Abdominal Vascular Emergencies: A Unified Approach

Emerg Med 39(10):20, 2007

The presentation may be vague, but one thing is clear: diagnosis and treatment must be swift or the patient will probably die. The author explores the evidence basis for the history and physical examination and presents a diagnostic algorithm that applies to three potentially devastating conditions.

By Joshua Broder, MD, FACEP

Abdominal aortic aneurysm (AAA), aortic dissection, and mesenteric ischemia are emergencies in the truest sense of the word. Clinicians find these conditions daunting because of their sometimes vague presentations, their extreme mortality and morbidity, and the time-sensitive nature of the diagnoses. The majority of patients who are not immediately diagnosed and treated die.

It is interesting to compare abdominal vascular emergencies with other disease processes, where diagnostic algorithms have been widely implemented to screen even low-risk patients. For example, low-risk patients with chest pain are generally screened through protocols and observation units, which is justified by the high incidence and high mortality of acute coronary syndromes. Ironically, the incidence of abdominal vascular emergencies as a group is also high and their case mortality risk is much higher than that of acute myocardial infarction (MI) (see table below). Although public health campaigns have declared “time is muscle” for acute MI, similar statements and protocols have not been issued regarding abdominal vascular emergencies.

In this article, I’ll review some common misconceptions about abdominal vascular emergencies, explore the evidence basis for history and physical examination findings, and present a diagnostic algorithm for these conditions. The unique characteristics of AAA, aortic dissection, and mesenteric ischemia will be discussed. However, the conditions will also be considered as a group because they affect similar at-risk populations and may be clinically indistinguishable on the basis of the history and physical examination.

LEADING CAUSE OF DEATH

Abdominal vascular emergencies rank in the top 15 causes of death in patients aged 50 and older. According to the Centers for Disease Control and Prevention, AAA and aortic dissection affect 5% of the population over age 65, with more than 11,000 ruptures occurring annually in the United States. Compared to these two conditions, mesenteric ischemia is relatively rare, affecting nine Americans in every 100,000, but this is a difficult diagnosis and it is likely underdiagnosed before death.

Although some risk factors for the conditions vary, advanced age, male gender, and tobacco smoking are warning signs in all three. Age is the most significant risk factor. However, if the patient is over age 50 and no other risk factors are present, that doesn’t justify discounting the possibility of an abdominal vascu- lar emergency.

On rare occasions, these conditions occur in younger patients with genetic predispositions or with other disease processes that increase their risk of a catastrophic vascular event.

UNDERLYING PATHOPHYSIOLOGIES

Although this article promotes a unified diagnostic approach to AAA, aortic dissection, and mesenteric ischemia, the pathophysiologies of these conditions are best discussed individually.

Abdominal aortic aneurysm. An AAA is defined as an aortic diameter greater than 3 cm (twice the normal size). Formation of an AAA is thought to be strongly associated with age, male gender, Caucasian race, family history of aneurysm, and tobacco smoking, according to a Veterans Affairs Cooperative Study of more than 70,000 U.S. veterans. Atherosclerotic disease in general is a risk factor, but contrary to what you might expect, diabetes is a negative risk factor for AAA.

Rupture of an aneurysm becomes progressively more likely as wall tension increases, and a dramatic increase in rupture rates occurs as aneurysm size exceeds 5 cm. Mortality with aneurysm rupture is primarily due to hemorrhagic shock.

Aortic dissection. Aortic dissection occurs as a tear in the intimal lining of the aorta develops and extends, usually distally in the direction of blood flow. High blood pressure, high aortic wall shear stress, and an intrinsically weak intimal layer due to connective tissue disorders are risk factors. Although this tear may ultimately extend through the muscular wall of the aorta (muscularis) and into the thin connective tissue layer surrounding the aorta (adventitia), it may be contained initially with no extravascular blood loss occurring. The extending intimal flap, however, frequently causes intravascular occlusion, resulting in end-organ hypoperfusion and early mortality. Examples include dissection into the celiac or mesenteric arteries (causing mesenteric ischemia), renal artery (causing renal hypoperfusion), major limb arteries (causing limb ischemia), carotid arteries (causing ischemic stroke), and coronary arteries (causing myocardial ischemia or infarction).

Retrograde dissection may damage the aortic valve, leading to acute aortic regurgitation, and dissection into the pericardium may result in pericardial tamponade. Death from hemorrhagic shock may occur if the tear violates the muscular layer of the aorta.

Data from the International Registry of Acute Aortic Dissection (IRAD) have refined our understanding of the condition by quantifying the rate of these complications. Dissection of the abdominal aorta alone is rare, accounting for only about 5% of dissections, but it may coexist with AAA and mesenteric ischemia. In fact, the IRAD database suggests that about 16% of type B dissections (those involving only the descending aorta) occur in the setting of an AAA greater than 6 cm in diameter, and approximately 5% are complicated by mesenteric ischemia.

Mesenteric ischemia. Mesenteric ischemia is actually a family of diseases encompassing both acute and chronic ischemia and arterial and venous occlusions. This article covers only acute arterial mesenteric is-chemia, which may occur by a number of mechanisms. For example, it may result from embolization of an occlusive thrombus, particularly in the setting of atrial fibrillation. It may also result from the in situ formation of a thrombus at the site of an existing partially obstructing atherosclerotic plaque. Or an advancing intimal flap from an aortic dissection may occlude the lumen or ostium of a blood vessel supplying the bowel.

Two other mechanisms for acute mesenteric ischemia include small bowel obstruction, in which strangulation of a bowel segment may occur, and generalized low-flow states, such as sepsis, cardiogenic shock, or hemorrhagic shock. Patients at risk for mesenteric is-chemia include those with atrial fibrillation, artificial heart valves, cardiomyopathy, and multiple abdominal surgeries. Advanced age is also a strong risk factor.

SUBTLE PRESENTATIONS

Although the classic presentations of AAA, aortic dissection, and mesenteric ischemia are readily recognized, most patients present with other symptoms. Consequently, a delay in diagnosis is the rule, not the exception (see table below). While being familiar with these classic presentations is essential, emergency physicians must also be astute enough to suspect these diseases in patients with far more subtle presentations if they are to make the early diagnosis that is critical in saving lives.

Rupture of an AAA, for example, may be surprisingly subtle in presentation. No less a clinician than William Osler reportedly stated, “There is no disease more conducive to clinical humility than aneurysm of the aorta.” A ruptured aneurysm classically presents with sudden onset of severe abdominal or back pain, or both, often accompanied by presyncope or syncope. However, presenting symptoms vary in emergency department patients, with many having only abdominal pain without syncope or back pain. Also, the time between symptom onset and emergency department presentation may be more than 24 hours in some cases.

Aortic dissection, similar to aortic aneurysm rupture, is described classically as the extremely rapid onset of severe chest and back pain or severe abdominal and back pain, with a tearing character noted. The IRAD database verifies the rapidity of onset (85% of patients) but calls other aspects of this presentation into question. A relatively low number of patients (25% of those with abdominal pain), for example, reported a “tearing” sensation; a higher number (33% of those with abdominal pain) reported less ominous descriptions such as “pressure.” Migratory pain, often considered an indication of progression of a dissection, was noted in only 20% to 25% of patients. Fewer than 5% presented with isolated abdominal pain. Among aortic dissection patients with abdominal pain as their predominant symptom, 18% presented more than six hours after symptom onset, and the mean time from symptom onset to diagnosis was 84 hours.

Acute mesenteric ischemia is also characterized as a rapid-onset disease with poorly localized severe abdominal pain, often described as “pain out of proportion to exam.” Studies cast doubt on this presentation, finding that an insidious onset of pain is common, occurring in up to one in five cases, and that pain is often described as well-localized or commensurate with examination findings.

Why the discrepancy between classic history and research findings? One explanation is that these diseases are often misdiagnosed, so subtle presentations may never be recognized, even after the patient’s death. In the past, because diagnostic work-ups for these diseases were difficult, often requiring angiography, clinicians may have been reluctant to subject patients with subtle presentations to risky tests. Today, with multidetector computed tomography (CT) and CT angiography scans available as primary diagnostic modalities, evaluation of less classic presentations is feasible, and more subtle or early presentations are more likely to be recognized.

PHYSICAL EXAMINATION FINDINGS

Unfortunately, a physical examination is too insensitive to rule out abdominal vascular emergencies reliably. However, if a patient has classic physical exam findings, that may increase pretest probability. But the absence of these findings should not be taken as justification for a more leisurely diagnostic evaluation.

Abdominal aortic aneurysm. The classic examination finding for AAA is a pulsatile abdominal mass, but this is present in only 80% of patients with unruptured aneurysms of 5 cm or larger. Thus, as many as one in five cases would be missed if clinicians relied on this finding before initiating a work-up. Obesity probably compromises sensitivity further, although its effect has not yet been studied. The sensitivity of abdominal palpation in ruptured AAA is also unknown, but rupture and intraperitoneal blood may adversely affect sensitivity.

Hypotension and tachycardia, often present in aortic rupture, are also unreliable. In a review of emergency department patients ultimately diagnosed with aortic rupture, fewer than half of those who died within two hours of arrival initially had hypotension and tachycardia. Thus, patients appearing to be hemodynamically stable should not receive a less urgent diagnostic evaluation if other signs and symptoms are compatible with AAA rupture.

Aortic dissection. The classic findings of aortic dissection include an extremity pulse deficit, aortic regurgitation murmur, and differential blood pressures in the extremities. However, these findings are either unstudied or have poor sensitivity and specificity. The IRAD database notes a pulse deficit in only about 20% of patients with aortic dissections and in only 13% of those presenting with abdominal pain alone. So the presence of normal pulses could disguise more than four out of five dissection cases. The reliability of a blood pressure differential to rule in or rule out aortic dissection is unknown, but in asymptomatic hypertensive patients, the normal difference in upper extremity blood pressures has been found to exceed 10 mm Hg in nearly one in five patients. So measuring blood pressures would likely result in both false positives and false negatives.

Instead of wasting precious time comparing blood pressures, which is unlikely to help with the diagnosis, a definitive imaging test should be performed in suspicious cases. Hypertension—while a clear risk factor for dissection—was present in only 63% of IRAD cases, suggesting that the absence of hypertension in emergency department patients cannot be relied on to exclude the diagnosis of aortic dissection.

Mesenteric ischemia. Classically, patients with mesenteric ischemia present with extreme pain disproportionate to physical exam findings, suggesting that the examination is normally benign. However, several studies have shown that peritonitis is a common initial presentation, occurring in 50% to 64% of cases. Although peritoneal findings such as rebound tenderness or guarding would no doubt result in a relatively rapid work-up and probable surgical consultation, they might reduce the physician’s concern for the time-sensitive lesion of mesenteric ischemia and instead prompt a search for infectious or inflammatory conditions or perforation. Rapid treatment is essential because a delay in surgery is strongly correlated with mortality.

A finding such as atrial fibrillation may increase suspicion for mesenteric ischemia but it lacks both sensitivity and specificity. Fewer than 50% of cases are due to embolic events from atrial fibrillation and a work-up for mesenteric ischemia should proceed regardless of the heart rhythm, if other features suggest its presence.

DIFFERENTIAL DIAGNOSIS

Because of the variability of the presentations of abdominal vascular emergencies and the poor sensitivity of classic history and examination findings, a broad net must be cast to capture cases. Moreover, the high morbidity and mortality of these disorders requires not only a thorough diagnostic work-up but also a rapid evaluation, so that critical interventions may be performed in time to make a meaningful difference.

Does every patient with abdominal pain need to be evaluated for these conditions? No. Patients who present with classic findings of other diseases or with benign history and exam findings may not need to be evaluated. Patients younger than 50 also have a low risk for a catastrophic vascular event, barring an unusual medical history. But for the remaining patients who have a nonspecific history and physical examination or worrisome findings, a single rapid diagnostic algorithm that can diagnose all of the vascular events and the more common emergency causes of abdominal pain should be used for every case.

The accelerated diagnostic algorithm described below can facilitate rapid diagnosis. This work-up uses laboratory testing, early bedside ultrasound, and prompt CT scanning without oral contrast to evaluate the patient.

STEP 1: LABORATORY TESTING

Immediate initiation of intravenous access for treatment and simultaneous blood sampling are mandatory. For the patient with acute severe abdominal pain, it may be wise to order a broad panel of laboratory testing both for diagnostic purposes and to obtain a surgical consultation. Laboratory testing for vascular emergencies is nonspecific and insensitive, but it may yield clues to these diagnoses, as well as offer alternative diagnoses. Although it seems logical that aortic aneurysm rupture would be accompanied by substantial anemia, a study of ruptured aortic aneurysms in the emergency department showed an initial hemoglobin level of 9 g/dl or higher in half of patients who died within two hours of arrival. In fact, even a normal hematocrit level may not offer strong reassurance in an at-risk patient, so rapid diagnostic imaging should proceed regardless of laboratory results.

Leukocytosis is a frequent finding in patients with mesenteric ischemia, but in the early hours of presentation this abnormality may not yet be apparent. Extreme leukocytosis (greater than 20,000 cells/mm3) should prompt suspicion of ischemia and infection. Perhaps the most sensitive early marker of mesenteric ischemia is an elevated lactate level. Lactate, a product of anaerobic metabolism of poorly perfused organs, is not specific to mesenteric ischemia but may be a sensitive indicator of the sick patient because an elevated lactate level may reflect sepsis, hemorrhage, or other shock states. In some institutions, a venous or arterial blood gas measurement can be rapidly obtained, with hematocrit and lactate levels available within minutes.

No laboratory tests exist that are specific for aortic dissection.

STEP 2: BEDSIDE IMAGING

Bedside ultrasonography for the evaluation of potential AAA should be the immediate second step in the accelerated diagnostic algorithm. Although ultrasound examination has an unacceptably low reported sensitivity for AAA rupture, studies of bedside ultrasonography by emergency physicians indicate that when an AAA is detected in the presence of acute abdominal pain, rupture has probably occurred. Bedside ultrasonography accelerates the disposition of the patient to the operating room and should be used as a triage tool early in the evaluation process, preferably as an extension of the physical examination and simultaneously with establishing intravenous access. Within minutes of the patient’s arrival, both an enlarged aorta and the presence of free peritoneal fluid can be determined (see image below). Either finding in a suspicious clinical context should prompt immediate surgical consultation.

Bedside x-ray films of the abdomen and chest play a limited role in the evaluation of a suspected vascular catastrophe. If a CT scan is quickly available, then that is the imaging study of choice. If CT scanning will be delayed, a portable, upright chest x-ray may be used to evaluate for free air. Abdominal films themselves are of very limited use because of poor sensitivity and specificity. Vascular calcifications may occasionally reveal the presence of AAA but x-ray films are not a reliable test.

Classic findings in mesenteric ischemia on x-ray films (for example, mural pneumatosis) are not sensitive and are predominantly late findings of bowel necrosis. They play little role in the early detection of mesenteric ischemia before a catastrophic injury cascade has begun. In fact, when ischemia is present, abdominal x-ray films more often result in nonspecific findings of ileus or apparent obstruction, which may falsely reassure the emergency physician of a serious, but not disastrous, cause of abdominal pain. These findings are not surprising—a poorly perfused bowel will cause peristalsis to cease, leading to an ileus or obstruction pattern.

Computed tomography is clearly more sensitive and specific for free air, obstruction, AAA, aortic dissection, and mesenteric ischemia than x-ray films (see images below). Because most institutions can now perform a multidetector CT scan of the abdomen in minutes, the potential time advantage of x-ray films is waning. However, plain films may still play a limited role in diagnosing unstable patients who are safer remaining in the emergency department for imaging.

STEP 3: COMPUTED TOMOGRAPHY IMAGING

Computed tomography scanning has excellent sensitivity and specificity for rupture and aortic dissection—almost 100% when an intravenous contrast medium is administered. It has improving sensitivity (96%) and specificity (94%) for mesenteric ischemia. Additionally, a CT scan has a high likelihood of revealing other serious causes of abdominal pain, including bowel obstruction and inflammatory or infectious etiologies.

The greatest dilemma facing the emergency physician is whether to perform a CT scan without contrast, with intravenous contrast alone, or with oral and intravenous contrast together. A growing body of literature has shown that CT scanning without oral contrast or with no contrast at all can still detect the most catastrophic abdominal events. A CT scan without intravenous contrast can detect the presence and size of an AAA or the presence of a substantial hemorrhage (see image below).

Other findings visible on a noncontrast CT scan include free air (pneumoperitoneum), small bowel obstruction, hemoperitoneum and retroperitoneal blood, and inflammatory changes. Intravenous contrast is useful in detecting active extravasation from a ruptured AAA. It may also reveal the intimal flap of aortic dissection, which may be invisible on noncontrast CT scan (see image below). Intravenous contrast also helps detect mesenteric ischemia by demonstrating branch arterial occlusion and regions of abnormal bowel wall enhancement, reflecting ischemic regions.

Oral contrast offers relatively few advantages for the detection of these catastrophic events and causes a time delay of two hours in many institutions. Although oral contrast may help detect ischemic bowel segments by delineating the thickness of the bowel wall, abnormal bowel can often be seen without oral contrast due to surrogate changes such as inflammatory stranding in surrounding fat. In addition, oral contrast may not reach the affected bowel segment if peristalsis is limited by ischemia. The possible slight improvement in diagnostic accuracy is overshadowed by the chance that the patient’s condition will deteriorate from diagnostic and therapeutic delay.

The harm to the patient from delay may not even be apparent in the emergency department. For example, the patient with mesenteric ischemia may remain hemodynamically stable in the emergency department, only to die days later from systemic inflammatory response syndrome because surgery was delayed. The urgency for diagnosis and treatment cannot be stressed enough.

Does failure to give oral contrast impair diagnosis if the patient’s pain does not have a vascular cause? Several studies of appendicitis and other inflammatory conditions suggest that oral contrast is not necessary for diagnosis. If intravenous contrast alone does not lead to a diagnosis but vascular causes appear less likely, a repeat CT scan with oral contrast can be performed.

Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) have excellent sensitivity and specificity for abdominal vascular emergencies. However, because of their limited availability and time delays, these tests should rarely be used in the emergency department. For patients with contraindications to iodinated CT contrast, the first option should be immediate noncontrast CT scan, not magnetic MRI or MRA. If noncontrast CT scan does not reveal a catastrophic event, then consider rapid MRI.

The box below summarizes the key points to keep in mind regarding CT scanning.

TREATMENT AND DISPOSITION

All of the conditions described above are traditionally treated with surgery, although interventional catheter-based therapies are being used more often for treatment of even ruptured AAA. For aortic dissections involving only the descending aorta, management in more than 70% of patients is by medical control of blood pressure using beta blockers and direct arterial vasodilators. Surgery is required in approximately 15% of patients; catheter-based therapies, such as stenting or fenestration of the intimal flap to improve end-organ perfusion, are performed in approximately 15% of patients.

When the patient is confirmed to have any of the catastrophic vascular diagnoses, the disposition is straightforward: immediate surgical consultation or transfer if a surgeon is unavailable. The more difficult decisions lie in those cases where no diagnosis is made following the algorithm described above. Both CT scan and MRI are highly sensitive and specific for aortic dissection and aneurysm rupture. However, imaging techniques have not been studied as well for the diagnosis of mesenteric ischemia, and the meaning of a negative examination in a patient with ongoing pain is unclear. Mesenteric ischemia is an evolving process that includes a gradient of disease, from mild ischemia to frank necrosis. Imaging and laboratory findings in early or mild disease may be negative, so repeat testing or observation may be necessary.

CHALLENGE FOR PHYSICIANS

Catastrophic abdominal vascular events are major causes of morbidity and mortality, particularly in patients over 50. Although these events are rare compared with leading causes of death such as acute coronary syndromes, their extreme case mortality and the imperative to diagnose and treat rapidly make them a challenge for the emergency physician. Their variable presentation requires a unified, rapid, and accurate diagnostic algorithm for all at-risk patients. Definitive imaging should be performed as early as possible in stable patients and early surgical consultation should be considered for all.

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