An aneurysm or aneurism (from Ancient Greek: ἀνεύρυσμα - aneurusma "dilation", from ἀνευρύνειν - aneurunein "to dilate"), is a localized, blood-filled dilation (balloon-like bulge) of a blood vessel caused by disease or weakening of the vessel wall.
Aneurysms most commonly occur in arteries at the base of the brain (the circle of Willis) and in the aorta (the main artery coming out of the heart, an aortic aneurysm). As the size of an aneurysm increases, there is an increased risk of rupture, which can result in severe hemorrhage, other complications or even death.
In a true aneurysm, the inner layers of a vessel have bulged outside the outer layer that normally confines them. The aneurysm is surrounded by these inner layers.
A false or pseudoaneurysm does not primarily involve such distortion of the vessel. It is a collection of blood leaking completely out of an artery or vein, but confined next to the vessel by the surrounding tissue. This blood-filled cavity will eventually either thrombose (clot) enough to seal the leak or rupture out of the tougher tissue enclosing it and flow freely between layers of other tissues or into looser tissues. Pseudoaneurysms can be caused by trauma that punctures the artery and are a known complication of percutaneous arterial procedures, such as arteriography, or of arterial grafting or of use of an artery for injection, such as by drug abusers unable to find a usable vein. Like true aneurysms, they may be felt as an abnormal pulsatile mass on palpation.
Aneurysms can be described by their shape. They have been described as either "fusiform" (resembling a narrow cylinder) or "saccular" (berry) (resembling a small sac), though alternatives have been proposed
Most frequent site of occurrence of cerebral aneurysms is in the anterior communicating artery, which is part of the circle of Willis. The next most common sites of cerebral aneurysm occurrence are in the internal carotid artery at the level of the posterior communicating artery, and at the ICA terminus.
Most (94%) non-intracranial aneurysms arise distal to the origin of the renal arteries at the infrarenal abdominal aorta, a condition mostly caused by atherosclerosis.
The thoracic aorta can also be involved. One common form of thoracic aortic aneurysm involves widening of the proximal aorta and the aortic root, which leads to aortic insufficiency. Aneurysms occur in the legs also, in particular in the deep vessels (e.g., the popliteal vessels in the knee).
Most frequent site of occurrence of cerebral aneurysms is in the anterior communicating artery, which is part of the circle of Willis. The next most common sites of cerebral aneurysm occurrence are in the internal carotid artery at the level of the posterior communicating artery, and at the ICA terminus.
Most (94%) non-intracranial aneurysms arise distal to the origin of the renal arteries at the infrarenal abdominal aorta, a condition mostly caused by atherosclerosis.
The thoracic aorta can also be involved. One common form of thoracic aortic aneurysm involves widening of the proximal aorta and the aortic root, which leads to aortic insufficiency. Aneurysms occur in the legs also, in particular in the deep vessels (e.g., the popliteal vessels in the knee).
Arterial aneurysms are much more common, but venous aneurysms do happen (for example, the popliteal venous aneurysm). GEN and VIVO.
Aneurysms can be classified by the underlying condition.
Many aneurysms are atherosclerotic in nature.
Another term used is "mycotic aneurysm". Some sources reserve this term for fungal infections only, while other sources use the term to describe bacterial infections as well.
While most aneurysms occur in an isolated form, the occurrence of berry aneurysms of the anterior communicating artery of the circle of Willis is associated with autosomal dominant polycystic kidney disease (ADPKD).
The third stage of syphilis also manifests as aneurysm of the aorta, which is due to loss of the vasa vasorum in the tunica adventitia.
minority of aneurysms are caused by a copper deficiency. Numerous animal experiments have shown that a copper deficiency can cause diseases affected by elastin] tissue strength . The lysyl oxidase that cross links connective tissue is secreted normally, but its activity is reduced, due, no doubt, to some of the initial enzyme molecules (apo-enzyme or enzyme without the copper) failing to contain copper.
Aneurysms of the aorta are the chief cause of death of copper deficient chickens, and also depleting copper produces aneurysms in turkeys.
Men who die of aneurysms have a liver content (of copper) that can be as little as 26% of normal. The median layer of the blood vessel (where the elastin is) is thinner but its elastin copper content is the same as normal men. The overall thickness is not different. The body must therefore have some way of preventing elastin tissue from growing if there is not enough activated lysyl oxidase for it. Men are more susceptible to aneurysms than young women, probably because estrogen increases the efficiency of absorption of copper. However, women can be affected by some of these problems after pregnancy, probably because women must give the liver of their babies large copper stores in order for them to survive the low levels of copper in milk. A baby’s liver has up to ten times as much copper as adult livers. Higher alcohol content enhances copper uptake, whilst zinc, iron and copper uptake diminish with increasing sugar and alcohol contents. Handling in iron or galvanized ironware is shown to deplete copper by almost 100% of initial levels and this has potential in health risk reduction applications. Excess intake of zinc can lead to deficiency of copper (hypocupremia). This happens because excess amounts of zinc in the body trigger reduced absorption of copper in the GI tract, which results in increased fecal loss of copper.
The occurrence and expansion of an aneurysm in a given segment of the arterial tree involves local hemodynamic factors and factors intrinsic to the arterial segment itself.
The aorta is a relatively low-resistance circuit for circulating blood. The lower extremities have higher arterial resistance, and the repeated trauma of a reflected arterial wave on the distal aorta may injure a weakened aortic wall and contribute to aneurysmal degeneration. Systemic hypertension compounds the injury, accelerates the expansion of known aneurysms, and may contribute to their formation.
Aneurysm formation is probably the result of multiple factors affecting that arterial segment and its local environment.
In hemodynamic terms, the coupling of aneurysmal dilation and increased wall stress is approximated by the law of Laplace. To be specific, the Laplace law applied to a cylinder states that the (arterial) wall tension is equal to the pressure times the radius of the arterial conduit (T = P x R). As diameter increases, wall tension increases, which contributes to more increase in diameter and risk of rupture. Increased pressure (systemic hypertension) and increased aneurysm size aggravate wall tension and therefore increase the risk of rupture. In addition, the vessel wall is supplied by the blood within its lumen in humans (although aorta has Vasa vasorum). Therefore[citation needed] in a developing aneurysm, the most ischemic portion of the aneurysm is at the farthest end, resulting in weakening of the vessel wall there and aiding further expansion of the aneurysm. Thus eventually all aneurysms will, if left to complete their evolution, rupture without intervention.
Diagnosis of a ruptured cerebral aneurysm is commonly made by finding signs of subarachnoid hemorrhage on a CT scan (Computed Tomography, sometimes called a CAT scan, a computerized test that rapidly X-rays the body in cross-sections, or slices, as the body is moved through a large, circular machine). If the CT scan is negative but a ruptured aneurysm is still suspected, a lumbar puncture is performed to detect blood in the cerebrospinal fluid (CSF). Computed Tomography Angiography (CTA) is an alternative to the traditional method and can be performed without the need for arterial catheterization. This test combines a regular CT scan with a contrast dye injected into a vein. Once the dye is injected into a vein, it travels to the brain arteries, and images are created using a CT scan. These images show exactly how blood flows into the brain arteries.
Throughout history, the treatment of arterial aneurysms has been surgical intervention, or watchful waiting in combination with control of blood pressure. In recent years, endovascular or minimally invasive techniques have been developed for many types of aneurysms.
At the current time, there are two treatment options for brain aneurysms: surgical clipping or endovascular coiling.
Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937. It consists of performing a craniotomy, exposing the aneurysm, and closing the base of the aneurysm with a clip. The surgical technique has been modified and improved over the years. Surgical clipping remains the best method to permanently eliminate aneurysms.
Endovascular coiling was introduced by Guido Guglielmi at UCLA in 1991. It consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. Once the catheter is in the aneurysm, platinum coils are pushed into the aneurysm and released. These coils initiate a clotting or thrombotic reaction within the aneurysm that, if successful, will eliminate the aneurysm. In the case of broad-based aneurysms, a stent is passed first into the parent artery to serve as a scaffold for the coils ("stent-assisted coiling").
At this point it appears that the risks associated with surgical clipping and endovascular coiling, in terms of stroke or death from the procedure, are the same. The ISAT trials have shown, however, that patients who have experienced aneurysmal rupture have a 7% lower mortality rate when treated by coiling than patients treated by clipping, when all other factors are equal. Coiled aneurysms, however, do have a higher recurrence rate as demonstrated by angiography. For instance, the most recent study by Jacques Moret and colleagues from Paris, France, (a group with one of the largest experiences in endovascular coiling) indicates that 28.6% of aneurysms recurred within one year of coiling, and that the recurrence rate increased with time. These results are similar to those previously reported by other endovascular groups. For instance Jean Raymond and colleagues from Montreal, Canada, (another group with a large experience in endovascular coiling) reported that 33.6% of aneurysms recurred within one year of coiling. The long-term coiling results of one of the two prospective, randomized studies comparing surgical clipping versus endovascular coiling, in particular the International Subarachnoid Aneurysm Trial (ISAT) show similar results. However, no studies to date have shown that the higher angiographic recurrence rate equals a higher rate of rebleeding. Thus far, the ISAT trials listed above show no increase in the rate of rebleeding, and show a persistent 7% lower mortality rate in subarachnoid hemorrhage patients who have been treated with coiling.. In ISAT, the need for late retreatment of aneurysms was 6.9 times more likely for endovascular coiling as compared to surgical clipping.
Patients who undergo endovascular coiling need to have annual studies (such as MRI/MRA, CTA, or angiography) to detect early recurrences, a practice that has not traditionally been performed with clipping. If a recurrence is identified, the aneurysm may need to be retreated with either surgery or further coiling. The risks associated with surgical clipping of previously coiled aneurysms are very high. Ultimately, the decision to treat with surgical clipping versus endovascular coiling should be made by a cerebrovascular team with extensive experience in both modalities.
Aneurysms are treated by either endovascular techniques (angioplasty with stent) or open surgery techniques. Open techniques include exclusion and excision. Exclusion of an aneurysm means tightly tying suture thread around the artery both proximally and distally to the aneurysm, to cut off blood flow through the aneurysm. If the aneurysm is infected or mycotic, it may then be excised (cut out and removed from the body). If uninfected, the aneurysm is often left in place. After exclusion or excision, a bypass graft can be placed, to ensure blood supply to the affected area. For some aneurysm repairs in the abdomen, where there is adequate collateral blood supply, bypass grafts are not needed.
For aneurysms in the aorta, arms, legs, or head, the weakened section of the vessel may be replaced by a bypass graft that is sutured at the vascular stumps. Instead of sewing, the graft tube ends, made rigid and expandable by nitinol wireframe, can be inserted into the vascular stumps and permanently fixed there by external ligature. New devices were recently developed to substitute the external ligature by expandable ring allowing use in acute ascending aorta dissection, providing airtight, easy and quick anastomosis extended to the arch concavity .Less invasive endovascular techniques allow covered metallic stent grafts to be inserted through the arteries of the leg and deployed across the aneurysm.
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