I. Overview
Intracranial aneurysms are mostly caused by localized congenital defects in the walls of cerebral arteries and on the basis of increased intraluminal pressure. Hypertension, cerebral atherosclerosis and vasculitis are related to the occurrence and development of aneurysms. Cerebral aneurysms are most often seen at the bifurcation of the arteries at the base of the brain. According to its location, 4/5 of them are located in the anterior half of the cerebral artery ring, with the internal carotid artery, posterior communicating artery and anterior communicating artery being the most common ones; the posterior half of the cerebral artery ring accounts for about 1/5 of them, occurring in the vertebrobasilar artery, posterior cerebral artery and its branches. Symptoms: When an aneurysm ruptures, there are often prodromal symptoms such as headache, followed by hemorrhagic symptoms, including severe headache, irritability, nausea and vomiting, followed by an increase in intracranial pressure. This may be accompanied by impaired consciousness and neurological localization of the corresponding area. If the aneurysm bleeds and forms a large hematoma, the condition deteriorates sharply and brain herniation crisis occurs. According to statistics, after the first rupture of an aneurysm, the mortality rate is as high as 30-40%, half of which die within 48 hours after the onset of the disease, and in 1/3 of the surviving cases, rebleeding may occur. CT scan can sometimes show the aneurysm lesion, and MRI examination can not only show the aneurysm, but also sometimes can see the attached thrombus. Once the diagnosis of cerebral aneurysm is made, surgical treatment should be performed in order to cure it and avoid the risk of hemorrhage. Minimally invasive treatment by aneurysm embolization or direct treatment of aneurysm by craniotomy can be used.
Etiology and pathology
The cause of aneurysm is not well understood. The theory of congenital defect of the arterial wall suggests that the arterial wall at the arterial bifurcation of the Willis ring in the skull is congenitally deficient in the subglottis layer. The theory of acquired degeneration of the arterial wall suggests that intracranial atherosclerosis and hypertension have caused the destruction of the intracranial elastic plate. The destruction of the elastic plate within the artery and its gradual bulging to form a cystic aneurysm. In addition, infectious lesions in the body such as bacterial endocarditis and pulmonary infections can cause infected aneurysms by shedding infectious emboli and eroding the cerebral artery wall; head trauma can also lead to aneurysm formation. However, all of them are rare in clinical practice.
Histological examination reveals only a layer of endothelium in the aneurysm wall, lack of smooth muscle tissue in the middle layer, and broken or absent elastic fibers. The aneurysm wall is infiltrated with inflammatory cells. Electron microscopy reveals the loss of elastic plates in the aneurysm wall. Giant aneurysms often have thrombosis or even calcification, and the straight emboli are layered in an “onion” shape. Aneurysms are cystic, spherical or berry-shaped. The aneurysm has a purplish-red appearance, and the wall is extremely thin, with intraoperative vortexes of blood flow visible. The top of the aneurysm is much weaker, and 98% of aneurysm bleeds are located at the top of the aneurysm. The ruptured aneurysm is surrounded by a hematoma, and the apex of the ruptured aneurysm is adherent to the surrounding tissue.
Aneurysms are classified according to their location as.
(i) aneurysms of the internal carotid artery system, which account for about 90% of intracranial aneurysms, including internal carotid artery-posterior communicating aneurysms, anterior artery-anterior communicating aneurysms, and middle artery aneurysms.
② vertebrobasilar system aneurysms, accounting for about 10% of intracranial aneurysms, including vertebral aneurysms, basilar aneurysms and posterior cerebral aneurysms. Aneurysms less than 0.5 cm in diameter are small, 0.6-1.5 cm in diameter are general, 1.6-2.5 cm in diameter are large, and those larger than 2.5 cm in diameter are huge. Smaller diameter aneurysms have more chances of bleeding. Intracranial multiple aneurysms account for about 20%, with two aneurysms being the most common and three or more.
Clinical manifestations
1.Aneurysm rupture and bleeding symptoms Small and medium-sized aneurysms without rupture and bleeding can be clinically asymptomatic. Once the aneurysm ruptures and bleeds, the clinical manifestation is severe subarachnoid hemorrhage, with rapid onset and severe headache, which is described as “head exploding”. The patient may have frequent vomiting, profuse sweating, and elevated body temperature; neck stiffness, and a positive Creutzfeldt-Jakob sign. There may also be impaired consciousness and even coma. Some patients have triggers such as exertion and emotional excitement before bleeding, while others have no obvious triggers or develop during sleep. In about 1/3 of patients, aneurysm rupture results in death due to untimely diagnosis and treatment. Most aneurysm ruptures are closed by clotting and the bleeding stops, and the condition gradually stabilizes. As the blood clot around the aneurysm rupture dissolves, the aneurysm may rupture and bleed again. Secondary bleeding occurs within 2 weeks of the first bleed. In some patients, the hemorrhage may invade the vitreous through the optic nerve sheath causing visual impairment. After subarachnoid hemorrhage, erythrocyte destruction produces 5-hydroxytryptamine, catecholamines and other vasoactive substances that act on cerebral blood vessels, resulting in vasospasm, with an incidence of 21% to 62%, mostly occurring 3-15 days after the hemorrhage. Local vasospasm occurs only in the vicinity of the aneurysm, and the patient’s symptoms are not obvious and only show up on cerebral angiography. Extensive cerebral vasospasm can lead to the occurrence of cerebral infarction, and the patient becomes unconscious, hemiplegic, or even dies.
2. Focal symptoms depend on the location of the aneurysm, adjacent anatomy and the size of the aneurysm. Arteriovenous nerve palsy is commonly seen in internal carotid artery-posterior communicating artery aneurysms and aneurysms of the posterior cerebral artery, manifesting as unilateral eyelid ptosis, pupil dilation, inversion, inability to see up or down, and loss of direct and indirect light responses. Sometimes focal symptoms appear before subarachnoid hemorrhage and are considered precursors to aneurysm hemorrhage, such as mild migraine and orbital pain followed by arteriovenous nerve palsy, at which time one should be alert to the ensuing subarachnoid hemorrhage. If an aneurysm hemorrhage in the middle cerebral artery forms a hematoma; or after an aneurysm hemorrhage in other parts of the brain, cerebral vasospasm cerebral infarction, the patient may develop hemiparesis, motor or sensory aphasia. If a giant aneurysm affects the visual pathway, the patient may have visual field impairment. After aneurysm hemorrhage, the condition varies in severity. To facilitate judgment of the condition, selection of the timing of imaging and surgery, and evaluation of the outcome.
The five levels of Hunt’s classification are often used internationally.
Grade I Asymptomatic, or with mild headache and neck stiffness.
Grade II: severe headache, cervical tonicity, no other neurological symptoms except for cerebral nerve paralysis such as motor heel nerve.
Grade 3 Mild impaired consciousness, agitation and mild cerebral symptoms.
Grade IV Semi-coma, hemiparesis, early decerebrate tonicity and vegetative disorders.
Grade V Deep coma, decerebrate, and endangered state.
IV. Examination
1. Determine whether there is subarachnoid hemorrhage. In the acute phase of hemorrhage, the positive rate of CT confirmation of SAH is extremely high, safe, rapid and reliable. One week after hemorrhage, CT ding is not easy to diagnose. Lumbar puncture may induce aneurysm rupture and bleeding, so it is generally no longer the first choice to confirm the diagnosis of SAH.
2.Because intracranial aneurysms are mostly located in the WiLLis arterial ring at the base of the skull, aneurysms less than 1.0 cm in diameter are not easily detected by CT. MRI is better than CT, and the flow space can be seen in the aneurysm; MRA can suggest different parts of aneurysm, and is often used for intracranial aneurysm screening. Three-dimensional CT (3D-CT) can understand the relationship between aneurysm and aneurysm-carrying artery from different angles and provide more information for surgical clamping of aneurysm decision.
Cerebral angiography is a necessary test to confirm the diagnosis of intracranial aneurysm, which is very important to determine the exact location, shape, internal diameter, number, vasospasm and surgical plan of the aneurysm, and DSA is clearer. A total cerebral angiogram with transfemoral artery cannulation can avoid missing multiple aneurysms. Cerebral angiography should be performed early when the disease is below grade III. Patients with grade III and above can wait until the disease is stable before performing angiography. Early angiogram to clarify the diagnosis and perform aneurysm embolization treatment or surgical clamping of aneurysm as soon as possible can prevent re-rupture and bleeding of aneurysm. If the first imaging is negative, the aneurysm may not be visualized due to cerebral vasospasm, and if there is a high suspicion of aneurysm, the imaging should be repeated after 3 months.
V. Treatment
Intracranial aneurysm should be treated surgically. About 70% of patients will die from aneurysm rebleeding with conservative treatment. Aneurysm embolization and microsurgery have reduced the surgical mortality rate of aneurysm to less than 2%.
1.Selecting the timing of surgery Once subarachnoid hemorrhage is detected, it should be contrasted and operated as early as possible.
2.Surgical method With the development of interventional technology, interventional treatment of aneurysm by spring-ring embolization has gradually become the most ideal method for intracranial aneurysm. Interventional treatment is less invasive, simple, safe, effective, fast recovery, less pain, less complications and significantly shorter hospital stay. Open clamping of aneurysms is the traditional treatment that neither blocks the aneurysm-carrying artery nor completely and utterly eliminates the aneurysm, and may be superior to embolization in some cases. Isolation, which involves clamping the aneurysm-carrying artery at both ends of the aneurysm, should be used with caution in cases where a good supply of side branches to the brain has not been demonstrated. The efficacy of aneurysm wall reinforcement is uncertain and should be used sparingly. After surgery, cerebral angiography should be repeated to confirm whether the aneurysm disappears.
After aneurysm rupture, the patient should rest in bed and minimize adverse sound and light stimulation, and the patient should be placed in ICU. Transcranial Doppler ultrasonography can monitor the changes of cerebral blood flow, which is helpful to observe the progress of the disease. Constipation should be treated with laxatives, maintenance of normal blood pressure, and appropriate sedation. Anti-vascular spasm treatment such as calcium antagonists is used. To prevent rebleeding from clot dissolution at the aneurysm rupture, larger doses of antifibrinolytic agents, such as aminocaproic acid; to inhibit the formation of fibrinolytic zymogen, are used with caution in patients with renal dysfunction, with the possibility of thrombosis as a side effect.