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AUTHOR INFORMATION |
Section 1 of 11  |
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
eMedicine Journal, January 25 2002, Volume 3, Number
1
|
INTRODUCTION |
Section 2 of 11  |
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.
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
- Chest pain is the most common presenting complaint in patients with an
aortic dissection. Consider thoracic aortic dissection in the differential
diagnosis of all patients presenting with chest pain.
- 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:
- 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.
- Iatrogenic causes (eg, cardiac catheterization)
|
DIFFERENTIALS |
Section 4 of 11  |
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
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:
- Chest x-ray (CXR): This study is abnormal in 80% of patients and is more
commonly abnormal in ascending aortic dissections (see Picture
1).
- 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.
- 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  |
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  |
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  |
Further Inpatient Care:
- Patients with symptomatic dissection should undergo immediate repair,
especially if it is leaking or expanding
- 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  |
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  |
|
BIBLIOGRAPHY |
Section 11 of 11
|
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Evaluation of Suspected Aortic Dissection. N Engl J Med 1993; 328(1): 35-43[Medline].
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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.
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