Aneurysms of Aorta
• Defined as abnormal localized dilatation of a blood vessel or wall of the heart.
• True Aneurysms: Bound by arterial wall or heart.
• False Aneurysms: Breach in wall of vessel, extravascular hematoma,
connection with lumen is retained, pulsating hematoma e.g. post myocardial
• Aneurysms are most important clinically when involve aorta.
• Two most important causes of aortic aneurysms are atherosclerosis and cystic
medial degeneration. However any artery may be involved by this condition if
wall gets weakened due to: trauma, congenital defects (Berry An), infections
e.g. Mycotic, Syphilis, Systemic diseases like vasculitis.
• Mycotic aneurysms: Due to septic embolization and weakening e.g. infective
endocarditis, due to extension from adjacent process and by circulating
organisms infecting the wall directly.
• Macroscopic types: Saccular, are spherical involving a portion of wall, 5-20
cm, partially or completely filled with thrombus. Fusiform, may involve up to
20 cm of the aortic wall.
Abdominal Aortic Aneurysms
• Atherosclerosis in men above 50 years of age the most
frequent cause which destroys the underlying tunica media
thereby weakening the wall.
• Abdominal aorta is most frequently affected, other parts
including arch of aorta, common iliac arteries and thoracic
aorta are also affected with less frequency.
• Part of abdominal aorta most commonly involved is below
the origin of renal arteries.
• Aneurysm is usually fusiform measuring 15 x 25 cm.
• Mural thrombosis is frequent which may be complete and
may involve the lumen partially. Aortic aneurysms may
also be accompanied by similar lesions in iliac arteries.
• Occasionally the origins of renal and superior mesenteric
artery may also be affected directly or by thrombosis. The
atheromatous lesions in the aneurysms are ulcerated with
mural thrombi. Atheroemboli can lodge in the vessels of
kidneys or lower extremities.
• Variants: two variants. 1- Inflammatory: characterized by
dense periaortic fibrosis containing an abundant
lymphoplasmacytic infiltration, many giant cells and
macrophages. Cause is uncertain.
• 2- Mycotic abdominal aneurysm: Aortic atherosclerotic
aneurysms infected by deposition of circulating organisms
in the wall, particularly salmonella gastroenteritis. This
leads to suppuration and further destruction of media.
Pathogenesis of Aneurysms.
• Atherosclerosis along with other factors in men above 50
years of age.
• Have been showing to be familial, in addition to the
familial factors responsible for atherosclerosis and
• Genetic defects e.g. Marfans syndrome in structural
components of aorta can also cause aneurysms and
• There is evidence that matrix metalloproteins and
plasminogen activators, which degrade extracellular matrix
contribute to aneurysm formation.
• Depend on location and size.
• Rupture into body cavities with massive hemorrhage.
• Occlusion of a branch vessel.
• Embolism from thrombosis or atheroma.
• Compression of surrounding structures, e.g. ureter.
• Presentation as abdominal mass.
• Tertiary syphilis is marked by cardiovascular and nervous
• Endarteritis obliterans involves small muscular arteries and
arterioles; most devastating when it involves the vasa
vasorum of aorta which can lead to aneurysm of thoracic
aorta along with dilatation of aortic annulus.
• Medial destruction is the key process in tertiary syphilis.
• Inflammatory process starts in the aortic adventitia, esp.
vasa vasorum, surrounded by lymphoplasmacytic
• There is ischemic injury to aortic media, patchy loss of
elastic tissue and smooth muscle cells followed by
inflammation and later on scarring.
• Aorta loses its elastic support, becomes dilated.
• Luetic involvement of aorta favors superimposed
atherosclerosis inducing further florid atheromatosis.
• Location in thoracic aorta an differentiate the luetic
aneurysms from those purely due to atherosclerosis.
• Luetic aortic aneurysms also cause, dilatation of aortic
valve ring, producing aortic valve insufficiency, valves get
damaged as well.
• Left ventricle becomes hypertrophied with consequent
marked cardiomegaly (cor bovinum).
• Both types of aneurysms produce signs and symptoms due
• Encroachment on mediastinal structures.
• Respiratory difficulties.
• Swallowing difficulties.
• Persistent cough- recurrent laryngeal nerve.
• Pain following erosion of ribs and vertebral bodies.
• Cardiac disease.
• Rupture of aneurysm.
• Aortic dissection is catastrophic disease, characterized by dissection of
blood in between and along the laminar planes of media forming blood
filled channel. Usually dilatation of aorta is minimal.
• Two groups of patients are affected e.g. men between 40-60 years in
whom chronic hypertension, second group consists of younger persons
having systemic or localized abnormality of connective tissue of aorta
e.g. Marfans syndrome.
• Dissection may occur as complication of arterial catheterization.
• Arterial dissections may occur in aorta or coronaries during
pregnancy, reason is unknown.
• Dissection is uncommon in advanced atherosclerosis due to scarring in
the tunica media of aorta.
• Starts mostly with intimal tear that occurs within 10 cm of
• Tears are usually 1-5 cm in length.
• Dissection may extend proximally or distally, may involve
the aorta up to the iliacs and femoral artery.
• Spreads along with laminar planes, between outer and
middle one third of the wall of aorta.
• The channel may again rupture in to the aorta through a
secondary tear (double barrel aorta), this avoids fatal extra
aortic rupture and fatal hemorrhage.
• Most common cause of death is rupture into one of the
• Clinical manifestations may also be due to extension of the
dissection to the origins of aortic branches, like coronary,
renal, mesenteric or iliac arteries causing obstructions to
• Histologically the most frequent and detectable lesion is
cystic medial degeneration. The lesions consist of elastic
tissue fragmentation and separation of elastic and
fibromuscular elements of tunica media that creates cleft
like or cystic spaces filled with amorphous extracellular
matrix. Inflammation is absent.
• Cystic medial degeneration is frequently found in patients
with Marfans syndrome.
• Cystic medial degeneration is frequently found at autopsy
in persons who had experienced no symptoms of
• Hypertension is the major risk factor, but contribution to
CMD is uncertain, no good correlation between CMD and
• Some dissections are due to inherited connective tissue
defects e.g. Marfans autosomal dominant disorder.
• Complications of Marfans syndrome include; aortic
dissection, aortic and mitral valve prolapse; other
manifestations include; skeletal and occular.
• The triggering factors for intimal tear and intramural
hemorrhage is unknown. But once the process has started,
hypertension plays an important role in the progression.
• Depend on level of aorta affected.
• Sudden onset of excruciating pain, beginning in the front
of chest, radiating to back, can be readily confused
clinically with that of acute myocardial infarction.
• The diagnosis may be based on various investigations,
including angiography, two dimensional cardiac
ultrasound, CT scan and MRI.
• Prognosis has recently improved due to development of
• Varicose veins have narrowed or abnormally dilated
lumina along with incompetence of valves leading to
venous stasis. These are tortuous, dilated, elongated and
• Loss of support of vessel walls and increased intramural
• Leg veins are affected due to posture, so occupations are
important in its aetiology.
• Prolonged erect posture also results in simple orthostatic
• Condition is more common over 50 years, obese people
and during pregnancy.
• There is marked variation in the thickness of the wall.
There may be thrombosis and valvular deformities.
• Microscopically changes consist of variations in thickness
of the wall caused by dilatations and compensatory
hypertrophy of smooth muscle and subintimal fibrosis.
• Venous stasis, congestion, oedema and thrombosis.
• Embolism is rare in contrast to deep vein thrombosis.
• Distension is painful.
• Persistent varicose veins produce oedema of legs along
with trophic changes leading to stasis dermatitis and
• Varicose veins are also seen in lower esophagus, in
patients of cirrhosis, due to portal hypertension.