71
Aortic Dissection
KEY CONCEPTS
• A ortic dissection most commonly presents as abrupt, sharp, severe pain
maximally intense at onset in the chest or back. There may be various
seemingly unconnected associated symptoms due to altered blood pres-
sure or insufficiency of disparate vascular beds.
• Definitive diagnosis is most commonly made with an imaging study such
as computed tomography of the aorta with intravenous contrast. A combi-
nation of standardized clinical assessment, chest x-­ray, and serum D-­dimer
testing can effectively rule out the condition in low-­risk patients.
• The critical immediate therapeutic actions are medical therapy to decrease
aortic sheer force and blood pressure control. Immediate surgical consulta-
tion is indicated.
• Surgical treatments, including endovascular stent placement, are advanc-
ing, leading to decreased mortality. This increases the importance and benefit
of early diagnosis in the emergency department setting.
FOUNDATIONS
Background and Importance
Aortic dissection is a lethal disease that can be difficult to diagnose.
The majority of patients present with abrupt, severe pain of the chest
or back, but a significant minority of patients present with different
symptoms that can mimic a variety of other more common conditions.
The average age of presentation is about 64 years and 65% are male.1
Approximately 5000 to 10,000 cases of aortic dissection are diagnosed
annually in the United States. Consequently, an individual emergency
physician can generally expect to see fewer than 1 case per year.
Anatomy, Physiology, and Pathophysiology
The aorta is composed of three layers: the inner endothelial intima,
the smooth muscle media, and the connective tissue outer adventitia.
In the media, elastic fibers composed of elastin and fibrillin intertwine
with collagen and smooth muscle cells, providing the viscoelastic prop-
erties that enable the aorta to distend, storing a portion of the stroke
volume and elastic potential energy during ventricular systole. The
aorta then recoils during diastole so that blood continues to be pro-
pelled to peripheral end organs.
The aorta emanates from the left ventricular outflow tract of the
heart, makes an approximate 180-­degree curve, and travels posteri-
orly within the mediastinum of the chest until it crosses through the
diaphragm. It assumes a retroperitoneal position within the abdomen
and continues inferiorly until it bisects into the common iliac arter-
ies at approximately the level of the umbilicus. Major arterial branches
include the brachiocephalic, left common carotid, and left subclavian
in the chest, and the celiac, superior mesenteric, bilateral renal and
Keith A. Marill
gonadal, and inferior mesenteric arteries in the abdomen. It provides
the major supply to the anterior spinal artery and lumbar spinal cord
via the artery of Adamkiewicz.
Aortic dissection is defined by separation of the media layer of the
aortic wall, generally with formation of a hematoma or false lumen.
This commonly occurs in the setting of degeneration of the medial
layer with associated inflammation. Aortic dissection is classified as
acute if it is diagnosed within 2 weeks of symptom onset, subacute if
diagnosed with 2 weeks to 3 months of onset, or chronic if greater than
3 months from onset.
Aortic dissection is commonly described with the Stanford classifi-
cation. Type A describes dissection involving the ascending aorta with
or without descending involvement, and Type B dissection is limited to
the descending aorta commencing distal to the left subclavian artery.
The less commonly used DeBakey classification separates dissections
into: type I, involving the ascending and descending aorta; type II,
involving only the ascending aorta; and type III, limited to the descend-
ing aorta (Fig. 71.1). These classification systems were proposed in part
to differentiate patients who required surgical or pharmacologic ther-
apy, though these delineations have blurred with modern therapeutic
advances including endovascular treatments.
Aortic dissection most commonly occurs due to a tear in the inti-
mal layer subsequent to a process that has weakened the aortic media.
Blood passes through the tear separating the intima from the media
or adventitia, creating a false lumen that can propagate in an antero-
grade or retrograde fashion. Propagation of aortic dissection can cause
complications such as visceral or neurologic malperfusion syndromes
due to compromise of branch vessels, pericardial tamponade, or acute
aortic insufficiency.
Intramural hematoma refers to hematoma formation within the
wall of the aorta without evidence of intimal aortic tear. The hematoma
may be localized or dissect along the plane of the aortic media. The risk
factors, presentation, and natural course of this variant generally mir-
ror those of typical aortic dissection due to intimal tear. However, over
half of intramural hematomas occur in the descending aorta as a result
of atherosclerotic disease or iatrogenic intravascular catheter manipu-
lation trauma.2 Intramural hematoma is most easily diagnosed with CT
angiography and may be missed with conventional angiography.
Penetrating atherosclerotic ulcer results from erosion of an intimal
atherosclerotic lesion. It is an alternative mechanism to intimal tear,
allowing blood to dissect into the media of the aortic wall or beyond.
This process develops gradually in elderly patients with extensive ath-
erosclerosis and often is heralded by chest or back pain and hyper-
tension. Ulceration may lead to hematoma formation in the dissected
media, or it can extend into the adventitia with pseudoaneurysm for-
mation and potential rupture. It is usually a localized process most
commonly occurring in the descending aorta without retrograde aortic
991
992 PART III  Emergency Medicine by System

Stanford

Type A Type B

DeBakey

Type I Type II Type III

Fig. 71.1 Acute aortic dissection classifications. The Stanford classification divides dissections into those
involving the ascending aorta from dissection originating there or proximal dissection of a more distal origin
(Type A), or those limited to the descending aorta (Type B). The DeBakey classification divides dissections into
those arising in the ascending aorta and extending distally beyond the innominate artery (Type I), arising in the
ascending aorta with extension limited to the level of the innominate artery take-­off (Type II), and arising at or
distal to the left subclavian artery take-­off with extension distally (Type III).

valve, pericardial, or branch vessel involvement and associated diffuse
symptoms and signs (Fig. 71.2).
About two-­thirds of aortic dissections are classified as type A,
and the remainder as type B. Hypertension is the most common risk
factor, present in a majority of patients.1 Both type A and B patients
may have a history of cardiac surgery, including aortic valve replace-
ment. Patients may have a history of aortic aneurysm or a prior aor-
tic dissection. Marfan syndrome is the connective tissue disease most
commonly associated with acute aortic dissection. Other associated
conditions include: atherosclerosis, a family history of thoracic aortic
disease with or without a defined genetic syndrome, bicuspid aortic
valve, coarctation of the aorta, a bovine-­type aortic arch, when the
brachiocephalic artery shares a common origin with the left common
carotid artery, and infectious disease such as syphilis. Activities and
events associated with increased aortic sheer force including crack
cocaine use, weight lifting, the peripartum period,3 and deceleration
trauma can rarely cause aortic dissection. Traumatic aortic dissection
most commonly occurs at the level of the left subclavian artery in the
proximal descending aorta because the aorta is tethered at this point
by the ligamentum arteriosum. Other causative genetic syndromes
include Turner, type 4 Ehlers-­Danlos, and Loeys-­Dietz. Fluoroquino-
lones interfere with collagen synthesis and increase the risk of aortic
dissection during treatment.4
CLINICAL FEATURES
Aortic dissection is classically characterized by an acute severe, sharp,
ripping or tearing, painful sensation in the chest or central upper back
 CHAPTER 71  Aortic Dissection 993

A B
Fig. 71.2  Pseudoaneurysm due to penetrating ulcer. A 66-­year-­old female presented with sharp chest pain
radiating to the interscapular area and was found to have a penetrating ulcer of her descending thoracic aorta
just beyond the left subclavian artery with a contained hematoma and blood in the mediastinum and left
chest. The patient was treated with emergent endovascular repair. (A) Cross-­sectional computed tomography
(CT) with contained hematoma (pseudoaneurysm) and left hemothorax, and (B) three-­dimensional CT angio-
gram rendering of aorta with pseudoaneurysm.

with maximal intensity from onset, and associated apprehension.5
When present, the pain generally radiates to the anterior chest or neck
when the ascending aorta is involved, and to the back, abdomen, or
down the legs when the pathology is in the descending thoracic aorta.
Migratory pain is described in about one-­third of cases. The radiation
and migration of pain often reflect the anatomic extension of the dis-
section. Emergency physicians may have little difficulty diagnosing
patients with a classic presentation. The challenge is that patients can
present with a spectrum of pain, and some patients have no pain at all
(Fig. 71.3). Additionally, many other symptoms may be present.
Other symptoms of type A dissection include lightheaded sensation
or syncope, and less commonly, dyspnea related to congestive heart
failure. Patients with either type A or B dissection may complain of
neurologic deficits related to cerebral or spinal cord compromise. Type
B dissection is considered complicated in the setting of refractory pain,
rapid aortic expansion or rupture, uncontrollable hypertension, or
insufficient perfusion of the renal, splanchnic, spinal, or lower extrem-
ity vasculature.
Signs of type A dissection include asymmetric pulse deficits,6 and
patients may present with hypertension, normotension, or hypoten-
sion. Pseudohypotension may occur when the blood pressure in one
arm is lowered due to subclavian artery compromise. Syncope occurs
in a minority of patients and is associated with increased mortality.
It is classically due to pericardial tamponade from retrograde dissec-
tion into the pericardial sac, but other causes include cerebrovascular
insufficiency, internal hemorrhage with hypovolemia, or dysrhythmia.
Tamponade may be evidenced by dilated neck veins, diminished heart
sounds, and decreased pulse or pulse pressure. A new diastolic mur-
mur in the lower left sternal border suggestive of aortic regurgitation
can occur when the dissection spans the aortic valve. All three compo-
nents of the classic triad—abrupt tearing pain, pulse deficits, and aortic
insufficiency—are seldom observed in a single patient.
Acute myocardial infarction due to coronary ostium compromise
may occur in type A dissection, with the majority of these cases involving
the right coronary artery ostium with infarction of the corresponding
inferior coronary territory. Left main occlusion is the second most com-
mon site (Fig 71.4). Rarely, patients may present with isolated congestive
heart failure when the dissection compromises aortic valve function.
The majority of patients with type B dissection have elevated blood
pressure greater than 150 mm Hg. Syncope and pulse deficits can occur
but are less common than with type A disease.
Neurologic symptoms and signs can occur in either type A or B
dissection.7 These include ischemic stroke, spinal ischemia leading to
temporary or permanent paralysis in 1% to 3% of patients, and isch-
emic peripheral neuropathy. Up to one-­third of patients who complain
of neurologic symptoms at dissection onset have no complaint of pain.
Gastrointestinal complications can also occur in either type A or B
disease. These can be due to fixed or dynamic arterial branch occlusion
or global hypoperfusion. Mesenteric ischemia is the most common
cause of death in type B disease. Gastrointestinal hemorrhage is less
common and can be due to ischemic bowel or fistula formation. Nau-
sea, vomiting, diaphoresis, and apprehension can be seen with all acute
dissections.
Information from the history and physical exam can be combined
systematically to estimate a combined risk of disease. The aortic dissec-
tion detection risk score (ADD) is a tool combining three domains of
clinical information to assess for the risk of acute dissection: high risk
conditions, pain features, and exam features (Table 71.1). Patients are
classified on a score of one to three, scoring one point if any items in
each of the three domains is positive. An ADD score of one or more is
95% sensitive for aortic dissection. Among patients with none of the
identified clinical risk factors on the ADD, half had a widened medi-
astinum on chest x-­ray. This suggests the ADD score and chest x-­ray
provide complementary information.
994 PART III  Emergency Medicine by System

A B
Fig. 71.3  Painless dissection presentation. A 64-­year-­old man with a history of atrial fibrillation on warfarin
presented with transient blurred vision without pain or complaints in his chest or elsewhere. Magnetic res-
onance angiogram (MRA) imaging revealed dissection involving the carotid artery. Subsequent computed
tomography angiogram (CTA) of the chest revealed a type B aortic dissection (A). Endovascular stenting was
performed without event. The patient re-­presented with chest pain 6 years later with an ascending dissection
requiring operative repair. (B) Computed tomography angiogram (CTA) demonstrating original type B dissec-
tion and new type A dissection.

hypertension associated with dissection may further suggest intracra-

DIFFERENTIAL DIAGNOSIS
The differential diagnosis for acute aortic dissection is broad and
includes many conditions more common than dissection. It is perhaps
most important to always consider the possibility of aortic dissection
when diagnosing these other conditions. Dissection may coincide with
or cause another condition on the differential. Some factors associated
with a delay in diagnosis include fever, normal blood pressure, female
sex, non-­white race, and previous cardiac surgery.
Acute myocardial ischemia or infarction is an alternative, more
common cause of chest pain or discomfort. In contrast to aortic dissec-
tion where pain is often at high intensity at onset, pain due to coronary
ischemia may be provoked by exertion and crescendo with subsequent
waxing and waning. It can sometimes be relieved by rest or nitroglyc-
erin. Myocardial ischemia may be associated with suggestive ECG
changes. Unfortunately, as noted, type A dissection can cause coronary
ostial compromise and subsequent myocardial infarction, leading to
misdiagnosis. Approximately one in every 1000 STEMIs is caused by a
type A dissection. Acute pericarditis presents with chest pain, which is
often positional, and evidence of pericardial effusion. Aortic dissection
should be considered in any patient with pericardial effusion, with or
without tamponade physiology, or new aortic regurgitation.
Pulmonary embolism can cause chest pain and syncope like aor-
tic dissection, but commonly associated pulmonary symptoms such
as shortness of breath or cough are absent in dissection. Patients
with aortic dissection and neurologic symptoms may appear to be
suffering from a primary central nervous system event such as isch-
emic or hemorrhagic stroke. Among patients with ischemic stroke,
approximately 1% are suffering from acute aortic dissection.8 Severe
nial hemorrhage.
Patients with mesenteric ischemia classically present with a soft abdo-
men and abdominal pain out of proportion to tenderness. This can also
be observed with acute type A or B dissection. Mesenteric ischemia may
present with bloody bowel movements, which is an uncommon finding
in acute dissection. Other intestinal conditions can cause acute abdomi-
nal pain, but often with localized abdominal exam findings.
Other vascular emergencies such as renal artery aneurysm can
present similarly to aortic dissection with severe pain and hyperten-
sion. These are important differentials, particularly in predisposed
patients such as those with type 4 Ehlers-­Danlos syndrome. Lumbar
spinal disc disease can cause back pain radiating to one or both legs
and associated neurologic compromise. These symptoms and signs are
usually more geographically constrained to this portion of the body as
compared to dissection.
DIAGNOSTIC TESTING
Diagnostic testing begins with bedside ultrasonography, which is
indispensable to assess for reversible catastrophic conditions such as
pericardial tamponade. Using a small footprint probe to allow access
between the ribs, the exam should focus on the heart, and thoracic and
abdominal aorta. The initial assessment should determine if there is a
pericardial effusion, and if so, if there evidence of right ventricular free
wall scalloping during diastole suggestive of tamponade physiology.
The aortic root should be assessed for dilatation, dissection, and visible
flap using the left parasternal long-­axis view. The descending aorta is
also inspected for dissection, flap, or dilatation.
 CHAPTER 71  Aortic Dissection 995

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

V1
A

B
Fig. 71.4  Acute dissection complicated by left main STEMI. A 46-­year-­old man presented with acute, severe
chest pain with vomiting and diaphoresis while lifting weights at the gym. Initial ECG (A) indicated acute
antero-­septal STEMI with reciprocal inferior ST depression. The patient was taken emergently to the cardiac
catheterization lab. After temporizing stenting of his left main coronary as well as the left anterior descending
and left circumflex arteries, he was taken to the operating room for aortic root graft replacement with CABG.
Intraoperative transesophageal echocardiogram (TEE) (B) reveals type A dissection of the ascending aortic
root extending to the aortic valve.

TABLE 71.1  Aortic Dissection Detection Risk Score

High-­Risk Conditions
Marfan Syndrome
Family history of aortic disease
Known aortic valve disease
Recent aortic manipulation
Known thoracic aortic aneurysm
 
 
 
Any positive attributes in each column yields a score of 1 for that column. Each column can have a score of 1 or 0. The total ADD score is the sum
of the 3 columns (on a scale of 0 to 3).
High-­Risk Pain Features High-­Risk Examination Features
Chest, back, or abdominal pain described as any of the following: Evidence of perfusion deficit:
Pulse deficit
Abrupt onset Systolic BP differential
Severe intensity Focal neurologic deficit (in
Ripping or tearing conjunction with pain)
Murmur of aortic insufficiency
(new and with pain)
Hypotension or shock state

Laboratory studies should be sent, including complete blood count,
serum chemistry and renal function, coagulation profile, and blood
typing. Additionally, clinicians should send serial troponin for patients
with pain suggestive of coronary ischemia, B-­type natriuretic peptide if
there are signs of heart failure, and urinalysis if there is any concern for
renal arterial involvement. None of these studies diagnose dissection,
but they help to rule out other etiologies and define the extent of
complications.
ECG may demonstrate STEMI due to coronary ostial compromise
by the dissection or associated flap. Voltage may be decreased due to
pericardial effusion. Left ventricular hypertrophy due to longstand-
ing hypertension may be present in 20% of cases. Nonspecific ST-­T
996 PART III  Emergency Medicine by System
changes may be observed, and these can delay the correct diagnosis
of dissection.9 There is no ECG finding highly accurate for dissection.
Chest x-­ray has a sensitivity of 67% for acute dissection. The most
sensitive chest x-­ray findings are a widened aortic silhouette or medi-
astinum where mediastinal widening was defined as a width of at least
8 cm at the level of the aortic knob or a mediastinal to chest width ratio
exceeding 0.25.7 Separation of aortic intimal calcification from the
external aortic wall and pleural effusion have sensitivities of 9% to 16%
and 16% to 37%, respectively. Two-­view versus one-­view chest x-­ray
technique does not improve sensitivity. Given the only fair sensitivity
of this test, it is crucial that emergency physicians not let a normal chest
x-­ray defer or delay further evaluation when dissection is suspected.
A variety of serologic tests have been investigated to diagnose aortic
dissection. Serum D-­dimer is the most useful at present. It is rapidly
performed and readily available due to its use to assess for pulmonary
embolism. At a test threshold of 500 ng/ml, the test is approximately
96% sensitive and 70% specific with a negative likelihood ratio of 0.05
for acute dissection.5 D-­dimer alone is insufficient to rule out acute
dissection confidently, but in concert with other information, it is use-
ful to assess the need for CT imaging.10,11 The combined strategy of
ADD=0 and negative D-­dimer was 99.7% sensitive for acute dissec-
tion.10 Specificity was 18%. Applied in practice, this means CT imaging
or equivalent could be avoided in 18% of the patients in whom dis-
section is considered, but not present. Conversely, in patients with an
ADD score of 2 or above, 4% of patients had an acute aortic syndrome
even if the d-­dimer was negative. This suggests that D-­dimer should
not be used in patients with a high clinical probability of dissection;
rather, these patients must receive an advanced imaging test.
Investigations of other candidate biomarkers for acute dissection
continue. These include smooth muscle myosin components, sol-
uble elastin fragments, microfibril fragments including fibrillin-1,
fibrin degradation products, and an interleukin receptor, ST2.12 None
have demonstrated sufficient sensitivity to rule out acute dissection
adequately.
The diagnosis of aortic dissection ultimately rests on diagnostic
imaging. Techniques with acceptable test characteristics include mul-
tidetector CT angiogram of the aorta (MDCTA), conventional angiog-
raphy, magnetic resonance angiography (MRA), and transesophageal
echocardiography (TEE). The choice of test used is based on multi-
ple factors, including accuracy, safety, contraindications, availability,
speed, convenience, ability to identify alternative diagnoses, and cost.
MDCTA is the initial imaging study in about three-­quarters of patients
today, followed by TEE.1 Often multiple tests are used. Goals of imag-
ing are to confirm the diagnosis, localize the tear, display the anatomy
and extent of the dissection flap, and determine whether prompt life-­
saving intervention is needed.
MDCTA is generally preferred throughout the United States
because it is readily available, fast, both sensitive and specific, and usu-
ally meets the previously stated goals. In the event of serious contrast
allergy requiring a prolonged pretreatment regimen, or inability to tol-
erate or fit on the CT scanner, then another modality must be used.
TEE may generally be the preferred alternative choice if it can be per-
formed expeditiously by a qualified specialist.
TEE offers some advantages over MDCTA. The TEE probe and
procedure are portable. In addition to being highly sensitive for the
identification of type A dissection, TEE is also useful when involve-
ment of the aortic valve and the status of the left ventricle, pericardial
space, and right and left coronary artery ostia are unknown. Transtho-
racic echocardiography (TTE) is useful if it demonstrates disease but is
insufficiently sensitive to rule out dissection.
MRA is rarely used for diagnosis of dissection because it takes lon-
ger to perform than MDCTA or TEE. Additionally, clinical staff must
maintain a distance from the potentially unstable patient during the
study, leading to safety issues. When used, it demonstrates excellent
spatial resolution and anatomic detail. Aortography is the historical
gold standard, but it is seldom the initial test for aortic dissection today
due to the ease and rapid acquisition of MDCTA in most instances. The
reported false-­negative rate for aortography ranges from 5% to 15%.
Aortography is valuable for the patient with STEMI but some presen-
tation characteristics suggestive of dissection. As time is essential for
percutaneous transluminal coronary angioplasty (PTCA) or stenting
for STEMI patients, the patient can be brought to the cardiac cathe-
terization lab and aortography performed at the initiation of the pro-
cedure in lieu of other imaging. The emergency physician must share
his or her concerns with the interventional cardiologist to plan this
diagnostic approach.
“Triple rule out” imaging refers to MDCTA protocol to assess
simultaneously for acute aortic dissection, myocardial infarction, and
pulmonary embolism. ECG gating freezes cardiac motion allowing
evaluation of the perivalvular area and coronary arteries. A broad spec-
trum of other chest and upper abdominal diseases also may be iden-
tified with this study. However, EPs seriously consider and test for all
three diagnoses in only about 3% of chest pain evaluations. There are
a host of limitations to this test including coronary calcifications or
stents, renal insufficiency, atrial fibrillation, inadequate heart rate con-
trol, contrast allergy, obesity, cost, and concern for radiation exposure.
MANAGEMENT
The initial primary goal of care in the emergency department setting is
to minimize dissection extension. This is accomplished by decreasing
the force of cardiac contraction and resulting aortic sheer forces, and
driving the heart rate down to 60 beats per minute or less. Acceleration
of aortic blood flow, dP/dt, is minimized while maintaining blood pres-
sure in the low normal range. Beta-1 adrenergic blockade therapy is the
preferred treatment (Table 71.2). Favored agents include esmolol infu-
sion due to its short 9-­minute half-­life and titratability, or metoprolol
or labetalol if esmolol is not readily available. Labetalol also provides
alpha-1 adrenergic blockade decreasing vascular tone and blood pres-
sure. A selective beta-1 receptor blocker such as esmolol or metoprolol
may be preferred for patients with chronic obstructive pulmonary dis-
ease (COPD) at risk for bronchospasm. Decreased cardiac contractility
can also be achieved with infusion of the calcium channel blockers dil-
tiazem or verapamil if beta blockers are contraindicated due to allergy
or severe pulmonary disease, or unavailable.
Blood pressure control is critical in the setting of dissection. Hypo-
tension should elicit an immediate search for potentially reversible
causes such as pericardial tamponade or internal hemorrhage. In addi-
tion to any temporizing interventions such as pericardiocentesis, blood
pressure may be supported with crystalloid infusion and vasopressors
to provide adequate perfusion of vital organs, targeting a mean arterial
pressure of 65 mm Hg. Norepinephrine or phenylephrine infusions
are preferred to maximize peripheral vasoconstriction and minimize
myocardial stimulation with resulting sheer stress. Antiadrenergic
infusions should be stopped.
Hypertension is commonly encountered in type B dissections and
must be treated with a target of 100 to 120 mm Hg systolic. Vasodilat-
ing agents such as nitroprusside can be infused, but only after initiation
of antiadrenergic therapy to blunt the force of myocardial contraction.
An ACE inhibitor such as enalaprilat may be beneficial, particularly if
there is renal artery compromise. An arterial catheter should be placed
in an uninvolved extremity to monitor and titrate therapy closely.
Analgesia is essential for patient comfort and to decrease pain-­
induced sympathetic discharge. Parenteral narcotics such as morphine,
 CHAPTER 71  Aortic Dissection 997

dissection generally requires expeditious surgical repair due to pro-

TABLE 71.2  Acute Aortic Dissection
gressive increasing risk of multiple complications, including rupture
Medications into the pericardial space, development of coronary or cerebral isch-
Medications Dosages (IV) emia, aortic regurgitation, congestive heart failure, or free rupture of
Contractile force the aorta into the thorax.
and BP control For patients with type A dissection complicated by malperfusion,
medical therapy, along with temporizing percutaneous reperfusion
Antiadrenergic using aortic stenting or fenestration, and selective branch stenting may
Esmolol 0.5 mg/kg over 1 minute, then 50 μg/kg/min infusion allow stabilization and reduce the risk of the operation. Repair of the
Increase by 50 μg/kg/min every 4 min to max. 300 patient’s ascending aorta may proceed after a period of recovery.
μg/kg/min Definitive aortic repair includes resection of the dissected aorta
Repeat 0.5 mg/kg boluses with each increase in segment and insertion of an aortic graft. Restoration of aortic valve
dosing competence is paramount in patients who develop aortic insufficiency.
This is usually achieved by resuspension of the native aortic valve or by
Labetalol 10–20 mg up to every 10 minutes, or 0.5-2 mg/min
aortic valve replacement, depending on the size of the aortic root and
infusion
the condition of the aortic valve leaflets. Reimplantation of the coro-
Metoprolol 2.5–5 mg every few minutes nary arteries to the new graft may also be necessary. Surgical mortality
has slowly decreased but remains substantial at 18% overall in major
Vasodilation
Nitroprusside Begin 0.25–0.5 μg/kg/min and increase to max. 10 centers.1
μg/kg/min The cornerstone of type B dissection treatment is blood pressure
Enalaprilat Begin 1.25 mg over 5 minutes, repeat up to 5 mg
control. Surgical intervention has been reserved for life-­threatening
every 6 hours
complications such as ischemia of both kidneys leading to reversible
renal failure, intestinal ischemia, limb ischemia, progressive aneurysm
Calcium channel
extension, impending or frank rupture, or intractable pain. However,
blockade
modern endovascular therapy using stent grafts and fenestration is
Diltiazem Begin 10–20 mg, then 5 mg/hr infusion evolving this paradigm. The goals of this therapy include reconstruc-
Infusion can be increased in 5 mg/hr increments up tion of the thoracic aorta segment containing the entry tear, induction
to 15 mg/hr of thrombosis of the false lumen, and reestablishment of the true aor-
Verapamil Begin 5 mg over 5 minutes, then repeat 5–10 mg up tic lumen and side-­branch flow. Aortic fenestration is indicated for
to every 15 minutes carefully selected patients with malperfusion syndrome due to branch
Or infuse 5 mg/hr with adjustment as needed artery occlusion, and to provide a reentry tear for a dead-­end false
lumen. A less invasive strategy using stents may be preferable to sur-
Analgesia (opioids) gery in higher-­risk candidates. Endovascular aortic repair may even be
Fentanyl 0.5–1 mcg/kg every 30 min as needed employed for uncomplicated type B dissections to prevent subsequent
Morphine 0.1 mg/kg every 1 hr as needed aneurysm formation, which is otherwise common.13
Surgery and endovascular interventions require coordinated teams
Vasopressor with expertise and experience to achieve success. Outcomes for type A
Norepinephrine Begin 5 μg/min and titrate up to mean arterial blood
dissection patients are generally better at high-­volume centers. How-
pressure goal of 65 mm Hg
ever, patient transfer incurs a delay in time-­sensitive care. Recent data
Phenylephrine Begin 50 μg/min and titrate up to mean arterial suggest regionalization of care with transfer a mean of 50 miles to high-­
blood pressure goal of 65 mm Hg volume centers is associated with lower operative mortality.14

fentanyl, or hydromorphone are reasonable choices. Fentanyl benefits
from a short half-­life allowing titratability and relatively minimal sec-
ondary decrease in blood pressure. These characteristics are particu-
larly valuable in the setting of hypotension.
Cardiac tamponade complicates up to approximately one-­fifth of
acute aortic dissections and carries a 50% mortality. Controlled cath-
eter drainage with a pigtail catheter can be performed with ED ultra-
sound guidance to temporize and allow time to prepare for definitive
operative care. We recommend insertion of an 8F pigtail catheter at the
fourth or fifth intercostal space at or just medial to the left midclavicu-
lar line aiming for the pericardial effusion visualized beyond the apex
of the heart. Once the catheter is inserted, 5 to 10 mL of hemopericar-
dium can be aspirated with close observation of the resulting hemody-
namics. Aspiration can be repeated as needed to attain a systolic blood
pressure of 80 to 90 mm Hg.
Definitive therapy of acute aortic dissection has been defined by the
type of dissection and continues to evolve, particularly due to advanc-
ing endovascular therapies. It is critical to consult surgical services as
soon as dissection is identified to develop a coordinated plan. Type A
DISPOSITION
Patients with acute aortic dissection generally require emergent surgi-
cal consultation and admission to the intensive care unit or operating
room for further care. Consultation with surgical subspecialties could
include cardiovascular surgery for type A dissections and vascular sur-
gery for type B dissections but may vary based on local practice and
resources.
The patient and family should be informed of the diagnosis and
gravity of the situation. Type A acute aortic dissection carries a mortal-
ity of 1% to 2% per hour immediately after the onset of symptoms. The
risk of death is increased in patients presenting with pericardial tam-
ponade, coronary artery involvement leading to myocardial ischemia
or infarction, or carotid artery involvement causing cerebral hypoper-
fusion. The most common causes of death are aortic rupture, stroke,
visceral ischemia, cardiac tamponade, and circulatory failure. The
long-­term 1-­and 3-­year survival reported in the IRAD in the surgically
treated patients surviving to hospital discharge are 96 ± 2.4% and 91 ±
3.9%, respectively, reflecting the timely surgical repair of the ascending
aortic dissection. Patients with type B acute aortic dissection without
998 PART III  Emergency Medicine by System
associated complications have a 30-­day mortality of 10%. However,
patients who develop ischemic complications with associated organ
malperfusion syndrome, renal failure, visceral ischemia, or contained
rupture often require urgent aortic repair, which carries a mortality of
20% by day 2 and 25% by day 30.
Survivors of aortic dissection require vigilant long-­term surveil-
lance with strict blood pressure control and monitoring. Patients who
retain patency in the false channel of the aorta after either medical
treatment or surgical repair have a significant risk of aneurysm forma-
tion and rupture of the false channel, especially in the first 6 months
after initial therapy. Expansion, rupture, or both are more common in
patients who are older and have poorly controlled hypertension and
COPD. Other potential complications include redissection and pro-
gressive aortic insufficiency. The emergency physician should have a
heightened level of concern and low threshold for definitive imaging
for patients who return to the ED with relevant complaints after prior
treatment for aortic dissection.
The references for this chapter can be found online at ExpertConsult.
com.