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Aneurysms.pptx
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- 2. •Cerebral aneurysms arepathologic focal dilatations of the cerebrovasculature that are prone to rupture. • Saccular, berry, or congenital aneurysms constitute 90% and located at branch points. • Dolichoectatic, fusiform, or arteriosclerotic aneurysms are elongated outpouchings of proximal arteries that account for 7% • Infectious or mycotic aneurysms are situated peripherally and comprise 0.5% of all cerebral aneurysms. • Other peripheral lesions include neoplastic aneurysms, rare sequelae of embolized tumor fragments, and traumatic aneurysms. • Trauma can also cause dissecting aneurysms Intracranial Aneurysm
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- 4. • Artery junctionpoints may become weak, causing ballooning of the blood vessel wall that can form a small sac or aneurysm.
- 10. • The integrityof the internal elastic lamina is compromised, with associated elastic defects in the adjacent layers of the tunica media and adventitia. • Muscular defects of the tunica media and minimal support of adjacent brain parenchyma augment the pathologic potential of chronic hemodynamic stress on the arterial wall. • Focal turbulence and discontinuity of the normal architecture at vessel bifurcations may account for the propensity of saccular aneurysm formation at these locations. Pathophysiology
- 11. Pathophysiology Distal aneurysms maybe smaller compared with proximal sites, yet the risk of rupture may be dissimilar due to the relatively thinner parent artery wall thickness. Abnormalities of the internal elastic lamina may be congenital or degenerative. Multiple conditions have been associated with cerebral aneurysms; they include the following: Autosomal dominant inherited polycystic kidney disease Fibromuscular dysplasia Arteriovenous malformations Osler-Weber-Rendu syndrome Coarctation of the aorta Other vascular anomalies Moyamoya syndrome Marfan syndrome Ehlers-Danlos syndrome, type IV Other collagen type III disorders Pseudoxanthoma elasticum Alpha1-antitrypsin deficiency Systemic lupus erythematosus
- 12. Pathophysiology Sickle cell anemia Bacterialendocarditis Fungal infections Neurofibromatosis type 1 Tuberous sclerosis Dolichoectatic aneurysms of proximal vessels most likely have an arteriosclerotic etiology. These tortuous, elongated dilatations devoid of a true aneurysmal neck. Infectious aneurysms typically are situated in distal branches of the middle cerebral artery (MCA; 75-80% of cases), reflecting the embolic origin of these lesions. Traumatic aneurysms may be located in peripheral cortical branches secondary to contact with the falcine edge or skull fractures associated with penetrating or closed head injury.
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- 14. • Headache: Thisis characterized by the acute onset of severe pain, which patients often describe as "the worst headache of my life.“ • Facial pain: Aneurysms may produce facial pain. • Manifestations of meningeal irritation: Neck pain or stiffness
- 15. • Alterations inconsciousness: The sudden elevation of ICP associated with aneurysmal rupture may lead to a severe decline in cerebral perfusion pressure, causing syncope (50% of cases). Confusion or mild impairment in alertness also may be noted. • Seizures: are present in 25% of aneurysmal SAH cases, with most events occurring within 24 hours of onset.
- 16. • Autonomic disturbanc es: Subarachnoid accumulation ofproducts of blood degradation may elicit fever. Nausea or vomiting, sweating, chills, and cardiac arrhythmias also may be present. • Visual symptoms: Blurring of vision, diplopia, or visual field defects may be present.
- 17. Investigation CT brain AneurysmalSAH may be detected in 90-95% of cases. MRI brain Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH, although the comparison of CT scan and MRI in detection of SAH is controversial. CT angiography Conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms. Aneurysm location, size, and morphology may be evaluated in the acute or chronic setting with this modality. Digital subtraction angiography with biplanar magnification views provides details that may be helpful in identifying an acutely ruptured aneurysm. Transcranial Doppler TCD facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow at the bedside. TCD has exhibited close correlation with angiography in the setting of vasospasm, typically manifesting 3-21 days following aneurysmal SAH.
- 18. Aim Allow thebrain to recover from initial insult ( bleeding) Prevent or treat other complication Vasospasm
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- 21. Fischer’s grading ofsubarachnoid haemorrhage Grade 1 No detectable blood on CT scan Grade 2 Diffuse thin SAH Vertical layers < 1 mm thickness Grade 3 Localised clot and/or thick SAH vertical layer > 1 mm thickness Grade 4 Intraventricular or intracerebral clot with diffuse or no subarachnoid haemorrhage Management
- 22. Nimotop • Calcium channelblockers (Nimodipine: , Verapamil (Isoptin) • Osmotic diuretic (Mannitol 20%) • Antiepileptics (Phenytoin) • Antihypertensives (Nitroprusside) • If surgery is delayed or contraindicated (antifibrinolytic agents) • Analgesics (acetaminophen) • Laxatives to prevent straining to avoid BP Medical Management
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- 25. • Clipping: Aneurosurgeon can operate on the brain by cutting open the skull, identifying the damaged blood vessel and putting a clip across the aneurysm. • This prevents blood from entering the aneurysm and causing further growth or blood leakage.
- 26. • Coiling: Aneurosurgeon or interventional radiologist can thread a tube through the arteries, as with an angiogram, identify the aneurysm, and fill it with coils of platinum wire or with latex. • This prevents further blood from entering the aneurysm and resolves the problem.