cerebral aneurysm anaesthesia

1. ANAESTHESIA FOR CEREBRAL
ANEURYSM
AND CEREBRAL PROTECTION
CONDUCTOR – DR KARUNA MA’AM
PRESENTER – DR HARINDRANATH

2. CONTENTS
• Definition of aneurysm
• Types
• Location
• Circle of Willis
• Aetiology
• Pathophysiology of SAH
• Symptoms associated with cerebral aneurysm & SAH.
• Grading of SAH
• Investigations & diagnosis
• Complications & management

3. DEFINITION
• An aneurysm is a localized or diffuse bulge or balloon like dilation of an
artery with a diameter of at least 50 % greater than the normal size of
the artery.
• It develops due to weakness in the vessel wall.
• TRUE ANEURYSM – abnormal dilation of an artery due to a weakened
vessel wall.
• FALSE ANEURYSM – external hematomas with persistent
communication to a leaking artery.

4. TYPES – BASED ON MORPHOLOGY
• SACCULAR ANEURYSM – rounded berry like outpouchings that arise
from arterial bifurcation points. Most commonly seen in circle of Willis.
• FUSIFORM ANEURYSM – elongated spindle shaped dilation of an
artery. Cylindrical & affects the entire circumference of the artery.
• DISSECTING ANEURYSM – due to separation of arterial wall layers
caused by blood entering the intima – media space after a tear in the
internal layer.These are pseudoaneurysms & are encapsulated, cavitated
para vascular hematomas that communicate with arterial lumen.

7. LOCATION
• Common location of cerebral aneurysm is on the arteries at
the base of brain, known as the Circle of Willis.
• Approximately , 85 % of cerebral aneurysms develop in the
anterior part of circle ofWillis.
•

9. • Blood supply to the brain by 4 major vessels which join together at the base
of brain forming CIRCLE OF WILLIS
1. Anterior cerebral artery.
2. Posterior cerebral artery.
3. Internal carotid artery.
4. Basilar artery.

10. WHY ANEURYSMS DEVELOP?
1. Congenital or familial inheritance.
2. Atherosclerosis.
3. Hypertension.
4. Connective tissue disorders.
5. Sickle cell anemia.
6. Infections.
7. Trauma.
8. Cigarette smoking , nicotine or alcohol abuse induced structural defect (i.e. a
decrease in the middle muscular layer -the tunica media of the arterial wall)
• Peak incidence – 40 to 60 years age , female >> males .

11. SYMPTOMS ASSOCIATED WITH CEREBRAL
ANEURYSMS AND SAH
• Headache
• Facial pain
• Neck pain or stiffness due to meningeal irritation.
• Aneurysmal rupture & SAH - sudden onset of severe headache,
meningism, transient or persistent loss of consciousness, epileptic
seizures, isolated cranial nerve palsy and focal neurological deficits.

12. PATHOPHYSIOLOGY OF SAH
• Rupture of aneurysm leads to free communication between intra-
arterial and subarachnoid spaces.
• Sudden increase in regional intracranial pressure (ICP) to a level equal
to that of systemic arterial pressure causes sudden onset of severe
headache and transient/permanent loss of consciousness.
• Spread of blood through the subarachnoid space causes headache,
meningism and subsequent development of hydrocephalus [as a
consequence of either impaired reabsorption of cerebrospinal fluid
(CSF) or formation of a blood clot in the ventricle].

13. • Blood clots and adhesions hinder the free spread of blood through the
subarachnoid space, supporting the formation of intracerebral haematomas.
• The blood (by oxyhaemoglobin and its breakdown products) in the subarachnoid
space contribute to cerebral vasospasm.
• SAH is usually accompanied by a decrease in CBF & cerebral metabolic rate (CMR)
& impaired cerebral autoregulation.
• Reactivity of the cerebral vasculature to changes in arterial carbon dioxide (CO2)
tension is usually preserved during SAH.
• CO2 reactivity becomes impaired only in patients with poor neurological condition.

14. • The three main predictors of mortality and dependence in
SAH are :
• 1. Impaired level of consciousness on admission.
• 2.Advanced age.
• 3. Large volume of blood on initial cranial computed
tomography (CT).

15. GRADING OF SAH
• World Federation of Neurological Surgeons (WFNS)
grading.
• Hees and Hunt grading.
• Fischer 4 point scale - best predictor of vasospasm.

16. GRADING OF SAH

17. INVESTIGATIONS

18. DIAGNOSIS
1. History.
2. CT scan shows 90 % c/o ruptured aneurysm. Unenhanced (no use of
contrast media) cranial CT is the initial diagnostic tool of choice in all
cases of suspected SAH
3. Lumbar puncture – Blood-containing CSF that does not clear during
continued flow and xanthochromic CSF are highly suspicious of SAH.
• The three methods of choice for detecting and delineating the
anatomy of intracranial aneurysms are
• (1) CT angiography after injection of contrast media
• (2) Magnetic resonance angiography
• (3) catheter angiography by direct intra-arterial catheterization (gold
standard)

19. COMPLICATIONS
• Major neurological complications post ruptured cerebral
aneurysms & aneurysmal SAH
1. Rebleeding
2. Cerebral vasospasm leading to ischemia
3. Hydrocephalus
4. Seizures
5. Cardiac dysfunction, systemic/pulmonary hypertension, neurologic
pulmonary edema, morphological ECG changes ST depression, high p
waves, QTc prolongation, arrhythmias likeVF/PSVT, peak cardiac
troponins.
• occur due to high sympathetic tone & release of catecholamine from
sympathetic nerve terminal seen in SAH
• 6. Hyponatremia(as a result of SIADH), hypocalcemia, hypomagnesemia

20. MANAGEMENT
• 1. NEUROPROTECTIVE STRATEGIES
• Adequate sedation
• Control of oxygenation & ventilation
• Avoidance of hypotension
• Maintenance of normoglycemia
• Prevention of hyperthermia
• 2. OCCLUSIONTHERAPY
• Surgical : craniotomy & clipping of aneurysm – early clipping within 72 hours
prevents rebleeding. Evacuation of SAH decreases incidence of vasospasm.
• Radiological endovascular coiling technique.

22. CEREBRAL ISCHEMIA &VASOSPASM
• Develop 3-4 days post SAH, lasting approximately 2 weeks.
• Large amount of blood on CT is a predictor for the development
of vasospasm.
Theories
1. Development of structural changes in blood vessels.
2. Immune mediated vasoconstriction.
3. Vasoconstrictive activity by the breakdown products of extravasted
blood products.
4. SAH induced changes in the biochemical medicated contraction &
relaxation of cerebral arterial smooth muscles.
• Causes neurological defecit.
• Diagnosed clinically & radiologically by angiography, transcranial

23. PROPHYLAXIS & THERAPY OF CEREBRALVASOSPASM
1. General measures
• Nimodipine- Calcium channel blocker, selective smooth muscle action, 60 mg
orally/ via nasogastric tube fourth hourly. Risk of thrombophlebitis so preferred
via central line administration if given IV.
• Mild sedation.
• Positive fluid balance.
• Avoidance of hypotensive episodes.
• Avoid hyponatremia.
• 2. Symptomatic treatment
• Triple H therapy
• Balloon angioplasty
• Intra-arterial papaverine

24. TRIPLE H THERAPY
• hypertension, hypervolemia and hemodilution.
• usually started in patients with an increase in transcranial Doppler
velocities (as a reflection of cerebral vasospasm), the development of
neurological deficits or both.
• Aim – is to increase CBF & increase CPP.
• For this purpose, systolic arterial pressure is increased (by administration
of IV fluid or cardiovasoactive drugs) to approximately 120–150 mm Hg
in unclipped and 160–200 mm Hg in clipped aneurysms.

25. • central venous pressure is maintained at 8–12 mm Hg (or pulmonary
artery wedge pressure at 15–18 mm Hg).
• contraindicated in patients with unclipped aneurysm.
• potentially life-threatening complications of triple-H therapy include
pulmonary oedema, myocardial ischaemia, respiratory insufficiency,
hyponatraemia.

26. PRE-OPERATIVE ANAESTHETIC MANAGEMENT
1. Pre-operative evaluation
• Electrolyte & cardiac abnormalities common during & after SAH.
• Serum concentrations of cardiac enzymes, biomarkers and 2- D
echocardiography should be performed.
• 2. Premedication
• Choice of the type ( e.g. benzodiazepine, barbiturate, and opioid) and
the dose of premedication drug will depend on clinical grade, ICP
level, respiratory status, co-morbidity, and chronic medication.
•

27. • Antianxiety drugs – to relieve anxiety which can increase the risk of
hypertension & aneurysmal rupture.
• Avoid respiratory depression as it will cause an increase in PaCO2 followed
by an increase in ICP.
• To maintain an adequate CPP – Nimodipine (for prophylaxis or treatment of
cerebral vasospasm) and any infusion of a vasoactive drug should be
administered.

28. • 3. Monitoring
• Standard monitoring – 5 lead ECG, pulse oximetry,
continuous intra- arterial pressure, Capnography, urine
output, body temperature.
• cardiovascular monitoring - pulmonary artery catheterization,
transoesophageal echocardiography, precordial Doppler.

29. • Neurophysiological monitoring for detection of cerebral function –
Cortical somatosensory-evoked potential (SSEP) used during aneurysm
surgery in the territory of both anterior and posterior cerebral
circulation and brainstem auditory-evoked potential (BAEP) used during
operations in the territory of the vertebral-basilar circulation.
• Detection of cerebral ischaemia by evoked potential monitoring helps in
adjustments in surgical technique (removal or replacement of a vascular
clip) & haemodynamic management (increasing blood pressure to
augment collateral perfusion during temporary or permanent vessel
occlusion).

30. • TIVA is the method of choice of anesthesia during
neurophysiological monitoring because IV anesthetics interfere
less with recordings of evoked potentials than volatile
anesthetics.
• Central venous catheter insertion - for guidance of
intravascular volume, for the injection of potent cardiovascular
drugs in c/o severe cardiovascular instability & for the
administration of mannitol (which may cause local inflammation
when administered through a smaller peripheral vein).

31. • Jugular venous bulb monitoring to detect cerebral venous oxygen
saturation & helps in early detection of cerebral ischaemia.
• 4. Brain relaxation
• Optimal brain relaxation and reduction in brain bulk help surgical
exposure, reduce the forces required for brain retraction & facilitate
clipping of the aneurysm.
• usually achieved by providing an adequate CPP, avoiding episodes of
hypotension and hypertension, administering the appropriate
anesthetic drugs at appropriate doses and concentrations, and
maintaining normo ventilation & adequate oxygenation.

32. • Pharmacological treatment – mannitol, frusemide.
• Other interventions - Adequate ventilation & oxygenation, CPP and acid–
base status, unobstructed cerebral venous return (check the patient’s head
position) & drainage of CSF (check patency of lumbar drain) should be
ensured.
• Volatile anesthetics and N2O should be discontinued and replaced by IV
anesthetic drugs like thiopentone (approximately 2–3 mg/kg iv bolus or
continuous infusion of thiopentone (approximately 4–5 mg /kg/hour)for its
cerebro- vasoconstrictive property.

33. CONDUCT OF ANESTHESIA
1. General principles
• The principal goals of the anesthetic management for
• aneurysm surgery include
1. control of the TMPG of the aneurysm.
2. preservation of adequate CPP and oxygen delivery.
3. avoidance of large and sudden swings in ICP.
4. providing conditions that allow optimal surgical exposure with least brain
retraction.
5. allowing rapid awakening of the patient.
• Laryngoscopy, tracheal intubation, positioning of the patient, placement of the pin
head-holder, raising of the bone flap are highly stimulating interventions assoc. with
increased risk of aneurysmal rupture.

34. • Sufficient doses of hypnotics (thiopentone or propofol), opioids, non-
depolarizing neuromuscular blocking agents (vecuronium, atracurium, cis
atracurium) & infiltration of the scalp with local anaesthetic at the sites
of pin placement.
• Maintain a lesser depth of baseline anesthesia and by prophylactic
administration of bolus doses of anesthetic (propofol or thiopentone
before placement of the pin head-holder) or cardiovascular depressant
drugs (esmolol or labetalol before laryngoscopy & tracheal intubation)
to abolish or blunt the hypertensive response to intense stimuli.

35. • 2. Choice of anesthetic drug
• Aim - avoid hypertensive episodes and ensure adequate CPP, maintain
physiological ICP and optimal brain relaxation.
• When MAP decreases in the presence of preserved cerebral
autoregulation, cerebral vessels dilate resulting in an increase in cerebral
blood volume and an increase in ICP.
• In patients of increased ICP, it is advisable to avoid all anesthetic drugs with
cerebro-vasodilatory potential (basically all volatile anesthetics and N2O)
and use drugs with cerebro-vasoconstrictive and cerebro-depressant
characteristics (basically all IV anesthetics with the exception of ketamine).

37. • 3. Management of CPP &TMPG of aneurysm
• CPP is calculated as the difference between mean arterial pressure
MAP and ICP [ CPP = MAP – ICP ].
•
• The TMPG (transmural pressure gradient) of the aneurysm is calculated
as the difference between the pressure within the aneurysm (equal to
MAP) and the pressure outside the aneurysm (equal to ICP) i. e. [TMPG
= MAP – ICP ].
• To maintain TMPG as low as possible to reduce the risk of aneurysm
rupture & CPP as high as needed to provide adequate cerebral
oxygenation.

38. • 4. Induction of anesthesia
• The main goals during induction of anesthesia are
(1) prevention of rupture of the aneurysm.
• (2) preservation of cerebral oxygenation.
• (3) prevention of an increase in ICP.
• Administer drugs that abolish or blunt the hypertensive response to
laryngoscopy and tracheal intubation (e.g. esmolol, labetalol and i.v.
lignocaine) and then proceed with tracheal intubation.

39. • Another approach is to provide a deep level of anesthesia (by high doses
of anesthetic drugs or by monitoring of depth of anesthesia) while
counteracting the anticipated decrease in blood pressure (and thus in
CPP) by a continuous infusion of a vasopressor (e.g. phenylephrine or
norepinephrine) from the beginning of induction of anesthesia.
• The deep level of anesthesia will prevent the hypertensive response to
laryngoscopy and tracheal intubation (reducing the risk aneurysm
rupture).
• The continuous infusion of a vasopressor will ensure adequate CPP
(reducing the risk of cerebral ischemia).

40. • 5. Respiratory management
• Normo ventilation is the goal.
• Transient & moderate hyperventilation should only be considered in
patients with increased ICP, as prolonged hyperventilation may cause
cerebral ischemia.
• PEEP should be used very restrictively ( increases ICP).

41. • 6. Induced hypotension
• A reduction in systemic arterial pressure decreases theTMPG of the
aneurysm and thereby the wall stress of the aneurysm.This may facilitate
preparation and clipping of the aneurysm, and help control bleeding.
• No longer recommended as it will critically impair cerebral perfusion,
especially in the presence of hypovolemia, and has been associated with
adverse outcome and a higher incidence of severe cerebral vasospasm.

42. • 7. Induced hypothermia – less than (22 degree Celsius)
cerebroprotective.
• 8. Prophylaxis of cerebral vasospasm
• Fluid management - Careful volume loading and maintenance of a slightly
higher than baseline MAP helps to reduce the incidence of postoperative
cerebral vasospasm.
• Intracisternal installation of papaverine after clipping of the aneurysm and
before closure of the dura is another attempt at preventing cerebral
vasospasm.Associated side effects include mydriasis, facial nerve palsy, signs
and symptoms resembling malignant hyperthermia, bradycardia and
hypotension.

43. • 9. Management of intraoperative aneurysm rupture.
• Can occur with an abrupt increase in the TMPG of the aneurysm (as a
consequence of either a sudden increase in blood pressure or an abrupt
decrease in ICP) or with surgical manipulation.
• The primary haemodynamic goal during rupture of an aneurysm is
maintenance of normovolemia.
• Temporary occlusion of cerebral arteries proximal and distal to the
aneurysm is an effective means of gaining control over ruptured aneurysms.

44. • Transient decrease in MAP to 40–50 mm Hg decreases wall shear stress,
reduces bleeding.
• At the same time, care should be taken to avoid cerebral ischemia.
• 10. Recovery
• Should be rapid & smooth.
• Hypertension ( risk of intracranial haemorrhage and oedema) should be
prevented by the prophylactic administration of the appropriate type and
dose of analgesic, anti-emetic, anti-shivering or anti-hypertensive drugs.

45. • Patients with preoperative Hunt and Hess grades III or IV or intraoperative
complications should not be extubated immediately after operation.
• Critically ill patients require intensive postoperative cardiopulmonary and
general supportive care.
• Early tracheostomy in comatose patients with poor prognosis

46. REFERENCES
• Butterworth, john.et al. Morgan and Mikhail. 6th ed.
• H.-J. Priebe et al.Aneurysmal subarachnoid haemorrhage and the anaesthetist. British
Journal of Anaesthesia 99 (1): 102–118 May 23, 2007.
• Astri Luoma, Ugan Reddy et al. Acute management of aneurysmal subarachnoid
haemorrhage. Continuing Education in Anaesthesia, Critical Care & Pain |Volume 13
Number 2 2013. Published by Oxford University Press on behalf of the British Journal of
Anaesthesia.
• Vishnu Gupta,Ashwani Kumar Choudhary et al. Journal of Anaesthesiology Clinical
Pharmacology | July-September 2014 |Vol 30 | Issue 3.

47. THANKYOU