Aortic dissection ( AD ) occurs when an injury to the deepest layer of the aorta allows blood to flow between the layers of the aortic wall, forcing a separate layer. In many cases, it is associated with sudden onset of chest or back pain, often described as "torn" in character. Also, vomiting, sweating, and a mild head may occur. Other symptoms can occur due to decreased blood supply to other organs such as stroke or mesenteric ischemia. Aortic dissection can quickly lead to death because there is insufficient blood flow to the heart or rupture of the aorta.
Aortic dissection is more common in those with a history of high blood pressure, a number of connective tissue diseases that affect the strength of blood vessel walls such as Marfan syndrome, bicuspid aortic valve, and previous cardiac surgery. Primary trauma, smoking, cocaine use, pregnancy, thoracic aortic aneurysm, arterial inflammation, and abnormal lipid levels are also associated with increased risk. Diagnosis is suspected based on symptoms with medical imaging such as computed tomography, magnetic resonance imaging, or ultrasound used to confirm and evaluate further dissection. The two main types are the Stanford A type that involves the first part of the aorta and the type B that does not.
Prevention is by controlling blood pressure and not smoking. Treatment of aortic dissection depends on the part of the aorta involved. Dissection involving the first part of the aorta usually requires surgery. Surgery can be performed either by opening in the chest or by repair of endovascular aneurysms; done from the inside of the blood vessels. Dissection involving the second part of the aorta can usually be treated with drugs that lower blood pressure and heart rate, unless there are complications.
Aortic dissection is relatively rare, occurring at an estimated rate of three per 100,000 people per year. This is more common in men than in women. The typical age at diagnosis is 63, with about 10% of cases occurring before 40. Without treatment, about half of people with type A die within three days and about 10% of people with type B die within a month. The first case of aortic dissection described is at the examination of King George II of England after his death in 1760. Surgery for aortic dissection was introduced in 1950 by Michael E. DeBakey.
Video Aortic dissection
Signs and symptoms
Approximately 96% of individuals with aortic dissection present with severe pain that has sudden onset. Pain can be described as a sensation of tobac, stabbing, or sharp; 17% of individuals feel the pain migrate when dissection extends into the aorta. The location of the pain is associated with the location of the dissection. Anterior chest pain is associated with dissection involving the ascending aorta, while interscapular pain (back) is associated with descending descending aorta. If the pain is pleuritic, it may show acute pericarditis caused by bleeding to the pericardial sac. This is a very dangerous occurrence, which suggests that an acute pericardial tamponade may be imminent. Pericardial tamponade is the most common cause of death from aortic dissection.
While the pain may be confused with the pain from myocardial infarction (heart attack), aortic dissection is usually unrelated to other signs that indicate myocardial infarction, including heart failure and ECG changes.
Individuals with diseased aortic disorders suffer from chronic disorders.
Less common symptoms seen in aortic dissection settings include congestive heart failure (7%), stupor (9%), stroke (6%), ischemic peripheral neuropathy, paraplegia, and heart attack. If the individual has an episode of fainting, about half the time is due to bleeding into the pericardium leading to pericardial tamponade.
The neurological complications of aortic dissection (ie stroke and paralysis) are caused by the involvement of one or more arteries that supply parts of the central nervous system.
If aortic dissection involves the abdominal aorta, a stomach aortic compromise is possible. In abdominal aortic dissection, the compromise of one or both renal arteries occurs in 5-8% of cases, whereas mesenteric ischemia (intestinal ischemia) occurs about 3% of the time.
Blood pressure
People with aortic dissection often have a history of high blood pressure; blood pressure varies greatly in presentation with acute aortic dissection, and tends to be higher in individuals with distal dissection. In individuals with proximal aortic dissection, 36% are present with hypertension, while 25% are present with hypotension. Proximal aortic dissection tends to be more associated with weakening of the vascular wall due to cystic medial degeneration. In those who come with distal aortic dissection (type B), 60-70% come with high blood pressure, while 2-3% come with low blood pressure.
Severe hypotension during presentation is a prognostic indicator of the grave. Usually associated with pericardial tamponade, severe aortic insufficiency, or aortic rupture. Accurate blood pressure measurement is important. Pseudohypotension (very low blood pressure measurements) can occur due to involvement of the brachiocephalic artery (supplying the right arm) or the left subclavian artery (supplying the left arm). Aortic_insufficiency Aortic insufficiency
Aortic insufficiency (AI) occurs in half to two thirds of ascending aortic dissection, and aortic aortic inastole heart murmur can be heard in about 32% of proximal dissection. The intensity (loudness) of the murmur depends on the blood pressure and may not be heard at low blood pressure.
There are many causes for AI in the setting of increased aortic dysfunction. Dissection can dilate the annulus of the aortic valve, so the valve leaflet can not wet the bed. Another mechanism is that dissection may extend to the aortic root and release a leaflet of the aortic valve. A third mechanism is that if there is a broad intimal tear, the intimal flap can prolapse to the LV outlet, causing intimalus intussusception into the aortic valve preventing proper valve closure.
Myocardial infarction
Myocardial infarction (heart attack) occurs in 1-2% of aortic dissection. The cause of infarction is the involvement of the coronary arteries, which supply the heart with oxygenated blood, in dissection. The right coronary artery is involved more often than the left coronary artery. If myocardial infarction is treated with thrombolytic therapy, mortality increases by more than 70%, mostly because bleeding to the pericardial sac causes cardiac tamponade.
Because aortic dissection may be present for emergency room physicians similar to myocardial infarction, clinicians should be careful to make a proper diagnosis before starting treatment for myocardial infarction since treatment regimens for myocardial infarction may be lethal in a person with aortic dissection..
Pleural effusion
Pleural effusion (collection of fluid in the space between the lungs and chest wall or diaphragm) can be caused by blood from aortic transient rupture or fluid due to an inflammatory reaction around the aorta. If pleural effusion develops due to aortic dissection, it is more common in the left hemithorax than right hemitorax.
Maps Aortic dissection
Cause
Aortic dissection is associated with hypertension (high blood pressure) and many connective tissue disorders. Vasculitis (inflammation of the arteries) is rarely associated with aortic dissection. It can also be a result of chest trauma. Approximately 72 to 80% of individuals present with aortic dissection have a history of previous hypertension. The use of illicit drugs with stimulants such as cocaine and methamphetamine is also a modifiable risk factor for AD. It could also be caused by smoking.
Bicuspid aortic valve (a type of congenital heart disease involving aortic valve) is found in 7-14% of individuals who have aortic dissection. This individual is susceptible to dissection in the ascending aorta. The risk of dissection in individuals with a bicuspid aortic valve is not associated with the degree of valve stenosis.
Connective tissue disorders such as Marfan syndrome, Ehlers-Danlos syndrome, and Loeys-Dietz syndrome increase the risk of aortic dissection. Similarly, vasculitides such as Takayasu arteritis, giant cell arteritis, polyarteritis nodosa, and Behcet's disease have been associated with subsequent aortic dissection. Marfan syndrome is found in 5-9% of individuals who have aortic dissection. In this subset, incidents in young individuals increase. Individuals with Marfan syndrome tend to have aortic aneurysm and are more susceptible to proximal dissection of the aorta.
Turner syndrome also increases the risk of aortic dissection, with dilatation of the aortic root.
Chest trauma that causes aortic dissection can be divided into two groups based on the causes: blunt chest trauma (usually seen in car accidents) and iatrogenic. The iatrogenic causes include trauma during cardiac catheterization or due to intra-aortic balloon pumps.
Aortic dissection may be the ultimate sequel of heart surgery. About 18% of individuals present with acute aortic dissection have a history of open heart surgery. Individuals who have experienced aortic valve replacement for aortic insufficiency are at very high risk because aortic insufficiency leads to increased blood flow in the rising aorta. This can cause dilation and weakening of the ascending aortic wall.
Syphilis only has the potential to cause aortic dissection at its tertiary stage.
Pathophysiology
Like all other arteries, the aorta consists of three layers, intima, media, and adventitia. Intima is in direct contact with blood in the vessels, and consists primarily of the layer of endothelial cells in the basement membrane; the media contains connective tissue and muscle, and the vessels are protected outside by adventitia, which consists of connective tissue.
In aortic dissection, the blood penetrates the intima and enters the media layer. High pressures tear apart separate media networks along the laminated plane separating the inner two-thirds and the outer third of the separate media. It can propagate along the aorta for variable distance forward or backward. The dissection that spreads to the iliac bifurcation (with the bloodstream) is called anterograde dissection and which spreads in the direction of the aortic root (opposite of the bloodstream) is called retrograd dissection. The initial tear is usually within 100 mm of the aortic valve, so retrograde dissection can easily harm the pericardium leading to hemopericardium. Anterograde dissection may spread throughout the aortic iliac bifurcation, break the aortic wall, or reshape into the intravascular lumen leading to the double-barrel aorta. The aortic double-barrel reduces blood flow pressure and reduces the risk of rupture. Rupture causes bleeding into the body cavity, and the prognosis depends on the area ruptured. Retroperitoneal and pericardial rupture are both possible.
The incidence of initiation in aortic dissection is a tear in the aortic intima layer. Because of the high pressure in the aorta, blood enters the media at the point of tear. The force of blood that enters the media causes tears to elongate. This can proximal (closer to the heart) or distal (distant from the heart) or both. Blood flows through the medium, creating a fake lumen (the actual lumen is the normal blood channel in the aorta). Separating the fake lumen from the true lumen is the intima tissue layer known as the intimal flap.
Most of the aortic disorders originate from the intimate tears either in the aorta up (65%), the aortic arch (10%), or just distal to the arteriosus ligamentum in the thoracic desendens (20%).
When blood flows into a lumen counterfeit, it may cause secondary tears in the intimate. Through this secondary tears, blood can return to the true lumen.
While it is not always clear why intima ruptures can occur, it often involves the degeneration of collagen and elastin that form the media. This is known as cystic medial necrosis and is most commonly associated with Marfan syndrome and is also associated with Ehlers-Danlos syndrome.
In about 13% of aortic dissection, there is no evidence of intact tears found. In this case, inciting instances are considered as intramural hematomas (caused by bleeding in the media). Since there is no direct relationship between the true lumen and the false lumen in this case, the diagnosis of aortic dissection by aortography is difficult if the cause is an intramural hematoma. Secondary aortic dissection due to intramural hematoma should be treated the same as that caused by intimal tears.
Diagnosis
Because of the various symptoms of aortic dissection, diagnosis is sometimes difficult. Attention should be increased in those with low blood pressure, neurological problems, and unequal pulsations.
While taking a good history of the individual may be very suggestive of aortic dissection, the diagnosis can not always be made by history and physical signs alone. Often, the diagnosis is made by visualizing the intimal flap on a diagnostic imaging test. Common tests used to diagnose aortic dissection include a chest CT scan with iodinated contrast material and a transesophageal echocardiogram. The proximity of the aorta to the esophagus allows the use of high-frequency ultrasound for better anatomical images. Other tests that may be used include aortogram or magnetic aortic resonance angiogram. Each of these tests has their pros and cons, and they lack the same sensitivity and specificity in the diagnosis of aortic dissection.
In general, selected imaging techniques are based on possible pretest diagnosis, availability of modality testing, patient stability, and test sensitivity and specificity.
D-dimer
Blood level D-dimer measurements may be useful in diagnostic evaluation. Levels less than 500 ng/ml can be considered as evidence against the diagnosis of aortic dissection, although these guidelines apply only in cases considered "low risk" and within 24 hours of symptom onset. The American Heart Association does not recommend using this test in making a diagnosis, because the evidence is still tentative.
Chest Rontgen
Chest radiographs can show a morphological changes in the thoracic aorta that can be seen in aortic dissection. Classically, the new mediastinal widening in radiography is of moderate sensitivity to detect rising aortic dissection; However, these findings have low specificity, as many other conditions can cause mediastinal dilation.
There are several other related radiographic findings:
- The "calcium mark" represents a clear separation of calcified intima from the outer aortic edge of more than 10 mm.
- Pleural effusions, more often in descending aortic dissection, and usually left on the left side.
- Other: destruction of aortic aorta, major left trunk bronchial depression, loss of paratracheal line, and tracheal deviation.
Importantly, about 12 to 20% of aortic dissection is undetectable by chest radiography; therefore, "normal" thoracic radiography does not rule out aortic dissection. If there is high clinical suspicion, more sensitive imaging tests (CT angiogram, MR angiography, or transesophageal echo) may be warranted.
Computed tomography
Computed tomography angiography is a noninvasive rapid test that provides an accurate three-dimensional view of the aorta. These images are produced by taking fast and thin chest and stomach pieces, and combining them on the computer to make cross-cuts. To describe the aorta with the accuracy required to make a proper diagnosis, the iodinated contrast material is injected into the peripheral vein. Contrast is injected and the scan is performed using the bolus tracking method. This type of scan is time for injection to capture contrast when entering the aorta. The scan then follows the contrast as it flows through the vessels. It has a sensitivity of 96 to 100% and a specificity of 96 to 100%. Losses include iodinated contrast material requirements and the inability to diagnose intima tear locations.
MRI
Magnetic resonance imaging (MRI) is also used for detection and assessment of aortic dissection, with 98% sensitivity and 98% specificity. Aortic MRI examination results in a three-dimensional aortic reconstruction, allowing the physician to determine the location of the intimal tear and involvement of the branch vessels, and to find the presence of secondary tears. This is a noninvasive test, does not require the use of iodinated contrast material, and can detect and measure aortic insufficiency rates.
The disadvantage of an MRI scan in the face of aortic dissection is that it has limited availability and is often only in a larger hospital, and a relatively time-consuming scan, which may be harmful to people who are already very unhealthy. Due to the high intensity magnetic field used during MRI, it is contraindicated in individuals with metal implants. In addition, many individuals experience claustrophobia while in the MRI scanning tube.
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Transesofageal echocardiogram (TEE) is a relatively good test in the diagnosis of aortic dissection, with a sensitivity of up to 98% and a specificity of up to 97%. This has been the preferred imaging modality for suspected aortic dissection. This is a relatively non-invasive test, which requires individuals to swallow the echocardiography probe. This is excellent in the evaluation of AI in the setting up of aortic dissection, and to determine whether the ostia (origin) of the coronary artery is involved. While many institutions provide sedation during transesophageal echocardiography to increase patient comfort, it can be done in cooperative individuals without the use of sedation. TEE deficiencies include the inability to visualize the distal ascending aorta (the beginning of the aortic arch), and the lower abdominal aorta located below the abdomen. TEE may be technically difficult for individuals with oesophageal stricture or varicose veins.
Aortogram
An aortogram involves placing a catheter in the aorta and injecting contrast material while taking X-rays from the aorta. This procedure is known as aortography. Previously considered a gold standard of diagnostics, it has been replaced by other less invasive imaging modalities.
Classification
Several different classification systems have been used to describe aortic dissection. One such classification is based on the chronicle and label of aortic dissection as hyperacute (& lt; 24 hours duration), acute (2-7 days), subacute (8-30 days), and chronic (& gt; 30 days). The commonly used system is based on the dissection anatomy or the duration of symptom onset before presentation. The Stanford system is used more generally now, as it is more aligned with patient management.
DeBakey
The DeBakey system, named after cardiothoracic surgeon Michael E. DeBakey, is an anatomical description of aortic dissection. It categorizes dissection based on where the original intima tears are located and the extent of dissection (localized either the rising aorta or descendent aorta or involving the aorta rising and falling.
- Type I - comes from ascending the aorta, and spreads at least to the arch of the aorta and often beyond it. It is most commonly seen in patients less than 65 years old and is the most deadly form of the disease.
- Type II - comes from the rising and limited aorta.
- Type III - comes from the descending aorta and rarely extends to the proximal, but will extend in the distal direction. Most common in elderly patients with atherosclerosis and hypertension.
Stanford
The Stanford classification is divided into two groups, A and B, depending on whether the aorta rises involved.
- A - involves the aorta up and/or aortic arch, and may be aortic desendens. Tears can be derived from an ascending aorta, aortic arch, or less frequently, on aorta desendens. These include DeBakey type I and II.
- B - involves aortic descending or curvature (distal to the left subclavian artery), without the aortic involvement up. These include DeBakey type III.
The Stanford classification is useful because following clinical practice, such as ascending aortic dissection generally requires primary surgical treatment, whereas Type B dissection is generally treated medically as a preliminary surgical treatment for complications.
The reason for the improvement of type A surgery is that elevated aortic surgery often involves the aortic valve, which, after losing its suspension support, the telescope into the aortic root, resulting in aortic disability. The valve should be resuspended to be repeated, as well as to repair or prevent coronary artery injury. Also, the dissection area is removed and replaced by a Dacron graft to prevent further dissection from occurring. However, Type B dissections are not repaired, from the point of view of death, by surgery, unless leaking, breaking, or compromising with other organs, such as the kidneys, occur.
Prevention
Among the risk factors recognized for aortic dissection, hypertension, high lipid levels (such as cholesterol) in the blood, and tobacco smoking are considered as preventable risk factors.
Improved aortic enlargement from an aneurysm or previously unrecognized and untreated aortic dissection is recommended when larger than 6 cm (2.4 inches) in size to reduce the risk of dissection. Improvement may be recommended when greater than 4.5 cm (1.8 inches) in size if the person has one of several connective tissue disorders or family history of a ruptured aorta.
Management
In acute dissection, treatment options depend on the location. For Stanford type A (ascending aortic) dissection, surgical management is superior to medical management. For uncomplicated type B (distal aortic) simple surgery (including abdominal aortic dissection), medical management is preferred over surgery.
The risk of death due to aortic dissection is highest in the first few hours after dissection begins, and decreases thereafter. Therefore, different therapeutic strategies for the treatment of acute dissection are compared with chronic dissection. Acute dissection is one in which individuals are present within the first two weeks. If the individual has survived from this window period, his prognosis increases. About 66% of all dissections are present in the acute phase. Individuals present two weeks after the onset of dissection are said to have chronic aortic dissection. These individuals have been selected as survivors of acute episodes and can be treated with medical therapy as long as they are stable.
Medication
Aortic dissection generally appears as a hypertensive emergency, and the primary consideration of medical management is strict blood pressure control. Target blood pressure should be a mean arterial pressure (MAP) of 60 to 75 mmHg, or the lowest tolerable blood pressure. The initial decline should be around 20%.
Another factor is to reduce the shear force dP/dt (the power of blood removal from the left ventricle). Handling long-term physical, emotional, and psychological pressure is important for controlling blood pressure.
Beta blockers are the first-line treatment for patients with acute and chronic aortic dissection. In acute dissection, fast-acting agents that can be administered intravenously and have an easier to adjust dose (such as esmolol, propranolol, or labetalol) are preferred. Vasodilators such as sodium nitroprusside can be considered for people with high blood pressure ongoing, but they should not be used alone, as they often stimulate a reflexive increase in heart rate.
Calcium channel blockers can be used in the treatment of aortic dissection, especially if contraindications to the use of beta blockers exist. Calcium channel blockers typically used are verapamil and diltiazem, due to the combined vasodilator and negative inotropic effects.
If the individual has refractory hypertension (persistent hypertension at a maximum dose of three different classes of antihypertensive agents), renal artery involvement in the aortic dissection area should be considered.
Surgery
Indications for aortic disorder surgical treatment include acute proximal aortic dissections and acute distal anesthesia disorders with one or more complications. Complications include the compromise of vital organs, rupture or rupture of the aorta, retrograde dissections to the aorta rise, and the history of Marfan syndrome or Ehlers-Danlos syndrome.
The goal in surgical management of aortic dissection is to resect (eliminate) the most damaged segment damaged from the aorta and to remove the entry of blood into the false lumen (both in the initial intimal tears and secondary tears along the vessels). While the excision of intima tears can be performed, it does not significantly alter the mortality rate.
The specific treatment used depends on the segment or segment of the aorta involved. Some treatments are:
- Open aortic surgery by replacing the damaged aorta part with a tubular graft (often made from Dacron) when no damage to the aortic valve is visible
- Bentall procedure - replacement of damaged aortic part and aortic valve replacement
- David's procedure - replacement of damaged aortic part and reimplantation of the aortic valve
- Improved chest endovascular aorta, minimally invasive surgical procedure usually combined with ongoing medical management
- Replacement of damaged aorta parts with unsolved vascular ring duct junctions: Vascular ring connector is a titanic ring used as a stent on a vascular graft to achieve rapid, blood-covered, and seamless anastomosis. The two grooves on the ring surface are for the fixation of the vascular and aortic graft. Ribbons used to bind rings provide a larger contact surface area than traditional stitching, thus providing a stronger anastomosis and better operating results.
A number of comorbid conditions increase the risk of surgical improvement of aortic dissection. These conditions include the following:
- Long-term preoperative evaluation (increase in length of time before surgery)
- Aged
- Complaints (eg coronary artery disease)
- Leakage of aneurysms
- Heart tamponade
- Shock
- History of myocardial infarction
- History of renal failure (acute or chronic renal failure)
Followup
Long-term follow-up in individuals who survive aortic dissection involves tight blood pressure control. The relative risk of late aortic aneurysm rupture is 10 times higher in individuals with uncontrolled hypertension, compared with individuals with systolic pressure below 130 mmHg.
The highest risk of death in the first two years after the acute event, and the individual should be followed during this time period. About 29% of late deaths after surgery are due to rupture of surgical aneurysms or other aneurysms. In addition, 17% to 25% incidence occurs in the formation of a new aneurysm, usually due to residual lumen lacer dilatation. This new aneurysm is more likely to break, because the walls are thinner.
Serial aortic imaging is recommended, with MRI being the preferred imaging technique.
Epidemiology
Establishing the incidence of aortic dissection has been difficult since many cases are only diagnosed after death (which may be caused by other causes), and are often initially misdiagnosed. Aortic dissection affects approximately 2.0-3.5 persons per 100,000 per year. Studies from Sweden show that the incidence of aortic dissection may increase. Men are more often affected than women: 65% of all people with aortic dissection are males. The median age at diagnosis was 63 years. In women before age 40, half of all aortic dissections occur during pregnancy (usually in the third trimester or early postpartum period). Dissection occurs in about 0.6% of pregnancies.
Prognosis
Of all people with aortic dissection, 40% died instantly and did not reach the hospital on time. The rest, 1% die every hour, making rapid diagnosis and treatment a priority. Even after diagnosis, 5-20% die during surgery or in the immediate postoperative period. In aortic surgery, if surgery is decidedly inappropriate, 75% die within 2 weeks. With aggressive treatment, 30-day survival for thoracic dissection may be as high as 90%.
History
The earliest documented aortic diagnosis case was associated with Frank Nicholls in his autopsy report of King George II of England, who was found dead on 25 October 1760; the report describes the dissection of the aortic arch and into the pericardium. The term "aortic dissection" was introduced by French physician J.P. Maunoir in 1802, and Renà ©  © Laennec labeled the condition of "dissecting aneurysm". London cardiologist Thomas Bevill Peacock contributed to the understanding of the condition by publishing two series of cases described in the literature thus far: 19 cases in 1843 and 80 in 1863. Typical symptoms of torn pain in the chest were recognized in 1855 when a case was diagnosed in life.
Surgery for aortic dissection was first introduced and developed by Michael E. DeBakey, Denton Cooley, and Oscar Creech, cardiac surgeons associated with Baylor College of Medicine, Houston, Texas, in 1954. DeBakey developed his own aortic dissection at age 97 2005, and underwent surgery in 2006. Endovascular treatment of aortic dissection was developed in the 1990s.
Society and culture
Ritter Rules
The ritter rule is a compilation of reminders, symptoms, and risk factors designed to prevent misdiagnosis of thoracic aorta dissection. The rule was named for actor John Ritter, who died of thoracic aortic dissection on September 11, 2003. Ritter was initially misdiagnosed and later treated for a heart attack. The Ritter Rules were developed by Dianna Milewicz, from the University of Texas Health Science Center in Houston, and jointly published in March 2010 by the John Ritter Foundation and Thoracic Aorta Disease Coalition.
References
External links
Source of the article : Wikipedia
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