44 A O R T I C A N E U R Y S M S C A R L O S E . D O N AY R E T here is no disease more conducive to clinical humility than aneurysm of the aorta. William Osler Aneurysmal enlargement of the human aorta with aneurysm formation can occur silently without symptoms, or it can present in dramatic fashion upon rupture. The increase in age of the general population, and the widespread use of imaging modalities such as computed tomography (CT) scan and ultrasound have resulted in greater identification of this potentially lethal pathologic process. The dilemmas that are faced by physicians when dealing with aortic aneurysms are the aims of this chapter: (1) identification of patients at risk of developing aortic aneurysms, (2) definition of the etiologic factors that place patients at increased risk of aneurysm rupture, (3) comparison of the outcomes and complications encountered in an elective, an urgent, and an emergent aneurysm operation, and (4) discussion of alternative forms of therapy that may be utilized in the high risk patient who has a large aortic aneurysm. CASE 1 ABDOMINAL PAIN AND A PULSATILE MASS A 68-year-old male was admitted with the chief complaint of abdominal pain. Four days before admission he developed epigastric and paraumbilical pain radiating to the back. This varied in intensity and was relieved by codeine pills. The pain in the lumbar region increased in severity 1 day before admission and began to involve the entire abdomen. He complained of nausea and vomiting, had a normal bowel movement before admission, and denied any urinary symptoms. His past medical history was significant for a prior myocardial infarction 12 years ago, and the use of nitroglycerin for the past 2 years for anginal complaints. Physical examination revealed a well-developed, well-nourished, acutely ill man with severe abdominal pain. BP, 120/85 mmHg; pulse, 110 bpm; respiration, 22 breaths/min. The abdomen showed moderate symmetrical distention, marked tenderness, and a sensation of fullness in the left lower quadrant, with some rebound pain. The liver and spleen were not palpable. There was no shifting dullness. A pulsatile mass was palpable at the level of the umbilicus. Bowel sounds were active. Rectal examination showed no tenderness or palpable masses. Femoral and radial pulses were 2+, but the popliteal and dorsalis pedis pulses were not found. Laboratory findings were Hct, 38%; WBC count, 14,000/mm3. Urine and stool were negative for blood. On ECG, an old inferior myocardial infarction was noted. The patient had two large IV catheters started, and he was cross-matched for 6 units of blood. An emergent abdominal CT was aborted when the patient’s blood pressure fell to 90 mmHg, and he was rushed to the operating room. At exploration, a large, contained retroperitoneal hematoma was encountered. Proximal aortic control was obtained at the diaphragmatic hiatus, the aneurysm was opened, and control of the iliac vessels was achieved with Fogarty balloon catheters. A 22-mm woven graft, impregnated with collagen, was used to repair the aorta. The patient required 4 units of PRBCs, 800 ml of Cell-Saver blood, 2 units of fresh frozen plasma, and 10 units of platelets. He arrived in the surgical ICU intubated, with a BP of 110/70 mmHg, a pulse of 120 bpm, and a urine output of 100 ml/hr. He did well during the next 3 days, requiring only 2 more units of PRBCs. But on the fourth day he had a maroon stool, his blood pressure declined to 90/50 mmHg, and his urine output fell. He was also found to have rebound tenderness in the left lower quadrant. Bedside sigmoidoscopy demonstrated ischemic colonic mucosa. He was again taken to the 319 3 2 0 V A S C U L A R S U R G E R Y operating room, where a gangrenous colon was found, and a left hemicolectomy with colostomy was performed. After a prolonged ICU stay, he was discharged home 7 weeks after his admission. CASE 2 ASYMPTOMATIC AROTIC ANEURYSM A 73-year-old, active male visited his family physician for a routine physical examination in order to qualify for a new life insurance policy. His medical history was significant only for hypertension, which was well controlled with a βblocker. He had smoked cigarettes for 40 years, but had stopped 5 years previously. His older brother, with no known medical problems, had died unexpectedly at home 6 months previously. Physical examination was unremarkable; no abdominal masses were detected. He had strong and prominent arterial pulses, but no bruits. A screening ultrasound demonstrated a fusiform abdominal aortic aneurysm, 5 cm in greatest diameter, and a 3-cm right popliteal artery aneurysm. The patient agreed to undergo an elective aortic aneurysm repair. A preoperative abdominal CT scan confirmed the 5-cm infrarenal aortic aneurysm and also demonstrated a 3.5-cm left common iliac artery aneurysm. The patient underwent an aortic/bi-iliac bypass and synthetic graft. His postoperative course was uneventful and he was discharged from the hospital 1 week later. Three months later he underwent an exclusion and bypass of his popliteal aneurysm with a reverse saphenous vein graft. A GENERAL CONSIDERATIONS n aneurysm is defined as a permanent, localized dilatation, 1.5 or more times the size of the normal arterial diameter. The normal aortic diameter gradually decreases in size from the thorax to the aortic bifurcation, is larger in men than women, and increases with age. The infrarenal aorta in men measures 2.2 cm in diameter compared to 1.9 cm for women; thus, 3 cm is a useful minimum size criterion. The aortic segment below the renal arteries is by far the most common location for aneurysm formation; 50% extend into and involve the iliac arteries. Dilatation of the aorta leads to vessel elongation, giving the aortic and iliac vessels a tortuous configuration. Concomitant femoral and popliteal aneurysms are present in 15% of patients diagnosed with aortic aneurysms (Case 2). The converse is also true, with 8% of patients presenting with a unilateral popliteal aneurysm having an aortic aneurysm. Over one-third are afflicted if bilateral popliteal aneurysms are present. Atherosclerosis is the major etiologic factor associated with abdominal aortic aneurysm (AAA) formation, but an evolving view based on several observations suggests a multifactorial causation. Most patients with aneurysms are elderly, and have evidence of significant atherosclerosis in the coronary arteries and carotid bifurcation. Occlusive vascular disease of the iliofemoral segments is encountered in 25%. However, a paradoxical observation must be explained. Why does atherosclerosis lead to stenosis or occlusion in certain vessels, but to aneurysmal dilatation of the aorta in the same patient? Atherosclerosis consists of a complex series of events, ranging from smooth cell migration and proliferation to cell necrosis with calcium deposition, as a response to arterial wall injury. Atherosclerotic plaque formation is accompanied by an arterial wall remodeling response, with subsequent arterial enlargement in an effort to prevent luminal stenosis. In the superficial femoral artery this enlargement response may be restricted by anatomic factors such as a tendinous adductor canal, predisposing this artery to stenosis rather than aneurysmal dilatation. The abdominal cavity does not place any anatomic restrictions on the atherosclerotic infrarenal aorta, and aneurysmal dilatation can proceed unencumbered. The same is true in the popliteal fossa with regard to popliteal aneurysms. Thus, it can be argued that atherosclerosis is fundamentally a dilating rather than a constricting disorder of arteries. Recent clinical observations and biochemical data suggest that aneurysm pathogenesis may be more complex than described above and possibly is related to a systemic connective tissue disorder. Patients with aneurysms are more prone to hernia formation and have a higher incidence of bilateral and recurrent hernias, as opposed to patients with aortic occlusive disease in whom inguinal herniation is unusual. This suggests that connective tissue abnormalities of both the abdominal wall and aortic wall result in hernias and aneurysms in the same patients. Elastin and collagen are structural proteins that play a critical role in the integrity of the aorta, and biochemical assays have shown decreased quantities of elastin and collagen in the wall of aneurysms. The major catabolic enzyme for the breakdown of elastin is a proteolytic enzyme, elastase. The amount of aortic elastase found in the walls of AAAs, multiple aneurysms, and ruptured AAAs is significantly higher when compared to aortas afflicted by occlusive disease. The activity of elastase is significantly modified by the proteinase inhibitor, α1-antitrypsin, which is found in significantly lower concentrations in patients with multiple and ruptured aneurysms. The inflammatory and smooth muscle cell reaction to atherosclerotic injury appears to be altered in patients with AAA with the creation of a proteolytic environment that favors elastin and collagen degradation. Loss of structural support in the aortic media of patients with AAA renders the aorta susceptible to expansion in both diameter and length. Other structural factors seem to favor aneurysmal formation in the infrarenal aorta. First, it has a smaller me- A O R T I C dial layer than the thoracic aorta and must tolerate a greater wall tension. Second, histologic studies have found a lack of vaso vasorum in the distal aorta. Third, laminated mural thrombus acts as a barrier to the diffusion of nutrients to the aortic wall. Under conditions in which the vasa vasorum are absent, the media is weakened by atherosclerotic plaque and impaired nutrition; atrophy of the arterial wall ensues and leads to aneurysmal degeneration. Once an aneurysm develops, its enlargement is governed by physical principles. In order to maintain a stable diameter, the vessel wall must exert a circumferential force that opposes the distending effects of pressure. This relation is described by the law of Laplace: T=P×r where T is circumferential wall tension, P is transmural pressure, and r is vessel radius. The distending force is given by the product of pressure and radius, while the retractile force offered by the arterial wall is tension. Laplace’s law has to be redefined because the arterial wall is not infinitely thin: S = P × ri/th, where S is the stress force developed by the stretched vessel, P is transmural pressure, ri is internal radius, and th is wall thickness. Using Laplace’s law, tripling the aortic radius from 2 to 6 cm results in a 12-fold increase in wall tension. (It is no mystery why blowing a balloon gets easier after a certain radius is achieved.) This helps explain why large aneurysms are more prone to rupture than small ones, and why hypertension is an important risk factor for rupture. K E Y P O I N T S • Inflammatory and smooth muscle cell reaction to atherosclerotic injury appears to be altered in patients with AAA with the creation of proteolytic environment that favors elastin and collagen degradation • Loss of structural support in aortic media of patients with AAA renders aorta susceptible to expansion in both diameter and length • Under conditions in which vasa vasorum are absent, media is weakened by atherosclerotic plaque and impaired nutrition; atrophy of arterial wall ensues and leads to aneurysmal degeneration • Large aneurysms are more prone to rupture than small ones; thus, hypertension is important risk factor for rupture M DIAGNOSIS ost AAAs (about 75%) cause no symptoms unless rapid expansion, leakage, or rupture occurs. They are usually detected during a routine physical examination, A N E U R Y S M S 3 2 1 when the patient undergoes an ultrasound or CT scan for an unrelated condition, during laparotomy, or by the patients themselves. It is important not to confuse an easily palpable pulsating aorta in a young, thin patient with an AAA. The lumbar-sacral curvature renders the aorta easily palpable in these individuals. In well-nourished patients, the abdominal examination can be improved if the abdominal wall is relaxed by having patients flex their knees and put their arms at their side. The presence of a prominent aortic pulsation should be searched for using light manual pressure. Most aneurysms will be palpable in the epigastrium or to the left of the umbilicus. Both lateral borders of the aneurysm should be marked and this distance measured. Physical examination overestimates the actual diameter of an aortic aneurysm by about 1 cm. If an aortic aneurysm is found, a thorough search for femoral and popliteal aneurysms must be carried out as there is an increased association of the two. A prominent and expansile popliteal pulse with the knee flexed 30–45 degrees is highly suggestive of an aneurysm. The diagnosis can be easily confirmed with an ultrasound of the knee. Rectal examination may, on occasion, reveal the transmitted pulsations of a large internal iliac aneurysm. Aneurysm rupture is defined as disruption of the aortic wall with extravasation of blood. The abrupt sensation of pain in the back, flank, or abdomen is characteristic of aneurysmal rupture or expansion. It is not certain why pain is produced by an expanding but intact aneurysm. The best explanation may be that sudden stretching of the layers of the aortic wall puts pressure on the adjacent somatic sensory nerves. The pain is usually severe and throbbing before rupture, but tends to become steady when rupture has occurred. It is usually located directly over the aneurysm, but radiation of the pain to the thigh, groin, or testicles is common. It must be remembered that hypotension and shock do not usually occur in the absence of rupture. Rupture appears to occur through the posterolateral aortic wall and into the retroperitoneal space (80%) and less commonly anteriorly into the free peritoneal cavity (20%). The incidence of an anterior type of rupture is probably higher than indicated because most of these patients die abruptly and do not reach the hospital. The severity of the accompanying hypotension and shock will depend on both the extent of the blood loss and the patient’s cardiovascular reserve. The classic presentation of ruptured AAAs includes abdominal and back pain, hypotension, and a pulsatile abdominal mass, but all three of these findings are present in only 20% of patients with a proven aortic rupture. However, over 90% of ruptured aneurysms produce abdominal pain of sudden onset, and over 50% of these patients also complain of back pain. In the stable patient with a ruptured abdominal aneurysm, a pulsatile mass is usually felt to the left of the midline. Since aneurysms usually rupture to the left base of the mesentery, the resulting hematoma often occurs to the left 3 2 2 V A S C U L A R S U R G E R Y and can be palpated above the umbilicus. If the hematoma dissects downward, it can present as a tender left lower quadrant mass. Distention in a hypotensive patient should arouse suspicion. Most patients with aneurysmal rupture will be distended from retroperitoneal or intraperitoneal blood, and a secondary intestinal ileus. Ecchymoses can result in the flank, scrotum, or thighs as blood dissects into the retroperitoneal plane. This physical finding occurs late and is usually not seen in the acute clinical scenario. Abdominal aortic aneurysms cause symptoms not only as a result of rupture and expansion, but also due to pressure on adjacent structures. Large AAAs can cause symptoms from local compression of the duodenum (early satiety, nausea, or vomiting), ureters (hydronephrosis), or iliac veins (venous thrombosis). Erosion of the vertebrae, which can lead to constant back pain, has also been reported, but this is more commonly seen with the now rare aneurysms of syphilitic origin. Acute ischemic symptoms can occur either from distal embolization of thrombotic debris contained within the aneurysmal sac or from aortic thrombosis. Embolism is much more common than acute thrombosis, but both combined occur in less than 5% of patients with AAA. In patients with distal emboli, a proximal aneurysmal source must always be considered, especially in those without apparent occlusive disease. Under rare circumstances, the AAA may erode and rupture into the inferior vena cava or one of the iliac veins, producing a large aortocaval or aortoiliac fistula. These patients present with acute lower extremity swelling and cyanosis, high output cardiac failure, and an abdominal machine-like murmur. Erosion into the duodenum can also occur, resulting in massive upper gastrointestinal bleeding with catastrophic results. Since most unruptured aortic aneurysms are asymptomatic until they expand or rupture, imaging studies are important to confirm the clinical diagnosis. Ultrasonography is the screening test of choice. Its advantages include a high degree of accuracy (95%), relatively low cost, noninvasiveness, and good patient compliance. However, the presence of intestinal gas often limits its usefulness in identifying the proximal extent of the AAA, determining iliac artery involvement, and locating the renal arteries, especially in obese patients. CT scan is also used in the evaluation of AAAs. It yields more data than ultrasound because it can show the relationship of the aneurysm to the renal vessels, the presence of iliac artery aneurysms, and may detect other undiagnosed intra-abdominal processes. Intravenous contrast is required to obtain usable images, and thus renal complications and allergic reactions to contrast media are possible. The use of angiography is limited in the diagnostic evaluation of AAA due to its invasiveness, documented allergic reactions, risk of dye induced renal failure, and cost. Furthermore, because aneurysms have layers of thrombus lining the lumen, angiography cannot be relied on to determine the diameter of an aneurysm or even establish its presence. It is used in the following situations: (1) when the aneurysm is thought to extend above the renal arteries, (2) in the patient with symptomatic iliofemoral disease, (3) in those with severe hypertension or impaired renal function, and (4) in the presence of a horseshoe kidney. A plain abdominal and lateral spine film can be obtained rapidly at the bedside, and in greater than 70% of cases the scattered plaques of calcification will outline the wall of an aortic aneurysm. Since symptomatic patients usually have an associated ileus, it is important to realize that any abdominal distention can make the ultrasound examination more difficult and often unreliable. A CT scan can be helpful but should only be obtained in the completely stable patient and only after suitable intravenous access and close monitoring have been established. Aortography is useless in this setting; it will not show the leak and may not even demonstrate an existing aneurysm. Furthermore, it is expensive, invasive, and time-consuming, and may lead to complications and volume depletion. Diagnosis is to be pursued only in the hemodynamically stable patient. In the unstable patient, rapid resuscitation and transport to the operating room take precedence. Two aneurysmal variants merit special mention. Inflammatory aortic aneurysms are characterized by dense periaortic fibrosis with an abundant inflammatory reaction that contains many macrophages and often giant cells. Patients present with back pain, fever, an elevated sedimentation rate, and hydronephrosis or urinary complaints due to ureteral involvement by this intense inflammatory reaction. Although its etiology is unknown, aneurysm repair reverses the process. Mycotic abdominal aneurysms are AAAs that have become infected by lodgment of circulating organisms (bacteria or fungi) in the arterial wall. The most common offender is Salmonella. In such cases suppuration further destroys the media, potentiating rapid dilatation and rupture. K E Y P O I N T S • Most AAAs (about 75%) cause no symptoms unless rapid expansion, leakage, or rupture occurs; usually detected during routine physical examination, when patient undergoes ultrasound or CT scan for unrelated condition, during laparotomy, or by patients themselves • Physical examination overestimates actual diameter of an aortic aneurysm by about 1 cm • Aneurysm rupture is defined as disruption of aortic wall with extravasation of blood • Classic presentation of ruptured AAA includes abdominal and back pain, hypotension, and a pulsatile abdominal mass, but all of these three findings are found in only 20% of patients with proven aortic rupture A O R T I C • Over 90% of ruptured aneurysms produce abdominal pain of sudden onset; over 50% of these patients also complain of back pain • Abdominal aortic aneurysms cause symptoms not only as a result of rupture and expansion, but also due to pressure on adjacent structures • Large AAAs can cause symptoms from local compression of duodenum (early satiety, nausea, or vomiting), ureters (hydronephrosis), or iliac veins (venous thrombosis) • Erosion of vertebrae, which can lead to constant back pain, has also been reported, but this is more commonly seen with aneurysms of syphilitic origin • Acute ischemic symptoms can occur either from distal embolization of thrombotic debris contained within aneurysmal sac or from aortic thrombosis • Embolism much more common than acute thrombosis, but both combined occur in less than 5% of patients with AAA • In patients with distal emboli, a proximal aneurysmal source must always be considered, expecially in those without apparent occlusive disease T DIFFERENTIAL DIAGNOSIS he diverse and nonspecific nature of the pain caused by an expanding or leaking aneurysm all too often leads to errors in diagnosis and causes delays that may be catastrophic. The final outcome in a patient presenting with a symptomatic AAA is positively impacted if the initial diagnosis is correct. A study showed that if the initial diagnosis was correct or an aneurysm was at least suspected from the onset, a 35% mortality rate was achieved. However, if the diagnosis was incorrect or a cardiopulmonary event occurred, the mortality rose to 75%. A ruptured aneurysm should be considered in any patient past middle age who presents with sudden onset of abdominal discomfort, back pain, or hypotension. A history or signs of atherosclerosis or associated risk factors should heighten suspicion. A normal electrocardiogram (ECG) helps to shift the focus away from the heart as the source of the patient’s collapse. However, it must also be remembered that in the typical atherosclerotic patient with an aneurysm, rupture can lead to hypovolemic shock and may precipitate myocardial ischemia. A careful abdominal examination should be performed and will identify the true cause of the chest pain in most patients who arrive at the emergency room complaining of angina pectoris due to blood loss and reflex tachycardia from a ruptured aneurysm. Systolic hypertension is not uncommon in elderly patients, and the normal blood pressure of 120/85 mmHg obtained initially in the patient in Case 1 has to be redefined as hypotension. AAA should not be confused with a dissecting aneurysm. Dissecting aneurysms usually begin in the thoracic aorta; the primary event is an erosion of the inner aortic A N E U R Y S M S 3 2 3 layers, which allows hemorrhage into the media. The blood then courses along this path parallel to the main bloodstream where it may force its way back into the aortic lumen with the formation of a false channel. Although dissecting aneurysms do produce an enlarged aorta, the process is completely separate from that seen with an expanding or leaking AAA. The main symptom of dissection is unbearable pain starting in the chest, sometimes radiating at first to the neck or back, but gradually extending down into the abdomen, and sometimes even to the hip or thigh. Diagnosis will be helped if the following points are remembered. The patient usually has a history of significant arterial hypertension of prolonged duration. A pulse examination and blood pressure determination should be carried out if possible in each limb. Discrepancies in pulses and pressures between the upper and lower or contralateral extremities are usually found and vary according to the distal extent of the dissection. If a renal artery is involved, there may be hematuria and perhaps a rise in the blood urea nitrogen (BUN) or creatinine. The limitation of blood flow to parts supplied by the affected arteries may lead to numbness, paresthesia, or even hemiplegia or paraplegia if the carotid or spinal arteries are involved. The main differences between an aortic dissection and a symptomatic AAA are the lack of initial pain in the chest without radiation to the abdomen, the presence of strong and equal pulses in the radial and femoral locations, and the absence of numbness, paresis, or hemiplegia in an AAA. Onset of back pain in patients with a symptomatic aneurysm is frequently initially diagnosed as renal colic. Both of these conditions can present with flank pain and radiation of the pain to the genital areas. The diagnosis of renal colic is highly questionable in the patient lacking a prior history of urinary complaints, and is found to have a normal urinalysis without microscopic hematuria, crystals, or sediments. Transient hypotension in these patients should not be attributed to a pain-mediated vagal episode or the onset of urinary sepsis. Abdominal x-rays and intravenous pyelograms should be inspected closely for the presence of calcifications outlining an aortic aneurysm. Lumbar pain after strenuous exercise, lifting, or working is a common complaint faced by primary care and emergency room physicians. Any elderly patient who presents with the onset of back pain should be carefully examined for the presence of a pulsatile abdominal mass. Lumbar films should be carefully examined for the presence of vascular calcifications or anterior vertebral erosions. The obese elderly patient in whom a reliable examination cannot be performed should have an abdominal ultrasound to exclude the presence of an aneurysm. The association of traumatic abdominal discomfort with hypotension can be explained by other conditions such as perforation of peptic ulcer or another viscus. However, a perforated viscus produces a board-like and 3 2 4 V A S C U L A R S U R G E R Y exquisitely tender, rigid abdomen. Mesenteric ischemia presents with abdominal pain out of proportion to the physical examination (excruciating pain with a soft abdomen) and intestinal emptying associated with bloody diarrhea. However, shock is usually a late and often lethal manifestation of mesenteric ischemia. Symptomatic aneurysms can also be confused with diverticulitis, since both can present with a tender left lower quadrant mass. One must remember diverticulitis is an inflammatory process, and is associated with fever, leukocytosis, and the presence of a nonpulsatile abdominal mass. Unless gross peritonitis exists, diverticulitis is not usually associated with shock. The expanding retroperitoneal hematoma caused by a ruptured AAA can, on occasion, dissect toward the right side, mimicking right-sided renal colic or even acute cholecystitis. Albert Einstein was discovered to have a grapefruit-sized aneurysm of the distal aorta during an abdominal exploration and underwent an “omentopexy” (aneurysm wrap). For the next 10 years he complained of occasional pain in the lower abdomen and back, and suffered from intermittent episodes of pain in the right upper quadrant that were labeled as chronic cholecystitis. He was admitted to Princeton Hospital on April 15, 1955 with generalized abdominal pain, which was most intense in the right upper quadrant. A clinical diagnosis of acute cholecystitis and leaking aortic aneurysm was made, but Einstein declined the recommended aortic surgery and expired 3 days later. Autopsy revealed a normal gallbladder and a huge abdominal aneurysm that had ruptured and hemorrhaged into the tissues around the gallbladder. This historical case can be used to emphasize the dictum that any abdominal pain in a patient with a previously diagnosed AAA should be suspected of being caused by rupture of the aneurysm. It should be remembered that 1. In elderly patients the possibility of a symptomatic AAA must be considered with any symptoms related to the abdomen or back 2. Any episode of hypotension in such patients should always be taken seriously 3. Thorough examination of the abdomen for the presence of pulsatile masses is mandatory, and should be supplemented with an abdominal ultrasound if the patient is hemodynamically stable K E Y P O I N T S • Ruptured aneurysm should be considered in any patient past middle age who presents with sudden onset of abdominal discomfort, back pain, or hypotension • In typical atherosclerotic patient with an aneurysm, rupture can lead to hypovolemic shock and may precipitate myocardial ischemia • Main symptom of dissection is unbearable pain starting in chest, sometimes radiating at first to neck or back, but gradually extending down into abdomen, and sometimes even to hip or thigh • Patient usually has history of significant arterial hypertension of prolonged duration; pulse examination and blood pressure determination carried out if possible in each limb • Discrepancies in pulses and pressures between upper and lower or contralateral extremities usually found and vary according to the distal extent of dissection • If renal artery involved, may produce hematuria and perhaps a rise in BUN or creatinine • Limitation of blood flow to parts supplied by affected arteries may lead to numbness, paresthesia, or even hemiplegia or paraplegia if carotid or spinal arteries involved • In elderly patients, possibility of symptomatic AAA must be considered with any symptoms related to abdomen or back • Any episode of hypotension in such patients should always be taken seriously • Thorough examination of abdomen for presence of pulsatile masses is mandatory, and should be supplemented with abdominal ultrasound if patient is hemodynamically stable T TREATMENT he dilemma is which patients with asymptomatic AAA should undergo elective operative treatment or, alternatively, careful nonoperative follow-up. The only risk factors independently predictive of rupture include the initial diameter of the aneurysm (large aneurysms expand more rapidly than small ones), elevated diastolic blood pressure (Laplace’s law), and the presence of chronic obstructive pulmonary disease (elastase and α1-antitrypsin). Using these three variables alone, the 5-year predicted rupture rate increases from 2% when all three risk factors are minimal to 100% when they are all present. Although 15–20% of small aneurysms do not expand substantially, 80% increase progressively in diameter and approximately 20% increase by more than 0.5 cm/yr. Unfortunately, it is impossible to predict the rate of expansion in any one patient; while some aneurysms are stable for years, others tend to expand rapidly. From clinical studies, it appears that for AAAs less than 4 cm in diameter the risk of rupture within 5 years is approximately 2%, with an increase to 25–40% for aneurysms larger than 5 cm. Data on risk of rupture for aneurysms in the 4–5-cm range are sparse, but such lesions have been reported to have a 5-year rupture rate of 3–12%. The mortality risk of elective aneurysm repair has decreased in the last two decades. Mortality has fallen from 12–15% to 3–5%, with some centers reporting an operative mortality of 2% or less, with a 5-year survival of 60% and a 10-year survival of 40%. Factors increasing the risk A O R T I C of elective surgery include coexisting cardiac disease, peripheral atherosclerosis, hypertension, decreased renal function, chronic obstructive pulmonary disease, obesity, and multiple previous surgeries. Elective operation is recommended for patients with AAAs that measure greater than 5 cm in diameter, are painful or tender, and have been documented to be enlarging. Distal embolization or obstruction of adjacent viscera are also indications for resection. Operations for smaller aneurysms (4–5-cm in diameter) should be performed in the low risk patient who has diastolic hypertension or who suffers from chronic obstructive pulmonary disease. Relative contraindications for small aneurysms include a recent myocardial infarction, congestive heart failure, severe angina pectoris, chronic renal failure, or life expectancy of less than 1 year. There is no argument that the mortality rate is increased in the patient who has to undergo an emergent aneurysm repair. The mortality rates for operations performed for ruptured aortic aneurysms differ because of significant variations in the hemodynamic status of the patient at the time of presentation. Patients who are not hypotensive and have small, contained hematomas have an operative mortality rate of 20%. The mortality rate doubles to 40% in those who present with hypotension but who respond to fluid resuscitation with restoration of blood pressure and urine output. Operative repair seeks to re-establish blood flow to the pelvis and lower extremities by utilizing a prosthetic vascular graft. Whenever possible, a tube graft is sutured below the renal arteries and above the aortic bifurcation, even in the presence of small iliac aneurysms, in order to shorten the length of the operation. If large or complex iliac aneurysms are encountered, a bifurcated graft is utilized and sutured to each iliac bifurcation. The hemodynamically stable patient with abdominal and back pain who is found to have an aneurysm represents a challenging management problem. Since symptoms are widely believed to represent acute aneurysm expansion and imminent rupture, immediate operation is generally accepted to be the proper course of action in an effort to avoid the complications associated with aneurysm rupture. It is recommended that once symptomatic, the hemodynamically stable AAA patient should undergo an emergent CT scan of the abdomen and pelvis under careful and close observation. The finding of blood in the retroperitoneum mandates immediate operation. In the absence of evidence of retroperitoneal bleeding, the patient at high operative risk due to pre-existing cardiopulmonary disease may benefit from a rapid and thorough preoperative assessment, and improvement of their cardiac, pulmonary, and renal function rather than from immediate operation. Thus, the key to a better outcome in the management of a patient with ruptured and unstable aneurysm is early diagnosis, aggressive resuscitation, and an early operation A N E U R Y S M S 3 2 5 with rapid control of bleeding. It should also be remembered that nearly every complication is more likely in an emergent rather than an elective operation. The incidence of renal failure after elective aortic aneurysm resection averages approximately 3% with a mortality rate of 45%, but the incidence of acute renal failure after operation for ruptured aneurysm averages 30% with a mortality rate of 75%. Sigmoid colon ischemia is a rare but devastating complication that is more likely to occur following repair of a ruptured AAA. It may result from embolization into, or ligation of the inferior mesenteric artery or the internal iliac arteries. Fortunately, the abundance of collateral flow to the sigmoid colon usually prevents this problem. Careful inspection of the sigmoid colon following graft replacement is essential and may be facilitated by Doppler examination of the bowel wall and mesentery. Postoperative colon ischemia should be suspected in the presence of cramping, abdominal pain, or early diarrhea (1–2 days after surgery), that usually contains blood. Prompt flexible sigmoidoscopy or colonoscopy should be performed. In most cases, patchy partial-thickness mucosal necrosis and sloughing can be detected. In the more severe cases of transmural infarction, early re-exploration is an indication of sigmoid ischemia. Paraplegia due to AAA repair is uncommon. Recovery from this complication is unusual and the mortality rate is high. Recently, a novel, minimally invasive approach has been introduced utilizing a stented graft to “exclude” AAA. This technique, which has been developed in animals, is now in human trials and consists of transfemoral placement of a thin walled prosthetic graft that is attached to the proximal aorta with an internal wire stent. This technique may further reduce the risk of elective AAA repair and may be especially appropriate for the high risk patient. K E Y P O I N T S • Only risk factors independently predictive of rupture include initial diameter of aneurysm (large aneurysms expand more rapidly than small), elevated diastolic blood pressure (Laplace’s law), and presence of chronic obstructive pulmonary disease (elastase and α1-antitrypsin) • Appears from clinical studies that for AAA less than 4 cm in diameter, risk of rupture within 5 years is approximately 2%, with increase to 25–40% for aneurysms larger than 5 cm • Data on risk of rupture for aneurysms in 4–5-cm range are sparse, but such lesions reported to have 5-year rupture rate of 3–12% • Elective operation recommended for patients with AAA measuring greater than 5 cm, are painful or tender, and documented to be enlarging • Distal embolization or obstruction of adjacent viscera also indicate resection 3 2 6 V A S C U L A R S U R G E R Y • Operations for smaller aneurysms (4–5 cm in diameter) should be performed in low risk patient who has diastolic hypertension or who suffers from chronic obstructive pulmonary disease • Relative contraindications for small aneurysms include recent myocardial infarction, congestive heart failure, severe angina pectoris, chronic renal failure, or life expectancy of less than 1 year A FOLLOW-UP successfully performed aneurysm repair will have little problem and generally will remain patent for the patient’s lifetime. Late presenting postoperative complications include graft infection and aorto-enteric fistula formation. Both of these complications require graft resection and extracavitary arterial reconstruction; unfortunately, they have a high mortality rate, usually greater than 50% despite appropriate treatment. Proximal or distal anastomotic disruption occurs due to arterial or graft degeneration or graft infection. A pseudoaneurysm, which is an expanding hematoma locally contained by surrounding connective tissue, is the usual end result. After 3-year follow-up, the incidence of pseudoaneurysm formation is 0.2% for the aortic anastomosis, 1% for iliac anastomoses, and 3% for femoral anastomoses. Patients should be followed with ultrasound or CT scan 5–10 years after repair to ensure that pseudoaneurysms are not forming. This can be addressed in an elective fashion before rupture occurs. SUGGESTED READINGS Cronenwett JL, Sargent SK, Wall MH et al: Variables that affect the expansion rate and outcome of small abdominal aortic aneurysms. J Vasc Surg 11:260, 1990 Covers the risk factors that are important to aneurysm enlargement, with an insightful audience discussion at the end. Ernst CB: Current concepts: abdominal aortic aneurysm. N Engl J Med 328:1167, 1993 Thorough review! Will fill in and reinforce the main topics covered in the chapter, and provide you with a fairly complete list of references. Marston WA, Ahlquist R, Johnson Jr G et al: Misdiagnosis of ruptured abdominal aortic aneurysms. J Vasc Surg 16:17, 1992 Addresses the most common errors that are made in diagnosing aortic aneurysms; surprisingly, the mortality was not negatively impacted as expected. Misdiagnosis probably preselected for patients that were able to withstand the delay and were better able to undergo surgical repair. QUESTIONS 1. Most abdominal aortic aneurysms? A. Produce vague symptoms such as back pain. B. Are detected on routine physical examination. C. Rupture when they are 4–6 cm in size. D. Occur without other manifestations of atherosclerosis. 2. The best screening test to determine whether an AAA is present is? A. Angiography. B. CT scan. C. Duplex-Doppler. D. MRI scan. 3. Which of the following is not predictive of the risk of AAA rupture? A. Size of the aneurysm. B. Elevated diastolic blood pressure. C. Chronic obstructive pulmonary disease. D. Transient ischemic attacks. 4. The most common cause of death after the successful repair of an AAA is? A. Cardiac arrest/cardiac failure. B. Paralysis from spinal ischemia. C. Infection. D. Hemorrhage. (See p. 604 for answers)