More than 90% of cerebral aneurysm occur at thefollowing locations-1-The origin of the posterior communicating artery2- The region of the anterior communicating artery3- Middle cerebral artery bifurcation4- apex of basilar artery5- internal carotid artery bifurcation.
Acquired vascular lesions secondary todegenerative changes in the muscular and elasticcomponents of the vessel wall. Usually occuring at the branching points of themajor cerebral vessels. A deficiency of type III collagen in arteries isassosiated with SAH.
Congenital influences may play a role. Disease processes associated with an increasedrisk of IA Polycystic kidney Hypertension Coarctation of the aorta Ehler- Danlos syndrome Fibromuscular disease smoking
Small – less than 12 mm 78% Large – 12-24 mm 20% Giant - 24mm 2% Majority of aneurysms that bleed are less than 1cm of diameter. Aneurysms that are less than .5 cm diameterhave less risk of bleeding.
Hypertension Pregnancy Smoking Heavy drinking Strenuous activity
Causes increase ICP Increased ICP causes decrease CBF Bleeding stops with decreased CBF Decreased consciousness 2 clinical scenarios are seen typically Return to normal ICP and CBF with return of function High ICP continues with low CBF
Grade 0 - Aneurysm is not ruptured Grade 1 - Asymptomatic, min. headache and sl. nuchalrigidity Grade 2 - Moderate to severe headache, nuchal rigidity, butno neurologic deficit other than cranial nerve palsy Grade 3 - Drowsiness, confusion, mild focal deficits Grade 4 - Stupor, mild or severe hemiparesis, possible earlydecerebrate rigidity, vegetative disturbances Grade 5 - Deep coma, decerebrate rigidity, moribundappearance
WFNS Grade GCS Score Motor DeficitI 15 AbsentII 13-14 AbsentIII 13-14 PresentIV 7-12 P or AV 3-6 P or A
It is very important to assess the degree of SAH.There are different grading scales for thispurpose. Modified Hunt and Hess grading scale is mostcommonly used because of ease of application. Extent of vasospasm is related to the amount ofsubarachnoid blood present. CT scan is graded according to the Fisher grade
Grade 1 – No blood detected Grade 2- Diffuse thin layer of subarachnoidblood ( vertical layers less than 1 mm thick) Grade 3 – Localised clot or thick layer ofsuarachnoid blood( vertical layer = 1 mm thick) Grade 4 – Intracerebral or intraventricular bloodwith diffuse or no subarachnoid blood
The clinical management of cerebral aneurysmscenters on the reduction of risk of hemorrhage inuruptured cases and of repeat hemarrhage inSAH. The major complications of SAH are –1- Aneurysmal rebleeding2- delayed cerebral ischemia secondary tovasospasm
Incidence of rebleeding is 14-30 % . Peak incidence at the end of the first week ofSAH. High risk of rebleed during angiography Assosiated with high rate of mortality andmorbidity.
Blood pressure control is of critical importancein reduction of risk of rebleeding. Antifibrinolytic agents have been usedsuccessfully to control rebleeding
Vasospasm is the leading cause of morbidity andmortality in patients who initially survive SAH Radiological evidence of vasospasm is noted in upto70% of patients . Clinical vasospasm occur in almost 30% of patients Clinical vasospasm occur after 4-9 days of SAH It typically does not occur after 2 weeks ofaneurysmal rupture.
Pathological changes occur are contraction ofvascular smooth muscles and thickening of thevessel wall Prostaglandins , biological amines , peptides , cyclicneucleotides , calcium , lipid peroxidation and freeredicals are implicated . Conventional cerebral angiography , xenon-enhanced CT and transcranial doppler is used toconfirm the presence of vasospasm
There is a correlation between the amount ofsubarachnoid blood after aneurysmal rupture andthe occurrence and severity of vasospasm Because of this , extensive removal of subarachnoidblood by early surgery is attempted to decrease theincidence of vasospasm. Nimodipine , a calcium channel blocker issuccessfully used .
Triple H therapy – hypertension , hypervolumiaand hemodilution is used in treatment ofvasospasm. A new method for symptomatic vasospasmincludes use of cerebral angioplasty to dilateconstricted major cerebral vessels.
Assesment of patients neuroloical condition andclinical grading of SAH A review of patient,s intracranial pathologicalconditions including CT scan and angiograms. Monitoring of ICP and transcranial dopplerultrasonography.
Evaluation of patients other systemic functions ,premorbid as well as present Systems known to affected by SAH Communication with the neurosurgeon regardingpositioning and special monitoring Optimisation of patient,s condition by correctingany biochemical and physiological condition
To assess the CNS , as we have discussed beforethere are grading scales-1. Modified Hunt and Hess grading2. WFNS grade scale3. Fisher grading of CT scan
The greater the clinical grade , more likelyvasospasm , elevated ICP , impaired autoregulationand disordered response to hypocapnia will occur Worse clinical grade is also assosited with cardiacarrythmia , myocardial dysfunction , hypovolumiaand hyponatremia.
ECG abnormalities Very common Many changes seen cannon t wave, Q-T prolongation, ST changes Autonomic surge may in fact cause somesubendocardial injury from increase myocardial walltension
Cardiac dysfunction does not appear to affectmorbidity or mortality (studies from Zaroff andBrowers) Prolonged Q-T with increased incidence ofventricular arrhythmias PVC’s are seen in 80% ECG changes occur during the first 48 hrs of SAH andcorrelate with amount of intracranial bleed.
ECG changes reflect the severity of neurogenicdamage and have not shown to contributeperioperative mortality and morbidity The decision to operate should not be influencedby these ECG changes.
Hydrocephalous Seizures 13% Vasospasm may be cause Increased risk of rebleed Treat and prophylaxis Headache, visual field changes, motordeficits
SIADH Cerebral salt wasting syndrome release of naturetic peptide hypovolemia, increased urine NA and volumecontraction Distinguish between the two and treataccordingly
Neurogenic pulmonary edema 1-2% with SAH Hyperactivity of the sympathetic nervous system Pneumonia in 7-12% of hospitalized patients withSAH
0-3 days post bleed appears to be optimal Improved outcome within 6 hours of rupturedespite high H/H grade If delayed, should be done after 10 days postbleed after fibrinolytic phase The results are worst with surgery performedbetween 7 to 10 days.
Avoid abrupt changes in BP Maintain CBF with normal to high blood pressure Avoid increase of ICP Assess immobility & vital signs control Achieve brain relaxation Allow for swift emergence & neurologic assessment Be prepared for disaster
Arterial blood pressure- beat to beat monitoringof MAP ECG- myocardial ischemia/ arrhythmia Pulse oximetry- systemic hypoxia EtCO2- trend monitor for Paco2/ detection of VAE Temperature- via oesophageal lead; to allowmodest, passive hypothermia(~35o C) Urine output- adequacy of renal function &hydration
Evoked potentials- intactness of specific CNSpathways Transcranial oximetry- noninvasive informationon regional cerebral oxygenation TCD ultrasonorgaphy
TCD is a indirect measure CBF It is unreliable as a measure of CBF in patients ofSAH because of changes in vessel diameter But it has become valuable for diagnosingvasospasm noninvasively before the onset ofclinical symptoms TCD has been successfully used in theperioperative management of patients withcerebral aneurysm.
Continuous TCD monitoring may improve the safetyof induced hypotension by correlating the bloodvelocity change to the decline in the bloodpressure. It has been used perioperatively to confirm thediagnosis of aneurysmal rupture.
Patients should receive their regular dose ofnimodipine and dexamethasone Tab Loarazepam 1-2 mg and tab rantac 150should be given in night before surgery To relieve anxiety inj midazolam in incrementaldose of 1 mg is given in the morning of surgery.
There is risk of rupture of aneurysm at the timeof induction due to high blood pressure duringtracheal intubation As a general principle , the patients bloodpressure should be reduced by 20-25% below thebaseline value and hypertensive response to thetracheal intubation should be alleviated.
Another useful approach is to balance the risk ofischemia from a decrease in CPP against thebenefit of a reduced chance of aneurysmalrupture from a decrease TMP. Conceptually induction phase is consisting of 2partsInduction to achieve loss of consciousness Thiopental ( 3- 5 mg/kg ) or propofol (1-2.5mg/kg ) in combination with fentanyl (3-7 ug/kg)or sufentanil(.3-.7 ug/kg) is suitable
Other alternatives include etomidate (.3-.4 mg/kg)and midazolam ( .1-.2mg/kg)Prophylaxis against rise in BP during laryngoscopy Many agents have been used successfully toalleviate hypertensive response of intubation.Fentanyl ( 5-10 ug/kg)Sufentanil ( .5-1 ug/kg)Esmolol (.5 mg/kg)Labetolol (10-20 mg)Intraveous or topical lidocaine (1.5-2 mg/kg)Second dose of thiopental ( 1-2 mg/kg)
Intravenous adjuncts are preferred in patientswith poor SAH grades whereas deep inhalationalanesthetics are preferred in patients with goodSAH grades.
Choice of muscle relaxant Vecuronium is most hemodyanamically stableand suitable muscle relaxant. Succinylcholine causes incease in ICP. Atracurium may cause hypotension. Pancuronium causes tachycardia andhypertension
The location and size of aneurysm generallydetermine the position of patient. Anterior circulation aneurysm are usuallyapproached using fronto-temporal incision with thepatient in supine position Basilar tip aneurysms are approached usingsubtemporal incision with the patient in lareralposition
Vertebral and basilar trunk aneurysms approached usingsuboccipital incision with the patient in sitting or parkbench position Avoid extreme positioning (extreme rotation or flexionof neck to avoid IJV compression) Padding/ fixing of regions susceptible to injury bypressure/ abrasion/ movement -groin, breasts, axillaryregion-falling extremities-knees kept in mild flexion to preventbackache postoperatively Mild head-up position (to aid venous cerebral drainage)
Elevation of contralateral shoulder by wedge/ roll(to prevent brachial plexus stretch injury if head isturned laterally) Meticulous attention to specific problems in prone/lateral/ parkbench/ sitting positions Care of ETT –easy intraoperative accessibility-fixed & packed securely toprevent accidental extubation, or abrasionsresulting from movement
Care of eyes- taped occlusively to prevent cornealdamage (from exposure/ irrigation with antisepticsolutions)APPLICATION OF SKULL PIN HOLDER FRAME Pain- provides maximal nociceptive stimulus- must be blocked adequately byi. deepening of anaesthesia (i.v. bolus ofthiopentone 1mg/kg or propofol 0.5 mg/kg)ii. analgesia (i.v. bolus of fentanyl 1-3mcg/kg or alfentanil 10-20 mcg/kg or remifentanil 0.25-1mcg/kg)
iii. local anaesthetic infiltration at pin siteiv. antihypertensive β-blockers e.g.Esmolol 1 mg/kg or Labetalol 0.5-1 mg/kg VAE- may occur with pin insertion
Positioning of Anaesthetist-optimal patient monitoring-access to airway/ intravenous & intraarteriallines
The goals during maintainance of anesthesia are -- To provide a relaxed or ‘slack’ brain that will allowminimum retraction pressure To maintain perfusion to the brain To reduce TMP if necessary during dissection of theaneurysm and final clipping Allow prompt awakening and assessment ofpatients with good SAH grades
MaintenanceCHOICE OF TECHNIQUEVolatile agents Intravenous agentsAdvantages Controlability/ predictability/ earlyawakeningGood control of CBF, ICP, & brainbulk-cerebrovasoconstriction↓ in ICPDisadvantages Poor control of CBF, ICP, & brainbulk-cerebrovasodilation↑ in ICPProlonged/ unpredictableawakeningMay interfere with D/D of delayedawakeningMay require emergent CT scanto rule out surgical complicationsType ofsurgerySimple, low risk of ↑ed ICP Complex, high risk of ↑ed ICP
MaintenanceCHOICE OF TECHNIQUEVolatile agents Intravenous agentsEarly institution ofmoderatehyperventilationMandatory OptionalConcurrent use withN2OIdeal agentUsually avoided-synergistic effects in ↑ing CBF &CMR-if used, ensure ↓in ICP byi. hyperventilationIi. osmotic diureticsIii. BP controlIv. adequate positioning/ cerebralvenous drainagev. lumbar drainageVi. Use of < 1 MAC (e.g. < 1.15% ofisoflurane)NoCan be used withoutsignificant problemsYes
Fluid Therapy Fluid therapy should be guided by intraoperative bloodloss, urine output and CVP/PAWP The aim is to maintain normovolumia beforeaneurysmal clipping and slight hypervolumia andhypertension after clipping. Avoidance of hyperglycemia (worsens consequences ofcerebral ischemia)
Avoidance of hypoosmolality – can cause brainoedemai. Target osmolality: 290-320 mOsm/kg)ii. Colloid oncotic pressure plays no significant rolein brain oedemaiii. Avoidance of glucose-containing & hypoosmolarsolutions (e.g. Ringer’s lactate, 254 mOsm/kg) Preferred solutions – crystalloids: 0.9% NaClcolloids: 6% HES (304 mOsm/kg)
Hematocrit- Target for >28% Warming of I.V. solutions– may be avoided topermit establishment of mild hypothermia (~350 C)for neuroprotection-must be essentially warmed at the end ofprocedure to ensure normothermia for emergencefrom anaesthesia
Hemodynamic control-Undesirable CNS arousal & hemodynamic activation mayoccur despite adequate depth of anaesthesia &analgesia-Consider use of i. Esmolol (1mg/kg: initial dose)ii. Labetalol (0.5-1mg/kg: initialdose)iii. Clonidine (0.5-1mcg/kg: initialdose) Moderate hypothermia (~350C)-may confer a degree of brain protection if ischemicevent occurs
Prevention1. No over hydration2. Sedation/ analgesia/ anxiolysis3. Avoidance of application of any noxious stimulus withsedation/ local anaesthesia4. Head-up position5. Osmotic agents (mannitol/ hypertonic saline)6. β-blockers/ clonidine/ lignocaine
7. Adequate hemodynamics: MAP, CVP, PCWP, HR8. Adequate ventilation: PaO2>100mmHg;PaCO2~35mmHg9. Minimal possible intrathoracic pressure10. Hyperventilation on demand (before induction)11. Use of total I.V. anaesthestic agents for induction& maintenance12. Avoidance of cerebral vasodilators (e.g.nitroglycerine)
Treatment1.Hyperventilation2.Osmotic agents3.CSF drainage (if ventricular/ lumbar catheter in situ)4.Augmentation of anaesthesia with I.V. anaestheticagents (e.g. propofol, thiopentone, etomidate)5.Adequate muscle relaxation6. Venous drainage (head-up/ avoidance of PEEP/reduction of inspiratory time)7.Mild controlled hypertension (if autoregulation ispresent)
5-7 minutes of occlusion with prompt reperfusionare usually well tolerated but this duration isinsufficient for clipping difficult or giant aneurysms A number of regimens have been used to extendthe occlusion duration High dose Mannitol 2g/kg SENDAI COCKTAIL - mannitol (500 ml of 20%solution) + vitamin E (500 mg) + dexamethasone(50 mg)
Pharmacological metabolic suppression bythiopentone ( 5-6 mg/kg) or etomidate (.4-.5mg/kg) Etomidate is preferred over thiopental due togreater hemodyanmic stability Moderate hypothermia has also been to extend theduration of tolerable occlusion
If the surgical procedure is uneventful , SAH grade Iand II patients should be extubated. Because hypertensive therapy is useful in reversingdelated cerebral ischemia from vasospasm , modestlevel of postoperative hypertension (<180mm hg )should not be aggressively treated. Depending on preoperative ventilatory status andduration and difficulty of surgical procedure
SAH grade III patients may or may not be extubated. Patients with preoperative SAH grade IV and Vusually require postoperative ventilatory support andneurointensive care.
In the postoperative period blood pressure should bemaintained above 140-150 mm hg and less than 180mm hg. To distinguish residual anesthesia from surgicalcause following general guidelines are useful1- Anesthesia causes global depression and any newfocal neurological deficit should alert to a surgicalcause
2-The effect of potent inhaled anesthetics shouldhave larly dissipated after 30-60 minutes3- patients whose pupils are midsized and having norespiratoty depression are unlikly to experience anarcotic overdose.4- unequal pupils not present before surgery alwayssuggest a surgical cause. Neurological assessment should be done every 15minutes in the recovery room.