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Current Status of Medical Therapy of Thoracic Aortic Aneurysm and Dissection Chapter | 22 245
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TABLE 22.5 Intravenous Agents for Treatment of Ascending Dissection [58].
Maintenance
Name Category Loading Dose
Sodium
nitroprusside
Nicardipine CCB 5 mg/h, increasing by
Clevidipine CCB 1–2 mg/h and can be
Propranolol β-Blocker 1–3 mg (given at
Esmolol β-Blocker 500 μg/kg bolus Continuous 50
Labetalol α- and
Diltiazem CCB 0.25 mg/kg IV bolus
Enalapril Vasodilator
Fenoldopam Dopamine
Vasodilator 0.3 to 3 μg/kg/min;
maximum limit for
an adult is 10 μg/kg/
min for 10 min
2.5 mg/h every 5 min
to a maximum of
15 mg/h
doubled every 90 s
until BP approaches
target
1 mg intervals over
1 min). Can be
repeated in not less
than every 4 h
20 mg over 2 min
β-blockers
ACE
inhibitor
D1 receptor agonist
then 40–80 mg every
10–15 min (maximum 300)
(up to 25 mg)
0.625–1.25 mg bolus 0.625–5 mg
0.03–0.1 μg/kg/min
initially
Dose Adverse Effects Caution
1–3 μg/kg/min Nausea, vomiting,
agitation, muscle twitching,
sweating, cutis anserina
and cyanide toxicity,
tachycardia
10 min
Downward
adjustment by
3 mg/h should
be attempted
after target BP is
reached
4-6 mg/h, max
21 mg/h
1–3 mg every 4 h Hypotension, nausea,
up to 200 μg/kg/
min
Continuous IV
at 2 mg/min
and titrate up to
5–10 mg/min
5–10 mg/h by
continuous
infusion
every 6 h
0.1–0.3 μg/kg/
min, maximum
1.6 μg/kg/min
Headache,
hypotension, nausea,
vomiting, tachycardia
Headache, atrial
fibrillation, insomnia,
nausea, fever, acute renal
failure
dizziness, cold extremities, reversible hair loss,
bradycardia
Hypotension, nausea,
dizziness, bronchospasm,
dyspepsia, and constipation, increases digoxin level
Vomiting, nausea, scalp
tingling, burning in throat,
dizziness, heart block,
orthostatic hypotension
Heart block, constipation,
liver dysfunction
Precipitates fall in BP in
high renin states, variable
response, renal failure
Tachycardia, hypotension,
headache, nausea, flushing,
hypokalemia, elevation of
IOP
In patients with
hepatic or renal
dysfunction
In patients with
advanced aortic
stenosis
In patients with allergies to soy products or
egg products, patients
with defective lipid
metabolism, advanced
aortic stenosis
In patients with
bradycardia or history
of CHF and bronchospasm. Maximum
initial dose should not
exceed 0.15 mg/h
In patients with CHF
or asthma or on
concomitant CCB
therapy
In patients with lung
disease, concomitant
CCB therapy
In patients with heart
failure, concomitant
β-blocker therapy
In patients with high
possibility of MI, renal
dysfunction
In patients with
glaucoma
ACE, angiotensin-converting enzyme; BP, blood pressure; CCB, calcium channel blocker; CHF, congestive heart failure; IOP, intraocular pressure; IV, intra-
venous; MI, myocardial ischemia.
Perhaps paradoxically to the novice clinician, controlling the blood pressure alone is not sufficient to control acute aortic dissection (see Fig. 22.7). Nitroprusside alone adequately controls blood pressure but does not attenuate the progression
of dissection. In fact, vasodilator therapy alone may increase dp/dt because of reflex sympathetic chronotropic and inotropic discharge in response to the decreased blood pressure. Thus, nitroprusside alone is not recommended for control of type
A dissection and has actually been demonstrated to increase ruptures in a dissected aorta [59]. Instead, the best results for
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FIGURE 22.7 Aortic pressure curves under various conditions. Curve (a), the administration of a vasodilator agent such as nitroprusside; curve (b), the
baseline state; curve (c), β-blockade administration. (a,b) Note the significant decrease in blood pressure and acceleration in heart rate at the expense of a
steeper slope of the ascending portion of the curve (representing increased dp/dt). (c) Although the degree of pressure lowering is usually smaller, the characteristic negative chronotropy and inotropy result in a blunted upstroke of the blood pressure curve, representing decreased impulse and dp/dt. Reprinted
with permission from Sanz J. Acute aortic dissection: anti-impulse therapy. In: Acute Aortic Disease. New York: Informa Healthcare; 2007. pp. 229–50.
controlling type A dissection are obtained with a combination of nitroprusside and propranolol [60]. The combination of
vasodilator with β-blockade diminishes sympathetic reflex and constitutes effective anti-impulse therapy.
In addition to the anti-impulse pharmacotherapy previously mentioned, it is important to control pain with intravenous
morphine. Pain itself can induce a hyperadrenergic state, exacerbating acute hypertension and increasing dp/dt.
There exist several situations in which patients with type A dissection cannot undergo surgical intervention and must
remain on medications: patients with complicated stroke [62,63], comorbid conditions (e.g., cancer, age) [64], prior aortic
valve replacement [65–67], and presentation to the hospital after 48–72 hours of the onset of dissection [68,69]. When a
patient is placed on chronic oral therapy, an afterload-reducing agent is preferred [such as hydralazine, an angiotensinconverting enzyme (ACE) inhibitor, or an ARB] along with a β-blocker.
CONCLUSIONS
The natural history of TAAs is one of progressive, inexorable expansion. Because most TAAs do not produce noticeable
symptoms, there exists a real threat of acute aortic catastrophe such as dissection or rupture. Because of the small risk
of surgical repair, surgical intervention should be reserved for those patients who are symptomatic or in whom imaging
reveals specific size or rate of expansion criteria. However, for those asymptomatic patients in whom imaging has revealed
a subthreshold TAA, clinicians are faced with the question of whether to prescribe pharmacotherapy in addition to lifestyle
modification (avoiding heavy lifting and straining). As this chapter details, there are several medications that act on various points in the proposed pathophysiologic pathways of aortic aneurysm development. Although some current guidelines
endorse starting medications to prevent aortic aneurysm expansion, it is worth keeping in mind that supporting clinical
evidence is conflicting and equivocal at best. Clinical studies have shown conflicting results for various classes of medications, including ARBs, β-blockers, tetracyclines, and statins. It will be increasingly important to conduct large, randomized
clinical trials with relevant clinical endpoints in patients specifically with non-Marfan TAA. Concurrently, a more thorough
understanding of the pathophysiologic basis of aneurysm formation is warranted to help direct more targeted, “individualized” treatment modalities.
At our Aortic Institute, we do not usually start β-blockers for TAA patients, but we do not stop them when they are
already in use and not causing marked side effects. Regardless of any putative aneurysm-related effects, β-blockers are
often a very appropriate part of an effective antihypertensive regimen and therefore important for patients with aneurysms.
Similarly, ACE and ARB medications may be a very appropriate part of a needed antihypertensive regimen. Also, we feel
that β-blockers may be protective at instants of potential instigation of aortic dissection in an enlarged vulnerable aorta.
See the schematic (Fig. 22.8) of the pathophysiologic mechanism that we believe leads to aortic dissection. We do feel that
β-blockers may have a role in blunting the acute hypertensive, epinephrine-mediated response that we feel triggers aortic
dissection in vulnerable patients (at times of severe physical or emotional stress). These associated roles for β-blockers,
ACEs, and ARBs imply that many of these drugs will be used, appropriately so, in TAA patients. It would be wrong, however, to presume that such medical therapy will slow aneurysm progression or reliably deter aortic dissection or rupture.
Such evidence is currently lacking.
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FIGURE 22.8 Conceptual pathway leading to acute aortic dissection. Overall schematic understanding of how aortic dissection picks a specific time to
occur. MMP, matrix metalloproteinase. Modified with permission from Elefteriades JA, Farkas EA. Thoracic aortic aneurysm clinically pertinent contro-
versies and uncertainties. J Am Coll Cardiol 2010;55:841–57.
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Chapter 23
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Organ Preservation During Open
Thoracoabdominal Reconstruction
Stephane Mahr, Marlies Stelzmüller, Tatjana Fleck, Kamen Dimitrov, Doris Hutschala, Günther Laufer,
Marek Ehrlich
Medical University of Vienna, Vienna, Austria
Chapter Outline
Background 251
Surgical Approach and Protection Techniques 251
Two-Staged Approach in Distal Aortic and TAAA Aneurysms 252
Cerebrospinal Fluid Drainage 252
Profound Hypothermic Circulatory Arrest 252
Major Drawback With Deep Hypothermia 252
Motor- and Somatosensory-Evoked Potentials 253
Left Heart Bypass Approach 253
Celiac Trunk and Superior Mesenteric Artery Perfusion 254
Renal Protection 254
Aortic Reconstruction With the Aim of Minimizing
Organ Ischemia 254
Extracorporeal Membrane Oxygenator 255
Conclusion 256
References 256
BACKGROUND
Descending thoracic aortic aneurysms still represent a potentially life-threatening situation. The afflicted population is
usually of older age and present at time of operation with various comorbidities such as hypertension, obstructive pulmonary disease, coronary heart disease, all of which have a significant impact on the surgical outcome.
Resection and graft replacement of the pathologically altered aorta is, in most patients, these days the preferred method
of treatment with excellent mid- and long-term results [1–3]. The operative techniques involved in thoracoabdominal aortic
aneurysm (TAAA) repair have evolved substantially over the last 20–30 years and the spectrum included single crossclamping proximal to the aneurysm side and exsanguination of the lower body in conjunction with a rapid autotransfusion
system in the early eighties, cardiopulmonary bypass (CPB), and the use of profound hypothermic circulatory arrest and
most recently the use of left heart bypass (LHB), permissive hypothermia, selective visceral organ perfusion, and cerebrospinal fluid (CSF) drainage [4–6].
The ultimate goal of these operations is to balance the need to resect and replace as much diseased aortic tissue as possible with the need to protect all aorta-related end organs. Due to the complexity and invasiveness of these aortic pathologies’ accurate planning and choice of organ protection method are of paramount importance. Organs at risk are the brain,
the spinal cord, and visceral organs including kidneys and lower extremities. Therefore, we describe our current strategies
for organ protection with special emphasis on cerebral, spinal, and visceral.
SURGICAL APPROACH AND PROTECTION TECHNIQUES
After defining the aortic pathology according to Crawford’s classification through computed tomography scan, the
appropriate strategy is chosen preoperatively with special emphasis on extracorporeal circuit (ECC) and visceral as
well as spinal cord protection. In Crawford II and III TAAA, a transperitoneal approach is chosen over a retroperitoneal
access. It is, in our opinion, a significantly quicker and safer approach because visceral damage can immediately been
discovered (e.g., malperfusion of the bowel). Furthermore, damage to the spleen can be immediately observed and
splenectomy can be easily approached to avoid bleeding complication intra- or postoperatively.
New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. http://dx.doi.org/10.1016/B978-0-12-809979-7.00023-7
Copyright © 2018 Elsevier Inc. All rights reserved.
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TWO-STAGED APPROACH IN DISTAL AORTIC AND TAAA ANEURYSMS
When the proximal part of the descending aorta shows great risk for clamping (due to massive atherosclerotic alteration
in the aortic wall or due to aortic diameters at the distal arch and/or proximal descending aorta), a two-stage approach is
recently favored in our department over a procedure where deep hypothermic circulatory arrest would be used. An elephant
trunk operation is first performed to be able to clamp and sew the descending prosthesis in a second stage. Only few hours
to days are necessary in between the two steps to assess neurologic and end organ function [7].
CEREBROSPINAL FLUID DRAINAGE
Randomized trials have shown reduction of paraplegia in extent I and II TAAAs, when CSF drainage was used [8].
A CSF catheter is placed 1 day before surgery in the third or fourth lumbar space to allow spinal fluid drainage and
monitoring of CSF pressure. The goal is to maintain CSF pressure in a range of less than 15 mmHg throughout the
procedure. It is also of paramount importance to keep the mean arterial pressure (MAP) between 80 and 100 mmHg in
the first postoperative period on the intensive care. CSF shall not be drained by more than 20 mL/h and the CSF catheter should be kept for the first three postoperative days. If a delayed neurologic deficit should appear after removal
of the drain, a new CSF drain must be reinserted immediately to decrease the CSF pressure. This should lead to the
prompt resolution of the neurologic deficit.
PROFOUND HYPOTHERMIC CIRCULATORY ARREST
Over the last three to four decades, several attempts have been made to address mostly the issue of ECC in this patientspecific cohort. Two primary approaches have basically emerged to maintain distal aortic perfusion, provide selective
visceral perfusion, and protect organ damage during the repair. The first one uses full CPB with a protective hypothermic strategy [9]. This technique is well accepted, especially in patients with distal arch or proximal descending aortic
aneurysms, where cross-clamping of the aorta is not feasible. There are several major technical advantages we have
noted using hypothermic CPB with circulatory arrest. The first is the opportunity to do an open proximal anastomosis.
This simplifies the operation (especially in redo aortic replacement as less dissection is required). In addition, the
open anastomosis allows a view of the interior of the aorta and any atheromatous debris is easily identified, and the
aorta is resected further proximally until there is normal, nondiseased intima if possible. We believe this decreases
the cerebral, visceral, or peripheral embolic potential as no residual atheromatous debris remains. Another advantage
is that the viscera are cooled and almost continuously perfused for maximal protection. The protective effect of profound hypothermia on visceral organ and spinal cord function after an ischemic interval induced by aortic clamping
has been demonstrated experimentally and in clinical studies [9]. According to these findings, only profound but not
mild or moderate hypothermia provides ample protection during the procedure. The kidneys are most sensitive to
ischemia than the liver or the bowel, and none of these organs are as vulnerable to ischemic damage as the spinal cord
[8]. In human beings, even severe visceral ischemic damage can often be managed (e.g., acute renal failure), although
some damage (e.g., extensive bowel infarction) may be incompatible with survival.
When this technique is applied, the left common femoral artery and vein are isolated through an oblique incision in the
skin crease of the groin. Heparin is administered to achieve an activated clotting time of more than 400 s (3 mg/kg). After
puncture and introduction of a guide wire to the right atrium of the heart under transesophageal echocardiographic (TEE)
guidance , a long venous cannula (28F–34F) is inserted through the left common femoral vein and the tip is positioned in
the right atrium also under TEE control. The femoral artery is cannulated with an 18F–22F short cannula. CPB is established and cooling is initiated (target temperature around 18°C). During the period of cooling, a catheter is preferentially
placed through the left inferior pulmonary vein or through the apex of the left ventricle for venting of the left heart, and the
head is packed in ice.
MAJOR DRAWBACK WITH DEEP HYPOTHERMIA
Despite good results with deep hypothermia in extensive TAAA repair, there has been a reluctance to adopt this technique, largely because of a perception that there is a vastly increased risk of bleeding and respiratory complications
with lower temperatures. However, in a series of TAAA operations performed by the Mount Sinai group, only platelet
transfusions were higher in the patients with deep hypothermia, and in the propensity-matched cohort there was no
difference between the mild and deep hypothermia groups in transfusions of red blood cells, fresh-frozen plasma, or
platelets [10].
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MOTOR- AND SOMATOSENSORY-EVOKED POTENTIALS
In certain centers, neuromonitoring with continuous motor-evoked potential (MEP) and somatosensory-evoked potential
(SSEP) has been widely applied during open TAAA repair to guide reimplantation of intercostal arteries and to optimize
distal aortic perfusion [11,12]. The main goal of neuromonitoring is to help identify ischemia in the anterior and lateral
spinal columns, which are sensitive to a decrease in oxygen supply.
A ≥75% consistent reduction from baseline evoked potential amplitude is considered to be significant. The method is
relying on electrical charges sent to the motor cortex through C3/C4 scalp electrodes, which evoke MEPs through the motor
pathway; values are recorded down the cord over multiple muscles in the upper and lower extremities for at least every
10–15 min. An upper extremity muscle (extensor digitorum communis) is recorded to help differentiate neurogenic impairment such as spinal and lower limb ischemia from nonspecific changes. Bilateral lower extremity muscles are recorded
using subdermal electroencephalographic (EEG) electrodes placed in the hamstring, tibialis anterior, and abductor hallucis
muscles. In addition, SSEPs consisting of electrical stimulus generated at the ulnar or tibial nerve that travels from the distal
extremity are recorded over the neck and scalp. In patients where the lower extremity tibial SSEPs are not present at the
ankle, subdermal EEG electrodes can be positioned behind the knee.
A decrease in MEP/SSEPs usually triggers incremental changes in MAP and CSF pressure. The MAP is then raised
from 80 up to 100 mmHg with norepinephrine and/or vasopressin infusions along with simultaneous decrease in CSF drain
pressure below 15 mmHg.
LEFT HEART BYPASS APPROACH
In patients with Crawford Type I or Type II extent with normal cardiac and pulmonary function an LHB approach is
implemented whenever possible [13]. One of the benefits of this technique is avoiding cerebral blood flow interruption.
We use LHB as a closed circuit with the addition of a reservoir to salvage shed blood (rapid infusion system). After
administration of heparin, 1 mg/kg access for this technique is achieved through the left pulmonary veins (angled-tip
cannula 18–24 French) or the left atrial appendage for drainage. The inflow line cannula (either coated extracorporeal
membrane oxygenation [ECMO] cannula [17–21 French] for distal body perfusion) can be inserted in the distal aorta
or in retrograde fashion through the femoral artery (caveat in chronic dissection cases). As shown in Fig. 23.1 LHB has
been established through one of the left pulmonary veins (alternatively through left atrial appendage) for drainage and a
cannula for the distal portion of the aorta after the aortic clamp. Out of the Y-connector, two additional lines are necessary for further visceral cannulation of the celiac trunk and superior mesenteric artery (SMA). Also renal perfusion setup
is indicated.
cold
renal
perfusion
left
heart
bypass
FIGURE 23.1 Left heart bypass setup.
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cold
renal
perfusion
FIGURE 23.2 Visceral perfusion.
left
heart
bypass
CELIAC TRUNK AND SUPERIOR MESENTERIC ARTERY PERFUSION
Visceral organ protection can be achieved through selective perfusion and is a well-established strategy [14].
The inflow line of the LHB circuit is equipped with a Y-connector to split blood going to the distal aortic cannula
and another line leading to two 9-French Pruitt balloon-tipped perfusion catheters for later delivery of selective visceral
perfusion to the celiac artery and SMA. Fig. 23.2 shows the now opened aorta and perfusion of visceral organs while performing either the distal anastomosis and/or reimplantation of intercostal arteries.
RENAL PROTECTION
Hospital mortality of patients undergoing TAAA repair is reduced when cold visceral perfusion is applied [15].
With a second extracorporeal pump, the renal perfusion is secured. Cold crystalloid renal perfusion is used
systematically when abdominal repair is necessary using an initial 500 mL followed by 200 mL lactated Ringer’s
solution with mannitol (12.5 g/L) and methylprednisolone (125 mg/L) at 4°C every 10 min during ischemic periods
[16]. Work published by Koksoy et al. showed superior protection with cold renal versus normothermic blood [17].
Further randomized trials showed no benefit using cold blood over cold crystalloid [18]. Restoring blood flow as soon
as possible is the ultimate goal.
AORTIC RECONSTRUCTION WITH THE AIM OF MINIMIZING ORGAN ISCHEMIA
After LHB is started at a flow rate of 500 mL/min, cross-clamp the aorta distal to the subclavian artery ideally with padded
aortic cross-clamp. A second aortic clamp is applied at the level of the middle third of the descending aorta (the higher
the better without compromising access for the proximal anastomosis). This approach provides ample flow into important
spinal arteries at the level TH7-L2 while performing the proximal anastomosis. LHB flow is raised at this stage to 1.5
and 2.5 mL/min to keep the patient’s MAP around 80 mmHg. A cell-saver device is used for collecting the shed blood. In
patients presenting with aortic dissection, differentiating between true and false lumen is substantial to excise the membrane. Now back-bleeding intercostal arteries are addressed meticulously and over sewn with prolene 3-0. Minimizing
blood loss and avoiding a steal phenomenon from spinal circulation is important for organ damage.
After choosing the appropriate size, a four-branched aortic graft (Coselli Prosthesis, Vascutek, Ireland) is chosen and
trimmed in size so that the distance between the proximal anastomosis of the aorta and the offspring of the visceral vessels
correlate. In general, a 24-, 26-, or 28-mm graft is used. This prosthesis features four side branches for individual attachment to the celiac, superior mesenteric, and both renal arteries. The major benefit of this product is that it allows sequential
artery reattachment and restoration of blood flow after each single performed anastomosis, elimination of aortic patch
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cold
renal
perfusion
FIGURE 23.3 Extracorporeal membrane oxygenation (ECMO) application and setup in thoracoabdominal setting.
ECMO
pseudoaneurysm formation, as well as early hemostasis. It is important when starting the anastomosis at the proximal aorta
to pay attention to the alignment of the offspring of the celiac graft with its corresponding vessel in order not to twist the
graft and avoid kinking.
After completion of the proximal anastomosis between the graft and the aortic cuff using a running suture polypropylene 4-0 in most cases, it is recommended to reinforce the circumference with multiple mattress sutures using
pledgeted polypropylene 4-0.
To address the distal part of the aorta, LHB is terminated and the remaining aorta is opened until the
bifurcation. Again retraction of the aortic wall with stay sutures eases access and facilitates over sewing back-bleeding
intercostal arteries. In a next step, Pruitt catheters are introduced into the orifice of the celiac trunk and SMA and perfused
with blood from the inflow line of the LHB with a continuous flow rate of 250 mL/min. In the same manner, the renal
arteries are perfused with cold crystalloid solution initially with a bolus of 500 mL followed by 200–400 mL every 10 min.
After identifying large and only little back-bleeding intercostal arteries between Th7 and L1, reimplantation of
these is performed in a side-to-side manner as an island patch. After this step, the proximal aortic cross-clamp can
be removed distally to restore reperfusion of these intercostal arteries and therefore minimize spinal cord ischemia.
In the same manner as described for the proximal anastomosis of the aorta now the distal anastomosis is performed
after trimming the graft to the appropriate length. At this stage, the aorta is deaired through one of the side branches
of the graft and each side graft is selectively clamped. Now the aortic clamp is carefully removed and blood flow is
restored to the lower extremities of the body. To reduce renal ischemic time, the right renal artery anastomosis is first
performed end-to-end, followed by the SMA, celiac trunk, and finally left renal artery. Before restoring blood flow
to each of these vessels, deairing is essential and perfusion catheters are removed only before tying the anastomosis.
Reversing heparin with protamine concludes this step.
EXTRACORPOREAL MEMBRANE OXYGENATOR
Patients presenting for TAAA repair with relevant pulmonary disease (e.g., COPD (chronic obstructive pulmonary disease)) need thorough evaluation preoperatively with regards to perfusion strategy. When intraoperative single lung ventilation results in insufficient peripheral oxygen saturation, the concept of LHB cannot be pursued and ECMO perfusion
represents an alternative without the necessity of full heparinization as in CPB.
Cannulation concept is a veno-arterial setting inserting a coated venous cannula (18–22 French) in the femoral vein
and an arterial coated cannula in the femoral artery (15–19 French) for partial ECMO support and only to raise oxygen
saturation and stabilizing hemodynamics. One major benefit arises during preparation the operative field when single lung
ventilation is necessary. In patients that do not tolerate single lung ventilation, ECMO flow can be initiated that facilitates
left lung manipulation during dissection. Fig. 23.3 shows the setup for circulatory support using ECMO instead of LHB.
Venous drainage was accomplished through percutaneous femoral vein access.
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