• The intracranial compartment has fixed volume. • Increases in volume of brain, blood, or CSF can lead to raised ICP, compromising

blood flow or causing herniation.• Both IV & volatile anesthetic agents reduce brain metabolism. Balance of this

effect with blood flow, because of flow metabolism coupling, determines extent of increase/decrease in CBF with a particular anesthetic agent.

• Cerebral preconditioning & augmentation of endogenous processes of repair, including both neurogenesis & diaschisis, are promising approaches to cerebral protection.

• Electrophysiologic & cerebral oxygenation/metabolism monitors are used perioperatively to assess cerebral function & to detect cerebral ischemia.

• Image-guided neurosurgical procedures used for diagnosis, 3D localization, & resection of intracranial lesions.

• Anesthesia for neurosurgical patients requires understanding of basic principles of neurophysiology & effects of anesthetic agents on intracranial dynamics.

1.Uncal2.Central (transtentorial)3.Cingulate (subfalcine)4.Transcalvarial 6.Tonsillar (downward cerebellar)5.Upward (upward cerebellar or upward

transtentorial)

Supratentorial herniation 1. Uncal – Ptosis, Hemiparesis, pupillary

asymmetry 2. Central (transtentorial) – unconsciousness,

decerebration, bradycardia, hypo/HTN 3. Cingulate (subfalcine) – leg weakness 4.Transcalvarial

• Hydrocephalus– Headache– Vomiting– Drowsiness– Visual disturbances

• Hemiparesis

• Cranial nerve deficits

• Gait disturbances

• Supratentorial tumors (meningiomas, gliomas, and metastatic lesions) change intracranial dynamics predictably.

• initially, when lesion is small & slowly expanding, volume-spatial compensation occurs by compression of CSF compartment & nearby cerebral veins.

• As lesion grows, compensatory mechanisms become exhausted, & further increase in tumor mass causes progressively greater rise in .

• Primary or metastatic tumors or chronic SDH can present as chronic mass lesions.

• Due to ability of intracranial compartment to compensate up to a point, patients may exhibit minimal neurologic dysfunction despite large mass, elevated ICP, & shifts in the position of brain structures.

• As the tumor enlarges - outstrip its BS, developing central hemorrhagic area that may expand rapidly, increasing ICP.

• Brain edema surrounding tumor increases effective bulk of tumor & represents additional portion of the brain that is not autoregulating.

• In such situations (compromised compliance), small increases in arterial pressure may produce large increases in CBF, which can markedly increase intracranial volume & ICP & cerebral ischemia/herniation.

• In addition to HTN, other causes of increased CBV such as 1.hypercarbia, 2.hypoxia, 3.vasodilating agents, 4. jugular venous obstruction, can adversely affect cerebral hemodynamics & must be avoided perioperatively.

• Intracranial tumors may be classified as 1.primary (those arising from the brain and its coverings) 2. metastatic. • Tumors can originate from any cell type within CNS. • Supratentorial tumors more common in adults & often

present with headache, seizures, or new neurologic deficits, whereas infratentorial tumors are more common in children & present with obstructive hydrocephalus & ataxia.

• Treatment & prognosis depend both on tumor type & location.

• Treatment may consist of surgical resection/debulking/chemotherapy/ radiation.

Astrocytoma • Often present in young adults with new-onset seizures. Upon

imaging, they generally show minimal enhancement with contrast.

• Surgical or radiation treatment of low-grade gliomas usually results in symptom-free long-term survival.

• Usually appears as a contrast-enhancing, well-demarcated lesion with minimal to no surrounding edema.

• Because of its benign pathologic characteristics, prognosis following surgical resection is generally very good; however, the location of the lesion, such as within the brainstem, may preclude resection.

• Gliobastoma multiforme (grade IV glioma) accounts for 30% of all primary brain tumors in adults.

• Imaging usually reveals a ring-enhancing lesion due to central necrosis as well as surrounding edema.

• Treatment typically involves debulking combined with radiation and chemotherapy.

• Due to microscopic infiltration of normal brain by tumor cells, resection alone is usually inadequate.

• Instead, treatment usually consists of surgical debulking combined with chemotherapy and radiation and is aimed at palliation, not cure. Despite treatment, life expectancy is usually on the order of weeks.

Oligodendroglioma • Arising from myelin-producing cells within CNS, account for only 6%

of primary intracranial tumors. • Classically, seizures predate appearance of tumor on imaging, often

by many yrs. • Calcifications are common & visualized on CT imaging. • Usually consists of mixture of oligodendrocytic & astrocytic cells. • Treatment & prognosis depend on the pathologic features. • Initial treatment involves resection since, early in the course,

consists of primarily oligodendrocytic cells, which are radioresistant.

• Due to presence of astrocytic cells, they commonly behave like anaplastic astrocytomas or glioblastoma multiforme later in their course.

Ependymoma • Arising from cells lining ventricles & central canal of spinal cord,

ependymomas commonly present in childhood & young adulthood. • Most common location is floor of 4th ventricle. • Symptoms include 1.obstructive hydrocephalus, 2.headache, 3.nausea, 4.vomiting, 5.ataxia. • Treatment consists of resection and radiation. Tumor infiltration

into surrounding tissues may preclude complete resection.

Primitive Neuroectodermal Tumor

• Diverse class of tumors including retinoblastoma, medulloblastoma, pineoblastoma, & neuroblastoma, all believed to arise from primitive neuroectodermal cells.

• Medulloblastoma is the most common pediatric primary malignant brain tumor & may disseminate via CSF to encompass spinal cord.

• Presentation of medulloblastoma is similar to ependymoma. • Treatment usually involves a combination of resection &

radiation given its high radiosensitivity.• Prognosis is very good in children, if there is disappearance of

tumor celIs within CSF.

Meningioma • Usually extra-axial (arising outside of the brain proper), slow-growing, well-circumscribed, benign tumors arising from arachnoid cap cells, not dura mater• Due to slow-growing nature, they can be very large at time of

diagnosis. • Occur anywhere arachnoid cap cells exist, most common near

sagittal sinus, falx cerebri, & cerebral convexity. • Usually apparent on plain radiographs & CT due to presence of

calcifications. • On MRI & conventional angiography, these tumors often receive

their blood supply from external carotid artery. • Surgical resection is mainstay of treatment. • Prognosis is usually excellent; however, some tumors may be

recurrent and require additional resection.

Pituitary Tumors • Arise from cells of anterior pituitary gland. • May occur along with tumors of parathyroids & pancreatic islet

cells as part of MEN 1. • Usually divided into functional (hormone secreting) &

nonfunctional. • Former usually present due to endocrine disturbance related to

hormone secreted by the tumor. • Functional tumors are usually smaller (<1 cm in diameter) at the

time of diagnosis (microadenomas). • Macroadenomas are usually nonfunctional, present with symptoms

related to their mass (headache/visual changes due to compression of optic chiasm), larger at diagnosis, usually >1 cm in diameter.

• Panhypopituitarism may be caused by either (compression of normal functioning pituitary).

• Apoplexy - abrupt onset of headache, visual changes, ophthalmoplegia, & altered mental status secondary to hemorrhage/necrosis/infarction within the tumor.

• Can invade cavernous sinus/ICA/compress various cranial nerves, causing an array of symptoms.

• Treatment depends on tumor type. • Prolactinomas are often initially treated medically with

bromocriptine. • Surgical resection transsphenoidally/open craniotomy

approach is often curative for most pituitary tumors.

Acoustic Neuroma

• Benign schwannoma involving vestibular component of cranial nerve VIII within internal auditory canal.

• Bilateral tumors may occur as part of neurofibromatosis type 2. • Common presenting symptoms - hearing loss, tinnitus &

disequilibrium. • Larger tumors, which grow out of the internal auditory canal & into

CP angle, may cause symptoms related to compression of cranial nerves, most commonly facial nerve (cranial nerve VII) & brainstem.

• Treatment usually consists of surgical resection +/- radiation. • Surgery usually involves intraoperative cranial nerve monitoring

with electromyography or brainstem auditory evoked potentials. • Prognosis is usually very good; however, recurrence of tumor is not

uncommon.

CNS Lymphoma

• Rare tumor that can arise as primary brain tumor, also known as microglioma, or via metastatis from systemic lymphoma.

• Primary CNS lymphoma can occur anywhere, most common in supratentorial locations (deep gray mater /corpus callosum).

• Primary CNS lymphoma thought to be associated with a variety of systemic disorders - SLE, Sjögren's syndrome, RA, immunosuppressed states, EBV.

• Symptoms depend on location of tumor. • Reasonable to wait to administer CTS, until after pathologic

findings are obtained as may be sensitive to steroids.

• CTS-associated tumor lysis prior to performing biopsy may result in failure to obtain an adequate sample to make diagnosis.

• Mainstay of treatment is chemotherapy (including intraventricularly delivered drugs) & whole-brain radiation.

• Prognosis is poor despite treatment.

Metastatic Tumor • Originate most often from primary sites in lungs or breasts. • Malignant melanoma, hypernephroma, & Ca colon also likely

to spread to brain. • Metastatic brain tumor is likely diagnosis when more than

one intracranial lesion is present.

• Lab tests should be ordered based on history & clinical findings, considering disease & complexity of Sx.

• Following are preoperative tests ordered:– Hb, TC – Platelet count – PT/APTT & INR [individualized] – Serum electrolytes, Blood sugar – Glycosylated hemoglobin (HbA1c) in patients with long standing

DM – BUN, Creatinine – TEE in patients scheduled for tumors in sitting position.– USG abdomen for polycystic kidney, pheochromocytoma

(Hemangioblastoma) .

1.Anti-convulsants 2. Antihypertensives 3.Steroids 4. Hypoglycaemic agents 5.Diuretics 6. Hormonal therapy7.Anticoagulants / antiplatelets NOTE:• Requirement of nondepolarizing muscle relaxants is increased

in patients on anticonvulsants• Lethargic patients do not receive premedication. • Patients who are alert and anxious may receive an anxiolytic

(e.g., midazolam 5 mg po) before coming to OR.

Evidence of midline shifts (>0.5 cm) on CT /MRI

suggests raised ICP.• Patients with intracranial pathology may be extremely

sensitive to CNS depressant effects of opioids & sedatives. • Drug-induced hypoventilation - accumulation of arterial CO2 increases

in ICP. • Considering potential adverse effects of preop medication,

pharmacologic premedication should be used sparingly, if at all, in patients with intracranial tumors.

• Preop depressant drugs best avoided in patients with diminished levels of consciousness.

• In alert adult patients with intracranial tumors, BZDs in small doses can provide anxiety relief without meaningfully affecting ventilation.

• Decisions to administer anticholinergic drugs or H2-receptor antagonists not influenced by presence/absence of increased ICP.

• ECG monitoring : necessary to detect responses related to intracranial tumors/ surgery. • ECG changes can reflect increased ICP or, more importantly, surgical

retraction or manipulation of the brainstem or cranial nerves. • CVS centers, RS control areas, nuclei of lower cranial nerves lie in

close proximity in brainstem. • Manipulation of brainstem may produce systemic HTN &

bradycardia/ hypotension & tachycardia. • Cardiac arrhythmias range from acute sinus arrhythmias to

ventricular premature beats/VT.

• Pulse oximetry is of obvious importance.

• Capnography : can facilitate ventilation & PaCO2 management as well as detecting VAE.

• In elderly & those with V/Q mismatch, et CO2 may correlate poorly with PaCO2.

• Nasopharyngeal /esophageal temperature monitored to prevent hyperthermia/uncontrolled hypothermia.

• Urine output also measured as indicator of perioperative fluid balance.

• Diuresis occurs following administration of osmotic/loop diuretics. • Reduced urine output – hypovolemia/release of ADH.• Needed in pts with diabetes insipidus/SIADH/aberrations of salt or

water physiology/ lengthy Sx anticipated & bladder distention is concern.

• IV access with large-bore catheters , given likelihood of bleeding & need for transfusion/ rapid administration of fluids.

• Measurement of intra-arterial blood pressure, ABG, CVP, recommended for major neurosurgical procedures.

• Arterial cannula is inserted before induction of anesthesia to continuously monitor ABP & estimate CPP.

• When pressure transducer is at midhead level (level of external auditory meatus), MAP approximates MAP at level of circle of Willis.

• CPP = difference btwn MAP & CVP in pts without intracranial HTN/ ICP in those with intracranial HTN.

• When cranium is open, ICP = atm pressure & CPP = MAP. • With direct arterial pressure monitoring, hemodynamic

consequences of pharmacologic agents administered during anesthesia recognized instantly.

Arterial catheter access for intraop ABG, hct, serum electrolytes, glucose, & osmolality. (to verify adequacy of hyperventilation).

Radial/femoral/brachial arteries suitable for short-term; after ulnar artery collateral blood flow is tested, cannulation of radial artery preferred.• CVP - reliable means of large-bore IV, monitor of fluid status. • When possible, CVP catheter should be inserted through

antecubital vein instead of jugular/subclavian veins. • Avoids increased ICP from both head-down position & decreased

cerebral venous outflow. • Position of antecubital central venous pressure verified by CXR,

transducer pressure waveform, or ECG.• TEE & PAC selectively used, eg. In pts with IHD.• Peripheral nerve stimulator : monitoring persistence of drug-

induced skeletal muscle weakness/paralysis.

• If paresis/paralysis of an extremity is associated with brain tumor, it is important to appreciate resistance (decreased sensitivity) to NDMR in paretic extremity, compared with normal extremity.

• Therefore, monitoring skeletal muscle paralysis on paretic limb may be misleading.

• In these instances, the altered muscle response to relaxants may reflect the proliferation of acetylcholine-responsive cholinergic receptors that can occur after denervation.

Preoperative ICP monitoring • Rarely used in patients for elective supratentorial tumor operations. • ICP monitoring is invasive procedure that can cause bleeding or infection. • When performed with LA before induction, can be uncomfortable to pt.

•

Hazards of Positioning Prone• Pressure over the eyeballs, pinna , genitalia • Kinking of the neck veins • Extreme flexion – endobronchial migration of the tube,

kinking • Brachial plexus , ulnar and sciatic nerve injuries

• Ventilation perfusion mismatch• Common peroneal nerve injury• Dependent pinna injury

• Achieved with drugs ( thiopental, etomidate, propofol) produce rapid, reliable onset of unconsciousness without increasing ICP. • In presence of raised ICP, thiopental is commonly used.• Alternative agents : propofol / midazolam depending on pt's condition. • Following induction sequence suggested: IV administration of thiopental

(3-5 mg/kg) or propofol (1.25-2.5 mg/kg), followed by opioid (fentanyl, 3-5 µg/kg) & muscle relaxant.

• In pts who have been vomiting due to raised ICP, cricoid pressure is applied during mask ventilation.

• If no airway difficulties anticipated, NDMR administered while controlled hyperventilation with 100% oxygen is instituted, with goal of decreasing PaCO2 to near 35 mm Hg.

• Administration of succinylcholine associated with modest, transient increases in ICP. (risk benefit assessment)

• Adequate depth & profound skeletal muscle paralysis should be achieved prior to laryngoscopy, (as movement can abruptly increase CBF, CBV & ICP).

• Abrupt, sustained increases in systemic blood pressure, particularly in areas of impaired cerebrovascular tone, may be accompanied by undesirable increases in CBF, CBV, and ICP, and followed by cerebral edema.

• To deepen, fentanyl administered in 50µg increments to total dose of 10µg/kg, depending on BP.

• Lidocaine (1.5 mg/kg) also administered IV 90sec before intubation to suppress laryngeal reflexes ( & other forms of intraop stimulation like placement of pinions, skin incision).

• Esmolol infusion / bolus may be used to reduce HR & BP response to DLscopy & intubation.

• Sustained hypotension must also be avoided (ischemia due to decreased CPP).

• New-onset seizures or repeat episodes of seizures are another possible origin of unexpected movement.

• ET intubation is performed as rapidly & smoothly as possible. • Patient's lungs are ventilated at a rate & tidal volume that maintain

PaCO2 near 35 mm Hg.

• Routine hyperventilation no longer recommended in neurosurgical patients due to risk of ischemia in some pathologic conditions. (surgical conditions should define PaCO2 level for each pt).

• Eg, in pts with significant intracranial HTN / using volatile agents, PaCO2 adjusted btwn 30-35 mmHg to reduce brain bulk.

• Opiods selected are usually fentanyl or remifentanil. • PEPP should be used with caution, attention paid to ICP, MAP & CPP effects.

MUSCLE RELAXANTSSUCCINYLCHOLINE• IV administration of succinylcholine activation of EEG & increases in CBF / ICP.• Cerebral effects Attributed to scoline-induced increase in

muscle afferent activity - cerebral stimulation. • Pts with compromised intracranial compliance, scoline shown

to increase ICP. • Not recommended for elective cases; but remains best agent

for achieving total paralysis for rapid-sequence intubation. • Anesthetic depth required to protect against ICP-elevating

effects of such noxious stimuli as well as scoline itself. • In Hemiplegic /paraplegic) pt, scoline avoided due to risk of

hyperkalemia.

• Agents that release histamine avoided (Histamine alone may lower BP & increase ICP, thus lowering CPP).

• When BBB disrupted, histamine can produce cerebrovasodilation & increases in CBF.

• Most benzylisoquinolinium compounds (d-tc, metocurine, atracurium, mivacurium) potential to release histamine.

• Doxacurium & cisatracurium produce minimal /no histamine release.

• Atracurium in intubating doses, reported to have no significant effect on ICP, BP, or CPP in neurosurgical patients.

• Steroidals (pancuronium, pipecuronium, vecuronium & rocuronium) may be better relaxants (do not directly affect ICP).

• Pancuronium does not produce an increase in CBF, CMRO2,ICP.

• However, pancuronium's vagolytic effects can increase HR & BP, & elevate ICP in pts with disturbed autoregulation.

• Pipecuronium, reported to have no significant effect on ICP or CPP in patients with intracranial tumors & no hemodynamic side effects.

• Vecuronium has no effect on ICP, HR/BP in neurosurgical pts. • To achieve relatively rapid airway control (within 90 seconds), a

priming dose of vecuronium (0.01 mg/kg) can be administered followed by a higher dose (0.10 mg/kg), or high doses of vecuronium (to 0.4 mg/kg) without hemodynamic consequence.

• Rocuronium also has no effect on ICP in neurosurgical pts, but may have mild vagolytic activity in higher doses (0.9 mg/kg).

MAINTENANCE

• Popular technique - continuous infusion of propofol with remifentanil / fentanyl. (shown to reduce ICP more effectively than iso/ sevo), propofol with remifentanil produced quicker emergence than des/sevo.

• In susceptible pts, risk of cerebral hypoperfusion greater when pts hyperventilated under propofol anesthesia.

• Nitrous oxide & volatile anesthetics potential to increase CBV & ICP as result of direct cerebral vasodilation.

• Nitrous oxide, 50 -70% in O2, administered by some to decrease total dose of IV agent / volatile agent.

• In elevated ICP / low compliance, some clinicians avoid nitrous oxide / high conc of isoflurane (> 1.0%).

• Opioid ,thiopental / propofol with midazolam / low-dose iso. • Peripheral vasodilating drugs (nitroprusside/nitroglycerin), may

increase CBV & ICP despite decrease in SBP (best used after craniotomy & opening dura).

• Spontaneous movement by pts must be prevented (dangerous increases in ICP/herniation/bleeding).

• In addition to adequate depths of anesthesia, skeletal muscle paralysis maintained.

MEASURES TO REDUCE ICPDiuretics: • Osmotic: Mannitol (0.25-1 g/kg iv), hypertonic saline.

Furosemide: 0.5-1 mg/kg iv, or 0.15-0.3 mg/kg with mannitol.Corticosteroids: • Dexamethasone (localized cerebral edema surrounding tumors;

requires 12-36 hrs).Adequate ventilation: • PaO2 100 mmHg, PaCO2 33-35 mmHg.

Optimize hemodynamics• (MAP, CVP, PCWP, HR): normotension, maintain CPP .Fluid therapy: Normovolemia before induction - prevent hypotension. Position improve cerebral venous return (neutral, head-up position).Drug-induced cerebral vasoconstriction (e.g., thiopental, propofol).Temperature control mild intraoperative hypothermia.CSF drainage to acutely reduce brain tension.

CLINICAL CONTROL OF RAISED ICP• Severe intracranial HTN - reflex arterial hypertension & bradycardia (Cushing's triad). • Reduction in SBP can further aggravate ischemia (reducing CPP).• Rapid brain dehydration & ICP reduction produced by administering

osmotic diuretic, mannitol / loop diuretic, furosemide.

Mannitol:• Infusion 0.25-1.0 g/kg. • Action begins within 10-15 mins, effective for approx 2 hrs. • Larger doses produce a longer duration of action but do not

necessarily reduce ICP more effectively (metabolic derangement). • Mannitol is effective when the blood-brain barrier is intact.

• By increasing osmolality of blood relative to brain, pulls water across intact BBB from brain to blood to restore the osmolar balance. • Shown to cause vasodilation of VSM, dependent on dose & rate of

administration. • Mannitol-induced vasodilation affects intracranial & extracranial

vessels & can transiently increase CBV & ICP while simultaneously decreasing SBP.

• Hence should be given slowly (10-minute infusion) in conjunction with maneuvers that decrease ICV (steroids / hyperventilation).

• Prolonged use of mannitol may produce 1.dehydration, 2.electrolyte disturbances, 3.hyperosmolality, 4.impaired renal function.

Hypertonic saline• Currently under investigation.• Shown to reduce ICP in animals & human studies may be more effective than other diuretics in certain conditions

(refractory intracranial HTN/ brain debulking ).• Alternative /adjunct to mannitol.

Potential Adverse Effects of IV AdministrationCENTRAL NERVOUS SYSTEM & SYSTEMIC1.Decreased level of consciousness 8. Hyperchloremic acidosis2.Hyperosmolality Hypernatremia 9. Coagulopathy3.Seizures 10. Rebound edema4.CHF 11. Phlebitis5.Central pontine myelinolysis 12. Renal failure6.Hypokalemia7.Subdural & intraparenchymal hemorrhagea

FUROSEMIDE• better agent in pts with impaired cardiac reserve.• Loop diuretic : reduces ICP by inducing systemic diuresis,

decreasing CSF production & resolving cerebral edema by improving cellular water transport.

• lowers ICP without increasing CBV or blood osmolality; but not as effective as mannitol.

• Can be given alone,initial dose (0.5-1 mg/kg) or lower dose with mannitol (0.15-0.30 mg/kg).

• combination of mannitol & furosemide diuresis more effective than mannitol alone in reducing ICP & brain bulk but causes more severe dehydration & electrolyte imbalances.

• Thus necessary to monitor electrolytes intraop & replace K as indicated.

CORTICOSTEROIDS• reduce edema around tumors; require many hrs/days before reduction in ICP. • Steroids preop frequently cause neurologic improvement that

precede ICP reduction.

Postulated MOA for steroidal reduction in brain edema • 1.brain dehydration, • 2.BBB repair, • 3.prevention of lysosomal activity, • 4.enhanced cerebral electrolyte transport, • 5.improved brain metabolism, • 6.promotion of H2O & electrolyte excretion, • 7.inhibition of phospholipase A2 activity.

Potential complications of continuous periop steroid

• 1.hyperglycemia, • 2.glucosuria, • 3.gastrointestinal bleeding, • 4.increased incidence of infection. • 5.electrolyte disturbances

• Therefore, the potential risks and benefits of continuous steroid administration need to be evaluated in these patients.

HYPERVENTILATION• reduces brain volume by decreasing CBF through cerebral vasoconstriction. • For every 1 mm Hg change in PaCO2, CBF changes by 2 mL/100

g/min. • Duration of effectiveness for lowering ICP as short as 4-6 hrs,

depending on pH of CSF. • Only effective when CO2 reactivity of cerebrovasculature intact.

• Impaired responsiveness to changes in CO2 in areas of vasoparalysis (associated with ischemia, trauma, tumor & infection).

• Target PaCO2 is 30-35 mmHg.

• By monitoring global cerebral oxygenation with, for example, SjVO2, therapeutic effectiveness of hyperventilation determined & more safely applied.

NOTE• Therapeutic goals are to maintain CPP & control intracranial dynamics so that cerebral ischemia,

edema, hemorrhage & herniation are avoided. • Severe hypotension results in cerebral ischemia & should be

treated with volume replacement, inotropes, or vasopressors as dictated by clinical need.

• Severe HTN, can worsen edema & cause IC hemorrhage & herniation.

• β2-adrenergic blockers propranolol & esmolol , combined αβ-adrenergic blocker labetalol effective in reducing SBP in pts with raised ICP with minimal or no effect on CBF / ICP.

FLUID THERAPY1.Do not dehydrate2.Avoid hypotonic solutions3.Colloids4.Blood5Avoid over-transfusion• Restricted fluid intake was traditional approach to IC

decompression therapy but now rarely used. • Severe fluid restriction over several days only modestly effective in

reducing oedema & can cause hypovolemia, hypotension, inadequate renal perfusion, electrolyte & acid-base disturbances, hypoxemia, reduced CBF.

• In pts who are dehydrated preop, IV volume must be restored to normal before induction to prevent hypotension.

• Relatively iso-osmolar solutions (NS, RL) do not adversely affect oedema (if intact BBB).

• Free water in hypo-osmolar solutions (0.45% NaCl) adversely affects ICP management.

• Hyper-osmolar solutions, 3% NaCL, initially tend to decrease brain water by increasing osmolarity of plasma.

• Regardless of solutions selected, any solution administered in large amounts can increase CBV & ICP.

• Blood loss should be corrected with PRBCs/ colloids supplemented with balanced salt solutions.

• Glucose-containing solutions should be used with caution since hyperglycemia, in CNS ischemia exacerbates neuronal injury.

• Replacement at approx 3:1 ratio (crystalloid:blood) to hct of approx 25-30%, depending on physiologic status.

POSITION• Neutral head position, elevated 15-30° to decrease ICP by improving venous drainage. • Flexing /turning of head may obstruct cerebral venous outflow

(dramatic ICP elevation, resolves with neutral head position).

PEEP• Can increase ICP (increases mean intrathoracic pressure, impairing

cerebral venous outflow & CO). • If PEEP required to maintain SpO2, applied cautiously & with

appropriate monitoring to minimize decreases in CO & increases in ICP.

• PEEP 10 cm H2O < used without significant increases in ICP / decreases in CPP.

• If higher levels of PEEP required to optimize SpO2, both CVP & ICP monitoring indicated.

TEMPERATURE• Intraop, modest degree of hypothermia, approx 34°C, way to

confer neuronal protection during focal ischemia. • Hypothermic techniques for febrile neurosurgical patients.• Hyperthermia particularly dangerous as it increases brain

metabolism, CBF & cerebral edema.

CSF DRAINAGE• To acutely reduce ICP, CSF drainage either by direct surgical

puncture of lateral ventricle /lumbar spinal catheter employed. • Lumbar CSF drainage used cautiously & only when dura open & pt

mildly hyperventilated to prevent acute brain herniation. • Brain tension can be effectively reduced by draining 10-20 mL of

CSF.

EMERGENCENeurologically intact preop & uneventful Intraop

• Smooth emergence• No coughing or straining

Neurologically compromised & extensive manipulations• Continue intubation & ventilation• Also if there is facial or neck swelling

Causes of Delayed Awakening 1.Preoperative low GCS 6.Surgical complications

2.Large tumor 7.Cerebral edema 3.Residual anesthetics 8.Hematoma 4.Metabolic / electrolyte disturbances 9. Pneumocephalus 5.Residual hypothermia 10.Vessel occlusion/ischemia

• IC hematoma & major cerebral edema most feared complications. • Emergence from anesthesia should be as smooth as possible, avoiding

straining/ bucking. • Bucking can cause HTN & elevated ICP, leading to postop hge &

cerebral edema. • Relaxants not reversed until head dressing applied. IV lidocaine (1.5

mg/kg) 90 seconds before suctioning & extubation . • Extubated only when fully reversed or awake & following commands.

If not responsive, not extubated. • Brief neurologic exam performed before & after extubation.• Pt positioned with head elevated 15-30°, shifted to recovery room

with oxygen by mask & SpO2 monitoring.

• General assertion states that larger the resection, lower the risk of recurrence of lesion & higher chance of pt's survival.

• But extensive tissue excision may favor occurrence of unpredictable degree of functio laesa, (depending on location).

• Neurological sequelae due to tumor excision may cause severe disability compromising pt's social life.

• Therefore, aim to remove max amount of lesion without impairing neurological function has pushed physicians & industry to develop sophisticated approaches performed in awake & responding pts, to evaluate neurological dysfunction before tissue removal.

• Awake craniotomy dates back to 2nd half 19th century, when only indication was epilepsy & Sx done under LA.

• Subsequently, surgical practice extended to resection of tumors involving functional cortex.

• In more recent years, indications further extended to removal of supratentorial tumors, regardless of cortical involvement.

• Awake Craniotomy evolved as direct consequence of following: 1.huge improvement of diagnostic tools; 2.impressive development of intraoperative functional neurosurgical

technology; 3.enhancement of anesthesia monitoring devices, 4.Pharmacokinetic & dynamic properties of new anesthetic agents &

delivery systems.

• Main advantage : intraop electrocorticography & mapping for accurate identification of brain areas controling motor function & speech.

• Allows maximal tumor resection with minimal postop deficits from retraction, edema &/or resection of eloquent tissue.

• Other advantages include :1.avoidance of GA 2. avoidance of more intensive monitoring intra-op & postop, 3. low complication rate, 4.reduction in resource utilization (shorter ICU & hospital stay).

• Functional mapping performed by stimulating brain with small electrical charge.

• Neuropsychologist then performs neurocognitive testing &/or monitors motor responses during mapping & later tumor resection.

• Intraop testing of language & motor function gold std.• Intraop monitoring severely inhibited by GA: some higher cortical

brain functions (i.e. speech) cannot be monitored during surgery.• "Awake craniotomy" is misleading term, as different Sx phases

require various levels of sedation & pt maintained completely awake only during mapping procedure & early resection of tumor.

• Preop selection, evaluation & preparation of pts different than GA. • Cooperative, able to participate in neurocognitive testing. • Must have uncomplicated airway, also candidate for GA. • Accurate detailed explanation of procedure (i.e. intraop sounds of

surgical instruments, head immobilization, voices...). • Regarding sequence of events during Sx & possible complications,

to minimize fear. (pt's confidence & agreement, cooperation fundamental factor for successful procedure).

• Like any craniotomy, adequate surgical exposure & brain relaxation required.

• Providing appropriate sedation & analgesia greatest challenge. • Continuous, rapid modulation of sedation & analgesia level

necessary to manage painful stimuli & cortical testing. • Adequate analgesia & sedation needed for head frame application,

skin incision, craniotomy & opening of dura. • Of utmost importance, pt must be awake & alert during brain

mapping, able to participate in complex neurocognitive testing.• Vital functions to be ensured, emergency support if deterioration of

clinical status occurs.• Positioning : comfortably with bolsters & additional padding.

Technique selected requires 1.optimal analgesia during nociceptive stimulations 2.sedation/anxiolysis, immobility/comfort during mapping & resection3. prevention of nausea, vomiting & seizures4.Maintenance of airway & adequate ventilation5.hemodynamic stability6.brain relaxation

Techniques described for more secure airwayprotection include (a) ETT & awakening without tube withdrawal (disallowing vocalization

testing); extubation & re-intubation after testing (b) placement, removal & replacement of LMA (c) Non-IPPV has also been described (CPAP, BiPAP).

• Whichever technique used, must anticipate respiratory complications (low SpO2, increase in EtCO2, hypoventilation/airway obstruction) & plan of action & required equipment to deal with difficult airway management.

• In asleep, awake, asleep techniques, initial phase of GA, with insertion of supraglottic airway device, followed by intraop awakening for language mapping during tumor resection & finally, back to GA during craniotomy closure.

• Sarang & Dinsmore retrospectively examined 3 techniques: (a)sedation with propofol, fentanyl, droperidol & midazolam

(b)propofol infusion, i.v. fentanyl & spontaneous ventilation LMA (c) propofol & remifentani, IPPV via a LMA. • Found that profound sedation & apnoea was possible in three

scenarios, must be vigilant to avoid.

• Limitations to NIPPV: nasal mask may be difficult to position, interfere with surgical field; pts may find it unpleasant.

• Successful use of pressure support ventilation described for pt with OSAS undergoing awake craniotomy.

1. Supraorbital2. Supratrochlear3. Zygomaticotemporal4. Auriculotemporal5. Greater occipital6. Lesser occipital• In addition, line of scalp incision infiltrated with LA.• Scalp blocks & infiltration with large volumes of LA carry potential

of toxicity in pts already prone to seizures. • Studies have shown LA absorbed rapidly & potentially toxic conc

achieved in some pts.

Propofol • 1st choice hypnotic • Can be administrated using target control infusion • With remifentanil, which has very short t1/2, rapid & fine

modulation of sedation depth• Accurate titration of both avoids devices for airways control.

Dexmedetomidine• Highly specific α2 adrenoreceptor agonist, recommended for use.• Advantage of providing sedation & analgesia without respiratory

depression.• Provides sedation closer to natural sleep, anxiolysis & analgesia,

decreasing need for opioids & antiHTN drugs.

α2 agonist clonidine often used as analgesic co-adjuvant

• Nerves blocked1.supraorbital, 2.supratrochlear, 3.zygomatico temporal, 4.auricuculotemporal, 5.posterior auricular, 5.lesser & greater occipital.• Total solution– 80ml

• 0.5% Bupivacaine – 40ml• 2% Lidocaine – 20ml• Adrenaline – 400 mcg(in

4ml saline)• Saline – 16ml

(a).Supraorbial & supratrochear - above eyebrow at midpoint, needle inserted perpendicular to skin, & medial margin of orbit.

(b) Auriculotemporal - 1.5cm anterior to tragus, perpendicular to skin.(c) Zygomatico temporal - midway btwn supraorbital ridge & post

margin of Zygoma; deep infiltration within temporalis & fascia.(d) Post auricular branches(greater auricular) - 1.5 cm posterior to ear

at level of tragus btwn skin & bone.(e) Greater & lesser occipital- along superior nuchal line approx

halfway btwn occipital protruberance & mastoid process; infiltration done with 22 G spinal needle.( all others with 23G)

• Remaining soultion used to infiltrate pin sites & line of incision, 15 mins before procedure & lasts atleast 4-5 hours.

• In lesions near motor cortex, electrical stimulation used to test motor function & map area.

• With speech, considerable inter-patient variability in location & cortical representation of speech areas.

• Intraoperative mapping of speech involves the identification of Broca’s area by producing speech arrest with cortical stimulation, & other speech areas by a series of naming & word/sentence comprehension tests using books or slides.

• Computer programs available that allow dysphasic patients to respond to images.

• In pts who are fluent in >1 language, localization problematic as multiple representation sites.

1.Seizures 2. Decreased level of consciousness3.Increased ICP 4. Neurological deficit5.HTN 6. Nausea & vomiting 7.Pain & loss of patient cooperation

• Onset of new seizures common presentation, esp during brain mapping (5-20 %), due to decreased levels of anticonvulsants /LA toxicity.

• Focal / general, usually self-limiting. • Protocols include prophylaxis with antiHTNs, anticonvulsants &

antiemetics to prevent these complications.