1. CBP: Aortic Dissection

2. Case
A 64 year old man presents to the emergency department complaining of sudden sharp 10/10 anterior chest pain with no radiation. His history is remarkable for hypertension, and type II diabetes, but no coronary artery disease or risk factors for venous thromboembolism. His BP is 180/100 on the left, and 162/80 on the right, with no pulsus paradoxus. HR 110, RR 22, O2 sat 96% on r/a, T Physical exam shows the patient to be in obvious discomfort, with a clear chest, normal heart sounds, no murmur, and a normal JVP. There are no focal neurological deficits. The electrocardiogram shows evidence of LVH, but no other abnormality. The chest x-ray is on it’s way.

3. Question 1
Please go over the ddx of chest pain

4. Differential diagnoses of Pt admitted to hospital with acute chest discomfort
G.I. disease
42%
Ischemic hearth disease
31%
Chest wall syndromes
28%
Pericarditis 4%
Pleuritis/Pneumonia 2% PE
Lung cancer
1.5%
Aortic aneurysm 1%
Aortic stenosis
Herpes zoster

5. Approach to the patient with chest discomfort
Stable/unstable
Symptoms
Physical examination
ECG
Lab works
Imaging

6. The importance of hystory
Duration of symptoms (i.e. angina 2-10 min, AMI > 30 min, aortic diss abrupt onset)
Quality of symptoms (i.e. AMI heaviness, sharp in pericarditis, ripping sens in AD)
Location (i.e. retrosternal with irradiation in AMI,interscapular for AD)

7. Physical examination General Appearance Vital signs
may suggest seriousness of symptoms.
Vital signs
marked difference in blood pressure between arms suggests aortic dissection
Palpate the chest wall
Hyperesthesia may be due to herpes zoster
Complete cardiac examination
pericardial rub
signs of acute AI or AS
Ischemia may result in MI murmur, S4 or S3
Determine if breath sounds are symmetric and if wheezes, crackles or evidence of consolidation

8. Troponin CK-MB Myoglobine
Labs
Troponin
CK-MB
Myoglobine

9. Imaging CXR (i.e. pneumonia, pnx, AD) CT (i.e. AD, PE)
TEE (signs of pulmonary hypertension, AD)
Aortogram (AD)

10. Question 1
Describe the most common classification systems of aortic dissection (Todd)

11. Classification systems for Thoracic Aortic Dissections
Time course: Acute vs. Chronic
Anatomical: Ascending, descending or both
Stanford:
Type A: Involving the ascending aorta (with or without descending aortic involvement)
Type B: Involving only the descending aorta
De Bakey:
I: Ascending and Descending aorta
II: Ascending Aorta only
III: Descending Aorta only

13. Question 2
Describe the pathophysiology of aortic dissection. (Ibrahim)

14. Pathophysiology of AAS
AAS=Acute Aortic Syndrome = Aortic Dissection (AD) (70%), Intramural Hematoma (IMH) (25-30%), Penetrating Atherosclerotic Ulcerations (PAU) (<5%). All may coexist together, esp. IMH and AD

15. Classic Aortic Dissection (AD)
3 layers of the large arteries, intima (innermost), media (middle), and adventitia (outermost). Trauma to endothelium in the intima layer (mostly chronic HTN+aging which leads to degeneration of the elastin in media, hence decreased wall ealsticity, increased wall stress and traumatic injury (La Place Law: Wall stress directly proportional to BP and radius and inversly proportional to wall thickness) --> endolthelial injury (entry point at the highest rate of rise of BP, dP/dT), flowing blood through into the diseased media, creating (False lumen), and leaving the original (True lumen), and (Intimal flap) in between.

16. -True Lumen: Round or oval, usually smaller, can be surrounded my calcified intima, permanent systolic pressure (doppler), for type B AD it feeds celiac A, SMA, and Rt Renal A.
-False: Crescent, usually larger, usually on the outer curvature of the Aorta in Type A, delayed contrast filling (20-60 sec), wedge around the true lumen and can loop around is a spiral pattern and form CT contrast image called (bird beak), thrombi and cobwebs (secondary flap, reminants of media collagenous materials) are common, Lt Renal A usually originates from False lumen in Type B AD.

17. Antegrade Propagation of AD
-According to the entry points. Note that re-entry or fenestrations can occur.
-Beside the progression to the branches (Brachiocephalic and carotids, subclavians, abdomenal, renal, and iliacs)

18. Retrograde Propagation (Type A)
-Pericardial effusion, coronary dissection, and aortic insufficiency. Also hemomediastinum, hemothorax and hemoperitoneum may occur.

19. -Green arrow is the entry point, Yellow is the False lumen
-Green arrow is the entry point, Yellow is the False lumen. Going from up downward, see how the false lumen wedge around the true lumen in spiral pattern.
-The lumen that is usually surrounded by another lumen is almost always the True lumen (Image 6)
-Image 7 shows the beak sign of the False lumen.

20. -Upper Image: brighter smaller True lumen (delayed filling of False lumen). See thrombus within false lumen
-Yellow arrow shows cobweb within False lumen.

21. Intramural Hematoma (IMH)
-Intramural bleeding within vasa vasorum of the media layer, I.e intact intima!
-Classified the same way as AD. Male=Female, unlike in AD.
-Mostly self-resolving (80%, esp if <2cm thick). Does not typically wedge around the True lumen in spirals like in AD. Upper image shows hyperdensity due to NECT study (can be mistaken as AD with thrombus in the false lumen). Lower images are CECT. Calicifications surround (like in AD) the True lumen.
-Higher mortality if >2cm think, >5cm length of Aorta involved, complicated by rupture into pericardium or pleura. Other complications include progression into AD in 18-47% of cases (worse if associated with PAU), rupture, formation of pseudoaneurysms.

22. Penetrating Atherosclerotic Ulcerations
-Always associated with athermatous plaque (mostly calcified) and within the descending aorta w/o intimal flap, usually multiple and smaller than AD and IMH, so Rx if required is usually endovascular. Patients almost always have atherosclerosis elsewhere, like CAD, CVD, and PAD, so although rarely cause classical AD, but patient may die of other causes of vasculopathy. Most common cause of saccular aneurysm, and in 40-50% may rupture. If associated with IMH then worse prognosis.
-Classified in the same way as AD.

23. -Already discussed above!

24. Question 3
List the major predisposing factors for aortic dissection. (Noemie)

25. Risk Factors
Most common RF
Peak incidence in 60-70s
M:F =2-5:1
Found in 7-14% of all dissection
Most common in 3rd trimester
Iatrogenic: 5% of all cases, Cardiac cath, AVR. aortic isthmus

26. Question 4
List the most common signs and symptoms of aortic dissection, and highlight the ones which have shown the best positive and negative likelihood ratios. (Erik)

27. Aortic Dissection Case Based Presentation: Utility of Hx, P/E, and CXR
Complications of therapy

28. List the most common signs and symptoms of aortic dissection, and highlight the ones which have shown the best positive and negative likelihood ratios.

30. Klompas, JAMA, 2002

34. The “naked” truth
Majority of data derived from retrospective chart reviews.
Significant selection bias – falsely inflating both sensitivity and specificity.
Do not reflect contemporary practice (lower threshold to scan with 64-MDCT, triple rule-out, etc.)

35. History
Most patients with [spontaneous] thoracic aortic dissection have severe pain of abrupt onset.
The absence of pain of sudden onset substantively decreases the probability of dissection (negative LR, 0.3; 95% CI, ); however, the study design of the reports precludes accurate assessment of the sensitivity and specificity of these features.

36. Physical
Pulse deficits (positive LR, 5.7; 95% CI, ) or focal neurological deficits (positive LR, ) greatly increase the likelihood of thoracic aortic dissection in the appropriate clinical setting.
The presence or absence of a diastolic murmur is not useful (positive LR, 1.4; negative LR, 0.9).

37. CXR
A normal aorta and mediastinum on chest radiograph helps exclude the diagnosis (negative LR, 0.3; 95% CI, ) but no particular radiographic abnormality is dependably present.

38. Bare bottom…
Clinical history, examination, and radiography can help rule in aortic dissection but are not sufficiently accurate to rule out the disease.

39. Question 5
List the main complications associated with acute aortic dissection, and briefly explain how they occur. (Neil)

40. Q: List five complications arising from aortic dissection.

41. Royal college question:
List 5 major complications of aortic dissection

42. Main complications 30 % get ischemic complications
In type I mortality due to complications increases 1% per hour
Etiology
Dynamic obstruction
Occlusion of true lumen by false lumen
Static obstruction
Compression, disruption, thrombosis

44. List of main complications
Tamponade
Acute severe Aortic insufficiency MI
CVA
Spinal infarct/paraplegia
Aortic rupture
Mesenteric/Renal/Limb ischemia
Pseudoaneurysm

45. Acute Severe Aortic Insuficiency
Widening of sinotubular junction causing improper coaptation
Diastolic leaflet prolapse from detachment of aortic leaflet commisural attachment
Intimal prolapse
Murmur is typically heard over R sternal border

46. Acute MI Occurs in 5 % of Type I dissections
Usually involves R coronary
Often presents as complete heart block or inferior /R sided MI
Mortality if you thrombolyse approaches 70%

48. Neuro complications CVA Spinal 10% of type I’s Carotid occlusion
5-10% of dissections present with syncope
Spinal
Intercostal arteries
Artery of Adamkiewicz
Can recover if treated early

49. Case cont’d…
The patient’s chest x-ray shows a wide mediastinum. In the meantime, the patient reports that he is in agony, and his BP rises to 200/120 on the left.

50. Question 6
What is the sensitivity and specificity of CXR for aortic dissection? List three CXR findings associated with the condition. (Federico)

51. CXR
Sensitivity 60-90%
Specificity 70%

52. CXR FINDINGS Widening of the mediastinum (63% type A, 56%type B)
Doubled shadow of the aortic wall
Disparity of the size in the ascending and descending aorta

53. Question 7
List the various modalities (other than chest x-ray) that can be used to diagnose aortic dissection, noting the sensitivity/specificity, advantages, and limitations of each (Omar)

54. Imaging modalities TTE, TEE, CT, Aortography
Perform better in high risk populations

55. Aortography Specificity/Sensitivity: 94% / 88% Pros: Cons:
Identify site of origin, branch artery involvement, AI, coronary extension
Cons:
Lengthy, large dye load, $$
invasive,
May fail to identify intramural hematoma

56. Computed Tomography Sensitivity/Specificity: 83-100% / 87-100%
Probably even better with newer generation, helical, multislice scanners
Accuracy may approach 100%

57. Computed Tomography Can identify: Non-invasive Cons:
intimal flap, branch vessel involvement, extent of dissection, false lumen patency, aortic size, pericardial effusion, end organ ischemia
Non-invasive
Cons:
Contrast material, cannot detect AI or visualize coronary artery dissection

58. MRI Sensitivity/Specificity: 95-100% / 98% Pros:
Less nephrotoxicity (Gadolinium)
Non invasive
Excellent visualization
New techniques allow for fast scan times (4 mins)

59. MRI
Cons:
Lengthy
Availability
Metallic hardware
Difficult to monitor

60. ECHO - Transthoracic Sens/Spec: 77-80% / 93-96% Pros: Cons:
Fast, inexpensive, available
Cons:
Operator dependant
Can only evaluate the aortic root and arch
Distal ascending Ao and descending Ao not assessed
Low sensitivity

61. ECHO - Transesophageal
Sens/Spec: 100% / 95%
Pros:
Rapid
Bedside test

62. ECHO - Transesophageal
Cons:
Cannot visualize abdominal aorta
Sedation
Relative CI’s: Chest trauma, varices, strictures, tumours
“Blind spot”
Right main stem bronchus obscures visualization of part of ascending aorta

63. Case cont’d
You’re now convinced this guy is dissecting, and decide to start treatment while waiting for the chest CT.

64. Question 8
Outline the principles behind medical management of aortic dissection, and explain the physiologic rationale of “anti-impulse” therapy. (Todd)

65. It’s not just blood pressure…it’s poor impulse control!
dP/dt
Change in pressure per
Unit of time

66. Anti-impulse therapy
Negative inotropy (and thus rate of rise of blood pressure, as well as mean and peak systolic pressure)
Negative chronotropy (fewer peak systolic pressures for the vulnerable vessel to experience)
Alpha blockade (prevent compensatory vasoconstriction)
Goal blood pressure: as low as possible without inducing organ failure….Systolic BP of 100, or MAP of
No great evidence; this would be a tough population to ethically randomize.

67. Pharmacologic options: with invasive monitoring
Esmolol: Beta blocker, bolus and infusion options
1 mg/kg (usually about 80 mg) bolus
mcg/kg/min
Labetalol: alpha-antagonistic properties
20 mg IV bolus (may require up to 80 mg over 10 min)
0.5-6 mg/min infusion
Propranolol: 1-10 mg bolus, followed by 3 mg/hr

68. Others
Nitroprusside: beware cyanide toxicity (at about 500 mcg/kg). Do not use without beta-blockade (reflex tachycardia)
0.5 mcg/kg/min, titrate in 0.5 increments to max 10 mcg/kg/min
ACE inhibitors may be used, but given the high risk of renal failure, and unreliable gut function depending upon the course of the dissection, they would not be plan A.
For patients who cannot tolerate beta blockers, non-DHP calcium channel blockers (verapamil or diltiazem) are viable options.

69. 4. Quit eating fast food and check into rehab. Again.

70. Case cont’d
You start an esmolol infusion and order morphine for his pain. You insert an arterial line into his left radial artery and decide to walk over to CT to talk to the radiologist.
On your way back from CT, you notice that the patient’s pressure is now 87/68 with a heart rate of 120, and large respiratory variations. When you ask the nurse how much esmolol the patient is on she tells you that she only gave the morphine before his pressure dropped.

71. Case cont’d
On exam, the patient appears confused, has distended neck veins, muffled heart sounds, and is peripherally cool. You put the echo probe on his chest and note a moderate-sized pericardial effusion with right atrial and ventricular diastolic collapse. You order a bolus, ask for a cardiac needle, and call the cardiac surgeon who organizes the OR and intraop TEE, and strongly advises against pericardiocentesis.

72. Question 9
Explain why pericardiocentesis may worsen outcome in cardiac tamponade secondary to proximal aortic dissection. (Neil)

74. BUT, not everyone dies SO….
If open communication with aortic root then pressure rises quickly and results in PEA and pericardiocentesis likely useless
BUT, not everyone dies SO….
Blood in pericardium leaks back through false lumen
Communication in some cases is transient
Stops due to thrombus or intimal flap

75. Pressure is the key
As tamponade increases the pressure gradient between the false lumen and the pericardium decreases which results in stasis and thrombus formation.
Tamponade also compresses the ventricles decreasing BP and dP/dT which reduces propagation of dissection

76. So why is a needle bad? By releasing tamponade you
Increase BP and dP/dT which can worsen dissection
Increase the gradient between the false lumen and pericardial space which may release thrombus or flap and result in an open communication with aorta
Both result in PEA which is usually non recoverable

77. Summary If stable, get to OR ASAP
If unstable, do pericardiocentesis, but consider only removing enough blood to maintain hemodynamic stability until the OR

78. Question 10
In what settings may it be preferable to delay or completely forego surgery in type A dissections? (Noemie)

79. Type A dissection
Ascending aortic dissection --> surgical emergency
Mortality 90% at 2 weeks if treated non-surgically 1
Most common cause of death in Int Reg of A.A.D. was aortic rupture and visceral ischemia
Circulation 2000; 102(19Suppl3):248-I252

80. Contraindications Stroke Relative contraindication
concerned about transformation into hemorrhagic stroke with anticoagulation and reperfusion
Ann Thorac Cardiovasc Sur 2009, 15(5):

81. Contraindications Delayed presentation: 48-72HR
Can optimize clinical condition prior to surgery
Observational 195 pts at Yale. Group A: Median 8.2 days to surgery.
Ann Thorac Surg 2007;83:

82. Contraindications Prior AVR Can operate semi-electively
Protected against AI
“Dissection cannot cross a
suture line” 1
RCA is protected by suture
Adhesions decrease chance of free rupture in pericardial sac
1. Ann Thorac Cardiovasc Sur 2009, 15(5):

83. Contraindications Comorbidities: Age, ARF, shock, redo surgery
If high risk surgery , could consider medical management
Ann Thorac Surg 2007;83:

84. Question 12
What are the indications for intervention in type B aortic dissection? (Ibrahim)

85. Indications for Intervention in Type B

86. Involvement of side branch compromising vital organ perfusion
Persistent Chest Pain
Involvement of side branch compromising vital organ perfusion
Impending rupture (Rapid aortic expansion, periaortic hematoma, hemomediastinum)
-In type B, must weigh risk vs benefit before proceeding with Sx, because mortality with medical Rx alone is 20% (higher with paraplegia (100%), hypotension/shock (67%, OR 24), aortic rupture (53%), leg ischemia (33%), absent chest/back pain (OR 3.5), side-branchvessel involvement (OR 3), renal A (50-70%), mesentric vessels (83%)). Mortality with surgery is 30% (higher in the last two (renal and mesentric involvement, 50-88%). Hence, still somewhat ill defined for Type B AD what’s the optimal Rx!, and thus, endovascular interventions may be suggested for lower mortality, but further studies needed to identify outcomes and clarify indications in larger numbers.

87. Endovascular Interventions
Branch vessel stent placement,
Percutaneous Aortic balloon Fenestration (PAF),
Aortic stent placement,
Stent-graft placement over the intimal entry tear restores normal blood flow in the true lumen and induces thrombosis of the false lumen
-1 and 2 will help in case of vital organ compromise d/t branch vessel involvement, esp if 4 can’t be performed due to large entry, failure to thombose completely, or very close to vital branch. 2 can be done within the aortic flap to decompress the false lumen if can’t be completely obliterated for same reasons to prevent re-expansion.

88. Indications for PAF (1) Mesentric ischemia;
(2) Renal failure or pain due to renal artery obstruction;
(3) Severe renovascular hypertension, which is difficult to control medically secondary to renal artery obstruction;
(4)Paraplegia or paraparesis due to spinal artery involvement;
(5) severe peripheral ischemia with rest pain or severe claudication
-All those are caused by due to obstruction of the feeding arteries by a flap or extension of the false lumen into the origin of the artery. For the latter, stent placement within the False lumen can be considered, usually using TEE or IVUS.
-For stents, Success rates %, 30 days mortality 25%. Long term outcomes are lacking, and largest study for PAF is only 40 pts (Hartnell and Gates, 2005)
-Advantages: (Based on retrospective data. Note there is no head to head prospective study for open vs EV Sx): Shorter time and less invasive, decreased LOS, ICU, lower short term mortality, less post-op complications including pulmonary, cardiac, renal, and neurologic, and downstream emblization. Eggebrecht et al showed only 14-18% of those complications , with 2 years survival approaching 90%, suggesting centers with better experience (>20 cases) have better outcomes. Failure to completely thrombose False lumen (in 25% of cases) may lead to re-expansion and dissection distal to the stent, hence close f/u +/- adjunctive intervention warranted!

89. Pawan et al, Ther Adv Cardiovasc Dis, 2008

90. Case cont’d
The patient goes to the OR where the TEE shows a dissection of the proximal aorta with mild aortic insufficiency, and a pericardial effusion with evidence of tamponade physiology. An urgent median sternotomy is performed and a tense pericardium is noted. After the patient is placed on cardiopulmonary bypass, the pericardium is opened, revealing a substantial amount of organized thrombus and blood. Further examination reveals a short, circumferential dissection of the proximal ascending aorta (see figure).

92. Case cont’d
The aortic root and valve were replaced with a stentless bioprosthetic composite graft, and the patient comes off-pump easily. The CSICU is full, and you agree to accept the patient to the ICU post-op.

93. Question 12
What are the main complications that occur post thoracoabdominal aortic surgery? (Erik)

94. Complications following Thoracoabdominal aneurysm repair by system involved

95. Respiratory Failure
Although there is continued focus on spinal cord ischemic injury and postoperative renal failure, postoperative respiratory failure remains the most commonly reported complication in the many published series.
Multiple etiologies: lung isolation, post-thoracotomy, diaphragmatic injury, phrenic nerve injury, TRALI, ARDS, etc.

96. Renal Failure Pre-AKIN/RIFLE classification.
In one analysis aortic cross-clamp time >100 minutes was the single intraoperative variable associated with postoperative renal failure (Kashyap et al., 1997).
Intraoperative hypotension (SBP <70 mm Hg for > 10 mins) trended toward significance with regard to postop renal failure, but was only significant in association with perioperative death.
Patients who experienced postoperative renal failure had an approximately 10-fold increased risk of perioperative death.

97. Neurological Events
Spinal cord injury of any sort remains one of the greatest fears after thoracoabdominal aneurysm repair.
Spinal cord injury is divided into immediate deficits and delayed deficits. Delayed-onset deficits continue to occur in some 10% of patients, and although these are often partial and reversible and with acceptable functional outcomes, continued vigilance to perioperative care, especially the avoidance of hypotension.

98. Cardiovascular Events
Cardiovascular complications occur in ~14% of patients:
myocardial infarction 4%
arrhythmia 8-10%
congestive heart failure 2%
unstable angina <1%
Standard clinical management.

99. Question 13
How would you manage a patient with signs of paraplegia post-thoracoabdominal aortic surgery? (Omar)

100. Paraplegia Nothing earth shattering here…
Try to correct, or at least limit, amount of ischemia to the cord
Increase MAP
Decrease spinal ICP

101. Paraplegia
Increase MAP till neurologic recovery is seen or limit of MAP reached
Safe upper limit of MAP defined by surgeon
Volume resuscitate
Transfuse, as needed
Liberal use of inotropic support
Esp with neurogenic shock
May require high doses

102. Paraplegia Lumbar CSF drains ICP goal of 8 – 12 Cap at 12 – 24hrs
Remove at 36 – 48 hrs