Aneurysm Pa Tho Physiology
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Omar Al-Nouri, DO General Surgery LUMC
Overview Background Classification Pathogenesis Aneurysm Types
Background The term aneurysm is derived from the Greek word aneurysma which means “widening” and is defined as a permanent and irreversible localized dilatation of a blood vessel, having at least 50% increase in diameter compared with the expected normal diameter. Ectasia is defined as a dilatation less than 50% of the normal diameter. In men, infrarenal aorta is normally between 14 and 24mm. In women, infrarenal aorta is normally between 12 and 21 mm. Therefore, abdominal aortic aneurysm (AAA) is diagnosed if the diameter is 3cm or larger in a man or 2.6 cm or larger in a women.
Background Aneurysms can develop at any location in the arterial tree, but are most commonly located in the aorta, followed by iliac, popliteal and femoral arteries.
Background The first elective operation for treatment of an aneurysm was performed by Antyllus in the 2nd century AD. He described ligation of the artery above and below the aneurysm, then incising the aneurysm sac and evacuating its contents. Endovascular aortic aneurysm repair EVAR dates back to 1991 when Juan Parodi introduced this as a treatment of AAA
Classification Aneurysms are classified into two main groups: true and false aneurysms. True aneurysms involve all three layers of the vessel wall False aneurysms do not have all 3 layers of the wall involved and typically involve a defect in the inner most two layers.
Classification Aneurysms are further classified by morphologic type The most common aneurysms are spindleshaped fusiform aneurysms Aneurysms that affect only part of the arterial circumference are termed saccular
Pathogenesis The pathogenesis of aneurysmal disease is a multi-factorial, complex process. More than 90% of aneurysms are associated with atherosclerosis. Aneurysms are more accurately referred to as degenerative, where an interaction of multiple factors rather than one single process is responsible for the destruction of the media of the vessel wall that leads to aneurysms formation. Congenital aneurysms associated with connective tissue disorders (i.e. Marfans, Ehlos-Danlers) are rare. Infected (mycotic) aneurysms are somewhat more common Dissecting aneurysms are applied to dissections with aneurysmal dilatation of the false lumen.
Pathogenesis Aneurysms are associated with alterations in the connective tissue of the vessel wall. The normal vessel wall is made up of lamellar units that consist of elastin, collagen (mainly types I and III) and vascular smooth muscle cells. Elastin fibers are most abundant in the media and are the main load-bearing component under most physiologic conditions. Collagen provides the tensile strength and is considered the “safety net”, acquiring load-bearing functions at higher pressures when elastin fails. In the normal aorta, there is a gradual but marked reduction in the number of medial elastin layers from the proximal thoracic aorta to the infrarenal aorta.
Pathogenesis Histologically, the aneurysms wall is thinned, with a marked decrease in the amount of medial elastin.
Biochemical studies show there is an increase in the collagen:elastin ratio in the aneurysms wall. Elastin fragmentation is the initial structural event and elastin depletion is completed early in aneurysm formation. Elastin degradation is a key step in the development of aneurysms, but collagen degradation is ultimately required for aneurysmal rupture.
Pathogenesis Proteolytic enzymes have also been shown to play a major role in aneurysms formation. There is increased expression and activity of matrix metalloproteinases (MMPs) in the wall of aneurysms. In AAAs, MMP activation favors elastin and collagen degradation. Interstitial collagen degradation accompanies increased expression of collagenases MMP-1 and MMP-13 in AAAs. Elastases MMP-2, MMP-9 and MMP-12 also have increased expression in aneurysmal aortic tissue.
Pathogenesis Increased serum levels of MMPs return to normal after aneurysmal repair. Another prominent histologic feature of aneurysms is the presence of an inflammatory infiltrate with a preponderance of plasma cells in the media and T cells in the adventia. These cells subsequently release a cascade of cytokines that result in the activation of many different proteases. Extensive lymphocytic and monocytic infiltrate in the media and adventia and deposition of IgG in the vessel wall further support the concept that aneurysm formation is autoimmune. An infectious cause of aneurysm formation has been suggested with as many as 55% of aortic aneurysms demonstrate Chlamydia pneumoniae.
Pathogenesis There is considerable evidence that genetics plays a role in aneurysm formation. Familial clustering is seen in 15% to 25% of patients undergoing AAA repair. Specific genetic abnormalities include decreased type III collagen in the aortic media of familial aneurysms, polymorphisms on the pro-α chain of type III collagen and deficiencies in α1-antitrypsin.
Pathogenesis Once an aneurysms forms its
enlargement is governed by Laplace's law. Laplace Law: T=PR For a given transmural pressure, the wall tension is proportionate to the radius. Thus, the larger the vessel radius, the larger the wall tension required to withstand a given internal fluid. HTN, increasing transmural pressure, is a major risk factor for rupture.
Pathogenesis The pathogenesis of degenerative aortic aneurysms is mulitfactorial involving disordered remodeling of the extracellular matrix, activation of proteolytic enzymes, chronic inflammation, genetic predisposition and biomechanical wall stress. Degenerative aneurysms account for more than 90% of aneurysmal disease
Abdominal Aortic Aneurysms Aortic aneurysms are most commonly located in the infrarenal aorta, with the segment immediately below the renal arteries usually being spared. The iliac arteries are involved in 40% of pts with AAA. In the U.S. between 3.5 and 6.6 per 1000 people have AAAs
Abdominal Aortic Aneurysms-Risk Factors Risk factors: Age, gender, race, tobacco use, and family history The frequency of aneurysms increases steadily in men older than 55 yrs, reaching a peak of 6% at 8o to 85 yrs. In women peak at 4.5% at older then 90 yrs. Male:female ratio is 4:1 to 5:1 in the 60 to 70 year age group, but beyond age of 80 it approaches 1:1. AAA is primarily a disease of elderly white men, with white males being two to three times more likely develop AAA than black males. Smoking is associated with 78% of AAAs and there is an 8:1 preponderance in smokers vs nonsmokers. There is an inverse relationship between DM and development of AAA. Pts with DM where two times less likely to develop AAA than those without DM.
Abdominal Aortic Aneurysms-Risk Factors The most frequent and lethal complication of AAAs is rupture. Rupture AAAs are the 13th leading cause of death in the United States. After rupture of an AAA, only half of patients arrive at the hospital alive. One studied showed, 50% reach the hospital alive, 7% died before surgery, 17% died during the operation and 37% died within 30 days of the operation for an overall mortality rate for open surgical repair of 45%
Abdominal Aortic Aneurysms-Risk Factors For AAAs between 5.5 and 6cm, the annual rupture risk is between 5 and 10%. AAAs between 6.o and 7.0cm the annual rupture risk is between 10% to 20%. AAAs >8cm have a 100% 5-year risk of rupture. Low risk for rupture: <5cm, <0.3cm/yr, no COPD, no Fmhx, normal BP, fusiform High risk for rupture: >6cm, >0.6cm/yr, severe COPD, +Fmhx, poorly controlled HTN, very eccenteric Recommended that repair of AAAs occurs when size >5.5 cm or growth of > 0.5cm/yr.
Abdominal Aortic AneurysmsDiagnosis Most asymptomatic aneurysms are
discovered on routine physical exam with the palpation of a pulsatile abdominal mass or during radiographic study. Chronic vague abdominal or back pain is the most common symptom, present in up to 30% of patients. Classic presentation of ruptured AAA present with the triad of sudden-onset midabdominal pain or flank pain, shock and the presence of a pulsatile mass. Most AAAs rupture on the left posterolateral wall, 2-4cms below renals
Abdominal Aortic AneurysmsDiagnosis Abdominal ultrasound is the most widely used noninvasive test for AAAs. Provides structural detail of the vessel and can accurately measure the size of the aneurysm in the longitudinal as well as cross-sectional directions. The thoracic and suprarenal aorta cannot be well visualized with U/S because of the overlying lung tissue.
Abdominal Aortic AneurysmsDiagnosis CT scan is the most precise test for imaging AAAs It can identify proximal and distal extent of the aneurysm, identify occlusive or aneurysmal dz in the renal, visceral and iliac arteries. Identify the size of the aortic lumen, amount and location of mural thrombus and presence of calcific dz.
Abdominal Aortic AneurysmsDiagnosis Spiral CT scanners w/ 3D CT angiography have largely replaced conventional angiography for evaluation of AAAs
Abdominal Aortic AneurysmsMedical Management Pt with low-risk AAAs that are being followed with serial CT exams, attempts are made to reduce expansion rate and rupture risk. Risk factor modification: smoking cessation, BP control and reduction of cholesterol, triglycerides and lipoproteins. Β-blocker use has failed to show a beneficial effect of slowing growth of aortic aneurysms. NSAIDs in experimental studies has shown to inhibit elastase-induced AAAs in rats through inhibition of COX2 and reduction of prostaglandin E2, interleukin-6, and MMP-9. MMP inhibitors have been proposed as another therapeutic approach to slow aneurysm expansion.
Abdominal Aortic Aneurysms Inflammatory aneurysm represent 5% of all infrarenal AAAs. Dense adhesions to the 3rd and 4th portion of the duodenum. Ureteral entrapment occurs in 25% of cases Mycotic aneurysms are caused by #1 Salmonella followed by #2 Staphylococcus. Abdominal pain, fevers and 50% will have positive blood cultures.
Iliac Artery Aneurysms Iliac artery aneurysms occur in
conjunction with AAAs in 40% of patients. Isolated iliac aneurysms are rare, accounting for less than 2% of all aortoilliac aneurysms. Much like AAAs, iliac aneurysms are associated with atherosclerosis. Marfans, Ehlers-Danlos, Kawasaki, Takayasu’s, cystic medial necrosis and arterial dissection. Most isolated iliac artery aneurysms involve the common iliac artery (70%) and the hypogastric artery (20%). Multiple iliac aneurysms occur in most patients are bilateral in 33% of pts.
Iliac Artery Aneurysms Clinical presentation is variable and because of their location in the pelvis, they are not easily palpable. Many pts have symptoms in the absence of rupture, which can caused by compression of adjacent pelvic structures (e.g. Bladder, colon, ureter, lumbosacral n.), but most present with lower abdominal and groin pain. Iliac aneurysms <3cm can be treated conservatively by serial radiologic exam. Iliac aneurysms >3.5cm are repaired if possible. Common iliac aneurysms associated w/ AAAs >2cm are repaired at the time of AAA repair. Internal iliac artery aneurysms can be treated with catheter based techniques by injecting embolization coils or use of thrombogenic material.
Femoral Artery Aneurysms Femoral artery aneurysms are the 2nd most common peripheral artery
aneurysm after popliteal. They are bilateral in 50% of pts and 92% of pts have concomitant aortoiliac aneurysm. True aneurysms are almost always degenerative atherosclerotic aneurysms, whereas pseudoaneurysms are commonly found after surgical revascularization or after percutaneous catherization. Diagnosis of FAAs are usually made by physical exam and confirmed by U/S. All true FAAs >2 cm need to be considered for repair because of risk for thromboembolic complications and increased risk of rupture. High risk of rupture is attributed to large FAAs and involvement of profunda femoris artery.
Popliteal Artery Aneurysms Popliteal artery aneurysms (PAAs)
are the most common peripheral aneurysms and account for 70% of the peripheral artery aneurysms. Early recognition is important due to the high risk of limb loss. Amputation rates in pts with acute thromboembolism due to PAAs have ranged from 0% to 30%. Almost all pts are men (97%), have contralateral aneurysms (50%) and have aortoiliac aneurysms (50%). Most PAAs are diagnosed with physical exam and confirmed with duplex scanning. Indications for repair: symptomatic dz, size >2 cm and aniographic evidence of distal embolization.
Upper Extremity Aneurysms Aneurysms of the upper extremity
are rare, accounting for 1% all peripheral aneurysms. Subclavian artery aneurysms are the most common of upper extremity aneurysms. Pts may feel neck, chest or shoulder pain from aneurysm expansion or rupture. Primary complication with subclavian aneurysm is distal emoblization to the upper extremity. Diagnosis can be established with duplex U/S or CT scan. Aortic arch and upper extremity angiography is necessary to define the extent of the disease.
Splanchnic Artery Aneurysms Aneurysms of the visceral branches of the abdominal aorta are three times more common then renal artery aneurysms and their clinical significance is a high mortality for ruptured aneurysms. The most common visceral artery aneurysm is splenic artery aneurysms. Women are four times more like to have splenic artery aneurysms than men. The incidence is also increased in multiparous women. As well as pts with splenomegaly and following orthotopic liver transplantation. Splenic artery aneurysms are usually diagnosed incidentally on CT scan. Indication for repair: symptomatic, pt is pregnant or in women of childbearing age.
Splanchnic Artery Aneurysms Hepatic artery aneurysms are divided into two types: extrahepatic
(true) aneurysms and intrahepatic (false) aneurysms. Degenerative atherosclerosis and fibroplasia are the most frequent causes of extrahepatic aneurysms. Most hepatic aneurysms require intervention because rupture is frequent and lethal. Superior mesenteric artery aneurysms are most commonly caused by degenerative atherosclerosis, but as many as 1/3 are cause by septic emboli. Herald bleeding and abdominal pain are the most typical presentations. Acute mesenteric ischemia due to thromboembolism is associated with rupture in 50% of pts.
Renal Artery Aneurysms Renal artery aneurysms are
uncommon and their rupture is rare. True renal artery aneurysms are most frequently caused by medial fibroplasia followed by degenerative atherosclerosis. Most frequent cause of false renal artery aneurysms are spontaneous or traumatic dissections. Indication for surgery: size >2 cm in women of childbearing age.
Overview Background Classification Pathogenesis Aneurysm Types
Background The term aneurysm is derived from the Greek word aneurysma which means “widening” and is defined as a permanent and irreversible localized dilatation of a blood vessel, having at least 50% increase in diameter compared with the expected normal diameter. Ectasia is defined as a dilatation less than 50% of the normal diameter. In men, infrarenal aorta is normally between 14 and 24mm. In women, infrarenal aorta is normally between 12 and 21 mm. Therefore, abdominal aortic aneurysm (AAA) is diagnosed if the diameter is 3cm or larger in a man or 2.6 cm or larger in a women.
Background Aneurysms can develop at any location in the arterial tree, but are most commonly located in the aorta, followed by iliac, popliteal and femoral arteries.
Background The first elective operation for treatment of an aneurysm was performed by Antyllus in the 2nd century AD. He described ligation of the artery above and below the aneurysm, then incising the aneurysm sac and evacuating its contents. Endovascular aortic aneurysm repair EVAR dates back to 1991 when Juan Parodi introduced this as a treatment of AAA
Classification Aneurysms are classified into two main groups: true and false aneurysms. True aneurysms involve all three layers of the vessel wall False aneurysms do not have all 3 layers of the wall involved and typically involve a defect in the inner most two layers.
Classification Aneurysms are further classified by morphologic type The most common aneurysms are spindleshaped fusiform aneurysms Aneurysms that affect only part of the arterial circumference are termed saccular
Pathogenesis The pathogenesis of aneurysmal disease is a multi-factorial, complex process. More than 90% of aneurysms are associated with atherosclerosis. Aneurysms are more accurately referred to as degenerative, where an interaction of multiple factors rather than one single process is responsible for the destruction of the media of the vessel wall that leads to aneurysms formation. Congenital aneurysms associated with connective tissue disorders (i.e. Marfans, Ehlos-Danlers) are rare. Infected (mycotic) aneurysms are somewhat more common Dissecting aneurysms are applied to dissections with aneurysmal dilatation of the false lumen.
Pathogenesis Aneurysms are associated with alterations in the connective tissue of the vessel wall. The normal vessel wall is made up of lamellar units that consist of elastin, collagen (mainly types I and III) and vascular smooth muscle cells. Elastin fibers are most abundant in the media and are the main load-bearing component under most physiologic conditions. Collagen provides the tensile strength and is considered the “safety net”, acquiring load-bearing functions at higher pressures when elastin fails. In the normal aorta, there is a gradual but marked reduction in the number of medial elastin layers from the proximal thoracic aorta to the infrarenal aorta.
Pathogenesis Histologically, the aneurysms wall is thinned, with a marked decrease in the amount of medial elastin.
Biochemical studies show there is an increase in the collagen:elastin ratio in the aneurysms wall. Elastin fragmentation is the initial structural event and elastin depletion is completed early in aneurysm formation. Elastin degradation is a key step in the development of aneurysms, but collagen degradation is ultimately required for aneurysmal rupture.
Pathogenesis Proteolytic enzymes have also been shown to play a major role in aneurysms formation. There is increased expression and activity of matrix metalloproteinases (MMPs) in the wall of aneurysms. In AAAs, MMP activation favors elastin and collagen degradation. Interstitial collagen degradation accompanies increased expression of collagenases MMP-1 and MMP-13 in AAAs. Elastases MMP-2, MMP-9 and MMP-12 also have increased expression in aneurysmal aortic tissue.
Pathogenesis Increased serum levels of MMPs return to normal after aneurysmal repair. Another prominent histologic feature of aneurysms is the presence of an inflammatory infiltrate with a preponderance of plasma cells in the media and T cells in the adventia. These cells subsequently release a cascade of cytokines that result in the activation of many different proteases. Extensive lymphocytic and monocytic infiltrate in the media and adventia and deposition of IgG in the vessel wall further support the concept that aneurysm formation is autoimmune. An infectious cause of aneurysm formation has been suggested with as many as 55% of aortic aneurysms demonstrate Chlamydia pneumoniae.
Pathogenesis There is considerable evidence that genetics plays a role in aneurysm formation. Familial clustering is seen in 15% to 25% of patients undergoing AAA repair. Specific genetic abnormalities include decreased type III collagen in the aortic media of familial aneurysms, polymorphisms on the pro-α chain of type III collagen and deficiencies in α1-antitrypsin.
Pathogenesis Once an aneurysms forms its
enlargement is governed by Laplace's law. Laplace Law: T=PR For a given transmural pressure, the wall tension is proportionate to the radius. Thus, the larger the vessel radius, the larger the wall tension required to withstand a given internal fluid. HTN, increasing transmural pressure, is a major risk factor for rupture.
Pathogenesis The pathogenesis of degenerative aortic aneurysms is mulitfactorial involving disordered remodeling of the extracellular matrix, activation of proteolytic enzymes, chronic inflammation, genetic predisposition and biomechanical wall stress. Degenerative aneurysms account for more than 90% of aneurysmal disease
Abdominal Aortic Aneurysms Aortic aneurysms are most commonly located in the infrarenal aorta, with the segment immediately below the renal arteries usually being spared. The iliac arteries are involved in 40% of pts with AAA. In the U.S. between 3.5 and 6.6 per 1000 people have AAAs
Abdominal Aortic Aneurysms-Risk Factors Risk factors: Age, gender, race, tobacco use, and family history The frequency of aneurysms increases steadily in men older than 55 yrs, reaching a peak of 6% at 8o to 85 yrs. In women peak at 4.5% at older then 90 yrs. Male:female ratio is 4:1 to 5:1 in the 60 to 70 year age group, but beyond age of 80 it approaches 1:1. AAA is primarily a disease of elderly white men, with white males being two to three times more likely develop AAA than black males. Smoking is associated with 78% of AAAs and there is an 8:1 preponderance in smokers vs nonsmokers. There is an inverse relationship between DM and development of AAA. Pts with DM where two times less likely to develop AAA than those without DM.
Abdominal Aortic Aneurysms-Risk Factors The most frequent and lethal complication of AAAs is rupture. Rupture AAAs are the 13th leading cause of death in the United States. After rupture of an AAA, only half of patients arrive at the hospital alive. One studied showed, 50% reach the hospital alive, 7% died before surgery, 17% died during the operation and 37% died within 30 days of the operation for an overall mortality rate for open surgical repair of 45%
Abdominal Aortic Aneurysms-Risk Factors For AAAs between 5.5 and 6cm, the annual rupture risk is between 5 and 10%. AAAs between 6.o and 7.0cm the annual rupture risk is between 10% to 20%. AAAs >8cm have a 100% 5-year risk of rupture. Low risk for rupture: <5cm, <0.3cm/yr, no COPD, no Fmhx, normal BP, fusiform High risk for rupture: >6cm, >0.6cm/yr, severe COPD, +Fmhx, poorly controlled HTN, very eccenteric Recommended that repair of AAAs occurs when size >5.5 cm or growth of > 0.5cm/yr.
Abdominal Aortic AneurysmsDiagnosis Most asymptomatic aneurysms are
discovered on routine physical exam with the palpation of a pulsatile abdominal mass or during radiographic study. Chronic vague abdominal or back pain is the most common symptom, present in up to 30% of patients. Classic presentation of ruptured AAA present with the triad of sudden-onset midabdominal pain or flank pain, shock and the presence of a pulsatile mass. Most AAAs rupture on the left posterolateral wall, 2-4cms below renals
Abdominal Aortic AneurysmsDiagnosis Abdominal ultrasound is the most widely used noninvasive test for AAAs. Provides structural detail of the vessel and can accurately measure the size of the aneurysm in the longitudinal as well as cross-sectional directions. The thoracic and suprarenal aorta cannot be well visualized with U/S because of the overlying lung tissue.
Abdominal Aortic AneurysmsDiagnosis CT scan is the most precise test for imaging AAAs It can identify proximal and distal extent of the aneurysm, identify occlusive or aneurysmal dz in the renal, visceral and iliac arteries. Identify the size of the aortic lumen, amount and location of mural thrombus and presence of calcific dz.
Abdominal Aortic AneurysmsDiagnosis Spiral CT scanners w/ 3D CT angiography have largely replaced conventional angiography for evaluation of AAAs
Abdominal Aortic AneurysmsMedical Management Pt with low-risk AAAs that are being followed with serial CT exams, attempts are made to reduce expansion rate and rupture risk. Risk factor modification: smoking cessation, BP control and reduction of cholesterol, triglycerides and lipoproteins. Β-blocker use has failed to show a beneficial effect of slowing growth of aortic aneurysms. NSAIDs in experimental studies has shown to inhibit elastase-induced AAAs in rats through inhibition of COX2 and reduction of prostaglandin E2, interleukin-6, and MMP-9. MMP inhibitors have been proposed as another therapeutic approach to slow aneurysm expansion.
Abdominal Aortic Aneurysms Inflammatory aneurysm represent 5% of all infrarenal AAAs. Dense adhesions to the 3rd and 4th portion of the duodenum. Ureteral entrapment occurs in 25% of cases Mycotic aneurysms are caused by #1 Salmonella followed by #2 Staphylococcus. Abdominal pain, fevers and 50% will have positive blood cultures.
Iliac Artery Aneurysms Iliac artery aneurysms occur in
conjunction with AAAs in 40% of patients. Isolated iliac aneurysms are rare, accounting for less than 2% of all aortoilliac aneurysms. Much like AAAs, iliac aneurysms are associated with atherosclerosis. Marfans, Ehlers-Danlos, Kawasaki, Takayasu’s, cystic medial necrosis and arterial dissection. Most isolated iliac artery aneurysms involve the common iliac artery (70%) and the hypogastric artery (20%). Multiple iliac aneurysms occur in most patients are bilateral in 33% of pts.
Iliac Artery Aneurysms Clinical presentation is variable and because of their location in the pelvis, they are not easily palpable. Many pts have symptoms in the absence of rupture, which can caused by compression of adjacent pelvic structures (e.g. Bladder, colon, ureter, lumbosacral n.), but most present with lower abdominal and groin pain. Iliac aneurysms <3cm can be treated conservatively by serial radiologic exam. Iliac aneurysms >3.5cm are repaired if possible. Common iliac aneurysms associated w/ AAAs >2cm are repaired at the time of AAA repair. Internal iliac artery aneurysms can be treated with catheter based techniques by injecting embolization coils or use of thrombogenic material.
Femoral Artery Aneurysms Femoral artery aneurysms are the 2nd most common peripheral artery
aneurysm after popliteal. They are bilateral in 50% of pts and 92% of pts have concomitant aortoiliac aneurysm. True aneurysms are almost always degenerative atherosclerotic aneurysms, whereas pseudoaneurysms are commonly found after surgical revascularization or after percutaneous catherization. Diagnosis of FAAs are usually made by physical exam and confirmed by U/S. All true FAAs >2 cm need to be considered for repair because of risk for thromboembolic complications and increased risk of rupture. High risk of rupture is attributed to large FAAs and involvement of profunda femoris artery.
Popliteal Artery Aneurysms Popliteal artery aneurysms (PAAs)
are the most common peripheral aneurysms and account for 70% of the peripheral artery aneurysms. Early recognition is important due to the high risk of limb loss. Amputation rates in pts with acute thromboembolism due to PAAs have ranged from 0% to 30%. Almost all pts are men (97%), have contralateral aneurysms (50%) and have aortoiliac aneurysms (50%). Most PAAs are diagnosed with physical exam and confirmed with duplex scanning. Indications for repair: symptomatic dz, size >2 cm and aniographic evidence of distal embolization.
Upper Extremity Aneurysms Aneurysms of the upper extremity
are rare, accounting for 1% all peripheral aneurysms. Subclavian artery aneurysms are the most common of upper extremity aneurysms. Pts may feel neck, chest or shoulder pain from aneurysm expansion or rupture. Primary complication with subclavian aneurysm is distal emoblization to the upper extremity. Diagnosis can be established with duplex U/S or CT scan. Aortic arch and upper extremity angiography is necessary to define the extent of the disease.
Splanchnic Artery Aneurysms Aneurysms of the visceral branches of the abdominal aorta are three times more common then renal artery aneurysms and their clinical significance is a high mortality for ruptured aneurysms. The most common visceral artery aneurysm is splenic artery aneurysms. Women are four times more like to have splenic artery aneurysms than men. The incidence is also increased in multiparous women. As well as pts with splenomegaly and following orthotopic liver transplantation. Splenic artery aneurysms are usually diagnosed incidentally on CT scan. Indication for repair: symptomatic, pt is pregnant or in women of childbearing age.
Splanchnic Artery Aneurysms Hepatic artery aneurysms are divided into two types: extrahepatic
(true) aneurysms and intrahepatic (false) aneurysms. Degenerative atherosclerosis and fibroplasia are the most frequent causes of extrahepatic aneurysms. Most hepatic aneurysms require intervention because rupture is frequent and lethal. Superior mesenteric artery aneurysms are most commonly caused by degenerative atherosclerosis, but as many as 1/3 are cause by septic emboli. Herald bleeding and abdominal pain are the most typical presentations. Acute mesenteric ischemia due to thromboembolism is associated with rupture in 50% of pts.
Renal Artery Aneurysms Renal artery aneurysms are
uncommon and their rupture is rare. True renal artery aneurysms are most frequently caused by medial fibroplasia followed by degenerative atherosclerosis. Most frequent cause of false renal artery aneurysms are spontaneous or traumatic dissections. Indication for surgery: size >2 cm in women of childbearing age.
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