14. EKG
  • 15. Management
    • Pt was immediately bolused with esmolol and titrated gradually to a bp of approximately 122/70.
    • Pt was transferred for surgery at 1:20 PM to SIUH
  • 16. Intraoperative TEE Ascend Aorta
  • 17. Intraoperative TEE – Aortic Arch
  • 18. Descend Aorta – Communication back into true lumen
  • 19. Descend Aorta – Multiple Intimal Flaps
  • 20. Intraoperative TEE
    • NO AI, NO Effusion
    • Proximal Dissection – Not involving sinus of valsalva
    • Concentric LVH
    • Multiple Dissection Flaps in Ascending and Descending Aorta
  • 21. Surgery
    • Dissected Ascending Aorta was dissected and replaced with a #22 mm Dacron interposition graft with a circumferential bypass
    • Pt. was hemodynamically stable post surgery.
    • Troponin at 21:51 - 1.28 (cutoff 0.5 for AMI)
  • 22. Course:
    • Labs:
    • 7/31: CK: 666 / 3563
    • 7/31: Troponin: 4.5
    • 7/31: MB: 25/ 27.9
  • 23. Hospital Course
    • Pt. was in ICU and became septic, ARF progressed to ESRD, Acute Liver Failure, developed mesenteric ischemia
    • Pt. was managed with pressors (Levophed) and was made DNR by family.
    • On 8/10: CT scan showed large pericardial effusion and dissecting aneurysm of the thoracic aorta.
        • Bun/Cr: 155/12.1
        • AST/ALT: 2360/1500
        • Patient coded, went into EMD and died.
  • 24. Aortic Dissection Zahir Rahman MD 10/14/02
  • 25. Classifications
    • Acute: when diagnosis is made within 2 weeks of initial onset of symptoms
    • Chronic: >2 weeks of symptoms
    • One third of patients fall into the chronic category.
  • 26. Common Classification Systems Braunwald
  • 27. Common Classifications of Aortic Dissection
  • 28. Variants of Aortic Dissection
  • 29. Predisposing Factors
    • Men/Female Ratio 2:1 to 5:1
    • Chronic Systemic HTN (62-78%)
    • Proximal Dissection:
      • Peak age 50-55 years
      • MC on initial presentation to have HTN 70%
    • Distal Dissection:
      • Peak Age 60-70 years
    • Direct Iatrogenic Trauma: 5% of cases
    • Indirect Trauma (eg sudden deceleration)
  • 30. Predisposing Factors
    • Hereditary Connective Tissue Diseases
      • Marfan Syndrome
      • Ehler Danlos Syndrome
    • Chromosomal Aberrations
      • Turners Syndrome
      • Noonans Syndrome
    • Aortic Diseases
      • Aortic Dilatation
      • Aortic Aneurysm
      • Anuloaortic ectasia
      • Aortic Arteritis
      • Bicuspid Aortic Valve
  • 31. Predisposing Factors
    • Females in 3 rd Trimester Pregnancy or 1 st Stage of Labor
    • Case Reports of:
      • Cocaine (Perron et al. Am J Emerg Med 1992)
      • Abrupt Discontinuation of Beta Blockers (Eber et al. Cardiology 1993; 83:128-131)
      • Probably Secondary to rapid rise in first derivative of pressure (dp/dt) on aortic wall.
  • 32. Cystic Medial Degeneration
    • Medial Degeneration predisposes dissection by decreasing cohesiveness of layers of aortic wall
      • More extensive in patients with:
        • HTN
        • Marfan Syndrome
        • Bicuspid Aortic Valves
      • But, even in other causes of dissection, medial degeneration is much greater than expected with normal aging.
  • 33. Pathogenesis
    • Intimal tears occur in regions of aorta subjected to greatest dp/dt and pressure fluctuations.
    • MC sites for initiation of intimal tear:
      • Ascending Aorta
      • 1 st Portion Descending Aorta
  • 34. Proposed Mechanism of Initiation of Dissection
  • 35. Natural History
    • Hydrodynamic forces propagate the dissection until rupture occurs either:
      • Back into the lumen of the aorta
      • Through the adventitia (causing death)
    • Mortality Rates if untreated:
      • 1-3% per hour
      • 90% within 3 months
    • Death usually caused by:
      • Acute aortic regurgitation
      • Major branch vessel obstruction
      • Aortic Rupture ( into pericardium, L pleural cavity, or mediastinum)
  • 36. Symptoms of Aortic Dissection According to a report on 464 patients from the International Registry of Acute Aortic Dissection. (Hagan et al. Jama 2000; 283:897-903)
  • 37. Clues to Proximal Dissection
    • Substernal chest pain
    • Neck, jaw, throat or face pain
    • Aortic Insufficiency
    • Decreased pulse or blood pressure in R arm
    • Decreased R carotid pulse
    • Pulse abnormalities are seen in 50% of proximal dissections
    • Ischemic EKG changes
    • AMI – Inferior (5%)
    • Marfans Syndrome
    • Hypotension
    • Syncope – 12%
    • CVA – 5-10%
  • 38. Aortic Regurgitation
    • AR in 18-50% cases
    • Diastolic murmur reported in 25% pts.
    • Acute Severe AR – 2 nd MC cause of death AD.
    • Murmur can wax and wane and intensity will vary with BP
    • 3 possible mechanisms for acute AR in dissection
    Hagan et al. IRAD. JAMA 2000;283:897-903.
  • 39. Mechanisms of Aortic Regurgitation in Proximal AD
  • 40. Hypotension with Proximal Dissection
    • Cardiac tamponade
    • Severe acute Aortic regurgitation with cardiogenic shock
    • Myocardial Infarction with resultant LV systolic dysfunction – usually RCA.
    • Acute Aortic Rupture.
    • Pseudohypotension by involving brachiocephalic artery
  • 41. Predicting Death in Type A Aortic Dissection (Mehta et al. Circulation. 2002;105:200-206)
    • Evaluated 547 patients enrolled in IRAD from Jan 1996 to Dec 1999.
    • In hospital mortality was 32.5%, 26.9% in surgically treated patients vs. 56.2% in medically treated patients
    • Rupture accounted for 33.3% of deaths
    • Neurological defecit - 13.9 % of deaths
    • Visceral ischemia/kidney failure (11.5%)
    • Cardiac Tamponade (7.9%)
  • 42. Clinical Variables Associated with High In-Hospital Mortality Rates. (Mehta et al. Circulation. 2002;105:200-206)
  • 43.
    • Interscapular pain
    • HTN less commonly associated about 35%
    • Left Pleural effusion
    • Pulse defecits are less frequent about 15%
    • Usually involve femoral or left subclavian
    • Spinal Cord Ischemia (10%)
      • Transverse Myelitis
      • Paraplegia
      • Quadriplegia
    Clues to Distal Dissection
  • 44. Clinical Prediction of Acute Aortic Dissection (von Kodolitsch et al, Arch Intern Med 2000;160:2977-2982)
    • Jan 1 1988 to Dec 31, 1996 41,495 presented to ED at Univ Hosp Eppendorf, Hamburg, Germany.
    • 250 constituted study group
      • CP, back pain or both within last 2 weeks
      • ACS or another diagnosis excluded
      • Of remaining patients, considered if suspicious for AD by 2 ED physicians.
    • 26 Clinical Variables to find any independent clinical predictors of dissection.
  • 45. (von Kodolitsch et al, Arch Intern Med 2000;160:2977-2982)
  • 46. (von Kodolitsch et al, Arch Intern Med 2000;160:2977-2982)
  • 47.
    • Aortic Pain: immediate onset, tearing or ripping character or both.
    • Mediastinal Widening
    • Pulse Differentials
    (von Kodolitsch et al, Arch Intern Med 2000;160:2977-2982)
  • 48. EKG
    • EKG: 1/3 exhibit LVH
    • EKG is important to rule out any ischemic changes or MI which would lead to an alternate diagnosis
    • EKG may display infarction
    • EKG – usually shows nonspecific ST-T wave changes.
  • 49. CXR
    • Widened Mediastinum suggestive but not diagnostic.
    • Seen Anywhere from 50% in most reports.
    • And in one report of 236 cases as high as: 90% (Spittell, Mayo Clinic Proc 68:642,1993.)
  • 50. Normal Aorta in CXR 3 years Prior
  • 51. Enlargement of the Aortic Knob A Case of Proximal Aortic Dissection
  • 52. Comparison of Imaging Modalities (Braunwald)
  • 53. Aortography
    • Sensitivity: 86-88%
    • Specificity: 75-94%
    • False negatives if intramural hematoma or thrombosis of false lumen
    • Good at detecting branch vessel involvement and Coronary Artery invovlvement.
  • 54. Thoracic Aortagram in AP view
  • 55. CT
    • Sensitivity 83-94%
    • Specificity of 100%
    • Spiral CT increased sensitivity to 96%
    • Non-invasive with rapid availability (MC initial imaging modality in IRAD pts)
    • Needs contrast to be effective
    • Disadvantages:
      • Cannot Detect AR
      • Does not detect Site of Intimal Tear well
      • Cannot detect Coronary Artery Involvement
  • 56. Contrast-Enhanced CT at level of Ventricle
  • 57. Left Anterior Oblique View Contrast Enhanced CT Intimal Flap originates beyond Left SC Artery
  • 58. TEE
    • Non-Invasive, Performed Quickly at Bedside
    • Sensitivity 98 – 99%
    • Specificity: 94 – 95% (biplane or multiplane TEE)
    • Good at detecting Coronary Artery Involvement
    • Disadvantage: does not evaluate distal ascending aorta and proximal arch (because of the interposition of air filled trachea and main stem bronchus)
  • 59. Descend Aorta – Communication back into true lumen
  • 60. MRI
    • Gold Standard for Diagnosis
    • Sensitivity and Specificity of 98-100%
    • Disadvantages:
      • Limited Availability
      • Limit the presences of monitoring and support devices
      • Relatively CI in unstable patients.
      • CI:
        • Pacemakers
        • Certain types of vascular clips
        • Older metallic heart valves
  • 61. RCA RSC LCA INTIMA TRUE LUMEN FALSE LUMEN PULMONARY TRUNK RSC
  • 62. Practical Assessment of Imaging Modalities
  • 63. Smooth Muscle Myosin Heavy Chain
    • AD causes extensive damage to the smooth muscle cells of the media releasing smooth muscle heavy chain into the circulation.
    • Serum Values:
      • 95 AD pts: 22.4 +/- 40.4 ug/L
      • 131 Volunteers: 0.9 +/- 0.4 ug/L
      • 48 AMI pts: 2.1 +/- 1.6 ug/L
      • 33 pts presented within 3 hrs of onset of AD: 51+/-52.3 ug/L
    • Serum Levels > 10 ug/L showed 100% specificity for Aortic Dissection.
    (Suzuki et al. Circulation 1996;93:1244-1249)
  • 64. MANAGEMENT
    • Therapy is targeted at halting the progression of the dissection
    • It is the course of the tear not the tear itself that leads to compromise of vasculature or rupture
    • Goal:
      • Reduction of SBP (100-120)
      • Dimunition of dp/dt (reflects force of LV ejection) through use of a beta blocker.
  • 65. Sodium Nitroprusside
    • Sodium Nitroprusside for acute reduction starting 10 – 20 mcg/min and titrated upward
    • Must initiate BB prior to instituion of Nipride due to its effect on raising dP/dT when used alone
    • Adding IV BB prior until desired effect such as HR 60 – 80s (propranolol 1 mg Q 3-5 minutes max 10 mg)
    • Then Q 4-6 hrs at a dose of 2 – 6 mg
  • 66. Labetolol
    • Effectively lowers dP/dT as well as reducing arterial pressure
    • Initial dose is 20mg followed by 40 to 80 mg Q 10 – 15 minutes (max 300mg IV)
    • Once BP controlled maintenance by continuous infusion
    • Infusion at 2mg/min titrating up to 5 –10 mg/min
  • 67. Esmolol
    • Ultra short acting BB for those with labile blood pressure or those that are surgical candidates. (Long acting medications may affect intraoperative bp management)
    • Load with 500 mcg/kg bolus
    • Infusion starts @ 50mcg/kg/min titrate to 200 mcg/kg/min for control
    • Controls dP/dT as well as blood pressure
    • Can be used in patients with uncertain risk for bronchospasm
  • 68. Contraindications to BB
    • Patients with severe Brady or AV block or bronchospasm BB may be CI
    • Calcium channel blockers specifically Cardizem and Diltiazem can be used if bronchospasm
    • Provide negative Inotrope and Chronotropic effects
    • If Dissection involves the renal arteries patients may develop high renin HTN
    • Treat with IV enalapril
  • 69. Other Considerations
    • Hypotension must ensure if its true or false
    • May be secondary to compromise of artery by dissection (pseudohypotension) so check both arms
    • If true hypotension may indicate rupture or tamponade
    • Fluids first then use levophed (norepinephrine) or phenylephrine (neosynephrine)
    • Dopamine should be avoided since it can raise dP/dT unless used at low doses for renal perfusion
  • 70. Cardiac Tamponade
    • Pericardiocentesis may be harmful
    • Retrospective study of 7 patients (6 hypotensive, 1 normotensive)
      • 3 of 4 with successful Pericardiocentesis died w/in 5-40 minutes of the procedure due to acute EMD
      • 0 of 3 w/o pericardiocentesis died prior to surgery
    Isselbacher et al, Circulation 1994: 90;2375-2378.
  • 71. Cardiac Tamponade
    • Increase in Intraaortic pressure after pericardiocentesis causing a reopening of the closed communication between the false lumen and pericardial space, leading to lethal cardiac tamponade.
    • Prudent to do Pericardiocentesis in AD only if in EMD or marked hypotension, and aspirate only enough pericardial fluid to raise bp.
  • 72. Indications for Definitive Surgical and Medical Therapy in AD
  • 73. Surgical Repair of Proximal Dissections
  • 74. Surgery
    • Preop mortality 3% if expedited and increases to 20% if prolonged
    • Objectives of surgery are to remove the most severely damaged segments of the aorta and to obliterate the false lumen by suturing the most proximal segment
    • Long term survival is not effected by failure to resect intimal tear (Miller et al. Journal Thoracic CV Surg 78:365;1979.
  • 75. Surgery with AR
    • In certain cases valve can be preserved by removing tear and resuspending leaflets
    • It avoids long term anticogulation
    • However if repair is unsuccessful or if patient had pre-existing valvular disease need AVR
    • In patients with Marfans need AVR
  • 76. Endovascular techniques
    • For treating high risk patients ( i.e. renal or visceral involvement) which carry a high operative mortality (>50%)
    • Balloon fenestration flow back to true lumen decompressing false lumen
    • Stenting of branch vessels compromised by dissection.
    • Intraluminal stent – grafts to close off the site of entry into false lumen and promote thrombosis.
    • 30 Day mortality for Proximal Dissections of intraluminal stents reported around 25%.
    • At present, about 13% of patients with AD get endovascular stenting.
  • 77. Long Term
    • Survival in PAD s/p repair who survive their hospital stay is:
      • 65-80% at 5 years
      • 50% at 10 years
    • MC cause of death in long-term survivors:
      • Rupture of the Aorta due to subsequent dissection or aneurysm formation.
    • Long Term Management:
      • Optimal BP control with Beta blockers
      • Periodic clinical and imaging assessments of Aorta
  • 78. Intramural Hematoma (H)
  • 79. Crescenteric Hematoma that does not Enhance confirming a intramural Hematoma that does not communicate with the Aortic Lumen.
  • 80. Evolution of a Penetrating atherosclerotic Ulcer of Aorta