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Management ofComplicated Acute Type AAortic Dissection: The Stanford Approach
https://t.me/med1917
distal extension, or ap fenestration) may then be performed as necessary. We
do not routinely perform aortography following repair unless a specic concern
persists.
377
Post-Operative Care
Aggressive resuscitation during and following central aortic repair is critical to
reverse metabolic derangement resulting from malperfusion and cardiopulmonary
bypass. Platelets and fresh frozen plasma are frequently required to address coagulopathy. Active warming may be required to maintain normothermia. Metabolic acidosis and elevated serum lactate are frequently present on arrival to the ICU and
should be monitored for correction with ongoing volume resuscitation. Persistent
metabolic acidosis should prompt re-evaluation for ongoing malperfusion or unrecognized bowel ischemia. A baseline neurologic status should be obtained within the
rst few hours in ICU; persistent obtundation or change in neurologic exam should
prompt immediate head CT.
Renal malperfusion due to static obstruction may persist following central repair.
Oliguria and rising serum creatinine from this entity is difcult to distinguish from
more typical acute kidney injury after cardiopulmonary bypass and transient lowow states. Devoted renal doppler ultrasound should be obtained in this setting.
Delayed renal artery stenting can be undertaken following initial resuscitation in an
attempt to salvage renal function.
Final Remarks
Complicated ATAAD represents a unique clinical challenge for aortic surgeons. The
heterogeneous spectrum of presentation precludes the application of a “one size ts
all” strategy. Despite specialized care at tertiary referral hospitals, surgical mortality
remains frustratingly high. Effective management requires a broad range of skills,
sound decision-making and institutional capability to perform both traditional open
surgery and hybrid endovascular interventions. Care of the complicated ATAAD
patient is frequently multidisciplinary, encompassing multiple consulting specialties to manage complications of malperfusion. Meticulous clinical decision-making
is a central theme in the determination of operative candidacy, strategy, and extent
of aortic repair in these patients, decisions which may mean the difference between
life and death. Finally, ATAAD patients require lifelong surveillance with crosssectional imaging for progressive aneurysmal dilation of the distal dissected aorta.
We strongly advocate for institution-based aortic teams to manage surveillance and
secondary interventions for the residual aorta. The “aortic team” consisting of cardiac and vascular surgeons and devoted cardiovascular Radiology specialists is a
critical asset in the longitudinal management of this complex patient subset.
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A. J. Pedroza and M. P. Fischbein
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A. J. Pedroza and M. P. Fischbein
Management ofType B Aortic Dissection
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AliKhoynezhad, TiffanyWorthington, RaffatJaber, JeffreyAltshuler,
andRodneyWhite
Introduction
Acute aortic dissection (AAD) is a devastating aortic catastrophe accounting for
more than 20 cases per million per year. AAD begins with a tear in the intimal layer
presumably due to existing wall weakness or an episode of high blood pressure.
Blood under pulsatile pressure subsequently forces the intimomedial tear to open
within the media of the aorta and dissects along into the media layers in the diseased
aortic wall, forming a false lumen(s). Temporal classication of AAD includes
hyperacute (within 24hours of onset), acute (1–14days after dissection), subacute
(15–90 days) or chronic (greater than 90 days from onset. Additionally, AAD is
classied by the location of the dissection. The Stanford classication system
divides acute aortic syndromes into two location categories: type A, when the intimomedial tear is in the ascending aorta, and type B when the intimomedial tear is in
the descending thoracic aorta [1]. This classication system is important for patient
triage, as typically all type A dissections should be evaluated for surgical intervention; however, type B lesions can often be managed with medical therapy alone.
Some experts disagree as to where the anatomic divide occurs for type A and type
B classication. The consensus is the origin of the left subclavian establishes the
divide, however other experts argue that arch dissection without a proximal extension should be managed conservatively [2].
In the absence of complicating factors such as rupture, malperfusion syndromes, rapid aortic expansion, and/or refractory pain (i.e., complicated acute
type B aortic dissection), acute type B aortic dissection (TBAD) can often be
treated with medical management alone. For those that exhibit these complications or high-risk features, immediate endovascular or open surgical intervention
A. Khoynezhad (*) · T. Worthington · R. Jaber · J. Altshuler · R. White
Department of Cardiovascular Surgery, MemorialCare Heart and Vascular Institute,
Long Beach, CA, USA
e-mail: akhoynezhad@memorialcare.org
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_27
381© Springer Nature Switzerland AG 2021
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is recommended. This chapter discusses the management of TBAD and when to
consider additional interventions.
A. Khoynezhad et al.
Presenting Signs andSymptoms
The typical patient with acute TBAD is a male patient, 60–70years old, with a
longstanding history of hypertension presenting to the emergency department with
sudden onset, ripping/tearing back, or abdominal pain. Chest pain is more common
for those with type A pathology; however up to 62% of those with TBAD may also
present with this complaint [3]. Patients 40–50years old with TBAD are less likely
to have a history of hypertension; instead, they often have a history of the bicuspid
aortic valve, Marfan syndrome, or another connective tissue disorder, or history of
prior aortic surgery [4]. Of patients presenting to the emergency department, 90%
reported this pain as severe or the worst pain of their lives [3]. One out of six patients
with acute aortic dissection may also describe a migratory quality to the pain [3].
In addition to complaints of pain, patients with aortic dissection may also report
more generalized complaints such as dyspnea, nausea, diaphoresis, nausea, and
vomiting. In the event of malperfusion syndrome, patients also may present with
symptoms specic to branch arteries that have been affected. Diminished perfusion
to cerebral vessels may lead to stroke or coma. If intercostal or segmental arteries
are affected, paraplegia or quadriplegia may be present. While patients with acute
ischemia of the superior mesenteric artery typically have substantial abdominal pain
and a poor prognosis, those with malperfusion to the lower extremities may take a
while to exhibit symptoms [5].
Signs and symptoms consistent with malperfusion syndrome may be persistent
or intermittent due to the dynamic nature of ow obstruction with the mobile intimal ap.
Physical exam ndings are often nonspecic and are not sufciently sensitive to
rule out aortic dissection, but it can be useful for raising the index of suspicion for
the presence of dissection and the need for emergent intervention [6]. ED physicians
were able to correctly suspect aortic dissection in only 65% of cases according to
one study [7]. Pulse decits are present in up to 31% of patients with TBAD and
signicantly raise the likelihood ratio of aortic dissection (LR 5.7) [3, 6]. The majority of patients (70%) presenting with TBAD are hypertensive (SBP >150mmHg)
[2]. The presence of hypotension is an ominous sign in a patient with dissection.
Prognosis
Once a patient develops an aortic dissection, the usual survival curve is signicantly
compromised. Although type A dissection is associated with an early mortality rate
of up to 50%, in patients with acute TBAD the mortality is 10–12% [8]. More recent
Management ofType B Aortic Dissection
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studies show all-comer hospital mortality of 8.8% for all acute TBAD [9]. Most of
these patients can be managed medically with antihypertensive medical therapy and
close follow-up imaging. This cohort of completely uncomplicated type B aortic
dissection do relatively well in early hospital stay with early mortality of 1.2–3% [9,
10]. This reduced mortality is mostly due to protocolization, dedicated aortic cen-
ters, and improved anti-impulsive management of these patients.
Patients with complicated acute TBAD have a substantially worse prognosis [11].
The early mortality is around 13% across North American medical centers and
one-year survival of 81% [12]. Unfortunately, up to 80% of survivors develop aneurysmal dilatation of the false lumen in the follow-up period with intervention
required in one-third of cases [13]. IRAD data suggest that about one in four patients
with TBAD died at the three-year mark regardless of the mode of therapy [14].
Three-year survival for those treated medically, surgically, and with the endovascular intervention were 77.6%, 82.8%, and 76.2%, respectively [14]. Independent predictors of mortality include aortic diameter >4cm, a patent false lumen, and partial
thrombosis of the false lumen [15].
383
Diagnostic Imaging
The diagnosis of acute aortic dissection in the emergency department remains a
clinical challenge. The classic presentation of dissection includes chest pain, which
is the second most common complaint in the emergency department. Of the approximately 4.4 million patients who present annually to the ED for chest pain, only
about 2000 have an aortic dissection [6, 16]. By this volume, an ED physician seeing 3000–4000 patients per year would encounter a patient with aortic dissection
once every three to four years [16].
The selection of diagnostic imaging depends on several factors, including patient
stability, availability of resources, and local expertise. The goals for imaging are to
conrm (or rule out) dissection rapidly, to evaluate the extent of the aortic injury,
locate intimal tears, conrm the presence of false lumen as well as any associated
thrombus formation, assess arterial branch involvement, identify aortic regurgitation and locate any signs of local rupture including pericardial or pleural effusion.
Chest x-ray ndings classically associated with aortic dissection include pleural
effusion, displaced intimal calcication, abnormal aortic contour, and widened
mediastinum. Unfortunately, sensitivity and specicity of chest X-ray for the diagnosis of aortic disease are limited (64% and 86% respectively); thus the presence or
absence of these ndings does not sufciently rule out dissection [17]. In 12.4% of
patients with aortic dissection, no chest X-ray abnormality was noted [3]. For this
reason, a chest X-ray should be avoided in the patient with suspected aortic disease,
as this may lead to further delay of denitive imaging.
Denitive imaging is crucial in the workup for aortic dissection. Imaging options
available include computed tomography angiography (CTA), transesophageal echocardiography (TEE), aortography, and magnetic resonance angiography (MRA).
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Aortography has lost popularity as a diagnostic imaging tool. Currently, angiography is used for diagnosis in <4% of cases [18]. It is associated with numerous disadvantages, including large contrast requirements (1mg/kg), the time it takes to
complete the procedure (up to 2h), and the usual risks associated with an invasive
procedure.
Sensitivity for CTA, TEE, and MRA are similar for the diagnosis of aortic dissection (98–100%). CTA is widely available and offers visualization of the entire
aorta. It is the rst choice for work up in aortic dissection and can often identify
intimal ap location, the extent of branch vessel involvement, and is relatively rapid
to perform. Disadvantages include the need for contrast administration and patient
transportation to the imaging suite. Due to the static nature of imaging, functional
assessment of the aortic valve cannot be performed with CTA.
MRA is not generally recommended as a rst-line imaging choice for suspected
acute dissection due to the extended duration of the study and the rarity of availability on an emergent basis.
TEE is an acceptable alternative for patients who are hemodynamically unstable
and unable to leave the emergency department for alternate imaging [2]. Advantages
include the ability to perform echocardiography at the patient bedside and acceptable sensitivity in identifying aortic pathology. TEE is more sensitive in detecting
type A pathology than type B (93.5% v 88.1%, respectively) [19].
A. Khoynezhad et al.
History ofSurgical Versus Medical Management
Morgagni initially described aortic dissection in the 1700s. For two hundred years,
although awareness persisted for the disease, treatment options for patients with
dissection were limited. Hirst etal. published a case series in 1958 describing 505
patients noting the manifestations, pathologic correlations, and historical aspects to
characterize further factors associated with aortic dissection [20]. Until the 1950s,
the management of aortic dissection was limited. After the landmark aortic operation by Drs. DeBakey and Cooley in the 1950s, TBAD became a surgically managed condition [21]. During that time, most patients with acute TBAD were offered
replacement of the descending thoracic aorta with an operative mortality of 30–40%.
In the 1960s, Wheat etal. started research on the effects of anti-impulsive therapy
[22]. To further evaluate medical treatments of aortic disease, researchers used a
variety of animal models. Dog models were used to assess the effects of the force of
contraction (dP/dT) and blood pressure control [23]. Male broad-breasted white
turkeys, which are naturally quite prone to aortic dissection, were used to assess the
effects of various medications on the elastin and collagen properties of aortic tissue.
The turkeys were fed B-aminopropionitrile (BAPN), which would cause medial
degeneration through the disruption of collagen cross-links and elastin bers in the
media of the turkey. The benecial effects of propranolol and hydralazine on aortic
elastin and collagen were identied through these models [24]. Through the 1970s,
medical management of uncomplicated TBAD became the standard of care as
Management ofType B Aortic Dissection
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availability of potent beta-blockers increased and comparative mortality to surgical
intervention favored a more conservative approach.
Early experience with the thoracic endovascular aortic intervention was initially
published in 1988 by Volodos etal. on the intervention of patients with a traumatic
aortic aneurysm [25]. In 1991, Juan Parodi published his experience with endovascular intervention for the treatment of an abdominal aortic aneurysm [26]. The following year, Dake etal. published cases of endovascular intervention in the thoracic
aorta [27]. Initial stent-grafts were designed using a 24F delivery system, were custom made for each case, and were used predominantly in patients with aortic aneurysm. White and co-workers used physicians-sponsored investigational device
exemptions for early evaluation of TEVAR for acute and chronic dissection in the
early 1990s [28]. This research laid the foundation for the studies that led to the rst
indication in the United States for thoracic endografts for patients with malperfusion by the FDA.This allowed Medtronic and Gore to obtain rapid approval for
malperfusion indication and was later used to cover additional thoracic indications
with the agreement to participate in post-market surveillance for other indications.
This led to rapid approval for numerous indications, faster than what would be
expected with individual studies. Cook is now doing a post-market study to get the
same approvals.
Through the late 1990s, less than ten percent of patients with TBAD were treated
with stent-grafts [29]. According to IRAD data in 2000, 20% of patients with type
B dissection underwent surgical therapy, 4.3% underwent percutaneous fenestration
or stenting [3]. In 2015, 8% underwent surgical intervention, 31% underwent endovascular intervention, and 63% were treated with medication alone [30]. This is in
contrast to today’s clinical practice, where the overwhelming majority of acute
TBAD offered an intervention, undergo aortic stent grafting.
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Initial Medical Management
Management options for patients with aortic dissection include medical, surgical, or
endovascular interventions. Regardless of the treatment approach considered, initial
intervention should be aimed at reducing the propagation of the dissection by
decreasing aortic wall stress [31]. This is achieved by controlling blood pressure
and left ventricular ejection force (dP/dT). Upon suspicion of aortic dissection in a
patient in the ED, the patient should be emergently assessed by the ED provider
with an abbreviated history and physical examination including the time of onset,
risk factors for aortic dissection, and assessment for ndings consistent with aortic
dissection. Two large-bore IVs should be established, supplemental oxygen administered, and the patient placed on a cardiac monitor. EKG, portable chest x-ray, and
lab work including type and cross are critical if massive transfusion is needed for
hemodynamic collapse.
Patients with uncomplicated type B aortic dissection should be admitted to the
cardiac intensive care unit with close monitoring including arterial line blood
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pressure monitoring, frequent neurologic status checks, urine output monitoring,
telemetry, supplemental oxygen, and pain control.
Initial management of acute type B aortic dissection
In the emergency department
(1) Establish two large-bore IVs (>18 gauge)
(2) Administer supplemental oxygen
(3) Cardiac monitoring, EKG, chest X-ray
(4) Obtain CBC, chemistry panel, coagulation panel, UA, CK, troponin, d-dimer
(5) Type and cross 10units packed red blood cells
(6) Early surgery consultation
Imaging
1. Computed tomography angiogram (CTA)
2. Echocardiogram
3. Magnetic resonance angiogram (MRA)
Blood pressure, heart rate, pain management
Goals: heart rate<60 beats/min, systolic blood pressure<100mmHg)
1. First line: beta-blockers
a. Esmolol (200–500mcg/kg IV loading dose)+25–50mcg/kg/min infusion (up to 300
mcg/kg/min max dose)
b. Labetalol (20mg IV bolus)+0.5–2mg/min IV infusion (up to 10mg/min max dose)
2. If hypertension persists: vasodilators
a. Nicardipine (2.5–5mg/h IV infusion titrated up to max dose 30mg/r)
3. Pain relief: morphine
Hemodynamically unstable patients
1. Tracheal intubation, mechanical ventilation
2. Blood pressure support with IV uids, PRBCs if rupture suspected
Studies suggest that 97% of patients with uncomplicated type B aortic dissection
will require at least one parenteral antihypertensive during admission [9]. Most
patients will require a regimen consisting of multiple antihypertensive medications
that require frequent titration to achieve a systolic BP less than 120mmHg [32]. All
patients with type B aortic dissection should be discharged on antihypertensive
medications.
First-line antihypertensive therapy includes beta-blockers such as labetalol,
esmolol, and metoprolol to reduce left ventricular contraction force (dP/dT) [33].
Adequate hemodynamic stabilization will reduce the risk of progression of dissection and help to reduce the risk of rupture [34]. In patients with contraindication
to beta-blockers such as asthma and heart failure, a trial of esmolol may be initiated,
the short half-life is typically well tolerated in patients with a history of pulmonary
disease. In the event esmolol is not well tolerated, non-dihydropyridine calcium
channel blockers can be used as an acceptable alternative [35]. A labetalol is an
attractive option for rst-line therapy due to the alpha- and beta- characteristics
which work to reduce both dP/dT as well as have vasodilatory properties. Caution
should be used in using beta-blockers in the presence of signicant acute aortic
valve insufciency due to the effects on compensatory mechanisms [2].
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