PATIENTS WITH ACUTE aortic disease who present to the emergency department (ED) represent some of the highest acuity patients that emergency clinicians will ever encounter in acute care settings (Wittels, 2011). Inaccuracies about the acute pathological conditions of aortic aneurysm and aortic dissection are found in the literature. These inaccuracies can often confuse clinicians about the correct naming and description of these conditions (Tilney, 2010). The goals of this two-part series about acute aortic conditions are to clarify inaccuracies clinicians may have seen in the literature, to assist clinicians in understanding of aortic pathology, and to identify unique characteristics that may assist emergency clinicians to anticipate emergent interventions for patients with an aortic aneurysm or dissection.

PATHOANATOMICAL OVERVIEW

Aortic aneurysms and dissections have two different types of anatomical pathology that can affect the patency and durability of the aorta. It is imperative to distinguish between these two conditions. Table 1 describes the nomenclature of nontraumatic aorta pathoanatomy as the aorta reacts to a certain mechanism and dilates (aneurysm), separates (dissection) layers of the aorta, or ruptures through one layer or all three layers (any condition that leads to intolerable aortic pressure; DynaMed, 2012a, 2012b; Hiratzka et al., 2010; Lederle, 2011; Tilney, 2010). Specific treatments are based on the layers of the aorta (see Figure 1) that are affected and the mechanism of aortic pathoanatomy.

Figure 1. Aortic wall layers. The innermost layer (tunica intima or interna), the middle layer (tunica media), and the outermost layer (tunica externa or adventitia). Copyright 2012 by Hypertension Diagnostics. Used with permission from Lippincott Williams & Wilkins.

Table 1. Nomenclature of nontraumatic aorta pathoanatomy

One common misnomer is for clinicians to use the terms "aneurysm" and "dissection" concurrently to describe a single acute condition-a "dissecting aneurysm" (Hiratzka et al., 2010). Aortic aneurysm and dissection are two different pathoanatomical conditions. Dissection may, and often does, occur without an aneurysm being present, and an aneurysm may, and often does, occur without dissection (Hiratzka et al., 2010). Although two separate processes, aortic aneurysm and dissection can coexist-as an aortic aneurysm and as an aortic dissection. Generally, this dual pathology occurs when patients with chronic aortic dissection develop dilation in the aortic wall. Over time, the outer wall of the false lumen further weakens because its inner layer has been dissected away, leading to a higher risk of developing aneurysm (Isselbacher, 2005). In turn, patients with a known, again chronic (unrepaired), thoracic aortic aneurysm can develop a thoracic dissection (Hiratzka et al., 2010). Also, patients who have had open or endovascular repair for an aortic pathoanatomical problem can develop either a late aneurysm or dissection 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 dilatation phenomenon of all wall layers (see Figure 2). Dilatation of an abdominal aneurysm becomes significant when the aortic diameter size exceeds 3 cm. A thoracic aneurysm is considered significant when the aorta diameter exceeds 5 cm or increases by 50%-150% (DynaMed, 2012a; Lederle, 2011; Olsson, Thelin, Stahle, Ekbom, & Granath, 2006). Most aneurysms involve the entire circumference of the aorta (Lewiss, Egan, & Shreves, 2011).

Figure 2. Thoracic and abdominal aneurysm. Copyright 2010-2011 by the

Changes primarily in the media layer of the aorta can lead to aortic aneurysm development. Because of the destructive effects to the elastin and collagen from risk factors, the thinned media layer dilates, increasing the expansile force on the aortic wall to the point of rupture through all three layers of the aorta. Rupture causes blood to flow into the mediastinum if the aneurysm is in the thorax and into the peritoneum or retroperitoneum if the aneurysm is below the diaphragm (Hiratzka et al., 2010; Isselbacher, 2005; Robinson & Taylor, 2009). There is tremendous variability in the literature regarding rupture risk estimation. These estimates mainly focus on abdominal aneurysms and cite that rupture risk range from 6% to 26% after the aneurysm exceeds 6 cm. This wide range of variation may indicate that other patient- and/or aneurysm-specific variables may affect rupture risk. Some independent predictors of rupture found in multivariate analysis include hypertension, tobacco use, chronic obstructive pulmonary disease (COPD), and gender. The risk of rupture is 4 times greater among women than among men. The threshold size of 5.5 cm for proposed surgical intervention may be too high for women because of the larger aneurysm size compared with the body size (Booher & Eagle, 2011; Brewster et al., 2003). The 5-year survival rate of patients with unrepaired thoracic aortic aneurysms greater than 6 cm ranges from 20% to 54%, with death due to rupture. Risk factors for rupture of thoracic aortic aneurysms are similar to abdominal aortic aneurysms and include increasing age, female gender, COPD, and, most importantly, increasing thoracic aortic diameter (Jonker et al., 2010).

Approximately 75% of aneurysms develop in the abdominal area of the aorta because of the decreased number of elastic lamellae as the aorta becomes more distal (Isselbacher, 2005; Norman & Powell, 2010). Mortality is less with abdominal aneurysms than with thoracic aneurysms (Booher & Eagle, 2011; Isselbacher, 2005). Two recent studies regarding the epidemiology of abdominal aneurysms have demonstrated a consistent, overall 30% reduction in the incidence of abdominal aneurysm rupture since 1988 due to early diagnosis and life-long surveillance, with the biggest reduction (36%) in the 65- to 84-year age group (Hadjibashi, Ng, Mirocha, Crossman, & Gewertz, 2011; Norman & Powell, 2010).

Aneurysms in the thoracic area occur less often, approximately 25% of the time, as thoracic aortic atherosclerosis is less common than abdominal aortic atherosclerosis (Hiratzka et al., 2010). Thoracic aneurysm identification is limited without imaging, as an expanding thoracic aneurysm cannot be felt through the rib cage (Jonker, 2010; Wittels, 2011). Often thoracic aneurysms are discovered unexpectedly on routine chest radiographs as an incidental finding (Booher & Eagle, 2011; Isselbacher, 2005). Because of the inability to diagnose asymptomatic thoracic aneurysms by physical examination, thoracic aneurysms often grow to the point that when they rupture, the outcome is fatal, immediately postrupture or postoperatively. For example, a nationwide study from Sweden (Olsson et al., 2006) analyzed 2,235 patients who presented with a ruptured thoracic aneurysm between 1987 and 2002; 87% of these patients died before making it to the operating room, and of the 297 patients who survived surgery, 35% died within 30 days. In a U.S. study that included 1,307 patients who underwent 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 abdominal aneurysms are comparable-approximately 50% of patients with a ruptured abdominal aneurysm die before reaching the hospital, and of those who do reach the hospital, the mortality rate is 80% (Sakalihasan, Limet, & Defawe, 2005).

The amount of blood loss into the mediastinum or peritoneum depends upon the size of the ruptured aneurysm and whether or not any tamponade has occurred. Smaller ruptures with less blood loss are sometimes referred to as "leaking" aneurysms. The patient may not exhibit signs and symptoms of shock at all (Lewiss et al., 2011). In the case of abdominal aneurysms, despite a large hole in the aorta, the patient may be stable because of tamponade within the retroperitoneum, preventing ongoing blood loss. However, not all patients with aneurysms will have a ruptured aneurysm. A hematoma can develop that is contained within the intimal or adventitial layers, and the patient will present with generalized chest or abdominal pain. Patients may present with symptoms that are not directly related to the aorta. End-organ symptoms such as extremity ischemia or stroke-like symptoms or abdominal pain due to mesentery ischemia may occur due to embolization of atherosclerotic debris from the aorta or the aneurysm itself (Hiratzka et al., 2010; Karalis, Chandrasekaran, Victor, Ross, & Mintz, 1991). Signs and symptoms of thrombi or emboli to distal arteries warrant the consideration of an aneurysm.

Figure 3 shows a coronal view image slice that was digitally enhanced from a real contrast computed tomographic (CT) angiogram of an 83-year-old man with a thoracic ascending aortic aneurysm, with no evidence of rupture. He presented with 24 hr of intermittent chest pain that radiated to the back and a history of myocardial infarction, with subsequent coronary artery bypass and grafting. Note the aortic dilatation extending into the arch.

Figure 3. Coronal (anterior) view image from contrast computed tomographic angiogram of an 83-year-old man with a thoracic ascending aortic aneurysm with no evidence of rupture.

Figure 4 shows a sagittal image slice that was digitally enhanced from a noncontrast CT scan of a 72-year-old man who presented with abdominal pain and had an abdominal aneurysm of approximately 8 cm in size. The patient did not receive contrast due to renal insufficiency. Note that the unruptured abdominal aneurysm is clearly visible. The white spots on the image are the calcium deposits of atherosclerosis.

Figure 4. Sagittal view image from noncontrast computed tomographic scan of a 72-year-old man with an ~8-cm abdominal aortic aneurysm with no evidence of rupture.

Figure 5 shows a single-slice axial view of a noncontrast CT scan of the same 8-cm abdominal aneurysm. The dark matter around the aorta is periaortic fat. This aneurysm has not ruptured because the fat remains intact. An abdominal aortic aneurysm can be identified without intravenous (IV) contrast. However, IV contrast assists in the detection of active hemorrhage.

Figure 5. Single-slice axial view of noncontrast computed tomographic scan of the 8-cm abdominal aneurysm shown in

Figure 6 shows an axial view image from a noncontrast CT scan showing the ruptured abdominal aneurysm of a 58-year-old man who presented with acute abdominal and left leg pain. The patient was hypotensive and tachycardic. Note that the entire left lower quadrant of the abdomen is filled with blood (blood without contrast appears a gray shade on the CT scan). Refer to the section on Imaging Considerations. This section highlights the rationale for why CT was not the safest study for this patient (see Part 2 of this article for Supplemental Digital Content).

Figure 6. Axial view image from a noncontrast computed tomographic scan showing a ruptured abdominal aneurysm of a 58-year-old man who presented with acute abdominal and left leg pain.

HISTORY

Genetic syndromes trigger aortic aneurysm formation (Booher & Eagle, 2011; Doney & Vilke, 2010; DynaMed, 2012a, 2012b; Isselbacher, 2005; Lederle & Simel, 1999; Lewiss et al., 2011; Wittels, 2011). Many of these conditions listed in Table 2 are not known when a patient presents to the ED or are very rare, so they do not play a significant role in identifying an aneurysm. Table 3 lists the history and physical findings that are more easily obtained in emergent situations (Booher & Eagle, 2011; Doney & Vilke, 2010; DynaMed, 2012a, 2012b; Isselbacher, 2005; Lederle & Simel, 1999; Lewiss et al., 2011; Wittels, 2011). Relying upon the signs and symptoms and suspecting an aneurysm in patients with a positive family history, or older men who smoked, are more paramount considerations (Lederle, 2011). The clinical presentation of a patient with an abdominal aneurysm more often than not is usually asymptomatic until rupture; however, if there are signs and symptoms, they are centered round gradual increase in abdominal pain. If present, symptoms may include vague, chronic abdominal pain, low back pain, or mid-abdominal or flank pain, which may radiate to back, groin, or scrotum. Pain is usually steady for hours to days and unaffected by movement. Additional pain characteristics related to pathoanatomy with abdominal aneurysms include sudden, acute abdominal or flank pain, pain associated with syncope, or shock if the aneurysm has ruptured. This triad is highly suggestive of a vascular catastrophe (Wittels, 2011). Severe lumbar region pain may suggest impending rupture (DynaMed, 2012b; Isselbacher, 2005). Varied pain patterns are accounted for by the fact that the rupture can occur in the retroperitoneum, peritoneum, or rarely even into the duodenum, bronchus, or vena cava (Lewiss et al., 2011). Abdominal palpation of a pulsatile mass has varied sensitivity (29%-76%) due to the retroperitoneal location of the aorta, aneurysm size, and obesity, but if it is found, then it is distinctive for an abdominal aneurysm (Ledele & Simel, 1999; Lewiss et al., 2011). If a pulsatile mass is not found, the possibility of finding an aneurysm should not be excluded, especially if the aneurysm is ruptured (Lederle & Simel, 1999).

Table 2. Genetically triggered aneurysm syndromes

Table 3. Common history and physical findings for aneurysm

The number of patients who present to the ED, with cardiac arrest due to a ruptured thoracic aneurysm is unknown, but, likely significant. Fortunately, for some patients, thoracic aneurysms are discovered during a routine visit to their primary care provider (Booher & Eagle, 2011). Chest pain occurs with leaking thoracic aneurysms, and severe chest or back pain with ruptured aneurysms (Wittels, 2011). Pain in the neck and jaw may arise with aortic arch aneurysms. Back and intrascapular and/or left shoulder pain correlates with descending thoracic aortic aneurysms. Symptoms of chronic heart failure can occur following dilatation of the aortic root and resulting aortic valve regurgitation (DynaMed, 2012a; Wittels, 2011). The patient may also have symptoms described as compressive symptoms related to increasing thoracic aneurysm size, which are listed in Table 4 (Booher & Eagle, 2011; DynaMed, 2012a; Isselbacher, 2005; Wittels, 2011).

Table 4. Compressive symptoms of thoracic aortic aneurysm

IMAGING CONSIDERATIONS

Along with a highly suggestive clinical presentation, the diagnosis of an aortic aneurysm and whether there is a rupture is guided by obtaining an image of the aorta. The manner in which this is accomplished is determined by whether or not the patient is demonstrating signs and symptoms of shock. When one considers the practice of routine population screening of the most likely candidates mentioned earlier, older men who smoked (Lederle, 2011), it is not uncommon to note that upon presentation the patient historically had an unruptured aneurysm that was being monitored. Logically considering that this aneurysm has now ruptured, diagnosis of the problem is relatively easy in these situations. Table 5 lists diagnostic imaging studies that should be considered when an aneurysm is on the differential diagnosis list (Booher & Eagle, 2011; Isselbacher, 2005; Lewiss et al., 2011; Sakalihasan et al., 2005). Essentially, bedside imaging studies using ultrasonography are indicated for patients demonstrating shock whereas CT, contrasted or not, is the most commonly ordered study in an acute situation if the patient is stable enough to tolerate transport to and from the CT scanner. A chest radiograph is useful only if a thoracic aneurysm is considered.

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

EMERGENCY MANAGEMENT

Emergent treatment will depend on whether or not there is aortic rupture. Patients with an intact aortic aneurysm may be discharged from the ED for follow-up with a cardiovascular surgeon (Lewiss et al., 2011). If the aneurysm is leaking and the patient is not displaying signs and symptoms of shock but is hypertensive, administration of medications to reduce ventricular ejection force (anti-impulse therapy) and blood pressure (antihypertensive therapy) to minimize loss of blood into the mediastinum (thoracic aneurysm) or peritoneum (abdominal aneurysm) may be recommended while expediting transport to surgery. However, anti-impulse, antihypertensive therapy is administered more often for aortic dissection than for an aortic aneurysm. These therapies will be discussed in Part 2 of this series.

If the patient presents with hemorrhagic/hypovolemic shock, then anti-impulse, antihypertensive therapy is contraindicated. These therapies are contraindicated because these medications would eliminate whatever minimal cardiovascular response is present. Rather, attention should be focused on restoring intravascular volume with crystalloids and packed red blood cells (PRBCs). Mostly, emergency-released, uncross-matched, untyped blood is used because of the emergent need. The goal of the intravascular volume replacement is to balance just enough aortic pressure to achieve perfusion without generating excessive blood pressure in order not to cause added blood loss through the rupture (permissive hypotension) (Doney & Vilke, 2010; Lewiss et al., 2011; Wittels, 2011). The volume of resuscitation fluids should be guided by end-organ function measured by mental status and urinary output and coronary artery perfusion measured by surrogates such as serial electrocardiograms, cardiac markers, and patient symptoms, maintaining the mean arterial pressure (MAP) at 60-65 mmHg. Overresuscitation can also lead to possible clot disruption, further increasing bleeding. Platelets and fresh frozen plasma may be needed, given the large volume of crystalloids and PRBCs, which lead to dilution of clotting factors. These patients should be transported to the operating room or transferred to a tertiary care facility with cardiovascular surgery capabilities (Wittels, 2011). Unfortunately, it is not uncommon for the patient to deteriorate rapidly en route during long transport times and experience cardiopulmonary arrest. Prognosis in this situation is poor (e.g., death) death (Isselbacher, 2005).

POSTOPERATIVE OUTCOMES

Decision making for selecting patients for aneurysm repair is influenced by estimates of aneurysm rupture risk, elective operative mortality risk, life expectancy, and patient preference (Brewster et al., 2003). Until recently, patients with aortic aneurysms would have needed open surgery for repair, which included a large incision and the temporary clamping of the aorta to anastomose a graft to the excised aneurysmal portions of the aorta. The main advantage to open repair is that it allows inspection of the ruptured aneurysm and possible aortic branches (Jonker et al., 2010). Since 2004, transluminally placed expanding endovascular stent-graft repair is usually preferred, as with the passage of the time, the skill of the surgeon has improved and the stents and dilator systems have become smaller and less stiff, which require less manipulation (Isselbacher, 2005Jonker 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 region of the aneurysm, excluding it from the circulation while allowing aortic blood flow to continue distally through the prosthetic stent-graft lumen (Isselbacher, 2005). Emergency clinicians may not pay a lot of attention to outcomes postsurgery; however, it is important to know some of the potential complications (Table 6) when emergent risk versus benefit, and consent discussions are taking place in the ED (Isselbacher, 2005; Jonker et al., 2010, 2011; Luebke & Brunkwall, 2010; Matsuda et al., 2011; van Prehn et al., 2008; Zoli et al., 2010). This is always a tense moment, as the patient does tend to have a sense of impending doom and exhibits a lot of fear and anxiety, especially when faced with the need to make a quick life-or-death decision. Decisions about optimal management are not always supported by clear scientific evidence. A patient who is clearly not a candidate for open aneurysm repair may not benefit from endovascular repair, as studies have shown no observed benefit from endovascular treatment. The primary outcome can be death from either endovascular stent grafting or no treatment at all (Rooke et al., 2011).

Table 6. Postoperative outcomes

UNIQUE ANATOMICAL DEVELOPMENTS OF ANEURYSMS

A tension hemothorax can occur from intrathoracic blood expanding from the ruptured aneurysm, as the enormous pressure that it creates then opens up the parietal pleura. Blood from the aorta moves into the pleural space, leading to progressive hemodynamic instability. The clinical team may not suspect or have any imaging results to prompt the diagnosis of ruptured aneurysm at this time. The patient is in distress, with a clinical examination showing the patient in obstructive shock and no breath sounds on one side. The shock results not only from the acute blood loss from the aneurysm but also from the increased intrathoracic pressure causing decreased cardiac output. Shock occurs in addition to respiratory distress, hypoxia, and acute loss of lung volume. Both conditions need emergent attention, including needle decompression, which is indicated on the basis of the limited information available but will not be effective, leading to the immediate need for a chest tube thoracostomy. However, most patients who are decompressed with insertion of a chest tube probably die because relief of the tamponade effect will lead to uncontrolled aortic bleeding. In the rare event of survival, emergent operative repair of the aneurysmal rupture is required (Pizon, Bissell, & Gilmore, 2010).

Aortoenteric Fistula

An aortoenteric fistula is an erosion of a segment of the aorta into an adjacent portion of the gastrointestinal (GI) tract and can occur as a primary event with abdominal aneurysms. However, it is frequently seen as a delayed complication (secondary) of aortic reconstructive surgery with prosthetic or homograft use. The incidence rate is less than 1% for unrepaired aneurysms and up to 2% for previously repaired aneurysms (Sakalihasan et al., 2005). The fistula occurs between the vascular graft and an adjacent portion of the GI tract, and it is commonly associated with graft infection. This anatomical development is rarely reported after endovascular aortic repair with stent grafting. The most common site in the GI tract is the duodenum. The average elapsed time between graft placement and fistula formation is 6 years (Doney & Vilke, 2010).

This anatomical development in the patient creates confusion at the time of presentation. The patient has massive GI bleeding and is in shock. Until an imaging study is completed, the diagnosis is a life-threatening GI bleed. It is very important to quickly discern the history of present illness centered on abdominal symptoms and any prior aorta surgical procedures and to conduct a physical examination to include rapid bedside ultrasonography. Secondary aortoenteric fistula may also present with fever, malaise, leukocytosis, focal findings of chronic wound or graft infection, or some combination of these. Because of the extreme mortality risk, the presence of GI bleeding in a patient with known abdominal aortic aneurysm, or history of aortic graft placement must be considered to have an aortoenteric fistula until proven otherwise (Doney & Vilke, 2010).

Esophagogastroduodenoscopy is the best initial study, as it can be easily done on an unstable patient at the bedside. However, in the presence of continued bleeding, this diagnostic test may be deferred to the surgical suite or may be impossible due to profuse bleeding. Computerized tomography with contrast is also crucial, as it helps define the relationship between the GI tract and the aorta or graft. Until surgery can be arranged, permissive hypotension is appropriate, given the stability of end-organ functioning such as normal mentation and no angina-type chest pain (Doney & Vilke, 2010).

Aortocaval Fistula

Similar in nature to aortoenteric fistulas, aortocaval fistulas are caused from rupture into the vena cava. The overall prevalence of this condition is 3%-6% (Sakalihasan et al., 2005). The shunting of blood from the high-pressure arterial system to the low-pressure venous system leads to venous hypertension and increased preload. Presentation depends upon the fistula caliber, anatomical position (proximal or distal), and time of onset (acute or chronic) (Melas, Saratzis, Saratzis, Lazaridis, & Kiskinis, 2011). This is seen clinically with a pattern of regional venous hypertension and stasis (lower extremity edema, hematuria, rectal bleeding), high-output cardiac failure, hypotensive shock, oliguria, and a machinery-like abdominal bruit/thrill (Akwei, Altaf, Tennant, MacSweeney, & Braithwaite, 2011; Melas et al., 2011). The increased venous hypertension impairs renal perfusion, leading to renal failure, especially if diagnosis is delayed or missed. This is the result of small fistulas that may be asymptomatic, leading to poor outcomes after surgery (Akwei et al., 2011).

Mega Aorta Syndrome

Most cases of mega aorta syndrome are symptomatic before catastrophic presentation. When the disease is recognized before rupture, the entire aorta can be replaced in stages, hence the name "elephant trunk procedure". The sequence and timing of the stages depend upon indication and condition of the patient (Wu, Mitchell, & Linklater, 2010).

Patients can also present with one segment of the mega aorta that has ruptured but the hematoma is contained as a large abdominal mass, 9 cm or greater. Imaging studies will show no or minimal peripheral blood flow. Rupture is the major risk with this condition, as the maximum wall tension for the thoracic aorta is reached at 6 cm, and at this point, 34% will rupture (Wu et al., 2010). The patient with mega aortic syndrome in cardiopulmonary arrest will present to the ED with a cardiac rhythm that quickly deteriorates from pulseless electrical activity to asystole.

CASE STUDY

Although this case highlights the development of one of the rare complications of an abdominal aortic aneurysm, aortoenteric fistula, it also emphasizes the focused approach to any patient who presents to the ED with a leaking or ruptured thoracic or abdominal aneurysm. With immediate recognition of the potential underlying pathoanatomy and degree of shock the patient is in, selecting the safest imaging study to confirm the diagnosis is crucial. Also understanding the balance between lower aortic pressure and end-organ perfusion to minimize aortic blood loss and positioning the patient quickly for surgical repair with a cardiovascular surgeon, survival and hopeful outcomes for patients with aortic aneurysms without catastrophic rupture, irreversible shock, and significant comorbidities can be possible (Mani et al., 2011).

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For more than 60 additional continuing education articles related to Emergency Care topics, go to http://NursingCenter.com/CE.