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  1. 1. 1 1 MAGDI AWAD SASI DISSECTING AORTIC A. Dissection, Aortic 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. The DeBakey classification divides 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. o Type III dissections are further divided into IIIa and IIIb. o Type IIIa refers to dissections that originate distal to the left subclavian artery but extend both proximally and distally, mostly 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. CLASSIFICATION DEBAKEY Type I Ascending aorta extending beyond arch Type II Ascending aorta only Type III a Descending aorta distal to left subclavian (above diaphragm) Type III b Descending aorta distal to LSA extending below diaphragm STANFORD  A – Ascending aorta  B – Not involving Ascending Aorta
  2. 2. 2 2 MAGDI AWAD SASI DISSECTING AORTIC A. Thoracic aortic dissections should be distinguished from aneurysms (ie, localized abnormal dilation of the aorta) and transections, which are caused most commonly by high-energy trauma . Race Aortic dissection is more common in blacks than in whites and less common in Asians than in whites. Sex The male-to-female ratio is 3:1. Age 75% of dissections occur in those aged 40-70 years, with a peak in 50-65 years
  3. 3. 3 3 MAGDI AWAD SASI DISSECTING AORTIC A. 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, which are 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
  4. 4. 4 4 MAGDI AWAD SASI DISSECTING AORTIC A. of the vasa vasorum also produces this disorder. Cystic medial necrosis is the hallmark histologic change associated with dissection in those with Marfan syndrome. Researchers have used the term cystic medial degeneration in elder patients. 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.
  5. 5. 5 5 MAGDI AWAD SASI DISSECTING AORTIC A. Mortality/Morbidity From 1-2% of patients with aortic dissection 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. SYMPTOMS: No one sign or symptom can positively identify acute aortic dissection (AAD). An estimated 38% of acute aortic dissections are missed on initial evaluation There are no validated clinical decision rules to help identify acute aortic dissection (ADD). The diagnosis is best made when there is high clinical suspicion given the overall evaluation of the patient, including the history, physical examination, and supporting tests including ECG, laboratory studies, and radiology. ". . . 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 symptom in patients with an aortic dissection. Consider thoracic aortic dissection in the differential diagnosis of all patients presenting with sudden chest pain. o The pain usually is described as ripping or tearing. o The sudden onset of chest pain has been shown to have a sensitivity of 84%. o 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.
  6. 6. 6 6 MAGDI AWAD SASI DISSECTING AORTIC A. o The pain of aortic dissection typically is abrupt onset. o Aortic dissection should be considered strongly in all patients reporting acute, sudden, and severe chest pain that is maximal at onset. o The nervi vascularis, bundles of nerve fibers found in the aortic adventitia, are involved in the production of pain. The description of the pain may indicate where the dissection arises. o 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. o 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. o 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: o Anterior chest pain - Ascending aortic dissection o Neck or jaw pain - Aortic arch dissection o Interscapular tearing or ripping pain - Descending aortic dissection o Chest pain o Myocardial infarction o Neurologic symptoms Syncope Stroke symptoms Altered mental status Limb paresthesias, pain, or weakness Hemiparesis or hemiplegia Horner syndrome o Dyspnea o Dysphagia
  7. 7. 7 7 MAGDI AWAD SASI DISSECTING AORTIC A. o Orthopnea o Anxiety and premonitions of death o Flank pain if renal artery is involved o Dyspnea and hemoptysis if dissection ruptures into the pleura SUMMARY=AAA is characterized by: 1. Acute chest pain with acute inferior MI 2. Acute LVF/PULMONARY ODEMA due to acute AR 3. Acute CVA AND wide mediastinum (aortic shadow widened) ABDOMINAL AORTA ANEURYSM Nonspecific abdominal symptoms (constipation,pain) Pulsating abdominal mass/backage Lower limbs intermittent cludication Physical Blood pressure may increase or decrease. o Hypertension may result from a catecholamine surge or underlying essential hypertension. o Hypotension is an ominous finding and may be the result of excessive vagal tone, cardiac tamponade, or hypovolemia from rupture of the dissection. o A blood pressure differential of greater than 20 mm Hg was an independent predictor of aortic dissection. A pressure differential of greater than 20 mm Hg should increase the suspicion of aortic dissection, but it does not rule it in. Significant interarm blood pressure differentials may be found in 20% of people without aortic dissection. Neurologic deficits are a presenting sign in up to 20% of cases. o The most common neurologic findings are syncope and altered mental status. o 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. o Other causes of syncope or altered mental status include strokes from compromised blood flow to the brain or spinal cord and ischemia from interruption of blood flow to the spinal arteries. o Peripheral nerve ischemia can manifest with numbness and tingling in the extremities.
  8. 8. 8 8 MAGDI AWAD SASI DISSECTING AORTIC A. o Hoarseness from recurrent laryngeal nerve compression also has been described from AAA (ASCENDING AORTA). o Horner syndrome is caused by interruption in the cervical sympathetic ganglia and presents with ptosis, miosis, and anhidrosis. o 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 examination 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 may be due to the following heritable diseases: A . Hereditary Connective Tissue Diseases Marfan Syndrome Ehler Danlos Syndrome B. Chromosomal Aberrations Turners Syndrome Noonans Syndrome C. Aortic Diseases
  9. 9. 9 9 MAGDI AWAD SASI DISSECTING AORTIC A. Aortic Dilatation Aortic Aneurysm Anuloaortic ectasia Aortic Arteritis Bicuspid Aortic Valve Hypertension or pulsatile blood flow can propagate the dissection. An estimated 50% of all cases of aortic dissection that occur in women younger than 40 years are associated with pregnancy. Syphilis may cause aortic dissection. Crack cocaine use may precipitate aortic dissection. Iatrogenic causes of aortic dissection include cardiac catheterization. Differential Diagnoses Aortic Regurgitation Pericarditis and Cardiac Tamponade Back Pain, Mechanical Pleural Effusion Gastroenteritis Pulmonary Embolism HypertensiveEmergencies Shock, Cardiogenic Myocardial Infarction Shock, Hypovolemic Thoracic Outlet Syndrome Pancreatitis Laboratory Studies Blood studies o Usually, the diagnosis is made before the blood work is returned; however, leukocytosis may be present. o BUN and creatinine are elevated if the dissection involves the renal arteries. o Troponin and creatine kinase (CK) can be elevated if the dissection has caused myocardial ischemia. o Decreases in the hemoglobin and hematocrit are ominous findings suggesting the dissection either is leaking or has ruptured. o Some studies suggest that D-dimer should be a part of the initial workup if aortic dissection is suspected.A negative result makes the presence of the disease less likely. o Hematuria, oliguria, and even anuria (<50 mL/d) may occur if the dissection involves the renal arteries. o Routine bloods – non diagnostic o D-dimer < 500ng/ml unlikely to be dissection
  10. 10. 10 10 MAGDI AWAD SASI DISSECTING AORTIC A. 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 . Keep this in mind when administering thrombolytics to patients with chest pain. ST elevation can be seen in Stanford type A dissections because 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. If the dissection involves the coronary ostia, it is the right coronary artery that is most commonly involved, leading to inferior ST-segment elevation pattern. DIAGNOSTIC EVALUATION  Chest radiograph  Tran thoracic echocardiogram  Tran esophageal echocardiogram*  Computed tomography*  Magnetic resonance imaging*  Aortography *Choice based on rapid availability and quality of performance
  11. 11. 11 11 MAGDI AWAD SASI DISSECTING AORTIC A. Chest radiography Findings are abnormal in 80% of patients and are abnormal in ascending aorta D. A widened mediastinum is sometimes difficult to identify on a portable anteroposterior (AP) radiograph. If the patient is hemodynamically stable and cooperative, an AP radiograph can be obtained at bedside. Look for a mediastinal width greater than 8 cm on AP chest radiograph. A tortuous aorta, common in hypertensive patients, may be hard to distinguish from a widened mediastinum(44-80%). If in doubt, a good posterior-anterior radiograph 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 specific radiographic sign. Calcium sign -Displaced intimal calcification (>10mm) from outer aortic wall– useful in older patients. Other radiologic abnormalities seen on chest radiography include the following: Left apical cap Tracheal deviation Depression of left main stem bronchus Esophageal deviation Loss of the paratracheal stripe Over 12% of the chest radiographs of patients with aortic dissection were read as normal. Several studies concluded that the overall diagnosis of aortic dissection is not determined by any one sign, rather a combination of all findings leads to suspicion of dissection.
  12. 12. 12 12 MAGDI AWAD SASI DISSECTING AORTIC A. TTE  Indicated as an initial test if patient is very unwell and other imaging not available.  Can be performed bedside ,Can detect intimal flap and AR  Limitation: No information beyond aortic root and early part of proximal aorta. TRANSESOPHAGEAL ECHO Procedure of first choice for dissection, if readily available Portability of equipment facilities in emergency to ER or ICU High sensitivity (98%) and specificity(97%) Limitations : Unable to visualize distal part of ascending Aorta (beginning of aortic arch) and descending Aorta below stomach .
  13. 13. 13 13 MAGDI AWAD SASI DISSECTING AORTIC A. Angiography Still considered by some as the diagnostic standard test for aortic dissection, it is being replaced by newer imaging modalities. Angiography leads to accurate diagnosis of aortic dissection in over 95% of patients and aids the surgeon in planning the repair operation because 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 . The use of contrast media may be harmful to patients who have renal insufficiency or an allergy to iodine. isdiagnoses 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 discerning the presence of a dissection difficult. Computed tomography (CT) scanning: The accepted diagnostic criterion standard, angiography, is being challenged by state-of-the-art CT angiography. With the advent of helical CT with multiplanar and 3D reconstruction and CT angiography, CT scanning is quickly replacing angiography as the diagnostic test of choice in many institutions Spiral CT scanning is associated with a higher rate of detection and better resolution than incremental CT scanning. High-quality 2D and 3D reconstructions are possible with spiral CT scanning, which greatly adds to the usefulness of this imaging modality. More importantly, imaging information, including the type of lesion, location of the pathologic lesion, extent of the disease, and evaluation of the true and false lumen 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.
  14. 14. 14 14 MAGDI AWAD SASI DISSECTING AORTIC A. Faster scanners have decreased the acquisition time to the range of a breath hold, resulting in less motion artifact from breathing. Drawbacks include the following: Transportation of a patient in potentially unstable condition from the ED, places the patient at risk. Requires the injection of iodinated contrast. The use of contrast material may harm a patient who has impaired renal function or an allergy to contrast media. No information on aortic regurgitation MRI MRI has over 90% sensitivity and greater than 95% specificity. It is the most sensitive method for diagnosing aortic dissection and has similar specificity to CT scanning. MRI shows the site of intimal tear, type and extent of dissection, and presence of aortic insufficiency, as well as the surrounding mediastinal structures. Other benefits are that MRI requires
  15. 15. 15 15 MAGDI AWAD SASI DISSECTING AORTIC A. no contrast medium and no ionizing radiation. It is the preferred modality for patients with renal failure and those with an allergy to iodine. Contrast-enhanced magnetic resonance angiography (CE-MRA) is a principle technique for evaluating the thoracic aorta. MRI is the preferred tool for imaging chronic dissections and postsurgical follow-up. Contrast 3D MRA is an accurate noninvasive imaging modality. It has the advantage of being able to evaluate the aortic valve more effectively than CT angiography. 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 scanning. Patients with permanent pacemakers cannot undergo MRI. Most patients with prosthetic heart valves or coronary stents can safely have an MRI. MRA • Good alternative to TEE or CT, if readily available • High sensitivity (98%) and specificity (98%) • Provides three dimensional reconstruction • Can detect site of intimal tear and involvement of branch vessels • Non-invasive; neither x-rays nor contrast needed • Limitation: claustrophobic, more costly, not readily available
  16. 16. 16 16 MAGDI AWAD SASI DISSECTING AORTIC A. Immediate management: 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 patient must be assessed frequently for hemodynamic compromise, mental status changes, neurologic or peripheral vascular changes, and development or progression of carotid, brachial, and femoral bruits. Aggressive management of heart rate and blood pressure should be initiated. Beta-blockers should be given initially to reduce the rate of change of blood pressure and the shear forces on the aortic wall. The target heart rate should be 60-80 beats per minute. The target systolic blood pressure should be 100-120 mm Hg.  Treat hypotension / hypertension – aim for MAP 60-70  Beta blockers eg esmalol, propranolol, labetalol  Vasodilators Na nitroprusside  Calcium channel blockers eg verapamil, diltiazem Indications for Definitive Surgical and Medical Therapy in AD
  17. 17. 17 17 MAGDI AWAD SASI DISSECTING AORTIC A.  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%.  Dissections involving the arch are more complicated that those involving only the ascending aorta because 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%.  The definitive treatment for type B dissections is less clear(distal D.).  Control blood pressure.  Mortality rate - the same medically treated or 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.  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.  The operative mortality rate is approximately 5%
  18. 18. 18 18 MAGDI AWAD SASI DISSECTING AORTIC A. Sodium Nitroprusside 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; 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 increases shear forces against aortic wall, thus increasing dP/dt. Objective is to keep heart rate at 60-80 bpm  Sodium Nitroprusside for acute reduction starting 10 – 20 mcg/min and titrated upward  Adding IV BB prior until desired effect such as HR 60 – 80s (propranolol 1 mg Q 3-5 minutes max 10 mg)  Then Q 4-6 hrs at a dose of 2 – 6 mg  0.5-3 mcg/kg/min IV; rates >4 mcg/kg/min may lead to cyanide toxicity Labetolol  Effectively lowers dP/dT as well as reducing arterial pressure  Blocks alpha-, beta1-, and beta2-adrenergic receptor sites, decreasing BP.   Initial dose is 20mg followed by 40 to 80 mg Q 10 – 15 minutes (max 300mg IV)  Once BP controlled maintenance by continuous infusion  Infusion at 2mg/min titrating up to 5 –10 mg/min Esmolol  Ultra short acting BB for those with labile blood pressure or those that are surgical candidates. (Long acting medications may affect intraoperative bp management)  Load with 500 mcg/kg bolus  Infusion starts @ 50mcg/kg/min titrate to 200 mcg/kg/min for control  Can be used in patients with uncertain risk for bronchospasm