Management of Symptomatic (Non-Ruptured) and Ruptured Abdominal Aortic Aneurysm

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Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm
Authors: Jeffrey Jim, MD, Robert W Thompson, MD

Section Editors: Joseph L Mills, Sr, MD, John F Eidt, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2017. | This topic last updated: Mar 08, 2017.
INTRODUCTION — Symptomatic abdominal aortic aneurysm (AAA) refers to any of a number of symptoms (eg,
abdominal pain, limb ischemia) that can be attributed to the aneurysm. The presence of symptoms increases the
risk for AAA rupture, and thus, for most patients with symptomatic AAA, repair should be performed. AAA rupture
can also occur in the absence of intervening symptoms. In the United States, rupture of an abdominal aortic
aneurysm occurs in approximately 15,000 patients per year [1]. Without repair, ruptured AAA is nearly always fatal.
In spite of significant advances in intensive care unit management and surgical techniques, mortality following repair
of ruptured AAA remains high [2]. Surgical outcomes may be improved using endovascular aneurysm repair
(EVAR), but aortic endografting under emergency circumstances presents many challenges. Increasing numbers of
institutions have initiated protocols for endovascular repair of ruptured AAA with promising results in small series,
but not all institutions are equipped to treat ruptured AAAs using minimally-invasive technology.
The management of symptomatic, non-ruptured and ruptured AAA will be reviewed. The diagnosis and
management of asymptomatic AAA and general technical issues of open surgical and endovascular aneurysm
repair are discussed elsewhere. (See "Clinical features and diagnosis of abdominal aortic aneurysm" and "Open
surgical repair of abdominal aortic aneurysm" and "Endovascular repair of abdominal aortic aneurysm" and
"Management of asymptomatic abdominal aortic aneurysm", section on 'Introduction'.)
ANEURYSM TERMINOLOGY — An abdominal aorta with a maximal diameter >3.0 cm is aneurysmal in most adult
patients. Abdominal aortic aneurysm (AAA) most often affects the segment of aorta below the renal arteries (figure
1); approximately 5 percent involve the renal or visceral arteries (figure 2). Most AAAs produce no symptoms. (See
"Overview of abdominal aortic aneurysm", section on 'Definitions and aortoiliac anatomy'.)
● Ruptured AAA – Aortic rupture is due to the weakening of the aortic wall leading to tearing of the aortic wall,
allowing blood to escape outside the confines of the aorta. (See "Clinical features and diagnosis of abdominal
aortic aneurysm", section on 'Ruptured AAA'.)
● Symptomatic (non-ruptured) AAA – Symptomatic AAA refers to any of a number of symptoms (eg,
abdominal/back/flank pain, limb ischemia) that can be attributed to the aneurysm. The presence of symptoms
increases the risk for rupture [3]. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section
on 'Symptomatic (nonruptured) AAA'.)
INITIAL MANAGEMENT — The initial management of the patient with symptomatic (non-ruptured) or ruptured AAA
is guided by the hemodynamic status. Hemodynamically unstable patients who are candidates for repair are
generally transferred directly from the emergency department to the operating room. Most patients with
symptomatic (non-ruptured) AAA are hemodynamically stable but will require admission to determine whether the
AAA is the source of the symptoms. Until the AAA can be excluded as a source of symptoms, the patient should be
observed in a monitored setting. For patients determined to have a symptomatic AAA, but for whom repair will be
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delayed to optimize associated medical conditions, we admit the patient to an intensive care unit setting. (See
'Emergent versus delayed repair of symptomatic aneurysm' below.)
Two large bore peripheral intravenous catheters should be placed in all patients (symptomatic non-ruptured or
ruptured AAA) for medication and fluid administration. In hemodynamically unstable patients with ruptured AAA,
indirect evidence from the trauma population and one observational study in patients with AAA suggest that
allowing a relatively low systolic blood pressure of 80 to 100 mmHg (permissive hypotension) may prevent further
tearing of the aorta and limit blood loss [4-6]. (See "Treatment of severe hypovolemia or hypovolemic shock in
adults".)
Pain control is an important part of management. It is important to keep the patient comfortable, but consciousness
should be maintained. In patients who remain severely hypertensive despite adequate pain control, short-acting
intravenous beta-blockers (eg, esmolol) can be used to titrate the blood pressure to normal values. (See "Pain
control in the critically ill adult patient".)
Laboratory studies including complete blood count, electrolytes, blood urea nitrogen, creatinine, liver function tests,
prothrombin time, partial thromboplastin time, and a type and cross-match should be obtained. If AAA repair will be
undertaken at the hospital to which the patient presented, packed red blood cells should be placed on hold for
possible transfusion in the operating room. In patients with ruptured AAA, the patient should have at least 10 units
of packed red blood cells available for transfusion, and the blood bank should be alerted to the potential need for
Fresh Frozen Plasma (FFP) or similar products (eg, PF24), or massive transfusion. Similar to trauma patients with
severe ongoing hemorrhage, patients with ruptured AAA requiring massive transfusion may require transfusion of
unmatched blood, and may benefit from packed red blood cell: FFP ratios ≤2:1 rather than higher ratios. (See
"Initial evaluation and management of shock in adult trauma" and "Massive blood transfusion", section on 'Trauma'
and "Clinical use of plasma components".)
APPROACH TO AAA ASSOCIATED WITH SYMPTOMS — Symptoms associated with AAA may or may not be
due to AAA rupture. A presumptive diagnosis of ruptured AAA, which is a surgical emergency, can be made in
patients known to have AAA or those with a newly diagnosed AAA who have hypotension and abdominal, flank, or
back pain. Although most patients with symptomatic (non-ruptured) AAA will require AAA repair, the timing of and
approach to repair differs depending upon the presenting symptoms which may be due to instability of the
aneurysm (impending rupture, thromboembolism), rapid expansion of the aneurysm causing abdominal discomfort,
or related to inflammatory or infected AAA causing systemic manifestations. The clinical and diagnostic features
that distinguish these are discussed in detail elsewhere. (See "Clinical features and diagnosis of abdominal aortic
aneurysm", section on 'Clinical features' and "Clinical features and diagnosis of abdominal aortic aneurysm", section
on 'Diagnosis'.)
Ruptured AAA — Although there are rare reports of patient survival following a contained rupture of abdominal
aortic aneurysm (AAA), in general, without repair, ruptured AAA is uniformly fatal, with death occurring usually
within hours and certainly within a week of rupture [7]. Thus, when ruptured AAA is identified, repair should be
undertaken emergently to give the patient the best chance for survival [3,8]. (See 'Initial management' above.)
Although AAA repair should be offered to most patients with ruptured AAA, some patients may be at such high risk
due to underlying comorbidities that comfort care is appropriate (See 'Decision for comfort care' below.)
Hemodynamically unstable patients with known AAA who present with classic symptoms/signs of rupture
(hypotension, flank/back pain, pulsatile mass) should be taken emergently to the operating room for immediate
control of hemorrhage and repair of the aneurysm. Efforts to obtain proximal aortic control in the operating room
should not be delayed waiting for type-specific blood components. For patients not previously known to have AAA,
time may permit a focused ultrasound exam to confirm that an aneurysm is present prior to abdominal exploration,
but this is not absolutely required (algorithm 1).
For hemodynamically stable patients suspected of having a ruptured AAA, computed tomography (CT) of the
abdomen confirms the rupture but is also important for evaluating whether an endovascular repair is feasible [9].
(See "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Imaging symptomatic patients' and
'Aneurysm repair' below.)
Impending rupture — Some patients without overt rupture on imaging studies have clinical symptoms or other
features on CT scan that may indicate that the aneurysm is rapidly changing in configuration (rapid expansion), or
at risk for "impending" rupture. Good risk surgical candidates should generally be repaired in an urgent manner.
Clinical features are discussed in detail elsewhere. (See "Clinical features and diagnosis of abdominal aortic
aneurysm", section on 'Clinical features' and "Clinical features and diagnosis of abdominal aortic aneurysm", section
on 'Ruptured versus nonruptured AAA'.)
Symptomatic (non-ruptured) AAA — Abdominal pain or other symptoms occurring in a patient known to have or
newly diagnosed with AAA can present a clinical dilemma. In surgical series, between 5 and 22 percent of AAA are
symptomatic [8,10-14]. Symptoms that may be related to AAA include abdominal pain or back pain, signs of acute
thromboembolism, and fever. In the absence of rupture, pain or other symptoms attributable to AAA may indicate
rapid expansion causing compression of adjacent structures, or an inflammatory or infected AAA [8,14-17]. In the
absence of overt or impending rupture, the symptomatic patient should be assessed to determine whether their
symptoms are related to the aneurysm, and although not well-studied, when no other cause is apparent, we agree
with major society guidelines that suggest urgent repair, provided the patient does not have comorbidities that
preclude repair [3] (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Are symptoms
related to AAA?' and "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Ruptured versus
nonruptured AAA'.)
Abdominal/back/flank pain — Patients presenting with abdominal/back/flank pain in association with AAA
should be admitted for further evaluation and monitoring. If an alternative diagnosis cannot be definitively
established, symptoms should be presumed to be due to the AAA and a vascular surgical consultation should be
obtained. The nature of the presenting symptoms should help determine whether the AAA is the source of the
symptoms or simply an incidental finding during work-up of another disease process.
Patients identified with another obvious source (eg, urinary calculi) for their symptoms, should undergo treatment of
the other acute disease process and the AAA should be managed electively as an asymptomatic AAA. An inpatient
vascular surgical consultation should nevertheless be obtained to confirm that the symptoms are not related to the
AAA and to evaluate the need for and timing of AAA repair depending upon the resolution of the acute process. The
determination of whether to proceed with elective repair depends upon the rupture risk, which is primarily
determined by aortic diameter. The presence of very large AAA (>6.0 cm) may warrant admission even if the
aneurysm is not felt to be the source of symptoms. (See "Management of asymptomatic abdominal aortic
aneurysm", section on 'Aneurysm diameter and rupture risk' and "Management of asymptomatic abdominal aortic
aneurysm", section on 'Very large aneurysm'.)
Thromboembolism — Patients with symptoms and signs of acute thromboembolism should be managed
according to the severity of symptoms (acute, subacute, or chronic limb ischemia). If thromboembolism is
associated with abdominal pain, for which there is no other conceivable source, the embolus may have originated
from a tear in the aortic wall and may be a sign of overt or impending aortic rupture. In the event of AAA rupture,
thrombectomy can be performed concurrently with AAA repair.
In the presence of AAA, a full evaluation should be performed to determine the source of the thromboemboli, and
should include an electrocardiogram, echocardiogram, contrast-enhanced CT of the aorta from the aortic valve to
the iliac bifurcation, and peripheral duplex ultrasound since distal embolization can also be related to concurrent
large vessel aneurysm (eg, popliteal artery aneurysm). If the clinical evaluation does not identify an alternative
source for thromboembolism, the AAA should be presumed to be the source.
In the absence of AAA rupture, acute ischemic symptoms due to lower extremity thromboembolism from the AAA
should be managed with anticoagulation, and thrombectomy (or lysis) as needed. If a lower extremity
revascularization procedure is needed, consideration should be given to concurrent AAA repair. Under some
circumstances AAA repair can be delayed; however, the risk of recurrent thromboembolism remains until the AAA is
repaired. (See "Overview of acute arterial occlusion of the extremities (acute limb ischemia)".)
Aortic infection — Patients with fever and other systemic manifestations that suggest infected aortic aneurysm
should be treated with urgent surgical debridement and vascular reconstruction. The clinical manifestations and
treatment of infected aneurysm are discussed elsewhere. (See "Overview of infected (mycotic) arterial aneurysm".)
Inflammatory aneurysm — A triad of chronic abdominal pain, weight loss, and elevated erythrocyte
sedimentation rate in a patient with an AAA is highly suggestive of an inflammatory aneurysm. Patients with
inflammatory aneurysms are often more symptomatic than patients with the more typical AAAs, but the incidence of
actual rupture may be lower [18]. In patients who present with symptoms, repair should be undertaken regardless of
aneurysm diameter. (See "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Infected
versus inflammatory AAA'.)
ANEURYSM REPAIR — Urgent or emergent AAA repair is generally indicated for patients with ruptured AAA and
symptomatic (non-ruptured) AAA, provided the risk for repair is not prohibitive [3,8]. The decision of whether or not
to offer repair to high-risk patients is discussed below. (See 'Decision for comfort care' below.)
Two methods of aneurysm repair are currently available: open surgery and endovascular aneurysm repair (EVAR).
● Open AAA repair – Open aneurysm repair involves replacement of the diseased aortic segment with a tube or
bifurcated prosthetic graft through a midline abdominal or retroperitoneal incision.
● EVAR – EVAR involves the placement of modular graft components delivered via the iliac or femoral arteries,
which line the aorta and exclude the aneurysm sac from the circulation.
Endovascular aneurysm repair reduces perioperative (30-day) morbidity and mortality following elective AAA repair
[19-24], and there is accumulating evidence that morbidity and mortality following repair of symptomatic [25] or
ruptured AAA may also be reduced [2,7,26-31]. A systematic review identified 23 observational studies with 7040
urgent or emergent open (n = 6300) or endovascular (n = 740) AAA repairs in patients with symptomatic (non-
ruptured) or ruptured AAA [25]. Emergency EVAR was associated with a significantly reduced perioperative (30-
day) mortality risk relative to open repair (pooled odds ratio [OR] 0.62, 95% CI 0.52-0.75).
To perform emergent endovascular AAA repair, the patient's aneurysm must meet anatomic criteria for EVAR and
the institution must have a defined program for emergency endovascular surgery. Abdominal CT, which is obtained
in hemodynamically stable patients, will determine whether the patient with symptomatic (non-ruptured) or ruptured
AAA is anatomically suited to endovascular aneurysm repair (EVAR). Although up to 70 percent of patients may be
candidates for EVAR, ruptured AAA is more often repaired with open surgical techniques, due to the limited number
of centers available to perform emergency EVAR. Transfer to a vascular center is appropriate for hemodynamically
stable patients who are anatomically suited to EVAR, particularly if the risk for open repair is high. (See 'Decision for
patient transfer' below and 'Risk assessment' below.)
The anatomic requirements for endovascular repair for non-ruptured and ruptured AAA are discussed elsewhere.
(See "Endovascular repair of abdominal aortic aneurysm", section on 'Anatomic suitability' and "Surgical and
endovascular repair of ruptured abdominal aortic aneurysm", section on 'Criteria for endovascular repair'.)
Risk assessment — The general assessment of perioperative risk for urgent/emergent repair of abdominal aortic
aneurysm is similar to that of elective AAA repair; however, the urgency of the clinical situation often precludes a
comprehensive evaluation. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Medical
risk assessment'.)
There have been many attempts to quantify the mortality risk associated with ruptured AAA. Various prediction
models are available, but, unfortunately, no one system or variable has proven to be reliable in predicting mortality
with certainty nor reliably support the decision to withhold intervention [32,33]. Factors that are associated with
increased mortality following open repair of ruptured AAA include hypotension with a systolic blood pressure <80
mmHg, advanced age (>80 years), cardiac arrest, loss of consciousness, creatinine >1.3 on admission, ischemic
heart disease, female sex, and hemoglobin <9.0 on admission [2,34-44]. There are no equivalent studies assessing
preoperative risk factors and endovascular aneurysm repair of ruptured AAA. One risk prediction model based upon
a population of United States Medicare beneficiaries (ie, >65 years of age), found that mortality following elective
AAA repair is predicted by comorbidities, gender, and age with no differential predictors between open or
endovascular repair [45].
For patients with several prognostic factors for poor outcome, the incidence of serious morbidity, such as dialysis
dependence, colonic ischemia, and myocardial infarction, is high and the need for surgery related to a complication
is also high. The presence of >3 prognostic factors increases the likelihood that the patient will require extended
care. For the patient who is older than 80, with renal dysfunction, loss of consciousness, and hemoglobin <9, the
chance of survival following open repair of ruptured AAA is almost zero [33]. The presence of multiple risk factors
for poor outcome in a patient of advanced age, especially those with a "Do Not Resuscitate" advanced directive or a
history of AAA repair refusal should lead to consideration for comfort care. (See 'Decision for comfort care' below.)
Emergent versus delayed repair of symptomatic aneurysm — The timing of AAA repair for hemodynamically
stable patients with symptomatic (non-ruptured) AAA remains a clinical challenge. Some patients may benefit from
optimization of their medical status prior to repair; however, a definitive recommendation that would suit every
clinical situation is not possible.
Several retrospective case series comparing open AAA repair under elective versus emergent circumstances for
symptomatic (non-ruptured) AAA have found significantly higher overall rates of perioperative morbidity and
mortality for emergent compared with urgent repair (overall 18 to 26 percent versus 4 to 5 percent) [8,46,47].
Another series found no deaths from rupture in patients with symptomatic AAA whose operations were delayed and
performed semi-electively [14]. The potential impact of endovascular repair in this subset of patients is unknown,
but is unlikely to alter the need for preoperative medical optimization that appears to be beneficial for some patients.
MORBIDITY AND MORTALITY — For symptomatic, non-ruptured AAAs, perioperative mortality rates are similar to
those of elective repair; however, the rates of postoperative complications and late survival are intermediate
compared with elective or ruptured AAA repair [48]. (See "Management of asymptomatic abdominal aortic
aneurysm", section on 'AAA repair' and "Endovascular repair of abdominal aortic aneurysm", section on
'Perioperative morbidity and mortality' and "Open surgical repair of abdominal aortic aneurysm", section on
'Morbidity and mortality'.)
The mortality associated with ruptured AAA may be as high as 90 percent when patients who die at home or upon
arrival to the hospital are taken into account. In spite of obvious improvements in pre-hospital care, cardiovascular
anesthesia, and critical care, surgical mortality following open repair of ruptured AAA has changed very little,
remaining at approximately 30 to 50 percent [49,50]. Although endovascular aneurysm repair may improve survival
following AAA rupture, this has not been definitively established. The complications of aneurysm repair and
mortality associated with ruptured AAA are discussed in detail elsewhere. (See "Surgical and endovascular repair of
ruptured abdominal aortic aneurysm", section on 'Complications' and "Surgical and endovascular repair of ruptured
abdominal aortic aneurysm", section on 'Mortality'.)
DECISION FOR PATIENT TRANSFER — Patients with AAA who require emergent or urgent aortic surgery for
ruptured or symptomatic (non-ruptured) AAA should be treated at a facility where surgical expertise and/or the
perioperative resources necessary for major aortic surgery are available (eg, operating room personnel, an
appropriately-trained surgeon, perioperative intensive care) [51]. For patients who present to a facility where these
are not available, transfer to a vascular center with higher levels of hospital resources (such as number of
physicians, nurses, and critical care beds) is appropriate and may result in lower mortality [52]. In a study of 35,367
patients in England in the United States, the lowest mortality for ruptured AAA was seen in teaching hospitals with
larger bed capacities and doing a greater proportion of cases with EVAR [53].
Improved outcomes for open surgical repair of ruptured AAA are correlated with surgeon experience with a higher
annual caseload of open aneurysm repair per year (non-ruptured and ruptured) correlating with improved outcomes
[54]. The shift toward endovascular therapies has reduced the exposure of the vascular surgeon-in-training to open
surgical repair of AAA. As a result, the number of qualified surgeons in the community experienced with open repair
of ruptured AAA is declining [55]. If an appropriate level of surgical care is not available at the institution to which
the patient initially presented, the patient should be transferred [51]. If transfer is chosen, the patient and their family
should be informed of the potential risk of deterioration during transfer, and the transfer should be accomplished as
quickly as possible.
Patients who have a high-risk for open AAA repair may be candidates for endovascular repair. However, for
endovascular repair to be undertaken, in addition to having appropriate hospital personnel in place, the institution
must have systems in place to support the endeavor. Resources that are needed include:
● Rapid availability of high-quality computed tomography
● Availability of trained support staff (nursing, scrub technicians, radiology technologists, anesthesia)
● Stock of available endovascular prostheses in a wide range of sizes, which are replenished continuously
● Available vascular surgeon appropriately-trained in advanced endovascular techniques
For most small hospitals and low-volume facilities, these requirements cannot be met. If an institution is not able to
perform emergency EVAR, an alternative approach is to provide open repair for hemodynamically unstable patients
and transfer for hemodynamically stable patients to an appropriate vascular center.
DECISION FOR COMFORT CARE — Some patients may refuse repair of a ruptured AAA, or are such poor
candidates for repair that they are not likely to survive or have a meaningful quality of life even if they recover from
the procedure. Although it remains disputed whether endovascular repair decreases mortality in patients with
ruptured AAA, patients who have factors associated with a poor prognosis for open AAA repair may have lower
rates of morbidity and mortality following EVAR for ruptured AAA, when repair is chosen. (See 'Risk assessment'
above.)
A decision must be made according to the wishes of the patient (if known) and family whether to proceed with repair
or provide comfort measures. Patients who will not undergo repair are kept pain-free and allowed to expire. In one
study of 21 patients, the average time to death following ruptured AAA without repair was seven hours [56]. In
another study of 57 patients with ruptured AAA who did not undergo surgical intervention, the median survival was
2.2 hours [57]. However, the survival after two hours was significantly different for patients who had shock or
required cardiopulmonary resuscitation (13 percent) compared with those who were stable but not treated due to
patient decision, comorbidity, age, or anatomic considerations. (See "Pain assessment and management in the last
weeks of life".)
SUMMARY AND RECOMMENDATIONS
● Symptomatic abdominal aortic aneurysm (AAA) refers to any of a number of symptoms (eg,
abdominal/back/flank pain, limb ischemia) that can be attributed to the aneurysm. In the absence of overt
rupture (defined as aortic wall disruption leading to escape of blood outside the confines of the aorta), the
presence of symptoms increases the risk for AAA rupture. AAA rupture can also occur in the absence of any
intervening symptoms. Without repair, ruptured AAA is nearly uniformly fatal. Of the 50 percent of patients with
ruptured AAA who reach the hospital for treatment, between 30 and 50 percent will die in the hospital in spite of
significant advances in intensive care unit management and surgical techniques. (See 'Introduction' above and
'Morbidity and mortality' above.)
● Initial management of patients with symptomatic (non-ruptured) and ruptured AAA includes the placement of
large bore peripheral intravenous catheters for medication and fluid administration, pain management, and
preparation for surgery. For patients with ruptured AAA, we suggest maintaining the systolic blood pressure
between 80 and 100 mmHg (permissive hypotension) rather than at higher levels prior to repair (Grade 2C).
Permissive hypotension may minimize further tearing of the aorta and reduce blood loss. (See 'Initial
management' above.)
● Although there are rare reports of patient survival following ruptured AAA without repair, in general, expectant
management of ruptured AAA is nearly uniformly fatal. Thus, when ruptured AAA is identified, repair should be
undertaken emergently to give the patient the best chance for survival. (See 'Ruptured AAA' above.)
● For patients with symptomatic (non-ruptured) AAA of any size or configuration who do not have a prohibitive
risk for repair, we agree with major society guidelines that suggest urgent AAA repair (open or endovascular),
rather than no repair (Grade 2C). In the absence of rupture, symptoms may indicate that the aneurysm is
rapidly changing, increasing the risk of rupture. Symptoms may include abdominal/back/flank pain, signs of
thromboembolism, or systemic symptoms related to infected or inflammatory aneurysm. (See 'Symptomatic
(non-ruptured) AAA' above.)
● Hemodynamically unstable patients with known AAA who present with classic symptoms/signs of rupture
(hypotension, flank/back pain, pulsatile mass) should be taken directly to the operating room for immediate
control of hemorrhage and repair of the aneurysm (algorithm 1). Efforts to obtain proximal aortic control in the
operating room should not be delayed waiting for type-specific blood components. For hemodynamically
unstable patients not previously known to have AAA, time may permit a focused ultrasound exam to confirm
that an aneurysm is present prior to abdominal exploration, but this is not absolutely required. For patients with
symptomatic (non-ruptured) or ruptured AAA who are hemodynamically stable, computed tomography (CT) of
the abdomen should be obtained to evaluate whether an endovascular repair is feasible. (See 'Ruptured AAA'
above and "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Imaging symptomatic
patients'.)
● Although many factors are associated with poor outcomes following repair of ruptured AAA, no scoring system
or variable has proven reliable in predicting mortality of ruptured AAA with certainty. Factors on admission that
are associated with increased mortality following open repair of ruptured AAA include hypotension, elevated
creatinine, low hematocrit, advanced age, and cardiac arrest. For older patients (>80 years) with multiple risk
factors in whom EVAR is not feasible, comfort care should be discussed with the patient and/or family as a
possible care option. (See 'Risk assessment' above and 'Decision for comfort care' above.)
● For patients with ruptured AAA, where appropriate facilities, personnel, equipment, and expertise are available
for endovascular aneurysm repair (EVAR), we suggest EVAR rather than open AAA repair, provided it is
anatomically feasible (Grade 2C). In appropriately selected patients, endovascular repair of ruptured AAA
appears to be associated with lower perioperative (30-day) morbidity and mortality. For patients with
symptomatic but non-ruptured AAA who have multiple risk factors for poor prognosis, we also suggest EVAR
rather than open repair (Grade 2C). Where endovascular aneurysm repair for emergency AAA repair is not an
option (eg, not anatomically feasible, lack of facilities or expertise), open repair at the initial facility by a surgeon
experienced with aortic surgery is appropriate. If no such surgeon is available, or the patient is a poor
candidate for open repair, transfer to a vascular center is appropriate. (See 'Decision for patient transfer' above
and 'Aneurysm repair' above and "Surgical and endovascular repair of ruptured abdominal aortic aneurysm",
section on 'Open surgical versus endovascular repair'.)
ACKNOWLEDGMENT — We are saddened by the death of Emile R Mohler, III, MD, who passed away in October
2017. UpToDate wishes to acknowledge Dr. Mohler's work as our Section Editor for Vascular Medicine.
Use of UpToDate is subject to the Subscription and License Agreement.
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https://aplicacionesbiblioteca.udea.edu.co:3925/contents/management-of-symptomatic-non-ruptured-and-ruptured-abdominal-aortic-aneurysm/print… 10/15
Topic 15191 Version 14.0
GRAPHICS
Anatomy abdominal aortic aneurysm
Graphic 60682 Version 13.0
Classification of abdominal aortic aneurysm
Abdominal aortic aneurysms (AAAs) are commonly described based on the relation to the renal
arteries.
Suprarenal AAA: The aneurysm involves the origins of one or more visceral arteries but
does not extend into the chest.
Pararenal AAA: The renal arteries arise from the aneurysmal aorta but the aorta at the level
of the superior mesenteric artery is not aneurysmal.
Juxtarenal AAA: The aneurysm originates just beyond the origins of the renal arteries.
There is no segment of nonaneurysmal aorta distal to the renal arteries, but the aorta at
the level of the renal arteries is not aneurysmal.
Infrarenal AAA: The aneurysm originates distal to the renal arteries. There is a segment of
nonaneurysmal aorta that extends distal to the origins of the renal arteries.
Algorithm for the diagnosis of abdominal aortic aneurysm
AAA: abdominal aortic aneurysm; H/P: history and physical; CT: computed tomography; OR: operating room; MRI: magnetic
resonance imaging.
* Systolic BP persists <90 mmHg, in spite of resuscitation.
¶ Intravenous contrast is not absolutely required to diagnose rupture, but is highly desired if endovascular repair is an option.
Δ Unrepaired, or prior open or endovascular repair.
◊ Ultrasound, abdominal CT, or MRI may be appropriate.
§ Can be performed at the bedside or in the operating room.
Contributor Disclosures
Jeffrey Jim, MD Consultant/Advisory Boards: Medtronic [Aortic interventions (endovascular devices)]. Robert W
Thompson, MD Nothing to disclose Joseph L Mills, Sr, MD Grant/Research/Clinical Trial Support: Cesca
Therapeutics [Critical limb ischemia (Hepatocyte growth factor)]; Voyager Trial [Peripheral artery disease
(Rivoxaraban)]. Consultant/Advisory Boards: AnGes [Critical limb ischemia (Hepatocyte growth factor)];
AstraZeneca [Peripheral artery disease (ticagrelor)]. Other Financial Interest: Elsevier; Rutherford [Vascular surgery
(Rutherford and Comprehensive Vascular and Endovascular Surgery textbooks)]. John F Eidt, MD Nothing to
disclose Kathryn A Collins, MD, PhD, FACS Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be provided
to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate
standards of evidence.
Conflict of interest policy

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Authors: Jeffrey Jim, MD, Robert W Thompson, MD

● Rapid availability of high-quality computed tomography

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1. http://hcupnet.ahrq.gov/HCUPnet (Accessed on May 11, 2012).

Topic 15191 Version 14.0

Anatomy abdominal aortic aneurysm

Graphic 60682 Version 13.0

Classification of abdominal aortic aneurysm

Graphic 90459 Version 2.0

Algorithm for the diagnosis of abdominal aortic aneurysm

Graphic 86821 Version 3.0

Conflict of interest policy

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