eMedicine Specialties > Emergency Medicine > Cardiovascular

Aneurysm, Abdominal: Treatment & Medication

Author: Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Contributor Information and Disclosures

Updated: Sep 8, 2009

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.

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

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

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

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.

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

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

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

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.

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

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

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

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.

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

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

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

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.

Adult

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

Pediatric

Administer as in adults

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

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.

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

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

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

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

More on Aneurysm, Abdominal

Overview: Aneurysm, Abdominal
Differential Diagnoses & Workup: Aneurysm, Abdominal
Treatment & Medication: Aneurysm, Abdominal
Follow-up: Aneurysm, Abdominal
Multimedia: Aneurysm, Abdominal
References

References

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Further Reading

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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