Intracranial anurysm

Intracranial anurysm

1. College Of Nursing Madras Medical College Chennai-03 INTRACRANIAL ANEURYSM PRESENTED BY EDWIN JOSE.L MSc(nursing) I YEAR College of nursing Madras medical college Chennai-03

2. INTRODUCTION Intracranial aneurysm represents an abnormal dilatation on the arterial wall of the cerebral vessel. Usually develops in a vessel segments ,most often near a bifurcation point with an underlying structural abnormalities. Approximately 85% of aneurysm are located in the anterior circulation of the circle of Willis. It represents a significant health concern predominantly because of significant morbidity and mortality associated with rupture and subarachnoid hemorrhage

3. CIRCLE OF VILLIS

4. Circle of willis The circle of Willis begins to form when the right and left internal carotid artery (ICA) enters the cranial cavity and each one divides into two main branches: the anterior cerebral artery (ACA) and middle cerebral artery (MCA). The anterior cerebral arteries are then united and blood can cross flow by the anterior communicating (ACOM) artery. The ACAs supply most midline portions of the frontal lobes and superior medial parietal lobes. The MCAs supply most of the lateral surface of the hemisphere, except the superior portion of the parietal lobe (via ACA) and the inferior portion of the temporal lobe and occipital lobe. The ACAs, ACOM, and MCAs form the anterior half, better known as the anterior cerebral circulation. Posteriorly, the basilar artery (BA), formed by the left and right vertebral arteries, branches into a left and right posterior cerebral artery (PCA), forming the posterior circulation. The PCAs mostly supply blood to the occipital lobe and inferior portion of the temporal lobe.

5. LAYERS OF BLOOD VESSEL

6. Definition – intracranial aneurysm Intracranial or cerebral aneurysm is an abnormal focal dilation of an artery in the brain that results from a weakening of the inner muscular layer (the intima) of a blood vessel wall. The vessel develops a "blister-like" dilation that can become thin and rupture without warning. The resultant bleeding into the space around the brain is called a subarachnoid  (SAH). This kind of hemorrhage can lead to a stroke, coma and/or death.

7. INTRACRANIAL ANEURYSM

8. INCIDENCE Aneurysm are most prevalent between the ages of 35-60years The female to male ratio is 3:2 , but before 40 male and female s are equally affected About 10-30%of patients can have multiple aneurysms About 3-5% of new strokes are due to aneurysm rupture related to subarachnoid hemorrhage

9. RISK FACTORS Alcohol abuse Cigarette smoking Female sex Genetic condition Hormonal therapy-estrogen therapy Older age Positive family history Uncontrolled hypertension

10. GENETIC AND OTHEr MEDICAL CONDITIONS ASSOCIATED WITH Aortic aneurysm Bicuspid aortic valve defects Coartcation of aorta Ehrler's-Danlos syndrome Fibromuscular dysplasia Hereditary hemorrhagic telangiectasis Intracranial arteriovenous malformation Klinefelter syndrome

11. CONT…… Marfan’s syndrome Microcephalic osteo dysplastic primordial dwarfism Neuro fibromatosis Noonan syndrome Pheochromocytoma Polycystic kidney disease Pseudo xanthoma elasticum Tuberous sclerosis Alpha –antitrypsin deficiency Alpha – glucosidase deficiency

12. TYPES OF INTRACRANIAL ANEURYSMS Saccular aneurysm Fusiform aneurysm Dissecting aneurysm Mycotic aneurysm

13. SACCULAR ANEURYSMS…… 90% of intracranial aneurysm are saccular or “berry shaped” and develop as a thin walled sac protruding from the arteries of the circle of willis or its main branch It consists of an out pouching of deficient collagenized tunica muscularis that protrudes through a localized defect in the internal elastic lamina Tunica muscularis and the elastic lamina terminate at the aneurysm neck and the aneurysm wall is very thin ,consisting of only intima and adventitia. 85% of saccular aneurysm are found at the polygon of Willis.

14. Cont ….. Anterior communicating artery – 30-35% Internal carotid artery – 30% (posterior communicating artery, carotid bifurcation, ophthalmic artery) Middle cerebral artery – 22% Posterior circulation -8-10% According to size it is grouped into Small < 10mm Large 10-25mm Gaint >25mm According to the neck width Small neck < 4mm Large neck > 4mm

15. FUSIFORM ANEURYSM

16. FUISIFORM ANEURYSMS…… Fusiform aneurysms are exaggerated arterial ectasia caused by atherosclerosis It occurs mostly in older patients It involves longer vessel segments They can lead to mass effect or ischemia, whereas rupture is uncommon.

17. DISSECTING ANEURYSMS…. Dissecting aneurysm are rare and in patients who with SAH have a poor natural history due to high rebleeding rate It usually seen on small perforated vessel due to chronic hypertension

18. MYCOTIC ANEURYSM It is very rare and develop from infection in the arterial wall often deriving from bacterial endocarditis Only distal branches of the cerebral arteries are commonly involved and the aneurysm are fusiform and eccentric without the neck that characterize saccular aneurysm.

19. Signs and symptoms Unruptured aneurysm : Most cerebral aneurysms do not show symptoms until they either become very large or rupture.  Small unchanging aneurysms generally will not produce symptoms.  A larger aneurysm that is steadily growing may press on tissues and nerves causing: pain above and behind the eye numbness weakness paralysis on one side of the face a dilated pupil in the eye vision changes or double vision.

20. Cont … Ruptured aneurysm: When an aneurysm ruptures (bursts), one always experiences a sudden and extremely severe headache (e.g., the worst headache of one’s life) and may also develop: double vision nausea vomiting Nuchal rigidity Photosensitivity- sensitivity to light Seizures loss of consciousness (this may happen briefly or may be prolonged) cardiac arrest.

21. Specific signs and symptoms Anterior communicating artery: This is the most common site of aneurysmal SAH (34%). Usually, ACoA aneurysms are silent until they rupture. Suprachiasmatic pressure may cause visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction. Neurological deficits in aneurysmal rupture may reflect intraventricular haemorrhage (79%), intraparenchymal haemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%).

22. Anterior cerebral artery: Aneurysms of this vessel, excluding ACoA , account for about 5% of all cerebral aneurysms. Most are asymptomatic until they rupture, although frontal lobe syndromes, anosmia, or motor deficits may be noted. Middle cerebral artery: Aneurysms of the middle cerebral artery,account for about 20% of aneurysms, typically at first or second division in the sylvian fissure. Aphasia, hemiparesis, hemisensory loss, anosognosia, or visual field defects may be noted.

23. Internal carotid artery: Besides PCoA aneurysms, aneurysms of the ICA, account for about 4% of all cerebral aneurysms. Supraglenoid aneurysms may cause ophthalmoplegia due to compression of cranial nerve (CN) III or variable visual defects and optic atrophy due to compression of the optic nerve. Chiasmal compression may produce bilateral temporal hemianopsia. Hypopituitarism or anosmia may be seen with giant aneurysms. Cavernous-carotid aneurysms exert mass effects within the cavernous sinus, producing ophthalmoplegia and facial sensory loss. Rupture of these aneurysms typically produces a carotid-cavernous fistula, SAH, or epistaxis.

24. Posterior communicating artery: Aneurysms present at the junction of the termination of the ICA and PCoA account for 23% of cerebral aneurysms they are directed laterally, posteriorly, and inferiorly. Pupillary dilatation, ophthalmoplegia, ptosis, mydriasis, and hemiparesis may result. Basilar artery: Basilar tip aneurysms,are the most common in the posterior circulation, accounting for 5% of all aneurysms. Clinical findings usually are those associated with SAH, although bitemporal hemianopsia or an oculomotor palsy may occur. Dolichoectatic aneurysms may cause bulbar dysfunction, respiratory difficulties, or neurogenic pulmonary edema.

25. Leaking aneurysm Sometimes an aneurysm may leak a small amount of blood into the brain (called a sentinel bleed).  Sentinel or warning headaches may result from an aneurysm that suffers a tiny leak, days or weeks prior to a significant rupture.  However, only a minority of individuals have a sentinel headache prior to rupture.

26. Common site of intracranial aneurysm

27. Cont ….. Most are located on or near the circle of Willis More than 90% are located are one of the following five sites The internal carotid artery at the level of posterior communicating artery Junction of the anterior cerebral and anterior communicating arteries Proximal bifurcation of the middle cerebral artery Junction of the posterior cerebral and basilar arteries Bifurcation of the carotid artery into the anterior cerebral and middle cerebral arteries.

28. Pathophysiology of intracranial aneurysm

29. Diagnostic evaluation History collection Physical examination Altered level of consciousness. Sluggish pupillary reaction. Motor and sensory dysfunction. Cranial nerve deficits (extraocular eye movements, facial droop, presence of ptosis). Speech difficulties and visual disturbance. Headache and nuchal rigidity or other neurologic deficits.

30. Cont …. Most cerebral aneurysms go unnoticed until they rupture or are detected during medical imaging tests for another condition.  Several tests are available to diagnose brain aneurysms and determine the best treatment. These include:  Computed tomography Magnetic resonance imaging Cerebral angiography Cerebrospinal fluid analysis Intra arterial digital substration angiography (IADSA) Magnetic resonance angiogram (MR Angiogram)

31. Computed tomography Reliable and simple diagnostic test for ruptured aneurysm Positivity rate is 98-100% of cases for up to 12 hours after onset and 93% in the first 24 hours Positive results decreases with time Findings: Appears as a well defined round hyperattenuating lesions ,most apparent on maximum intensity projection images

32. Subarachnoid hemorrhage . Frontal intraparenchymal hematoma with rupture into the ventricular system. Left rounded density that suggests aneurysm formation with acute rupture.

33. Fisher’s grade - sah

34. Magnetic resonance imaging T1 – most of the patent aneurysms appear as flow void or they may show heterogeneous signal intensity In thrombosed aneurysms the appearance depends on the age of clot within the lumen T2 – typically hypodensed - laminated thrombus may show a hyper intensed rim

35. MRI brain axial T1 and T2 images showing acute phase haemorrhage in right temporoparietal region with mass effect and midline shift.

36. CEREBRAL ANGIOGRAPHY It is widely used modality for imaging and screening intracranial aneurysm In this 100ml of contrast medium is injected intravenously at a flow rate of 4ml/sec Changes in attenuation values are measured with a region of interest with the internal carotid arteries and spinal scan is automatically started

37. large vertebral junction aneurysm  extravasation from the aneurysms

38. Cerebrospinal fluid analysis Done in patient in whom CT reveals no abnormalities but hav strong clinical history of SAH Bloody CSF that fails to clear with continued egress of CSF suggests SAH Presence of xanthochromia ,a yellowish discoloration of the cerebrospinal fluid representing bilirubin from the breakdown of haemoglobin Blood from SAH that occurred more than 12 hours before the spinal tap will results in xanthochromic CSF where fresh blood occurs with trauma

39. Intra arterial digital substration angiography (IADSA) Most sensitive tool for the detection of intracranial aneurysm and should be performed with in 24 hours from bleeding Used to demonstrate the aneurysm ,its neck ,size, location, associated cortical branches, vasospasm, and additional aneurysm Performed with selective injection of ICA and vertebral arteries in order to investigate entire cerebral vasculature

40. Intra arterial digital substration angiography (IADSA)

41. MAGNETIC RESONANCE ANGIOGRAM It is another use full modality ,sensitivity for smaller aneurysm i.e. <3mm False negative and false positive aneurysm detected on MRA were mainly located in skull bone and middle cerebral artery It shows information about brain tissue and adjacent structure in relationship to the aneurysm

42. MAGNETIC RESONANCE ANGIOGRAPHY

43. Complication of aneurysm rupture Re-rupture, rebleeding Cerebral vasospasm Delayed ischemic complications and stroke Hydrocephalus Seizures Central nervous system infections Volume disturbances Osmolar disturbances Cerebral sodium depletion SIADH Pulmonary oedema Cardiac arrythmias Takotsubo cardiomyopathy

44. management Medical management Unruptured aneurysm: Studies shows that there is correlation between modifiable risk factors such as hypertension and smoking and aneurysm rupture Bed rest FFP Vitamin K Antiseizure drugs Analgesic agents Aspirin was successful in reducing aneurysm wall inflammation

45. Surgical management Patients with a ruptured intracranial aneurysm should be treated as soon as possible after the haemorrhage to prevent rebleeding and to provide adequate medical treatment of vasospasm Surgical clipping Detachable coils- endovascular coiling

46. Surgical clipping In 1937 Walter Dandy, an American neurosurgeon introduced method of “clipping” ,who applied V shaped silver clip to the neck of an internal carotid artery aneurysm. Since then variety of aneurysm clips have been evolved Aneurysm is clipped through a craniotomy ,a small metal clip made up of titanium is then applied to neck of the aneurysm Aneurysm clips comes in all different shapes and sizes and the choice is based on the size and location of the aneurysm Clip has a spring mechanism which allows the two jaws of the clip to close around either side of the aneurysm thus occluding the aneurysm

47. Surgical clipping

48. Endovascular coiling During 1980’s ,endovascular treatment of aneurysm with balloon was done which has high rate of rupture In 1991, Guido Guglielmi ,an American neuroradiologist invented platinum detachable micro-coil which was approved by FDA in 1995. Guglielmi detachable coil are soft wire spiral originally made out of platinum These coils are deployed into the aneurysms via a microcatheter inserted through the femoral artery and advanced into the brain Once the coil are released into the aneurysm the blood flow pattern within the aneurysm is altered and the slow and sluggish remaining blood flow leads to thrombosis

49. GUGLIELMI DETACHABLE COIL

50. Flow diversion Flow diversion bridge the aneurysm neck and divert the blood flow away from the aneurysm sac ,due to impedance created by the mesh of the implant Reduction of the blood flow into the aneurysmal sac causes stasis of blood flow into the aneurysm which leads to thrombosis and healing of the aneurysm

51. FLOW DIVERSION

52. Nursing management Nursing assessment: Altered level of consciousness. Sluggish pupillary reaction. Motor and sensory dysfunction. Cranial nerve deficits (extraocular eye movements, facial droop, presence of ptosis). Speech difficulties and visual disturbance. Headache and nuchal rigidity or other neurologic deficits.

53. Nursing diagnosis Ineffective tissue perfusion related to bleeding or vasospasm. Impaired Physical Mobility related to weakness ,paraesthesia Impaired verbal communication related to impaired cerebral circulation Dist urbed sensory perception related to altered sensory reception, transmission, integration Self care deficit related to neuromuscu lar impairment Risk for impaired swallowing related to neuromuscular impairment

54. Improving cerebral tissue perfusion Monitor closely for neurologic deterioration, and maintain a neurologic flow record. Check blood pressure, pulse, level of consciousness, pupillary responses, and motor function hourly; monitor respiratory status Implement aneurysm precautions (immediate and absolute bed rest in a quiet, nonstressful setting; restrict visitors) E levate the head of bed 15 to 30 degrees or as ordered. Avoid any activity that suddenly increases blood pressure or obstructs venous return ( eg , Valsalva maneuver, straining), Apply antiembolism stockings or sequential compression devices. Observe legs for signs and symptoms of deep vein thrombosis tenderness, redness, swelling, warmth, and edema.

55. Releiving sensory perception Keep sensory stimulation to a minimum. Explain restrictions to help reduce patient’s sense of isolation. Relieving  anxiety Inform patient of plan of care. Provide support and appropriate reassurance to patient and family.

56. Monitoring and managing complications Assess for and immediately report signs of possible vasospasm, and administer calcium channel blockers or fluid volume expanders as prescribed. Maintain  seizure  precautions and maintain airway and prevent injury if a  seizure  occurs. Administer  antiseizure medications as prescribed, phenytoin is medication of choice. Monitor for onset of symptoms of hydrocephalus Monitor for and report symptoms of aneurysm rebleeding. Rebleeding occurs most often in the first 2 weeks. Symptoms include sudden severe headache, nausea, vomiting, decreased level of consciousness, and neurologic deficit. Administer medications as ordered. Hyponatremia:   monitor sodium level.

57. Discharge and home care guidelines Teach patients and family members about disease condition Medical treatments Assistive devices Follow-up environment

58. Thank you