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Vascular Closure Devices and Thrombosis Chapter | 30 445
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[36] Sen T, Astarcioglu MA, Kilit C, Amasyali B. Successful thrombolytic treatment of a mobile thrombus on atrial septal defect occluder device. Acta
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[37] Homma S, Di Tullio MR, Sacco RL, Smith C, Mohr JP. Surgical closure of patent foramen ovale in cryptogenic stroke patients. Stroke
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[40] Krasuski RA, Hart SA, Allen D, Qureshi A, Pettersson G, Houghtaling PL, Batizy LH, Blackstone E. Prevalence and repair of intraoperatively
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[41] Kotowycz MA, Therrien J, Ionescu-Ittu R, Owens CG, Pilote L, Martucci G, Tchervenkov C, Marelli AJ. Long-term outcomes after surgical versus
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Chapter 31
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Management Strategies for Thrombosis
of Major Abdominal Aortic Branches:
The Superior Mesenteric and Renal
Arteries
Mohammed Aladdin, Moshe S. Fuksbrumer and Allyne Topaz
The Brooklyn Hospital Center, Brooklyn, NY, United States
INTRODUCTION
Acute thrombotic and thromboembolic occlusions of the superior mesenteric artery (SMA) account for life-threatening
scenarios leading to irreversible damage to the intestinal wall with a mortality as high as 60%e100%. Renal artery
thrombosis constitutes another, albeit rare, life-threatening vascular condition. The marked difference in their prevalences
can be attributed to the different anatomic exit angles from the abdominal aorta of these vessels and to their different
distances from the heart. The hallmark of both conditions is thrombosis associated with stable or unstable atherosclerotic
plaque. Accordingly, erosion or rupture of a plaque are common underlying pathologic processes that account for thrombus
formation and accumulation. Other common etiologies are thrombus embolization and hypercoagulopathy. Thromb us
formation can also be precipitated by acute vascular events or cardiovascular changes [1].
This chapter describes the complex etiologic role of thrombus in the clinical presentation of the aforementioned
vascular conditions. The content covers the available diagnostic modalities and reviews the roles of pharmacotherapy,
endovascular interventions, and surgical treatment. Several sample cases are presented to illustrate the typical clinical
issues. As thrombus removal leads to restoration of antegrade blood flow, the therapeutic strategies described herein play a
critical role in the inhibition of ischemia-induced injuries to the intestines and kidneys, thus preventing further devastating
damage to these vital organs [2,3].
ANATOMY
The three major mesenteric arteries that perfuse the small and the large intestines are: (1) the celiac trunk, which supplies
the hepatobiliary system, spleen, and proximal small bowel; (2) the SMA, which supplies the small intestine and proximal
middle colon; and (3) the inferior mesenteric artery (IMA), which supplies the distal colon and the rectum. Collateral blood
vessels connecting the celiac trunk, the SMA, and the IMA maintain blood flow to the intestines in chronic atherosclerotic
vascular disease and serve an important role in the event of an acute occlusion of one of these mesenteric arteries,
particularly the SMA.
PATHOPHYSIOLOGY OF ACUTE MESENTERIC ISCHEMIA
SMA occlusion secondary to atherosclerotic plaque accounts for about 70% of all acute mesenteric ischemia (AMI) cases [4].
Thrombotic occlusion usually appears as a thrombus superimposed on a heavily calcified and occlusive lesion at the
ostium of the SMA. Approximately 30%e50% of cases are caused by arterial thromboembolism [5]. Due to the large
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vessel lumen and the unique shallow downward anatomic exit from the abdominal aorta, the SMA is susceptible to cardiac
thromboembolism. Sources of cardiac embolism are myocardial infarction, atrial fibrillation, dilated cardiomyopathy,
infective throm botic endocarditis, and thrombotic atherosclerotic plaques of the aortic wall. Approximately 15%e30% of
cases are caused by thrombosis [6]. Unsurprisingly, pati ents with SMA occlusion commonly have a history of atherosclerotic disease involving the coronary, cerebrovascular, and peripheral arterial vessels [7].
In those patients, acute SMA thrombosis represents dynamic pathologic changes that affect chronic atherosclerotic
lesions.
Acute vascular events can enhance the impact of these pathologic changes as well. Consequently, total cessation of
flow with complete vessel occlusion can ensue [8].
The severity of thrombus-induced ischemic injury directly relates to the number of blood vessels involved and is
inversely proportional to the volume of the mesenteric artery blood flow. Other variables that influence the disease severity
include systemic blood pressure, duration of the ischemia, and the number of interconnecting vessels. While blockage of
the IMA may not affect blood flow to the intestine because of the existing supporting collateral vessels, the SMA is more
frequently affected, and interruption of blood flow can lead to detrimental ischemia. With advanced ischemia, the intestinal
mucosal layer loses its integrity, resulting in the release of bacteria and toxins into the circulation. Sepsis, cardiac failure,
and organ failure occur prior to the advancement of necrosis of the intestine’s wall. Further ischemia and hypoxia drive the
cyanotic wall and the fluid can be released into the peritoneal cavity, which leads to transmural necrosis, a condition with
much worse prognostic outcomes [9].
Clinical Presentation
The clinical presentation of acute SMA is nonspecific and variable; most patients, however, present with severe abdominal
pain disproportionate to the physical examination. Symptoms range from acute sudden-onset severe abdominal pain to
less-defined pain. A diagnostic feature of AMI is a history of abdominal angina or postprandial pain that occurs about
10e20 min after meals and can last 1e3 h. Patients may also have a history of chronic abdominal pain that persists from
several weeks to months, often followed by an acute abdominal insult [10]. In 75% of reported cases, patients with acute
SMA may also have associated bloody stool. Other symptoms include nausea and vomiting in about 75% of cases, and
25% of patients display abdominal distension and gastrointestinal bleeding as primary symptoms.
Diagnosis
Physical Examination
The physical examination depe nds on the course of the disease. Palpation may demonstrate a range of mild tenderness to a
generalized guarding. Fever, hypotension, tachycardia, tachypnea, and change in mental status can be encountered. Foul
breath may be noted with bowel infarction, from the putrefaction of undigested gastrointestinal material.
Laboratory Studies
Laboratory markers can be unreliable and nonspecific to acute SMA [11e15]. While markers carry inherent limitations,
they can be used to track responses to treatmen t. Proposed biomarkers in humans include D-dimer [16,17], which has a
higher sensitivity relative to other markers;
binding protein. Overall, studies have shown that markers are significantly upregulated in patients with AMI compared
with control patients [19].
Imaging
L-lactate [18]; D-lactate; glutathione S-transferase; and intestinal fatty acid
As of this writing, imaging is the most effective way to diagnose AMI. Color Doppler ultrasound is an established
bedside technology for the identification of flow-limiting plaque and associated thrombosis [20]. Conventional mesenteric
angiography (CMA) images that depict abrupt occlusion of the SMA with absence of coll aterals are indicative of acute
mesenteric thrombosis. CMA is currently the gold standard for imaging AMI with 100% sensitivity and specificity.
Computed tomographic angiography (CTA) also provides excellent and accurate imaging modality [21] with a sensitivity
of 96%e100% and specificity of 89%e94% [22,23]. Other modalities include vascular ultrasound and selective
mesenteric angiography, previously regarded as the gold standard of diagnosis. Magnetic resonance angiography (MRA)
provides an alternative to CTA with a sensitivity of 100% and a specificity of 90%. Advantages include the noninvasive
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mechanism and absence of the radiation associated with CTA [24,25]. Nevertheless, a significant limitation of MRA relates
to the longer time required to complete scans in comparison with CTA. For patients with impaired renal function or chronic
kidney disease in whom contrast load is an issue of concern, CO
angiography is a valid option.
2
Treatment
The critical elements of initial therapy include volume resuscitation, hemodynamic monitoring, administration of broadspectrum antibiotics, and adequate pain control [26e29].
Surgery
In instances in which peritonitis develops during thrombolysis, the vascular treatment should be postponed and surgical
evaluation should be obtained [30,31]. Surgical managemen t in acute mesenteric thrombosis is indicated w hen the
diagnosis is suspected in the presence of peritonitis. Laparotomy with resection of the ischemic bowel, open thrombectomy, a nd temporary c lo sure with early second-look surgery (within 48 h) is indicated. Intraoper at ive assessment of
necrotic bowel with extensive resection may be required, with avoidance of bowel anastomosis in the septic patient. A
planned second-look procedure for evaluation of bowel ischemia progression is associated with a significant reduction in
morbidity and mortality. The management of arterial embolism consists of midline laparotomy with access of the SM A
at the mesenteric root. After proximal and distal control tra nsverse arteriotomy is performed,followedbyembolectomy.
Bypass procedures with native or synthetic grafts, including supraceliac to superior mesenteric trunk, renal mesenteric
bypass, or retrograde common iliac bypass, ar e options [32].
Endovascular Treatment
With the rapid development of user-friendly reliable percutaneous devices since the late 1990s, endovascular intervention
has been established as the primary management option for AMI in patients without advanced bowel ischemia [33].
Mechanical Thrombectomy
The user-friendly aspiration catheters are most effective in instances of total cessation of blood flow. However, while this
modality is effective in small blood vessels of 2e4 mm, it is ineffective in large thrombus burden and large vessels. The
Penumbra catheter also relies on suction and can be used in blood vessels of 6e7 mm. Mechanical thrombectomy with
power-based mechanical devices and stent thrombus-capturing platforms alone or in combination with thrombus-aspiration
catheters offer prompt recanalization, clot removal, and prevention of distal embolism [34].
Thrombolytic Therapy
Thrombolytic therapy is an expedient and effective treatment for AMI as it has the potential to resolve the clot completely
and consequently decrease the risk of thrombotic distal embolization as well as possibly obviating surgery. Even if only
partial thrombus dissolution is achieved, these pharmacologic agents serve as adjunct therapy to surgery by sparing at least
some portion of the ischemic bowel segments.
For effective treatment, initiation of therapy should be done within at least 8 h of the beginning of the acute abdominal
pain [35]. The patient should be admitted to the intensive care unit while thrombolytic therapy is administered, allowing for
continuous monitoring of vital signs, signs of active bleeding, and neurological changes [36]. Because the severity of the
intestinal ischemia relates to the function of compensating collaterals [37,38], the course of this treatment depends on the
duration of ischemia and extent of thrombosis. The primary complication requiring consideration is excessive bleeding.
Other complications include development of pseudo-aneurysm and contrast-induced nephropathy [39]. The usefulness and
efficacy of thrombolytic therapy notwithstanding, there are minor and major contraindications for this therapy.
Table 31.1 displays indications for endovascular interventions in the SMA.
TABLE 31.1 Indications for Endovascular Interventions for Superior Mesenteric Artery (SMA) Thrombosis
l Visceral ischemia with demonstration of SMA thrombus with or without underlying atherosclerotic plaque
l Angiographic evidence of flow-limiting thrombus with impending vessel closure
l Computed tomography scan demonstrating SMA thrombosis
l Ultrasound scanning and Doppler velocity demonstrating significant SMA flow disturbances
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Selective Thrombolytic Agents
Streptokinase
The is a protein produced by group B hemolytic streptococci and purified for clinical use. Its dose is a 250,000-U (2.5-mg)
intraarterial bolus or a low-dose continuous infusion with 5000e10,000 U/h. Its half-life is 12e18 min. This is more cost
effective and carries a low risk of allergic reaction (w3%). Sufficient dose must be given to overcome possible
neutralization with antibiotics to streptococcus. Streptokinase acts on bound and free plasminogen.
Urokinase
Urokinase is an enzyme cultured from human kidney cells. The typical dose is 200e250 U given as an intraarterial bolus.
This is followed by infusion with a dose of 60,000e120,000 U/h. Urokinase has a half-life of about 15e20 min and can act
on both bound and free plasminogen.
Tissue Plasminogen Activator
This is a recombinant human serine protease that binds to fibrin and is activated by cleavage of arginineeisoleucine. This
binding then activates plasminogen by cleaving at Arg560eVal561. The typical dose is 10e20 mg administered in a slow
intraarterial bolus. This is then followed by a subsequent dose of 0.5e 2.00 mg administered every hour. This thrombolytic
agent has a relatively short half-life of 2e6 min. It is fibrin selective and acts primarily on fibrin-bound plasminogen. It is
the most expensive treatment as of this writing.
The primary and secondary efficacies of thrombolytic treatment are reflected both angiographically and clinically.
Angiographic patency of the treated SMA indicates adequate reestablishment of blood flow to the corresponding intestine
segments. The clinical outcomes include decreased or disappearance of abdominal pain, maintenance of normal vital signs,
and normal blood work panel. Other indicators of clinical success include no signs of peritonitis, no requirement for any
type of surgical intervention, and early hospital discharge.
The following illustrative cases represent typical cases of diagnosis and management of acute total thrombotic
occlusion of the SMA.
CASE STUDIES
Case 1: A 55-year-old female presented with acute abdominal pain and hypotension. Clinical examination revealed
disproportionate abdominal pain in the physical exam. Increased white count with a left shift, increased lactic acid level,
and serum creatinine level were found. Abdominal noncontrast computed tomography (CT) scan demonstrated significant
vascular calcification at the origin of the SMA. This was followed by contrast CT, which demonstrated total occlusion of
the SMA. Successful recanalization of the occluded SMA was performed with combined therapeutic strategy: pharmacotherapy with heparin and tissue plasminogen activator (tPA) thrombolysis followed by primary stenting of the origin of
the SMA. The patient had a prolonged recovery without any complications (Figs. 31.1e31.4).
FIGURE 31.1 Axial contrast CT scan of an abdomen demonstrates complete occlusion of the origin and the proximal portion of the superior mesenteric
artery, as indicated by the red arrow.
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FIGURE 31.2 Sagittal image of CT angiogram demonstrates occlusion of the origin of the superior mesenteric artery by calcified plaque.
FIGURE 31.3 Aortogram in lateral view demonstrates occlusion of proximal portion of the superior mesenteric artery (SMA) with reconstitution of the
SMA as indicated by arrows.
Case 2: A 70-year-old female presented with acute abdominal pain. An aortic abdominal angiogram demonstrated acute
thrombotic occlusion of the distal SMA. Dedicated therapy included administration of tPA followed by balloon angioplasty, which restored adequate antegrade flow in the SMA. This revasc ularization strategy resulted in proper clinical
improvement (Figs. 31.5 and 31.6).
Altogether, the optimal treatment remains debatable. However, in an effort to discern the contemporary recommendations for treatment, Zhao and colleagues performed a systematic literature review of 28 articles with a total of 1110
patients with AMI treated between 2000 and 2013. They concluded that endovascular treatment may serve as a first-line
therapy for select patients when there is a low suspicion for intestinal necrosis. Open surgery should be reserved for
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FIGURE 31.4 Selective superior mesenteric artery (SMA) angiogram in lateral view showing successful recanalization and stenting of the occluded
portion of the SMA as indicated by the arrow.
FIGURE 31.5 Selective frontal angiogram of the superior mesenteric artery demonstrates distal acute occlusion by thrombus.
emergency conditions requiring exploratory laparotomy. The hybrid technique may be an especially effective approach for
treating AMI, with low morbidity and mortality, although further studies are required comparing it with open surgery and
endovascular technique [31].
ACUTE RENAL ARTERY THROMBOSIS
Acute renal artery thrombosis (ART) is a rare, yet critical and often misdiagnosed, condition. Renal artery thrombosis was
first described by Von Recklinghausen in 1861 [40]. The thrombosis can be caused by atherosclerosis of the renal artery,
cardiac embolism associated with myocardial infarction or atrial fibrillation, infective thrombotic endocarditis, thrombotic
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FIGURE 31.6 Selective angiogram of the superior mesenteric artery (SMA) demonstrated successful recanalization of the occluded SMA after tissue
plasminogen activator thrombolysis and adjunct balloon angioplasty.
atherosclerotic plaque of the aorta, hypercoagulopathy, and trauma. Importantly, in kidney transplant recipients, ART is a
devastating complication of renal transplantation that can result in graft loss if not detected early. Surgical and technical
errors are the major cause of renal artery thrombosis [41].
Thus, unfortunately, due to the significant challenges in establishing accurately an early diagnosis, renal thrombosis
often leads to serious sequelae of acute renal failure, uncontrolled hypertension, and renal infarction [42,43]. The
symptoms of disease are nonspecific, as about 97% of patients report abdominal or flank pain. Other symptoms include
nausea, vomiting, and fever, which can occur in 20% of the patients [44]. The patient can rapidly develop severe electrolyte
imbalance and exhibit symptoms and findings of congestive heart failure. Because of difficulties in making an early
diagnosis of acute renal thrombosis or thrombotic embolus, serious consequences such as acute renal failure, worsening
congestive heart failure, and hypertension may rapidly develop. The differential diagnosis is also nonspecific and includes
acute pyelonephritis, renal cell carcinoma, and renal colic [45,46]. Thrombosis involvement of both renal arteries accounts
for about 16% of cases, mostly in patients with coagulation disorders [47]. In about 40% of cases, patients present with
microscopic hematuria [48]. Notably, clinical awareness is required to detect in posterenal stenting patients the ominous
development of thrombosis, which can represent either early or late renal stent thrombosis.
Diagnosis
Initial diagnosis can be obtained by utilization of noninvasive methods such as duplex sonography of the renal artery;
however, it carries a very low sensitivity of about 11%. Nuclear medicine studies such as renal isotope scans can indicate
abnormalities 97% of the time [48]. Abdominal CT with intravenous contrast is considered a highly useful imaging
modality for detection of ART, providing the baseline renal function is normal. Angiogram with CO
diagnostic modality, especially when the baseline renal function is severely impaired or in cases of known contrast allergy.
Altogether, in the clinical setting of renal artery thrombosis, with the presence of abdominal pain, unstable hemodynamic
condition, and abnormal blood chemistry, early accurate diagnosis is essential to preserve kidney function, which is the
primary objective of all effective treatment strategies.
Treatment
Once the diagnosis is established, initial administration of intravenous heparin bolus followed by drip is recommended.
The percutaneous endovascular approach is an important treatment strategy [49,50]. Table 31.2 displays the indications for
renal artery endovascular interventions. Direct catheter-based thrombolytic treatment offers selective engagement into the
thrombosed vessel, followed by administration of intrarenal thrombolytic agent. This strategy can incorporate balloon
angioplasty, mechanical thrombectomy, and stent deployment as deemed necessary. Rapid restoration of adequate antegrade renal artery flow should lead to successful clinical outcome.
is another valid
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TABLE 31.2 Indications for Endovascular Interventions for Renal Artery Thrombosis
l Renal artery thrombosis with or without underlying atherosclerotic plaque
l Renal artery thrombosis causing:
l hemodynamic instability or compromise with uncontrolled and/or malignant hypertension
l impaired and/or deteriorating renal function
l congestive heart failure and pulmonary edema
l Angiographic demonstration of flow-limiting thrombus with impending acute or subacute total vessel closure
l Computed tomography scan demonstrating thrombosis in a single or bilateral renal arteries
l Ultrasound scanning and Doppler velocity study demonstrating significant flow disturbances
The representative Case 3 herein describes renal artery thrombosis. A 50-year-old female presented with severe hypertension and acute renal failure. Abdominal CT images followed by abdominal aortogram demonstrated complete
thrombotic occlusion of the left renal artery 1 cm from its origin. Selective renal arteriography demonstrated the pathophysiologic etiology that accounted for the occlusion: spontaneous dissection of an atherosclerotic plaque and resultant
severe thrombosis. The tailored treatment included successful thrombus dissolution and recanalization with administration
of heparin and tPA followed by primary stenting. Adequate patency of the target vessel and successful restoration of
antegrade flow were achieved (Figs. 31.7e31.10).
FIGURE 31.7 Coronal CT angiogram image showing an occluded left renal artery as indicated by the arrow.
FIGURE 31.8 Aortagram lateral view showing occlusion of the proximal left renal artery as indicated by the arrow.
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FIGURE 31.9 Selective left renal artery angiogram showing dissection of the left renal artery as indicated and acute thrombus occluding the posterior
division of the left renal artery (circle).
FIGURE 31.10 Angiogram after stenting of the left renal artery demonstrates marked patency of the stent and adequate flow restoration. The final stage
of this angiogram [not shown] demonstrated excellent patency of the renal artery.
SUMMARY
The SMA and the renal arteries are major aortic branches, both perfusing vital organs. Thrombosis of these vessels
constitutes a major deleterious clinical development, which calls for timely diagnosis.
Acute occlusive mesenteric ischemia is subdivided per pathophysiologic characteristics into acute mesenteric arterial
embolism and acute mesenteric arterial thrombosis. Acute mesenteric arterial thrombosis is commonly encountered in
clinical practice. AMI resulting from mesenteric arterial thrombosis is a life-threatening cardiovascular complication with
symptoms ranging from sudden-onset abdominal pain to vague symptoms of several days’ duration. This condition is
associated with mortality rates as high as 70%e90%, despite standard therapies of anticoagulation and surgical exploration. ART, while a rare clinical occurrence, is caused by the same pathophysiologic mechanisms. Delayed or erroneous
diagnosis can lead to severe u ncontrolled hypertension, electrolyte abnormalities, congestive heart failure, and kidney loss.
Expeditiously applied specific thrombus-targeting strategies in the form of thrombolytic pharmacotherapy, catheter-based
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