Presentation on Sub arachnoid HG and aneurysm surgery

1. Aneurysm surgery
Presenter:
Dr. Junayed Safar mahmud
IMO, Department of Neurosurgery
National Institute of Neurosciences and Hospital

2. Cerebral Aneurysm
• An aneurysm is an outward bulging, likened to a bubble or balloon,
caused by a localized, abnormal, weak spot on a blood vessel wall.
• An intracranial aneurysm, also known as a brain aneurysm, is a
cerebrovascular disorder in which weakness in the wall of a cerebral
artery or vein causes a localized dilation or ballooning of the blood
vessel.
• Prevalence:
• Estimated prevalence of incidental aneurysms range from 1-5% of the
population.
• Ratio of ruptured:unruptured (incidental) aneurysm is 5:3 to 5:6 (rough
estimate is 1:1, i.e. 50% of these aneurysms rupture)
• Unruptured intracranial aneurysms are more common in women (≈3:1 ratio)
and in the elderly, and only 2% of aneurysms present during childhood.

3. • Etiology of Aneurysms:
• congenital predisposition (e.g. defect in the muscular layer of the arterial wall,
referred to as a medial gap)
• “atherosclerotic” or hypertensive: presumed etiology of most saccular aneurysms,
probably interacts with congenital predisposition
• embolic: as in atrial myxoma
• infectious – so called “mycotic aneurysms”
• Traumatic aneurysms
• associated with other conditions
• In case of cerebral blood vessels,
• There is less elastic in the tunica media and adventitia of cerebral blood vessels,
• the media has less muscle, the adventitia is thinner,
• Lies in Sub. Arachnoid space with little support structure.

4. Types of Cerebral Aneurysms
According to size
• Small aneurysms have a diameter
of less than 15 mm.
• Larger aneurysms include those
classified as
• large (15 to 25 mm),
• giant (25 to 50 mm), and
• super-giant (over 50 mm)
According to shape
• Berry (saccular) aneurysms
• appear as a round outpouching and
are the most common form of
cerebral aneurysm.
• Fusiform aneurysms
• widening of a segment of an artery
around the entire blood vessel, rather
than just arising from a side of an
artery's wall.
• Microaneurysms
• also known as Charcot–Bouchard
aneurysms, typically occur in small
blood vessels (less than 300
micrometre diameter)

5. Location of cerebral aneurysms
Saccular aneurysms location:
• 85–95% in carotid system, with the following 3 most common
locations:
• a) ACoA (single most common): 30% (ACoA & ACA more common in males)
• b) p-comm: 25%
• c) middle cerebral artery (MCA): 20%
• 5–15% in posterior circulation (vertebro-basilar)
• a) ≈ 10% on basilar artery: basilar bifurcation, AKA basilar tip, is the most
common, followed by BA-SCA, BA-VA junction, AICA
• b) ≈ 5% on vertebral artery: VA-PICA junction is the most common
• 20–30% of aneurysm patients have multiple aneurysms
Fusiform aneurysms are more common in the vertebrobasilar system.

6. Presentation of cerebral aneurysms
Major rupture
• most commonly produces SAH, which may be accompanied by:
• Intracerebral hemorrhage: occurs in 20–40% (more common with
aneurysms distal to the Circle of Willis, e.g. MCA aneurysms)
• Intraventricular hemorrhage: occurs in 13–28%
• carry a worse prognosis (64% mortality).
• Distal PICA aneurysms: may rupture directly into 4th ventricle through the
foramen of Luschka
• a-comm aneurysm: rupture through the lamina terminalis into the anterior 3rd or
lateral ventricles
• Distal basilar artery or carotid terminus aneurysms: may rupture through the
floor of the 3rd ventricle (rare)
• Subdural blood occurs in 2–5%

7. Presentation other than major rupture
• mass effect
• giant aneurysms: including brain stem compression producing hemiparesis and cranial
neuropathies
• cranial neuropathy
• oculomotor (3rd nerve) palsy (ONP): occurs in ≈ 9% of p-comm aneurysms
• compressive optic neuropathy with ophthalmic artery aneurysms
• chiasmal syndromes due to ophthalmic, a-comm, or basilar apex aneurysms
• intra- or suprasellar aneurysm producing endocrine disturbance due to pituitary gland or
stalk compression
• minor hemorrhage: warning or sentinel hemorrhage
• small infarcts or transient ischemia due to distal embolization
• seizures: at surgery, an adjacent area of encephalomalacia may be found
• headache without hemorrhage
• Has been attributed to aneurysmal expansion, thrombosis, or intramural bleeding, all without
rupture
• incidentally discovered

8. Aneurysmal Rupture
Sub-Arachnoid
Haemorrhage

9. Outcome of aneurysmal SAH
• 10–15% of patients die before reaching medical care
• mortality is 10% within first few days
• 30-day mortality rate was 46% in one series, and in others over half the patients
died within 2 weeks of their SAH
• causes of mortality
• a) 25% die as a result of medical complications of SAH
● neurogenic pulmonary edema
● neurogenic stunned myocardium
• b) about 8% die from progressive deterioration from the initial hemorrhage
• among patients surviving the initial hemorrhage treated without surgery,
rebleeding is the major cause of morbidity and mortality, the risk is ≈ 15–20%
within 2 weeks.
• of those reaching neurosurgical care, vasospasm kills 7%, and severe deficit in 7%
• ≈ 66% of those who have successful aneurysm clipping never return to the same
quality of life as before the SAH

10. Clinical Features (Symptoms)
Headache:
• The most common symptom, present in up to 97% of cases
• Usually severe (classic description: “the worst headache of my life”)
and sudden in onset (paroxysmal).
• The H/A may resolve spontaneously (sentinel hemorrhage or warning
headache; they occur in 30–60% of patients presenting with SAH).

11. • Meningismus:
• Nuchal rigidity, Kernig sign, Brudzinski sign
• Hypertension
• Focal Neurological Deficit
• Aphasia, Hemiparesis, hemiplegia
• Oculomotor palsy, etc.
• Ocular haemorrhage
• subhyaloid (preretinal) hemorrhage: seen funduscopically in 11–33% of cases
• (intra)retinal hemorrhage: may surround the fovea
• hemorrhage within the vitreous humor (Terson syndrome). Occurs in 4–27% of
cases of aneurysmal SAH, usually bilateral.
Clinical Features (Signs)

12. Obtundation or coma :
May be due to the following conditions,
• Increased ICP
• damage to brain tissue from intraparenchymal hemorrhage (may also
contribute to increased ICP)
• Acute Hydrocephalus, due to intraventricular hg.
• Diffuse ischemia (may be secondary to increased ICP)
• Seizure
• Low blood flow (reduced CBF) due to reduced cardiac output
Clinical Features (Signs)

13. Work up of Suspected SAH (Diagnose SAH)
• non-contrast high-resolution Ct scan
• A good quality (e.g. n o motion artifact) non-contrast high -resolution CT will detect SAH in ≥
95% of cases if scanned within 48 hrs of SAH.
• CT also assesses
• Hydrocephalus : occurs acutely in 21% of aneurysmal ruptures
• Hematoma
• infarct: not sensitive in first 24 hours after infarct
• CT can predict aneurysm location based on the pattern of blood in ≈ 78% of cases
• Lumbar puncture
• The most sensitive test for SAH. False positives – traumatic taps
• opening pressure: elevated
• non-clotting bloody fluid that does not clear with sequential tubes. cell count: RBC count usually
>100,000 RBCs/mm3. Compare RBC count in first to last tube (should not drop significantly)
• xanthochromia: yellow coloration of CSF supernatant
• Caution: lowering the CSF pressure may possibly precipitate rebleeding by increasing the
transmural pressure . Therefore remove only a small amount of CSF (several ml) and use a
small (≤ 20 Ga) spinal needle.

14. • Magnetic resonance angiography (MRA)
• sensitivity is 87% an d specificity is 92% for detecting intracranial aneurysms (IAs)
(compared to catheter DSA)
• CT angiography (CTA)
• prospective study shows CTA detects 97% of aneurysms (compared to catheter DSA)
• safe and effective when used as the initial and sole imaging study for ruptured and
unruptured cerebral aneurysms.
• Catheter angiogram or Digital subtraction angiography (DSA)
• The gold standard for evaluation of cerebral aneurysms.
• Demonstrates source (usually aneurysm) in ≈ 80–85%; remainder are so-called “SAH
of unknown etiology”
• Shows if radiographic vasospasm is present
• assesses primary feeding arteries, collateral flow in case of a need for arterial
sacrifice.
Work up of Suspected SAH (Source of SAH)

15. Clinical Grading of SAH (Hunt & Hess)

16. Clinical Grading of SAH (WFNS)

17. Management of Aneurysmal SAH

18. Initial Management of SAH
• Admit to Monitored bed with hourly neuro check
• NPO in preparation for surgery or intervention
• Early aggressive fluid therapy to head off CSW
• NS+20 mEq KCl/L at ≈ 2 ml/kg/hr (typically 140–150 ml/hr)
• Prophylactic anticonvulsants : levetiracetam recommended
• Sedation with propofol
• Analgesics: Fentanyl, 25–100mcg (0.5–2 ml) IVP
• Dexamethasone: may help with H/A and neck pain.
• Anti-emetics: Ondansetrone 8 hours for 1–2 days
• Calcium channel blockers: nimodipine 60 mg PO/NG q 4 hrs initiated within 96
hrs of SAH. IV administration is equally as effective where available. Oral
nimodipine should be administered to all patients with aSAH.
• Antifibrinolytic therapy (?) : reduce risk of rebleeding, Increases incidence of VS.

19. • H2 blockers (e.g. ranitidine) or proton pump inhibitors
• stool softener in patients able to take PO
• statins: No clinical benefit
• Oxygenation :
• 2L/min per Nasal Cannulla
• in ventilated patient: strive for normocarbia and pO2 >100 mm Hg
• Temperature: maintain normothermia by Tylenol and cooling measures
• HTN: SBP 120–160 mm Hg is a guideline with unclipped aneurysm
• Investigations:
• ABG, Electrolyte, CBC, PT, APTT on admission and daily (electrolyte 12 hourly if
CSW)
• Serum glucose for strict control.
• Chest x ray daily
Initial Management of SAH

20. Treatment option for aneurysms
Surgical treatment option for Aneurysms
• Microvascular clipping: the surgical gold standard. Surgical placement of a clip
across the neck of the aneurysm to exclude the aneurysm from the circulation
• wrapping or coating the aneurysm:
• with muscle: the first method used to surgically treat an aneurysm
• with cotton or muslin: Rebleeding rate similar to natural history
• with plastic resin or other polymer: the risk was slightly lower than the natural history
• teflon and fibrin glue
• Trapping of aneurysm with or without bypass
• by direct surgical means (ligation or clip occlusion), or some combination. May also
incorporate vascular bypass (e.g. EC-IC bypass) to maintain flow distal to trapped segment.

22. Endovascular techniques to treat the aneurysm
• thrombosing the aneurysm
• “coiling” with Guglielmi electrolytically detachable coils
• Onyx HD 500 has been used for wide-necked or giant ICA aneurysms
• “flow diversion” with “covered stents” (tightly woven stents) which promotes
thrombosis of the aneurysm.
• trapping:
• effective treatment requires distal AND proximal arterial interruption
• proximal ligation
Treatment option for aneurysms

24. Factors to consider (Coiling vs clipping)
• health care environment / equipment available
• skill set and experience of the neurosurgeon and interventionalist
• greater annual numbers of aneurysms treated by individual practitioners were significantly
related to decrease in morbidity
• anatomy and location of the aneurysm
• favourable dome/neck ratio versus wide neck aneurysms
• MCA aneurysms may be difficult to coil because of a branch near the neck
• Basilar apex: favours coiling
• associated Haematoma: surgery allows both evacuation of haemorrhage and aneurysm
• symptoms due to mass effect: clipping
• younger age: lower risk of surgery, and lower lifetime risk of recurrence than
with coiling
• clinical state / comorbidities
• good outcome seen in 63% clip vs. 46% coil in poor grade (WFNS IV/V) pts
• patients on anticoagulation (e.g. Plavix) favor endovascular treatment

25. Aneurysm Treatment Decisions
Unruptured Aneurysm:
• Lifetime risk for a 20-year-old with an UIA to be 16%, which drops o
to 5% for a 60-year-old.
• A more recent study estimates the annual rupture rate to be ≈ 1%.

26. Timing of aneurysm surgery
Early surgery advocated for the following reasons:
• If successful, virtually eliminates the risk of rebleeding which occurs
most frequently in the period immediately following SAH
• Facilitates treatment of vasospasm which peaks in incidence between
days 6–8 post SAH (never seen before day 3) by induction of arterial
hypertension and volume expansion
• Allows lavage to remove potentially vasospasmogenic agents from
contact with vessels, including use of thrombolytic agents
• Although operative mortality is higher, overall patient mortality is
lower

27. Factors that favor choosing early surgery include:
• good medical condition of patient
• good neurologic condition of patient (Hunt and Hess (H&H) grade ≤ 3)
• large amounts of subarachnoid blood, increasing the likelihood and
severity of subsequent vasospasm.
• conditions that complicate management in face of unclipped aneurysm:
e.g. unstable blood pressure; frequent and/or intractable seizures
• large clot with mass effect
• Early rebleeding, especially multiple rebleeds
• Indications of imminent rebleeding

28. Per operative techniques and Neuroprotection
Brain Relaxation:

29. Cerebral Protection During Surgery
Cerebral protection by increasing the ischemic tolerance of the CNS
• Drugs that mitigate the toxic effects of ischemia without reducing
CMRO2
• Calcium channel blocker : Nimodipine
• Free radical scavangers : antioxidants
• Mannitol : transiently increasing CBV and decreasing blood viscosity
• reduction of CMRO2
• by reducing the electrical activity of neurons
• barbiturates: Thiopental Na
• Isoflurane
• By reducing maintainance energy of neurons
• Mild hypothermia (33 deg.)
• Deep hypothermia (18 deg.) – upto 1 hr of circulatory arrest can be tolerated.

30. Adjunctive cerebral protection techniques
• Systemic hypotension:
• usually used during final approach to aneurysm
• Because of the potential danger of hypoxic injury to brain and other organs, some
surgeons avoid this method.
• “focal” hypotension: using temporary aneurysm clips
• specially designed with low closing force to avoid intimal injury
• if a long segment of the ICA is being trapped, administer 5000 U IV heparin to
prevent thrombosis and subsequent emboli
• <5 mins temporary clip occlusion: no further intervention
• up to 10 or 15 mins occlusion: administer IV brain protection anesthesia (e.g.
thiopental, propofol, and/or etomidate)
• >20 mins occlusion: not tolerated (except possibly ICA proximal to p-comm),
bypass grafting around the segment to be occluded
Cerebral Protection During Surgery

31. Prevention of intraoperative rupture

32. Post OP order for aneurysm clipping
• Transfer to ICU (neuro unit if available) when stable
• Neuro check q 1 hr,
• O2: 2 L per NC / Ventilator orders
• activity: bed rest (BR) with HOB elevated 20–30°
• incentive spirometry q 2 hrs while awake (do not use following
transsphenoidal surgery)
• IVF: NS+ 20 mEq KCl/L @ 90 ml/hr

33. Post OP order for aneurysm clipping

34. Vesospasm protection
• Dopamin Drip, Norepinephrin, Dobutamin, phenylephrine