Aortic dissection resident survival guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D.; Chetan Lokhande, M.B.B.S [2]; Pratik Bahekar, MBBS [3]

Aortic dissection resident survival guide Microchapters
Overview
Classification
Causes
FIRE
Diagnosis
Treatment Medical Surgical
Do's
Dont's

Overview

Aortic dissection (AD) is a disruption of the medial layer of the aorta triggered by intramural bleeding. It is commonly due to an intimal tear that causes tracking of blood in a dissection plane within the media. Blood accumulation results in a separation of the aortic wall layers with ensuing formation of a true lumen and a false lumen with or without communication between the two. Aortic dissection is a medical emergency and can quickly lead to death if not managed urgently. Patients classically present with abrupt onset of severe, knife-like chest (most common), back, or abdominal pain. Other important features that increases the probability of aortic dissection include pulse deficits, systolic blood pressure differences between limbs, focal neurologic deficits, new aortic murmurs, shock, and a history of connective tissue disease and aortic valve disease. CT, MRI, or transesophageal echocardiography (TEE) may be used for the diagnosis AD, although CT is preferred because of it's speed, excellent sensitivity, and superiority in diagnosing arch vessel involvement. Serial imaging is recommended to monitor for progression of the dissection. After excluding possible aortic regurgitation, intravenous beta-blockers should be initiated in all patients to reduce the systolic blood pressure (SBP) to 100 to 120 mmHg and controlling the heart rate, to minimize the shear stress on the aortic wall. Treatment depends on the anatomic location of the dissection and complications. Uncomplicated type B dissections should be treated medically whereas type A dissections and complicated type B dissections should be treated surgically. Complications of AD include aortic regurgitation, myocardial ischaemia or infarction, pleural effusion, stroke, mesenteric ischemia, and acute kidney injury.

Classification

DeBakey and Stanford systems are the commonly used systems to classify aortic dissection.

Proximal Dissections

Originate in the ascending aorta and may propagate to involve the aortic arch, and possibly part of the descending aorta (include Debakey type I and II, and Stanford type A)

Distal Dissections

Originate in the descending aorta (distal to left subclavian artery) and propagate distally, rarely extends proximally (include Debakey type IIIa and IIIb, and Stanford type B)

Click here for the detailed classification schemes.

Causes

Life Threatening Causes

Aortic dissection is a life-threatening condition and must be treated as such irrespective of the underlying cause.

Common Causes

• Hypertension (underlying cause in 70%)
• Pre-existing aortic diseases or aortic valve disease
• Blunt chest trauma
• Complication of cardiac procedures
• Connective tissue disorders
• Vasculitis
• Intravenous drug use (cocaine and amphetamines)

Click here for the complete list of causes.

FIRE: Focused Initial Rapid Evaluation

A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.
Boxes in red signify that an urgent management is needed.

Abbreviations: AVR: Aortic valve replacement; BP Blood Pressure, CCU: Coronary care unit; CHF: Congestive cardiac failure; CXR: Chest X-ray; EKG: Electrocardiogram; MI: Myocardial infarction; OR: Operating room; TAVR: Transcatheter aortic valve replacement; TEE: Transesophageal echocardiogram; TTE: Transthoracic echocardiogram; HEENT: Head eye ear nose throat

Identify cardinal findings that increase the pretest probability of acute aortic dissection ❑ Chest pain or back pain or abdominal pain ❑ Sudden in onset ❑ Tearing or sharp in quality ❑ Increasing in intensity ❑ Unexplained syncope ❑ Focal neurological deficits ❑ Unequal pulses or BPs in the limbs ❑ Perfusion deficits ❑ Refractory hypertension (decreased renal perfusion) ❑ Tensed abdomen ❑ Progressive metabolic acidosis ❑ Increasing liver enzymes

Does the patient have the following findings which require urgent management? ❑ Hemodynamic instability: ❑ Hypotension ❑ Cold extremities ❑ Peripheral cyanosis ❑ Mottling ❑ Altered mental status ❑ Oliguria ❑ High risk features Presence of 2 or more high risk features, requires immediate surgical management. ❑ Difference in the blood pressure in both extremities ❑ Signs of shock (hypoperfusion) ❑ Pulse deficit involving carotid, femoral or subclavian arteries ❑ Diastolic murmur suggestive of aortic regurgitation ❑ Marfan's syndrome ❑ Signs suggestive of stroke ❑ Aortic disorder ❑ Aortic valve disease ❑ Recent aortic manipulation

Yes

No

Assess the following things simultaneously ❑ Assess hemodynamic stability ❑ Order urgent TEE and look for the following features: ❑ Pericardial effusion ❑ Regional wall motion abnormality (RWMA) ❑ Dilated root ❑ Aortic regurgitation (AR)

Continue with the diagnostic approach below

Does the patient have hypotension

Yes

No

❑ Assess airway, breathing, and circulation ❑ Place a cardiac monitor to monitor cardiac rhythm ❑ Intra-arterial BP monitoring ❑ Secure 2 large-bore intravenous lines (IVs) ❑ Monitor oxygen, respiration, blood pressure, and urine output ❑ Frequently assess, hemodynamic compromise, mental status changes, neurologic or peripheral vascular changes ❑ Monitor development or progression of carotid, brachial, and femoral bruits ❑ Indwelling urethral catheter is used to monitor urine output ❑ Obtain blood samples for, ❑ CBC, electrolytes ❑ Cardiac enzymes to rule out MI ❑ Blood group and cross match

Titrate BP between 90-120 mm Hg ❑ Control heart rate by betablockers before lowering BP by other agents, as other agents can lead to reflex tachycardia and worsening of aortic dissection ❑ Esmolol ❑ 500 micrograms/kg intravenous initially, followed by 50 micrograms/kg/min for 4 min ❑ If necessary increase infusion up to 200 micrograms/kg/min ❑ Metoprolol ❑ 5 mg intravenously every 5-10 minutes ❑ If necessary increase up to a maximum dosage of 15 mg/total dose ❑ Substitute non-dihydropyridine calcium channel blockers or vasodilators or labetalol if betablockers are contraindicated ❑ Diltiazem ❑ 0.25 mg/kg intravenous bolus initially then 5-10 mg/hr infusion ❑ If necessary increase dose to 15 mg/hr ❑ Verapamil ❑ 0.05 to 0.1 mg/kg IV bolus ❑ Nitroprusside ❑ 0.3 to 0.5 micrograms/kg/min IV initially then increase by 0.5 micrograms/kg/min ❑ If necessary increase dose to a maximum of 15 mg/hr ❑ Labetalol ❑ 1-5 mg/min IV infusion

Can aortic dissection be confirmed?

Yes

No

Type A dissection

Type B dissection

Obtain a secondary imaging study, if there is a high clinical suspicion

❑ Transfer to a cardio-thoracic unit for the surgical management

❑ Initiate medical management unless there is ❑ Leaking of dissection ❑ Rupture of dissection ❑ Malperfusion to any organ

Complete Diagnostic Approach

A complete diagnostic approach should be carried out after a focused initial rapid evaluation is conducted and following initiation of any urgent intervention.

Characterize the symptoms: ❑ Chest pain ❑ Tearing, ripping, sharp. stabbing, or knife-like ❑ Sudden onset and increasing in intensity ❑ Worsened by deep breathing or cough and relieved by sitting upright (suggestive of hemorrhage into the pericardial sac). ❑ Neck, throat, and jaw pain ❑ Abdominal pain or back pain (think of associated mesenteric ischemia) ❑ Syncope in 50% of cases (suggestive of hemorrhage into the pericardial sac causing pericardial tamponade) ❑ Palpitation ❑ Rapid, weak pulse ❑ Dyspnea ❑ Rapid breathing ❑ Orthopnea ❑ Hemoptysis (suggestive of compression of and erosion into the bronchus) ❑ Stridor (suggestive of compression of the airway) ❑ Flank pain ❑ Oliguria/ anuria (suggestive of involvement of the renal arteries causing pre-renal kidney injury). ❑ Nausea and vomiting ❑ Dysphasia(suggestive of pressure on the esophagus) ❑ Hematemesis ❑ Gastrointestinal bleeding ❑ Altered mental status ❑ Symptoms suggestive of stroke e.g. paraplegia, numbness and tingling (suggestive of involvement of cerebral or spinal arteries) ❑ Horner's syndrome (suggestive of compression of the superior cervical ganglia) ❑ Drooping of eyelids (ptosis) ❑ Decreased or no sweating (anhidrosis) ❑ Miosis ❑ Hoarseness of voice (suggestive of compression of the recurrent laryngeal nerve) ❑ Claudication (suggestive of iliac artery occlusion) ❑ Painless dissection (15 – 55 %)(unexplained syncope, stroke or congestive heart failure (CHF))

Obtain a detailed history: ❑ Past medical history ❑ Hypertension (most important risk factor present in >70% of patients) ❑ Pheochromocytoma ❑ Family history ❑ Connective tissue disorder ❑ Marfan syndrome ❑ Ehlers-Danlos syndrome ❑ Loeys-Dietz syndrome ❑ Polycystic kidney disease ❑ Anatomic defects ❑ Biscuspid aortic valve ❑ Aortic valve disease ❑ Aortic root disorders ❑ Aortic aneurysm ❑ Coarctation of aorta ❑ Iatrogenic ❑ Recent aortic manipulation ❑ Chronic steroid usage ❑ Immunosuppressive therapy ❑ Social history ❑ Cocaine abuse ❑ Heavy weight lifting ❑ Trauma ❑ Other genetic disorders ❑ Turners syndrome (usually due to bicuspid aortic valve) ❑ Familial thoracic aneurysm and dissection syndrome ❑ Inflammatory vasculitis ❑ Takayasu arteritis ❑ Giant cell arteritis ❑ Behcet's arteritis ❑ Pregnancy ❑ Aortitis

Examine the patient: ❑ Vitals ❑ Pulse ❑ Tachycardia (suggestive of pain, aortic insufficiency, pericardial tamponade, and aortic rupture if associated with severe hypotension) ❑ Wide pulse pressure (suggestive of acute aortic insufficiency) ❑ Pulsus paradoxus (suggestive of pericardial tamponade) ❑ Pulse deficit involving carotid, femoral or subclavian artery ❑ Absent femoral pulse ❑ Blood pressure ❑ Difference in the blood pressure in both extremities ❑ Hypertension (due to pain and catecholamine surge) ❑ Hypotension (grave prognostic indicator, suggestive of pericardial tamponade, severe aortic insufficiency, or aortic rupture) ❑ Signs of shock (hypoperfusion) ❑ Hypotension (SBP < 90 mm of Hg or drop in mean arterial pressure >30 mm of Hg) ❑ Altered mental status ❑ Cold and clammy extremities ❑ Oliguria (urine output <0.5mL/kg/hr) ❑ HEENT examination ❑ Increased JVP (suggestive of heart failure) ❑ Horner's syndrome ❑ Hoarseness due to compression of the left recurrent laryngeal nerve ❑ Swelling of the neck and face (suggestive of superior vena cava syndrome) ❑ Cardiovascular examination ❑ Faint early diastolic murmur (suggestive of acute aortic regurgitation, vs. loud decrescendo diastolic murmur of chronic AR) ❑ Pericardial friction rub (suggestive of pericarditis) ❑ Clicks (suggestive of pseudoprolapse/true prolapse of mitral and/or tricuspid valve) ❑ Beck's triad (suggestive of cardiac tamponade) ❑ Hypotension (suggestive of decreased stroke volume) ❑ Jugular venous distension (suggestive of venous hypertension due to decrease cardiac output) ❑ Muffled heart sounds (suggestive of fluid inside the pericardium) ❑ Respiratory examination ❑ Kussmaul's sign (Paradoxical increase in jugular venous pressure with inspiration - Suggestive of tamponade) ❑ Decreased movement of the chest ❑ Stony dullness to percussion (suggestive of hemothorax and / or pleural effusion ❑ Diminished breath sounds ❑ Crackles / crepitations / rales (suggestive of pulmonary edema due to acute aortic insufficiency) ❑ Stridor and wheezing (suggestive of compression of the airway) ❑ Decreased tactile fremitus (suggestive of pleural effusion) ❑ Abdominal examination ❑ Ascites ❑ Neurological examination ❑ Altered mental status ❑ Extremity tingling and numbness (suggestive of nerve compression) ❑ Focal neurological deficits (signs suggestive of stroke) ❑ Extremity examination ❑ Peripheral edema ❑ Claudication

Consider alternate diagnosis: ❑ Aortic regurgitation ❑ Aortic stenosis ❑ Aortic aneurysm ❑ Atherosclerotic or cholesterol embolism ❑ Cardiac tamponade ❑ Cardiogenic shock/hypovolemic shock/hemorrhagic shock ❑ Esophageal perforation or rupture ❑ Hypertensive emergencies ❑ Musculoskeletal pain ❑ Mediastinal tumors ❑ Myocardial infarction ❑ Myocarditis ❑ Pancreatitis ❑ Peptic ulcer disease or perforating ulcer ❑ Pleural effusion ❑ Pulmonary embolism

Focused bedside pre-test risk assessment ❑ High risk conditions ❑ Marfan syndrome ❑ Connective tissue disease ❑ Family history of aortic disease ❑ Known aortic valve disease ❑ Recent aortic manipulation ❑ Known thoracic aortic aneurysm ❑ Aortic disorder ❑ High risk pain features ❑ Chest, back, or abdominal pain ❑ Abrupt onset ❑ Severe intensity ❑ Ripping, tearing, sharp, or stabbing ❑ High risk exam features ❑ Perfusion deficits ❑ Pulse deficit ❑ Systolic blood pressure differential ❑ Focal neurological deficit ❑ Murmur of aortic insufficiency ❑ Hypotension or shock

Low pre-test probability (No features present) High threshold for aortic imaging

Intermediate pre-test probability (1 feature present) Intermediate threshold for aortic imaging

High pre-test probability (2 or more features present) Immediate surgical evaluation and expedited aortic imaging

❑ Can an alternate diagnosis be identified?

❑ Order an EKG ❑ Does EKG show ST elevation ?

Yes

No

No

Yes

❑ Consider immediate surgical consultation and do aortic imaging as soon as possible

Treat accordingly

❑ Is there evidence of: ❑ Unexplained hypotension? ❑ Widened mediastinum on CXR?

❑ Can an alternate diagnosis be identified?

❑ Treat like a primary acute coronary syndrome (ACS) ❑ If perfusion deficits are present then consider immediate coronary reperfusion therapy ❑ Identifiable culprit lesion on coronary angiography?

No

Yes

No

Yes Treat accordingly

No

❑ Check risk factors for Thoracic aortic disease (TAD) ❑ Advanced age ❑ Risk factor for aortic diseases ❑ Syncope ❑ Do a detailed aortic imaging for thoracic aortic disease

Detailed and accelerated aortic imaging

❑ Aortic Imaging ❑ Transesophageal echocardiography (TEE) (preferred in unstable patients) ❑ Computed tomography(chest to pelvis; better visualization of aortic branch involvement) ❑ Magnetic resonance imaging(chest to pelvis)

❑ Can aortic dissection be confirmed by imaging study

Yes

No

❑ Start appropriate therapy

❑ Obtain a secondary imaging study if there is high clinical suspicion, even if the initial aortic imaging studies are negative

Treatment

Medical Treatment

Shown below is an algorithm summarizing the medical management of aortic dissection according to the 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for Diagnosis and Management of patients with Thoracic Aortic Disease.

Confirmed aortic dissection ❑ Check whether dissection occurred in ascending aorta

Yes

Consider surgical management

No

❑ Start Medical management

❑ Check Vitals ❑ Blood pressure in both arms ❑ Take the highest reading for treatment or goal therapy ❑ Is patient hemodynamically stable ?

Yes

No

❑ Control rate and pressure ❑ Beta blockers Betablockers are contraindicated in hypersensitivity, bradycardia, heart block, uncompensated heart failure, hypotension, asthma, severe chronic obstructive pulmonary disease ❑ Esmolol ❑ 500 micrograms/kg intravenous initially, followed by 50 micrograms/kg/min for 4 min ❑ If necessary increase infusion up to 200 micrograms/kg/min ❑ Metoprolol ❑ 5 mg intravenously every 5-10 minutes ❑ If necessary increase up to a maximum dosage of 15 mg/total dose OR ❑ Substitute non-dihydropyridine calcium channel blockers or vasodilators or labetalol if betablockers are contraindicated Calcium channel blockers are contraindicated in hypersensitivity, hypotension, second- or third-degree atrioventricular block, sick sinus syndrome, left ventricular dysfunction, pulmonary congestion ❑ Diltiazem ❑ 0.25 mg/kg intravenous bolus initially then 5-10 mg/hr infusion ❑ If necessary increase dose to 15 mg/hr ❑ Verapamil ❑ 0.05 to 0.1 mg/kg IV bolus ❑ Vasodilators ❑ Nitroprusside Nitroprusside is contraindicated in hypersensitivity, poor cerebral ischemia or coronary perfusion ❑ 0.3 to 0.5 micrograms/kg/min IV initially then increase by 0.5 micrograms/kg/min ❑ If necessary increase dose to a maximum of 15 mg/hr ❑ Labetalol ❑ 1-5 mg/min IV infusion ❑ Goal heart rate should be 60 beats per minute ❑ Goal systolic BP 90-120 mm of Hg ❑ Pain control ❑ Use Opiates ❑ Morphine sulphate ❑ 2-5 mg intravenously every 5-30 minutes or as needed

❑ Type A dissection ❑ Is a surgical emergency, do an expedited surgical consultation Surgery is relatively contraindicated in hemorrhagic stroke ❑ Maintain euvolemic status ❑ Intravenous fluid replacement ❑ Maintain mean arterial pressure (MAP) of 70 mm of Hg ❑ Rule out the following complications using imaging studies: ❑ Pericardial tamponade ❑ Rupture of aorta ❑ Aortic insufficiency ❑ Myocardial infarction Stanford A type dissection

❑ Type B dissection ❑ Uncomplicated dissection are treated medically ❑ Intravenous fluid replacement ❑ Maintain mean arterial pressure (MAP) of 70 mm of Hg ❑ Start vasopressors, if the patient remains hypotensive ❑ Complicated aortic dissection is treated surgically ❑ Leaking dissection ❑ Rupture ❑ Malperfusion to a vital organs ❑ Refractory hypertension (decreased renal perfusion) ❑ Tensed abdomen ❑ Progressive metabolic acidosis ❑ Increasing liver enzymes ❑ Rupture in the pericardial sac(rare) ❑ Beck's triad (cardiac tamponade) ❑ Imaging studies to find out contained rupture ❑ Perform Transthoracic echocardiogram (TTE) to assess cardiac function Stanford B type dissection

❑ Can the cause of hypotension respond to surgical management

❑ Monitor vitals closely ❑ Maintain systolic BP <120 mm of Hg

No

Yes

Consider surgical management

Yes

No

❑ Check if dissection involves ascending aorta

Yes

No

❑ Control blood pressure ❑ Intravenous vasodilator

❑ Monitor vitals closely ❑ Maintain systolic BP <120 mm of Hg

❑ Check for any complications which might require surgery ❑ Malperfusion ❑ Progressing dissection ❑ Expansion of aortic aneurysm ❑ Uncontrolled or refractory hypertension

Yes

❑ Consider surgical management

No

❑ Switch to oral medications ❑ Betablockers ❑ Antihypertensive regimen ❑ Follow up in the outpatient ❑ Start long-term antihypertensive drug therapy, usually including β-blockers, calcium channel blockers, and ACE inhibitors. ❑ Avoidance of strenuous physical activity. ❑ MRI may be done before discharge and repeated at 6 mo and 1 yr, then every 1 to 2 yrs.

Surgical Treatment

Shown below is an algorithm summarizing the surgical management of aortic dissection according to the Guidelines for Diagnosis and Management of patients with Thoracic Aortic Disease.

❑ Imaging study confirms aortic dissection ❑ Check whether dissection occurred in ascending aorta

No

Yes

❑ Assess suitability for surgery ❑ Patient stable for pre-op testing?

No

Medical management

Yes

❑ Age > 40?

No

Yes

❑ Assess need for pre-operative coronary angiography ❑ Known CAD? ❑ Significant risk factors for CAD?

No

Yes

❑ Perform angiography Is significant CAD detected on angiography?

No

Yes

❑ Plan for CABG at the time of aortic dissection repair

❑ Perform urgent operative management

❑ Perform intra-operative assessment of aortic valve by Transesophageal echocardiography (TEE) for presence of one of the following: ❑ Aortic regurgitation ❑ Dissection of aortic sinuses

No

Yes

❑ Perform graft replacement of ascending aorta ± aortic arch

❑ Perform graft replacement of ascending aorta ± aortic arch ❑ Consider repair/replacement of aortic valve

Do's

History and Examination

• For pre-test risk determination include information about:
  • Medical History
  • Family history and ask specifically for family history of aortic dissection or thoracic aneurysm
  • Pain history
• Do a detailed physical examination to identify findings for certain high risk conditions like:(class I, level of evidence B)
  • Marfan's syndrome
  • Loeys-Dietz syndrome
  • Ehlers-Danlos syndrome
  • Turner's syndrome
  • Connective tissue disorder
• Check for genetic mutations predisposing to dissection:(class I, level of evidence B)
  • Fibrillin 1 (FBN1)
  • Transforming growth factor, beta receptor I (TGFBR1)
  • Transforming growth factor, beta receptor II(TGFBR2)
  • Alpha-actin-2(ACTA2)
  • Myosin-11 (MYHH11)
• Ask about recent aortic or surgical or catheter manipulation.(class I, level of evidence C)
• Ask in detail about the pain. Include the following: (class I, level of evidence B)
  • Onset of pain whether abrupt or instantaneous
  • Severity of pain
  • Quality of pain whether ripping, tearing, stabbing or sharp.
• Check for the following features on examination:(class I, level of evidence B)
  • Pulse deficits
  • Blood pressure (systolic) difference of above 20 mm of Hg in limbs
  • New onset aortic regurgitation features
  • Focal neurological deficits
• Patients less than 40 years of age and presenting with sudden onset chest, abdominal or back pain should be evaluated for high risk conditions.
• Patients presenting with features of syncope along with features of dissection should have a detailed neurological examination and cardiovascular examination to rule out pericardial tamponade and other neurological deficits.(class I, level of evidence C)

Screening Tests

• Do a transesophageal echocardiography (TEE) in the emergency room. This is the preferred approach. If the patient is hemodynamically unstable, then a transesophageal echo can be performed in the operating room after the patient has been induced and is being prepared for surgery.
• Do a magnetic resonance imaging contrast aortography (MRI) only if:
  • A patient who has chronic chest pain who is hemodynamically stable
  • A chronic dissection
• Do an EKG when patients presents with symptoms of dissection.(class I, level of evidence B)
• Treat the patient as an acute cardiac event, if ST elevation is present in EKG then, unless the patient has high risk factors for acute dissection.
• Perform coronary angiography, followed by thrombolysis or percutaneous coronary intervention, if EKG shows ST elevation with no dissection features.
• Do order a X-ray for all patients with intermediate risk and a low risk to rule out alternate diagnosis.(class I, level of evidence C)
• Evaluate high risk patients by transesophageal echocardiogram, computed tomography or magnetic resonance imaging to rule out dissection.(class I, level of evidence B)
• Obtain a secondary imaging study, if the initial aortic imaging studies are non conclusive, and there is a high clinical suspicion.(class III, level of evidence C)

Initial Management

• Medical management should be aimed at decreasing aortic wall stress.(class I, level of evidence C)
• Titrate beta blocker to maintain heart rate of 60 beats/ minute.(class I, level of evidence C)
• Use nondihyropyridine calcium channel blockers to control rate, if beta blockers are contraindicated.(class I, level of evidence C)
• Use angiotensin converting enzyme and other vasodilators to maintain end organ perfusion, if BP remains above 120 mm of Hg, after medical treatment.(class I, level of evidence C).

Definitive Management

• Do a definitive aortic imaging study, if chest X-ray demonstrates widened mediastinum.
• Aim to curtail heart rate less than 60 beats/minute and systolic blood pressure between 90 and 120 mm of Hg.
• Use sodium nitroprusside as the first line for the treatment of hypertension. Nicardipine, nitroglycerin and fenoldopam can also be used.
• Use esmolol in asthma, congestive heart failure or chronic obstructive pulmonary disease.
• Use labetalol to maintain heart rate and blood pressure, it prevents usage of another vasodilator.
• Do a pericardiocentesis for pericardial bleeding and dissection related hemopericardium.
• Do a plasma smooth muscle myosin heavy chain protein, D-dimer and high sensitive C-reactive protein to rule out alternate diagnosis.
• Order a surgical consultation for all patients once diagnosed with aortic dissection. This applies to patients presenting with dissection at any location. (class I, level of evidence C)
• Do an emergent repair in acute dissection of ascending aorta to prevent complications like rupture.(class I, level of evidence C)
• Consider surgical repair for all type A dissections as they involve the aortic valve. type A|Ascending aortic dissections (Type A Stanford)]] often involve the aortic valve, which having lost its suspensory support, telescopes down into the aortic root, resulting in aortic incompetence. This needs re-suspending to re-seat the valve and repair / prevent coronary artery injury. The area of dissection is removed and replaced with a dacron graft to prevent further dissection from occurring.
• Suspect malperfusion in type B aortic dissection, if following sings are present, Refractory hypertension (decreased renal perfusion), tensed abdomen, progressive metabolic acidosis, increasing liver enzymes (impaired perfusion of truncus coeliacus, mesenteric arteries).
• Consider medical management for type B dissections, unless there is leaking, rupture or compromise to other organs, e.g. kidneys and life threatening conditions like perfusion deficit, dissection enlargement, aneurysm enlargement or blood pressure refractory to treatment.(class I, level of evidence C)
• Do a MRI before discharge and repeat at 6 mo and 1 yr, then every 1 to 2 yr.

Dont's

• Don't delay aortic imaging even if chest x-ray is negative (class III, level of evidence C).
• Don't use beta blocker in patients having aortic regurgitation as they may block the tachycardia caused by compensation.
• Don't use nitroprusside without a β-blocker or calcium channel blocker otherwise dissection worsens because of reflex sympathetic activation. This causes vasodilation which can increase ventricular inotropy and aortic shear stress.
• Don't use vasodilator before heart rate is controlled otherwise there would be reflex tachycardia which would increase the stress on aorta and worsening the dissection.
• Hemorrhagic stroke is a relative contraindication to urgent surgical intervention done for type A tears, as intraoperative heparinization and restoration of cerebral blood flow can worsen ongoing stroke outcomes.
• Avoid strenous physical exercise.
• Avoid antihypertensives that act mainly by vasodilation (hydralazine, minoxidil).
• Avoid β-blockers that have intrinsic sympathomimetic action (acebutolol, pindolol).

References