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_3860_Библиотеки_им_академика_М_И_Перельмана
.pdf
414 C. W. Bakal and S. Sprayregen
https://t.me/med1917
A
FIGURE 33-2. Angiodysplasia in proximal ascending colon in a 63-year-
old woman with a history of multiple previous episodes of brisk lower
gastrointestinal bleeding. A: There is simultaneous opacification of the
ileocolic artery and vein during the arterial phase of the selective injection,
consistent with an early draining vein and arteriovenous shunting. B: Magnification view better demonstrates the prominent, early draining vein
(
black arrow
increased tortuosity and caliber of the terminal ileocolic branch. C: Venous
C
phase demonstrates marked prominence of the ileocolic vein (
) as well as a subtle associated vascular tuft (
white arrow
arrow
B
), with
).
Vascular Diseases of the Lower Gastrointestinal Tract
https://t.me/med1917
415
A B
FIGURE 33-3. A 63-year-old woman with recurrent episodes of lower gastrointestinal bleeding. A: Hypervascular lesion in the
jejeunum (
B: Barium enema performed 1 week after angiogram demonstrates a submucosal mass (
schwannoma was resected.
differentiated from AV malformations by the circumscribed nature of the angiographic blush as well as the
presence of mass effect. Angiography may be helpful for
small bowel myomas because their extramucosal location
may prevent visualization on a small bowel barium series.
Arterial encasement may be seen with malignancies.
Meckel’s diverticulum accounts for 1% of cases of GI
arrowhead
) with prominent draining vein (
arrow
). Because of the mass effect, this was thought to represent a tumor.
white arrow
). At laparotomy, a
tortuous vessels at its distal aspect and arising from the
distal SMA. The vitellointestinal artery also may have a
number of side branches along its entire length and
exhibit no appreciable tortuosity. Demonstration of a
Meckel’s diverticulum requires a high index of suspicion
and may require the use of superselective catheteriza-
11,12
tion.
bleeding and usually is seen in young patients (younger
than 20 years of age), presenting as repeated episodes of
brisk lower GI hemorrhage. In adults, it usually presents
as slower, chronic GI bleeding.
99m
Tc pertechnetate abdominal scans can localize ectopic gastric mucosa and
thus may be helpful in diagnosis. The scans are considered a sensitive technique for localization in children, but
the sensitivity and specificity in adults are limited.
Angiographic localization thus can play an important
role. Meckel’s diverticulum is usually found in the terminal ileum, supplied by a persistent vitellointestinal artery
(Fig. 33-4). Classically, this artery was described as an
elongated artery without branching, having a group of
■ Mesenteric Ischemia
Ischemic diseases of the GI tract that are of interest to the
vascular and interventional radiologist are caused primarily by compromise of SMA flow. Inadequate blood
10
flow causing ischemia to all or part of the small intestine
and right half of the colon can occur acutely or chronically. In the acute form, there is generally loss of viability
of varying portions of the bowel supplied by the SMA,
which may cause an abdominal catastrophe. Mesenteric
angiography followed by transcatheter therapy or laparo-
416 C. W. Bakal and S. Sprayregen
https://t.me/med1917
FIGURE 33-4. Meckel’s diverticulum. Vitellointestinal artery
supplies the diverticulum (
arrows
).
tomy needs to be performed promptly to decrease morbidity and mortality. Conversely, chronic mesenteric ischemia generally occurs without loss of tissue viability
because collateral filling can compensate. The diagnosis
of chronic mesenteric ischemia is often made after other
entities are excluded, with angiography reserved for late
in the workup.
Acute mesenteric ischemia
Acute mesenteric ischemia generally occurs in elderly patients with significant comorbidities. It has a high mortality, because it is often diagnosed too late. Patient survival
requires a high clinical suspicion and an aggressive approach to both diagnosisand therapy. Theocclusive forms
of acute mesenteric ischemia are SMA embolus, SMA
thrombosis, and superior mesenteric vein (SMV) thrombosis. Nonocclusive mesenteric ischemia (NOMI) occurs
in the SMA distributionas aresult ofpathologic vasospasm
initiated by decreased cardiac output, typically because of
myocardial infarction or pulmonar y edema. Mesenteric
vasoconstriction is a normal response to low cardiac output states; it can persist as pathologic vasospasm after the
inciting clinical event has resolved.
13
The essentials of
management include medical resuscitation, obtaining a
plain film, early and liberal use of angiography and administration of transcatheter vasodilators whenever possible. In the occlusive forms of the disease, laparotomy usually is performed to revascularize the bowel. Frankly
infarcted segments are resected, and questionably viable
segments are left in place. These questionable segments
should be evaluated (and resected if they have progressed
to infarction) at a “second look” operation performed 24
hr later.
Abdominal pain is present in 75 to 90% of patients who
have acute mesenteric ischemia. Classically, the pain is
described as “out of proportion” to the physical find-
14
ings.
Usually, abdominal distension and leukocytosis are
present. Frank GI bleeding is unusual, although most
patients have occult blood in the stool. Bowel-wall edema
ensues with marked intravascular volume depletion,
hemoconcentration, and shock. Fluid exudate is seen in
the bowel lumen. Injury persisting less than 6 hr generally causes reversible damage, but after 12 to 24 hr, inflammation and hemorrhage intensify and usually lead to
transmural infarction and gangrene. Laboratory tests for
acute mesenteric ischemia, including complete blood
count (CBC) and peritoneal fluid analysis, are not helpful in establishing or excluding the diagnosis of ischemia.
An obstructive series should be the initial examination
in a patient with suspected acute mesenteric ischemia.
The role of the plain film in suspected acute mesenteric
ischemia is to exclude other causes of abdominal pain,
especially a perforated viscus.
26% of cases of frank intestinal infarction.
15
Plain films are normal in
16
Nonspecific
signs occur late in the course of disease and are present
in one third of cases. These signs include adynamic ileus,
thickened bowel wall in the SMA distribution with “pinky
printing,” pseudoobstruction or obstruction, and formless loops of bowel. Plain film findings that are more
specific for mesenteric ischemia occur late and include
pneumatosis, portal venous gas, rigid formless loops, and
thickened bowel wall (thumbprinting). Pneumatosis although highly suggestive, is uncommon, occurring in 5%
of cases. The presence of portal venous gas is associated
with a 75% mortality.
17,18
Although small bowel barium studies can determine
the presence of persistent ischemic segments postoperatively or in chronic disease, barium plays no role in the
workup of acute mesenteric ischemia. Computed tomography (CT) has been used increasingly as the initial
study in the workup of abdominal pain. It is sensitive for
intramural air and bowel-wall thickening and can be used
to include or exclude alternate etiologies of pain. The
role of CT in the acute workup of mesenteric ischemia is
https://t.me/med1917
still evolving. It is currently not sufficiently sensitive
enough for use in the workup of primary acute vascular
insufficiency.
19
The use of relatively large amounts of intravenous contrast and the need for oral contrast agents
may preclude performing an adequate arteriogram. We
consider arteriography the gold standard because of its
high diagnostic accuracy and because of the ability to
deliver pharmacologic agents into the mesenteric artery.
In patients with suspected acute mesenteric ischemia, arteriography should be performed expeditiously after the
abdominal plain film.
If acute mesenteric ischemia is the leading suspected
diagnosis, CT should not be performed; however, if other
etiologies of abdominal pain are suspect and CT is performed, it is essential that the CT signs of mesenteric
ischemia be recognized. CT findings include abrupt vascular cutoffs with nonenhancement of mesenteric vessels.
Thrombosis of the SMA or SMV may be seen as an intravascular filling defect, and bowel wall enhancement
may be reduced or absent. Thrombosis of the SMV usually presents with enlargement of the SMV with low-density thrombus, which is well defined by a perivascular rim
(Fig. 33-5). There may be engorgement of the mesenteric
veins. Bowel wall findings include intramural hemorrhage or thickening of the bowel wall, dilatation of the
small intestine, and right and transverse colon (Fig. 33-6).
Pneumatosis, mesenteric venous gas, and portal venous
gas all are sensitively depicted by CT (Fig. 33-7). A normal
CT does not rule out mesenteric ischemia.
Historically, acute mesenteric ischemia has been reported to have a 70 to 90% mortality rate. An aggressive
management protocol using early angiography and transcatheter papaverine has been associated with a decreased mortality of 45%, with most survivors sustaining
minimal bowel loss.
13,20
Angiography can differentiate
Vascular Diseases of the Lower Gastrointestinal Tract 417
FIGURE 33-6. Dilated, thickened loops of bowel on computed
tomography in a patient with acute mesenteric ischemia.
(Courtesy of Ellen Wolf, M.D.)
between the occlusive and nonocclusive forms of the
disease, determine the nature and site of occlusion,
evaluate perfusion of the vascular bed distal to the occlusion, and be followed by intraarterial infusion of vasodilators. The presence of shock is an absolute contraindication to the use of vasodilators. If the patient is receiving
vasopressors, the diagnosis of nonocclusive mesenteric
ischemia cannot be made with certainty because these
agents produce splanchnic vasoconstriction which mimics NOMI. Thus, shock and vasopressor infusions are
relatively strong contraindications to angiography. In patients on vasopressors, diagnostic angiography may be
performed if superior mesenteric artery embolus is suspected in the specific setting of acute abdominal pain
and a cardiac arrhythmia.
FIGURE 33-5. Superior mesenteric vein (SMV) thrombosis.
Contrast-enhanced computed tomography demonstrates filling
defect in the SMV with an enhanced perivascular rim (
arrow
FIGURE 33-7. Intramural air seen on computed tomography
in a 75-year-old man with advanced acute mesenteric ischemia. This patient died of extensive bowel necrosis. (Courtesy
of Ellen Wolf, M.D.)
).
418
https://t.me/med1917
C. W. Bakal and S. Sprayregen
Acute mesenteric ischemia is a true angiographic
emergency. The angiographic technique is straightforward. Lateral and anteroposterior (AP) aortography are
performed to note the status of the celiac and mesenteric
artery origins and arterial collateral filling patterns. Aortography is also valuable for visualizing any extramesenteric events, such as renal arter y embolus, which can
produce a similar clinical picture to mesenteric ische-
14
mia.
In addition to the occlusive and nonocclusive processes that specifically affect the SMA, aortic dissection can
also cause mesenteric ischemia.
Selective superior mesenteric arteriography is performed after the aortogram is completed. Low osmolar
contrast is used primarily because of the tenuous clinical
condition of most of these patients. The diagnostic study
should be performed without pharmacologic enhancement: administration of IA vasodilators such as papaverine (sometimes used for better delineation of the venous
phase in anatomic mapping studies) could ameliorate
the vasospasm seen in NOMI, precluding the diagnosis.
Traditional film screen techniques are well accepted, although increasing numbers of angiographers are using
high-resolution (1024 ⫻ 1024) nonsubtracted digital arteriography. It is essential to administer enough contrast
and film out far enough for visualization of the venous
phase (e.g., 6–8mL/sec, total volume 50–60 mL, covering
30 sec).
SMA embolus is the most frequent form of mesenteric
ischemia (50% of cases). The source of the embolus is
usually the left ventricle. Patients who have atrial fibrillation or who were recently cardioverted are at high risk.
Angiographically, the embolus presents as a sharp,
rounded filling defect and occurs most often at branch
points, especially the middle colic artery (Fig. 33-8). About
18% of emboli will lodge at the SMA origin, where they can
be difficult to differentiate from acute thrombosis.
21,22
Emboli lodging proximal to the ileocolic artery are considered major. Considerable vasospasm is often present,
which puts the bowel at additional risk.
13,23
After making
the diagnosis, a transcatheter vasodilator infusion is begun immediately in the angiography suite to ameliorate
vasospasm and is continued throughout and after laparotomy (papaverine, 60-mgbolus followedby 60mg/hr infusion). Extramesenteric emboli can occur inup to one fifth
of patients with SMA embolus and should not be overlooked clinically in the course of diagnosing the patient’s
abdominal pain. In 10% of patients, minor emboli occur
in the terminal SMA distal to the ileocolic artery origin or
distally in branches ofthe superior mesenteric artery. If no
peritonitis is present, patients may be managed with no
specific therapy or with transcatheter papaverine and followed clinically without laparotomy. The role of regional
thrombolysis in treating acute mesenteric artery embolus
appears promising and its use is increasing; however, the
use of lytic agents is not universally accepted and remains
controversial. Several case reports and small series have
documented the use of urokinase inselected patients.
24–29
Lysis may be effective in patients with recent onset of abdominal pain and a normal abdominal plain film and
should only be continued if there is significant improvement of the angiographic signs and the clinical symptoms
within the first hour of the start of the IA infusion.
24
SMA thrombosis occurs in elderly patients with underlying atherosclerotic disease. These patients usually have
a history of peripheral vascular disease or coronary or
cerebrovascular comorbidity and also may have a preceding chronic course of abdominal pain (intestinal angina).
Thrombosis usually occurs at the origin of the superior
mesenteric artery as an extension or exacerbation of aortic atherosclerosis (Fig. 33-9). SMA thrombosis is a relatively rare cause of acute mesenteric ischemia.
NOMI typically occurs in critically ill patients in intensive care units and is frequently associated with a preceding episode of myocardial infarction of congestive heart
failure. The incidence of NOMI probably has decreased
with the increased use of calcium channel blockers in the
intensive care unit. Unless complicated by peritonitis,
surgery is contraindicated in this disease, which is treated
with transcatheter papaverine for 24 to 48 hr (Fig. 33-10).
The initial (nonpapaverine enhanced) arteriogram may
demonstrate diffuse narrowing of the SMA trunk and
branches, narrowing at branch origins, a “string of sausages” appearance of the mesenteric arterial branches,
spasm of the arcades, or impaired filling of the intramural vessels (Fig. 33-11).
29
Mesenteric venous thrombosis can be acute, subacute,
or chronic and is idiopathic in 20% of cases (Fig. 33-12).
Known etiologies include hypercoagulable states,neoplastic disease, peritonitis, surgery (e.g., splenectomy, pancreatectomy), and trauma. There is an association with
deep venous thrombosis. Mesenteric venous thrombosis
appears to have a better prognosis than arterial forms of
mesenteric ischemia, with a mortality of about 32%.
Mortality and morbidity may be reducedeven further with
prompt heparinization. This disease has a more variable
onset than the arterial forms of mesenteric ischemia, and
extensive venous collaterals appear to prevent infarction
of bowel in most cases. If no peritoneal signs are present,
intravenous heparin should be given. The presence of
peritoneal signs mandates a laparotomy. If only a short
ischemic segment of bowel is found, it is resected and
heparin is given. Ifa viable long ischemic segment is found
and the superior mesenteric vein is patent, then heparin
and an intraarterial papaverine drip are given. A “secondlook operation” can be performed. In the presence of
long ischemic segments and mesenteric vein occlusion,
thrombectomy also is indicated. Long segments of nonviable bowel must be resected, and total parenteral nutrition may be needed. Thrombolysis for acute mesenteric
venous thrombosis has been administered through the
30
A
https://t.me/med1917
B
C
FIGURE 33-8. Patient with atrial fibrillation and several hours of acute
abdominal pain. A: There are dilated bowel loops and questionable intramural and portal vein gas (
cutoff of the superior mesenteric artery (SMA) trunk (
superior mesenteric arteriogram demonstrates embolus lodging in the
main SMA trunk at the level of the middle colic artery, with absent distal
arrow
filling (
embolus proved fatal.
). A papaverine infusion was begun preoperatively, but the
arrows.
) B: Lateral aortogram demonstrates
arrow
). C: Selective
420 C. W. Bakal and S. Sprayregen
https://t.me/med1917
FIGURE 33-9. Lateral aortogram in an elderly patient with
acute superior mesenteric artery (SMA) thrombosis.
SMA31and directly into the superior mesenteric vein
through a transjugular, intrahepatic approach
32
in case
reports; results have been promising. With thewidespread
use of CT, an increasing number of patients with asymptomatic, incidental mesenteric venous thrombus have been
identified; the presence of such incidental cases suggests
that mesentericvenous thrombosis may be associated with
a very wide clinical spectrum of clinical illness.
The term colonic ischemia usually is reserved for a different, more benign condition than acute superior mesenteric ischemia. Colonic ischemia is generally a transient
disease with low mortality, although it can be fulminant.
It usually occurs in the presence of a “low flow” state and
is believed to be associated with small-vessel disease in the
distribution of the IMA. Plain film signs include thumbprinting in the descending colon as a result of clinical
edema or hemorrhage. Escherichia coli 0157:H7 infection
is thought to be one etiology. The diagnosis is usually
confirmed by endoscopy; angiography is not indicated.
Chronic mesenteric ischemia
Chronic mesenteric ischemia or “intestinal angina” occurs when there is chronic occlusion of at least two of
three celio-mesenteric arteries (Fig. 33-13).
33
The etiol-
A B
FIGURE 33-10. Nonocclusive mesenteric ischemia. A: There is diffuse spasm of the superior mesenteric artery (SMA) and its
branches. There is poor filling of the SMA branches B: After an overnight transcatheter papaverine infusion, there is marked
resolution with improved branch filling.
Vascular Diseases of the Lower Gastrointestinal Tract 421
https://t.me/med1917
FIGURE 33-11. “String of sausages” appearance in another
patient with nonocclusive mesenteric ischemia (NOMI).
ogy is usually atherosclerotic. The chronic time course of
stenosis leading to occlusion allows for extensive collateralization. (In situ thrombosis of a stenotic SMA may rarely
lead to an acute exacerbation and to a clinical presentation of acute mesenteric ischemia.) Intestinal angina occurs when the metabolic demand of the bowel outstrips
the ability of the compromised arteries to deliver blood
and oxygen. Patients typically complain of intense abdominal pain after eating, which may lead to “food fear,”
with consequent marked weight loss. Malabsorbtion and
abdominal bruit may develop. The diagnosis of chronic
mesenteric ischemia is frequently one of exclusion, made
after other possible etiologies of pain and weight loss
(such as pancreatic neoplasm) are eliminated. Angiography is usually invoked late in an extensive workup and
is confirmatory. The difficulty of making this diagnosis is
exacerbated because two- and even three-vessel celiomesenteric arterial occlusion has been seen and reported in
asymptomatic patients. Conventional therapy is surgical,
FIGURE 33-12. Patient with 2 weeks of moderate abdominal
pain. There is superior mesenteric vein (SMV) thrombosis. Note
arrow
absence of the superior mesenteric vein (
ence of collaterals in the duodenum (
of the portal vein, with nonopacified blood from the splenic vein
curved arrow.
(
)
arrowhead
) and the pres-
). There is filling
for example, aortomesenteric or iliac-mesenteric bypass.
Percutaneous transluminal angioplasty (PTA) has been
used for atherosclerotic SMA stenoses, with some authors
reporting 80 to 90% initial success; secondary patency
and a 1- to 2-year clinical success rate for SMA PTA is
reported as high as 60 to 80%.
34–36
SMA stents may be
important in achieving an effective result. Bypass surgery
appears more durable than PTA (possibly because of the
tendency to perform multiple-vessel bypasses) but most
likely has a higher morbidity.
37
Thus, some recommend
PTA primarily for use in candidates who are at high risk
for surgery. The use of metallic stents probably increases
the success rate of PTA.
38,39
Median arcuate ligament compression (celiaccompres-
sion syndrome) of the superior aspect of the celiac trunk
422 C. W. Bakal and S. Sprayregen
https://t.me/med1917
A
FIGURE 33-13. Symptomatic chronic mesenteric ischemia.
Aortogram demonstrates occlusion of the celiac and mesenteric arteries in the lateral (A) and the frontal projections (B).
Significant atherosclerotic plaque is seen in the aorta and left
renal artery. Large collateral is responsible for mesenteric per-
C
fusion (C).
B
Vascular Diseases of the Lower Gastrointestinal Tract
https://t.me/med1917
423
is usually asymptomatic and is thought to occur frequently. A bandlike superior indentation of the celiac
artery is pathognomonic. PTA is not usually effective or
indicated for median arcuate ligament syndrome.
■ Summary
Angiographic techniques play an important role in the
diagnosis and management of lower GI hemorrhage and
mesenteric ischemia. Timely and knowledgeable consultation with the interventional radiology service can make
a huge impact on patient outcome.
References
1. Winzelberg GC, Froelich JW, McKusick KA, et al. Radionuclide
localization of lower gastrointestinal hemorrhage. Radiology 1981;
139:465–469.
2. Alavi A. Detection of gastrointestinal bleeding with 99m Tc-sulfur
colloid. Semin Nucl Med 1982;12:126–128.
3. Baum S, Nusbaum M. The control of gastrointestinal hemorrhage
by selective mesenteric arterial infusion of vasopressin. Radiology
1971;98:497–505.
4. Kornblith PL, Boley SJ, Whitehouse BS. Anatomy of the splanchic
circulation. Intestinal ischemia. Surg Clin North Am 1992;72:1–30.
5. Seppanen SK, Leppanen MJ, Pimenoff G, Seppanen JM. Microcatheter embolization of hemorrhages. Cardiovasc Intervent Radiol
1997;20:174–179.
6. Gordon RL, Ahl KL, Kerlan RK, et al. Selective arterial embolization for control of lower gastrointestinal bleeding. Am J Surg 1997;
174:24–28.
7. Boley SJ, Sprayregen S, Sammartano RJ, et al. The pathophysiologic
basis for the angiographic signs of vascular ectasias of the colon.
Radiology 1977;125:615–621.
8. Athanasoulis CA. Therapeutic applications of angiography. N Engl
J Med 1980;302:117–120.
9. Schmidt SP. Boskind JF, Smith DC, Catalano RD. Angiographic
localization of small bowel angiodysplasia with use of platinum
coils. J Vasc Interv Radiol 1993;4:737–739.
10. Schwartz MJ, Lewis JH. Meckel’s diverticulum: pitfalls in scintigraphic detection in the adult. Am J Gastroenterol 1984;79:611– 618.
11. Okazaki M, Higashihara H, Saida Y, et al. Angiographic findings of
Meckel’s diverticulum; the characteristic appearance of the vitellintestinal artery. Abdom Imaging 1993;18:15–19.
12. Mitchell AWM, Spencer J, Allison DJ, Jackson JE. Meckel’s diverticulum: angiographic findings in 16 patients. AJR Am J Roentgenol
1998;170:329–333.
13. Boley SJ, Brandt LJ, Veith FJ. Ischemic disorders of the intestines.
Curr Probl Surg 1978;15:1.
14. Bakal CW, Sprayregen S, Wolf EL. Radiology in intestinal ischemia:
angiographic diagnosis and management. Surg Clin North Am
1992;72:125–142.
15. Wolf EL, Sprayregen S, Bakal CW. Radiology in intestinal ischemia—plain film, contrast, and other imaging studies. Surg Clin
North Am 1992;72:107–124.
16. Smerud MJ, Johnson CD, Stephens DH. Diagnosis of bowel infarction: a comparison of plain films and CT scans in 23 cases. AJR
Am J Roentgenol 1990;154:99–103.
17. Tomchik FS, Wittenberg J, Ottinger LW. The roentgenographic
spectrum of bowel infarction. Radiology 1970;96:249.
18. Liebman PR, Patten MT, Manny J, et al. Hepatic-portal venous gas
in adults; etiology, pathophysiology and clinical significance. Ann
Surg 1978;187:281–287.
19. Taourel PG, Deneuville M, Pradel JA, et al. Acute mesenteric ischemia: diagnosis with contrast-enhanced CT. Radiology 1996;199:
632–636.
20. Kaleya RN, Sammartano RJ, Boley SJ. Aggressive approach to acute
mesenteric ischemia. Surg Clin North Am 1992;72:157–182.
21. Boley SJ, Feinstein FR, Sammartano R, et al. New concepts in the
management of superior mesenteric artery embolus. Surg Gynecol
Obstet 1981;153:561.
22. Clark RA, Gallant TE. Acute mesenteric ischemia: angiographic
spectrum. AJR Am J Roentgenol 1984;142:555.
23. Laufman H. Significance of vasospasm in vascular occlusion [thesis]. Northwestern University Medical School, Chicago, 1948.
24. Simó G, Echenagusia AJ, Camúñez F, et al. Superior mesenteric
artery arterial embolism: local fibrinolytic treatment with urokinase. Radiology 1997;204:775–779.
25.
Schoenbaum
artery embolism: treatment with intraarterial urokinase. J Vasc In-
terv Radiol 1992;3:485–490.
26. Gallego AM, Ramirez P, Rodriguez JM, et al. Role of urokinase in
the superior mesenteric arter y embolism. Surgery 1996 Jul;120:
111–113.
27. Fuentes FT, Muerza GS, Belda AE, et al. Successful intrarterial
fragmentation and urokinase therapy in superior mesenteric artery
embolism. Surgery 1995;117:712–714.
28. Badiola CM, Scoppetta DJ. Rapid revascularization of an embolic
superior mesenteric artery occlusion using pulse-spray pharmacomechanical thrombolysis with urokinase. AJR Am J Roentgenol
1997;169:55–77.
29. Siegelman SS, Sprayregen S, Boley SJ. Angiographic diagnosis of
mesenteric arterial vasoconstriction. Radiology 1974;112:533.
30. Boley SJ, Kaleya RN, Brandt LJ. Mesenteric venous thrombosis. Surg
Clin North Am 1992;72:183–202.
31. Poplausky MR, Kaufman JA, Geller SC, et al. Mesenteric venous
thrombosis treated with urokinase via the superior mesenteric artery. Gastroenterology 1996;110:1633–1635.
32. Rivitz M, Geller, SC, Hahn C, Waltman AC. Treatment of acute
mesenteric venous thrombosis with transjugular intramesenteric
urokinase infusion. J Vasc Interv Radiol 1995;6:219–228.
33. Cunningham CG, Reilly LM, Stoney R. Chronic visceral ischemia.
Surg Clin North Am 1992;72:231–244.
34. Allen RC, Martin GH, Rees CH, Rivera FJ, et al. Mesenteric
angioplasty in the treatment of chronic mesenteric ischemia. J Vasc
Interv Surg 1996;24:415–421.
35. Hallisey MJ, Deschaine J, Ilescas FF, et al. Angioplasty for the relief
of visceral ischemia. J Vasc Interv Radiol 1995;(6):785–791.
36. Matsumoto AH, Tegtmeyer CJ, Fitzcharles EK, et al. Percutaneous
transluminal angioplasty of visceral arterial stenoses: results and
long term clinical follow-up. J Vasc Interv Radiol 1995;6:165–174.
37. Rose SC, Quigley TM, Raker EJ. Revascularization for chronic mesenteric ischemia: comparison of operative arterial bypass grafting
and percutaneous transluminal angioplasty. J Vasc Interv Radiol
1995;6:339–349.
38. Trost DW. Stents and angioplasty for relief of mesenteric ischemia.
Presented at “Advances in vascular intervention and CO
York City, May 30, 1997.
39. Liermann DD. The use of stents in the mesenteric arteries. Presented at “Advances in vascular intervention and CO
City, May 30, 1997.
SW, Pena C, Koenisberg P, et al. Superior mesenteric
.” New
2
.” New York
2
Соседние файлы в папке Библиотека им академика М.И. Перельмана