Home

helps physicians and healthcare professionals

Erectile Dysfunction

helps physicians and healthcare professionals

Doctor123.org

helps physicians and healthcare professionals
Home Erectile Dysfunction Erectile Dysfunction Drugs

Aortic Dissection


BASICS


DESCRIPTION


  • Classically an intimal tear in the aorta resulting in hematoma formation. Accumulating blood in false lumen of arterial wall leads to propagation of a dissection. Alternatively, may begin as an intrawall hematoma without intimal tear.
  • Stanford classification (most widely used and frequently guides management)
    • Type A: involves ascending aorta or ascending aorta and aortic arch regardless of site of intimal tear
    • Type B: involves descending aorta
    • Type non-A, non-B: isolated aortic arch involvement
  • DeBakey classification (based on origin site)
    • Type 1: originates in ascending aorta, propagates at least as far as aortic arch
    • Type 2: involves only ascending aorta
    • Type 3: originates in descending aorta, may propagate proximately to the arch or distally to the abdominal aorta
  • Svensson classification
    • Class 1: classic dissection with true and false lumen
    • Class 2: intramural hematoma or hemorrhage
    • Class 3: subtle dissection without hematoma
    • Class 4: atherosclerotic plaque rupture and ulceration
    • Class 5: iatrogenic
  • Synonym(s): dissecting aneurysm, dissecting hematoma

EPIDEMIOLOGY


Predominant age varies with cause. About 68% are male and 79% Caucasians (1). Older patients usually have atherosclerosis, whereas younger patients should be investigated for an underlying cause. Type A dissection occurs in patients with an average age of 60 years. Type B dissection patients are generally older. Patients with Marfan syndrome have a mean age of 36 years.  
Incidence
3/100,000 people per year  
Prevalence
United States:  
  • Diagnosed in 1/10,000 patients admitted to hospital
  • Found in 1/350 patients at autopsy
  • Numbers may be slightly higher due to unexplained deaths at home or in hospital without autopsy.

ETIOLOGY AND PATHOPHYSIOLOGY


  • In most cases, dissection develops in the absence of an aneurysm, but the false lumen that can be created during dissection can later expand to form an aneurysm. In patients with inherited connective tissue disease, abnormal or deficient proteins lead to weakening of vessel walls. Bicuspid aortic valves may also lead to an acquired dysfunction of vascular walls and smooth muscle cells. Histologic investigations of postmortem and biopsy specimens reveal cystic medial necrosis, especially in those patients with known preexisting aneurysms.
  • Although the exact sequence of events is controversial, an aortic dissection is likely the result of multiple pathologic processes. Stress on the aortic wall from hypertension; intimal damage with subsequent tear, rupture, or ulceration of atherosclerotic plaques; and the involvement of vasa vasorum and intramural hematoma may be contributory. Expansion of the false lumen with blood may cause compression of the true lumen, causing hypoperfusion of distal organs.

Genetics
Up to 20% of patients with th6oracic aneurysm or dissection were found to have first-degree relatives with aneurysm or dissection. Studies have found that the TGFBR1 and TGFBR2 genes are related to aneurysm and dissection in isolated cases and in patients with Marfan syndrome. Other research has found ACTA2 gene mutations to be involved in isolated and familial dissections and aneurysms.  

RISK FACTORS


  • Most common associated factors: hypertension (~70% of patients), old age, atherosclerosis, previous cardiovascular surgery, particularly repair of aneurysm or dissection
  • Collagen abnormalities: Marfan syndrome, Ehlers-Danlos syndrome (particularly type IV)
  • Recreational drug use: smoking, cocaine, methamphetamine
  • Inflammatory vasculitis: Takayasu arteritis, giant cell arteritis, Beh §et disease, syphilis
  • Congenital cardiovascular anomalies (Turner syndrome, bicuspid aortic valve, coarctation of aorta, Erdheim cystic medial necrosis, familial ectopia lentis, tetralogy of Fallot)
  • Trauma (catheters, motor vehicle accidents, vascular surgery, intra-aortic balloon pump)
  • Pregnancy (usually has underlying vascular pathology)

GENERAL PREVENTION


  • Medical management of precipitating risk factors such as hypertension, smoking cessation, lipid control (2)[C]
  • Surveillance of aortic root and replacement when appropriate in patients with collagen disorders (e.g., Marfan, Ehlers-Danlos) (2)[C]. In addition Marfan patients should receive β-blockade to reduce aortic dilatation (2)[B].

COMMONLY ASSOCIATED CONDITIONS


See "Risk Factors."  

DIAGNOSIS


HISTORY


  • A high level of clinical suspicion is essential.
  • A typical patient is a hypertensive male aged 60 to 80 years unless coexisting connective tissue disorders are present.
  • A positive family history raises index of suspicion.
  • Subjective complaints: 85% of patients report abrupt onset of pain. Pain is often described as sharp, less often as tearing or ripping. 90% of patients stated that the pain was "severe" or "worst ever." Patients with type A dissections more often report chest pain. Patients with type B dissections more often report back and abdominal pain.
  • Painless dissection may occur. Hypoperfusion may manifest as syncope, cerebrovascular events. Dissection may occasionally present as acute heart failure, angina/MI, paresis, or bowel ischemia.

PHYSICAL EXAM


  • Hypotension and shock are usually seen with type A dissections (may be normotensive).
  • Hypertension is more common with type B dissections.
  • Pulse deficit; with unequal pulses in up to 1/3 of cases
  • New murmur and findings of aortic regurgitation
  • Signs of congestive heart failure
  • Limb ischemia
  • Spinal cord syndromes/neurologic deficits
  • Features of tamponade

DIFFERENTIAL DIAGNOSIS


Myocardial infarction, pericarditis, pericardial tamponade not from aortic dissection, angina or atherosclerotic embolism, pulmonary embolism, pneumonia, pleurisy, acute pancreatitis or cholecystitis, penetrating duodenal ulcer, Mallory-Weiss tear or esophageal rupture, mediastinal pathology, musculoskeletal pain  

DIAGNOSTIC TESTS & INTERPRETATION


  • A normal EKG and chest x-ray cannot be used to rule out the diagnosis if clinical suspicion is high.
  • EKG may show the following:
    • Normal findings in up to 1/3 of patients
    • Nonspecific ST-T changes (~40%), left ventricular hypertrophy (~25%)
    • Ischemic changes (~15%), acute MI (~3%), old MI with Q waves (~7%)
  • D-Dimer has been suggested as a serologic marker of dissection. In the first 24 hours, a low D-Dimer can rule out aortic dissection with an accuracy of 95% (3)[C],(4)[B].
  • Other possible novel markers for aortic dissection include a combination of elastin fragments, and smooth-muscle myosin heavy-chain protein.
  • A chest X-ray should be performed (2)[C]:
    • Normal findings in ~15% of patients
    • Widening of the mediastinum (~60%), abnormal aortic outline (~50%)
    • Abnormal cardiac silhouette (~25%), calcified or displaced aorta (~15%)
    • Pleural effusion (~19%)
  • Studies suggest that CT scan with IV contrast, transesophageal echocardiography, and MRI each provides ~95% sensitivity and specificity for diagnosis:
    • MRI has limited availability, is not suitable for unstable patients, and is contraindicated with specific types of pacemakers and metal implants; it is first line for long-term follow-up of aortic dissection (2)[B],(5)[A].
    • A CT scan may better rule out dissection in those patients where clinical suspicion and pretest probability are both low (2)[B],(5)[A].
    • Transesophageal echocardiography can be done at the bedside of an unstable patient in 15-20 minutes, and it can offer additional information about heart and aortic valve function (2)[B],(5)[A].
    • Based on availability and speed of diagnosis; CT scans remain the modality of choice.
    • If there is a high probability of aortic dissection, a second diagnostic test should be obtained if the first is negative or inconclusive (2)[C].
  • Both MRI and CT scans can be used by clinicians to assess the extent, size, and location of the dissection, as well as involvement of the branches off the aorta, although some sources suggest an MRI as the preferred modality for precise anatomic definition.

Diagnostic Procedures/Other
Contrast angiography can be used specifically as a diagnostic tool, especially when visceral perfusion defects are suspected. Angiography may also be used as an entry point into endovascular treatment of dissection.  
Test Interpretation
  • ~60% of intimal tears occur in the proximal ascending aorta. The remaining incidence of tears occur between the origin of the left subclavian artery and ligamentum arteriosum, descending aorta (20%), aortic arch (10%), and abdominal aorta.
  • Although medial necrosis is found in aging aortas, it is more extensive in patients who develop aortic dissections.
  • Cystic medial necrosis is seen in patients with defects in elastin and connective tissue organization (e.g., Marfan, Ehlers-Danlos).
  • Death usually is due to rupture and tamponade.

TREATMENT


Due to the acute nature of an aortic dissection, there are no randomized controlled trials related to treatment and management.  

GENERAL MEASURES


Patients should be monitored in an intensive care unit (6)[C]. Intubation, mechanical ventilation, and arterial BP monitoring is preferred, particularly in unstable patients (7)[C]. Adequate pain control should be achieved with morphine (6)[C]. If surgical repair of aneurysm is indicated, do not delay repair to evaluate for coronary artery disease and valvular dysfunction. Prompt correction of hypotension and identification of the cause are essential.  

MEDICATION


For an uncomplicated (i.e., lack of hemodynamic instability or branch vessel involvement) dissection of descending aorta (Stanford B), medical therapy is indicated, whereas urgent surgery is needed for type A (1)[C],(2)[B]. Surgical evaluation should be obtained regardless of the classification (2)[C].  
First Line
The cornerstone of medical management is BP control by using intravenous β-blockers, (propranolol, metoprolol, labetalol, or esmolol); titrated to a heart rate of ≤60 BPM (2,3)[C].  
Second Line
  • For patients with contraindications for β-blockade, calcium channel blockers with negative inotropic and chronotropic effects (verapamil, diltiazem) may be used (2,7)[C].
  • If hypertension is refractory to initial therapies (i.e., systolic BP >120), then ACE inhibitors or nitroprusside can be considered, but the patient should be evaluated for a possible surgical intervention at that time (2,3)[C].
  • Use of direct vasodilators such as hydralazine should be avoided.

SURGERY/OTHER PROCEDURES


  • Stanford A type dissection
    • Surgery is the treatment of choice for type A dissections (80% treated surgically) to prevent aortic rupture and cardiac tamponade, while relieving any aortic regurgitation that may be present (1)[C],(2)[B].
    • Patients who are not appropriate surgical candidates (comorbid medical conditions, patient choice, very advanced age) have an in-hospital mortality of 50% at 30 days.
    • Surgical correction aims to resect the ascending aorta and arch, and replace them with a conduit graft (2,7)[C].
    • Other procedures including repair or replacement of aortic valves and coronary arteries may be done depending on the extent of the dissection (2,7)[C].
  • Stanford B-type dissection:
    • A surgical resection of the aorta for type B is generally associated with worse outcomes than medical management (2)[C].
    • Surgical indications for Stanford B include the following: continued aortic expansion; impending aortic rupture; occlusion of major aortic branch to renal, mesenteric, or iliac arteries; persistent and recurrent chest pain; and periaortic or mediastinal hematoma (3)[C].
  • Poor prognostic factors for surgical success: age >70 years; abrupt-onset chest pain; hypotension, shock, or tamponade at presentation; renal failure; pulse deficit; abnormal ECG, ST-segment elevation; history of aortic valve replacement; and renal and/or visceral ischemia (8)
  • Stenting of complicated type B dissections seems to be a reasonable and safe alternative to surgical management, although further follow-up is needed (9)[B].

INPATIENT CONSIDERATIONS


Admission Criteria/Initial Stabilization
Admit to ICU, intubate hemodynamically unstable patients. If present, determine etiology of hypotension: blood loss, tamponade, heart failure.  

ONGOING CARE


FOLLOW-UP RECOMMENDATIONS


Patient Monitoring
  • Maintain systolic BP at ≤120 mm Hg, as tolerated. β-Blockers are first-line (1,3,7)[C].
  • Prior to discharge, thoracic MRI or chest CT scan should be obtained and followed at 1, 3, and 12 months, and then yearly to assess for complications (1)[A],(7)[C].
  • During follow-up, carefully attend to signs and symptoms of recurrent dissection.

DIET


NPO until surgical evaluation is complete and patient is classified as medical therapy only.  

PATIENT EDUCATION


Depending on etiology, emphasis must be placed on risk factors and prevention of recurrence: smoking cessation, BP control with β-blockers, avoidance of strenuous activity.  

PROGNOSIS


Hospital survival estimate, treated medically and surgically: 70%. Type A dissections treated surgically show a 90% survival rate at 3 years. Survival at 10 years is similar for both medically and surgically treated patients. Dissection recurrence risk: 5 years: 13%; 10 years: 23%.  

COMPLICATIONS


Recurrence, localized saccular aneurysm, cardiac tamponade, aortic valvular insufficiency, progressive aortic enlargement. Stent placement risks include paraplegia, stroke, embolization, side-branch occlusion, and infection.  

REFERENCES


11 Thrumurthy  SG, Karthikesalingam  A. The diagnosis and management of aortic dissection. BMJ.  2011;344:d8290.22 Hiratzka  LF, Bakris  GL, Beckman  JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. Circulation.  2010;121(13):e266-e369.33 Braverman  AC. Aortic dissection: prompt diagnosis and emergency treatment are critical. Cleve Clin J Med.  2011;78(10):685-696.44 Bossone  E, Suzuki  T, Eagle  KA, et al. Diagnosis of acute aortic syndromes: imaging and beyond. Herz.  2012;38(3):269-276.55 Shiga  T, Wajima  Z, Apfel  CC, et al. Diagnostic accuracy of transesophageal echocardiography, helical computed tomography, and magnetic resonance imaging for suspected thoracic aortic dissection: systematic review and meta-analysis. Arch Intern Med.  2006;166(13):1350-1356.66 De Le ³n Ayala  IA, Chen  YF. Acute aortic dissection: an update. Kaohsiung J Med Sci.  2012;28(6):299-305.77 Erbel  R, Alfonso  F, Boileau  C, et al. Diagnosis and management of aortic dissection. Eur Heart J.  2001;22(18):1642-1681.88 Mehta  RH, Suzuki  T, Hagan  PG, et al. Predicting death in patients with acute type A aortic dissection. Circulation.  2002;105(2):200-206.99 Nienaber  CA, Kische  S, Ince  H, et al. Thoracic endovascular aneurysm repair for complicated type B aortic dissection. J Vasc Surg.  2011;54(5):1529-1533.

ADDITIONAL READING


Nair  HC. Transesophageal echocardiography evaluation of thoracic aorta. Ann Card Anaesth.  2010;13(2):186.  

SEE ALSO


Ehlers-Danlos Syndrome; Hypertension, Essential; Hypertension, Secondary and Resistant; Marfan Syndrome  

CODES


ICD10


  • I71.00 Dissection of unspecified site of aorta
  • I71.01 Dissection of thoracic aorta
  • I71.03 Dissection of thoracoabdominal aorta
  • I71.02 Dissection of abdominal aorta

ICD9


  • 441.00 Dissection of aorta, unspecified site
  • 441.01 Dissection of aorta, thoracic
  • 441.03 Dissection of aorta, thoracoabdominal
  • 441.02 Dissection of aorta, abdominal

SNOMED


  • dissection of aorta (disorder)
  • dissection of thoracic aorta (disorder)
  • Dissecting aneurysm of thoracoabdominal aorta
  • Dissection of abdominal aorta (disorder)
  • Distal aortic dissection (disorder)
  • Type I dissection of thoracic aorta (disorder)
  • Type II dissection of thoracic aorta (disorder)

CLINICAL PEARLS


  • Acute pain is reported by 90% of patients with aortic dissections. The pain is more often sharp but may be tearing and is located in the chest, abdomen, or back. Maintain a high level of suspicion and act quickly if the diagnosis of aortic dissection is suspected.
  • Survival at 10 years is similar for both medically and surgically treated patients.
  • If there is a high probability of aortic dissection, a second diagnostic test should be obtained if the first is negative or inconclusive.
Copyright © 2016 - 2017
Doctor123.org | Disclaimer