Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3734_Библиотеки_им_академика_М_И_Перельмана
.pdf
Part II
https://t.me/med1917
Imaging and Initial Management of Acute
Aortic Syndromes
Initial Medical Management ofAcute
https://t.me/med1917
Aortic Syndromes
AbigailR.Benkert andJeffreyG.Gaca
Introduction
Acute aortic syndrome encompasses three life-threatening diseases: aortic dissection, intramural hematoma, and penetrating atherosclerotic aortic ulcer. When
symptom onset is within 14 days of inciting event, the presentation is deemed
‘acute.’ All diseases within the acute aortic syndrome eventually lead to the breakdown of the aortic intima and media [1]. Lesions are classically described based on
their location within the thoracic aorta. A lesion involving the ascending aorta is
Stanford A (DeBakey type I–II); those not involving the ascending aorta are Stanford
B (DeBakey type III). For this chapter, we will use the Stanford nomenclature.
Acute aortic dissection (AAD) occurs when an intimal tear results in formation
of a dissection plane and disruption of the medial layer. This results in separation of
the aortic wall layers and subsequent formation of true and false lumens [2]. The
false channel is contained by the outer medial and adventitial layers. However, the
intimal tear (dissection ap) can extend both proximally and distally with each cardiac cycle, potentially compromising ow within branch arteries. When the outer
aortic wall weakens, aortic rupture is possible. The International Registry of Acute
Aortic Dissection (IRAD) reports that of patients presenting with AAD, 67% presented with type A dissections (TAAD) [3]. The mortality of type A dissection is
1–2% per hour after early symptom onset, and survival appears to depend upon the
degree of communication and the wall stress present in the false lumen [4].
Intramural hematoma (IMH) most commonly occurs in the descending aorta and
is characterized by rupture of the vaso vasorum into the aortic media, with subsequent hematoma formation [3]. Functionally, the hematoma within the aortic wall
does not freely communicate with the lumen and has restricted ow [5]. The absence
A. R. Benkert · J. G. Gaca (*)
Division of Cardiothoracic Surgery, Department of Surgery, Duke University Medical Center,
Durham, NC, USA
e-mail: jeffrey.gaca@duke.edu
J. S. Coselli et al. (eds.), Aortic Dissection and Acute Aortic Syndromes,
https://doi.org/10.1007/978-3-030-66668-2_9
119© Springer Nature Switzerland AG 2021
120
https://t.me/med1917
of an intimal lesion distinguishes aortic IMH from a peri-aortic hematoma that may
be associated with a penetrating aortic ulcer (PAU). IMH accounts for 10–25% of
acute aortic syndromes and the overall long-term prognosis is more favorable than
that of patients with AAD [2]. However, several studies suggest that 30–40% of
IMH evolve into AAD, with the greatest risk at 8 days from symptom onset [2].
Penetrating aortic ulcer (PAU) refers to ulceration of an atherosclerotic plaque,
which penetrates through the elastic lamina and into the aortic media. The location
of PAU is predominantly in the descending aorta (85–90%). While the true prevalence of the disorder is unknown, it is estimated to represent 2–7% of all acute aortic
syndromes [3]. These lesions, left untreated, can lead to progressive aortic enlargement and aneurysm development. Propagation of the ulcerative process may lead to
IMH, pseudoaneurysm, AAD, or aortic rupture [2].
A. R. Benkert and J. G. Gaca
Presentation andDiagnosis
Given the high mortality associated with missed and delayed diagnoses of acute
aortic syndromes, a high clinical suspicion and diagnosis as early in the disease
process as possible is paramount.
Acute Aortic Dissection
The most important risk factor precipitating acute aortic dissection is systemic
hypertension, which increases the stress on the aortic wall. Seventy-seven percent of
patients presenting with AAD have co-morbid hypertension [3]. Aortic dissection
most commonly occurs in men, representing two-thirds of affected patients. Women,
when affected, tend to be older (mean 67 vs. 63years) [3]. Less common precipitating risk factors include atherosclerosis, known aortic aneurysm, previous cardiac
surgery, connective tissue disorders (Marfan’s, Loeys-Dietz), and cocaine use.
Patients commonly present with a chief complaint of acute onset severe chest or
back pain. The pain is typically abrupt in onset and is at its most severe at the time
of onset. Most frequently described as sharp [3], it can also be tearing, ripping, and
stabbing in nature. In TAAD, the pain is usually retrosternal, whereas in distal dissections the pain is more often localized interscapular and in the back. Of note,
symptoms can deceptively be intermittent [1]. Up to 30% of patients later found to
have AAD were initially suspected to have other conditions such as myocardial
infarctions or pulmonary embolus. Therefore, acute aortic dissection should remain
on the differential diagnosis for patients presenting with unexplained syncope,
stroke, acute onset congestive heart failure, and acute ischemia of extremities or
viscera, even when the typical chest pain is not the leading symptom [4]. Recurrent
chest or back pain typically indicates extension, expansion, or rupture of the
dissection.
Initial Medical Management ofAcute Aortic Syndromes
https://t.me/med1917
Physical examination should focus on ndings that help increase suspicion for
dissection and represent high-risk features, as well as signs of end-organ dysfunction. A detailed pulse examination, including carotid, radial, and femoral pulses can
indicate the extent of disease. Syncope, stroke, and other neurologic symptoms may
occur in up to 40% of patients with proximal aortic dissection, yet these initial
symptoms can often mask the diagnosis [3]. Differential upper extremity pulses
suggest involvement of the brachiocephalic branch arteries. Iliofemoral involvement can result in lower extremity pulse loss, the most drastic of which is pulseless
bilateral lower extremities in the case of complete obstruction of the iliac bifurcation. A complete cardiac exam should be completed, with particular attention to
whether there is new-onset diastolic (aortic regurgitation) murmur or signs of pericardial involvement including presence of pericardial friction rub, jugular venous
distension, or pulsus paradoxus consistent with tamponade. After aortic rupture,
aortic regurgitation is the second most common cause of death, with patients frequently presenting with heart failure and cardiogenic shock [2]. Branch artery compromise can also lead to malperfusion of the bowel (acute abdomen and acidosis)
and kidneys (rising blood urea nitrogen/creatinine and oliguria).
121
Intramural Hematoma
The clinical presentation of IMH is similar to that of AAD.Distinguishing between
the two entities cannot be made clinically and requires tomographic imaging [6].
Penetrating Aortic Ulcer
Clinical manifestations of PAU are similar to AAD. However, patients tend to be
older and more frequently have a history of tobacco abuse, hypertension, coronary
artery disease, chronic obstructive pulmonary disease, and concurrent abdominal
aneurysms. Symptoms typically occur once the PAU reaches the adventitia; therefore, symptoms are assumed to indicate an emergency.
Initial Medical Management
There remains a lack of evidence for initial targeted medical management of acute
aortic syndromes. As there are no randomized controlled trials or meta-analyses, the
recommendations that follow are provided by a consensus of opinions (Class I,
Level C).
The aim of medical management in acute aortic syndromes is to prevent aortic
rupture, and in the case of IMH and PAU, to prevent progression to AAD.While
122
https://t.me/med1917
denitive interventions vary based upon the classication and type of acute aortic
syndrome, all patients presenting with acute aortic syndrome are initially managed
medically. Upon suspicion of diagnosis, the primary goal is to reduce blood pressure, heart rate, and force of cardiac ejection (dp/dt). Carefully monitored and
aggressive management is essential to prevent rupture, as the main cause of death is
not the initial tear, but related to the extension of the dissection with ultimate rupture
and death due to hemorrhage or cardiac tamponade [1, 7].
A. R. Benkert and J. G. Gaca
Anti-impulse Therapy
Current medical management is largely derived from the seminal work of Wheat
etal. [7] as well as Simpson and Taylor [8]. Wheat etal. constructed an ex vivo
model of aortas using Tygon tubing coated internally with rubber cement to demonstrate the primary goals of pharmacological management of acute aortic syndromes
[7]. The contractile force of the myocardium, expressed as change in pressure over
time (dp/dt) or as the initial upstroke of the arterial pressure curve, is largely responsible for the initiation and propagation of the dissection. The strength of the pulsation, rather than hypertension or high blood ow alone, leads to progression. Thus,
the goals of medical management are to reduce blood pressure, as well as to reduce
the left ventricular ejection force (dp/dt) and shear stress [7]. When fed
B-aminopropionitrile fumarate (BAPN), a drug that mediates reduction in the tensile strength of the aorta by inhibiting lysyl oxidase, the Broad-Breasted White turkey develops iatrogenic aortic dissection. Simpson etal. investigated the effects of
various pharmacologic strategies on the risk of aortic rupture in this model [8].
These studies demonstrate that blood pressure control alone is not adequate to prevent aortic rupture. Rather, beta-blocker therapy acts to reduce both blood pressure
as well as chronotropy and inotropy, subsequently reducing dp/dt and the risk of
rupture.
Initial medical therapy should aim to decrease wall stress (anti-impulse therapy)
in order to limit extension of the dissection and reduce the risk of developing endorgan damage and rupture. Heart rate and blood pressure should be lowered to the
lowest tolerable levels while ensuring adequate cerebral, coronary, and renal perfusion; typical heart rate goals are <60 bpm and systolic blood pressure goals are
100–120 mmHg. Intravenous short-acting agents should be administered and
titrated using electronic monitoring of blood pressure, heart rate, and EKG.Consistent
with European Society of Cardiology Guidelines, IRAD observed that over a period
of 17years, patients with both type A and type B AAD received signicantly greater
use of beta blockers (88% and 91%, respectively) [9].
First-line management is with intravenous (IV) beta-blocker therapy, with dosing as seen in Table1. In patients with potential intolerance to beta-blockers (asthma,
bradycardia, signs of heart failure), esmolol is a reasonable choice due to its short
half-life (9min) [1]. In patients who are truly beta-blocker intolerant, verapamil or
diltiazem may be useful to decrease blood pressure without causing reex
Initial Medical Management ofAcute Aortic Syndromes
https://t.me/med1917
123
tachycardia. If the systolic blood pressure is still greater than 120mmHg after betablocker therapy, vasodilator therapy is recommended. This should only be done
once heart rate is consistently less than 60bpm. Agent options include nitroprusside
and nicardipine, with dosing as seen in Table 1. In patients with an emergent or
urgent indication for operation, anti-impulse therapy for hypertensive patients
should be continued as the patient progresses to the operating room. In those patients
who do not have an indication for immediate intervention and will be treated medically, such as those with an uncomplicated Type B aortic dissection (TBAD), the
initial goal of therapy is to eliminate pain. In addition to anti-impulse therapy,
Table 1 Intravenous agents for initial medical management of acute aortic syndromes [1, 10]
Medication
First line: beta-blockers
Esmolol •
Labetalol • Both alpha
Mechanism
of action Formulation Bolus dose
Cardioselective
• Negative
inotropy and
chronotropy
and
betablockade,
plus
vasodilation
• Negative
inotropy and
chronotropy
2.5g/250mL 250–
500mcg/kg
200mg/200mL 20mg over
2min; then
20–80mg
bolus every
10min
(max
300mg)
Maintenance
dose Notes
•
50–200mcg/
kg/min
titrated to
maximum
dose of
300mcg/kg/
min
0.5–2mg/min • Caution in
Caution in
patients with
heart failure,
asthma, or
concomitant
calcium channel
blocker therapy
Use cautiously
•
in setting of
acute aortic
regurgitation as
will block
compensatory
tachycardia
•
Onset of action:
2min. Duration
of action:
10–20min
patients with
lung disease or
concomitant
calcium channel
blocker therapy
• Adverse events
include
vomiting, throat
burning, heart
block,
orthostatic
hypotension
• Onset of action:
5min. Duration
of action: 6h
(continued)
124
https://t.me/med1917
Table 1 (continued)
Medication
If resistant to beta-blockers
Verapamil •
Diltiazem •
Vasodilators
Nitroprusside • Relaxes
Nicardipine •
Mechanism
of action Formulation Bolus dose
Reduces
SVR
• Depresses
contractility
Reduces
SVR
• Negative
inotropy
arterial
smooth
muscle
•
Reduces
SVR and
PVR
Selectively
relaxes
arterial
smooth
muscle
•
Reduces
SVR
A. R. Benkert and J. G. Gaca
Maintenance
dose Notes
120mg/250mL 0.1mg/kg
over 2min
250mg/250mL 0.25mg/kg
over 2min,
then
0.35mg/kg
over 2min
50mg/250mL 0.25–0.5mcg/
50mg/250mL 5mg/h 2.5–5mg/h
2–5mcg/kg/
min
5–15mg/h •
kg/min
titrated to
maximum
8mcg/kg/min
titrated to
maximum
15mg/h
•
Onset of action:
1–5min
Caution in
patients with
heart failure or
concomitant
beta-blocker
therapy
Adverse events
•
include liver
dysfunction
• Onset of action:
2–5min
Adverse effects
•
include reex
increase in
contractility and
dp/dt; in a
patient with
aortic dissection,
this mandates
concomitant use
of beta-blocker
•
Caution in
patients with
hepatic or renal
dysfunction
• Can cause
cyanide toxicity
• Effect dissipates
in 1–2min
• No effect on AV
conduction
• Has long
duration of
action: 4–6h
• Can increase
V/Q mismatch
and produce
hypoxemia
Initial Medical Management ofAcute Aortic Syndromes
https://t.me/med1917
proper management of pain is an important factor in management. Morphine sulfate
is typically the drug of choice due its reliable and predictable effects, safety prole,
ease of reversibility and ease of titration with the intravenous formulation.
A toxicology screen should be considered in all patients presenting with acute
aortic syndrome, particularly if there are no known predisposing factors. Patients
who develop aortic dissection as a result of cocaine intoxication should not receive
non-selective beta blockers alone as this may lead to unopposed alpha stimulation,
thus worsening hypertension [2]. Treatment of cocaine-related acute aortic syndromes should aim to reverse the centrally mediated nervous system stimulation.
After initial therapy with IV agents for a period of 12–24h, the goal of medically
managed dissection patients is to transition them to an effective oral anti- hypertensive
regimen. The patients are transitioned to an oral regimen consisting of beta blockers, calcium channel blockers, and/or alpha antagonists as the IV regimen is weaned
in a monitored setting with the same blood pressure and heart rate goals as above.
In addition, all medically managed aortic syndrome patients should undergo repeat
cross-sectional imaging (CT scan) at approximately 24–48h after presentation. A
small percentage of aortic pathology managed medically may progress to diagnoses
requiring surgical intervention. For example, an ascending IMH may progress to
TAAD, or a TBAD may have retrograde extension and evolve into a TAAD.This
progression of disease is usually signied by a change in the patient’s
symptomatology.
While there are no high-quality data on the efcacy of initial medical management for all patients with acute aortic syndrome, anti-impulse therapy remains a
Class I recommendation. Anti-impulse therapy addresses the primary precipitating
risk factor (hypertension) leading to acute aortic syndromes, as well as reduces the
aortic shear stress and risk of disease propagation in the initial period following
presentation. Prior to denitive intervention for type A disease, reduction of propagation to further branch arteries reduces associated morbidity and mortality.
In-hospital mortality rates are less than 10% for medically managed uncomplicated
acute type B dissection [10] and as many as 10% of type B IMH lesions may completely resolve with appropriate beta-blockade [11]. However, long-term data from
IRAD demonstrate that the 3-year survival rate for patients managed medically is
only 78% [12]. Recently, the trend has favored endovascular intervention even for
acute uncomplicated TBAD, though this is not supported by randomized data.
125
Volume Management
For patients who present with hypotension, the cause should be evaluated prior to
uid volume resuscitation. Alternative causes include hemopericardium with tamponade, valvular dysfunction, or left ventricular systolic dysfunction, all of which
126
https://t.me/med1917
require further intervention. Pseudohypotension, which occurs when blood pressure
is measured in an extremity with circulation compromised by the dissection, should
be ruled-out prior to initiation of medical therapy. In the case of aortic rupture or
cardiac tamponade, the initial management includes rapid volume resuscitation as a
temporizing measure prior to immediate operative management. Despite high central venous pressure with cardiac tamponade, volume administration will improve
cardiac lling against the external pressure within the pericardial space.
Pericardiocentesis is associated with adverse outcomes, potentially due to rebound
increase in intra-aortic pressure, but may be performed for those who cannot survive
until surgery [13].
A. R. Benkert and J. G. Gaca
Complication-Specic Approach
Acute aortic syndromes are described as ‘complicated’ when there is malperfusion
of a vascular bed. Complicated dissections account for approximately 15–20% of
cases and can result in malperfusion of the brain, heart, viscera, spinal cord, and
limbs [10]. Complicated disease portends a poor prognosis; in patients with limb
ischemia or renal/mesenteric malperfusion versus those without, mortality is twice
as high [13]. Malperfusion syndromes can be further classied as dynamic or static
based on the mechanism of impaired blood ow. Dynamic occlusion occurs when
the orice of the aortic branch vessel is occluded by the mobile aortic dissection
ap, thus leading to occlusion of the true lumen by the false lumen. In this case,
fenestration of the intimal ap and/or treatment of the primary tear with thoracic
endovascular aortic repair (TEVAR) can depressurize the false lumen and restore
ow [10]. Static malperfusion occurs when the dissection ap extends into the aortic side branch, thus occluding the distal vessel. Branch vessel stenting in addition
to TEVAR is typically necessary in this case to resolve the malperfusion syndrome [10].
In cases of malperfusion, a ‘complication-specic approach’ is recommended.
Patients presenting with an acute TAAD, in whom the associated malperfusion is a
more signicant threat to life, restoration of ow to the occluded vascular bed is
recommended prior to repair of the dissection. When considering delay of TAAD
repair, all factors related to the presentation must be taken into account in order to
judge the risk of rupture and death associated with the delay. These factors include
the acuity of symptoms, the presence of continual chest or back pain despite adequate anti-impulse therapy, the degree of aortic insufciency or tamponade, and the
presence of heart failure. In the scenario of complicated acute TBAD, medical management alone is not sufcient, and these dissections should be treated immediately
(usually by endovascular therapy or extra-anatomic bypass). Figures1 and 2 display
the algorithms for management of complicated acute aortic syndromes.
Following is a discussion of initial management of patients presenting with various manifestations of complicated dissection.
Initial Medical Management ofAcute Aortic Syndromes
https://t.me/med1917
127
Type A Aortic Dissection
Complicated
Non-focal
Surgical repair
Neurologic Malperfusion
Dense hemiparesis
Medical management
Visceral malperfusion
Viable bowel
Endovascular repair +/-
branch vessel
revascularization, followed
by surgical repair
Necrotic bowel
Medical management
Extremity malperfusion
Pulseless and insensate
Restore extremity blood
flow
Pulseless but sensorimotor
intact
Type A dissection repair
Fig. 1 Management approach for patients presenting with acute type A aortic dissection
Type B Aortic Dissection
Uncomplicated
Medical Management +/-
elective TEVAR
Visceral malperfusion
TEVAR +/-
fenestration/stenting
Complicated
Extremity malperfusion
TEVA R + extra-anatomic
bypass/stenting
Uncomplicated
Surgical repair
Fig. 2 Management approach for patients presenting with acute type B aortic dissection
Neurologic Complications
Among patients within IRAD, 6% of patients with TAAD also presented with a
stroke. These patients commonly presented with syncope, shock, or pulse decit
[3]. Patients presenting with altered sensorium and delirium are common, however these symptoms do not necessarily indicate a cerebrovascular accident
(CVA). If these patients have a non-focal neurologic exam, immediate repair of
TAAD should not be delayed in order to investigate a possible CVA.However, a
dense hemi- paretic CVA is a particularly poor prognostic sign that may make
operative repair prohibitively risky. Management of patients with an acute aortic
syndrome complicated by CVA remains controversial as immediate surgical
repair carries a risk of hemorrhagic conversion, while conservative management
is associated with a high incidence of early mortality [14]. Paraplegia and spinal
cord malperfusion is a presenting manifestation in 2–5% of patients with AAD
[15]. Prior to repair, there is no specic way to revascularize the spinal cord.
These patients should undergo immediate repair of TAAD as resolution of
Соседние файлы в папке Библиотека им академика М.И. Перельмана