eMedicine Specialties > Emergency Medicine > Cardiovascular

Aneurysm, Abdominal

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Updated: Sep 8, 2009

Introduction

Background

Abdominal aortic aneurysm (AAA) is a relatively common, potentially life-threatening condition. Most cases are asymptomatic and are often detected as an incidental finding using diagnostic imaging obtained for other reasons. There is a wide spectrum of clinical presentations and abdominal aortic aneurysm should be considered in the differential diagnosis for a number of symptoms.

Abdominal aortic aneurysm is usually the result of degeneration in the media of the arterial wall, resulting in a slow and continuous dilatation of the lumen of the vessel. In fewer than 5% of cases, abdominal aortic aneurysm is caused by mycotic aneurysm of hematogenous origin. In these cases, local invasion of the intima and media gives rise to abscess formation and aneurysmal dilation of the vessel. Gram-positive organisms most commonly cause mycotic aneurysm. As with aneurysm of the thoracic aorta, abdominal aortic aneurysm may be described as fusiform, which is circumferential, or saccular, which is more localized.

The lateral view clearly shows calcification of both walls. Abdominal aortic aneurysm can be diagnosed with certainty.

Pathophysiology

After age 50, the normal diameter of the infrarenal aorta is 1.5 cm in women and 1.7 cm in men. An infrarenal aorta that is 3 cm in diameter or larger is considered an abdominal aortic aneurysm (AAA), even if asymptomatic. Approximately 90% of abdominal aortic aneurysms are infrarenal.

The 3 layers comprising the normal aorta are the intima, media, and adventitia. Structural and elastic properties of major arteries are mostly imparted by the media, which is composed of smooth muscle cells surrounded by elastin, collagen, and proteoglycans. Abdominal aortic aneurysm develops following degeneration of the media due to atherosclerotic changes. The degeneration ultimately may lead to widening of the vessel lumen and loss of structural integrity. While abdominal aortic aneurysm is known to primarily involve the media, the exact etiology is not known.

Most abdominal aortic aneurysms occur in association with advanced atherosclerosis. Atherosclerosis may induce abdominal aortic aneurysm formation by causing mechanical weakening of the aortic wall with loss of elastic recoil, along with degenerative ischemic changes, through obstruction of the vasa vasorum. Many patients with advanced atherosclerosis do not develop AAA, while some patients having no evidence of atherosclerosis do. The observed association between atherosclerosis and AAA is probably not causative; however, atherosclerosis may represent a nonspecific secondary response to vessel wall injury that is induced by multiple factors.

Frequency

United States

Ruptured AAA is the 13th-leading cause of death in the United States, causing an estimated 15,000 deaths per year. The incidence of AAA is 2-4% in the adult population, and 11% of cases in that subset occur in males older than 65 years. Despite increased survival following diagnosis, incidence and crude mortality seem to be increasing.

Mortality/Morbidity

In 1988, 40,000 surgical reconstructions for abdominal aortic aneurysm (AAA) were performed in the US, with substantial mortality differences between elective versus emergency operations. As elective aneurysm repair has a mortality rate drastically lower than that associated with rupture, the emphasis must be on early detection and repair free from complications.

Race

White males have the highest incidence of AAA.

Sex

Males are affected 7 times more often than females.

Age

AAA occurs most commonly in patients between age 65 and 75 years, and it is more frequent in men smokers.

Clinical

History

Abdominal aortic aneurysms (AAAs) are usually asymptomatic until they expand or rupture. Patients may experience unimpressive back, flank, abdominal, or groin pain for some time prior to rupture. Isolated groin pain is a particularly insidious presentation. This occurs with retroperitoneal expansion and pressure on either the right or left femoral nerve. This symptom may be present without any other associated findings, and a high index of suspicion is necessary to make the diagnosis.

• Expanding AAA causes sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the chief complaint, and pain may be a less significant symptom to the patient.
• Patients with a ruptured AAA may present in frank shock as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension.
• At least 65% of patients with ruptured AAA die from sudden cardiovascular collapse before arriving at a hospital.
• Patients at greatest risk for AAA are those who are older than 65 years and have peripheral atherosclerotic vascular disease.
• A history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension often is elicited.
• Less frequent causes of AAA include Marfan and Ehlers-Danlos syndromes, collagen vascular diseases, and mycotic aneurysm.
• Patients who have a first-degree relative with AAA are at increased risk.
• It is important to note progressive symptoms (eg, abdominal or back pain, vomiting, syncope, claudication). These should alert the clinician to the possibility of expansion with imminent rupture.

Physical

• While abrupt onset of pain due to AAA may be quite dramatic, associated physical findings may be very subtle.
• Patients may have normal vital signs in the presence of a ruptured AAA due to retroperitoneal containment of hematoma.
• Presence of a pulsatile abdominal mass is virtually diagnostic but is found in less than half of cases. It is more commonly seen with a ruptured aneurysm. In an obese abdomen, an AAA is more difficult to palpate. Even in 25% of patients known to have an aneurysm, vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery.
• Misdiagnosis is fairly common because the classic presentation of pain associated with hypotension, tachycardia, and a pulsatile abdominal mass is present in fewer than 30-50% of cases. The leading misdiagnosis is renal colic, as dissection of the renal artery may produce flank pain and hematuria.
• Presence of an abdominal bruit or lateral propagation of the aortic pulse wave offer subtle clues and may be more frequently found than the pulsatile mass.
• The clinician need not be afraid of properly palpating the abdomen because no evidence exists that aortic rupture can be precipitated by this maneuver.

Causes

• Patients at greatest risk for AAA are those who are older than 65 years and have peripheral atherosclerotic vascular disease.
• A history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension often is elicited. The US Preventive Services Task Force recommends ultrasonography screening in men aged 65-75 years who have ever smoked.¹  
• Less frequent causes of AAA include Marfan and Ehlers-Danlos syndromes, collagen vascular diseases, and mycotic aneurysm.
• Patients who have a first-degree relative with AAA are at increased risk.

Differential Diagnoses

Other Problems to Be Considered

Gastrointestinal bleed
Ischemic bowel
Nephrolithiasis
Musculoskeletal pain
Perforated gastrointestinal ulcer
Pyelonephritis
Pancreatitis

Workup

Laboratory Studies

No specific laboratory studies exists that can be used to make the diagnosis of abdominal aortic aneurysm (AAA). Laboratory testing may be used to aid in diagnosis of other pathology or diagnose associated medical disorders.

Imaging Studies

More than 80% of patients with ruptured abdominal aortic aneurysm (AAA) present without previous diagnosis of AAA, which contributes to an initial misdiagnosis rate of 24-42%. A rational approach to diagnostic evaluation is predicated on a high degree of suspicion. Options for radiologic evaluation of AAA include plain radiography, ultrasonography, CT scan, MRI, and angiography.

• Ultrasonography
  • Ultrasonography is the standard imaging tool; if performed by trained personnel, it has a sensitivity and specificity approaching 100% and 96%, respectively, for the detection of infrarenal AAA.
  • Bedside emergency ultrasonography should be performed without delay if AAA is suspected. Elderly patients with abdominal pain are prime candidates for bedside ultrasonography screening.
  • Ultrasonography is noninvasive and may be performed at the bedside. Ultrasonography can be used to detect free peritoneal blood.
  • Limitations of the study are few but do include inability to detect leakage, rupture, branch artery involvement, and suprarenal involvement. Also, ability to image the aorta is reduced in the presence of bowel gas or obesity.
  • The primary role of ultrasonography is to screen patients at risk for AAA, to determine the size of the aneurysm, and to observe the aneurysm over time.
  • Significant portions of abdominal aorta (at least one third of its length) are not visualized on bedside emergency ultrasonography in 8% of nonfasted patients.² This rate is higher than reported for fasted patients receiving elective ultrasonography for evaluation of their aortas.

Ultrasonogram of a patient with an abdominal aortic aneurysm. This aneurysm was best visualized on a transverse or axial image. This patient underwent a conventional abdominal aortic aneurysm repair.

• Plain radiography
  • Plain radiographs often are obtained on patients with abdominal complaints before the diagnosis of AAA has been entertained. Using this method to evaluate patients with AAA is difficult because the only marginally specific finding, aortic wall calcification, is seen less than half of the time. Aortic wall calcification may appear without aneurysm rim calcification, which leads to a high false-negative rate.
  • Do not order plain radiography for the sole purpose of evaluating suspected AAA because it wastes time, delays care, and places the patient at risk for aortic rupture and death because of its low diagnostic yield.

Radiograph shows calcification of the abdominal aorta. The left wall is clearly depicted and appears aneurysmal; however, the right wall overlies the spine.

• CT
  • CT scan sensitivity for detecting AAA is nearly 100%, and the study offers certain advantages over ultrasonography in defining aortic size, rostral-caudal extent, involvement of visceral arteries, and extension into the suprarenal aorta. CT scanning permits visualization of the retroperitoneum, is not limited by obesity or bowel gas, detects leakage, and permits concomitant evaluation of the kidneys.
  • Spiral CT scan allows 3-dimensional imaging of abdominal contents, enhancing the ability to detect branch vessel and adjacent organ involvement.
  • Major disadvantages of CT scanning include technician availability, cost, longer study time, exposure to contrast, and the need to send patients out of the department for an extended time.

CT demonstrates an abdominal aortic aneurysm. The aneurysm was noted during workup for back pain, and CT was ordered after the abdominal aortic aneurysm was identified on radiographs. No evidence of rupture is seen (same patient as in Media file 2).

• MRI
  • MRI permits aorta imaging comparable to CT scanning and ultrasonography without subjecting the patient to dye load or ionizing radiation. The technique may offer superior imaging of branch vessels compared to CT scan or ultrasonography, but it is less valuable in assessing suprarenal extension and is not suitable in patients who are unstable. MRI may have a role in very stable patients with a severe dye allergy.
  • Lack of widespread availability, need for a stable patient, incompatibility with monitoring equipment, and high cost limit its applicability.

MRI of a 77-year-old man with leg pain believed to be secondary to degenerative disk disease. During evaluation, an abdominal aortic aneurysm was discovered.

• Angiography
  • Angiography is useful in determining aortic anatomy and has been advocated for preoperative use if suspicion of suprarenal or thoracic aneurysm, femoral or popliteal aneurysm, renal artery stenosis, unexplained impairment of renal function, occlusive iliofemoral disease, or visceral ischemia exists.
  • The test is limited by its invasiveness, cost, lack of operator availability, time involved, and risk of complications (eg, bleeding, perforation, embolization). Routine use of angiography in evaluation of AAA is not recommended.
  • Digital subtraction angiography (DSA) requires less time, uses less contrast material, and is less invasive than conventional angiography. The technique is not widely available and offers no real advantage over conventional CT scanning.

Treatment

Prehospital Care

• Prehospital care of patients having symptoms compatible with or suggestive of aortic aneurysm or dissection consists of assuring adequate breathing, maintaining oxygenation, treating shock, and obtaining useful information concerning history in order to expedite treatment on ED arrival. All patients with suspected aortic aneurysm should receive 100% oxygen along with continuous ECG and vital sign monitoring while en route to hospital. Large-bore IVs (14- or 16-gauge) should be inserted en route if possible.
• Establishing diagnosis in the field is usually difficult or impossible, but certain salient features of aortic aneurysm or dissection may be observed. Both can pose a threat to life if not quickly recognized and treated. Patients older than 50 years with sudden onset of abdominal pain should be presumed to have a ruptured abdominal aortic aneurysm (AAA) and should receive attentive airway management and vigorous fluid resuscitation, as indicated.
• Patient presentation during the prehospital phase of care differs depending on whether the aneurysm is acutely expanding or leaking or whether it involves the thoracic or abdominal aorta. Radio communication with the receiving hospital permits the medical control physician to direct care, and it facilitates selection of a capable destination hospital while permitting the ED to mobilize appropriate resources.
• The physician directing prehospital care should request transport to a facility capable of operative treatment of an aortic aneurysm in the rare event that the diagnosis can be suspected based on prehospital information.
• Use of military antishock trousers (MAST) to reverse shock due to ruptured AAA may seem beneficial, but it may actually be detrimental. While their application theoretically offers temporary stabilization by compressing the leaking AAA and expanding hematoma, an undesirable reduction in cardiac output also occurs. Expedient transport of patients who are unstable is a therapeutic imperative for those who are deteriorating.

Emergency Department Care

• Abdominal, back, or flank pain of sudden onset is characteristic of a rapidly expanding or ruptured abdominal aortic aneurysm (AAA). The diagnosis should be entertained whenever a patient older than 50 years presents with abdominal pain, particularly when pain is associated with syncope or signs of hemorrhagic shock.
• Examine patients suspected of having AAA for the presence of a pulsatile mass, which, if present, mandates immediate surgical intervention.
• Manage hemorrhagic shock with fluid resuscitation, blood transfusion, and immediate surgical consultation.
• Treatment for coagulopathy may be initiated in the ED for patients on warfarin or heparin.
• AAA rupture is believed to occur when the mechanical stress acting on the wall exceeds the strength of the wall tissue.
  • Wall tension can be calculated using the Laplace Law for wall tension: P x R/W, where P = mean arterial pressure (MAP), R = radius of the vessel, and W = wall thickness of the vessel.
  • AAA wall tension is a significant predictor of pending rupture. The actual tension in the AAA wall appears to be a more sensitive predictor of rupture than aneurysm diameter alone.
  • For these reasons, the clinician may wish to achieve acute blood pressure control in patients with AAA and elevated blood pressure.
  • Agents commonly used include antihypertensive agents and analgesics.
  • Patients with leaking AAAs, if normotensive, do not require pharmacotherapy.
  • In the setting of hypotension, reduction of blood pressure may be contraindicated.
• Initial therapeutic goals include elimination of pain and reduction of systolic blood pressure to 100-120 mm Hg, or to the lowest level commensurate with adequate vital organ (cardiac, cerebral, renal) perfusion.
  • Whenever systolic hypertension is present, beta-blockers can be used to reduce arterial dP/dt.
  • To prevent exacerbations in tachycardia and hypertension, treat patients with IV morphine sulfate. This reduces the force of cardiac contraction and the rate of rise of the aortic pressure (dP/dT) and may thus delay rupture.

Consultations

• Screening men beginning at 65 years reduces the mortality from rupture and is cost-effective.³ Open thoracic and abdominal aneurysm repair has a mortality rate of around 8%, with myocardial infarction being a frequent cause of death.³ Preoperative reduction of cardiac risk by cardiac investigations and beta-blockade may reduce this mortality rate. Autologous transfusion techniques, such as acute normovolemic hemodilution and interoperative cell salvage, reduce the need for allogeneic blood and the complications associated with open surgery. Minimally invasive endovascular repair is now possible for 40% of AAA and an increasing proportion of thoracic aneurysms.^3,4
• The combination of screening, reduced preoperative risk, and new minimally invasive techniques extend aortic aneurysm treatment into an increasingly elderly population.
• Urgency of consultation is dictated by the stability of the patient. In patients who are stable but without symptoms, the diagnostic workup takes precedence. Consider consulting a radiologist to determine whether ultrasonography, CT scan, or MRI would be the most appropriate study.
• Follow-up with a vascular surgeon is warranted if the abdominal aorta exceeds 3 cm in diameter or if any segment is greater than 1.5 times the diameter of an adjacent section.
• Patients having abdominal aortic aneurysm (AAA) smaller than 4 cm in diameter require serial ultrasonography twice per year. If the diameter increases by more than 0.5 cm over 6 months, or if it exceeds 4 cm, surgical repair usually is warranted.
• Immediately consult a surgeon for symptomatic patients with AAA. If hemodynamically stable, imaging modalities may be considered following discussion with surgical consultant.
• In cases that involve patients who are unstable, immediately consult a surgeon. Then, notify anesthesia and operating room personnel. Bedside ultrasonography may be obtained while awaiting definitive treatment; however, it should not delay surgery. CT scanning is not appropriate in patients who are unstable.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Antihypertensives

Used to reduce arterial dP/dt. For acute reduction of arterial pressure, the potent vasodilator sodium nitroprusside is very effective. To reduce dP/dt acutely, administer an IV beta-blocker in incremental doses until a heart rate of 60-80 beats/min is attained. When beta-blockers are contraindicated, such as in second- or third-degree atrioventricular block, consider using calcium channel blockers.

Esmolol (Brevibloc)

Ultra–short-acting beta 2-blocker, particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Can be discontinued abruptly if necessary. Normally used in conjunction with nitroprusside. May be useful as a means to test beta-blocker safety and tolerance in patients with history of obstructive pulmonary disease who are at uncertain risk for bronchospasm from beta-blockade. Elimination half-life is 9 min.

Dosing

Adult

Loading dose infusion: 250-500 mcg/kg/min IV for 1 min, followed by a 4-min maintenance infusion of 50 mcg/kg/min; repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min (for 4 min) if therapeutic effects not observed in 5 min; repeat sequence up to 4 times prn
As desired BP is approached, omit loading infusion and reduce incremental dose in maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min or lower; may increase interval between titration steps from 5-10 min if desired

Pediatric

Not established

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; A-V conduction abnormalities

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely

Labetalol (Normodyne, Trandate)

Blocks alpha-1 beta 1-, and beta 2-adrenergic receptor sites, decreasing BP.

Dosing

Adult

20 mg (0.25 mg/kg for 80-kg patient) IV over 2 min initially, follow with 20-80 mg q10-15min until BP controlled
Maintenance dose: 2 mg/min infusion; titrate to 5-20 mg/min; not to exceed a total dose of 300 mg

Pediatric

Not established

Interactions

Labetalol decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia, resulting from nitroglycerin use, without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes

Contraindications

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction present; in elderly patients, a lower response rate and higher incidence of toxicity may be observed

Propranolol (Inderal, Betachron E-R)

Class II antiarrhythmic nonselective beta-adrenergic receptor blocker. Has membrane-stabilizing activity and decreases automaticity of contractions. Propranolol is not suitable for emergency treatment of hypertension. Do not administer IV in hypertensive emergencies.

Dosing

Adult

40-80 mg PO bid initially; increase as required to usual range of 160-320 mg/d; up to 640 mg/d may be required

Pediatric

0.5 mg/kg/d PO divided bid/qid and increase gradually q3-7d; usual dosage range is 2-4 mg/kg/d divided bid; not to exceed 2 mg/kg/d

Interactions

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; A-V conduction abnormalities

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely

Metoprolol (Lopressor)

Selective beta 1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG. When considering conversion from IV to PO dosage forms, use ratio of 2.5 mg PO to 1 mg IV metoprolol.

Dosing

Adult

100 mg/d PO qd or divided bid/tid initially; increase at 1-wk intervals prn up to a total of 450 mg/d prn

Pediatric

Not established

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of metoprolol, possibly resulting in decreased pharmacologic effects; toxicity of metoprolol may increase with coadministration of sparfloxacin, phenothiazines, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives; metoprolol may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; A-V conduction abnormalities; asthma

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG

Nitroprusside (Nitropress)

Causes peripheral vasodilation by direct action on venous and arteriolar smooth muscle, thus reducing peripheral resistance. Commonly used IV because of its rapid onset and short duration of action. Easily titrated to desired effect. Nitroprusside is light sensitive and both bottle and tubing should be wrapped in aluminum foil. Prior to initiating nitroprusside, administer a beta-blocker to counteract physiologic response of reflex tachycardia that occurs when nitroprusside is used alone. This physiologic response will increase the shear forces against the aortic wall, thus increasing dP/dT. Objective is to keep heart rate between 60-80 bpm.

Dosing

Adult

0.5-3 mcg/kg/min IV; rates >4 mcg/kg/min may lead to cyanide toxicity

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic and atrial fibrillation or flutter

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, nitroprusside levels may increase and can cause cyanide toxicity; sodium nitroprusside has the ability to lower blood pressure and thus should be used only in those patients with mean arterial pressures >70 mm Hg

Analgesics

Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet and prevent exacerbations in tachycardia and hypertension.

Morphine sulfate (Astramorph, Infumorph)

DOC for narcotic analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Like fentanyl, morphine sulfate is easily titrated to desired level of pain control.
Morphine sulfate administered IV may be dosed in a number of ways and is commonly titrated until desired effect obtained.

Dosing

Adult

Initial: 0.1 mg/kg IV/IM/SC
Maintenance: 5-20 mg/70 kg q4h IV/IM/SC

Pediatric

0.1-0.2 mg/kg/dose IV/IM/SC q2-4h prn

Interactions

Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine

Contraindications

Documented hypersensitivity; hypotension; potentially compromised airway where establishing rapid airway control would be difficult

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate

Follow-up

Further Inpatient Care

• Patients require admission when they are unstable or symptomatic, when they have significant comorbid conditions, or when the diagnosis is uncertain.
• Elderly patients or those with preexisting conditions (eg, emphysema, hypertension, congestive heart failure, coronary artery disease, cerebrovascular disease, renal insufficiency) may require stabilization prior to elective surgery.
• Asymptomatic patients with inflammatory abdominal aortic aneurysm (AAA) or AAA in association with distal emboli, pain, or bowel obstruction require emergent repair regardless of aneurysm size.
• The two primary methods of AAA repair are open and endovascular.
• Open AAA repair requires direct access to the aorta through an abdominal incision. The open repair method is well established as definitive, having been in used for over 50 years.
• Endovascular repair first became practical in the 1990s and is now an established alternative to open repair. Endovascular repair of an AAA involves gaining access to the lumen of the abdominal aorta, usually via small incisions over the femoral vessels. An endograft, typically a cloth graft with a stent exoskeleton, is placed within the lumen of the AAA extending distally into the iliac arteries. The graft serves to contain aortic flow and decrease the pressure on the aortic wall, leading to a reduction in AAA size over time and a decrease in the risk of aortic rupture.

Further Outpatient Care

• Close follow-up is required after endovascular repair with serial CT scans performed at 1, 6, and 12 months, and then yearly to ensure that the graft is effective.
• Patients with incidental abdominal aortic aneurysm (AAA) that is less than 3 cm require no further follow-up. If the AAA is 3-4 cm, annual ultrasound imaging should be used to monitor for further dilatation. AAAs 4-4.5 cm should be evaluated by ultrasound every 6 months, and patients with AAAs greater that 4.5 cm in diameter should be referred to a vascular surgeon.

Transfer

• Surgical repair should be performed as expediently as possible by an experienced surgeon.
• Transfer of an unstable patient with AAA should only occur if the sending facility is incapable of operative care. Personnel skilled at resuscitation should accompany the transfer.
• Consideration can be given to transfer stable asymptomatic patients after appropriate imaging studies have excluded rupture, expansion, or leak.

Prognosis

• The prognosis is guarded in patients who suffer rupture prehospital. More than 50% do not survive to the ED; of those who do, survival rate drops by about 1% per minute. However, survival rate is good in the subset of patients who are not in severe shock and who receive timely, expert surgical intervention.

Patient Education

• For excellent patient education resources, visit eMedicine's Circulatory Problems Center and Cholesterol Center. Also, see eMedicine's patient education articles Aortic Aneurysm, High Cholesterol, and Cholesterol FAQs.

Miscellaneous

Medicolegal Pitfalls

• Patients who complain of back, flank, groin, or abdominal pain but have stable vital signs and do not appear ill present diagnostic challenges. They may be sent home or kept for extended periods in the ED while waiting for diagnostic testing for suspected ureterolithiasis or other benign abdominal conditions. If AAA ruptures and shock ensues, morbidity and mortality increase dramatically. Emergency physicians have been held liable for failure to diagnose AAA and obtain appropriate consultation in these situations. A high index of suspicion is necessary to avoid this medical-legal pitfall.

Multimedia

Media file 1: Radiograph shows calcification of the abdominal aorta. The left wall is clearly depicted and appears aneurysmal; however, the right wall overlies the spine.

Media file 2: The lateral view clearly shows calcification of both walls. Abdominal aortic aneurysm can be diagnosed with certainty.

Media file 3: CT demonstrates an abdominal aortic aneurysm. The aneurysm was noted during workup for back pain, and CT was ordered after the abdominal aortic aneurysm was identified on radiographs. No evidence of rupture is seen (same patient as in Media file 2).

Media file 4: Arteriogram demonstrates an infrarenal abdominal aortic aneurysm. This arteriogram was obtained in preparation of an endovascular repair of the aneurysm (same patient as in Media file 2).

Media file 5: Lateral arteriogram demonstrates an infrarenal abdominal aortic aneurysm. Demonstration of the superior mesenteric artery, inferior mesenteric artery, and celiac artery on the lateral arteriogram in important to completely evaluate the extent of the aneurysm.

Media file 6: Arteriogram after successful endovascular repair of an abdominal aortic aneurysm.

Media file 7: Ultrasonogram of a patient with an abdominal aortic aneurysm. This aneurysm was best visualized on a transverse or axial image. This patient underwent a conventional abdominal aortic aneurysm repair.

Media file 8: MRI of a 77-year-old man with leg pain believed to be secondary to degenerative disk disease. During evaluation, an abdominal aortic aneurysm was discovered.

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Keywords

abdominal aneurysm, abdominal aortic aneurysm, AAA, mycotic aneurysm, abscess formation, atherosclerosis, smoking, chronic obstructive pulmonary disease, COPD, hypertension, syncope, shock, cyanosis, sudden cardiovascular collapse, peripheral atherosclerotic vascular disease, Marfan syndrome, Ehlers-Danlos syndrome, collagen vascular diseases, mycotic aneurysm, claudication, pulsatile abdominal mass, abdominal bruit, aortic rupture

Contributor Information and Disclosures

Author

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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