Aortic Dissection - Yudi Her Oktaviono, MD, PhD, FIHA.pdf

8/18/2019 Aortic Dissection - Yudi Her Oktaviono, MD, PhD, FIHA.pdf

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Aortic Dissection

Kriswanto , MD

Yudi Her Oktaviono , MD. PHD

Departement of cardiologyDr. Soetomo General Hospital - Airlangga University

Surabaya - indonesia


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Historical Note

• Recognized since 16 th century.

• Lannaec (French physician) introduced term Dissection aneurysm in 1819.


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• King George 2 of Great Britain died (october 25,1760) while training on the

commode and was the first well documented case of an aortic dissection.


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Historical Note

• First successful outcome of modern treatment of aortic dissection was attributed to

Dr. DeBakey in his report, 1955 and later he devised a classification that is widely

used today as Debakey classification.


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Anatomy of aorta


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Overview of vessel histology

Tunica intimaendothelium

basement membraneinternal elastic lamina

Tunica mediacircular smooth muscle

external elastic lamina

Tunica adventitia

endotheliumbasement membrane

ARTERY VEIN

CAPILLARY


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Large or elastic arteries

A = tunica intima (interna) B = tunica media C = tunica adventitia (externa)

Aorta–section – H&E – 4x objective


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arrowheads = elastic fibers arrows = nuclei of smooth muscle

Aorta–section – H&E– high magnification

With H&E, elastin fibers and smooth muscle cells are hard to discern. Underhigh power, focus up and down with the fine focus knob, and look for fibersthat are birefringent (they look like they glow). These are elastin fibers.


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Verhoeff ’s stain is used to visualize elastin fibers because it stainsthem purple-black. How many layers of elastin fibers can you countin the tunica media?

Large vessels are so thick that they must have their own bloodsupply. This is the vasa vasorum.

Aorta–section – Verhoeff ’s stain for elastin fibers– 4x objective

A = tunica intima (interna) B = tunica media C = tunica adventitia (externa) arrowheads = vasavasorum


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1.25


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Percentage 60% 10-15% 25-30%

Type DeBakey I DeBakey II DeBakey III

Stanford A Stanford B

Proximal Distal

Classification of aortic dissection

Classification


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Incidence

• Ranges from 2-10 per 100,000 person-years

• Evidence of dissection is found in 1-3% of all autopsies

• International Registry of Acute Aortic Dissection (IRAD)

– 65% men – mean age 63yrs

– Women tend to present older (67 vs. 60yrs)

• Highest incidence in patients 50 to 70 years old.• Male-to-female ratio 2:1

• Half of dissections in females before age 40 occur duringpregnancy


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Mortality

• When left untreated…

– 33% of patients die within the first 24 hours

– 50% die within 48 hours

– ~75% die within 2-weeks


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Aortic dissection mimickers

– Myocardial ischemia due to an acute coronary syndrome with or without ST segmentelevation

– Pericarditis

– Pulmonary embolus

– Aortic regurgitation without dissection

– Aortic aneurysm without dissection – Musculoskeletal pain

– Mediastinal tumors

– Pleuritis

– Cholecystitis

– Atherosclerotic or cholesterol embolism

– Peptic ulcer disease or perforating ulcer

– Acute pancreatitis


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Predisposing factors

• Older patients – HTN (72% of IRAD patients)

• Younger patients – Pre-existing aneurysm (13%) – Inflammatory disease (giant cell, takayasu, RA, syphilitic aortitis)

– Collagen disorders (Marfan’s [50% of pts


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Clinical Features

• Abrupt onset of severe, sharp or "tearing" posterior chest or back pain (70-90%)

• Pulse deficit

– weak/absent carotid, brachial, or femoral pulse resulting fromintimal flap or compression by hematoma

• HTN at initial presentation is more common in those with a type Bdissection (70 vs 36%)


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Clinical presentation


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Clinical presentation


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If dissection involves ascending aorta…

• Acute aortic insufficiency --> diastolic decrescendo murmur, hypotension,or heart failure (1/2 to 2/3 of pts)

• Acute MI due to coronary occlusion (1-2%). RCA most commonly involved (Lmain sudden death) and, in infrequent cases, leads to complete heartblock.

• Tamponade• Hemothorax (if extends through adventitia)

• Stroke (if involves carotids)

• Horner syndrome (compression of superior cervical sympathetic ganglion)or vocal cord paralysis (compression of the left recurrent laryngeal nerve)


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DIAGNOSTIC

EKG Findings

• normal (31%)

• nonspecific ST--T wave changes (30-42%)

– (commonly, LVH and strain patterns associated with HTN)• ischemic changes (15%)

• acute MI (5%)

• >98% do not show ST elevation

***Based on 464 IRAD patients


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Labs

• D-dimer ? – 14-center international study of 220 patients (87 with AD, 133 controls)

– D-dimer levels 3213 ±1465 and 3574 ± 1430 for type A and Brespectively

– Sensitivity 96.6%, Specificity 46.6%

– Possibility that D-dimer could be used to help rule-out aortic dissection

Suzuki et. al. Diagnosis of Acute Aortic Dissection by D-Dimer. Circulation 2009; 119,

2702-2707


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Chest X Ray


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ImagingSummary of specialized imaging techniques Angiography CT MRI TEE

Sensitivity Poor Average Excellent Excellent

Specificity Good Good Excellent Good

Site of tear Good Poor Excellent Good

AorticRegurgitation

Excellent Useless Excellent Excellent

Pericardialeffusion

Useless Poor Excellent Good

Coronaries Excellent Useless** Good Average

Modified from Cigarroa JE et al.


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ECHOCARDIOGRAPHY

0.50


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TEE

0.21


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CT Scan


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Angiography

• First definitive test for aortic dissection

• Traditionally considered “the gold standard”

• Involves injection of contrast media into the aorta – Identifies the site of the dissection

– Major branches of the aorta – Communication site between true & false lumen

– Can detect thrombus in the false lumen

• Disadvantages – Not very practical in critically ill patients

– Nephrotoxic contrast

– Risks of an invasive procedure


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Medical management

• Basic management – Type A dissection surgery

– Type B dissection medical management, TEVAR

• Surgery -- prevents medial extension reaching the pericardium

and producing fatal tamponade or worsening other complications


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Medical therapy

• Reduce systolic BP to 100 to 120 mmHg or the lowest level that is tolerated

• IV Beta blockers – Propanolol (1-10 mg load, 3mg/hr)

– Labetalol (20 mg bolus, 0.5 to 2 mg/min)

• If SBP remains >100mmHg, nitroprusside should be added – Do not use without beta blockade

– Avoid hydralazine


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Bentall procedure


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What is the optimal treatment


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TEVAR


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1.20


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Long Term Outcome

• Type A

– Survival at 5 yrs – 68%

– Survival at 10 yrs – 52 %

• Type B

– 5 yrs – 60 - 80%

– 10 yrs – 40 – 80%

– Spontaneous healing of dissection is uncommon


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Long-Term Management

• Medical therapy – Oral Beta-blockers (reduces aortic wall stress)

– Keep BP < 135/80 mmHg (combination therapy)

– Avoidance of strenuous physical activity

• Serial imaging – Thoracic MR scan prior to discharge

– f/u scans at 3, 6, and 12 months

– Subsequent screening studies done every 1-2 yrs if no evidence of progression


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Overview

• Incidence of aortic dissection is at least 2000 new cases per year

• Peak incidence is in the sixth to seventh decade

• Men are affected twice as commonly as women

• Mortality in the first 48 hours is 1% per hour – Early diagnosis is essential


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Pathophysiology

• The chief predisposing factor is degeneration of collagen and elastin inthe aortic intima media

• Blood passes through the tear into the aortic media, separating the

media from the intima and creating a false lumen

• Dissection can occur both distal and proximal to the tear


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Classification

• Debakey system – Type I

• Originates in the ascending aorta, propagates to the aortic arch and beyond it distally

– Type II• Confined to the ascending aorta

– Type III• Confined to the descending aorta, and extends distally, or rarely retrograde into the aortic

arch


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Classification

• The Stanford system

– Type A

• All dissections involving the ascending aorta

– Type B• All other dissections regardless of the site of the primary intimal tear

– Ascending aortic dissections are twice as common as descending


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Predisposing factors

• Age, 60-80 yrs old

• Long standing history of hypertension – 80% of cases have co-existing HTN

• Takayasu’s arteritis

• Giant cell arteritis

• Syphilis

• Collagen disorders – Marfan syndrome (6-9% of aortic dissections)

– Ehlers-Danlos syndrome


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Other Risk Factors

• Congenital Cardiac Anomalies

– Bicuspid aortic valve (7-14% of cases)

– Coarctation of the aorta

• Cocaine

– Abrupt HTN, due to catecholamine release

• Trauma

• Pregnancy (50% of dissections in women


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Clinical Symptoms

• Severe, sharp, “tearing” posterior chest pain or back pain (occurs in 74-90% of pts)

– Pain may be associated with syncope, CVA, MI, or CHF

– Painless dissection relatively uncommon

• Chest pain is more common with Type A dissections

• Back or abdominal pain is more common with Type B dissections


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Physical Exam

• Pulse deficit

– Weak or absent carotid, brachial, or femoral pulses

– these patients have a higher rate of mortality

• Acute Aortic Insufficiency

– Diastolic decrescendo murmur

– Best heard along the right sternal border


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Clinical signs

• Acute MI – RCA most commonly involved

• Cardiac tamponade

• Pleural effusions

• Hypertension or hypotension• Hemothorax

• Variation in BP between the arms (>30mmHg)

• Neurologic deficits – Stroke or decreased consciousness


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Clinical Signs

• Involvement of the descending aorta

– Splanchnic ischemia

– Renal insufficiency

– Lower extremity ischemia – Spinal cord ischemia


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Diagnosis

• Generally suspected from the history and PE

• In a recent study in 2000, 96% of acute dissection patients could be identified basedupon a combination of three clinical features – Immediate onset of chest pain

– Mediastinal widening on CXR – A variation in pulse and/or blood pressure (>20 mmHg difference between R & L arm

• Incidence >83% when any combination of all three variables occurred


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Differential Diagnosis

• Acute Coronary Syndrome

• Pericarditis

• Pulmonary embolus

• Pleuritis

• Cholecystitis

• Perforating ulcer


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Diagnostic Tests

• EKG – Absence of EKG changes usually helps distinguish dissection from angina

– Usually non-specific ST-T wave changes seen

• CXR

• Cardiac Enzymes


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Chest X-Ray

• May show widening of the aorta with ascending aorta

dissections

– Present in 63 % of patients with Type A dissections


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Diagnostic Imaging

• Not performed until the patient is medically stable

• Has been a dramatic shift from invasive to non-invasive diagnosticstrategy

• Spiral CT scan

• TEE

• MRI

• Angiography


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Imaging

• Can identify aortic dissection and other features such as:

– Involvement of the ascending aorta

– Extent of dissection

– Thrombus in the false lumen

– Branch vessel or coronary artery involvement

– Aortic insufficiency

– Pericardial effusion with or without tamponade

– Sites of entry and re-entry


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Spiral CT

• Sensitivity 83%

• Specificity 90 - 100%

• Two distinct lumens with a visible intimal flap can be identified

• Advantages – Noninvasive

– Readily available at most hospitals on an emergency basis – Can differentiate dissection from other causes of aortic widening (tumor, periaortic hematoma, fat)

• Disadvantages – Sensitivity lower than TEE and MRI

– Intimal flap is seen < 75% of cases

– Nephrotoxic contrast is required

– Cannot reliably detect AI, or delineate branch vessels


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TTE

• First used to diagnose aortic dissections in the ’70s

• Sensitivity 59-85%, specificity 63-96%

• Image quality limited by obesity, lung disease, and chest wall

deformities


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TEE

• Sensitivity 98% Specificity 95%

• Advantages

– Close proximity of the esophagus to the thoracic aorta

– Portable procedure

– Yields diagnosis in < 5 minutes

– Useful in patients too unstable for MRI

– True and false lumens can be identified

– Thrombosis, pericardial effusion, AI, and proximal coronary arteries can be readily visualized


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TEE

• Lower specificity attributed to reverberations atherosclerotic vessels orcalcified aortic disease producing echo images that resemble an aorticflap

• Disadvantages – Contraindicated in patients with esophageal varices, tumors, or strictures

– Potential complications: bradycardia, hypotension, bronchospasm


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MRI

• Most accurate noninvasive for evaluating the thoracic aorta

• Sensitivity 98%

• Specificity 98%

• Advantages – Safe

– Can visualize the whole extent of the aorta in multiple planes – Ability to assess branch vessels, AI, and pericardial effusion

– No contrast or radiation

• Disadvantages – Not readily available on an emergency basis

– Time consuming

– Limited applicability in pts with pacemakers or metallic clips


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Treatment

• Acute dissections involving the ascending aorta are considered surgical

emergencies

• Dissections confined to the descending aorta are treated medically

– Unless patient demonstrates continued hemorrhage into the pleural or

retroperitoneal space


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Surgical Options

• Excision of the intimal tear

• Obliteration of entry into the false lumen proximally

• Reconstitution of the aorta with interposition of a synthetic

vascular graft


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Type A Dissections

• Operative mortality varies from 7-35%

• 27% post-op mortality

– Patients who died had a higher rate of in-hospital complications suchas strokes, renal failure, limb ischemia, & mesenteric ischemia


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Poor prognostic factors

• Hypotension or shock

• Renal failure

• Age> 70 yrs

• Pulse deficit

• Prior MI• Underlying pulmonary disease

• Preoperative neurologic impairment

• Renal and/or visceral ischemia

• Abnormal EKG, particularly ST elevation


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Aortic Dissection

Matt White

February 8, 2010

Morning Report


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Aortic Dissection

• Background

• Epidemiology

• Clinical characteristics

• Diagnostic Modalities• Treatment


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History

• First known case was King George II on October, 25, 1760• First successful repair by Dr. Michael DeBakey in 1955.• ". . . spontaneous tear of the arterial coats is associated with

atrocious pain, with symptoms, indeed, in the case of the aorta of angina pectoris and many instances have been mistaken for it" – William Osler, 1910.


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Mechanism

• Primary event is a tear in the aortic intima.

• Degeneration of aortic media, or cystic medial necrosis, is felt to be aprerequisite nontraumatic aortic dissection

• Blood passes into the aortic media through the tear, separating the intimafrom the media and creating a false lumen.

Uncertain whether the initiating event is a primary rupture of the

intima with secondary dissection of the media, or hemorrhage

within the media and subsequent rupture of the overlying intima


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Mechanism (cont’d)

• Propagation of the dissection can occur both distal andproximal to the initial tear,

• Complications of dissection: – ischemia (coronary, cerebral, spinal, or visceral)

– aortic regurgitation

– Pericardial effusion/cardiac tamponade


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Nomenclature

DeBakey classification system• Type I - Originates in ascending aorta, propagates at least to the aortic arch

and often beyond it distally.• Type II – Originates in and is confined to the ascending aorta.• Type III – Originates in descending aorta, rarely extends proximally but will

extend distally.

Daily (Stanford) classification system• Divided into 2 groups; A and B depending on whether the ascending aorta is

involved.• A = Type I and II DeBakey• B = Type III DeBakey


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Aortic Dissection

• Background

• Epidemiology




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Aortic Dissection

• Background

• Epidemiology




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Aortic Dissection

• Background

• Epidemiology




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Pre-OR management

• Virtually all non-shocked patients require medicalmanagement prior to surgery

• Aim of medical management:

– reduce the absolute pressure on the damaged aortic media – Reduce the rate of rise of that pressure (dP/dT).


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Medical management

• Blood pressure control



• Pain control


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Main goals of medical management

• Systolic BP < 100 mmHg.

• Pain free.

• Adequate renal perfusion (urine output > 30 ml/hr).

• No evidence of cerebral hypoperfusion.• Minimized shear stress (β-blocked to < 55/min).


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Antihypertensive choice

• Labetalol for beta blockade

• Nitroprusside if HR controlled but SBP still >100mmHg


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Antihypertensive choice

• Start with β-blockers

• use of a vasodilator in isolation will actually increaseaortic shear stress by widening the pulse pressure and

the dP/dT of left ventricular ejection.


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References

• Davies, Crispin; Bashir, Yaver; Shively. CardiovascularEmergencies. London, GBR: BMJ Publishing Group, 2001. p151-172

• Manning, Warren. Clinical manifestations and diagnosis of aortic

dissection. UptoDate• Suzuki et. al. Diagnosis of Acute Aortic Dissection by D-Dimer.

Circulation 2009; 119, 2702-2707

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