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.
