eMedicine World Medical Library
This Page is Brought to You by eResidency.net
 
(advertisement)

Dissection, Aortic

Home | Search | Contents | A-Z Index | Tools | Updates | Medline | Cover | Dictionary | GetCME | Rate this topic | Help
 eMedicine Journal > Emergency Medicine > Cardiovascular > Dissection, Aortic
 Author Information | Introduction | Clinical | Differentials | Workup | Treatment | Medication | Follow-up | Miscellaneous | Pictures | Bibliography
Click here to take a CME test We are offering CME for this topic. Click on the GetCME button to take CME (Your first test is Free!) Click here to win a PDA

AUTHOR INFORMATION Section 1 of 11    Click here to go to the top of this page Click here to go to the next section in this topic

Authored by John Wiesenfarth, MD, MS, FACEP, FAAEM, Assistant Chief, Department of Emergency Medicine, Kaiser-Permanente Hospital Sacramento/Roseville; Assistant Professor, Division of Emergency Medicine, University of California at Davis

John Wiesenfarth, MD, MS, FACEP, FAAEM, is a member of the following medical societies: American Medical Association, and Wilderness Medical Society

Edited by Joseph J Sachter, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Barry Brenner, MD, PhD, Chairman, Department of Emergency of Medicine, Professor, Departments of Emergency Medicine and Internal Medicine, University of Arkansas for Medical Sciences

Author's Email: John Wiesenfarth, MD, MS, FACEP, FAAEM Click here to view conflict-of-interest information on the author of this topic
Editor's Email: Joseph J Sachter, MD, FACEP

eMedicine Journal, January 25 2002, Volume 3, Number 1
INTRODUCTION Section 2 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

Background: Much has been written on the subject of aortic dissections, from the first well-documented case of aortic dissection, when King George II of England died while straining on the commode, to the first successful operative repairs by DeBakey in 1955, to modern techniques of diagnosing and repairing thoracic aortic dissections.

Aortic dissection is the most common catastrophe of the aorta, 2-3 times more common than rupture of the abdominal aorta. When left untreated, about 33% of patients die within the first 24 hours, and 50% die within 48 hours. The 2-week mortality rate approaches 75% in patients with undiagnosed ascending aortic dissection.

Dissections of the thoracic aorta have been classified anatomically by 2 different methods. The more commonly used system is the Stanford classification, which is based on involvement of the ascending aorta and simplifies the DeBakey classification.

The Stanford classification divides dissections into 2 types, type A and type B.

  • Type A involves the ascending aorta (DeBakey types I and II); type B does not (DeBakey type III).

  • This system also helps delineate treatment. Usually, type A dissections require surgery, while type B dissections may be managed medically under most conditions.
  • The DeBakey classification divides the dissections into 3 types.

  • Type I involves the ascending aorta, aortic arch, and descending aorta.

  • Type II is confined to the ascending aorta.

  • Type III is confined to the descending aorta distal to the left subclavian artery.

  • Type III dissections are further divided into IIIa and IIIb.

  • Type IIIa refers to dissections that originate distal to the left subclavian artery but extend both proximally and distally, most above the diaphragm.

  • Type IIIb refers to dissections that originate distal to the left subclavian artery, extend only distally and may extend below the diaphragm.
  • Thoracic aortic dissections should be distinguished from aneurysms (localized abnormal dilation of the aorta) and transections, which are caused most commonly by high-energy trauma.

    Pathophysiology: The essential feature of aortic dissection is a tear in the intimal layer, followed by formation and propagation of a subintimal hematoma. The dissecting hematoma commonly occupies about half and occasionally the entire circumference of the aorta. This produces a false lumen or double-barreled aorta, which can reduce blood flow to the major arteries arising from the aorta. If the dissection involves the pericardial space, cardiac tamponade may result.

    Cystic medial necrosis

    The normal aorta contains collagen, elastin, and smooth muscle cells that contribute the intima, media, and adventitia to the layers of the aorta. With aging, degenerative changes lead to breakdown of the collagen, elastin, and smooth muscle and an increase in basophilic ground substance. This condition is termed cystic medial necrosis. Atherosclerosis that causes occlusion of the vasa vasorum also produces this disorder. Cystic medial necrosis is the hallmark histologic change associated with dissection in those with Marfan syndrome.

    Cystic medial necrosis was first described by Erdheim in 1929. Sources disagree over the accuracy of this term in the elderly, since the true histopathologic changes are neither cystic nor necrotic. Researchers have used the term cystic medial degeneration.

    Early on, cystic medial necrosis described an accumulation of basophilic ground substance in the media with the formation of cystlike pools. The media in these focal areas may show loss of cells (ie, necrosis). This term still is used commonly to describe the histopathologic changes that occur.

    Dissection sites

    The most common site of dissection is the first few centimeters of the ascending aorta, with 90% occurring within 10 centimeters of the aortic valve. The second most common site is just distal to the left subclavian artery. Between 5% and 10% of dissections do not have an obvious intimal tear. These often are attributed to rupture of the aortic vasa vasorum as first described by Krukenberg in 1920.

    Diseases leading to aortic dissection

    Certain diseases, such as Marfan, Ehlers-Danlos, and other connective tissue diseases, affect the media of the aorta and make it prone to dissection. Pulsatile flow and high blood pressure contribute to propagation of the dissection.

    Diseases that weaken the aortic wall predispose the patient to aortic dissection. Shearing forces separate the layers in the media of the aorta. Intimal rupture occurs at points of fixation along the aorta where hydraulic stress is maximal.

    Frequency:

    • In the US: The true incidence of dissection is difficult to estimate. Most estimates are based on autopsy studies. One population-based study estimated the incidence at roughly 6 new aneurysms per 100,000 person years. Evidence of dissection is found in 1-3% of all autopsies.

    Mortality/Morbidity:

    • From 1-2% die per hour for the first 24-48 hours.
    • Aortopathy may be present in heritable diseases such as Marfan syndrome, Ehlers-Danlos syndrome, annuloaortic ectasia, familial aortic dissections, adult polycystic kidney disease, Turner syndrome, Noonan syndrome, osteogenesis imperfecta, bicuspid aortic valve, coarctation of the aorta, and connective-tissue disorders. It is also seen in heritable metabolic disorders such as homocystinuria and familial hypercholesterolemia.
    • Incidence is increased in pregnancy and syphilis. Thoracic aortic dissection also is associated with crack cocaine use and iatrogenic causes, such as cardiac catheterization.

    Race: Aortic dissection is more common in blacks than in whites and less common in Asians than in whites.

    Sex: Male-to-female ratio is 3:1.

    Age: Approximately 75% of dissections occur in those aged 40-70 years, with a peak in the range of 50-65 years.
    CLINICAL Section 3 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    History: ". . . spontaneous tear of the arterial coats is associated with atrocious pain, with symptoms, indeed, in the case of the aorta of angina pectoris and many instances have been mistaken for it." - William Osler, 1910

      • The pain usually is described as "ripping" or "tearing."
      • This description is not universal, and some patients present with only mild pain, often mistaken for musculoskeletal conditions, located in the thorax, groin, or back.
      • The pain of aortic dissection typically is distinguished from the pain of acute myocardial infarction (AMI) by its abrupt onset.
      • Aortic dissection should be considered strongly in all patients complaining of acute, sudden, and severe chest pain that is maximal at onset.
      • The truly sudden onset of chest pain is seen in few other conditions. Spiegel and Wassermann found that acute stretching of the aortic wall produces pain.
      • The nervi vascularis, bundles of nerve fibers found in the aortic adventitia, are involved in the production of pain.
    • Assess the following characteristics of pain:
      • Severity
      • Character
      • Timing, including rate of onset, duration, and frequency of episodes
      • Migration, including aggravating or alleviating factors and associated symptoms
    • The description of the pain may indicate where the dissection arises.
      • Anterior chest pain and chest pain that mimics AMI usually are associated with anterior arch or aortic root dissection. This is caused by the dissection interrupting flow to the coronary arteries, resulting in myocardial ischemia.

      • Pain that is described in the neck or jaw indicates that the dissection involves the aortic arch and extends into the great vessels of the arch.

      • Tearing or ripping pain that is felt in the intrascapular area may indicate that the dissection involves the descending aorta. The pain typically changes as the dissection evolves.
    • Aortic dissection is painless in about 10% of patients. Painless dissection is more common in those with neurologic complications from the dissection and those with Marfan syndrome.

    • Presenting signs and symptoms in acute thoracic aortic dissection include the following:
      • Anterior chest pain - Ascending aortic dissection

      • Neck or jaw pain - Aortic arch dissection

      • Interscapular tearing or ripping pain - Descending aortic dissection

      • Chest pain

      • Myocardial infarction
      • Neurologic complaints

      • Syncope

      • Cerebrovascular accident (CVA) symptoms

      • Altered mental status

      • Limb paresthesias, pain, or weakness
      • Hemiparesis or hemiplegia

      • Horner syndrome

      • Dyspnea

      • Dysphagia

      • Orthopnea

      • Anxiety and premonitions of death
      • Flank pain if renal artery is involved
      • Dyspnea and hemoptysis if dissection ruptures into the pleura

    Physical:

    • Blood pressure may increase or decrease.
      • Hypertension may result from a catecholamine surge or underlying essential hypertension.
      • Hypotension is an ominous finding and may be the result of excessive vagal tone, cardiac tamponade, or hypovolemia from rupture of the dissection.
    • Neurologic deficits are a presenting sign in up to 20% of cases.
      • The most common neurologic findings are syncope and altered mental status.
      • Syncope is part of the early course of aortic dissection in about 5% of patients and may be the result of increased vagal tone, hypovolemia, or dysrhythmia.
      • Other causes of syncope or altered mental status include CVAs from compromised blood flow to the brain or spinal cord and ischemia from interruption of blood flow to the spinal arteries.
      • Peripheral nerve ischemia can present with numbness and tingling in the extremities.
      • Hoarseness from recurrent laryngeal nerve compression also has been described.
      • Horner syndrome is caused by interruption in the cervical sympathetic ganglia and presents with ptosis, miosis, and anhidrosis.
      • Superior vena cava syndrome, caused by compression of the superior vena cava from a large distorted aorta, may occur.
    • Dyspnea may be caused by congestive heart failure or tracheal or bronchial compression.
    • Dysphagia from compression of the esophagus may be present.
    • Findings suggestive of cardiac tamponade, such as muffled heart sounds, hypotension, pulsus paradoxus, jugular venous distension, and Kussmaul sign, must be recognized quickly.
    • Other diagnostic clues include a new diastolic murmur, asymmetrical pulses, and asymmetrical blood pressure measurements. Pay careful attention to carotid, brachial, and femoral pulses on initial exam and look for progression of bruits or development of bruits on reexamination.
    • Physical findings of a hemothorax may be found if the dissection ruptures into the pleura.

    Causes: Aortic dissection is more common in patients with hypertension, connective-tissue disorders, congenital aortic stenosis or bicuspid aortic valve, and in those with first-degree relatives with history of thoracic dissections. These diseases affect the media of the aorta and predispose it to dissection.

    • Aortopathy due to heritable diseases

      • Marfan syndrome

      • Ehlers-Danlos syndrome

      • Annuloaortic ectasia

      • Familial aortic dissections

      • Adult polycystic kidney disease

      • Turner syndrome

      • Noonan syndrome

      • Osteogenesis imperfecta

      • Bicuspid aortic valve

      • Coarctation of the aorta

      • Connective-tissue disorders

      • Metabolic disorders (eg, homocystinuria, familial hypercholesterolemia)
    • Hypertension or pulsatile blood flow can propagate the dissection.
    • Pregnancy
    • Syphilis
    • Crack cocaine use
    • Iatrogenic causes (eg, cardiac catheterization)
    DIFFERENTIALS Section 4 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    Aortic Regurgitation
    Aortic Stenosis
    Back Pain, Mechanical
    Gastroenteritis
    Hernias
    Hypertensive Emergencies
    Myocardial Infarction
    Myocarditis
    Myopathies
    Pancreatitis
    Pericarditis and Cardiac Tamponade
    Peripheral Vascular Injuries
    Pleural Effusion
    Pulmonary Embolism
    Shock, Cardiogenic
    Shock, Hemorrhagic
    Shock, Hypovolemic
    Thoracic Outlet Syndrome


    Other Problems to be Considered:

    Musculoskeletal chest pain

    WORKUP Section 5 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    Lab Studies:

      • Usually, the diagnosis is made before the blood work is returned; however, leukocytosis may be present.
      • BUN and creatinine are elevated if the dissection involves the renal arteries.
      • Creatine phosphokinase (CPK) is elevated if the dissection has caused myocardial ischemia.
      • Decreases in the hemoglobin and hematocrit are ominous findings suggesting the dissection either is leaking or has ruptured.
      • Hematuria, oliguria, and even anuria (<50 mL/d) may occur if the dissection involves the renal arteries.

    Imaging Studies:

      • Findings suggesting hemothorax may be found if the dissection ruptures into the pleura (see Picture 2).
      • Widened mediastinum: Radiographic findings in acute thoracic dissection include a widened mediastinum in many cases (see Picture 3).

        • Recently, the International Registry of Acute Aortic Dissection published data on 464 patients that showed only 25% presenting with this finding.

        • A widened mediastinum is sometimes difficult to identify on a portable anteroposterior (AP) CXR. If the patient is hemodynamically stable and cooperative, an AP film can be obtained at bedside.

        • Look for a mediastinal width >8 cm on AP CXR.

        • A tortuous aorta, common in hypertensive patients, may be hard to distinguish from a widened mediastinum. If in doubt, a good posterior-anterior CXR is recommended.

        • The differential diagnosis of a widened mediastinum includes tumor, adenopathy, lymphoma, and enlarged thyroid.
      • Abnormal (ie, blunted) aortic knob was observed in 66% of patients in one study.
      • Ring sign (displacement of the aorta >5 mm past the calcified aortic intima) is considered a very specific radiographic sign.
      • Other radiologic abnormalities seen on CXR include the following:

        • Left apical cap

        • Tracheal deviation

        • Depression of left main stem bronchus

        • Esophageal deviation

        • Loss of the paratracheal stripe
      • One study concluded that it was not any one sign that determined the overall diagnosis, rather a combination of all findings that led to suspicion of dissection.
    • Angiography: Still considered by some as the criterion standard test for aortic dissection, it is being replaced by newer imaging modalities.
      • Angiography accurately diagnoses aortic dissection in over 95% of patients (see Picture 4) and aids the surgeon in planning the repair operation, as blood vessels of the arch can be assessed easily. Benefits include visualization of the true and false lumens, intimal flap, aortic regurgitation, and coronary arteries.
      • Drawbacks include the following:

        • The procedure is invasive.

        • The patient must be transported to the radiology department, leaving the ED.

        • The use of contrast media may be harmful to patients who have renal insufficiency or an allergy to iodine.

        • Misdiagnoses can occur if the false channel is thrombosed. In this instance, the false lumen and intimal flap may not be visualized. Possible simultaneous opacification of the true and false lumens may make it difficult to discern whether a dissection is present.
    • Computed tomography (CT): With the advent of helical CT with multiplanar and 3D reconstruction, CT is quickly replacing the angiogram as the criterion standard in many institutions.
      • Prospective studies have shown a sensitivity of 83-94% with a specificity of 87-100%.

      • Spiral CT is associated with a higher rate of detection and better resolution than incremental CT. High-quality 2D and 3D reconstructions are possible with spiral CT, which greatly adds to the usefulness of this imaging modality.

      • More importantly, imaging information, including the type of lesion, location of the pathologic lesion, and extent of the disease, can be assessed quickly and help the surgeon plan the operation.

      • This information helps determine if hypothermic circulatory arrest is necessary for surgery; this procedure increases the complexity, length, morbidity, and mortality associated with surgery.

      • Helical CT images usually are acquired within 1-2 breath holds.
      • Drawbacks include the following:

        • Transportation of a patient in potentially unstable condition from the ED, even for the relatively short time needed for this procedure, places the patient at risk.

        • The use of contrast material may harm a patient who has impaired renal function or an allergy to contrast media.

        • CT scan provides no information on aortic regurgitation.
    • Echocardiography
      • With its increasing acceptance and use in the ED, ultrasound is becoming a very valuable diagnostic aid, although transthoracic echocardiography (TTE) has a much lower sensitivity (80%) and lower specificity (90%) than angiography.

      • TTE is most useful in ascending aortic dissections, especially those closest to the aortic root and within a few centimeters of the aortic valve. Sensitivity is highest in this location.

      • ECG also is useful in diagnosing cardiac tamponade and aortic regurgitation.

      • Benefits include its rapid, simple bedside use in the ED and its noninvasive nature.

      • Drawbacks include the lack of sensitivity and specificity, especially with arch and descending aortic dissections, and dependence on operator experience.
      • Transesophageal echocardiography (TEE) has greater sensitivity and specificity than transthoracic echocardiography (in the range of 97-99% and 97-100%, respectively).

        • Advantages include its quick and easy bedside use in the ED, which makes it ideal for patients in unstable condition.

        • TEE detects involvement of the coronary arteries, aortic insufficiency, and cardiac tamponade.

        • It is a relatively quick study to perform and relatively noninvasive.

        • The main drawback of TEE is its strong dependence on operator experience.

        • Other drawbacks are that false positives can occur from reverberations in the ascending aorta and that the upper ascending aorta and arch may not be visualized well, leading to false negatives.

        • TEE cannot be performed in patients with esophageal varicosities or stenosis. If the study is negative and clinical suspicion remains high, a second diagnostic test is recommended.
    • Magnetic resonance imaging (MRI)
      • MRI has over 90% sensitivity and greater than 95% specificity. MRI shows the site of intimal tear, type and extent of dissection, and presence of aortic insufficiency.

      • Other benefits are that MRI requires no contrast medium and no ionizing radiation.
      • Drawbacks include the following:

        • MRI is not readily available at most institutions, requiring transportation of patients in unstable condition away from the ED.

        • MRI requires much more time to acquire images than CT.

        • Patients with permanent pacemakers cannot undergo MRI. Most patients with prosthetic heart valves or coronary stents can safely have an MRI.

    Other Tests:

    • ECG: All patients with suspected thoracic aortic dissection should have an ECG.
      • In acute thoracic dissection, ECG can mimic the changes seen in acute cardiac ischemia. In the presence of chest pain, these signs can make distinguishing dissection from AMI very difficult (see Picture 5). Keep this in mind when administering thrombolytics to patients with chest pain.
      • ST elevation can be seen in Stanford type A dissections, as the dissection interrupts blood flow to the coronary arteries.

        • The incidence of abnormal ECG findings is greater in Stanford type A dissections than in other types of dissections.

        • In one study, 8% of patients with type A dissections had ST elevation, while no patients with type B dissections had ST elevation.

        • More commonly, the ECG abnormality is ST depression.
    TREATMENT Section 6 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    Prehospital Care:

    • Assure adequate breathing, maintain oxygenation, treat shock, and obtain useful historic information.
    • Establishing the diagnosis in the field is usually difficult or impossible, but certain salient features of aortic dissection may be observed. It is life threatening if not quickly recognized and treated.
    • Radio communication with the receiving hospital permits the medical control physician to direct care and select a capable destination hospital while permitting the ED to mobilize appropriate resources.
    • In the rare event that the diagnosis can be made based on prehospital information, the physician directing prehospital care should request transport to a facility capable of operative treatment of an aortic dissection.

    Emergency Department Care:

    • The mortality rate of patients with aortic dissection is 1-2% per hour for the first 24-48 hours. Initial therapy should begin when the diagnosis is suspected. This includes 2 large-bore intravenous lines (IVs), oxygen, respiratory monitoring, and monitoring of cardiac rhythm, blood pressure, and urine output.

    • Clinically, the physician should reassess the patient frequently for hemodynamic compromise, mental status changes, neurologic or peripheral vascular changes, and development or progression of carotid, brachial, and femoral bruits.
    • Urgent surgical intervention is required in type A dissections.
      • The area of the aorta with the intimal tear usually is resected and replaced with a Dacron graft.

      • The operative mortality rate is usually less than 10% and serious complications are rare with ascending aortic dissections.

      • The development of more impermeable grafts, such as woven Dacron, collagen-impregnated Hemashield (Meadox Medicals, Oakland, NJ), aortic grafts, and gel-coated Carbo-Seal Ascending Aortic Prothesis (Sulzer Carbomedics, Austin, TX) has greatly enhanced the surgical repair of thoracic aortic dissections.

      • With the introduction of profound hypothermic circulatory arrest and retrograde cerebral perfusion, the morbidity and mortality rates associated with this highly invasive surgery have decreased.

      • Dissections involving the arch are more complicated that those involving only the ascending aorta, as the innominate, carotid, and subclavian vessels branch from the arch. Deep hypothermic arrest usually is required. If the arrest time is less than 45 minutes, the incidence of central nervous system complications is less than 10%.
    • Retrograde cerebral perfusion may increase the protection of the central nervous system during the arrest period.
      • Mortality rate of aortic arch dissections is about 10-15%, with significant neurologic complications occurring in another 10%.

      • The mortality rate is influenced by the patient's clinical condition.
    • The definitive treatment for type B dissections is less clear.
      • Uncomplicated distal dissections may be treated medically to control blood pressure.

      • Distal dissections treated medically have the same or lower mortality rate as those treated surgically.

      • Surgery is reserved for distal dissections that are leaking, ruptured, or compromising blood flow to a vital organ.

      • Acute distal dissections in patients with Marfan syndrome usually are treated surgically.

      • Inability to control hypertension with medication is also an indication for surgery in those with a distal thoracic aortic dissection.

      • Patients with a distal dissection are usually hypertensive, emphysematous, or older.

      • Long-term medical therapy involves a beta-adrenergic blocker combined with other antihypertensive medications. Avoid antihypertensives (eg, hydralazine, minoxidil) that produce a hyperdynamic response that would increase dP/dT (ie, alter the duration of P or T waves).

      • Survivors of surgical therapy also should receive beta-adrenergic blockers.
    • Definitive treatment involves segmental resection of the dissection with interposition of a synthetic graft.
      • When thoracic dissections are associated with aortic valvular disease, replace the defective valve.

      • With combined reconstruction-valve replacement, the operative mortality rate is approximately 5% with a late mortality rate of less than 10%.

      • Operative repair of the transverse aortic arch is technically difficult, with an operative mortality rate of 10% despite induction of hypothermic cardiocirculatory arrest.

      • Repair of the descending aorta is associated with a higher incidence of paraplegia than repair of other types of dissections because of interruption of segmental blood supply to the spinal cord.
      • Operative mortality rate is approximately 5%.

    Consultations:

    • Once a thoracic dissection is suspected, consult a thoracic surgeon.
      • Since many patients with this disorder have concomitant medical illness, consult the patient's primary care physician to expedite preoperative preparation.
      • Early consultation is encouraged when ordering further imaging studies if the patient requires rapid operative intervention.
    • Consult a radiologist prior to obtaining aortography.
    MEDICATION Section 7 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    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.

    Whether systolic hypertension or pain is present, beta-blockers are used to reduce arterial dP/dt.

    To prevent exacerbations of tachycardia and hypertension, treat patient with IV morphine sulfate. This reduces the force of cardiac contraction and the rate of rise of the aortic pressure (dP/dT). It then retards the propagation of the dissection and delays rupture.

    Drug Category: Antihypertensives -- These agents are 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. Sublingual nifedipine successfully treats refractory hypertension associated with aortic dissection.
    Drug Name
    Esmolol (Brevibloc) -- Ultra-short-acting beta 2-blocker, particularly useful in patients with labile arterial pressure, especially if surgery is planned, because it 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 of bronchospasm from beta-blockade. Elimination half-life is 9 min.
    Adult Dose Loading dose infusion: 250-500 mcg/kg/min 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 Dose Not established
    Contraindications Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock, AV conduction abnormalities
    Interactions Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; sparfloxacin, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives may increase cardiotoxicity; digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents may increase toxicity
    Pregnancy C - Safety for use during pregnancy has not been established.
    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 withdrawn abruptly; withdraw drug slowly and monitor patient closely
    Drug Name
    Labetalol (Normodyne, Trandate) -- Blocks alpha-, beta 1-, and beta 2-adrenergic receptor sites, decreasing BP.
    Adult Dose Initial dose: 20 mg (0.25 mg/kg for 80-kg patient) IV over 2 min; follow with 20-80 mg q10-15min until BP controlled
    Maintenance dose: 2 mg/min continuous infusion; titrate up to 5-20 mg/min; not to exceed a total dose of 300 mg
    Pediatric Dose Not established
    Contraindications Documented hypersensitivity; cardiogenic shock, AV block, uncompensated CHF, pulmonary edema, bradycardia; reactive airway disease
    Interactions Decreases effects of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia associated with nitroglycerin use without interfering with hypotensive effects; cimetidine may increase blood levels; glutethimide may decrease effects by inducing microsomal enzymes
    Pregnancy C - Safety for use during pregnancy has not been established.
    Precautions Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction; in elderly patients, lower response rate and higher incidence of toxicity may be observed
    Drug Name
    Propranolol (Inderal, Betachron E-R) -- Class II antiarrhythmic nonselective beta-adrenergic receptor blocker. Has membrane-stabilizing activity and decreases automaticity of contractions. Not suitable for emergency treatment of hypertension. Do not administer IV in hypertensive emergencies.
    Adult Dose 40-80 mg PO bid initially; increase to usual range of 160-320 mg/d prn; up to 640 mg/d may be required
    Pediatric Dose 0.5 mg/kg/d PO divided bid/qid; increase gradually q3-7d; usual dosage range is 2-4 mg/kg/d divided bid; not to exceed 16 mg/kg/d
    Contraindications Documented hypersensitivity; uncompensated CHF, bradycardia, cardiogenic shock, and AV conduction abnormalities
    Interactions Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; may increase toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines
    Pregnancy B - Usually safe but benefits must outweigh the risks.
    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
    Drug Name
    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 Dose 100 mg/d qd or divided bid/tid initially; increase at 1-wk intervals prn; not to exceed 450 mg/d prn
    Pediatric Dose Not established
    Contraindications Documented hypersensitivity; uncompensated CHF, cardiogenic shock, bradycardia, and AV conduction abnormalities
    Interactions Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effects; sparfloxacin, phenothiazines, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives may increase toxicity; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
    Pregnancy B - Usually safe but benefits must outweigh the risks.
    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 drug slowly; during IV administration, carefully monitor BP, heart rate, and ECG
    Drug Name
    Nitroprusside (Nitropress) -- Causes peripheral vasodilation by direct action on venous and arteriolar smooth muscle, thus reducing peripheral resistance. Commonly used IV because of rapid onset and short duration of action. Easily titratable to reach desired effect. Light sensitive; both bottle and tubing should be wrapped in aluminum foil. Prior to initiating nitroprusside, administer beta-blocker to counteract physiologic response of reflex tachycardia that occurs when nitroprusside used alone. This physiologic response will increase shear forces against aortic wall, thus increasing dP/dT. Objective is to keep heart rate at 60-80 bpm.
    Adult Dose 0.5-3 mcg/kg/min; rates >4 mcg/kg/min may lead to cyanide toxicity
    Pediatric Dose Administer as in adults
    Contraindications Documented hypersensitivity; subaortic stenosis, idiopathic hypertrophic; atrial fibrillation or flutter
    Interactions None reported
    Pregnancy C - Safety for use during pregnancy has not been established.
    Precautions Caution in increased intracranial pressure, hepatic failure, severe renal impairment, and hypothyroidism; in renal or hepatic insufficiency, levels may increase and can cause cyanide toxicity; sodium nitroprusside has ability to lower BP and thus should be used only in patients with mean arterial pressures >70 mm Hg
    Drug Category: Analgesics -- Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and prevent exacerbations of tachycardia and hypertension.
    Drug Name
    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 easily titrated to desired level of pain control. If administered IV, may be dosed in a number of ways; commonly titrated until desired effect obtained.
    Adult Dose Initial dose: 0.1 mg/kg IV/IM/SC
    Maintenance dose: 5-20 mg/70 kg q4h IV/IM/SC
    Pediatric Dose 0.1-0.2 mg/kg q2-4h prn
    Contraindications Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult
    Interactions Phenothiazines may antagonize analgesic effects; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects
    Pregnancy C - Safety for use during pregnancy has not been established.
    Precautions Avoid 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 Section 8 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    Further Inpatient Care:

    • Symptomatic patients require admission to a center experienced in cardiopulmonary bypass and operative care.
    • Completely asymptomatic patients may have their repair performed electively but may require admission to expedite their evaluation or for preoperative stabilization of their condition.
    • Patients with chest pain should undergo serial ECGs and CPK determinations if AMI is indicated.

    Further Outpatient Care:

    • Follow-up examinations with radiologic studies are recommended at 3-month intervals for the first year and every 6 months for the next 2 years.
    • After this, follow up annually.

    Transfer:

    • Symptomatic patients require care at a facility equipped to perform cardiopulmonary bypass with aortic and/or valvular repair.
    • Contact the receiving physician as soon as possible to transfer patients before their condition deteriorates.
    • Early airway management is indicated in the presence of hemoptysis or stridor.
    • If coronary insufficiency is suspected, nitrates may be used, but therapy with thrombolytic agents and aspirin should be avoided.
    • Patients should be monitored and accompanied by personnel capable of resuscitation.
    • If a prolonged ground transport time is anticipated, consider air transport.

    Prognosis:

    • On the basis of his experience, Crawford has stated that "no patient should be considered cured of the disease."
    • The 5-year survival rate is about 75% whether the patient is treated medically or surgically.
    • The 10-year survival rate is between 40% and 69% for both surgically and medically treated dissections.
    • In the pretreatment era, the 1-year survival rate was 5-10%.
    • Reoperation may be necessary for late complications.
    MISCELLANEOUS Section 9 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    Medical/Legal Pitfalls:

    • Failure to diagnose the disease in patients presenting with chest pain
    • Failure to avoid using thrombolytics in the patient presenting with chest pain and ECG changes
      • Multiple case reports describe patients who received thrombolytics and were found later to have a dissection. The diagnosis of aortic dissection can be very subtle.
      • The diagnosis depends on clinical suspicion, with contributory history, physical exam, and imaging studies.
      • Obtaining a chest radiograph prior to thrombolytics is considered prudent.
      • Checking blood pressures in both arms and listening for carotid bruits also can help diagnose aortic dissection prior to thrombolytics. The entire clinical picture must be taken into account.
    PICTURES Section 10 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic

    Caption: Picture 1. X-ray of a patient with aortic dissection (Courtesy of Dr. K. London, University of California at Davis Medical Center)
    Click to see larger picture Click to see detailView Full Size Image
    Click to ZoomeMedicine Zoom View (Interactive!)
    Picture Type: X-RAY
    Caption: Picture 2. X-ray of a patient with aortic dissection presenting with hemothorax
    Click to see larger picture Click to see detailView Full Size Image
    Click to ZoomeMedicine Zoom View (Interactive!)
    Picture Type: X-RAY
    Caption: Picture 3. X-ray demonstrating widened mediastinum in a patient with aortic dissection
    Click to see larger picture Click to see detailView Full Size Image
    Click to ZoomeMedicine Zoom View (Interactive!)
    Picture Type: X-RAY
    Caption: Picture 4. Angiogram demonstrating dissection of the aorta (See Picture 3 for the chest x-ray of this patient.)
    Click to see larger picture Click to see detailView Full Size Image
    Click to ZoomeMedicine Zoom View (Interactive!)
    Picture Type: Photo
    Caption: Picture 5. Electrocardiogram of a patient presenting to the ED with chest pain who has been diagnosed with aortic dissection
    Click to see larger picture Click to see detailView Full Size Image
    Click to ZoomeMedicine Zoom View (Interactive!)
    Picture Type: ECG
    BIBLIOGRAPHY Section 11 of 11   Click here to go to the previous section in this topic Click here to go to the top of this page

    • Bickerstaff L, Pairolera P, Hollier L: Thoracic Aortic Aneurysm: A Population Based Study. Surgery 1982; 92: 1103-1108[Medline].
    • Chen K, Varon J, Wenker OC, et al: Acute thoracic aortic dissection: the basics. J Emerg Med 1997 Nov-Dec; 15(6): 859-67[Medline].
    • Cigarroa J, Isselbacher E, DeSanctis R: Diagnostic Imaging in the Evaluation of Suspected Aortic Dissection. N Engl J Med 1993; 328(1): 35-43[Medline].
    • DeBakey M, Cooley D, Creech O: Surgical Considerations of Dissecting Aneurysm of the Aorta. Ann Surg 1955; 142: 586-612.
    • DeBakey M, Cooley D: Successful Resection of Aneurysm of Thoracic Aorta and Replacement by Graft. JAMA 1953; 152: 673-676.
    • DeSanctis R, Doroghazi R, Austen G: Aortic Dissection. N Engl J Med 1987; 317(17): 1060-66[Medline].
    • Erbel R, Engberding R, Roelandt J: Echocardiography in the Diagnosis of Aortic Dissection. Lancet 1989; 1: 457-461[Medline].
    • Erdheim J: Medionecrosis Aorte Idiopathica Apitca. Virchows Arch Pathol Anat 1930; 276: 187-229.
    • Hagan PG, Nienaber CA, Isselbacher EM: The International Registry of Acute Aortic Dissection (IRAD): New Insights Into an Old Disease. JAMA 2000; 283: 897-903.[Medline].
    • Jagannath AS, Sos TA, Lockhart SH: Aortic dissection: a statistical analysis of the usefulness of plain chest radiographic findings. - Lockhart SH 1986 Dec; 147(6): 1123-6[Medline].
    • Krukenberg E: Beitrage zur Frage des Aneurysma Dissecans. Beitr Pathol Anat Allerg Pathol 1920; 67: 329-351.
    • Nichols F: Observations Concerning the Body of His Late Majesty. Philos Trans Lond 1762; 52: 265-275.
    • Pansini S, Garliardotto P, Pompei E: Early and Late Risk Factors in Surgical Treatment of Acute Type A Aortic Dissection. Ann Thorac Surg 1998; 66: 779-784[Medline].
    • Ponraj P, Pepper J: Aortic dissection. Br J Clin Pract 1992 Summer; 46(2): 127-31[Medline].
    • Prokop EK, Palmer RF, Wheat MW Jr: Hydrodynamic forces in dissecting aneurysms. In-vitro studies in a Tygon model and in dog aortas. Circ Res 1970 Jul; 27(1): 121-7[Medline].
    • Safi H, Miller C, Reardon M: Operation for acute and Chronic Aortic Dissection:Recent Outcome with Regard to Neurologic Deficit and Early Death. Ann Thorac Surg 1998; 66(2): 402-411[Medline].
    • Sarasin F, Gaspoz J, Junod A, et al: Detecting Acute Thoracic Aortic Dissection in the Emergency Department: Time Constraints and the Choice of the Optimal Diagnostic Test. Ann Emerg Med 1996; 28(3): 278-288[Medline].
    • Spiegel EA, Wassreman S: Experimentalstudien uber die Entsehungdes Aortenschmerzes und seine Leitung zum zentralnervensystem. Ztschr F. d. ges. Exper Med 1926; 52: 180-196.
    • Svensson L, Crawford E, Hess K: Experience With 1509 Patients Undergoing Thoracoabdominal Aortic Operations. J Vasc Surg 1993; 17: 357-370[Medline].
    • Wooley C, Sparks E, Boudoulas H: Aortic pain. Prog Cardiovasc Dis 1998; 40(6): 563-589[Medline].

    NOTE:
    Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER
    eMedicine Journal, January 25 2002, Volume 3, Number 1

    Dissection, Aortic excerpt

    Copyright 2002, eMedicine.com, Inc.
     eMedicine Journal > Emergency Medicine > Cardiovascular > Dissection, Aortic
    Home | Search | Contents | A-Z Index | Tools | Updates | Medline | Cover | Dictionary | GetCME | Rate this topic | Help
    Click here to take a CME test We are offering CME for this topic. Click on the GetCME button to take CME (Your first test is Free!) Click here to win a PDA