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IV. Dissection
Fig. 16.8. Localised dissection secondary to an intramural hae-
matoma (arrow). The majority of these dissections present pro-
gression to formation of a pseudoaneurysm
influencing increased wall stress. Finally, increased false
lumen pressure was another important factor implying
false lumen enlargement. The high false lumen pressure
was due, in the majority of cases, to a large entry tear
without distal emptying flow or a reentry site of similar
size. It is often impossible to identify the reentry tears;
thus, they were considered to be indirect signs of high
false lumen pressure by TEE when the velocity of the
echocardiographic contrast in the false lumen was slow
and the contrast moved up and down for several cycles
(Figs. 16.6, 16.7). MRI also permitted assessment of
time and false lumen flow at different levels of the aorta, which helps to define whether the sizes of the entry
and reentry tears are similar.
A suspicious, though not very specific, finding of
high pressures in the false lumen is when the true lumen is compressed by the false lumen and the ratio is
under 1: 5. The lesser dilatation of the false lumen in
operated type A dissection patients is due to the small
entry tear size and the tear is often located in the distal
part of the ascending aorta prosthesis. These pathophysiologic data of aortic dissection evolution may be
of great interest for selecting asymptomatic patients
who would benefit more from endovascular treatment
in the subacute phase of aortic dissection.
On the other hand, evolution of dissection at some
level of the aorta occurs in approximately 25% of haematomas [5]. The majority of dissections are localised
and only are 20% classic. Extension, echolucency and
thickness of the haematoma are variables related to aortic dissection evolution, most of which are asymptomatic and evident in the first 3±6 months after onset of the
intramural haematoma. Small intimal tears can be iden-
tified on TEE and in a small proportion of cases trigger
a dissection. Localised dissections (Fig. 16.8) evolve to
pseudoaneurysm, disappearance of the intimal flap and
produce an ulcerlike image. Some authors have suggested poor prognosis for haematomas presenting this
evolution. In our series, two of the 17 images had disappeared at 6 months and only one case presented progressive dilatation and was treated with endovascular
therapy.
Knowledge of the pathophysiology of aortic dissection is essential to understand the short- and long-term
evolution, complications and most appropriate therapeutic management. Genetical or acquired structural alterations, secondary to the atherosclerotic process, are
the causal substrate of most dissections. Nevertheless,
the most therapeutically controllable variables are those
secondary to the decrease in wall stress, both by hypertensive therapy and by surgical or endovascular treatment.
References
1. Ambos MA, Rothberg M, Lefleur RS, Weiner S, McCauley
DI. Unsuspected aortic dissection: the chronic ªhealedº
dissection. Am J Roentgenol 1979; 132:221±225.
2. Dalen JE, Pape LA, Cohn LH, Koster JK, Collins JJ. Dissection of the aorta. Pathogenesis, diagnosis and treatment. Prog Cardiovasc Dis 1980; 23:237±245.
3. Erbel R, Oelert H, Meyer J, et al. Effect of medical and
surgical therapy on aortic dissection evaluated by transesophageal echocardiography. Circulation 1993; 87:1604±
1615.
4. Ergin MA, Phillips RA, Galla JD, et al. Significance of distal false lumen after type A dissection repair. Ann Thorac
Surg 1994; 57:820±825.
5. Evangelista A, Dominguez R, Sebastia C, et al. Long-term
follow-up of aortic intramural hematoma. Circulation
2003; 108:583±589.
6. Fann JI, Sarris GE, Mitchell RS, et al. Treatment of patients with aortic dissection presenting with peripheral
vascular complications. Ann Surg 1990; 212:705±713.
7. Guo D, Hasham S, Kuang S-Q, et al. Familial thoracic aortic aneurysms and dissections. Genetic heterogeneity with
a major locus mapping to 5q 13-14. Circulation 2001;
103:2461±2468.
8. Hagan PG, Nienaber CA, Isselbacher EM, et al. The international registry of acute aortic dissection (IRAD): new
insights into an old disease. JAMA 2000; 283:897±903.
9. Hirst AE, Gore I. Is cystic medionecrosis the cause of dissecting aortic aneurysm? Circulation 1976; 53:915±916.
10. Januzzi J, Sabatine MS, Eagle KA, et al. Iatrogenic aortic
dissection. Am J Cardiol 2002; 89:623±626.
11. Junoven T, Ergin MA, Galla JD, et al. Risk factors for rupture of chronic type B dissection. J Thorac Cardiovasc
Surg 1999; 117:776±786.
12. Larson EW, Edwards WD. Risk factors for aortic dissection. A necropsy study of 161 cases. Am J Cardiol 1984;
53:849±855.
13. Marui A, Mochizuki T, Mitsui N, Koyama T, Kimura F,
Horibe M. Towards the best treatment for uncomplicated
patients with type B acute aortic dissection. Circulation
1999; 100:II275±280.
A. Evangelista, T. Gonzlez-Alujas Chapter 16 Pathophysiology of Aortic Dissection
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173
14. Mehta RH, Suzuki T, Hagan PG, et al. Predicting death in
patients with acute type A aortic dissection. Circulation
2002; 105:200±206.
15. Moore NR, Parry AJ, Trottman-Dickenson B, Pillai R,
Westaby S. Fate of the native aorta after repair of acute
type A dissection; a magnetic resonance imaging study.
Heart 1996; 75:62±66.
16. Nienaber CA, Eagle KA. Aortic dissection: new frontiers
in diagnosis and management. Circulation 2003; 108:628±
635.
17. Roberts WC, Honing HS. The spectrum of cardiovascular
disease in the marfan syndrome: A clinico-morphologic
study of 18 necropsy patients and comparison to 151 previously reported necropsy patients. Am Heart J 1982;
104:115±135.
18. Nienaber CA, Sievers HH. Intramural hematoma in acute
aortic syndrome more than one variant of dissection? Circulation 2002; 106:284±285.
19. Pacifico L, Spodick D. ILEAD-ischemia of the lower
extremities due to aortic dissection: the isolated presentation. Clin Cardiol 1999; 22:353±356.
20. Prokop EK, Palmer RF, Wheat MW Jr. Hydrodynamic
forces in dissecting aneurysms. In vitro studies in a tygon
model and in dog aortas. Circ Res 1970; 27:121±127.
21. Roberts WC. Aortic dissection: Anatomy, consequences
and causes. Am Heart J 1981; 101:195±214.
22. Roberts CS, Roberts WC. Dissection of the aorta associated with congenital malformation of the aortic valve. J
Am Coll Cardiol 1991; 17:712±716.
23. Robicseck F, Thubrikar MJ. Hemodynamic considerations
regarding the mechanism and prevention of aortic dissection. Ann Thorac Surg 1994; 58:1247±1253.
24. Schlatmann TJM, Becker AE. Pathogenesis of dissecting
aneurysm of aorta. Comparative histopathologic study of
significance of medial changes. Am J Cardiol 1977; 39:21±
26.
25. Sueyoshi E, Sakamoto I, Hayashi K, Yamaguchi T, Imada
T. Growth rate of aortic diameter in patients with type B
aortic dissection during the chronic phase. Circulation
2004; 110:II-256±261.
26. von Kodolitsch Y, Aydin MA, Loose R, et al. Predictors of
aneurysm formation after surgery of aortic coarctation. J
Am Coll Cardiol 2002; 39:617±624.
27. Wheat MW. Acute dissecting aneurysms of the aorta diagnosis and treatment ± 1979. Am Heart J 1980; 99:373±387.
Surgical Treatment
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of Acute Type B Dissection
Marc Schepens, Karl Dossche
Chapter
17
Contents
17.1 Introduction ......................
17.2 Indications for Surgery ................ 175
17.3 Surgical Techniques .................. 176
17.3.1 General Considerations ........... 176
17.3.2 Use of Soft Clamps, Teflon Felt and Glue . 177
17.3.3 Access ..................... 177
17.3.4 Perfusion Techniques ............ 177
17.3.5 Atriofemoral Bypass (Left Heart Bypass) . 178
17.3.6 Extracorporal Circulation
(Partial or Total, Deep Hypothermic
Circulatory Arrest) ..............
17.4 Surgical Steps ...................... 178
17.5 Malperfusion ...................... 179
17.6 Results .......................... 179
17.7 Conclusion ....................... 180
175
178
17.1 Introduction
Most cases (80%) [1] of acute type B aortic dissections
can be treated medically. This is also the case for acute
intramural hematoma type B and for penetrating aortic
ulcus. The aim of medical treatment consists of hemodynamic monitoring, lowering the blood pressure with
beta-blockers and vasodilators. Beta-blockers reduce
dP/dt and therefore control the ejection of blood from
the heart. Prognosis treated as such is not bad: in-hospital mortality is about 11% [1] underscoring the fact
that medical treatment alone is justified. Because almost
all dissected aortas will dilate and become aneurysmatic
over time, it is essential that patients who were initially
treated medically have long-life aortic surveillance in
order to detect aneurysmal dilatation in time. However,
in some circumstances of acute type B aortic dissection,
acute intramural hematoma type B or penetrating ulcus,
medical treatment is insufficient and surgical treatment
should be added.
17.2 Indications for Surgery
Surgical treatment is mandatory in patients with:
1. Rupture (Fig. 17.1): This will occur usually into the
left chest and/or mediastinum, mostly from the
upper portion of the descending thoracic aorta.
However, it can happen all along the thoracoabdominal aorta. It is not exceptional to appreciate also a
right-sided hematothorax. Moderate pleural effusion
(often bilateral) is a common finding even in an uncomplicated acute type B dissection and therefore
does not by itself present a surgical indication [2].
2. Uncontrollable hypertension and/or pain despite
maximal medical therapy (with modern drug regimes these circumstances are rare).
3. Malperfusion: Fortunately malperfusion is a rare
phenomenon because reentries occur spontaneously
causing automatic relief. All side branches of the
aorta, starting from the intercostal arteries and ending somewhere at the iliac arteries, are at risk for
malperfusion. The mechanisms of malperfusion as
classified by Beregi et al. [3] and Gaxotte et al. [4]
lie in the extension of the dissecting process into the
side branch, the narrowing of the side branch by the
Fig. 17.1. A ruptured type B dissection on computed tomogra-
phy (CT) scan
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IV. Dissection
Fig. 17.2. This patient had an uneventful type B aortic dissec-
tion initially treated with antihypertensive drugs. He developed
sudden hoarseness owing to the rapid expansion of the postdissection aneurysm. The dissection extended retrogradely into
the arch. The image on the left shows a CT scan with an
thrombosed or expanded false lumen, intussusception of the inner layers into the side branch or combinations. This can lead to clinical pictures such as
spinal cord problems (paraplegia or paraparesis), intestinal infarction, renal failure, ischemia of the lower extremities or combinations. These can occur
acutely but also progressively. The main problem is
that malperfusion does not always manifest itself by
a clear-cut clinical sign. On the contrary, it often
happens unnoticed, causing important time delay. It
should be clear that the function of the end organ is
at risk when malperfusion occurs; therefore, aggressive diagnostic testing (intra-arterial angiography) is
mandatory. Renal failure and mesenteric infarction
contribute to the high mortality in acute type B aortic dissection [1, 5±7].
4. Rapidly expanding aortic diameter might become
evident on consecutive plain chest X-rays but is better appreciated on repetitive computed tomography
(CT) scans.
5. Acute hoarseness: This can be an alarming sign of
rapid expansion of the dissected aorta in the neighborhood of the left recurrent laryngeal nerve. If this
occurs, an urgent CT scan or an MRI scan is mandatory (Fig. 17.2).
acutely distended and dissected aortic arch. The image in the
middle shows the preoperative angiography. He underwent an
emergency arch and proximal descending aorta replacement
using extracorporeal circulation. On the right is the postoperative CT scan (at 3 months)
to the spinal cord. Only rarely is replacement of the distal descending or the total thoracoabdominal aorta required. In this way the risk of spinal cord problems is
reduced. Mostly the dissected aorta is only moderately
enlarged in the acute phase. The operation for acute
distal aortic dissection should be tailored to address the
specific problem necessitating the intervention. In most
circumstances the distal repair can be performed in the
chest.
Only if there are indications on preoperative diagnostic tests that the rupture is localized low or that the
complete thoracoabdominal aorta is acutely enlarged is
a complete descending thoracic aortic or thoracoabdominal aortic replacement indicated. Resecting all the
17.3 Surgical Techniques
17.3.1 General Considerations
Open surgical repair in acute type B aortic dissection
should be seen as a life-saving procedure that aims at
the repair by insertion of a tubular Dacron prosthesis at
the proximal descending thoracic aorta and the restoration of the blood flow into the true lumen. Replacing
the proximal one third of the descending thoracic aorta
(Fig. 17.3) eliminates most likely the site of aortic rupture and is unlikely to interfere with the blood supply
Fig. 17.3. A short interposition graft in the proximal descending
thoracic aorta in a case of ruptured type B dissection
M. Schepens, K. Dossche Chapter 17 Surgical Treatment of Acute Type B Dissection
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177
dissected aorta should not be attained in the acute settings but certainly is the goal in the case of chronic dissections.
17.3.2 Use of Soft Clamps, Teflon Felt and Glue
It is advisable not to use the regular aortic clamps on
an acutely dissected aorta owing to the extreme friability. Instead, straight or angled rubber-shod Fogarty aortic clamps can be used. Owing to the fragility of the
acute dissected aorta, it might be safe to use reinforcement of the suture lines with Teflon felt (either posteriorly, circumferentially, externally or internally or both)
(Fig. 17.4) or to use glue, like gelatin±resorcin±formalin
(Microval, Saint-Just-Malmont, France) or BioGlue
(Cryolife, Kennesaw, GA, USA) [8]. When glue is used,
it is important that all layers are completely dry before
the application. It is much safer to transect the aorta
completely circumferentially not only at the proximal
suture line but also distally. This will overcome suturing
the esophageal wall (reducing the risk of late aorto-esophageal fistula) and will also ensure that all layers of
the dissected aortic wall are included into the anastomosis (which is not always so obvious in acute dissection).
In chronic dissections in which the intimal membrane has become fibrotic and scarred, it is advisable
to resect the membrane over a short distance and to suture the graft to the outer coat of the aorta. This fenestration of the dissecting membrane is essential in
chronic dissections at the distal and also at the proximal suture line. In acute aortic dissection (within
2 weeks after the onset) in contrast, all aortic layers
should be sutured together and blood flow should be
rerouted into the true lumen. This will allow the true
lumen to expand completely, thereby also maximizing
flow to compromised side branches. At the proximal
aortic stump it is important to ascertain which is the
true and which is the false channel: this can be done by
temporarily opening the aortic cross-clamp (in the case
of simple cross-clamping or left heart bypass).
17.3.3 Access
The chest of the patient is in the right lateral decubitus
position with the pelvis rotated posteriorly for optimal
access to the left femoral vessels. One can choose between a single thoracotomy, a double thoracotomy
(through either a double or a single skin incision) or a
thoracophrenolaparotomy (Fig. 17.5). It is important to
choose the correct approach to achieve optimal control.
Usually we prefer the fifth intercostal space (upper side
of the sixth rib) for repair of the descending thoracic
aorta: this approach allows for arch control and distally
up to the level of the tenth thoracic level. More distal
control and visibility in the area of the hiatus might become difficult or even problematic. In these circumstances one could add a second (lower) thoracotomy
through the same skin incision. Therefore, the anterior
aspect of the skin incision should be sloped down towards the costal arch. If the aortic arch needs to be
partially or totally replaced simultaneously (which is
exceptional in the case of acute type B dissection), we
prefer the fourth intercostal space (upper side of the
fifth rib): through this incision even the ascending aorta
can be reached. Under these circumstances it will be
very difficult if not impossible to reach the lower half
of the descending thoracic aorta. This means that a second lower chest incision is mandatory if the planned
repair extends to this region.
If a thoracoabdominal repair is anticipated, it will
depend on the type of the aneurysm which approach is
chosen but in general a thoracophrenolaparotomy is
suitable. A low left-sided tenth- or eleventh-rib
approach is useful for type IV thoracoabdominal repair
and also for creating a surgical reentry in the region of
the ostia of the visceral vessels.
Fig. 17.4. Teflon felt is used to reinforce the aortic stumps
(either externally or internally and between the layers)
17.3.4 Perfusion Techniques
Despite the fact that in the early experience most interventions were performed using simple cross-clamping
(or clamp-and-sew technique), this technique is now no
longer used because it causes difficult-to-control proximal hypertension with its detrimental effects on the
heart and brain, extreme distal hypotension and ischemia of a major portion of the body including kidneys,
guts and spinal cord. More important, it has been determined that 20±30 min is the safe time period of aortic
occlusion (at normothermia); this time period is insufficient for performing complex repairs, which is always
the case in acute type B dissection.
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IV. Dissection
Fig. 17.5. Access possibilities: left posterolateral thoracotomy (for proximal repair); middle thoracophrenolaparotomy (for thora-
coabdominal resection); right lumbotomy (for creating an abdominal reentry)
17.3.5 Atriofemoral Bypass (Left Heart Bypass)
Most surgeons actually use the left heart bypass. In this
system, oxygenated blood is withdrawn from the left atrium (through the left atrial appendage or through the
pulmonary vein) and reperfused via the left femoral artery into the lower body half, thereby reducing the ischemic time period of all distal organs, including the
spinal cord. Although in chronic aneurysm one can
cannulate the descending thoracic aorta, this is contraindicated in patients with acute type B dissections necessitating surgical repair. Using heparin-bonded pump
circuits avoids systemic heparinization. Owing to extensive heat loss the temperature of the body will decrease
to about 32 8C, which is an additional advantage; the
built-in heat exchanger allows for rewarming at the end
of the procedure. Maintenance of distal perfusion during clamping is the major advantage of this atriofemoral bypass: abdominal organs, including guts and kidneys, do not become ischemic. Also the ischemia of the
spinal cord is limited, reducing the incidence of paraplegia/paraparesis [9, 10]. When the aortic segment
containing the visceral arteries is excluded from the circulation by clamps, selective perfusion through side
branches allows the visceral arteries to be perfused continuously. Proximal clamping of the aortic arch should
not be a problem because theoretically the arch is not
involved in the dissection (although the hematoma may
spread around the arch, making identification of structures less reliable). Distally again it is important to use
soft clamps so as not to damage the fragile aortic wall;
an open distal anastomosis can be performed after having stopped the pump.
17.3.6 Extracorporeal Circulation (Partial or Total,
Deep Hypothermic Circulatory Arrest)
Using extracorporeal circulation via the femoro-femoral
(or pulmonary-femoral) route necessitates complete heparinization. Optimal organ protection can be achieved
by cooling the patient. By using deep hypothermic circulatory arrest (isoelectric encephalogram, nasopharyngeal and rectal temperature at about 18 8C or lower), we
can perform so-called ªopenº anastomoses: the application of clamps becomes unnecessary and end-to-end
anastomoses can be performed in a bloodless field, on
a flaccid aorta, which makes identification of all aortic
layers easier. Intraoperative damage to the lung should
be avoided because it will compromise the postoperative
respiratory status. We think that a ªno touchº technique
is important: only a posterior strip of the aorta needs
to be free from adherent lung tissue to allow for a longitudinal incision (this principle also applies to left heart
bypass).
17.4 Surgical Steps
After having installed the bypass (e.g., left heart bypass), control over the proximal and distal aorta is established using umbilical tapes or vessel loops. Encircling an acutely dissected aorta should be performed
with extreme care. In the case of replacement of the
proximal part of the descending thoracic aorta, the
proximal clamp should be placed on the aortic arch, between the left subclavian artery and the left carotid artery. Soft clamps are also used at the distal clamping re-
M. Schepens, K. Dossche Chapter 17 Surgical Treatment of Acute Type B Dissection
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gion. The aorta is opened longitudinally, the edges retracted with stay sutures. Back-bleeding intercostal vessels can be oversewn in the higher thoracic part but it
is advisable to reimplant intercostals in the lower thoracic area if major parts of the thoracic or thoracoabdominal aorta are to be replaced [8]. On the other
hand, reimplantation of intercostal vessels in a very friable dissected aortic wall might be hazardous. Some
authors consider reimplantation in these circumstances
even contraindicated [11]. Complete transection of the
proximal aorta is performed and the layers are identified and reconstructed (using Teflon or glue). It is important to have a nice cuff of aortic tissue projecting
out of the clamp: this makes repair and control of
bleeding easier. Finally a woven Dacron prosthesis is
anastomosed in an end-to-end fashion. This anastomosis can be tested by removing the proximal clamp and
occluding the vascular graft. Deairing is important to
avoid air entering into the head vessels. If hemostasis is
judged acceptable, the prosthesis is sized at its correct
length and the distal end is anastomosed to the aorta
similarly to the proximal anastomosis. Finally all
clamps are removed and antegrade flow is restored.
Since the acutely dissected aorta mostly is not enlarged,
it is not so evident to cover the prosthesis with aortic
wall; if desired one can use a poly(tetrafluoroethylene)
or a bovine pericardium patch, but it is not mandatory.
17.5 Malperfusion
In the past creating a surgical reentry was the treatment
of choice for malperfusion, but actually endovascular
catheter-based interventions are the primary option
[12]. Surgeons dealing with aortic problems should,
however, keep themselves abreast of the technique of
creating a surgical reentry because endovascular interventions might fail or be unsuccessful. Of course it can
be performed at any aortic level; it was most frequently
used at the level of the upper abdominal aorta in order
to relieve malperfusion of the viscera. It was described
for the first time by Shaw [13] in 1955. We prefer a low
thoracophrenolaparotomy entering the chest at the level
of the tenth or eleventh rib. The diaphragm can be left
intact at its anterior aspect, while the posterior part can
be divided circumferentially. Using this approach allows
for access to and control of the lower thoracic aorta
and the complete abdominal aorta up to the aortic bifurcation. The peritoneum need not be opened except
for inspection of the viability of the viscera at the end
of the procedure (in case of doubt). Once control over
the proximal (just above the diaphragm) and distal aorta (eventually one do not need to clamp distally) is established (again using soft clamps), the dissected aorta
is incised longitudinally over a short segment at the level of the compromised side branches. It is wise to avoid
Fig. 17.6. Creating an abdominal reentry
incision in the dissected part (the ªblueº part) because
otherwise suturing may become problematic; the nondissected part will have a normal color. The intimal flap
is excised in both directions as far as possible (Fig.
17.6). Of course, the use of one or even two cell-savers
is mandatory because back-bleeding from all side
branches will obstruct clear vision. When parts of the
intimal flap are no longer obstructing the ostia of the
main side branches (it is very important to have clear
access to all the ostia), the aorta is closed, preferably
with Prolene 5 ´ 0, over two strips of Teflon. This suture
line deserves utmost attention. The procedure mostly
takes no longer than 20±30 min of aortic clamping, so
no bypass is needed. However, if a tube graft insertion
is planned, we would advise using an adjunct (left heart
bypass). If at the end of the procedure the viability of
the affected organs is not restored adequately (flow
probes or Doppler imaging might help to assess this),
extra-anatomic bypass (e.g., axillobifemoral) can be
added. In the case of lower-extremity malperfusion, one
can choose to insert a small abdominal tube graft into
the abdominal aorta or just create an abdominal reentry
as described before. Femoro-femoral cross-over or axillobifemoral bypass can be an alternative.
Because the left renal artery is often affected by the
dissecting process, we completely agree with Borst et al.
[2] that unilateral malperfusion of this kidney can be
accepted without intervention. Acute onset paraplegia
after acute type B aortic dissection without involvement
of other vascular territories remains a controversial indication for creating reentry because we think that in
most cases the spinal cord deficit will be irreversible.
17.6 Results
Medical treatment of acute type B aortic dissection offers a 30-day mortality of about 10% [1]. Historical series have shown in the past varying results: Masuda et
al. [14] described a 6.5% hospital mortality and Appelbaum et al. [15] 32%.
Results of surgically treated acute type B dissection
should be interpreted with caution. If surgery is reserved for complicated patients with malperfusion, mortality will be high, while in other series in which sur-
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IV. Dissection
gery is the routine treatment of uncomplicated acute
type B dissections, one might expect a low mortality
rate. It has been shown that the preoperative status has
a tremendous impact on surgical outcome and results:
Genoni et al. [16] have shown that rupture, shock and
malperfusion are significant predictors of poor survival.
Nevertheless some series report zero mortality in patients treated surgically for acute type B dissection with
a 5- and 10-year survival of 80 and 57%, respectively
[17]. They suggest that earlier surgery for these patients
might be indicated.
17.7 Conclusion
In view of recent progress in endovascular treatment of
acute type B dissections with its less invasive character
and excellent good initial and medium-term results,
open repair becomes less and less the first option in
complicated acute type B dissections. Nevertheless it
must remain an important pillar in the treatment of
acute complicated type B dissections. We must not forget that endovascular treatment can fail or it can be inadequate. Owing to the fact that surgery for acute
type B dissections is difficult, often during the night
and without optimal anesthesiological support, it should
be reserved to aortic centers where a large number of
acute and elective patients are treated with all treatment
modalities.
References
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14. Masuda Y, Yamada Z, Morooka N, et al. Prognosis of patients with medically treated aortic dissections. Circulation 1991; 84:III7±13.
15. Appelbaum A, Karp RB, Kirklin JW. Ascending vs descending aortic dissections. Ann Surg 1976; 183:296±300.
16. Genoni M, Paul M, Tavakoli R, et al. Predictors of complications in acute type B aortic dissection. Eur J Cardiothorac Surg 2002; 22:59±63.
17. Lansman SL, Hagl C, Fink D, et al. Acute type B aortic
dissection: surgical therapy. Ann Thorac Surg 2002;
74:S1833±1835.
Surgical Treatment of Chronic
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Descending Aortic Dissection
Michael J. Jacobs
Chapter
18
Contents
18.1 Introduction ......................
18.2 Indications for Surgery ................ 181
18.3 Surgical Techniques .................. 182
18.3.1 Access ..................... 182
18.3.2 Thoracic Approach .............. 182
18.3.3 Thoracoabdominal Approach ........ 184
18.3.4 Abdominal Approach ............ 184
18.4 Adjunctive Procedures ................. 184
18.5 General Considerations: Pitfalls During Surgery . 185
18.6 Additional Surgical Techniques ........... 185
18.6.1 Descending Thoracic Postdissection
Aortic Aneurysms ..............
18.6.2 Thoracoabdominal Aneurysms ....... 186
18.7 Complications ...................... 186
18.7.1 Stroke ..................... 186
18.7.2 Paraplegia ...................186
18.7.3 Renal Failure ................. 186
18.7.4 Visceral Ischemia ............... 187
18.7.5 Pulmonary Complications .......... 187
18.8 Conclusion ....................... 187
181
185
18.1 Introduction
The definition of descending aortic dissection is clear,
indicating a dissected descending thoracic or thoracoabdominal aorta following an acute onset of an intimal
tear. More debatable is the term ªchronic,º which in
general is used if the dissection is older than 2 weeks.
It seems more appropriate to apply the term ªearly
chronic-phase,º for the first 2±4 weeks following the
acute phase of 2 weeks, on the basis of the instability of
the patient and the friable quality of the aorta in these
weeks. In this chapter only the chronic phase is addressed, indicating more than 6 weeks after the dissection. Descending aortic dissection can be limited to the
descending thoracic aorta but most often extends to the
abdominal aorta and even the iliac and femoral arteries.
Currently available techniques for open surgery and adjunctive protective measures will be described.
18.2 Indications for Surgery
In patients with uncomplicated chronic type B dissection there is no need for surgical intervention and adequate blood pressure management and regular anatomic
assessment by means of computed tomography or magnetic resonance are performed. ªUncomplicatedº basically means that the aorta is not dilated or growing in
time. It rarely occurs that in chronic, not dilated dissected aortas, the patient develops acute ischemic events
like intestinal ischemia, renal failure or paraplegia.
The main concern in chronic type B dissection is
aortic dilatation, which will ultimately determine the indication for surgery. The initial aortic diameter at the
time of the dissection and the fate of the false lumen
have an important influence on the development of aneurysm formation. It has been shown that the predominant predictors for aortic enlargement in the chronic
phase are the existence of a maximum aortic diameter
of or greater than 40 mm during the acute phase and a
patent primary entry site in the thoracic aorta [1].
Others [2] also showed that a patent false lumen and an
initial diameter of 40 mm or more were independent
predictors for chronic phase enlargement (larger than
60 mm) and aortic rupture.
Table 18.1 summarizes the different morphologic features at the time of the acute intimal tear. The nondilated aorta with a thrombosed false lumen will have the
best prognosis, whereas the dilated aorta with a patent
false lumen will likely develop an aneurysm. It is obvious that dissected aortic aneurysms carry a higher
risk compared with aortic dissections.
In summary, the indication for surgical repair of
chronic descending aortic dissection depends on the
diameter of the aorta. Subsequently, from a surgical
point of view, the dissected aorta becomes a thoracic
aortic aneurysm (TAA) or a thoracoabdominal aortic
182
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IV. Dissection
Table 18.1. Possible morphologic features of the aorta at the
time of acute type B aortic dissection
Aortic dissection Fate of lumen Remarks
Nondilated aorta Open true and false
Nondilated aorta Thrombosed false
Nondilated aorta Thrombosed true
Dissected aortic
aneurysm
Dilated aorta Open true and false
Dilated aorta Thrombosed false
Dilated aorta Thrombosed true
lumens
lumen
lumen
Fate of lumen Remarks
lumens
lumen
lumen
Most common
Best prognosis
Unco mmon
Most common
Best prognosis
Unco mmon
aneurysm (TAAA). In fact, 25% of descending and
TAAAs are postdissection dilatations [3].
Prosthetic replacement of a TAA or a TAAA is indicated if the diameter exceeds 6 cm. In Marfan patients
the threshold is accepted at 5 cm. Additional indications
for surgery comprise aorta-related symptoms like back
pain and rapid, progressive aortic dilatation.
18.3 Surgical Techniques
18.3.1 Access
Surgical access is dependent on the extent of the aortic
replacement. Figure 18.1 schematically depicts the different TAAs and TAAAs. Table 18.2 summarizes the surgical access for the corresponding aneurysms. Figure
18.2 depicts a giant post-type B dissection thoracic aneurysm. Figure 18.3 shows a perforation of the aortic
wall and only thrombus in the false lumen prevented
free rupture. Figure 18.4 illustrates the implanted polyester graft.
It is obvious that the majority of type B, C and D
descending thoracic aneurysms can be treated by endovascular techniques; these modalities are described elsewhere in this book. Descending thoracic aneurysms
with distal arch involvement can be treated by hybrid
techniques in which an endograft covers the supraaortic
arteries following bypass reconstruction of these arteries.
Table 18.2. Surgical access for the corresponding aneurysms
Extent of aneurysm Access
Descending thoracic aorta,
proximal part Ôdistal aortic
arch (Fig. 18.1 a, b)
Descending thoracic aorta,
mid+distal parts
(Fig. 18.1c)
Descending thoracic aorta,
entire (Fig. 18.1 d)
Thoracoabdominal types I,
II, III according to Crawford
Thoracoabdominal type IV Laparotomy/left anterior thora-
Left thoracotomy, fourth intercostal space
Fifth intercostal space
Fifth intercostal space
Thoracolaparotomy, sixth intercostal space
cotomy, eighth intercostal
space
18.3.2 Thoracic Approach
In open repair, type A and B descending thoracic aneurysms require a surgical approach via the fourth intercostal space. If, however, the aneurysm extends to the
diaphragm, the fifth intercostal space will provide adequate exposure. In some cases it is necessary to resect
the rib in order to extend the surgical working field.
The left lung is intubated with a selective bronchus
blocker or double lumen tube, allowing collapse of the
lung. In a substantial number of cases, the left lung is
adherent to the aneurysm as a result of local fibrous reaction following dissection and dilatation. It is recommended to limit the surgical dissection of the lung as
much as possible and only prepare the cross-clamp positions and the area of aortotomy.
Since the intimal tear is located at the level of the
left subclavian artery in the majority of patients it is
necessary to prepare a cross-clamp position proximal to
the left subclavian artery. Indeed, it might be possible
to clamp the aorta just distal to the subclavian artery,
but often this approach does not provide enough ªnormal,º nondissected aortic tissue to perform a secure
anastomosis. During dissection of the aortic arch and
left subclavian and carotid arteries, careful attention is
paid to the vagus and recurrent nerve. The nerve can
be dissected free from the aortic wall and secured with
a vessel loop. In all cases we prefer to transect the Botalli duct, allowing more access for the proximal clamp.
Safe clamping between the left carotid and the subclavian arteries requires circular dissection of the transverse
aortic arch. Opening of the pericardium, posterior to
the phrenic nerve, not only provides access to the left
atrium or pulmonary vein, but also allows easier dissection at the inner curve of the aortic arch. After the inner and outer curves have been dissected, the final
clamp position between the carotid and subclavian arteries can be prepared by two fingers encircling the aortic arch. During preparation of the distal clamp posi-
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