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Article: TME200169 Date: July 18, 2012 Time: 19:28

Advanced Emergency Nursing JournalVol. 34, No. 3, pp. 216–229

Copyright C© 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins

CasesO F N O T EColumn Editor: Theresa M. Campo, DNP, APN, NP-C, CEN

Acute Aortic Emergencies—Part 1Aortic Aneurysms

Ann White, MSN, RN, CCNS, CEN, CPEN

Joshua Broder, MD, FACEP

AbstractThis article is a 2-part series about patients with aortic emergencies. Patients with acute aorticdisease who present to the emergency department represent some of the highest acuity patientsthat emergency clinicians will ever encounter in acute care settings. Part 1 focuses on aorticaneurysms in the thorax or abdomen. An aortic aneurysm involves transverse dilatation, leading torupture and hemorrhage. Diagnosis is largely based on clinical presentation and carefully selectedimaging studies. Emergency interventions are guided by whether or not the patient is hypertensiveor in shock. For patients in shock, attention should focus on restoring intravascular volume whilenot generating excessive blood pressure. Open surgical intervention or endovascularly placed stentgrafting should then be expedited. Both options are not without complications, most commonlybeing stroke, paraplegia, and death. Part 2 will explore aortic dissection. Key words: aorta, aortic,aneurysm, dissection, emergency department

PATIENTS WITH ACUTE aortic diseasewho present to the emergency depart-ment (ED) represent some of the high-

est acuity patients that emergency clinicianswill ever encounter in acute care settings(Wittels, 2011). Inaccuracies about the acute

Author Affiliations: Department of Advanced ClinicalPractice, Duke University Hospital, Clinical AssociateFaculty, Duke University School of Nursing, Durham,NC (Ms White); and Division of Emergency Medicine,Duke University Medical Center (Dr Broder).

Disclosure: The authors report no conflicts of interest.

Corresponding Author: Ann White, MSN, RN, CCNS,CEN, CPEN, Department of Advanced Clinical Prac-tice, Duke University Hospital, Clinical Associate Fac-ulty, Duke University School of Nursing, DUMC 3677,Durham, NC 27710 ([email protected]).

DOI: 10.1097/TME.0b013e31826133b0

pathological conditions of aortic aneurysmand aortic dissection are found in the liter-ature. These inaccuracies can often confuseclinicians about the correct naming and de-scription of these conditions (Tilney, 2010).The goals of this two-part series about acuteaortic conditions are to clarify inaccuraciesclinicians may have seen in the literature,to assist clinicians in understanding of aorticpathology, and to identify unique character-istics that may assist emergency clinicians toanticipate emergent interventions for patientswith an aortic aneurysm or dissection.

PATHOANATOMICAL OVERVIEW

Aortic aneurysms and dissections have twodifferent types of anatomical pathology that

Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

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July–September 2012 � Vol. 34, No. 3 Acute Aortic Emergencies—Part 1 217

can affect the patency and durability ofthe aorta. It is imperative to distinguish be-tween these two conditions. Table 1 de-scribes the nomenclature of nontraumaticaorta pathoanatomy as the aorta reacts to acertain mechanism and dilates (aneurysm),separates (dissection) layers of the aorta, orruptures through one layer or all three layers(any condition that leads to intolerable aorticpressure; DynaMed, 2012a, 2012b; Hiratzkaet al., 2010; Lederle, 2011; Tilney, 2010). Spe-cific treatments are based on the layers of theaorta (see Figure 1) that are affected and themechanism of aortic pathoanatomy.

One common misnomer is for cliniciansto use the terms “aneurysm” and “dissec-tion” concurrently to describe a single acutecondition—a “dissecting aneurysm” (Hiratzkaet al., 2010). Aortic aneurysm and dissec-tion are two different pathoanatomical condi-tions. Dissection may, and often does, occurwithout an aneurysm being present, and ananeurysm may, and often does, occur withoutdissection (Hiratzka et al., 2010). Although

Table 1. Nomenclature of nontraumaticaorta pathoanatomy

Pathoanatomy Mechanism

Aneurysm Dilatation of the aortaincluding all wall layers,with a diameterexceeding 3(abdominal) to 5 cm(thoracic), or50%–150% increase

Transverse process:leading to rupture

and hemorrhageintomediastinum orperitoneum

Bleeding eventDissection Pathological separation of

layers of the aortaLongitudinal process:

often no bloodleaves the vessel

Ischemia event

Figure 1. Aortic wall layers. The innermost layer(tunica intima or interna), the middle layer (tunicamedia), and the outermost layer (tunica externa oradventitia). Copyright 2012 by Hypertension Di-agnostics. Used with permission from LippincottWilliams & Wilkins.

two separate processes, aortic aneurysm anddissection can coexist—as an aortic aneurysmand as an aortic dissection. Generally, thisdual pathology occurs when patients withchronic aortic dissection develop dilation inthe aortic wall. Over time, the outer wall ofthe false lumen further weakens because itsinner layer has been dissected away, lead-ing to a higher risk of developing aneurysm(Isselbacher, 2005). In turn, patients witha known, again chronic (unrepaired), tho-racic aortic aneurysm can develop a thoracicdissection (Hiratzka et al., 2010). Also, pa-tients who have had open or endovascularrepair for an aortic pathoanatomical problemcan develop either a late aneurysm or dissec-tion at the site of manipulation, anastomosis,or implanted device borders (Bonser et al.,2011; Trimarchi et al., 2010).

AORTIC ANEURYSM: BACKGROUND

The mechanism of an aneurysm is a dilatationphenomenon of all wall layers (see Figure 2).Dilatation of an abdominal aneurysm becomessignificant when the aortic diameter size ex-ceeds 3 cm. A thoracic aneurysm is consid-ered significant when the aorta diameter ex-ceeds 5 cm or increases by 50%–150% (Dy-naMed, 2012a; Lederle, 2011; Olsson, The-lin, Stahle, Ekbom, & Granath, 2006). Mostaneurysms involve the entire circumferenceof the aorta (Lewiss, Egan, & Shreves, 2011).



218 Advanced Emergency Nursing Journal

Figure 2. Thoracic and abdominal aneurysm.Copyright 2010-2011 by the Merck Manual.Used with permission from Lippincott Williams &Wilkins.

Changes primarily in the media layer of theaorta can lead to aortic aneurysm develop-ment. Because of the destructive effects tothe elastin and collagen from risk factors, thethinned media layer dilates, increasing the ex-pansile force on the aortic wall to the point ofrupture through all three layers of the aorta.Rupture causes blood to flow into the medi-astinum if the aneurysm is in the thorax andinto the peritoneum or retroperitoneum if theaneurysm is below the diaphragm (Hiratzka etal., 2010; Isselbacher, 2005; Robinson & Tay-lor, 2009). There is tremendous variability inthe literature regarding rupture risk estima-tion. These estimates mainly focus on abdom-inal aneurysms and cite that rupture risk rangefrom 6% to 26% after the aneurysm exceeds6 cm. This wide range of variation may in-dicate that other patient- and/or aneurysm-specific variables may affect rupture risk.Some independent predictors of rupturefound in multivariate analysis include hyper-tension, tobacco use, chronic obstructive pul-monary disease (COPD), and gender. The riskof rupture is 4 times greater among womenthan among men. The threshold size of 5.5cm for proposed surgical intervention maybe too high for women because of the largeraneurysm size compared with the body size(Booher & Eagle, 2011; Brewster et al., 2003).The 5-year survival rate of patients with unre-paired thoracic aortic aneurysms greater than6 cm ranges from 20% to 54%, with death due

to rupture. Risk factors for rupture of thoracicaortic aneurysms are similar to abdominal aor-tic aneurysms and include increasing age, fe-male gender, COPD, and, most importantly,increasing thoracic aortic diameter (Jonkeret al., 2010).

Approximately 75% of aneurysms developin the abdominal area of the aorta because ofthe decreased number of elastic lamellae asthe aorta becomes more distal (Isselbacher,2005; Norman & Powell, 2010). Mortalityis less with abdominal aneurysms than withthoracic aneurysms (Booher & Eagle, 2011;Isselbacher, 2005). Two recent studies regard-ing the epidemiology of abdominal aneurysmshave demonstrated a consistent, overall 30%reduction in the incidence of abdominalaneurysm rupture since 1988 due to earlydiagnosis and life-long surveillance, with thebiggest reduction (36%) in the 65- to 84-yearage group (Hadjibashi, Ng, Mirocha, Cross-man, & Gewertz, 2011; Norman & Powell,2010).

Aneurysms in the thoracic area occur lessoften, approximately 25% of the time, asthoracic aortic atherosclerosis is less com-mon than abdominal aortic atherosclerosis(Hiratzka et al., 2010). Thoracic aneurysmidentification is limited without imaging, as anexpanding thoracic aneurysm cannot be feltthrough the rib cage (Jonker, 2010; Wittels,2011). Often thoracic aneurysms are discov-ered unexpectedly on routine chest radio-graphs as an incidental finding (Booher & Ea-gle, 2011; Isselbacher, 2005). Because of theinability to diagnose asymptomatic thoracicaneurysms by physical examination, thoracicaneurysms often grow to the point that whenthey rupture, the outcome is fatal, immedi-ately postrupture or postoperatively. For ex-ample, a nationwide study from Sweden (Ols-son et al., 2006) analyzed 2,235 patients whopresented with a ruptured thoracic aneurysmbetween 1987 and 2002; 87% of these pa-tients died before making it to the operatingroom, and of the 297 patients who survivedsurgery, 35% died within 30 days. In a U.S.study that included 1,307 patients who under-went surgery for ruptured thoracic aneurysm,the perioperative mortality rate was 28% for




open repair and 28% for endovascular repair(Goodney et al., 2011). Data for abdominalaneurysms are comparable—approximately50% of patients with a ruptured abdominalaneurysm die before reaching the hospital,and of those who do reach the hospital, themortality rate is 80% (Sakalihasan, Limet, &Defawe, 2005).

The amount of blood loss into the medi-astinum or peritoneum depends upon thesize of the ruptured aneurysm and whetheror not any tamponade has occurred. Smallerruptures with less blood loss are sometimesreferred to as “leaking” aneurysms. The pa-tient may not exhibit signs and symptomsof shock at all (Lewiss et al., 2011). In thecase of abdominal aneurysms, despite a largehole in the aorta, the patient may be stablebecause of tamponade within the retroperi-toneum, preventing ongoing blood loss. How-ever, not all patients with aneurysms will havea ruptured aneurysm. A hematoma can de-velop that is contained within the intimal oradventitial layers, and the patient will presentwith generalized chest or abdominal pain. Pa-tients may present with symptoms that are notdirectly related to the aorta. End-organ symp-toms such as extremity ischemia or stroke-likesymptoms or abdominal pain due to mesen-tery ischemia may occur due to embolizationof atherosclerotic debris from the aorta or theaneurysm itself (Hiratzka et al., 2010; Karalis,Chandrasekaran, Victor, Ross, & Mintz, 1991).Signs and symptoms of thrombi or emboli todistal arteries warrant the consideration of ananeurysm.

Figure 3 shows a coronal view image slicethat was digitally enhanced from a real con-trast computed tomographic (CT) angiogramof an 83-year-old man with a thoracic ascend-ing aortic aneurysm, with no evidence of rup-ture. He presented with 24 hr of intermit-tent chest pain that radiated to the back anda history of myocardial infarction, with sub-sequent coronary artery bypass and grafting.Note the aortic dilatation extending into thearch.

Figure 4 shows a sagittal image slice thatwas digitally enhanced from a noncontrast

Figure 3. Coronal (anterior) view image fromcontrast computed tomographic angiogram of an83-year-old man with a thoracic ascending aorticaneurysm with no evidence of rupture.

CT scan of a 72-year-old man who presentedwith abdominal pain and had an abdominalaneurysm of approximately 8 cm in size. Thepatient did not receive contrast due to renalinsufficiency. Note that the unruptured ab-dominal aneurysm is clearly visible. The whitespots on the image are the calcium depositsof atherosclerosis.

Figure 5 shows a single-slice axial view ofa noncontrast CT scan of the same 8-cm ab-dominal aneurysm. The dark matter aroundthe aorta is periaortic fat. This aneurysm hasnot ruptured because the fat remains intact.




Figure 4. Sagittal view image from noncontrastcomputed tomographic scan of a 72-year-old manwith an ∼8-cm abdominal aortic aneurysm with noevidence of rupture.

An abdominal aortic aneurysm can be identi-fied without intravenous (IV) contrast. How-ever, IV contrast assists in the detection ofactive hemorrhage.

Figure 6 shows an axial view image from anoncontrast CT scan showing the rupturedabdominal aneurysm of a 58-year-old manwho presented with acute abdominal and leftleg pain. The patient was hypotensive andtachycardic. Note that the entire left lowerquadrant of the abdomen is filled with blood

Figure 5. Single-slice axial view of noncontrastcomputed tomographic scan of the 8-cm abdom-inal aneurysm shown in Figure 4.

Figure 6. Axial view image from a noncontrastcomputed tomographic scan showing a rupturedabdominal aneurysm of a 58-year-old man who pre-sented with acute abdominal and left leg pain.

(blood without contrast appears a gray shadeon the CT scan). Refer to the section on Imag-ing Considerations. This section highlightsthe rationale for why CT was not the safeststudy for this patient (see Part 2 of this articlefor Supplemental Digital Content).

HISTORY

Genetic syndromes trigger aortic aneurysmformation (Booher & Eagle, 2011; Doney& Vilke, 2010; DynaMed, 2012a, 2012b;Isselbacher, 2005; Lederle & Simel, 1999;Lewiss et al., 2011; Wittels, 2011). Many ofthese conditions listed in Table 2 are notknown when a patient presents to the ED orare very rare, so they do not play a signifi-cant role in identifying an aneurysm. Table 3

Table 2. Genetically triggered aneurysmsyndromes

• Marfan syndrome• Turners syndrome• Loeys-Dietz syndrome• Bicuspid aortic valve• Familial thoracic aortic aneurysm syndrome




lists the history and physical findings thatare more easily obtained in emergent situa-tions (Booher & Eagle, 2011; Doney & Vilke,2010; DynaMed, 2012a, 2012b; Isselbacher,2005; Lederle & Simel, 1999; Lewiss et al.,2011; Wittels, 2011). Relying upon the signsand symptoms and suspecting an aneurysmin patients with a positive family history, orolder men who smoked, are more paramountconsiderations (Lederle, 2011). The clinicalpresentation of a patient with an abdomi-nal aneurysm more often than not is usu-ally asymptomatic until rupture; however,if there are signs and symptoms, they arecentered round gradual increase in abdomi-nal pain. If present, symptoms may includevague, chronic abdominal pain, low backpain, or mid-abdominal or flank pain, whichmay radiate to back, groin, or scrotum. Painis usually steady for hours to days and unaf-fected by movement. Additional pain charac-teristics related to pathoanatomy with abdom-

Table 3. Common history and physicalfindings for aneurysm

Patient historyAtherosclerosisHyperlipidemiaHypertensionTobacco useAortic arteritisChronic aortic dissectionSigns and symptomsAbdominal aneurysm—gradual increase in

abdominal pain, back pain, sudden painindicating rupture, gastrointestinalbleeding, pulsatile mass (varied sensitivity)

Thoracic aneurysms—chest pain, diastolicmurmur, heart failure, shortness of breath,hoarseness, difficulty swallowing, jugularvein distention, trachea deviation

AgeThoracic aneurysm appears more in older

age and rises rapidly inMen >55 yearsWomen >70 years

GenderMen: 10 times more likely than in women

inal aneurysms include sudden, acute abdom-inal or flank pain, pain associated with syn-cope, or shock if the aneurysm has ruptured.This triad is highly suggestive of a vascularcatastrophe (Wittels, 2011). Severe lumbarregion pain may suggest impending rupture(DynaMed, 2012b; Isselbacher, 2005). Variedpain patterns are accounted for by the factthat the rupture can occur in the retroperi-toneum, peritoneum, or rarely even into theduodenum, bronchus, or vena cava (Lewisset al., 2011). Abdominal palpation of a pul-satile mass has varied sensitivity (29%–76%)due to the retroperitoneal location of theaorta, aneurysm size, and obesity, but if it isfound, then it is distinctive for an abdomi-nal aneurysm (Ledele & Simel, 1999; Lewisset al., 2011). If a pulsatile mass is not found,the possibility of finding an aneurysm shouldnot be excluded, especially if the aneurysm isruptured (Lederle & Simel, 1999).

The number of patients who present to theED, with cardiac arrest due to a ruptured tho-racic aneurysm is unknown, but, likely signif-icant. Fortunately, for some patients, thoracicaneurysms are discovered during a routinevisit to their primary care provider (Booher& Eagle, 2011). Chest pain occurs with leak-ing thoracic aneurysms, and severe chest orback pain with ruptured aneurysms (Wittels,2011). Pain in the neck and jaw may arise withaortic arch aneurysms. Back and intrascapu-lar and/or left shoulder pain correlates withdescending thoracic aortic aneurysms. Symp-toms of chronic heart failure can occur follow-ing dilatation of the aortic root and resultingaortic valve regurgitation (DynaMed, 2012a;Wittels, 2011). The patient may also havesymptoms described as compressive symp-toms related to increasing thoracic aneurysmsize, which are listed in Table 4 (Booher &Eagle, 2011; DynaMed, 2012a; Isselbacher,2005; Wittels, 2011).

IMAGING CONSIDERATIONS

Along with a highly suggestive clinical pre-sentation, the diagnosis of an aortic aneurysmand whether there is a rupture is guided by




Table 4. Compressive symptoms of thoracicaortic aneurysm

Hoarseness: Due to left recurrent laryngealnerve stretching

Stridor: Due to tracheal or bronchialcompression

Dyspnea: Due to lung compressionDysphagia: Due to esophageal compressionEdema: Due to superior vena cava

compression

obtaining an image of the aorta. The man-ner in which this is accomplished is deter-mined by whether or not the patient is demon-strating signs and symptoms of shock. Whenone considers the practice of routine popula-tion screening of the most likely candidatesmentioned earlier, older men who smoked(Lederle, 2011), it is not uncommon to notethat upon presentation the patient historicallyhad an unruptured aneurysm that was be-ing monitored. Logically considering that thisaneurysm has now ruptured, diagnosis of theproblem is relatively easy in these situations.Table 5 lists diagnostic imaging studies thatshould be considered when an aneurysm ison the differential diagnosis list (Booher &Eagle, 2011; Isselbacher, 2005; Lewiss et al.,2011; Sakalihasan et al., 2005). Essentially,bedside imaging studies using ultrasonogra-phy are indicated for patients demonstratingshock whereas CT, contrasted or not, is themost commonly ordered study in an acute sit-uation if the patient is stable enough to tol-erate transport to and from the CT scanner.A chest radiograph is useful only if a thoracicaneurysm is considered.

EMERGENCY MANAGEMENT

Emergent treatment will depend on whetheror not there is aortic rupture. Patients withan intact aortic aneurysm may be dischargedfrom the ED for follow-up with a cardiovas-cular surgeon (Lewiss et al., 2011). If the

aneurysm is leaking and the patient is not dis-playing signs and symptoms of shock but ishypertensive, administration of medicationsto reduce ventricular ejection force (anti-impulse therapy) and blood pressure (antihy-pertensive therapy) to minimize loss of bloodinto the mediastinum (thoracic aneurysm) orperitoneum (abdominal aneurysm) may berecommended while expediting transport tosurgery. However, anti-impulse, antihyperten-sive therapy is administered more often foraortic dissection than for an aortic aneurysm.These therapies will be discussed in Part 2 ofthis series.

If the patient presents with hemorrhagic/hypovolemic shock, then anti-impulse, an-tihypertensive therapy is contraindicated.These therapies are contraindicated becausethese medications would eliminate whateverminimal cardiovascular response is present.Rather, attention should be focused on restor-ing intravascular volume with crystalloidsand packed red blood cells (PRBCs). Mostly,emergency-released, uncross-matched, un-typed blood is used because of the emer-gent need. The goal of the intravascular vol-ume replacement is to balance just enoughaortic pressure to achieve perfusion withoutgenerating excessive blood pressure in or-der not to cause added blood loss throughthe rupture (permissive hypotension) (Doney& Vilke, 2010; Lewiss et al., 2011; Wittels,2011). The volume of resuscitation fluidsshould be guided by end-organ function mea-sured by mental status and urinary outputand coronary artery perfusion measured bysurrogates such as serial electrocardiograms,cardiac markers, and patient symptoms, main-taining the mean arterial pressure (MAP) at60–65 mmHg. Overresuscitation can also leadto possible clot disruption, further increasingbleeding. Platelets and fresh frozen plasmamay be needed, given the large volume ofcrystalloids and PRBCs, which lead to dilutionof clotting factors. These patients should betransported to the operating room or trans-ferred to a tertiary care facility with cardio-vascular surgery capabilities (Wittels, 2011).Unfortunately, it is not uncommon for the




Table 5. Diagnostic imaging studies to detect thoracic or abdominal aneurysms

Diagnostic test Utility, benefits, and limitations

Chest radiograph Useful to detect thoracic aneurysm—Characterized by wideningmediastinum, enlarged aortic knob, and tracheal deviation; smalleraneurysms or even some large ones may not produce any abnormalfindings

Bedsideultrasonography

Useful to detect and size thoracic or abdominal aneurysms (sensitivity andspecificity approaching 100% for abdominal aneurysms; accurate withsize measurement)—Mostly, only feasible study for patients in shock;able to detect peritoneal rupture but not reliable in distinguishinghemorrhage that is mostly retroperitoneal

Transesophageal/transthoracicechocardiogram

Useful to detect features of thoracic aneurysm in conjunction with bedsideultrasonography for patient in shock—Complimentary tool to evaluateaortic root involvement, as this area not imaged or sized well withcross-sectional computed tomography due to asymmetry and cardiacmotion; however, limited in evaluation of entire ascending aorta, arch,and descending aorta so should not be the sole study

Helical computedtomography withintravenouscontrast

Useful to detect and size thoracic or abdominal aneurysms—Forasymptomatic patients not in shock or whether ultrasonography istechnically limited or cannot eliminate the presence of rupture; candisplay presence of blood within thrombus (predictive marker ofimpending rupture), extravasation of contrast indicative of rupture,useful to determine intervention approach—endovascular or opensurgery as provides anatomical detail, entire aorta should be scanned todetect disease in more than one location (occurs up to 20% of time),axial images of tortuous aorta (common in the elderly) may overestimatesize of aneurysm

Magnetic resonanceimaging/angiography

Useful to detect and size thoracic or abdominalaneurysms—Non-nephrotoxic contrast material, excellent anatomicaldetail (better than computed tomography to image aortic root), not veryuseful for acute diagnosis in emergency department for relativelyunstable patient but more so for long-term surveillance

patient to deteriorate rapidly en route dur-ing long transport times and experience car-diopulmonary arrest. Prognosis in this situa-tion is poor (e.g., death) death (Isselbacher,2005).

POSTOPERATIVE OUTCOMES

Decision making for selecting patients foraneurysm repair is influenced by estimatesof aneurysm rupture risk, elective operativemortality risk, life expectancy, and patientpreference (Brewster et al., 2003). Until re-cently, patients with aortic aneurysms wouldhave needed open surgery for repair, which

included a large incision and the tempo-rary clamping of the aorta to anastomose agraft to the excised aneurysmal portions ofthe aorta. The main advantage to open re-pair is that it allows inspection of the rup-tured aneurysm and possible aortic branches(Jonker et al., 2010). Since 2004, translumi-nally placed expanding endovascular stent-graft repair is usually preferred, as with thepassage of the time, the skill of the sur-geon has improved and the stents and dilatorsystems have become smaller and less stiff,which require less manipulation (Isselbacher,2005 Jonker et al., 2011; Rooke et al., 2011;Scali et al., 2011). Older patients with more




comorbidities tolerate this procedure better.The stent graft serves to bridge the regionof the aneurysm, excluding it from the cir-culation while allowing aortic blood flow tocontinue distally through the prosthetic stent-graft lumen (Isselbacher, 2005). Emergencyclinicians may not pay a lot of attention to out-comes postsurgery; however, it is importantto know some of the potential complications(Table 6) when emergent risk versus benefit,and consent discussions are taking place inthe ED (Isselbacher, 2005; Jonker et al., 2010,2011; Luebke & Brunkwall, 2010; Matsudaet al., 2011; van Prehn et al., 2008; Zoli etal., 2010). This is always a tense moment, asthe patient does tend to have a sense of im-pending doom and exhibits a lot of fear andanxiety, especially when faced with the needto make a quick life-or-death decision. Deci-sions about optimal management are not al-ways supported by clear scientific evidence.A patient who is clearly not a candidate foropen aneurysm repair may not benefit fromendovascular repair, as studies have shownno observed benefit from endovascular treat-ment. The primary outcome can be deathfrom either endovascular stent grafting or notreatment at all (Rooke et al., 2011).

UNIQUE ANATOMICAL DEVELOPMENTS OFANEURYSMS

Several unique anatomical developments canoccur in patients with thoracic or abdominalaneurysms that can confuse the clinical pre-sentation and impact care in the ED. Famil-iarity and recognition of these conditions areparamount.

Tension Hemothorax

A tension hemothorax can occur from in-trathoracic blood expanding from the rup-tured aneurysm, as the enormous pressurethat it creates then opens up the parietalpleura. Blood from the aorta moves into thepleural space, leading to progressive hemo-dynamic instability. The clinical team may notsuspect or have any imaging results to prompt

the diagnosis of ruptured aneurysm at thistime.. The patient is in distress, with a clinicalexamination showing the patient in obstruc-tive shock and no breath sounds on one side.The shock results not only from the acuteblood loss from the aneurysm but also fromthe increased intrathoracic pressure causingdecreased cardiac output. Shock occurs inaddition to respiratory distress, hypoxia, andacute loss of lung volume. Both conditionsneed emergent attention, including needle de-compression, which is indicated on the basisof the limited information available but willnot be effective, leading to the immediateneed for a chest tube thoracostomy. How-ever, most patients who are decompressedwith insertion of a chest tube probably die be-cause relief of the tamponade effect will leadto uncontrolled aortic bleeding. In the rareevent of survival, emergent operative repairof the aneurysmal rupture is required (Pizon,Bissell, & Gilmore, 2010).

Aortoenteric Fistula

An aortoenteric fistula is an erosion of asegment of the aorta into an adjacent por-tion of the gastrointestinal (GI) tract and canoccur as a primary event with abdominalaneurysms. However, it is frequently seen asa delayed complication (secondary) of aorticreconstructive surgery with prosthetic or ho-mograft use. The incidence rate is less than 1%for unrepaired aneurysms and up to 2% forpreviously repaired aneurysms (Sakalihasanet al., 2005). The fistula occurs between thevascular graft and an adjacent portion of theGI tract, and it is commonly associated withgraft infection. This anatomical developmentis rarely reported after endovascular aortic re-pair with stent grafting. The most commonsite in the GI tract is the duodenum. The av-erage elapsed time between graft placementand fistula formation is 6 years (Doney &Vilke, 2010).

This anatomical development in the patientcreates confusion at the time of presentation.The patient has massive GI bleeding and is inshock. Until an imaging study is completed,




Table 6. Postoperative outcomes

Outcome/incidence Mechanism

Stroke: 4%–10% chance, incidence fairlyequal between open repair andendovascular groups

Urgent situations do not allow optimal preoperativeplanning and screening

Physicians may be less cautious because of urgency ofsaving the person’s life

Hypovolemia as a result of blood loss may contribute toinsufficient cerebral perfusion

Cerebral embolization of atherosclerotic plaques duringmanipulation of catheters, guide wire, or endograftsin the diseased aortic arch

Air emboliPreexisting cervical carotid and vertebrobasilar artery

diseaseParaplegia: Based on the size of the

aneurysm, probability of paraplegiaincreases from 2% when less thaneight segmental arteries are sacrificedto 13% when ≥13 segmental arteriesare sacrificed

Endovascular repair precludes revascularization of thesegmental artery pairs that supply blood flow tostructures around and inside the spinal canal (spinalcord) at each segmental level

Open repair also precludes revascularization as the aortais excised and a graft is placed that does not routinelyperfuse the spinal cord

A more distal aneurysm location involving theabdominal aorta increases risk

When a large number of input or collateral arteries areremoved, irreversible ischemia occurs

30-day mortality: Significantly lower inpatients treated with endovascularrepair (19%) than in patients treatedwith open repair (33%). (These dataare based on patients with rupturedthoracic aneurysm.)

ExsanguinationCardiac complications, i.e., myocardial infarction

(endovascular repair 4%; open repair 11%)Multiorgan failureInfectious complications

Endoleak: When two endovascularstents are placed next to each otherand an imperfect seal at the proximallanding zone (area in aorta wherestent is deployed) occurs allowingblood to flow around the stent graft;present in at least 11% of patients

Death possible from rupture of the stented aneurysm oradjacent aorta, perforation of the aortic wall by thebare portion of the stent graft, or an infected stentgraft

Risk to endograft-related complications may increasewith emergency procedures due to the possiblelimited availability of the optimal endograft size

Hypovolemic shock may decrease the diameter of theaorta through the sympathetic response of peripheralvasoconstriction, which may complicate andcontribute to inadequate preoperative endograftsizing

the diagnosis is a life-threatening GI bleed. Itis very important to quickly discern the his-tory of present illness centered on abdom-inal symptoms and any prior aorta surgicalprocedures and to conduct a physical exami-nation to include rapid bedside ultrasonogra-

phy. Secondary aortoenteric fistula may alsopresent with fever, malaise, leukocytosis, fo-cal findings of chronic wound or graft in-fection, or some combination of these. Be-cause of the extreme mortality risk, the pres-ence of GI bleeding in a patient with known




abdominal aortic aneurysm, or history of aor-tic graft placement must be considered tohave an aortoenteric fistula until proven oth-erwise (Doney & Vilke, 2010).

Esophagogastroduodenoscopy is the bestinitial study, as it can be easily done on an un-stable patient at the bedside. However, in thepresence of continued bleeding, this diagnos-tic test may be deferred to the surgical suite ormay be impossible due to profuse bleeding.Computerized tomography with contrast isalso crucial, as it helps define the relationshipbetween the GI tract and the aorta or graft.Until surgery can be arranged, permissive hy-potension is appropriate, given the stability ofend-organ functioning such as normal menta-tion and no angina-type chest pain (Doney &Vilke, 2010).

Aortocaval Fistula

Similar in nature to aortoenteric fistulas, aor-tocaval fistulas are caused from rupture intothe vena cava. The overall prevalence of thiscondition is 3%–6% (Sakalihasan et al., 2005).The shunting of blood from the high-pressurearterial system to the low-pressure venoussystem leads to venous hypertension and in-creased preload. Presentation depends uponthe fistula caliber, anatomical position (prox-imal or distal), and time of onset (acute orchronic) (Melas, Saratzis, Saratzis, Lazaridis,& Kiskinis, 2011). This is seen clinically witha pattern of regional venous hypertensionand stasis (lower extremity edema, hema-turia, rectal bleeding), high-output cardiacfailure, hypotensive shock, oliguria, and amachinery-like abdominal bruit/thrill (Akwei,Altaf, Tennant, MacSweeney, & Braithwaite,2011; Melas et al., 2011). The increased ve-nous hypertension impairs renal perfusion,leading to renal failure, especially if diagno-sis is delayed or missed. This is the result ofsmall fistulas that may be asymptomatic, lead-ing to poor outcomes after surgery (Akwei etal., 2011).

Mega Aorta Syndrome

Another unique anatomical development ofan aneurysm is the development of mega aorta

syndrome described as a diffuse aneurysmaldilation to greater than 6 cm in diameter ofthe entire aorta. The disease progression isslow, occurring over years.

Most cases of mega aorta syndrome aresymptomatic before catastrophic presenta-tion. When the disease is recognized beforerupture, the entire aorta can be replaced instages, hence the name “elephant trunk pro-cedure”. The sequence and timing of thestages depend upon indication and condi-tion of the patient (Wu, Mitchell, & Linklater,2010).

Patients can also present with one segmentof the mega aorta that has ruptured but thehematoma is contained as a large abdominalmass, 9 cm or greater. Imaging studies willshow no or minimal peripheral blood flow.Rupture is the major risk with this condition,as the maximum wall tension for the thoracicaorta is reached at 6 cm, and at this point,34% will rupture (Wu et al., 2010). The pa-tient with mega aortic syndrome in cardiopul-monary arrest will present to the ED with acardiac rhythm that quickly deteriorates frompulseless electrical activity to asystole.

CASE STUDY

A 65-year-old man arrived in a small-community ED. His chief complaint was se-vere, sudden abdominal pain, followed by alarge volume of bloody stool per rectum. Thefollowing vital signs were obtained upon ar-rival: blood pressure, 88/62; heart rate, 118;respiratory rate, 18; O2 saturation, 98% on2 L; and temperature, 37.4◦ C. A history ofan unrepaired abdominal aortic aneurysm,measured at 5 cm 1 year ago, was con-firmed. Physical examination demonstratedthat the patient had abdominal tendernessand a palpable mass with abnormal pulsa-tions. Peritoneal signs of rebound and guard-ing were present. Peripheral pulses werediminished in the lower extremities.

The patient quickly had two more episodesof bloody stool per rectum, measuring ap-proximately 500 ml. The patient was resus-citated with 2 L of normal saline and 2units of PRBCs. On the basis of the patient’s




instability and a known history of aneurysm,the emergency medicine physician confirmeda ruptured aortic aneurysm and free bloodin the peritoneum via ultrasound. Immediatetransfer of the patient was arranged after con-sulting with a cardiovascular surgeon, whoagreed with the probable differential diagno-sis of a ruptured abdominal aortic aneurysmwith aortoenteric fistula.

Transport via paramedic emergency med-ical services (EMS) was quickly arranged tothe closest tertiary acute care hospital 40miles away. The EMS transport orders in-cluded maintaining the patient’s MAP at 60–65 mmHg in an attempt to reduce the amountof blood flowing from the aorta while main-taining end-organ perfusion with an IV ad-ministration of normal saline at 75 ml perhour. If the patient demonstrated any signsof increased shock, the IV administration wasto be increased and medical control was tobe notified to consider the administrationof emergency-released uncross-matched, un-typed PRBCs, which were available duringtransport.

The patient arrived at the tertiary acute careED with the following vital signs: blood pres-sure 90/56 (MAP 67), pulse 100, respiratoryrate 22, 98% on a 15-L nonrebreather mask,and 37.2 ◦C temperature. The patient wasconscious and alert, but retching and vom-iting, and having continuous bloody stool perrectum. The patient was immediately trans-ported to the operating room area, sitting ona bedpan due to the continuous blood comingfrom his rectum and in a high Fowler’s posi-tion vomiting into a basin. Because of the aor-toenteric fistula, the patient underwent opensurgery for repair of the aneurysm and fistula.The patient tolerated the procedure well anddid not develop any complications.

CASE DISCUSSION AND SUMMARY

Although this case highlights the develop-ment of one of the rare complications of anabdominal aortic aneurysm, aortoenteric fis-tula, it also emphasizes the focused approachto any patient who presents to the ED with

a leaking or ruptured thoracic or abdominalaneurysm. With immediate recognition of thepotential underlying pathoanatomy and de-gree of shock the patient is in, selecting thesafest imaging study to confirm the diagno-sis is crucial. Also understanding the balancebetween lower aortic pressure and end-organperfusion to minimize aortic blood loss andpositioning the patient quickly for surgical re-pair with a cardiovascular surgeon, survivaland hopeful outcomes for patients with aor-tic aneurysms without catastrophic rupture,irreversible shock, and significant comorbidi-ties can be possible (Mani et al., 2011).

Part 2 of this series will discuss the uniquecharacteristics of patients with aortic dis-section and highlight the challenging deci-sion making in diagnosis and the complex-ity of emergent management to include anti-impulse, antihypertensive therapy.

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