awake craniotomy

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Anesthetic safety in awake craniotomyPresented byMohamad Abdulrazik El saaid

Under supervision of

Professor Amir Ibrahim Mohamad SalahDoctor Mohamad Anwar El ShafeiDoctor Mostafa Gamal Eldin MahranIntroductionAwake craniotomy literally means a procedure where the patient is awake during critical portions of the surgery so that his vital functions such as speech and movement can be monitored continuously.

Maintain Anesthetic Goal Ensure1.Adequate patient comfort. 1.Patient Safety.2.Analgesia. 2.Control and maintainance 3.Immobility. of critical functions.4.Patient co-operation.

Advantage of awake craniotomy

1.Intraoperative Electrocorticography:

It is the gold standard for defining epileptogenic zones in clinical practice.

2.Cortical Mapping:

Recording the electric currents that result from muscle contractions in order to identify motor areas of the cortex

Language areas are identified from the verbal responses of an awake patient.

Intraoperative electrocorticography

electrodes placed directly on the exposed surface of the brain to record electrical activity from the cerebral cortex.

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Cortical Mapping

Electromyography (EMG)3Nerve Supply of head and neckFace sensory innervation is supplied by three branches of trigeminal nerve (Opthalmic, Maxillary, Mandibular).Front and Side of the neck by cervical plexus.Posterior head and neck by cervical nerves.

Opthalmic Frontal nerve Supaorbital & Supratrochlear N.

Maxillary Zygomaticotemporal Nerve.

Mandibular Auriculotemporal Nerve.

Cervical plexus Lesser & Greater Occipital N.

neurophysiologyPoor anesthetic technique which allows coughing, straining, hypotension, exaggerated hypertension, hypoxia and hypercarbia will seriously damage the critically ill brain.

Better results can be obtained by careful monitoring of the patient and attention to simple details than by complex pharmacological interventions.Intracranial pressure [ICP]:The principle constituents within the skull are brain (80%), blood (12%) and cerebro-spinal fluid (8%).Normally range (5-13 mmHg).

Hatmanns solution

Compound sodium lactate CSLUsed as systemic alkalinizer & fluid & electrolyte replenisher

Contraindicated in

DM lactateCongestive heart failure7Cerebral Perfusion Pressure [CPP]:Cerebral perfusion pressure [CPP] is defined as the difference between mean arterial and intracranial pressures.

CPP = MAP ICP

Normal cerebral perfusion pressure is 80mmHg, but when reduced to less than 50mmHg there is metabolic evidence of ischemia and reduced electrical activity.Regulation of Cerebral Blood Flow :The normal cerebral blood flow is 45-50 ml/100g/min. In decompensated brain as a result of major intracranial pathology, increases or decreases in CBF will in turn lead to a significant rise or fall in ICP. Cerebral Blood Flow [CBF]:Chemical regulation.Myogenic regulation.Neurogenic regulation.Viscosity effect.Vasoactive agents.I.Chemical Regulation3. PaO2: From 60 to more than 300 mmHg have little influence on CBF. When the PaO2 is less than 60 mmHg, CBF increases rapidly. 1. PaCO2: Co2 causes cerebral vasodilatation.CBF changes 1 to 2 ml/100g/min for each 1 mmHg change in PaCO2 . CO2 CBF , CO2 CBF. This response is attenuated below a PaCO2 of 25 mmHg.2. CMR:2.Anesthetic agents: anesthetic agents suppress CMR, with exception of ketamine and nitrous oxide.3.Temperature: CMR decreases by 6 to 7% per Celsius of temperature reduction.1. Functional State: Extreme increase in epileptic fit.

PaCo2

Hyperventilation can lead to a mean reduction in ICP of 50% within 2-30 mins.

CBF influnced by respiratory acidosis greater than by metabolic acidosis becauseCo2 diffuses freely across BBB but H+ is not

CMR

Increased neuronal activity -- increased local brain metabolism,Increase in CMR --- proportional change in CBF.10II. Myogenic autoregulation:Autoregulation maintains a constant blood flow between MAP 50mmHg and 150mmHgIII. Neurogenic regulation:There is extensive innervation on the larger cerebral arteries. IV. Viscosity effect:Within the normal range (33-45%) , there is only trivial alteration of CBF.V. Vasoactive agents:Inhalational agents:Volatile anesthetis agents cause cerebral vasodilation in dose dependant waySystemic vasodilators:Most drugs that cause hypotension causes cerebral vasodilation Catecholamine Agonist/Antagonist. Above and below the autoregulatory plateau, CBF is pressure dependent and varies linearly with CPP

11Catecholamines 1. 1-Agonists:

Little direct influence on CBF in humansNorepinephrine may cause vasodilatation when the BBB is defective.

2. 2-Agonists: As (Dexmedetomidine and Clonidine).

CBF, with analgesic and sedative effects.

3. -Agonists:

In large doses CBF.

4. -Blockers:

No effect .

5. Dopamine:

Its effect on CBF and CMR has not been defined with certainty.

Preoperative evaluationIndication of awake craniotomy1. Anatomical indications:

Lesions in or adjacent to motor or speech area. as cortical stimulation allows accurate planning of the resection margin.

2. Physiological indications:

Stimulation of deep brain nuclei in treatment of intractable movement disorders such as parkinsons disease and dystonias.

Accurate location of the stimulating electrodes can most be confirmed in awake patient.

3. Pharmacological indications:

To avoid drugs used in GA, as in awake patients, it allows better electrocoricography results that make the resection margins safe.13Contraindications of Awake craniotomy1. Patient refusal.2. Inability to communicate .3. Low occipital tumors.4. Significant dural invasion.5. Pediatric patients with insufficient understanding and ability to cooperate. 6. Significant psychiatric illness.7. Medical conditions that would prevent lying still for several hours.8. Medical conditions that would compromise the patients ability to lie sedated for prolonged periods without developing hypoxemia or hypercarbia.9. Inexperienced neurosurgeon is absolute contraindication.

2. (Decreased level of consciousness, Profound confusion, Mental retardation, Severe language barrier, Emotional instability.)

4. as severe pain may occur on resection of the tumor dural portion.

7. rheumatological or movement disorders.

8. morbid obesity or severe obstructive pulmonary disease.

14Preoperative psychological preparation:

Psychological preparation is one of the most crucial aspects of operating on patients under local anesthesia. the patient has to be reassured that the awake part of the procedure will be painless.

Laboratory evaluation

Special attention to therapeutic levels of antiepileptic drugs as it doubles after surgery.

Airway evaluation:

Conversion from local anethesia to GA can occur at any moment.

because of its short-acting effect. Some authors recently discouraged benzodiazepine administration before awake craniotomy because these types of drugs may reduce pharyngeal muscular tone, influence cognitive function, and minimize epileptic foci.

Opioid administration and dura mater or cerebral vessels traction may induce intractable nausea and vomiting. Vomiting is extremely dangerous during surgery due to risk of aspiration

It induces mild sedation, hemodynamic stability due to blunting of the adrenergic response, as well as analgesic and antiemetic effect.

. Antisalivation effect but it may be troublesome for awake patients.

15Premedication:

1. Seditives:

Midazolam is the best benzodiazepine for awake craniotomies.

2. Antiemetics and Antacids.

3. 2-Agonists:

Analgesic and sedetive effect with blunting of adrenergic response.

4. Anticholinergics:

Antisalivation effect may be troublesome for some patients.

5. Anticonvulsants.

6. Dexamethasone:

To decrease possible brain edema.

7. Antibiotics.

Seditives

Negative effects as (respiratory depression , paradoxical agitation , interfere with ECoG , minimize epileptic foci)

Clonidine is a good alternative.

2. Opiod and dural traction nausea and vomiting risk of aspiration, rise in ICP16Intraoperative managementI. Preparation of the operating room.

II. Positioning.

III. Scalp Block:

6 Scalp nerves should be blocked + Wound infiltration + Dural block

A. Timing and duration: done at least 20 minutes prior to skin incision, lasts for 3-4 hours. B. Technique: A scalp block is performed using approximately 2.5 to 5 ml bupivacaine 0.25% to 0.5% with epinephrine 1: 200.000 at each site. Injection is performed with a 1.25 inch 25 gauge needle.

As with any awake technique, delays and technical problems in the operating theatre should be avoided. Staff should be aware of the presence of an awake patient, all devices and medications should be ready.

It is usually prefered to allow the patients to position themselves on the operating table before institution of sedation or anesthesia so that they may lie in the most comfortable position.

17I. Scalp Nerves block1. Supraorbital Nerve Block:

Blocked with 2 ml of local

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