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Aortic EmergenciesCarrie Fales, MD

Steven Nakajima, PharmD

No Financial Disclosures

ED or No ED? Objectives

AAA and Aortic dissections Overview

Classification/Pathophysiology

Diagnostics

Management

Disposition

Who is in the audience?

Are you a:

A. Nurse

B. Paramedic

C. Physician

D. NP or PA

E. Respiratory therapist

F. Pharmacist

G. Other

Aortic Emergencies

Abdominal Aortic Aneurysm (AAA)

Aortic Dissection

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https://my.clevelandclinic.org/health/articles/heart-blood-vessels-aorta/aortic-aneurysm-aortic-dissection?view=print https://my.clevelandclinic.org/health/articles/heart-blood-vessels-aorta/aortic-aneurysm-aortic-dissection?view=print

Vessel AnatomyIntima = endothelial layer

Media = smooth muscle; elastin, collagen, and proteoglycans

Adventitia = collagen

Aneurysm vs. Dissection DefinitionsAneurysm

Focal dilatation in an artery

Greater than 1.5x normal diameter

True aneurysms have expansion of all layers of vessel wall

False aneurysms/pseudo aneurysms contained only by adventitia or surrounding soft tissue, ruptured media

Dissection

Blood entering media and splitting the layers of the aorta

Avoid ‘dissecting aneurysm’ terminology

Abdominal Aortic Aneurysm (AAA) Classification Classification of abdominal aortic aneurysms in reference to renal arteries Suprarenal, Pararenal, Juxtarenal, Infrarenal

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Abdominal Aortic Aneurysm

90% of AAA originate below renal arteries Due to rebound systolic pressure forces and turbulent flow

at bifurcation causing mechanical stresses

Low elastin content in this region

Area more prone to atherosclerosis

Comparable to proximal aorta and bicuspid valve

Abdominal Aortic Aneurysm

Defined as aneurysm at ≥3.0cm

Repair considered at ≥5.0cm

After age 50 years, the normal diameter of the infrarenalaorta 1.5 cm in women 1.7 cm in men

Risk of rupture directly related to size < 4 cm aneurysm, < 2% risk per year 4-5 cm, 1-5% 5-6 cm, 3-15% 6-7 cm, 10-20% > 7 cm, 20-50%

Risk Factors Male

Smoking history

Family history

Chronic obstructive pulmonary disease (COPD)

Previous aneurysm repair or peripheral aneurysm (popliteal or femoral)

Coronary artery disease

Hypertension

Marfan syndrome, Ehlers-Danlos syndrome, and collagen-vascular diseases

Mycotic aneurysm

Cystic medial necrosis

Arteritis

Trauma

Anastomotic disruption producing pseudo aneurysms

Smoking

ED or NO ED? Abdominal Aortic Aneursyms

Classic triad of back/abdominal/flank pain, hypotension, and palpable pulsatile mass only present 30% of the time

Most AAAs asymptomatic until time of rupture

15,000 deaths per year in US

Up to 30% of patients in ED misdiagnosed Common renal colic, diverticulitis, GI bleed

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Pre hospital Care

Advanced Life Support level care

IV access

EKG and cardiac monitoring

Treat hypoxia with oxygen

Treat hypotension with IVFs

Thorough neurologic exam

Physical Exam

Thorough physical exam- abdominal, neuro, cardiac, pulmonary

Abdominal bruit 5-10%

Palpation of pulsating mass Neither sensitive or specific

Size dependent

Patient dependent

Differential Diagnosis

Acute coronary syndrome

Cholecystitis, cholelithiasis, choledocholithiasis

Pancreatitis

Peptic ulcer disease, gastritis, GERD

GI bleed

Musculoskeletal back pain

Renal colic

Diverticulitis

Evaluation

BMP

CBC

Coagulation studies

Type and screen/cross

Also consider cardiac enzymes, LFTs, lipase, UA with other diseases in differential

EKG

Diagnostic Studies

X-ray Rarely can see calcification

Used to identify alternative diagnoses

Diagnostic Studies

CT

Nearly 100% sensitive and specific

Can detect extra luminal blood Retroperitoneal hemorrhage identification 77-

100% sensitive

Helpful for surgical planning

Radiation

Time consuming

Not ideal for unstable patient

IV contrast not necessary but does provide more information

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Diagnostic Studies

Ultrasound

ED bedside US ideal

Advantages Readily available Very sensitive and specific Lack of radiation

Disadvantages Operator dependent Inadequate to identify retroperitoneal blood, most

common area of AAA rupture

Bedside Ultrasound

Use 3.5 MHz curvilinear transducer

Measure outer wall to outer wall

Measure proximally and distally

Transverse (9 o’clock) and sagittal/longitudinal (12 o’clock) planes

If AAA found, look for free fluid with FAST

Biggest hurdles Bowel gas Obesity IVC vs. aorta

Transverse Proximal

Transverse Distal

Sagittal/Longitudinal Proximal

Sagittal/Longitudinal Distal

Treatment and Disposition

Surgical emergency

Early surgical evaluation and involvement

Resuscitate hypotensive patients with blood products

Treat hypertension with beta blockers

Question #1

The majority of isolated AAAs are infrarenal in location.

a. True

b. False

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Question #1- Answer

The majority of isolated AAAs are infrarenal in location.

a. True

b. False

Question #2

All of the following are risk factors for aortic aneurysm EXCEPT:

a. Hypertension

b. Age over 65

c. Cigarette smoking

d. Atherosclerosis

e. Diabetes

Question #2- Answer

All of the following are risk factors for aortic aneurysm EXCEPT:

a. Hypertension

b. Age over 65

c. Cigarette smoking

d. Atherosclerosis

e. Diabetes

Question #3

In what percentage of patients presenting with abdominal aortic aneurysm is an alternative, incorrect diagnosis initially made by physicians?

a. 10% b. 30% c. 50% d. 80%

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Question #3- Answer

In what percentage of patients presenting with abdominal aortic aneurysm is an alternative, incorrect diagnosis initially made by physicians?

a. 10% b. 30% c. 50% d. 80%

Question #4

The absence of a pulsatile abdominal mass excludes the diagnosis of aortic aneurysm.

a. True

b. False

Question #4- Answer

The absence of a pulsatile abdominal mass excludes the diagnosis of aortic aneurysm.

a. True

b. False

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Aortic Dissection Aortic Dissection

Subset of acute aortic syndromes Aortic intramural hematoma

Penetrating atherosclerotic ulcer

Aortic dissection

Aortic Dissection

Aortic dissection diagnosis missed in ED setting 16-38% of the time More likely to be missed for walk-in patients compared to EMS

arrived patients

Area for medical risk and litigation

High morbidity and mortality Type A Dissection

1-2% mortality per hour in first 48 hours 50% mortality day three 80% mortality day fourteen

Type B dissection 10-70% mortality at day 30 based on risk factors and medical co-

morbidities

Aortic Dissection

2/3 of aortic dissections are Stanford type A

1/3 of aortic dissections are Stanford type B Approximately 30% will be classified as complicated

dissections radiographic evidence of thoracic aortic rupture (eg, blood

outside the aortic wall)

ischemia involving the viscera, kidneys, spinal cord, or lower extremities

persistent pain

rapid expansion in the distal arch or proximal descending aorta to a total aortic diameter of > 4.5 cm

Classification

Acute vs chronic

14 days of symptoms

DeBakey type I, II, or III

I- ascending aorta, arch, descending aorta

II- only ascending aorta

III- only descending aorta

Stanford A or B

A- any involvement of ascending aorta

B- only descending aorta

Classification

Class 1 – classic aortic dissection: separation of intima from media and/or adventitia with intimal flap

Class 2 – intramural hematoma: hemorrhage within aortic wall without obvious intimal flap

Class 3 – subtle-discrete dissection: localized intimal tear with no dissection flap or medial hematoma

Class 4 – penetrating atherosclerotic ulcer: usually localized to descending aorta with significant atheroma; found usually in the adventitia with localized hematoma or saccular aneurysm. May convert to classic aortic dissection

Class 5 – iatrogenic or traumatic dissection: following cardiac catheterization or cardiac surgery or decelerating chest trauma

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Aortic Dissection

Approximately 10,000 patients in US per year Likely underestimate because of retrospective data and

autopsy data

Most commonly 40-70 year olds

Men 3x more likely than women

Women tend to present later and with worse outcomes

Risk Factors

Hypertension

Cocaine

Pregnancy

Trauma

Congenital: Aortic coarctation, Bicuspid valve, Connective Tissue Disorders- Marfan, Ehlers-Danlos, Turner Syndrome

Iatrogenic: Heart surgery, Aortic valve replacement, Catheterizaiton

ED or No ED? Clinical History

International Registry of Acute Aortic Dissection [IRAD]Hagan PG. JAMA 2000, 283:897

464 patients

12 centers

Database of clinical information

Clinical features, treatment, and outcomes

Classic symtomatology: abrupt and severe chest pain that radiates to back

ripping, tearing sensation

feeling of impending doom

Pre hospital Care

Advanced Life Support level care

IV access

EKG and cardiac monitoring

Treat hypoxia with oxygen

Treat hypotension with IVFs

Thorough neurologic exam

International Registry of Acute Aortic Dissection- History

Male 65.3%

Mean age* 63 years

Type A 62.3%

Hypertension 72.1%

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International Registry of Acute Aortic Dissection- Symptoms

Pain present is 95.5% of patients

Chest pain 72.7%

Anterior chest pain 60.9%

Back pain 53.2%

Abdominal pain 29.6%

International Registry of Acute Aortic Dissection- Pain

Abrupt onset 84.4%

‘Worst pain ever’ 90.6%

Sharp 64.4%

Tearing or ripping 50.6%

Radiating 28.3%

Migratory 16.6%

Physical Exam

Thorough physical exam- neuro, cardiac, pulmonary

Need high index of suspicion

Aortic insufficiency murmur (32%)

Pulse deficit in radial and/or femoral arteries (15%)

Hypertension (49%)

Hypotension (18%)

Check bilateral upper extremity blood pressure A difference of 20 mm Hg between arms is considered positive and can be

suggestive of an aortic dissection However, 20% of the population will have a blood pressure differential

without an aortic dissection

Differential DiagnosisThink about aortic dissection with any chest pain, back pain, abdominal pain, syncope, acute neurologic deficit with pain

Broad differential:

Myocardial infarction/acute coronary syndrome

Pericardial effusion, tamponade, pericarditis

Pneumonia

Esophageal rupture

Pneumothorax

Pulmonary embolism

Stroke

Musculoskeletal

Spinal cord injury

Intra-abdominal process

Evaluation

BMP

CBC

Coagulation studies

Type and screen/cross

Also consider cardiac enzymes, LFTs, lipase, UA with other diseases in differential

D-dimer Multiple studies to use as screening tool but none validated

Diagnostic Studies

EKG Nondiagnostic and not specific or sensitive Q waves

ST abnormalities

T wave abnormalities

No abnormalities

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Diagnostic Studies

Chest x-ray

There is no single radiographic finding that accurately predicts the presence of aortic dissection.

Wide mediastinum 66.1%Abnormal aortic contour 49.6%Pleural effusion 19.2%Wall calcification displacement 14.1%Normal CXR 12.4%

Wide Mediastinum

Abnormal Aortic Contour Calcification

Diagnostic Studies

CT Imaging modality of choice

High sensitivity

Identifies alternative diagnoses

Identifies false lumen and additional anatomy Dissection flap

Extension of flap into great vessels

Signs of rupture

Signs of end organ damage

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Diagnostic Studies

Transesophageal echocardiography Requires experienced operator and operator dependent

Usually requires sedation or anesthesia

Evaluates pericardial effusion, left ventricular dysfunction, aortic insufficiency

John A Elefteriades et al. Open Heart 2015;2:e000169©2015 by British Cardiovascular Society

Branch Vessel Compromise

Myocardial infarction

Stroke

Spinal cord infarction

Mesenteric and renal ischemia

Limb ischemia

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Aortic Valve Dysfunction

Aortic insufficiency

Acute pulmonary edema

Pericardial tamponade

ED or No ED?

Treatment

Pain management

Anti-hypertensive therapy Goal to reduce force on intimal flap

Negative inotropic effect

Goal HR <60 and BP <100-120

dP/dT (derivative of pressure / derivative of time) Concept

dP/dT

Antihypertensives

IDEAL Parenteral medications Short acting (fast onset/off-set)

Easily titrated (IV > oral, SL, IM)

Predictable BP reduction (avoid large drop in BP that causes hypoperfusion)

Favorable side effect profile

Patient-specific

β-BlockersDrug Mechanism Dose ADME Pearls

Labetalol β1-β2-α1 antagonist

(↓ HR, SVR)

Bolus: 10-20mg q10

1-6mg/min

On: 2-5min

Off: 2-6hr

-Precipitous ↓ BP-Fluid overload

Esmolol β1-antagonist

(↓ HR, contractility)

Bolus: 500 µg/kg

50–300 µg/kg/min

On: 60s

Off: 10-20min

-First line in aortic dissection-May bolus with increase-Premixed

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Esmolol

• Primarily decreases HR– Usually for aortic dissection

• Bolus: – 500 mcg/kg over 1 minute

• Infusion: 50-300 mcg/kg/min– Titrate by 50 mcg/kg/min

q5 minutes to BP AND HR– Reduce dose if HR <50

Labetalol

• Bolus: – 5-20 mg over 2 minutes– Boluses generally for

acute ischemic stroke

• Infusion: 1-6 mg/min– Titrate by 1 mg/min q5

minutes to BP AND HR– Reduce dose if HR <50

Calcium Channel Blockers

Drug Mechanism Dose ADME Pearls

Nicardipine

Drug Mechanism Dose ADME Pearls

Nicardipine 2nd GenPeripheral L-type selective CCB

(↓ SVR)

2.5-15 mg/hr

On: 5-15min

Off: 4-6hr

-Cerebral and coronary activity-Fluid overload

Clevidipine 3rd Gen Peripheral L-type selective CCB

(↓ SVR)

1-21 mg/hr On: 2-4 min

Off: 5-15 min

-In lipid = 2 kcal/mL-Esterase-Soy/Egg allergy

Nicardipine

• Infusion: 5 -15 mg/hr– Titrate by 2.5 mg/hr

q5 - 15 minutes to BP goal

• May cause reflex tachycardia– Ensure patient is

adequately β-blocked first

Clevidipine

• Infusion: 1-21 mg/hr– Double dose every 90

seconds, as BP approaches goal may increase dose by less than double

– T1/2= 1 minute

Nitric Oxide Donors

Drug Mechanism Dose ADME Pearls

Sodium Nitroprusside

arterial/veno-vasodilator

0.3-10 µg/kg/min

On: 3s

Off: 1-2 min

-Coronary steal-Cyanide toxicity; avoid in liver/renal- ↑ ICP

Nitroglycerine Venous > arterial vasodilator

5-400 µg/min

On: 2-5 min

Off: 10-20min

-Premixed-Variable response to Δ-HA, flushing-PDEs

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Sodium Nitroprusside

Protect from light!

Titration- very fast onset Start: 0.3 mcg/kg/min

Increase every minute by 0.5 mcg/kg/min

Max dose 10 mcg/kg/min

Monitor for cyanide toxicity Dyspnea, SpO2, AMS

Toxicity of Sodium Nitroprusside

Cyanide

Thiocyanate

Methemoglobin

Disposition

Admission to ICU

Surgical intervention vs. medical management Generally surgical intervention for Type A dissections and

medical management for Type B dissections

Endovascular repair vs. open repair Thoracic endovascular aortic repair (TEVAR)

Question #1

To decrease shear force, which of the following should be the initial medical therapy for aortic dissection?

a. Esmolol

b. Clevidipine

c. Nicardipine

d. Nitroprusside

Question #1- Answer

To decrease shear force, which of the following should be the initial medical therapy for aortic dissection?

a. Esmolol

b. Clevidipine

c. Nicardipine

d. Nitroprusside

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Question #2

Acute aortic syndrome encompasses all of the following EXCEPT:

a. Aortic aneurysm

b. Aortic dissection

c. Intramural hematoma

d. Penetrating atherosclerotic ulcer

Question #2- Answer

Acute aortic syndrome encompasses all of the following EXCEPT:

a. Aortic aneurysm

b. Aortic dissection

c. Intramural hematoma

d. Penetrating atherosclerotic ulcer

Question #3

The Stanford type B dissection refers to:

a. DeBakey type I and II dissection

b. Dissection of the ascending aorta only

c. Dissection of both the ascending and descending aorta

d. Dissection of the descending aorta only

Question #3- Answer

The Stanford type B dissection refers to:

a. DeBakey type I and II dissection

b. Dissection of the ascending aorta only

c. Dissection of both the ascending and descending aorta

d. Dissection of the descending aorta only

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Question #4

All of the following are risk factors for aortic dissection or rupture, EXCEPT:

a. hypertension

b. Marfan syndrome

c. known connective tissue disorder

d. cocaine

e. diabetes

Question #4- Answer

All of the following are risk factors for aortic dissection or rupture, EXCEPT:

a. hypertension

b. Marfan syndrome

c. known connective tissue disorder

d. cocaine

e. diabetes

Thank you

References available upon request