Anaesthesia for supratentorial tumor surgeries
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Transcript of Anaesthesia for supratentorial tumor surgeries
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• 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.
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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
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• Hydrocephalus– Headache– Vomiting– Drowsiness– Visual disturbances
• Hemiparesis
• Cranial nerve deficits
• Gait disturbances
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• 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.
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• 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.
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• 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.
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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.
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• 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.
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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.
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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.
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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.
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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.
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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.
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• 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.
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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.
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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.
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• 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.
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• 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) .
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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.
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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.
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• 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.
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• 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.
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• 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).
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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.
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• 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.
•
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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
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• Ventilation perfusion mismatch• Common peroneal nerve injury• Dependent pinna injury
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• 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)
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• 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.
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• 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.
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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.
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• 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).
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• 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).
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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.
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• 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.
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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.
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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.
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• 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.
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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
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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.
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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.
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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.
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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.
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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.
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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.
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• 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.
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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.
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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.
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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
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• 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.
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• 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.
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• 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.
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• 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.
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• 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).
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• 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.
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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).
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• 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.
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• 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.
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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.
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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
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• 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
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(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.
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• 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.
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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.
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