Acute Arterial Occlusion of a Limb
Essentials of Diagnosis
- Sudden pain in an extremity.
- Generally associated with some element of neurologic
dysfunction with numbness, weakness, or complete paralysis.
- Absent extremity pulses.
General Considerations
Acute occlusion may be due to an embolus or to thrombosis
of a diseased atherosclerotic segment. Arterial to arterial emboli such as in
the cerebrovascular tree can occur, but emboli large enough to occlude proximal
arteries in the lower extremities are almost always from the heart and tend to
lodge at the bifurcation of major arteries. Over 50% of the emboli from cardiac
sources go to the lower extremities, 20% to the cerebrovascular circulation, and
the remainder to the upper extremities and mesenteric and renal circulation.
Atrial fibrillation is the usual cause of the thrombus; other causes are
valvular disease or ischemic heart disease where thrombus has formed on the
ventricular surface of a transmural myocardial infarct.
Emboli from arterial sources such as arterial ulcerations
or calcified excrescences are usually small and go to the distal arterial tree
(toes).
The typical patient with primary thrombosis has had
a history of claudication and now has an acute occlusion. If the stenosis has
developed over time, collateral blood vessels will develop, and the resulting
occlusion may only reduce walking distance or cause minimal increase in
symptoms.
Clinical Findings
Symptoms and Signs
The most common symptom is sudden onset of extremity pain,
often accompanied by neurologic dysfunction, which can be numbness or paralysis
in extreme cases. With popliteal occlusion, symptoms may only affect the foot.
With proximal occlusions, the whole leg may be affected. Signs include absence
of pulses in the arteries distal to the occlusion and signs of severe arterial
ischemia, such as pallor on elevation, coolness of the extremity, mottling, and
impaired neurologic function with hyperesthesia progressing to anesthesia
accompanied with paralysis.
Laboratory Findings
These include little or no flow with Doppler examination of
the distal vessels. Imaging, if done, shows an abrupt cutoff of the vessel
involved. Blood work may indicate systemic acidosis.
Imaging
Whenever possible, imaging should be done in the operating
room because a delay in obtaining angiography, MRA, or CTA may jeopardize the
viability of the tissue at risk (see arteriogram). However, in cases with only
modest symptoms and light touch of the extremity is maintained, imaging may be
helpful in expediting the revascularization procedure by identifying the exact
areas of occlusion and delineating distal vessel patency.
Treatment
Immediate revascularization is the treatment of choice in
all cases of symptomatic acute arterial thrombosis. Evidence of neurologic
injury, including loss of light touch sensation, indicates that collateral flow
is inadequate to maintain limb viability and revascularization should be
accomplished within 3 hours. Longer delays carry a significant risk of
irreversible tissue damage. This risk approaches 100% at 6 hours.
Heparin
As soon as the diagnosis is made, heparin should be
administered (5000–10,000 units) intravenously. This helps prevent propagation
of the clot. Heparin may also help relieve associated spasm of the vessels.
There may be some reduction in symptoms with aggressive anticoagulation, but
revascularization will still be required. Patients in atrial fibrillation need
to continue taking anticoagulants until cardioversion can be attempted.
Surgical Intervention
General anesthesia is usually indicated in these patients;
local anesthesia may be used in extremely high-risk patients if the exploration
is to be limited to the common femoral artery. In extreme cases, it may be
necessary to perform embolectomy from the femoral popliteal and even the pedal
vessels to revascularize the limb. Intraoperative thrombolysis with tissue
plasminogen activator (TPA) may be used to lyse a clot in the distal arterial
tree.
Endovascular Techniques
Chemical thrombolysis with TPA may be done but often
requires 24 hours or longer to fully lyse the thrombus. This approach can be
taken only in patients with an intact neurologic exam. An echocardiogram should
be done to identify additional clot in the atrium. If an additional clot is
found, it is a relative contraindication to thrombolysis because of the risk of
subsequent emboli from the lysed cardiac clot. Catheter-based mechanical
thrombolysis may be an excellent alternative.
Complications
Complications of revascularization of an acutely ischemic
limb can include severe acidosis and myocardial arrest. In cases where several
hours have elapsed but recovery of viable tissue may still possible, significant
levels of lactic acid, potassium, and other harmful agents may be released into
the circulation during revascularization. Pretreatment of the patient with
sodium bicarbonate prior to reestablishing arterial flow is required. Surgery in
the presence of thrombolytic agents and heparin carries a high risk of
postoperative wound hematoma.
Prognosis
There is a 10–25% risk of amputation with acute arterial
occlusion, and a 25% or higher in-hospital mortality rate. Prognosis for acute
occlusion of an atherosclerotic segment is generally much better because the
collateral flow can maintain extremity viability. The longer term survival
reflects the overall condition of the patient. In high-risk patients, an acute
arterial occlusion suggests a dismal prognosis.
Occlusive Cerebrovascular Disease
Essentials of Diagnosis
- Sudden onset of a neurologic deficit consistent with
unilateral cortical ischemia; weakness and numbness of an extremity, aphasia,
dysarthria, or unilateral blindness (amaurosis fugax).
- Bruit heard loudest in the mid neck.
General Considerations
Unlike the other vascular territories, symptoms of
occlusive cerebrovascular disease are predominantly due to emboli. Transient
ischemic attacks (TIAs) are the result of small emboli and are the earliest
manifestation of carotid stenosis (see illustration). These transient symptoms
are thought to demonstrate plaque instability, and the risk of additional emboli
causing permanent deficits are high. Twenty-five percent or more of all strokes
may be due to emboli. In the absence of atrial fibrillation, approximately 90%
of these emboli originate from the proximal internal carotid artery. Lesions in
the carotid siphon, the common carotid, and the proximal great vessels are far
less common.
Clinical Findings
Symptoms and Signs
Generally, the ischemic symptoms of TIAs last only a few
minutes but may continue up to 24 hours. Emboli to the retinal artery cause
unilateral blindness which, when transient, is termed "amaurosis fugax."
Posterior circulation symptoms referable to the brainstem, cerebellum, and
visual regions of the brain are due to atherosclerosis of the vertebral basilar
systems and are much less common.
Signs of cerebrovascular disease include bruits in the
mid-cervical area with reduced or absent arm pulses. While bruits in the neck in
older patients and generalized atherosclerosis are important signs of
cerebrovascular disease, they are not specific for narrowing within the vessel.
There is poor correlation between the degree of stenosis and the presence of the
bruit. Furthermore, absence of a bruit does not exclude the possibility of
carotid stenosis. Nonfocal symptoms, such as dizziness and unsteadiness, seldom
are related to cerebrovascular atherosclerosis.
Imaging
Duplex ultrasonography is the imaging modality of choice
with a high specificity and sensitivity for detecting and grading the degree of
stenosis at the carotid bifurcation (see ultrasound); (see ultrasound).
Excellent depiction of the full anatomy of the cerebrovascular circulation from
arch to cranium can be obtained with either MRA or CTA. Each of these modalities
may have false-positive or false-negative findings. Since the decision to
intervene in cases of carotid stenosis depends on an accurate assessment of the
degree of stenosis, it is recommended that at least two modalities be used to
confirm the degree of stenosis. Cerebral angiography is reserved for cases that
cannot be resolved by these less invasive imaging modalities.
Treatment
Asymptomatic Patients
Patients with no neurologic symptoms but with carotid
stenosis on imaging will benefit from carotid intervention if they are
considered to be at low risk for intervention and their expected survival is
greater than 5 years. Recommendation for intervention also presumes that the
treating institution has a stroke rate in asymptomatic patients that is
acceptable (< 3%). Large studies indicate a reduction in stroke from 11.5% to
5.0% over 5 years with surgical treatment of asymptomatic carotid stenoses of
greater than 60%. However, the usual practice is to only treat those patients
who have greater than 80% stenosis.
Symptomatic Patients
Patients with TIAs or strokes from which they have
completely or nearly completely recovered will benefit from carotid intervention
if the carotid stenosis, ipsilateral to the event, has a stenosis of  70%, and they are
likely to derive benefit with a stenosis of 50–69%. In these situations, carotid
endarterectomy has been shown to have a durable effect in preventing further
events.
Complications
The primary complication of carotid intervention is stroke
due to embolization of plaque material during the procedure. The American Heart
Association has recommended upper limits of acceptable combined morbidity and
mortality for these interventions: 3% for asymptomatic, 5% for those with TIAs,
and 7% for patients with previous stroke. Results that do not match these
guidelines will jeopardize the therapeutic benefit of carotid intervention.
Carotid Endarterectomy
In addition to stroke risk, carotid endarterectomy carries
a 10% risk of transient cranial nerve injury (usually the vagus or hypoglossal
nerve) and 1–2% risk of permanent deficits. There is also the risk of
postoperative neck hematoma, which can cause acute compromise of the airway.
Coronary artery disease exists as a comorbidity in most of these patients.
Myocardial infarction rates after carotid endarterectomy are approximately
5%.
Angioplasty and Stenting
Carotid angioplasty and stenting has been advocated as an
alternative to carotid endarterectomy. Angioplasty and stenting offers the
advantage of avoidance of both cranial nerve injury and neck hematoma. However,
emboli are more common during angioplasty in spite of the use of embolic
protection devices during the procedure. The Carotid Revascularization
Endarterectomy versus Stent Trial (CREST), sponsored by the National Institutes
of Health, randomized patients to undergo carotid endarterectomy or angioplasty;
this study should determine the role of stenting in carotid disease.
Recurrent Carotid Stenosis
Scarring of the arterial wall at the site of the
intervention after both angioplasty and endarterectomy may create recurrent
stenosis. These lesions tend to be less embologenic, and treatment need not be
as aggressive as for primary disease. The cranial nerve risk for these patients
may be higher with repeat endarterectomy than with angioplasty of the narrowed
segment.
Prognosis
Prognosis for patients with carotid stenosis who have had a
TIA or small stroke is poor without treatment; 25% of these patients will have a
stroke with most of the events occurring in the first year of follow-up.
Patients with carotid stenosis without symptoms have an annual stroke rate of
just over 2%. Risk factor modification with antiplatelet agents is not nearly as
effective in preventing stroke as removing the stenosis. Symptomatic patients
most likely have unstable plaques with ulceration or they have had a recent
progression of the stenosis. This suggests that prospective ultrasound screening
would be valuable in timing intervention in asymptomatic patients. Approximately
10% of asymptomatic patients have evidence of plaque progression in a given
year. Concomitant coronary artery disease is common and is an important factor
in these patients both for perioperative risk and long-term prognosis.
Aggressive risk factor modification should be prescribed for patients with
cerebrovascular disease regardless of planned intervention.
Visceral Artery Insufficiency (Intestinal Angina)
Essentials of Diagnosis
- Severe postprandial abdominal pain.
- Weight loss with a "fear of eating."
General Considerations
Acute visceral artery insufficiency results from
either embolic occlusion or primary thrombosis of at least one major mesenteric
vessel. Ischemia can also result from nonocclusive mesenteric vascular
insufficiency, which is generally seen in patients with low flow states, such as
congestive heart failure, or who are in shock. A chronic syndrome occurs
when there is adequate perfusion for the viscera at rest but ischemia occurs
with severe abdominal pain when flow demands increase with feeding. Because of
the rich collateral network in the mesentery, generally at least two of the
three major visceral vessels (celiac, superior mesenteric, inferior mesenteric
arteries) are affected before symptoms develop. Ischemic colitis, a
variant of mesenteric ischemia, usually occurs in the distribution of the
inferior mesenteric artery. The intestinal mucosa is the most sensitive to low
perfusion and will slough if underperfused. The clinical presentation is similar
to inflammatory bowel disease. Ischemic colitis can occur postoperatively,
particularly after aortic aneurysm resection or aorto-femoral bypass for
occlusive disease, when there is sudden reduction in blood flow to the inferior
mesenteric artery.
Clinical Findings
Symptoms and Signs
Acute Intestinal Ischemia
Patients with primary thrombosis often give an antecedent
history consistent with chronic intestinal ischemia. The key finding with acute
mesenteric ischemia is severe, steady epigastric and periumbilical pain with
minimal or no findings on physical examination of the abdomen. A high white cell
count, lactic acidosis, hypotension, and abdominal distention may aid in the
diagnosis.
Chronic Intestinal Ischemia
Patients are generally over 45 years of age and may have
evidence of atherosclerosis in other vascular beds. Symptoms consist of
epigastric or periumbilical postprandial pain lasting 1–3 hours. To avoid the
pain, patients limit food intake and may develop a fear of eating. Weight loss
is universal.
Ischemic Colitis
Characteristic symptoms are left lower quadrant pain and
tenderness, abdominal cramping, and mild diarrhea, which is often bloody.
Imaging and Colonoscopy
In patients with acute or chronic mesenteric
ischemia, a CTA or MRA can demonstrate narrowing of the proximal visceral
vessels. In acute mesenteric ischemia from a nonocclusive low flow state,
angiography is needed to display the typical "pruned tree" appearance of the
distal visceral vascular bed (see arteriogram). Ultrasound scanning of the
mesenteric vessels may show proximal obstructing lesions in laboratories that
have experience with this technique.
In patients with ischemic colitis, colonoscopy may
reveal segmental inflammatory changes, most often in the rectal sigmoid and
splenic flexure where collateral circulation may be poor.
Treatment
A high suspicion of acute mesenteric ischemia dictates
immediate exploration to determine bowel viability. If the bowel remains viable,
bypass can be done from the aorta to the celiac and the superior mesentery
artery. In cases where bowel viability is questionable or bowel resection will
be required, the bypass can be done with autologous vein, or with PTFE. Recent
reports suggest a surprisingly low incidence of graft infection in these cases.
The mainstay of treatment of ischemic colitis is maintenance of hydration until
collateral circulation becomes well established.
For the treatment of nonocclusive mesenteric disease,
vasodilators can be delivered through a catheter in the mesenteric arteries.
In chronic visceral ischemia, angioplasty and stenting of
the proximal vessel may be beneficial depending on the anatomy of the stenosis.
Should an endovascular solution not be available, an aorto-visceral artery
bypass is the preferred management. The long-term results are highly durable.
Visceral artery endarterectomy is reserved for cases with multiple lesions where
bypass would be difficult.
Prognosis
The combined morbidity and mortality rates are 10–15% from
surgical intervention in these debilitated patients. However, without
intervention both acute and chronic visceral ischemia are uniformly fatal.
Adequate collateral circulation usually develops in those who have ischemic
colitis; the prognosis for this entity is better than chronic mesenteric
insufficiency.
| Acosta S et al. Clinical implications for the
management of acute thromboembolic occlusion of the superior mesenteric artery:
autopsy findings in 213 patients. Ann Surg. 2005 Mar;241(3): 516–22. [PMID:
15729076] |
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Acute Mesenteric Vein Occlusion
The hallmarks of acute mesenteric vein occlusion are
postprandial pain and evidence of a hypercoagulable state. Acute mesenteric vein
occlusion presents similarly to the arterial occlusive syndromes but is much
less common. Patients at risk include those with a systemic hypercoagulable
state, such as that observed with paroxysmal nocturnal hemoglobinuria or protein
C, protein S, or antithrombin deficiencies. These lesions are difficult to treat
surgically, and thrombolysis is the mainstay of therapy. Long-term
anticoagulation is required for these patients.
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Thromboangiitis Obliterans (Buerger's Disease)
Essentials of Diagnosis
- Typically occurs in young male cigarette smokers.
- Distal extremities involved with severe circulatory
insufficiency.
- Thrombosis of the superficial veins may occur.
- Amputation will be necessary unless the patient stops
smoking.
General Considerations
Buerger's disease is a segmental, inflammatory, and
thrombotic process of the distal most arteries and occasionally veins of the
extremities. Pathologic examination reveals arteritis in the affected vessels.
The cause is not known but it is rarely seen in nonsmokers. Arteries most
commonly affected are the plantar and digital vessels of the foot and lower leg.
In advanced stages, the fingers and hands may become involved. Fortunately, the
incidence of Buerger's disease seems to have decreased in the past decade.
Clinical Findings
Symptoms and Signs
Buerger's disease may be initially difficult to
differentiate from routine peripheral vascular disease, but in most cases, the
lesions are on the toes and the patient is younger than 40 years old. The
observation of superficial thrombophlebitis may aid the diagnosis. Because the
distal vessels are usually affected, intermittent claudication is not common
with Buerger's disease, but rest pain, particularly pain in the distal most
extremity (ie, toes), is frequent. This pain often progresses to tissue loss and
amputation, unless the patient stops smoking. The progression of the disease
seems to be intermittent with acute and dramatic episodes followed by some
periods of remission.
Imaging
MRA or invasive angiography can demonstrate the
obliteration of the distal arterial tree typical of Buerger's disease.
Differential Diagnosis
In peripheral vascular disease, the onset of tissue
ischemia tends to be less traumatic than in Buerger's disease, and symptoms of
proximal arterial involvement, such as claudication, predominate.
Symptoms of Raynaud's disease may be difficult to
differentiate from Buerger's disease. Repetitive atheroemboli may also mimic
Buerger's disease and may be difficult to differentiate. It may be necessary to
image the proximal arterial tree to rule out sources of arterial emboli.
Treatment
Smoking cessation is the mainstay of therapy and will halt
the disease in most cases. As the distal arterial tree is occluded,
revascularization is not possible. Sympathectomy is rarely effective.
Prognosis
If smoking cessation can be achieved, the outlook for
Buerger's disease may be better than in patients with premature peripheral
vascular disease. If smoking cessation is not achieved, then the prognosis is
generally poor, with amputation of both lower and upper extremities the eventual
outcome.
| Olin JW. Thromboangiitis obliterans (Buerger's
disease). N Engl J Med. 2000 Sep 21;343(12):864–9. [PMID: 10995867] |
Abdominal Aortic Aneurysms
Essentials of Diagnosis
- Most aortic aneurysms are asymptomatic until rupture.
- Abdominal aortic aneurysms measuring 5 cm are palpable in
80% of patients.
- Back or abdominal pain with aneurysmal tenderness may
precede rupture.
- Rupture is catastrophic; hypotension; excruciating
abdominal pain that radiates the back.
General Considerations
Dilatation of the infrarenal aorta is a normal part of
aging. The aorta of a healthy young man measures approximately 2 cm. An aneurysm
is considered present when the aortic diameter exceeds 3 cm, but aneurysms
rarely cause any problems until their diameter exceeds 5 cm. Abdominal aortic
aneurysms are found in 2% of men over 55 years of age; the male to female ratio
is 8:1. Ninety percent of abdominal atherosclerotic aneurysms originate below
the renal arteries. The aneurysms usually involve the aortic bifurcation and
often involve the common iliac arteries.
Inflammatory aneurysms happen when an inflammatory peel,
similar to the inflammation that occurs with retroperitoneal fibrosis, surrounds
the aneurysm and encases the retroperitoneal structures, which include the
duodenum and, occasionally, the ureters (see photograph).
Clinical Findings
Symptoms and Signs
Asymptomatic
Although 80% of 5-cm infrarenal aneurysms are palpable on
routine physical examination, most aneurysms are discovered as incidental
findings on ultrasound or CT imaging during the evaluation of unrelated
abdominal symptoms.
Symptomatic
Pain
Aneurysmal expansion may be accompanied by pain that is
mild to severe midabdominal discomfort often radiating to the lower back. The
pain may be constant or intermittent and is exacerbated by even gentle pressure
on the aneurysm sack. The pain may also accompany inflammatory aneurysms.
Rupture
The sudden escape of blood into the retroperitoneal space
causes severe pain, a palpable abdominal mass, and hypotension. Free rupture
into the peritoneal cavity is a lethal event. Most aneurysms have a thick lining
of blood clot, which can break away, float with the blood to a small peripheral
artery where it occludes blood flow (embolism). Although this phenomenon is
rare, multiple localized areas of poor peripheral blood flow (blue toe
syndrome), should prompt a search for an aneurysm.
Laboratory Findings
Even with a contained rupture, there may be little change
in routine laboratory findings. The hematocrit will be normal, since there has
been no opportunity for hemodilution.
Aneurysms are associated with the cardiopulmonary diseases
of elderly male smokers, which include coronary artery disease, carotid disease,
renal impairment, and emphysema. Preoperative testing may indicate the presence
of these comorbid conditions.
Imaging
Abdominal ultrasonography is the diagnostic study of choice
for initial diagnosis (see ultrasound). In approximately three-quarters of
patients with aneurysms, curvilinear calcifications outlining portions of the
aneurysm wall may be visible on plain films of the abdomen or back. CT scans
provide a more reliable assessment of aneurysm diameter and should be done when
the aneurysm nears the diameter threshold for treatment. Contrast-enhanced CT
scans show the arteries above and below the aneurysm (see CT Scan). The
visualization of this vasculature is essential for planning repair.
Screening
There are now data to support using abdominal ultrasound to
screen 65- to 74-year-old men, but not women, who have a history of smoking.
Repeated screening does not appear to be needed.
Treatment
Aneurysmal Rupture
If the rupture and bleeding are confined to the
retroperitoneum, the combination of low blood pressure and retroperitoneal
containment may arrest the blood loss long enough for the patient to undergo
urgent operation. Endovascular repair represents the best opportunity for
survival because the retroperitoneal blood clot is left intact. Patients who
have free rupture of the aneurysm into the peritoneum do not survive long enough
to undergo surgical repair.
Elective Repair
In general, elective repair is indicated for aortic
aneurysms > 5.5 cm in diameter or aneurysms that have undergone rapid
expansion (> 5 mm in 6 months). Symptoms such as pain or tenderness may
indicate impending rupture. These patients need to undergo aneurysm repair
regardless of the aneurysm's diameter. Improving outcomes with endovascular
techniques have caused some experts to recommend treatment of smaller aneurysms.
Current studies are ongoing to determine whether this may be appropriate.
Inflammatory Aneurysm
The presence of peri-aortic inflammation (inflammatory
aneurysm) is not an indication for surgical treatment, unless there is
associated compression of retroperitoneal structures, such as the ureter.
Interestingly, the inflammation that encases an inflammatory aneurysm recedes
after either endovascular or surgical aneurysmal repair.
Assessment of Operative Risk
Aneurysms appear to be a variant presentation of systemic
atherosclerosis. Some assessment of coronary risk for aneurysm intervention is
essential prior to planning procedures. A 2004 trial demonstrated minimal value
in addressing stable coronary artery disease prior to aneurysm resection.
However, in patients with significant symptoms of coronary disease, the coronary
disease should be treated first. Aneurysm resection should follow shortly
thereafter because there is a significant increase risk in aneurysm rupture
after the coronary procedures. In patients with concomitant carotid stenosis,
there is no benefit in repairing asymptomatic carotid disease prior to aneurysm
resection.
Open Surgical Resection versus Endovascular Repair
In open surgical aneurysm repair, a graft is sutured to the
non-dilated aorta above and below the aneurysm. This involves an abdominal
incision, extensive dissection, and interruption of aortic blood flow. The
mortality rate is low in centers that have a high volume for this procedure and
it is performed in good risk patients. Older, sicker patients may not tolerate
the cardiopulmonary stresses of the operation. With endovascular repair, a
stent-graft is used to line the aorta and exclude the aneurysm. The anatomic
requirements to securely achieve aneurysm exclusion vary according to the
performance characteristics of the specific stent-graft device. In general,
successful attachment requires a segment of non-dilated aorta (neck) between the
renal arteries and the aneurysm to be at least 15 mm in length, and device
insertion requires iliac arteries to be at least 7 mm in diameter.
Complications
Myocardial infarction, the most common complication, occurs
in up to 10% of patients who undergo open aneurismal repair. The incidence of
myocardial infarction is substantially lower with endovascular repair. For
routine infrarenal aneurysms, renal injury is unusual; however, when it does
occur, it is a significant complicating factor in the postoperative period.
Respiratory complications are similar to those seen in most major abdominal
surgery. Gastrointestinal hemorrhage, even years after aortic surgeries, may
suggest the possibility of graft enteric fistula; the incidence of this
complication is higher when the initial surgery is performed on an emergency
basis.
Prognosis
The mortality rate for an open elective surgical resection
is 1–5%. Of those who survive surgery, approximately 60% are alive at 5 years;
myocardial infarction is the leading cause of death. The decision to repair
aneurysms in high-risk patients has been made easier with the reduced
perioperative morbidity and mortality of the endovascular approach. In the
long-term, difference between open and endovascular repair in perioperative
mortality are relatively small compared with the mortality rates associated with
the usual comorbid conditions.
Mortality rates of untreated aneurysms vary with aneurysm
diameter. The mortality rate among patients with large aneurysms who have not
undergone surgery, has been defined as follows: 12% annual risk of rupture with
an aneurysm 6
cm in diameter and a 25% annual risk of rupture in aneurysms of 7 cm diameter. In general, a
patient with an aortic aneurysm has a threefold greater chance of dying of a
consequence of rupture of the aneurysm than of dying of the surgical
resection.
At present, endovascular aneurysm repair may be less
definitive than open surgical repair. The subsequent behavior of the
endovascularly repaired aneurysm depends on how successfully it has been
excluded from the circulation, as demonstrated by the absence of
contrast-enhanced blood on CT within the space between the stent-graft and the
aneurysm wall. Complete exclusion lowers the pressure in the aneurysm sac, which
causes the aneurysm to shrink. On the other hand, direct leakage of
contrast-enhanced blood into the aneurysm (endoleak, types 1 and 3) is
associated with high aneurysm sac pressure, a low rate of aneurysm shrinkage,
and a persistent risk of rupture. Indirect leakage of blood through persistent
lumbar and inferior mesenteric branches of the aneurysm (endoleak, type 2)
produces an intermediate picture with somewhat reduced pressure, slow shrinkage
and low rupture risk. However, type 2 endoleak warrants close observation
because aneurysm dilatation and rupture can occur.
Recources: Current Medical Diagnosis &
Treatment 2008
Stephen J.
McPhee, Maxine A. Papadakis, and Lawrence M. Tierney, Jr., Eds.
Ralph
Gonzales, Roni Zeiger, Online Eds.
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