Abdominal aortic aneurysm, also written as AAA and often pronounced 'triple-A', is a localized dilatationof the abdominal aorta, that exceeds the normal diameter by more than 50%. The normal diameter of the infrarenal aorta is 2 cm. It is caused by a degenerative process of the aortic wall, but the exact etiologyremains unknown. It is most commonly located below the kidneys (infrarenally; 90%), other possible locations are above or at the level of the kidneys (suprarenal and pararenal). The aneurysm can extend to include one or both of the iliac arteries. An aortic aneurysm may also occur in the thorax.
An abdominal aortic aneurysm occurs most commonly in older individuals (between 65 and 75), and more in men and smokers. There is moderate evidence to support screening in individuals with these risk factors. The majority of abdominal aortic aneurysms do not cause symptoms. Symptomatic and large aneurysms (>5.5 cm in diameter) are considered for repair.
The most important complication of an abdominal aortic aneurysm is rupture, which is most often a fatal event. An abdominal aortic aneurysm weakens the walls of the blood vessel, leaving it vulnerable to bursting open, or rupturing, and spilling large amounts of blood into the abdominal cavity, leading to only minutes of life remaining.[1]
Famous Patients, Famous Operations, 2002 : The Case of the Scientist with a Pulsating Mass Albert B. Lowenfels, MD A 69-year-old white male scientist consulted his physician because of pain in the upper abdomen. For a number of years he had suffered from attacks of upper abdominal pain, which usually lasted for 2-3 days and were often accompanied by vomiting. These attacks usually occurred about every 3 or 4 months. The patient was a pipe smoker and slightly overweight. The rest of his history was noncontributory. On physical examination, his physician noted a pulsating mass deep in the center of the abdomen. Who is this mystery patient?The patient is Albert Einstein (Figure), considered to be the most influential person of the 20th century and ranked as one of the top scientists of all time. Albert Einstein, who was born in 1879 in Ulm, Germany, died in Princeton, New Jersey, in 1955 at the age of 76. The immediate cause of death was a ruptured abdominal aneurysm. In December 1948, Dr. Rudolph Nissen, famous for developing a widely used operation to prevent esophageal reflux, performed an exploratory laparotomy on Einstein at the Brooklyn Jewish Hospital. At that time, a "grapefruit-sized" aortic aneurysm was discovered to be the cause of Einstein's abdominal pain.
During that era, ligation of the abdominal aorta had already proved to be ineffective, and replacing the aorta with a graft was still a decade away. The only available treatment was to attempt to reinforce the aortic wall and delay the inevitable rupture. Polyethene cellophane is a tissue irritant, producing marked fibrosis. Dr. Nissen wrapped the visible anterior portion of the aneurysm with this type of cellophane, in the hopes of stimulating an intense fibrous tissue reaction that would strengthen the bulging aortic wall. Einstein recovered from the operation, and after a 3-week hospital stay, returned to his home in Princeton, New Jersey. Following this palliative operation, Einstein lived for 5 more productive years with only minor symptoms. In 1952, he was offered and declined the presidency of Israel. He published his last scientific paper in 1954, in the Annals of Mathematics. During this period he had occasional back pain and pain in his right upper quadrant, labeled as "chronic cholecystitis." On Tuesday, April 12, 1955, Einstein developed abdominal pain, which became more severe on the following day. Although Einstein must have realized that the aneurysm had finally burst, he initially refused hospitalization. He finally agreed to be admitted to the Princeton Hospital, only because he felt he was becoming too much of a burden at home. He was seen by Frank Glenn, MD, then Chief of Surgery at New York Hospital, who diagnosed cholecystitis and a leaking abdominal aneurysm. Glenn recommended resection of the aneurysm, even though the operation was new. At that time, Dr. Glenn had only done a few such operations, using cadaver grafts to replace the aorta. Einstein refused surgery, saying: "I want to go when I want. It is tasteless to prolong life artificially. I have done my share, it is time to go. I will do it elegantly."[1] Five years after surgery, the patient collapsed at home and was rehospitalized. Although he had intermittent bouts of generalized abdominal pain requiring morphine for relief, he had pain-free intervals when he appeared to be quite comfortable. The pain became localized to the right upper quadrant, where a palpable mass was noted. Five days after admission, he developed labored breathing and expired at 1:15 AM on April 18, 1955. An autopsy, performed by Thomas Harvey, MD, revealed a normal gallbladder and a huge abdominal aneurysm. Harvey reported that compression of the gallbladder from hemorrhage had simulated an attack of cholecystitis.[2] Was wrapping Einstein's aneurysm with cellophane useful, or just a sham operation?A recent review of life expectancy in persons turned down for elective aneurysm surgery showed a median survival of only 9 months in patients with aneurysms larger than 7 cm.[3] Einstein lived for over 5 years; perhaps wrapping the aorta did prolong his life.What would have been the anticipated outcome if Einstein had been operated on?In 1955, although resection of aortic aneurysms had been practiced since 1951, resection of a ruptured aneurysm, especially after a previous aortic wrapping procedure, would have had a prohibitively high mortality rate.How would Einstein's aneurysm be diagnosed today?There are now many ways to visualize the abdominal aorta and to determine the relation of the diseased aorta to the renal and iliac vessels. Formerly, arteriography was commonly used to detect and evaluate aneurysms, but this procedure has been replaced by computerized tomographic angiography or by magnetic resonance angiography. These newer procedures are rapid, accurate, and provide crucial information about the relationship of the aneurysm to the renal and iliac vessels.[4]Today, any patient without a serious medical contraindication who has an aortic aneurysm greater than 5 cm is a candidate for surgery. Einstein would have certainly been referred for surgery at the time of his initial symptoms because his "grapefruit-sized" aneurysm was at least 12 cm in diameter. When performed as an elective procedure, the operative mortality rate is about 5%, increasing dramatically to about 50% if the aneurysm has ruptured. Operating on aneurysms smaller than 5 cm does not seem to improve long-term survival. Until a few years ago, the operation of choice would have been resection of the aneurysmal mass, followed by replacement with a prosthetic graft.[5] But recently, endovascular grafts have been developed that are inserted via the femoral artery, positioned within the aneurysm, and secured with self-expanding stents or hooks. This procedure is becoming increasingly popular because it is less stressful for the patient and reduces the length of hospitalization.[6] The long-term results of this procedure need additional evaluation to assess the frequency of complications, such as leakage around the graft.[7] What happened to the world's most famous brain?It disappeared rather mysteriously after the autopsy, and was discovered to have been secretly hidden by Thomas Harvey, the pathologist who performed the 1955 autopsy! Forty years later, at age 86, Harvey, along with a journalist, drove Einstein's brain across the United States to be given to Einstein's granddaughter. Michael Paterniti, the driver, describes the brain's discovery and final trip inDriving Mr. Albert: A Trip Across America With Albert Einstein's Brain.[8]EtiologyThe exact causes of the degenerative process remain unclear. There are, however, some theories and risk factors defined.
ScreeningA clinical practice guideline by the U.S. Preventive Services Task Force "recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men age 65 to 75 years who have ever smoked".[11][12] This is a grade B recommendation[13]. A re-analysis of the meta-analysis estimated a number needed to screen of approximately 850 patients.[14] The largest of the randomized controlled trials on which this guideline was based studied a screening program that consisted of[15]:
This trial reported significant short[15] ( number needed to screen after 4 years of approximately 590 to prevent nonfatal ruptured AAA plus AAA-related deaths[16]) and long term[17] ( number needed to screen after 7 years of approximately 280 to prevent nonfatal ruptured AAA plus AAA-related deaths) benefit and cost effectiveness.[18] Subsequent randomized controlled trials also found benefit:
In the U.S., effective January 1, 2007, provisions of the SAAAVE Act (Screening Abdominal Aortic Aneurysm Very Efficiently) now provide a free, one-time, ultrasound AAA screening benefit for those qualified seniors. Men who have smoked at least 100 cigarettes during their life, and men and women with a family history of AAA qualify for the one-time ultrasound screening. Enrollees must visit their healthcare professional for their Welcome to Medicare physical within six months of enrolment in order to qualify for the free screening. The Welcome to Medicare Physical Exam must be completed within the first six months of Medicare eligibility, but there is no published time limit thereafter for completion of the AAA screening. Providers who perform the physical and order the AAA screening need to document the AAA risk factors.[21] [edit]Manifestations and DiagnosisAAAs are commonly divided according to their size and symptomatology. An aneurysm is usually considered to be present if the measured outer aortic diameter is over 3 cm (normal diameter of aorta is around 2 cm). The natural history is of increasing diameter over time, followed eventually by the development of symptoms (usually rupture). If the outer diameter exceeds 5.5 cm, the aneurysm is considered to be large. For aneurysms under 5.5 cm, the risk of rupture is low, so that the risks of surgery usually outweigh the risk of rupture. Aneurysms less than 5.5 cm are therefore usually kept under surveillance until such time as they become large enough to warrant repair, or develop symptoms.[6][9]The vast majority of aneurysms are asymptomatic. The risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery. Possible symptoms include low back pain, flank pain, abdominal pain, groin pain or pulsating abdominal mass.[22] The complications include rupture, peripheral embolisation, acute aortic occlusion, and aortocaval (beteween the aorta and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination, a palpable abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.[7] As most of the AAAs are asymptomatic, their presence is usually revealed during an abdominal examination for another reason - the most common being abdominal ultrasonography. A physician may also detect the presence of an AAA by abdominal palpation. Ultrasonography provides the initial assessment of the size and extent of the aneurysm, and is the usual modality for surveillance. Preoperative examinations include CT, MRI and special modes thereof, like CT/MR angiography. Angiography may be useful also, as an additional method of measurement for the planning of endoluminal repair. Note that an aneurysmal aorta may appear normal on angiogram, due to thrombus within the sac. [edit]RuptureThe clinical manifestation of ruptured AAA can include low back, flank, abdominal or groin pain, but the bleeding usually leads to a hypovolemic shock with hypotension, tachycardia, cyanosis, and altered mental status. The mortality of AAA 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.[23] The bleeding can be retroperitoneal or intraperitoneal, or the rupture can create an aortocaval or aortointestinal (between the aorta and intestine) fistula.[6]. Flank ecchymosis (appearance of a bruise) is a sign of retroperitoneal hemorrhage, and is also called the Grey-Turner sign.[7] Ruptured AAA is a clinical diagnosis: the presence of the triad of abdominal pain, shock and pulsatile abdominal mass makes the diagnosis; no further investigations are required for diagnostic purposes, and imaging should not delay surgery. The operative mortality has slowly decreased over several decades but remains higher than 40%.[24] [edit]TreatmentThe treatment options for asymptomatic AAA are immediate repair, surveillance with a view to eventual repair, and conservative management. There are currently two modes of repair available for an AAA: open aneurysm repair (OR), and endovascular aneurysm repair (EVAR).
New endovascular devices are being developed that are able to treat more complex and tortuous anatomies.[35] |
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