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Death occurs immediately after traumatic rupture of the thoracic aorta 75%–90% of the time since bleeding is so severe, and 80–85% of patients die before arriving at a hospital. Of those who live to reach a hospital, 23% die at the time of or shortly after arrival. In the US, an estimated 7,500–8,000 cases occur yearly, of which 1,000–1,500 make it to a hospital alive; these low numbers make it difficult to estimate the efficacy of surgical options. However, if surgery is performed in time, it can offer a chance of survival.
Though there is a concern that a small, stable tear in the aorta could enlarge and cause complete rupture of the aorta and heavy bleeding, this may be less common than previously believed as long as the patient's blood pressure does not get too high.
Traumatic aortic rupture is treated with surgery. However, morbidity and mortality rates for surgical repair of the aorta for this condition are among the highest of any cardiovascular surgery. For example, surgery is associated with a high rate of paraplegia, because the spinal cord is very sensitive to ischemia (lack of blood supply), and the nerve tissue can be damaged or killed by the interruption of the blood supply during surgery.
A less invasive option for treatment is endovascular repair, which does not require open thoracotomy and can be safer for people with other injuries to organs.
Since high blood pressure could exacerbate an incomplete tear in the aorta or even separate it completely from the heart, which would almost inevitably kill the patient, hospital staff take measures to keep the blood pressure low. Such measures include giving pain medication, keeping the patient calm, and avoiding procedures that could cause gagging or vomiting. Beta blockers and vasodilators can be given to lower the blood pressure, and intravenous fluids that might normally be given are foregone to avoid raising it.
Mortality from aortic rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.
Conservative management is indicated in people where repair carries a high risk of mortality and in patients where repair is unlikely to improve life expectancy. The mainstay of the conservative treatment is smoking cessation.
Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceeds the risk of rupture. As an AAA grows in diameter, the risk of rupture increases. Surveillance until an aneurysm has reached a diameter of 5.5 cm has not been shown to have a higher risk as compared to early intervention.
Injuries to the aorta are usually the result of trauma, such as deceleration and crush injuries. Deceleration injuries almost always occur during high speed impacts, such as those in motor vehicle crashes and falls from a substantial height. Several mechanical processes can occur and are reflected in the injury itself. A more recently proposed mechanism is that the aorta can be compressed between bony structures (such as the manubrium, clavicle, and first rib) and the spine. In the ascending aorta (the portion of the aorta which is almost vertical), one mechanism of injury is torsion (a two-way twisting).
No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs. Blood pressure and lipids should, however, be treated per usual.
Aortic ruptures can be repaired surgically via open aortic surgery or using endovascular therapy (EVAR), regardless of cause, just as non-ruptured aortic aneurysms are repaired. An aortic occlusion balloon can be placed to stabilize the patient and prevent further blood loss prior to the induction of anesthesia.
There are inconsistencies in the terminology of aortic injury. There are several terms which are interchangeably used to describe injury to the aorta such as "tear", "laceration", "transection", and "rupture". "Laceration" is used as a term for the consequence of a tear, whereas a "transection" is a section across an axis or cross section. For all intents and purposes, the latter is used when a tear occurs across all or nearly all of the circumference of the aorta. "Rupture" is defined as a forcible disruption of tissue. Some disagree with the usage of "rupture" as they believe it implies that a tear is incompatible with life; however, the term accurately gauges the severity of tears in the aorta. A rupture can be either complete or partial, and can be classified further by the position of the tear.
Currently, there is controversy over whether or not inheritance truly plays a role in FAD, and if so which gene it acts upon. FAD does not come from strictly one predisposing factor, such as hypertension. It is suggested that the combination of environmental factors along with genetics may contribute to causing FAD. Before newer and more effective cures and therapies can be developed, first the specific gene mutation must be identified. Until such a gene is determined, scientists say patient education, and physician awareness is vital. Currently scientists have found animal models to be beneficial in understanding the pathology behind FAD. In the future there is hope to develop drugs that will better support and strengthen the aortic wall. Endovascular methods of treatment are becoming increasingly popular, and scientists hope to use this technique in both acute and chronic cases.
The risk of aneurysm enlargement may be diminished with attention to the patient's blood pressure, smoking and cholesterol levels. There have been proposals to introduce ultrasound scans as a screening tool for those most at risk: men over the age of 65. The tetracycline antibiotic doxycycline is currently being investigated for use as a potential drug in the prevention of aortic aneurysm due to its metalloproteinase inhibitor and collagen stabilizing properties. In contrast, fluoroquinolones antibiotics are being investigated as a potential contributor to aortic aneurysms, given their tendency to break down collagen fibrils.
Anacetrapib is a cholesteryl ester transfer protein inhibitor that raises high-density lipoprotein (HDL) cholesterol and reduces low-density lipoprotein (LDL) cholesterol.
Anacetrapib reduces progression of atherosclerosis, mainly by reducing non-HDL-cholesterol, improves lesion stability and adds to the beneficial effects of atorvastatin
Elevating the amount of HDL cholesterol in the abdominal area of the aortic artery in mice both reduced the size of aneurysms that had already grown and prevented abdominal aortic aneurysms from forming at all. In short, raising HDL cholesterol is beneficial because it induces programmed cell death. The walls of a failing aorta are replaced and strengthened. New lesions should not form at all when using this drug.
Endovascular treatment of aortic aneurysms is a minimally invasive alternative to open surgery repair. It involves placement of an endo-vascular stent through small incisions at the top of each leg into the aorta.
As compared to open surgery, EVAR has a lower risk of death in the short term and a shorter hospital stay but may not always be an option. There does not appear to be a difference in longer term outcomes between the two. After EVAR, repeat procedures are more likely to be needed.
Better results are only in uncomplicated, elective descending thoracic and infrarenal aorta. Moreover, recent USA data from 2006–2007 of isolated descending thoracic aorta aneurysms found 23% of ideal candidate (uncomplicated, elective descending aortic aneurysms) underwent to TEVAR, the remaining 77% underwent open surgical repair.
Of all people with aortic dissection, 40% die immediately and do not reach a hospital in time. Of the remainder, 1% die every hour, making prompt diagnosis and treatment a priority. Even after diagnosis, 5–20% die during surgery or in the immediate postoperative period. In ascending aortic dissection, if surgery is decided to be not appropriate, 75% die within 2 weeks. With aggressive treatment, 30-day survival for thoracic dissections may be as high as 90%.
Type 1 and Type 2 FAD call for the same treatment: immediate surgery to replace the aorta. Surgery is required due to the high risk of mortality. Type 3 is less severe and requires the maintenance of blood pressure through diet and exercise. Upon diagnosing someone with FAD intravenous antihypertensive treatment is frequently used. Often intravenous sodium nitroprusside is used for its efficiency in lessening the pulsatile load thus reducing blood pressure. Reducing this force slows the progression of the dissection. Surgical success depends on age, severity of symptoms, postoperative organ dysfunction and stroke. Surgical intervention is always indicated in Type 1 cases. Aortic surgery is palliative, not curative. The goal is to merely to prevent rupture, restore blood flow, and fix any aortic valve dysfunction. Post operative protocols include frequent monitoring of the aorta diameter. Statins and beta blockers are also popular treatments used to reduce future plaque build up and blockage of epinephrine receptors as a way to control heart rate and blood pressure.
Long term treatment should also include regular check ups every 3 to 6 months. A CT scan or MRI is recommended, along with required chest x-rays. Antihypertensive therapy with beta adrenergic antagonists is required regardless of medical versus surgical treatment. Ten to twenty percent of those who choose surgical intervention are re-operated on due to compression, aneurysm development or blood leakage.
The size cut off for aortic aneurysm is crucial to its treatment. A thoracic aorta greater than 4.5 cm is generally defined as aneurysmal, while a size greater than 6 cm is the distinction for treatment, which can be either endovascular or surgical, with the former reserved for pathology at the descending aorta.
Indication for surgery may depend upon the size of the aneurysm. Aneurysms in the ascending aorta may require surgery at a smaller size than aneurysms in the descending aorta.
Treatment may be via open or via endovascular means.
In an acute dissection, treatment choice depends on its location. For Stanford type A (ascending aortic) dissection, surgical management is superior to medical management. For uncomplicated Stanford type B (distal aortic) dissections (including abdominal aortic dissections), medical management is preferred over surgical.
The risk of death due to aortic dissection is highest in the first few hours after the dissection begins, and decreases afterward. Because of this, the therapeutic strategies differ for the treatment of an acute dissection compared to a chronic dissection. An acute dissection is one in which the individual presents within the first two weeks. If the individual has managed to survive this window period, his prognosis is improved. About 66% of all dissections present in the acute phase. Individuals who present two weeks after the onset of the dissection are said to have chronic aortic dissections. These individuals have been self-selected as survivors of the acute episode and can be treated with medical therapy as long as they are stable.
In most cases, isolated diaphragmatic rupture is associated with good outcome if it is surgically repaired. The death rate (mortality) for diaphragmatic rupture after blunt and penetrating trauma is estimated to be 15–40% and 10–30% respectively, but other injuries play a large role in determining outcome.
Each year in the United States, some 45,000 people die from diseases of the aorta and its branches. Acute aortic dissection, a life-threatening event due to a tear in the aortic wall, affects 5 to 10 patients per million population each year, most often men between the ages of 50 and 70; of those that occur in women younger than 40, nearly half arise during pregnancy. The majority of these deaths occur as a result of complications of thoracic aneurysmal disease.
A significant complication of diaphragmatic rupture is traumatic diaphragmatic herniation: organs such as the stomach that herniate into the chest cavity and may be strangulated, losing their blood supply. Herniation of abdominal organs is present in 3–4% of people with abdominal trauma who present to a trauma center.
For individuals who survive the initial crush injury, survival rates are high for traumatic asphyxia.
Incidence rates of cranial aneurysms are estimated at between 0.4% and 3.6%. Those without risk factors have expected prevalence of 2–3%. In adults, females are more likely to have aneurysms. They are most prevalent in people ages 35 – 60, but can occur in children as well. Aneurysms are rare in children with a reported prevalence of .5% to 4.6%. The most common incidence are among 50-year-olds, and there are typically no warning signs. Most aneurysms develop after the age of 40.
Evidence for the treatment of thoracic outlet syndrome as of 2014 is poor.
Inflammatory aortic aneurysm (IAA), also known as Inflammatory abdominal aortic aneurysm (IAAA), is a type of abdominal aortic aneurysm (AAA) where the walls of the aneurysm become thick and inflamed. Similar to AAA, IAA occurs in the abdominal region. IAA is closely associated and believed to be a response to and extensive peri-anuerysmal fibrosis, which is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process IAA accounts for 5-10% of aortic aneurysms. IAA is occurs mainly in a population that is on average younger by 10 years than most AAA patients. Some common symptoms of IAA may include back pain, abdominal tenderness, fevers, weight loss or elevated Erythrocyte sedimentation rate (ESR) levels. Corticosteroids and other immunosuppressive drugs have been found to decrease symptoms and the degree of peri-aortic inflammation and fibrosis
Incidence rates are two to three times higher in males, while there are more large and giant aneurysms and fewer multiple aneurysms. Intracranial hemorrhages are 1.6 times more likely to be due to aneurysms than cerebral arteriovenous malformations in whites, but four times less in certain Asian populations.
Most patients, particularly infants, present with subarachnoid hemorrhage and corresponding headaches or neurological deficits. The mortality rate for pediatric aneurysms is lower than in adults.
Although the exact cause is unknown, some risk factors associated with individuals with IAA are:
Tobacco Use: Cigarette smoking and other forms of tobacco use appear to increase your risk of aortic aneurysms. In addition to the damaging effects that smoking causes directly to the arteries, smoking contributes to the buildup of fatty plaques in your arteries (atherosclerosis) and high blood pressure. Smoking can also cause your aneurysm to grow faster by further damaging your aorta.
Hardening of the arteries (atherosclerosis). Atherosclerosis occurs when fat and other substances build up on the lining of a blood vessel, increasing your risk of an aneurysm.
Infection in the aorta (vasculitis). In rare cases, abdominal aortic aneurysm may be caused by an infection or inflammation that weakens a section of the aortic wall.
There are many causes of TOS. The most frequent cause is trauma, either sudden (as in a clavicle fracture caused by a car accident), or repetitive (as in a legal secretary who works with his/her hands, wrists, and arms at a fast paced desk station with non-ergonomic posture for many years). TOS is also found in certain occupations involving lots of lifting of the arms and repetitive use of the wrists and arms.
One cause of arterial compression is trauma, and a recent case involving fracture of the clavicle has been reported.
The two groups of people most likely to develop TOS are those suffering from neck injuries due to traffic accidents and those who use computers in non-ergonomic postures for extended periods of time. TOS is frequently a repetitive stress injury (RSI) caused by certain types of work environments. Other groups which may develop TOS are athletes who frequently raise their arms above the head (such as swimmers, volleyball players, dancers, badminton players, baseball pitchers, and weightlifters), rock climbers, electricians who work long hours with their hands above their heads, and some musicians.