Aortic dissection ppt
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An aortic dissection is a tear in the inner layer of the aorta that allows blood to flow between the layers of the aortic wall, creating a false passageway. It is a medical emergency that requires prompt diagnosis and treatment. Type A dissections, which involve the ascending aorta, require emergency surgery while type B dissections, involving only the descending aorta, are generally treated medically with blood pressure control. Surgical treatment of type A dissections aims to remove the damaged aortic segment and restore blood flow through the aorta using a graft.
Aortic dissection ppt
- 2. Aortic dissection • An aortic dissection is a tearing of the layers within the aortic wall, classically associated with sudden- onset chest or back pain, a pulse deficit, and mediastinal widening on a chest radiograph. • Depending on size and degree of aortic involvement, it may result in marked hemodynamic instability and, often, a rapid death.
- 4. • Prompt diagnosis and appropriate treatment are critical to maximize the possibility of survival. • Significant dissections are often fatal and rarely survive to clinical attention; • majority of dissections seen in the critical care environment are either Subacute, contained, or sparing the major aortic vessels.
- 5. • Anatomy of injury in aortic dissection • The tear usually originates in the intima. • It then propagates into the media creating a false channel for blood to flow and hematoma to form. • The dissection process may alternatively originate with hemorrhage in the media that secondarily causes disruption of the intima
- 7. • In 70% of patients, the intimal tear, which is the beginning of the dissection, occurs in the ascending aorta. • In 20% of patients it occurs in the descending thoracic aorta, • in 10% of patients it occurs in the aortic arch. • Only rarely is an intimal tear identified in the abdominal aorta.
- 8. DeBakey classifications of aortic dissection • The two classification systems most commonly used both have anatomic as well as management implications.
- 9. • The DeBakey classification describes • three types of dissection : Type I: extends from aortic root to beyond the ascending aorta • Type 11: involves only the ascending aorta • Type Ill: Begins distal to the takeoff of the left subclavian artery and has two subtypes • Type III A: limited to the thoracic aorta • Type 111 B: extends below the diaphragm
- 11. • The Stanford classification has two types of dissection • Type A: involves the ascending aorta • TYPE B: involves the descending aorta, distal to the left subclavian artery
- 12. • Approximately 75% of patients with ruptured aortic aneurysm will reach an emergency department alive. • Whereas for aortic dissection 40% die immediately. • Furthermore, only 50% to 70% will be alive 5 years after surgery depending on age and underlying cause.
- 13. • For untreated acute dissection of the ascending aorta the mortality rate is 1 % to 2% per hour after onset. • For type A dissections treated medically it is 20% within the first 24 hours and 50% by 1 month after presentation. • Even with surgical intervention the mortality rate for type A dissection may be as high as 10% after 24 hours and nearly 20% 1 month after repair.
- 14. • type B dissection is less dangerous than type A, it is still associated with an extremely high mortality. • The 30-day mortality rate for an uncomplicated type B dissection approaches 10%. • patients with type B dissection who have complications such as limb ischemia, renal failure, or visceral ischemia have a 2-day mortality upwards of 20% and may prompt the need for surgical intervention
- 15. Risk factors
- 16. • Hypertension: • Present in 70% to 90% of patients with acute dissection. • Advanced age: • Mean of 63 years in the International Registry of Acute Aortic Dissection (IRAD). • Male sex: • Represented by 65% of patients in the IRAD. • Family history: • Recently recognized is a genetic, nonsyndromic familial form of thoracic aortic dissection
- 17. • Trauma (deceleration/torsional injury) . • Congenital and inflammatory disorders: • Present as Marfan syndrome in almost 5% of total patients in the IRAD • and half of those patients under age 40 years
- 18. Other associated congenital disorders • Ehlers-Danlos syndrome, Loeys-Dietz syndrome, • bicuspid aortic valve, • aortic coarctation, • Turner syndrome, Takayasu and giant-cell aortitis, relapsing polychondritis (Behcet disease, spondyloarthropathies),
- 19. • confirmed genetic mutations known to predispose to dissections • (TGFBRI, TGFBRP, FBNI, ACTAP, or MYHI I ) .
- 20. • Pregnancy • Associated with 50% of dissections in women under age 40 and most frequently occurring in the third trimester. • This might be attributable to elevations in cardiac output during pregnancy that cause increased wall stress.
- 21. Circadian and seasonal variations • Producing a higher frequency of dissection in the morning hours and in the winter months. • Iatrogenic • Occurring as a consequence of invasive procedures or surgery, especially when the aorta has been entered or its main branches have been cannulated, such as for cardiopulmonary bypass
- 22. • The common clinical signs and symptoms of aortic dissection
- 23. Pain • The most common presenting symptom is chest pain, occurring in up to 90% of patients with acute dissection. • Classically, for type A dissections, sudden onset of severe anterior chest pain with extension to the back occurs that is described as ripping or tearing in nature
- 24. • The pain is usually of maximal intensity from its inception and is frequently unremitting. • It may migrate along the path of the dissection. • The pain of aortic dissection may mimic that of myocardial ischemia. • Patients with type B dissections are more likely to be seen with back pain ( 64%) alone.
- 25. Syncope • Syncope is a well-recognized clinical feature of dissection, occurring in up to 13% of cases. • Impairments of cerebral blood flow can be due to Acute hypovolemia, low cardiac output, or dissection-involvement of the cerebral vessels.
- 26. • Patients with a presenting syncope were significantly more likely to die than were those without syncope (34% vs. 23%), • likely because of the frequent correlation with associated • cardiac tamponade, • stroke, • decreased consciousness, • and spinal cord ischemia.
- 27. Neurologic symptoms • 17% of patients were seen initially with neurologic symptoms, 53% of which represented ischemic stroke. • Neurologic complications may result from hypotension, malperfusion, distal thromboembolism, or nerve compression. • Acute paraplegia as a result of spinal cord malperfusion has been described as a primary manifestation in 1% to 3% of patients. • Up to 50% of neurologic symptoms may be transient
- 28. Cardiovascular manifestations • The heart is the most frequently involved end- organ in acute proximal aortic dissections. • Acute aortic regurgitation may be present in 41 % to 76% of patients with proximal dissection caused by widening of the aortic annulus resulting in incomplete valve closure • actual disruption of the aortic valve leaflets from the dissection flap
- 29. • Clinical manifestations of dissection- related aortic regurgitation span from • mere diastolic murmurs without clinical significance • to overt congestive heart failure • and cardiogenic shock.
- 31. Myocardial ischemia or infarction • May result from compromised coronary artery flow by an expanding false lumen that compresses the proximal coronary or by extension of the dissection flap into the coronary artery ostium. • This occurs in 7% to 19% of patients with proximal aortic dissections. • Clinically, these present as electrocardiographic changes consistent with primary myocardial ischemia and/or infarction. • MI IS DANGEROUS FOR A PATIENT OF AORTIC DISSECTION
- 32. • Cardiac tamponade is diagnosed in 8% to 10% of patients seen with acute type A dissections. • It is associated with a high mortality and should prompt consideration for emergent drainage and aortic repair. • Hypertension occurs in greater than 50% of patients with dissection, more commonly with distal disease. Ongoing renal ischemia can produce severe hypertension
- 33. • Hypotension/shock may present in up to 20% of patients with dissection. • This may be a result of cardiac tamponade from aortic rupture into the pericardium, • dissection, or compression of the coronary arteries, acute aortic regurgitation, • acute blood loss, • true lumen compression by distended false lumen, or an intra- abdominal catastrophe. • Cardiogenic shock In approximately 6% of cases. • This can be due to acute aortic regurgitation or ongoing myocardial ischemia
- 34. • Peripheral vascular complications • Can manifest as pulse and/or blood pressure differentials or deficits and occur in approximately one third to one half of patients with proximal dissection. • Etiology is partial compression, obstruction, thrombosis, or embolism of the aortic branch vessels, resulting in cerebral, renal, visceral, or limb ischemia. • Peripheral pulse deficits should alert the clinician to possible ongoing renal or visceral ischemia unable to be detected from physical examination or laboratory values alone
- 36. Pulmonary complications • May manifest as pleural effusions, which occur most frequently on the left. • Causes include rupture of the dissection into the pleural space or weeping of fluid from the aorta as an inflammatory response to the dissection
- 37. Laboratory abnormalities associated with aortic dissection • Laboratory data are usually unrevealing, but anemia from blood loss into the false lumen can occur. • A moderate leukocytosis (10,000-14,000 white cells per mL) is sometimes seen. • Lactic acid dehydrogenase and bilirubin levels may be elevated because of hemolysis within the false lumen.
- 38. • Disseminated intravascular coagulation has been reported. • Currently, randomized controlled data do not support the use of D-dimers or experimental serum markers • (plasma smooth muscle myosin heavy chain protein, high-sensitivity C-reactive protein)
- 39. Imaging modalities used to diagnose aortic dissection • On the basis of clinical risk factors and conditions, presentation, and associated examination findings, patients are stratified into Low- intermediate- or high- risk categories
- 40. Further work-up is dictated by this pretest probability index. • Some patients with acute dissection initially have no high-risk features, creating a diagnostic dilemma. • According to most recent guidelines, if a clear alternative diagnosis is not established after the initial evaluation, then obtaining a diagnostic aortic imaging study should be considered
- 41. • Although lacking specificity, a chest radiograph should be obtained as part of the initial diagnostic evaluation. • • A radiograph abnormality is seen in up to 90% of patients with aortic dissection; • most frequent is widening of the aorta and mediastinum
- 42. • Other findings may include a • localized hump on the aortic arch, • displacement of calcification in the aortic knob, and pleural effusions. • However, approximately 40% of radiographs in acute dissection lack a widened mediastinum, and as many as 16% are normal. • Thus a negative radiograph must not delay definitive aortic imaging in patients deemed at high risk for aortic dissection by initial screening
- 45. • (CT), (MRI), and (TEE) Are all highly accurate imaging modalities that may be used to make the diagnosis; • all can provide acceptable diagnostic accuracy. • Transthoracic echocardiography has limited diagnostic accuracy
- 50. Aortography • Which was once the test of choice, is no longer used routinely because it is invasive and time- consuming and involves exposure to intravenous contrast dye. • The most recent comparative study with nonhelical CT, MRI, and TEE showed 100% sensitivity for all modalities, with better specificity of CT (100%) as compared with TEE or MRI
- 51. • A recent metaanalysis found that all three imaging techniques provided equally reliable results.
- 52. • It should be noted, however, that the diagnosis of acute aortic dissection can be difficult and occasionally cannot be absolutely excluded by a single imaging study. • If a high clinical suspicion exists despite initially negative imaging, then consideration should be given to a second imaging modality.
- 53. Diagnosis could be confused with Aortic dissection • Acute myocardial infarction • Pulmonary embolism • Acute cholycystitis • Pleuritis • Pericarditis • Atherosclerotic emboli Cerebrovascular accidents . . Acute aortic regurgitation • Thoracic nondissecting aneurysm . Mediastinal cysts or tumors Cholecystitis .
- 54. Differentiate between the management of Stanford type A and type B dissections • An acute type A dissection is a surgical emergency • medical management is critical to halt progression of dissection while diagnostic work-up takes place
- 55. • Pain management • gradual down-titration of blood pressure • are critical to prevent extension of dissection
- 56. • blood products and intravascular access should be available in event of aortic rupture. • Patients with uncomplicated type B dissection are preferably managed medically with B- blockers and other antihypertensive agents. Surgical intervention has no demonstrable superiority • except in cases of • failed medical management manifesting as malperfusion, • aortic expansion with potential for imminent rupture, • or intractable pain
- 57. • Ongoing advances with less invasive interventions (endovascular stent grafts and endovascular fenestration procedures) suggest an expanded role for interventional management in treatment of acute type B dissection, especially in experienced centers.
- 58. The strategies for medical management of dissection and commonly used medications The goals of medical therapy are to treat pain, to aggressively control blood pressure, to determine need for surgical or endovascular intervention.
- 59. • Patients who are seen with hypotension should receive the following: • Prompt but judicious volume resuscitation and hemodynamic support with intravenous vasopressors to maintain a goal mean arterial pressure of 70 mm Hg . • Rapid search for underlying etiology (tamponade, myocardial dysfunction, acute hemorrhage) • Emergent surgical consultation for operative management
- 60. • In those who are seen initially with hypertension, • the blood pressure should generally be lowered to a systolic of 100 to 120 mm Hg, • to a mean of 60 to 65 mm Hg, • or to the lowest level that is compatible with perfusion of the vital organs. • The aortic wall stress is affected by • the heart rate, • blood pressure, • velocity of ventricular contraction .
- 61. • The ideal antihypertensive regimen must decrease blood pressure without increasing cardiac output through peripheral vasodilatation. • This is because an increased cardiac output can increase flow rates producing higher aortic wall stress and thus propagating dissection
- 62. • Intravenous B-blockers (commonly esmolol, labetalol, propranolol, or metoprolol) are considered the first-line medical stabilization regimen because they affect all three parameters without increases in cardiac output and aortic wall stress. • In patients who are unable to tolerate B- blockade, nondihydropyridine calcium channel antagonists (verapamil, diltiazem) offer an acceptable alternative
- 63. • Often, single-drug therapy alone is inadequate to optimize blood pressure management. • Adequate pain control is essential not only for patient comfort but also to decrease sympathetic mediated increases in heart rate and blood pressure. • This may be accomplished with intravenous opioid analgesics.
- 64. • If B-blockade and adequate pain control are ineffective to control blood pressure, • addition of a rapidly acting, easily titratable intravenous vasodilator, such as nitroprusside should be considered.
- 65. • Other agents, such as Nicardipine, nitroglycerin, and fenoldopam are also acceptable. Vasodilator therapy without prior B-blockade may cause reflex tachycardia and increased force of ventricular contraction leading to greater wall stress and potentially causing false lumen propagation; therefore adequate B-blockade must be established first, before the vasodilator is initiated.
- 66. The surgical approach for repair of Stanford type A dissection. • The purpose of surgery is to • resect the aortic segment containing the proximal intimal tear, • to obliterate the false channel, • and to restore aortic continuity with a graft or by reapproximating the transected ends of aorta. • For patients with aortic insufficiency, it may be possible to resuspend the aortic valve, but in some cases replacement of the aortic valve is necessary.
- 67. • In some cases of proximal dissection, reimplantation of the coronary arteries is required. • If a DeBakey type II dissection is present, entire dissected aorta should be replaced. • Surgery to repair an aortic dissection generally requires cardiopulmonary bypass and, often, deep hypothermic circulatory arrest.
- 68. Recent alternatives to surgical repair o • An endovascular technique of stent-grafting and/or balloon fenestration may be used for initial surgical treatment of some dissections. • Indications for open or endograft treatment are based on anatomic features of the lesion, clinical presentation and course, patient comorbidities, and anatomic constraints related to endograft technology
- 69. • Dissections pose a complex situation because branches of aorta may be perfused from either true or false lumen. • Often, both true and false lumens are patent and some of visceral, renal, or lower extremity vessels are fed by one channel and remainder by other. • Consideration must be given to how blood flow reaches vital organs before considering treatment of a dissection with an endovascular stent-graft
- 71. • For type B dissection, an increasing number of reports show better results with endovascular repair versus open surgical repair.
- 72. • However, longer-term (5 year) data are needed to fully assess potential impact of stent- grafting for acute dissection, • including Effects on survival, • clinical outcomes, • and long-term aortic remodeling.
- 74. The use of fenestrated endografts • A new era in treatment of aortic dissections. • Unsuitable anatomy is a significant barrier to use of endovascular stent-grafts for most forms of aortic disease, • where ostia of major vessels would otherwise be partially or completed covered with deployment of a stent-graft
- 75. The use of fenestrated endografts • Using preoperative Three-dimensional CT aortic reconstruction customized stents can be constructed, • featuring holes (fenestrations) or side- branches matched to patient-specific anatomy to ensure perfusion to major aortic branch vessels.
- 76. • The use of fenestrated endografts • Current trials are underway in Europe and United States for their use for complex aneurysmal disease, and expectations are high for similar application to aortic dissection