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_3850_Библиотеки_им_академика_М_И_Перельмана
.pdf
292
https://t.me/med1917
VI. Aortic Hematoma and Ulcers
abc
e f
d
Fig. 28.2. A 68-year-old man who presented with a thoracic pain with dyspnea that
was suggestive of pulmonary embolism. The CT examination revealed an intramural
hematoma (IMH).
thickening of the aortic wall on the posterior side of the aortic arch. Next to the aorta
a small amount of pleural fluid is visible.
the level of the convexity of the aortic arch: a small round ulcerlike lesion is seen
within the IMH.
descending aorta: a tiny irregularity of the intima is seen on the left side of the aorta.
d Sagittal multiplanar reconstruction view of the descending aorta that shows the ex-
tent of the IMH.
increased in size (
has evolved to a large aortic ulcer (
g
face-shaded view (
aorta
In a meta-analysis of the literature, Maraj et al. [43]
reported that IMHs were diagnosed in 81% of cases
with CT and, with TEE, MRI or a combination of the
two in the remainder of the cases. This distribution,
different to that reported in the RAD for the diagnosis
of aortic dissection, probably reflects the better accuracy of CT in detecting this disease. However, the advantage of CT and especially MD-CT for the assessment
of IMHs has not been specifically reported.
Many reports described the imaging features of
IMHs with echocardiography and emphasized the accuracy of this technique [33, 44]. However, in many cases
a Axial image without contrast enhancement: high attenuation
b Axial image with contrast enhancement at
c Axial image with contrast enhancement at the middle part of the
e±g CT scan 2 months later: the ulcer in the aortic arch has slightly
e) while the irregularity at the middle part of the descending aorta
f). These two lesions are well displayed on the sur-
g). This patient was treated by means of stenting the descending
the hypoechoic appearance of IMHs on TEE-TTE makes
it difficult to differentiate IMHs from atheromatous plaques and may account for the poorer accuracy of echography in detecting IMH.
MRI may be used in the acute phase to detect IMHs.
They appear with a high signal value on T2-weighted
images and low signal intensity on T1-weighted images.
The excellent tissue contrast of MRI, especially for
blood, makes it a highly accurate method for screening
IMHs. However, MRI will overall help to diagnose IMHs
in the subacute phase (after 1 week) because of the typical high signal of blood on T1-weighted images [35].
F. Thony et al. Chapter 28 The Current Optimal Imaging Modality for Evaluating Acute Aortic Syndromes
https://t.me/med1917
293
CT is certainly the most efficient diagnostic imaging
modality for IMHs (Fig. 28.2) [7, 12]. The high attenuation level of acute bleeding is typical of an IMH and
the excellent spatial resolution of this technique allows
for detection of subtle hematomas. However, it may be
sometimes difficult on a CT scan to prove this diagnosis
if the hematoma is very thin, or without a high attenuation value. Furthermore, if only images after contrast
enhancement are acquired, the aortic wall thickening
may simulate an atheromatous involvement of the aorta.
This is the main reason why every aortic examination
indicated for an acute aortic syndrome systematically
requires images before and after intravenous contrast
enhancement.
The management strategy of thoracic pains suggestive of an acute aortic syndrome should systematically
include a CT (or MRI) examination in the case of a
normal or noncontributory echocardiographic examination. This condition is mandatory for detecting IMHs.
It may explain why the incidence rate varies from 10 to
30% in series reported in the literature [37, 44, 45].
IMHs are unstable lesions that may spontaneously
heal or evolve to a dissection, an ulcer (Fig. 28.2) or a
thoracic rupture [46]. Thus, they have to be carefully
monitored by means of two or three CT examinations
during the first week, 2 weeks later and then after 1 and
3 months. This follow-up will be assumed with CT and
MRI and will continue for years because ulcers and intimal lesions associated with IMHs may evolve to aortic
pseudoaneurysms or rupture.
The therapeutic strategy is not consensual. For some
authors, type A IMHs are indicated for surgical repair
[44, 46±48], while for others [36, 45] medical treatment
is justified. Type B IMHs are medically treated but
some of them may benefit from a stenting of the aorta
[37]. Morphologic examinations have to detect and localize all the intimal lesions because it will be instrumental to plan the stent-graft treatment. If an endovascular treatment is planned, measurements of the aorta
and visualization of the aorto-iliac route have to be ruled out. For this thoraco-abdominal aortic investigation,
CT and MRI are the appropriate imaging tools.
28.4 Imaging of Aortic Ulcers
Atherosclerotic ulcers represent an unremarkable evolution of atheromatous lesions, frequently seen in the abdominal aorta and iliac arteries, which are usually
stable over time and rarely prone to complications.
Most aortic ulcers are incidentally discovered and are
confined to the inner part of the aortic wall. However,
in the thoracic aorta some of them may penetrate deeply into the wall and cause a localized or dissecting
IMH (Fig. 28.3), a dissection or an aortic rupture. This
specific evolution was first described by Stanson et al.
[40], who defined penetrating ulcers as atherosclerotic
lesions with an ulceration that penetrates the external
elastic lamina. Even though these lesions will not be responsible for an acute aortic syndrome, their natural
history may be a pseudoaneurismal evolution or distal
embolisms [49±52] and thus they need to be monitored
over a long period.
Penetrating ulcers occur in elderly patients with severe atherosclerotic lesions. The role of imaging investigations is to detect the lesion(s), to search for signs of
complications (bleeding or dissection) or to estimate
the risk for complications (aneurismal evolution, embolisms), to give information on the entire aorta and iliac
arteries for therapeutic strategy and to monitor patients
regularly thereafter. This implies three-dimensional
noninvasive imaging with high spatial resolution.
MD-CT allows for detection of aortic ulcers even if
they are small. It is efficient for the evaluation of their
penetration and bleeding in or out of the aortic wall.
Visualization of calcifications is of importance for grading the penetration of the ulcer through the arterial
wall [49, 50]. If stent-grafting is indicated, it will help
therapeutic management with sizing and investigation
of the aorto-iliac route (diameter of iliac arteries, atheromatous lesion with a risk of embolism, tortuous arteries) [53, 54]. If surgical treatment is indicated, the
imaging evaluation will search for other aortic ulcers to
determine the length of the aortic segment that will be
replaced.
Although MRI is not currently used in acute aortic
syndromes, it may be helpful for investigation of aortic
ulcers because many of these severely atherosclerotic
patients suffer from chronic renal failure and will not
be eligible for MD-CT. MRI is accurate for the investigation of aortic ulcers, especially for IMHs complicating
aortic ulcers (Fig. 28.3) [55] but does not demonstrate
aortic calcifications. Furthermore, some ulcer craters
may be missed on spin-echo images because of stagnant
blood flow within the ulcer [49]; thus, complementary
sequences such as gadolinium-enhanced magnetic resonance angiography must be used [51].
Penetrating aortic ulcers are more difficult to identify with TEE although this examination may be helpful
in the evaluation of a hematoma or dissection complicating the aortic ulcers [56]. Besides, there is only one
series published in the literature about echocardiography in the diagnosis of penetrating ulcers [56].
28.5 Conclusion
Which imaging modality is more appropriate to investigate acute aortic syndromes depends, for a given
pathology, on imaging criteria requested for the diagnosis, information relevant in patient management and on
the ability of an imaging modality to provide them.
294
https://t.me/med1917
VI. Aortic Hematoma and Ulcers
a
b
de
Over the past 2 decades technical improvements of
imaging modalities have increased exponentially and
make it difficult to give at the moment the state of the
art of imaging in acute aortic syndromes. Finally, in a
medical facility, the best way to investigate acute aortic
syndromes will depend on the quality of imaging equipment, the skill and experience of physicians with an
imaging technique, and diagnostic and therapeutic
strategies elaborated for patient management.
References
1. Vilacosta I, Roman JA. Acute aortic syndrome. Heart
2001; 85:365±368.
2. Van der Loo B, Jenni R. Acute aortic syndrome: proposal
for a novel classification. Heart 2003; 89:928.
3. von Kodolitsch Y, Nienaber CA, Dieckmann C, Schwartz
AG, Hofmann T, Brekenfeld C, Nicolas V, Berger J, Meinertz T. Chest radiography for the diagnosis of acute aortic syndrome. Am J Med 2004; 116:73±77.
4. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D,
Karavite DJ, Russman PL, Evangelista A, Fattori R, Suzuki
T, Oh JK, Moore AG, Malouf JF, Pape LA, Gaca C, Sechtem U, Lenferink S, Deutsch HJ, Diedrichs H, Marcos y
Robles J, Llovet A, Gilon D, Das SK, Armstrong WF, Deeb
GM, Eagle KA. The International Registry of Acute Aortic
Dissection (IRAD): new insights into an old disease.
JAMA 2000; 283:897±903.
5. Moore AG, Eagle KA, Bruckman D, Moon BS, Malouf JF,
Fattori R, Evangelista A, Isselbacher EM, Suzuki T, Nienaber CA, Gilon D, Oh JK. Choice of computed tomography,
transesophageal echocardiography, magnetic resonance
imaging, and aortography in acute aortic dissection: International Registry of Acute Aortic Dissection (IRAD).
Am J Cardiol 2002; 89:1235±1238.
6. Hirst AE Jr, Johns VJ Jr, Kime SW Jr. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine 1958;
37:217±279.
7. Yoshida S, Akiba H, Tamakawa M, Yama N, Hareyama M,
Morishita K, Abe T. Thoracic involvement of type A aortic
dissection and intramural hematoma: diagnostic accuracy7comparison of emergency helical CT and surgical find-
ings. Radiology 2003; 228:430±435.
8. Nienaber CA, von Kodolitsch Y, Nicolas V, Siglow V, Piepho A, Brockhoff C, Koschyk DH, Spielmann RP. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1±9.
9. Cigarroa JE, Isselbacher EM, DeSanctis RW, Eagle KA. Diagnostic imaging in the evaluation of suspected aortic
dissection. Old standards and new directions. N Engl J
Med 1993; 328:35±43.
c
Fig. 28.3. A 89-year-old man who was
hospitalized because he felt faint, without
thoracic pain.
a deformation of the aortic border (ar-
rows) on the frontal (
projections.
formed 8 days after the patient's admission. T1-weighted sequences in the axial
(
c) and sagittal (d) plans demonstrate a
high signal thickening on the posterior
part of the aortic wall (arrows), related
to a subacute bleeding in the aortic wall.
The extent of this hemorrhage within the
aortic wall is limited to a few centimeters.
ble on the MIP reconstruction of the
gadolinium-enhanced magnetic resonance angiograph (arrowheads). This
disease is likely an aortic ulcer complicated by a localized hemorrhage. It explains the patient's symptoms 1 week before
a, b The chest X-ray shows
a) and lateral (b)
c±e MRI examination per-
e A slight ulcerlike lesion is visi-
F. Thony et al. Chapter 28 The Current Optimal Imaging Modality for Evaluating Acute Aortic Syndromes
https://t.me/med1917
295
10. Sharma U, Ghai S, Paul SB, Gulati MS, Bahl VK, Rajani
M, Mukhopadhyay S. Helical CT evaluation of aortic aneurysms and dissection: a pictorial essay. Clin Imaging
2003; 27:273±280.
11. Prokop M. Multislice CT angiography. Eur J Radiol 2000;
36:86±96.
12. Rubin GD. MDCT imaging of the aorta and peripheral
vessels. Eur J Radiol 2003; 45:S42±49.
13. Willoteaux S, Lions C, Gaxotte V, Negaiwi Z, Beregi JP.
Imaging of aortic dissection by helical computed tomography (CT). Eur Radiol 2004; 14:1999±2008.
14. Hartnell GG. Imaging of aortic aneurysms and dissection:
CT and MRI. J Thorac Imaging 2001; 16:35±46.
15. Pereles FS, McCarthy RM, Baskaran V, Carr JC, Kapoor V,
Krupinski EA, Finn JP. Thoracic aortic dissection and aneurysm: evaluation with nonenhanced true FISP MR angiography in less than 4 minutes. Radiology 2002;
223:270±274.
16. Sommer T, Fehske W, Holzknecht N, Smekal AV, Keller E,
Lutterbey G, Kreft B, Kuhl C, Gieseke J, Abu-Ramadan D,
Schild H. Aortic dissection: a comparative study of diagnosis with spiral CT, multiplanar transesophageal echocardiography, and MR imaging. Radiology 1996; 199:347±352.
17. Silvey SV, Stoughton TL, Pearl W, Collazo WA, Belbel RJ.
Rupture of the outer partition of aortic dissection during
transesophageal echocardiography. Am J Cardiol 1991;
68:286±287.
18. Mehta RH, Bossone E, Evangelista A, O'Gara PT, Smith
DE, Cooper JV, Oh JK, Januzzi JL, Hutchison S, Gilon D,
Pape LA, Nienaber CA, Isselbacher EM, Eagle KA. International Registry of Acute Aortic Dissection Investigators.
Acute type B aortic dissection in elderly patients: clinical
features, outcomes, and simple risk stratification rule.
Ann Thorac Surg 2004; 77:1622±1628.
19. Khan IA, Nair CK. Clinical, diagnostic, and management
perspectives of aortic dissection. Chest 2002; 122:311±328.
20. Rizzo RJ, Aranki SF, Aklog L, Couper GS, Adams DH,
Collins JJ Jr, Kinchla NM, Allred EN, Cohn LH. Rapid
noninvasive diagnosis and surgical repair of acute ascending aortic dissection. Improved survival with less angiography. J Thorac Cardiovasc Surg 1994; 108:567±574.
21. Kern MJ, Serota H, Callicoat P, Deligonul U, Lee WH,
Aguirre F, Lew B, Barner H, Willman V. Use of coronary
arteriography in the preoperative management of patients
undergoing urgent repair of the thoracic aorta. Am Heart
J 1990; 119:143±148.
22. Miller JS, Lemaire SA, Coselli JS. Evaluating aortic dissection: when is coronary angiography indicated? Heart
2000; 83:615±616.
23. Nienaber CA, Eagle KA. Aortic dissection: new frontiers
in diagnosis and management: part I: from etiology to diagnostic strategies. Circulation 2003; 108:628±635.
24. Fallenberg M, Juergens KU, Wichter T, Scheld HH, Fischbach R. Coronary artery aneurysm and type-A aortic dissection demonstrated by retrospectively ECG-gated multislice spiral CT. Eur Radiol 2002; 12:201±204.
25 Vernhet H, Serfaty JM, Serhal M, McFadden E, Bonnefoy E,
Adeleine P, Revel D, Douek P. Abdominal CT angiography
before surgery as a predictor of postoperative death in acute
aortic dissection. AJR Am J Roentgenol 2004; 182:875±879.
26. Williams DM, Lee DY, Hamilton BH, Marx MV, Narasimham DL, Kazanjian SN, Prince MR, Andrews JC, Cho KJ,
Deeb GM. The dissected aorta: part III. Anatomy and
radiologic diagnosis of branch-vessel compromise. Radiology 1997; 203:37±44.
27. Gaxotte V, Cocheteux B, Haulon S, Vincentelli A, Lions C,
Koussa M, Willoteaux S, Asseman P, Prat A, Beregi JP. Relationship of intimal flap position to endovascular treatment of malperfusion syndromes in aortic dissection. J
Endovasc Ther 2003; 10:719±727.
28. Markl M, Draney MT, Hope MD, Levin JM, Chan FP, Alley
MT, Pelc NJ, Herfkens RJ. Time-resolved 3-dimensional
velocity mapping in the thoracic aorta: visualization of 3directional blood flow patterns in healthy volunteers and
patients. J Comput Assist Tomogr 2004; 28:459±468.
29. Nitatori T, Yokoyama K, Hachiya J, Yoshino A, Yamakami
N, Katase S, Ichikawa T. Fast dynamic MRI of aortic dissection: flow assessment by subsecondal imaging. Radiat
Med 1999; 17:9±14.
30. Dake MD, Kato N, Mitchell RS, Semba CP, Razavi MK,
Shimono T, Hirano T, Takeda K, Yada I, Miller DC. Endovascular stent-graft placement for the treatment of acute
aortic dissection. N Engl J Med. 1999; 340:1546±1552.
31. Quint LE, Platt JF, Sonnad SS, Deeb GM, Williams DM.
Aortic intimal tears: detection with spiral computed tomography. J Endovasc Ther 2003; 10:505±510.
32. Yamada T, Tada S, Harada J. Aortic dissection without intimal rupture: diagnosis with MR imaging and CT. Radiology 1988; 168:347±352.
33. Mohr-Kahaly S, Erbel R, Kearney P, Puth M, Meyer J. Aortic intramural hemorrhage visualized by transesophageal
echocardiography: findings and prognostic implications. J
Am Coll Cardiol 1994; 23:658±664.
34. Sueyoshi E, Matsuoka Y, Imada T, Okimoto T, Sakamoto I,
Hayashi K. New development of an ulcerlike projection in
aortic intramural hematoma: CT evaluation. Radiology
2002; 224:536±541.
35. Murray JG, Manisali M, Flamm SD, et al. Intramural hematoma of the thoracic aorta: MR image findings and their
prognostic implications. Radiology 1997; 204:349±355.
36. Kaji S, Nishigami K, Akasaka T, et al. Prediction of progression or regression of type A aortic intramural hematoma by
computed tomography. Circulation 1999; 00:II281±286.
37. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis of aortic intramural hematoma with and without penetrating
atherosclerotic ulcer: a clinical and radiological analysis.
Circulation 2002; 106:342±348.
38. Cambria RP. Regarding ªAnalysis of predictive factors for
progression of type B aortic intramural hematoma with
computed tomographyº. J Vasc Surg 2002; 35:1295±1296.
39. Muluk SC, Kaufman JA, Torchiana DF, Gertler JP, Cambria
RP. Diagnosis and treatment of thoracic aortic intramural
hematoma. J Vasc Surg 1996; 24:1022±1029.
40. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating
atherosclerotic ulcers of the thoracic aorta: natural history
and clinicopathologic correlations. Ann Vasc Surg 1986;
1:15±23.
41. Hayashi H, Matsuoka Y, Sakamoto I, Sueyoshi E, Okimoto
T, Hayashi K, Matsunaga N. Penetrating atherosclerotic ulcer of the aorta: imaging features and disease concept.
Radiographics 2000; 20:995±1005.
42. Rubinowitz AN, Krinsky GA, Lee VS. Intramural hematoma of the ascending aorta secondary to descending thoracic aortic penetrating ulcer: findings in two patients. J
Comput Assist Tomogr 2002; 26:613±616.
43. Maraj R, Rerkpattanapipat P, Jacobs LE, Makornwattana P,
Kotler MN. Meta-analysis of 143 reported cases of aortic
intramural hematoma. Am J Cardiol 2000; 86:664±668.
44. Nienaber CA, von Kodolitsch Y, Petersen B, et al. Intramural hemorrhage of the thoracic aorta. Diagnostic and
therapeutic implications. Circulation 1995; 92:1465±1472.
45. Song JK, Kim HS, Kang DH, et al. Different clinical features of aortic intramural hematoma versus dissection involving the ascending aorta. J Am Coll Cardiol 2001;
37:1604±1610.
46. von Kodolitsch Y, Csosz SK, Koschyk DH, Schalwat I,
Loose R, Karck M, Dieckmann C, Fattori R, Haverich A,
Berger J, Meinertz T, Nienaber CA. Intramural hematoma
of the aorta: predictors of progression to dissection and
rupture. Circulation 2003; 107:1158±1163.
296
https://t.me/med1917
VI. Aortic Hematoma and Ulcers
47. Kurimoto Y, Morishita K, Kawaharada N, Fukada J, Asai
Y, Abe T. Initial management of acute type-a aortic dissection with a thrombosed false lumen: a retrospective cohort study. Surg Today 2004; 34:652±657.
48. Robbins RC, McManus RP, Mitchell RS, et al. Management
of patients with intramural hematoma of the thoracic aorta. Circulation 1993; 88:1±10.
49. Harris JA, Bis KG, Glover JL, Bendick PJ, Shetty A, Brown
OW. Penetrating atherosclerotic ulcers of the aorta. J Vasc
Surg 1994; 19:90±98.
50. Kazerooni EA, Bree RL, Williams DM. Penetrating atherosclerotic ulcers of the descending thoracic aorta: evaluation with CT and distinction from aortic dissection. Radiology 1992; 183:759±765.
51. Levy JR, Heiken JP, Gutierrez FR. Imaging of penetrating
atherosclerotic ulcers of the aorta. AJR Am J Roentgenol
1999; 73:151±154.
52. Tittle SL, Lynch RJ, Cole PE, Singh HS, Rizzo JA, Kopf
GS, Elefteriades JA. Midterm follow-up of penetrating ul-
cer and intramural hematoma of the aorta. J Thorac Cardiovasc Surg 2002; 123:1051±1059.
53. Kos X, Bouchard L, Otal P, Chabbert V, Chemla P, Soula
P, Meites G, Joffre F, Rousseau H. Stent-graft treatment of
penetrating thoracic aortic ulcers. J Endovasc Ther 2002;
9:II25±31.
54. Schoder M, Grabenwoger M, Holzenbein T, Domanovits
H, Fleischmann D, Wolf F, Cejna M, Lammer J. Endovascular stent-graft repair of complicated penetrating atherosclerotic ulcers of the descending thoracic aorta. J Vasc
Surg 2002; 36:720±726.
55. Yucel EK, Steinberg FL, Egglin TK, Geller SC, Waltman
AC, Athanasoulis CA. Penetrating aortic ulcers: diagnosis
with MR imaging. Radiology 1990; 177:779±781.
56. Vilacosta I, San Roman JA, Aragoncillo P, Ferreiros J,
Mendez R, Graupner C, Batlle E, Serrano J, Pinto A, Oyonarte JM. Penetrating atherosclerotic aortic ulcer: documentation by transesophageal echocardiography. J Am
Coll Cardiol 1998; 32:83±89
Management of Aortic Hematomas
https://t.me/med1917
and Ulcers: Evaluation Scoring
Jean-Franois Heautot, Vincent Tran Dinh,
Bertrand De Latour, Jean-Philippe Verhoye
Chapter
29
Contents
29.1 Introduction ......................
29.2 Therapeutic Principles ................. 297
29.2.1 Medical Treatment .............297
29.2.2 Surgical Treatment ............. 297
29.2.3 Endovascular Treatment .......... 298
29.3 Evolutive Risk Factors .................298
29.3.1 Clinical Risk Factors ............ 298
29.3.1.1 Difficulties in Blood Pressure Control . 298
29.3.1.2 Persistent or Recurrent Pain ....... 298
29.3.2 Anatomo-radiologic Risk Factors .... 298
29.3.2.1 Site ......................298
29.3.2.2 Aorta Diameter ...............298
29.3.2.3 Hematoma Thickness ........... 298
29.3.2.4 Intimal Lesion ............... 298
29.3.2.5 Effusions ................... 299
29.4 Management Strategy ................. 299
29.4.1 Type A ....................299
29.4.2 Type B .................... 299
29.4.3 Gravity Score ................ 299
29.4.4 Decision Algorithm ............ 300
29.5 Conclusion ....................... 300
297
29.1 Introduction
The management of intramural hematomas (IMH) and
atherosclerotic penetrating ulcers (APU) of the aorta relies, as that of aortic dissections, on the localization of
the lesion according to the Stanford classification,
type A being located on the ascending aorta, and
treated surgically, type B on the descending aorta, and
treated medically. Recent publications [1±4] have suggested that medical therapy could be successfully applied to type A IMH in high-surgical-risk patients. Besides, advances in endovascular techniques allow a
more aggressive approach of complicated type B. These
new management trends make necessary a score to predict low-risk type A and high-risk type B.
After a literature review of therapeutic modalities
and risk factors, we propose an evolutivity risk score
and a decisional algorithm for IMH and APU management.
29.2 Therapeutic Principles
29.2.1 Medical Treatment
Medical treatment is based on the control of systolic
blood pressure to decrease the chance of rupture. At
the acute phase (first 2 weeks) it is mandatory to administrate a beta blocker via an intravenous route. The
patient is to be monitored in an intensive care unit,
with continuous measurement of systolic blood pressure, with an arterial line if needed. If the blood pressure is difficult to control, a calcium channel antagonist,
or a nitrate, can be used. Systolic blood pressure must
be lower than 120 mmHg, and bursts are to be avoided
by a strict rest in bed.
Analgesia must control pain. Morphine can be given
if required by the intensity of the pain, but persisting
or aggravating pain must lead to the search for a potential evolution by repeating computed tomography (CT)
scanner control.
A pericardial effusion at the initial stage mandates
an ultrasound control twice a week, and particular clinical attention with respect to the risk of tamponade.
After the acute phase, oral administration of antihypertensive drugs can be initiated. Systolic blood pressure
control remains the key aim of the medical management.
29.2.2 Surgical Treatment
Surgical treatment is based on the currently validated
techniques of replacement of the pathologic segment.
The basic principle is to realize prostheto-aortic sutures
in areas of normal wall, sometimes reinforced by a Teflon banding according to the fragility of the aortic wall.
The sealing of the suture can be completed by the use
of biological glues (cf. previous chapters).
298
https://t.me/med1917
VI. Aortic Hematoma and Ulcers
Because of an older age, and a greater frequency of
comorbidities [5], the surgical risk is higher in patients
with IMH or APU than that of patients with aortic dissection.
The open repair requires local excision and graft interposition. This is a major undertaking in a population
of patients with a high incidence of comorbidity, with a
high risk of complications including paraplegia and cerebrovascular accident. Thus, the desire to prevent
spontaneous complications of the disease's course by
open surgery must be cautiously considered with respect to the patient status, and the patient and his or
her family duly informed. In this respect, endovascular
techniques afford an encouraging alternative to treat intimal lesions of the descending aorta [6].
29.2.3 Endovascular Treatment
Today, endovascular treatment is mainly available for the
descending aorta. It relies on stent-grafts. Their main use
is to provide protection from the risk of rupture in the
case of an intimal lesion. The landing zone must include
a sufficient proximal and distal area of normal aortic
wall. It seems preferable to use completely covered
stent-grafts, without bare stents or hooks. Given the intima fragility, it seems unwise to use a modeling balloon to
complete the stent-graft deployment.
Up to now, systematic use of stent-grafts in IMH
without an intimal lesion has not been validated. Only
randomized studies could justify such a therapeutic
strategy.
This technique requires a careful imaging protocol
in order to better select the feasibility of the endovascular access (quality of the iliac arteries), and the diameter and length of the stent-graft [7±9]. The main
branches must be precisely located with respect to the
lesion, specially the subclavian and left carotid proximally, and the celiac and superior mesenteric distally.
This technique should be offered to elderly patients
at high surgical risk for conventional surgical repair.
Ideal anatomic targets are localized lesions with normal-sized, minimally angulated, cylindrical proximal
and distal landing zones of adequate length. Adequate
vascular access in terms of arterial size and lack of excessive tortuosity and occlusive disease is also critical
for a safe and successful stent-graft deployment [10].
Complications (namely paraplegias) are less frequent
than with conventional surgical repair.
29.3 Evolutive Risk Factors
The assessment of evolutive risk factors will determine
the therapeutic strategy. The evolution must be assessed
with repeated imaging controls, principally a CT scan-
ner. Screening at the end of the first week, 1 and
6 months, 1 year and yearly thereafter until complete
normal restitution seems a reasonable and safe protocol. An intermediate control can be necessary in the
case of modifications. At the chronic phase, MRI can be
proposed as an alternative. The choice of the imaging
modality depends on the local equipment and expertise.
29.3.1 Clinical Risk Factors
29.3.1.1 Difficulties in Blood Pressure Control
This is a pejorative factor which, without justifying an
interventional attitude in itself, leads to a more aggressive management, especially in the presence of an intimal lesion.
29.3.1.2 Persistent or Recurrent Pain
Thoracic pain difficult to control is a significant risk
factor in all the studies. It represents a syndrome of
menace of rupture if it is associated with an increase of
pericardial or pleural effusions [5].
29.3.2 Anatomo-radiologic Risk Factors
29.3.2.1 Site
The site of the IMH or APU defines the type, A or B.
Type A and proximal type B have a worse outcome than
distal type B [5, 11±13].
29.3.2.2 Aorta Diameter
It is commonly accepted that the cutoff diameters for
surgery of aneurisms (ascending 50±55 mm, descending
60±70 mm) can be applied to IMH and APU.
29.3.2.3 Hematoma Thickness
A thickness greater than 7 mm defines the hematoma.
A thickness greater than 10±12 mm is a factor of a bad
outcome [11]. In the study by Song et al. [1] it is the
only independent predictor for adverse outcomes
(death, aortic surgery, and overt aortic dissection) in
type A IMH, with an 11-mm cutoff value.
29.3.2.4 Intimal Lesion
By definition there is always an intimal lesion in the
APU. In IMH, intimal lesions most often represent ostial disruptions (mainly of intercostal arteries) called
ªulcerlike projections.º They are more frequent on the
descending aorta than on the ascending aorta. Their onset during the course of the disease is a predictor of
worse outcome [4]. Different thresholds of size and
J.-F. Heautot et al. Chapter 29 Management of Aortic Hematomas and Ulcers: Evaluation Scoring
https://t.me/med1917
299
depth have been proposed. In the study by Ganaha et
al. [5], the cutoff was a diameter of 20 mm and a depth
of 10 mm.
The presence of an intimal tear can foretell the evolution towards overt dissection [5]; thus, it must be
searched for with great care [14, 15], the smallest ones
necessitating close scrutiny for detection. Careful follow-up of the evolution must always be done.
29.3.2.5 Effusions
Pleural or pericardial effusions can witness transudation of the IMH or a hemothorax. In the absence of
characteristic thrombus hyperdensity on the CT scanner
image, it is difficult to distinguish serous or hemorrhagic nature without pleural puncture. More than their
existence in itself, their increase is a predictor of rupture [5, 6].
29.4 Management Strategy
IMH usually appear on aortas with little atheroma lesions, oppositely to APU. So, evolution towards a frank
dissection is frequent in the case of IMH, by media
splitting, whereas in the case of UPA, fibrous changes
of the aortic wall due to atheroma limit the extension
of the dissecting process. Evolution towards localized
dissection can be completely silent [1, 2].
Association of persistent or recurrent pain, evolving
serous or hemorrhagic effusion, and dynamic instability
constitute a syndrome of menace of rupture. APU carry
a high risk or rupture, whereas in the case of IMH,
without an intimal lesion, the healing process is not infrequent. So, to us, the strategy in the acute phase will
essentially rely on the existence or not of an intimal lesion, and rupture risk factors. This justifies a close
imaging follow-up, systematic in the case of an asymptomatic patient, and in case of clinical change in the
case of a symptomatic patient.
At the chronic phase, in both cases, patient followup must aim at looking for aneurism evolution, generally fusiform in the case of IMH without an intimal lesion, sacciform in other cases.
studies and timed surgical repair in cases with complications must remain the rule [1±3].
Aggressive management is recommended for APU,
and suspicion for rupture must be maintained during
the acute phase. Type A APU should be treated surgically.
29.4.2 Type B
Medical management is recommended for type B APU
[16]. Stent-grafts permit a higher degree of protection
against rupture than medical therapy alone. Because
APU affect older persons, one must consider the patient's age, overall physical condition, and anticipated
life expectancy in the decision to use operative treatment. If patients tolerate medical management without
clinical deterioration, they may continue conservative
follow-up care with reasonable safety [10]. This medical
treatment is permissible in high-surgical-risk patients,
when a close clinical and imaging follow-up is possible,
in uncomplicated forms, and when the aorta diameter
is smaller than 50 mm.
29.4.3 Gravity Score
On the basis of the analysis of literature, the authors
suggest a gravity score based on two clinical items and
four radiological items to compose a gravity score. Each
item is weighted by its severity in terms of prediction
of risk.
Clinical items
Persistent or recurrent thoracic pain in spite
of best medical treatment
Increasing effusion 1
Radiological items
Type A 2
Intimal tear 1
Increase of aorta diameter 1
Increase of IMU thickness or APU depth 1
2
29.4.1 Type A
Surgery remains the only treatment option for hemodynamically unstable patients with type A lesions.
Medical treatment of type A IMH without an intimal
tear, bed rest with antihypertensive treatment to minimize the risk of evolution towards frank dissection, can
only be conceived in the case of important comorbidity
and in the absence of menace of rupture. Supportive
medical treatment with frequent follow-up imaging
The lowest score is 0 and the maximum score is 8. If
the score is more than or equal to 3, prediction of rupture is high and treatment (type A surgical, type B endovascular) is indicated. If the score is below 3, the risk
is low. Medical treatment is the rule in type B. It can be
applied to type A (i.e., good control of pain and blood
pressure, without radiological evolution despite repeated CT scanner controls).
300
https://t.me/med1917
VI. Aortic Hematoma and Ulcers
29.4.4 Decision Algorithm
In view of recent publications [6, 17, 18], the authors
suggest the following:
Type A Intimal lesion Surgery
Type A No intimal lesion;
no comorbidity;
risk score less than 3
Type B Intimal lesion; risk score 3
or more
Type B No intimal tear; risk score
less than 3
Medical treatment
Stent-graft
Medical treatment
29.5 Conclusion
Whom to treat?
The key is whether there is an intimal tear [16].
Studies have demonstrated that IMH without an intimal
tear evolve in the short term and can be reabsorbed or
progress to classic dissection or aortic rupture.
Long-term follow-up is mandatory to detect aneurismal evolution, even in the absence of an intimal lesion,
because of the aortic wall stress [16].
Most studies describing IMH have used very small
study populations; thus, owing to the paucity of clinical
experience with IMH, the optimal therapy for this condition is still largely undefined.
These are provisional recommendations regarding
the treatment of penetrating ulcers. As more knowledge
is acquired, better understanding of this disease could
lead to a more accurate definition of risk factors.
References
1. Song JM, Kim HS, Song JK, Kang DH, Hong MK, Kim JJ,
Park SW, Park SJ, Lim, TH, Song MG. Usefulness of the
initial non invasive imaging study to predict the adverse
outcomes in the medical treatment of acute type A aortic
intramural hematoma. Circulation 2003; 108(Suppl 1):
II324±328.
2. Song JK, Kim HS, Kang DH, Lim TH, Song MG, Park SW,
Park SJ. Different clinical features of aortic intramural hematoma versus dissection involving the ascending aorta. J
Am Coll Cardiol 2001; 37:1604±1610.
3. Song JK, Kim HS, Song JM, Kang DH, Ha JW, Rim SJ,
Chung N, Kim KS, Park SW, Kim YJ, Sohn DW. Outcomes
of medically treated patients with aortic intramural hematoma. Am J Med 2002; 113:181±187.
4. Kaji S, Akasaka T, Katayama M, Yamamuro A, Yamabe K,
Tamita K, Akiyama M, Watanabe N, Tanemoto K, Morioka
S, Yoshida K. Long-term prognosis of patients with type B
aortic intramural hematoma. Circulation 2003; 108(Suppl
1):II307±311.
5. Ganaha F, Miller DC, Sugimoto K, et al. Prognosis of aortic intramural hematoma with and without penetrating
atherosclerotic ulcer: a clinical and radiological analysis.
Circulation 2002; 106:342±348.
6. Troxler M, Mavor AI, Homer-Vanniasinkam S. Penetrating
atherosclerotic ulcers of the aorta. Br J Surg 2001;
88:1169±1177.
7. Sailer J, Peloschek P, Rand T, Grabenwoger M, Thurnher
S, Lammer J. Endovascular treatment of aortic type B dissection and penetrating ulcer using commercially available stent-grafts. AJR Am J Roentgenol 2001; 177:1365±
1369.
8. Cambria RP, Brewster DC, Lauterbach SR, Kaufman JL,
Geller S, Fan CM, Greenfield A, Hilgenberg A, Clouse
WD. Evolving experience with thoracic aortic stent graft
repair. J Vasc Surg 2002; 35:1129±1136.
9. Schoder M, Grabenwoger M, Holzenbein T, Domanovits
H, Fleischmann D, Wolf F, Cejna M, Lammer J. Endovascular stent-graft repair of complicated penetrating atherosclerotic ulcers of the descending thoracic aorta. J Vasc
Surg 2002; 36:720±726.
10. Demers P, Miller DC, Mitchell RS, Kee ST, Chagonjian L,
Dake MD. Stent-graft repair of penetrating atherosclerotic
ulcers in the descending thoracic aorta: mid-term results.
Ann Thorac Surg 2004; 77:81±86.
11. Moizumi Y, Komatsu T, Motoyoshi N, Tabayashi K. Clinical features and long-term outcome of type A and type B
intramural hematoma of the aorta. J Thorac Cardiovasc
Surg 2004; 127:421±427.
12. Evangelista A, Dominguez R, Sebastia C, Salas A, Permanyer-Miralda G, Avegliano G, Gomez-Bosh Z, Gonzalez-Alujas T, Garcia del Castillo H, Soler-Soler J. Prognostic value of clinical and morphologic findings in shortterm evolution of aortic intramural haematoma. Therapeutic implications. Eur Heart J 2004; 25:81±87.
13. von Kodolitsch Y, Csosz SK, Koschyk DH, Schalwat I,
Loose R, Karck M, Dieckmann C, Fattori R, Haverich A,
Berger J, Meinertz T, Nienaber CA. Intramural hematoma
of the aorta: predictors of progression to dissection and
rupture. Circulation 2003; 107:1158±1163.
14. Quint LE, Platt JF, Sonnad SS, Deeb GM, Williams DM.
Aortic intimal tears: detection with spiral computed tomography. J Endovasc Ther 2003; 10:505±510.
15. Macura KJ, Corl FM, Fishman EK, Bluemke DA. Pathogenesis in acute aortic syndromes: aortic dissection, intramural hematoma, and penetrating atherosclerotic aortic
ulcer. AJR Am J Roentgenol 2003; 181:309±316.
16. Tittle SL, Lynch RJ, Cole PE, Singh HS, Rizzo JA, Kopf
GS, Elefteriades JA. Midterm follow-up of penetrating ulcer and intramural hematoma of the aorta. J Thorac Cardiovasc Surg 2002; 123:1051±1059.
17. Maraj R, Rerkpattanapipat P, Jacobs LE, Makornwattana P,
Kotler MN. Meta-analysis of 143 reported cases of aortic
intramural hematoma. Am J Cardiol 2000; 86:664±668.
18. Motoyoshi N, Moizumi Y, Komatsu T, Tabayashi K. Intramural hematoma and dissection involving ascending aorta: the clinical features and prognosis. Eur J Cardiothorac
Surg 2003; 24:237±242; discussion 242.
Endograft Management
https://t.me/med1917
of Aortic Hematomas and Ulcers
David M. Williams, Bora Peynircioglu
Chapter
30
Contents
30.1 Introduction ......................
30.2 Pathological Description ............... 301
30.3 Imaging Features .................... 302
30.4 Principles of Treatment ................304
30.5 Intimal Defect Without IMH ............. 304
30.6 Intimal Defect with IMH ............... 304
30.7 IMH Without Intimal Defect ............. 305
30.8 Treatment Results ................... 305
30.9 Conclusion ....................... 306
301
30.1 Introduction
In evaluating a symptomatic patient with intramural hematoma (IMH) of the thoracic aorta, the clinician is occasionally presented with difficult and unanswerable
questions such as these: Is an intimal defect present or
not? Does it have a bearing on the hematoma? If a definite defect is present, is it an intimal tear related to an
incipient classic dissection, or is it a penetrating ulcer?
How do these distinctions help us decide proper patient
management? That these distinctions do matter has
been established by the Stanford group, who found that
IMH in symptomatic patients was significantly more often associated with disease progression when accompanied by penetrating ulcer than when not [4].
IMH or intramural hemorrhage of the thoracic aorta
is a condition representing localized hemorrhage within
the aortic media. When the term is used strictly, no intimal defect such as a tear or an ulcer is present. In
practice, the term is loosely used to mean a mostly
thrombosed false lumen regardless of intimal defect.
Furthermore, it may be difficult by imaging means to
completely exclude an intimal defect. When the intimal
defect is identified, it may be difficult to classify it. The
literature reflects these difficulties by a commonly encountered vagueness or even inconsistency in the description of how the diagnosis of strict IMH was confirmed, or an intimal defect excluded, or an atherosclerotic etiology verified.
In clinical practice, several authors have noted that
patients with IMH share a clinical profile and prognosis
with patients with a classic dissection affecting the
same aortic territory [6, 7, 11]. Most aortic dissections
have intimal tears in classic locations near the sinotubular ridge in the ascending aorta or just beyond the attachment of the ligamentum arteriosum in the descending aorta [8]. Whether patients with IMH would, if not
treated medically, progress to full-blown dissection
complete with the classic spectrum of ªentryº tears has
not been established.
The penetrating atherosclerotic ulcer of the thoracic
aorta was described in classic papers by Stanson et al.
[9] and Cooke et al. [1] nearly 20 years ago. Numerous
authors have contributed to the literature on ulcers
since that time, bearing on the presentation, natural
history, and treatment of this troublesome lesion.
Nevertheless, uncertainty in the pathophysiology of the
ulceration, nonspecific features of the lesion at aortography and computerized tomography (CT) examination, and frequent appeal to imaging (most of which is
unavailable to reviewer and reader alike) rather than
histological proof of disease all contribute to day-to-day
practical uncertainties in identifying and treating the
penetrating ulcer.
30.2 Pathological Description
The distinguishing pathological feature of this lesion is
a localized ªulceration,º a gaping communication between the lumen and the medial layer of the aorta,
which can result in external rupture or intramural hemorrhage. When intramural hemorrhage accompanies the
ulcer, it lies within the aortic media and therefore comprises an aortic dissection. Two surgical specimens of
ulcers were depicted in the Mayo papers: a longitudi-
Соседние файлы в папке Библиотека им академика М.И. Перельмана