CEREBRAL ANEURYSMS for examination .pptx

High top notch examination notes on cerebral aneurysm

1. CEREBRAL ANEURYSMS Presented By, Athullya C Medical Surgical Nursing Govt. College of Nursing, Kottayam

2. DEFINITION A cerebral aneurysm is a saccular outpouching of a cerebral artery. Rupture of a cerebral aneurysm usually results in a SAH .

3. INCIDENCE Approximately 10-15 million Americans have an intracranial aneurysm, most of which are small, innocuous and do not bleed throughout life. Each year in the US, there are approx. 30,000 new cases of SAH secondary to rupture of an intracranial aneurysm. Cerebral aneurysm is most prevalent in the 35-60 yrs of age group, with 50 yrs being the mean age of occurrence. Aneurysmal SAH occurs more often in women than in men (3:2). Approx. 15-20% of people with aneurysm will have multiple aneurysms.

4. ETIOLOGY Precise etiology of aneurysm is unclear. Extrinsic factors Congenital factors Genetic factors Theories on etiology of cerebral aneurysm: A congenital / developmental defect exists in the medial & adventitial layers of the artery in the circle of Willis. This assumption has been found with scientific basis in postmortem persons without aneurysms. Results in the formation and rupture of intracerebral aneurysm

5. The degenerative theory : The intima covered only by the adventitia bulges from a local weakness. By late midlife, stress causes vessel ballooning and rupture. There is a predisposition to aneurysm formation in individuals with HTN and those with connective tissue diseases (causing fragility of the arterial wall). Head trauma can result in traumatic intracranial aneurysms due to a localized arterial tear. Bacterial & fungal infections have also been known to cause infectious (mycotic) aneurysms. Atherosclerotic aneurysms can form in vessel walls that have been damaged by deposits of atheromatous material, resulting in fusiform aneurysms.

6. CLASSIFICATION Classification based on size: Small  15mm Large  15-25mm Giant  25-50mm Super-giant  >50mm

7. PARTS OF ANEURYSM

8. Classification based on shape and etiology: Berry Aneurysm  Most common type  Berry shaped with a neck or stem

9. Saccular Aneurysm  Any aneurysm having a saccular outpouching. Fusiform Aneurysm  An outpouching of an arterial wall, but without a stem.

10. Traumatic Aneurysm  An aneurysm resulting from traumatic head injury (accounts a small number). Mycotic (Infectious) Aneurysm  Rare type caused by septic emboli from infections such as bacterial endocarditis. May lead to aneurysmal formation. Charcot-Bouchard Aneurysm  Microscopic aneurysmal formation associated with HTN involving the basal ganglia and brain stem.

11. Dissecting Aneurysm  Aneurysm related to atherosclerosis, inflammation or trauma.  An aneurysm in which intimal layer is pulled away from the medial layer and blood is forced between the layers.

12. A true aneurysm is defined as an abnormal, localized and permanent dilatation, of all three layers of an arterial wall. Dilatation is typically greater than 150% of its original size. A false aneurysm (or pseudoaneurysm) results from a tear or injury to the vessel wall, where blood leaks out and is contained by surrounding tissues rather than the vessel itself. True aneurysms are a form of vessel dilation, whereas false aneurysms involve a contained rupture. Difference between True Aneurysm and False / Pseudo-Aneurysm

13. LOCATION Cerebral Aneurysms usually occur at the bifurcations and branches of the large arteries at the base of the brain at the circle of Willis. 85% of aneurysms develop in the anterior part of the circle of Willis. The remaining 15% are found in the posterior circulation, known as the vertebrobasilar system.

14. Most common sites of aneurysms are the following: Internal carotid artery (ICA) at the bifurcation with the anterior communicating artery ( ACoA ) ICA and origin of the posterior communicating artery ( PoCA ) First major bifurcation of the middle cerebral artery (MCA) Bifurcation of the ICA into the MCA and anterior cerebral artery (ACA) Junction of the PCoA and the posterior cerebral artery (PCA) Bifurcation of the basilar artery Origins of three cerebellar arteries

15. PATHOPHYSIOLOGY At the time of aneurysmal rupture, blood under high pressure is forced into the subarachnoid space at the base of the brain (circle of Willis area), spreading by way of the Sylvian fissures into the basal cisterns. Less often, the aneurysm ruptures into one of the following areas of the brain , resulting in the formation of hematoma:  The brain parenchymal tissue – Intracerebral hematoma  The ventricles - Intraventricular hematoma  The subarachnoid space - Subarachnoid hematoma  The subdural space - Subdural hematoma

16. When rupture occurs, it usually occurs at the thin walled dome of the aneurysm causing blood to enter into the subarachnoid space. Tissue pressure surrounding the aneurysm stops the bleeding, and fibrin, platelets and fluid form a plug which seals off the site of bleeding. The resulting clot can occlude the area or interfere with CSF absorption. The released blood is an irritant to the brain tissue, setting up an inflammatory response that enhances cerebral edema. Concurrent with the time of rupture, significant SAH occurs, raising ICP toward the MAP and lowering cerebral perfusion pressure.

17. These hemodynamic changes probably account for the transient loss of or altered level of consciousness. Clinically, a stroke syndrome , with associated increased ICP develops. The specific signs and symptoms associated with the event depend on the location of the haemorrhage and the degree of increased ICP.

18. Stroke syndromes are specific patterns of neurological signs and symptoms that indicate a particular area of the brain or its blood supply has been damaged by a stroke. Examples include the  Middle Cerebral Artery (MCA) syndrome , which commonly causes weakness in the face and arm, difficulty with language, and neglect, and  Top-of-the-Basilar syndrome , which can lead to disorientation, unresponsiveness, and visual deficits.  These syndromes help medical professionals pinpoint the location and extent of the stroke, guiding diagnosis and treatment. 

19. SIGNS AND SYMPTOMS BEFORE RUPTURE OF BLEEDING Most patients are completely asymptomatic until the time of bleeding. In approx. 40% of cases, there are warning signs (PRODROMAL SIGNS) that are either ignored or attributed to other causes. Prodromal signs may suggest the location of an aneurysm or enlargement of the lesion. Prodromal signs are  Sudden severe headache (sentinel headache), stiff neck, vision changes (blurred or double vision), sensitivity to light, pain behind or above the eye, nausea & enlarged pupil.

20. Localized signs and symptoms includes: Oculomotor nerve palsy (CN III) Dilated pupil (Loss of light reflex) Possible ptosis EOM deficits with possible diplopia Pain above and behind the eyes Localized headache EOM deficits of the trochlear (IV) or abducens (VI) CN Small, intermittent, aneurysmal leakage of blood that may result in generalized headache, neck pain, upper back pain, nausea and vomiting.

21. AFTER RUPTURE OR BLEEDING At the time of rupture or bleeding blood is forced into the subarachnoid space. Violent headache  Subjective data of patient : Explosive or “Worst headache of my life”. Immediate loss of consciousness or decreased LOC Vomiting (common)

22. Other signs and symptoms includes: CN deficits (CN III, IV & VI) Signs of meningeal irritation  Nausea & vomiting  Stiff neck, pain in the neck & back  Blurred vision or photophobia (Signs of meningeal irritation appears 4-8 hrs after SAH & mild temperature elevation also accompany SAH) Signs of stroke syndrome  Hemiparesis, hemiplegia, aphasia & cognitive deficits Due to cerebral edema & increased ICP  Seizures, HTN, bradycardia & widening pulse pressure Due to pituitary dysfunction secondary to irritation or edema  Diabetes insipidus & Hyponatremia

23. INVESTIGATIONS History & neurological examination CT scan  Without contrast media within the first 48 hrs of aneurysmal rupture Cerebral angiography MRI or Magnetic resonance angiography Lumbar puncture CSF analysis TCD – Transcranial Doppler Hunt-Hess Classification system

24. HUNT AND HESS CLASSIFICATION OF CLINICAL GRADES OF CEREBRAL ANEURYSM GRADE DESCRIPTIVE CRITERIA I Alert, oriented and asymptomatic II Alert, oriented, headache & stiff neck III Lethargic or confused, minor focal deficits (hemiparesis) IV Stupor, moderate to severe focal deficits (hemiplegia) V Comatose & severe neurological deficits (posturing)

25. MEDICAL MANAGEMENT “Treatment of choice for a cerebral aneurysm is surgery”. INITIAL APPROACH TO MEDICAL MANAGEMENT Complete bed rest and institution of aneurysm precautions Application of elastic hose &/or sequential compression boots Maintenance of normal fluid volume BP control Drug therapy  Anticonvulsants, stool softeners, steroids, analgesics, sedatives & calcium channel blockers Monitoring of neurological signs for changes &/or development of complications

26. Complete bed rest & aneurysm precautions The purpose of aneurysm precautions is to prevent elevations in BP, which could lead to rebleeding. Typical Aneurysm precautions : Providing quiet environment that controls & minimizes stress Admit to a quiet, single room – Remove telephone - The door should be kept partially closed. Control natural and artificial light by means of turning blinds or pulling shades to prevent direct light into the room.

27. Reading, watching TV and listening to the radio are allowed, provided they do not upset or overstimulate the patient. Maintain the patient on bed rest with head of bed at 30 degree at all times. Visitors are limited to immediate family / significant others. Place an “Aneurysm Precautions” sign on the door. ANEURYSM PRECAUTIONS Visitors & non-unit staff should check with nurse before entering room Only close family members may visit the patient No more than 2 visitors may visit at a time Keep the door partially closed Avoid exciting or upsetting the patient Check with the nurse before offering food/drink to patient

28. Monitor and document neurological signs and vital signs as ordered. Provide diet as ordered – Alert patients can feed themselves unless contraindicated. Constipation and straining at stool should be prevented.  Establish a bowel program – stool softeners, gentle laxatives  Keeping bedside commode  Avoid enemas Apply high thigh elastic hose.  Apply air boots (sequential compression boots)  Observe the legs for signs& symptoms of DVT.  Report abnormal findings immediately.

29. Assist with hygienic care as necessary. Administer care gently (Gentle back care, ROM exercise)  Helps prevent overstimulation and increasing BP & risk of rebleeding. Discourage or control any activity that initiates Valsalva’s maneuverer (coughing, straining at stool, pushing up in bed with the elbows, turning with the mouth closed). Administer analgesics for headache as ordered. Maintain an accurate I/O record  To maintain normothermia & to avoid hypovolemia (it increases the risk of vasospasm).

30. Elastic hose & Sequential compression boots Due to immobility from bed rest, the risk for DVT & PE is increased. Thigh high elastic hose & sequential compression boots are applied to decrease the incidence of these problems. Once the aneurysm is secured by clipping, low-dose heparin may be safely instituted for 3-4 days postoperative. SCD

31. Fluid volume control Goal of medical management is to maintain fluid volume within a normal range (euvolia). Reasons for maintaining fluid volume is that dehydration increases haemoconcentration, which is thought to increase the incidence of cerebral vasospasm. If cerebral edema is present, a regimen of a moderate fluid restriction & steroids is usually ordered. Mannitol may be ordered to decrease the cerebral edema. If a mass effect is present from a subdural, intracerebral or other hematoma  Early surgical evacuation.

32. BP control In the early hors or days after rupture, BP is commonly elevated, reflecting a physiological response to a rise in ICP. As ICP is decreased, the BP also decreases. If the BP continues to be elevated owing to increased ICP from the mass effect of cerebral edema or a hematoma, mannitol may be administered. The drug is beneficial for 2 reasons:  It decreases cerebral edema & neurological deficits  It improves cerebral blood flow Decreased cerebral edema lowers the ICP and BP.

33. HTN is controlled to prevent rebleeding. The goal of therapy is to maintain the systolic blood pressure at about 150mmHg. SBP above this level are usually treated with drugs such as:  Labetalol  Nicardipine These drugs effectively lower the pressure without sudden drops in the systolic pressure and are easily titrated.

34. Drug therapy Calcium channel blockers – Nimodipine is routinely given for 21 days following SAH. “Nimodipine enhance collateral blood flow & improve long term outcome”. Anticonvulsants are given as a prophylaxis against seizures. Stool softeners prevent constipation & straining at stool. Use of steroids is controversial, but it is beneficial for treatment of cerebral edema & the inflammatory effects of meningeal irritation. Analgesics – Acetaminophen or codeine to control headache. Sedatives – Phenobarbital for agitated patients (at risk for elevated BP)

35. Monitoring for complications In the acute phase, patient will be managed in the ICU for the early detection of complications. The major complications of aneurysms are:  Aneurysmal rupture/Bleeding  Cerebral vasospasm  Hydrocephalus Other problems associated with aneurysmal rupture/bleed are reflected in lab studies & results of EKG.

36. Blood studies WBC count often elevated – 15,000 -18,000 as a result of meningeal irritation. Haematocrit, fibrin and platelet levels, bleeding time & osmolality – indicator of the development of cerebral vasospasm. Electrolytes : Hyponatremia develops due to SIADH or salt-wasting. Blood gas levels : Monitor adequacy of oxygenation .

37. EKG Changes related to hypothalamic dysfunction result in elevated serum catecholamine levels. Catecholamines stimulates anti-adrenergic receptors in the myocardium, possibly causing ST changes, prolonged QRS, prolonged Q-T interval & tall T waves. EKG changes may be consistent with subendocardial damage & sometimes myocardial ischemia.

38. SURGICAL MANAGEMENT Surgery is the treatment of choice for a ruptured or bleeding cerebral aneurysm. The goal of surgery is to prevent rebleeding by sealing off the aneurysm so that aneurysm is totally obliterated with a clip or other method such as muslin wrapping. Timing of surgery Past  Wait approximately 2 weeks before scheduling surgery. ( Rationale : The patient was a better surgical candidate once cerebral edema had subsided & is medically stabilized. Also, at this point, slackness of the brain allowed for easy dissection. )

39. Earlier surgery within 48-72hrs after haemorrhage for those who are in good neurological condition based on the Hunt and Hess classification system. Patients with clinical grades I & II, and some with clinical grade III are selected for early surgery. The remaining patients with grade III aneurysm & those with grades IV & V aneurysm are deferred for later surgery. Benefits of early surgery are: Results in superior management in patients with anterior circulation aneurysm & basilar tip aneurysm Allows for removal of basal cistern clots associated with vasospasm Permits institution of hypervolemic/hypertensive treatment for postoperative vasospasm without the risk for rebleeding.

40. Surgical approaches & considerations The surgical approach and method of aneurysmal obliteration depends on the location and characteristics of the aneurysm. A aneurysm with a stem or neck is usually managed with a surgical clip on the stem or neck. Depending on the location of the aneurysm, more than one clip may be necessary to obliterate it. The surgeons may choose from a wide selection of commercial clips of different sizes, shapes & angulation.

41. For aneurysm that are difficult to reach, the surgeon may have to modify a clip to accommodate the vessels and structures at the aneurysmal site. Before permanent clips are positioned, a temporary clip is applied to assess the effect of clipping on the blood supply to other areas. Temporary clips are softer and are gold-tipped. When the adequacy of vascular territory circulation is verified, the permanent clips are then applied. Intraoperative cerebral angiography, digital subtraction angiography or cerebral blood flow studies may be conducted to verify the adequacy of circulation & the security of clip or other methods of aneurysmal obliteration.

42. Some aneurysm such as Fusiform aneurysm are not amenable to clipping, because of their shape or location. So, here aneurysm is surgically wrapped in muslin , which provides support to the weakened arterial wall. Another approach is “Ligation of the aneurysm” , with subsequent aspiration. If multiple aneurysm are present, it may not be possible to obliterate all lesions at one surgery. Based on CT scan & angiography, 1 st priority to site that has bled. With an aneurysm involving ACA, special precautions must be taken to prevent injury to the small perforating vessels emitting from this area. If these sites are compromised, the patient will either not awaken or memory deficits & personality changes will be prominent.

43. In case of mycotic aneurysm, treatment of antibiotics helps in disappearance of the lesions. But, if aneurysm remains and enlarges, surgical excision is necessary. Asymptomatic aneurysm (less than 10mm in diameter) have low risk of rupture, whereas those with diameters of >10mm have higher risk of rupture. So, asymptomatic aneurysm with diameter 10mm or more should be treated surgically. Patients whose aneurysm have been obliterated at the time of rupture need to be monitored because these aneurysm may recur.

44. ENDOVASCULAR BALLOON THERAPY It is a relatively new treatment modality used for treatment of selected cerebral aneurysm and arteriovenous malformations. With interventional radiology this procedure is done. Here, catheter – “Super selective catheter” are passed into the vascular lesions by a percutaneous transfemoral approach. These catheters has the ability to enter vessels that are inaccessible with normal catheters. The traditional gold standard for treatment of cerebral aneurysm remains intracranial surgical clipping or clamping.

45. Newer treatment options offered are “Balloon occlusion of the aneurysm & balloon occlusion of the parent vessel“.

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