Psychiatric Drugs and Anesthesia


T. Peck, A. Wong, E. Norman. Anaesthetic implications of psychoactive drugs. Continuing Education in Anesthesia. Crit Care Pain, 10 (2010), pp. 177–181

Summary of perioperative advice for patients taking psychotropic drugs

Drug group Examples of drug Perioperative concerns Withdrawal symptoms Preoperative discontinuation recommendations
TCAs Amitriptyline, imipramine, dosulepin Muscarinic, histaminergic, and α-adrenergic blocking effect Yes Discontinue
SSRIs Venlafaxine, fluoxetine Anti-cholinergic effect Yes Can continue
Avoid serotonin crisis precipitants
MAOIs Phenelzine, moclobemide Avoid indirect-acting sympathomimetics Yes Irreversible MAOI—discontinue 2 weeks before surgery
Avoid serotonin crisis precipitants Reversible MAOI—discontinue on day of surgery
Mood stabilizers Lithium Prolongation of NMB drugs No Discontinue 24 h before surgery
Reduction in anaesthetic agent requirements
Avoid NSAIDs
Carbamazepine Inducer of cytochrome P450 system No Can continue
Valproate Interferes with platelet function No Can continue
Typical antipsychotics Prochlorperazine, chlorpromazine Cholinergic, α1-adrenergic, and histaminergic blocking effect Yes Can continue
Caution desflurane
Atypical antipsychotics Quatiepine, risperidone α1-adrenergic blocking effect Yes Can continue
BDZs Lorazepam, temazepam Sedative Yes Can continue



The Awake Craniotomy

Notes from Gupta/Gelb ch 20 “Perioperative Management of Awake Craniotomy” and Oxford Handbook of Anesthesia



-Tumor or lesion near eloquent areas of brain

-steroetactic and DBS for Parkinson’s

-epilepsy surgery



-either local + sedation, or GA with i/o wake up, or combination of sedation + awake



-good rapport with patient essential

-determine if patient will tolerate, mentally, lying flat for long period (especially challenging in children)

-obesity, reflux and highly vascular tumors may also caution against


Cortical Mapping

-Cortical mapping = electrical stim to recognize sensitive areas, can ID motor, sensory, speech

-despite mapping, many surgeons prefer fully awake to ensure no neurodeficits post op

-intraop ECoG (electrocorticography) may be used to ID epileptogenic focus


I/O Management

-routine a-line, foley (if long)

-positioning in comfort is key, head best positioned with 3 pin fixator under local (minimize movement, max airway control)

-always have access to airway

-Multiple techniques: local, local + sedation, asleep awake asleep with GA and I/O wake up  (for more complex/extensive)

-Skin, scalp, pericranium and periosteum of skull –> extensive sensory innervation; use field block or scalp block (see prior post).  Dura has extensive innervation, so anesthestize nerve trunk near middle meningeal and edges of cranium (see scalp block post).

-Precedex and Remi, both good choices for short-acting pain control and sedation without profound respiratory depression (especially precedex).

-Anti-emetics important –> especially for temporal lobe epilepsy surgery –> highly emotogenic.


Airway Control

-many techniques, from spon vent without devices to ETT and LMA.

-Risk of coughing during removal of LMA or ETT when dura open!

-ETT/LMA allow more precise monitroing of ETCO2

-Can be difficult to reintubate, and ETT makes assessing verbal responses difficult/impossible

-Alternative: Soft nosopharyngeal airway (with 25% cocaine paste as per Gupta/Gelb), can remain in place throughout procedure and monitor ETCO2, oxygen through other nostril. Risky in obese patients.


I/O Problems

– Uncooperative patient, cardiovascular (htn, hypotension, tachy), excessive sedation–>increased PaCO2–>Edema, resp depression, loss of airway, brain swelling, seizures(tx with propofol 20-40mg, or iced saline spray to cortex), pain, Local toxicity

-Patients with mass effect tumors -> most at risk for PaCO2 related brain swelling


Scalp Blocks

From Pinosky ML, Fishman RL, Reeves St et al. the effect of bupivacaine skull block on the hemodynamic response to craniotomy. Anesth Analg 1996; 83:1256-1261.

After induction of anesthesia, baseline hemodynamic variables were recorded and the skull block was performed 5 min before head pinning. The supraorbital and supratrochlear nerves were blocked with 2 mL of solution as they emerged from the orbit with a 23-gauge needle introduced above the eyebrow perpendicular to the skin. The auriculotemporal nerves were blocked bilaterally with 5 mL of solution injected 1.5 cm anterior to the ear at the level of the tragus; the needle was introduced perpendicular to the skin and infiltration was made deep to the fascia and superficially as the needle was withdrawn. The postauricular branches of the greater auricular nerves were blocked with 2 mL of solution between skin and bone, 1.5 cm posterior to the ear at the level of the tragus (Figure 1). The greater, lesser, and third occipital nerves were blocked with 5 mL of solution using a 22-gauge spinal needle, with infiltration along the superior nuchal line, approximately halfway between the occipital protuberance and the mastoid process (Figure 2).

scalp blocks - AA1996
Suprorbital foramen is palpable just medial to mid-eyebrow, the supratrocheal foramen is not often palpable, instead find supraorbital and go 1cm medial.

scalp blocks - AA1996_FIG2


Skull dermatomes
Skull dermatomes

Anesthesia for Epilepsy Surgery


Background and Pathophys

  • 0.5% to 1% of general pop
  • recurrent seizure activity
  • 30% of patients have no relief from meds –> surgery
  • Altered regulation of electric activity, symptom of underlying process/disease
    • interictal spikes on eeg
    • impaired GABA inhibition, altered neurotransmitters
  • Generalized = both hemispheres, get LOC; Partial  = one area of brain, no impair consc.; Complex partial = one area then spreads and lose consc., most common, includes temporal lobe epilepsy

Surgery for patients with severe medication related side effects, TLE is most response to surgery

Pre-Op Assessment

  • Get drug levels, assess for side effects from meds (see table)
  • c/w anti-epileptics periop, giving benzos is acceptable most times but check with surgeon for plan


  • communicate to surgeon regarding recording cerebral activity, activating epileptic focus and cortical mapping
  • Electorcorticography (ECoG) = grid electrode over cortex, map foci of epilepsy
    • GA with techniques to minimize effect on ecog

Anesthesia effects on Electrophysiology of Brain

  • Dose related! in general, low dose = proconvulsant, high dose = anticonvulsant
  • Thiopental is anticonvulsant
  • Methohexital and Etomidate = proconvulsant; used to activate foci
  • Propofol
    • activate EEG in temporal lobe epilepsy
    • can produce seizures and opisthotonos in non-epileptic patients
    • dose dependent ==> activates EEG in low dose, burst suppression (anticonvulsant) in higher clincal dose
  • Diazepam / Benzos : anticonvulsant
  • Inhalationals: low-dose iso is best, isoelectric at 2 MAC, sevo and des similiar
    • high dose enflurane + elevated paCO2 =  seizures!
  • Nitrous: dose dependent changes in EEG, high % = anti-convulsant

Typical Plan:

  • GA + surgical needs, consider similar to craniotomy
  • Volatile + short opioid good choice to minimize epileptic activity
  • prop + remi not studied well on ECoG
  • Scalp block + opioid/N2O + precedex
  • To provoke a seizure for surgery use small dose:
    • methohexital
    • thiopental
    • propofol
    • alfentanil

I/O seizures that are not provoked on purpose –> look for HTN, Tachy, increased ETCO2

  • deepen and bolus prop

Be a bloke, don’t provoke:

  • avoid aforementioned proconvusl drugs
  • light anesth and hypoxemia is bad, co2 normal range
  • Metabolic: low sugarl, calcium or Mag, any out of whack Na, uremia
  • Hematomas and hx of poor controlled epilepsy (duh)


  • Neurosurg ICU to monitor for and minimize risk of p/o seizures

The Back of the Brain

The Three Sphinxes of Bikini – Dali

Notes from ch 18, Gupta/Gelb, Anesthesia for posterior fossa lesions:

Posterior Fossa –> master controller of CV and respiratory fx


  • tumors most common, 60% of all kid tumors
  • adults: acoustic neuroma, mets (lung/breast), meningioma, hemangioblastoma
    • heamngioblastoma can be a/w occult pheochromocytoma
  • Acoutstic neuroma -> CN 8, small via retromastoid, large lesions via suboccipital, goal to preserve cocholear and facial nerve fx
  • Chiari
    • type 1 = cerebellar tonsils in cervical spine canal (teens)
    • type 2 = inferior vermis herniates through foramen magnum
    • lower cranial nerve dysfx => stridor, resp distress, dysphagia, aspiration
  • Trigeminal neuralgia (tic douloureux) – small vessles wraps nerve ->neuralgia

Pre-Op Eval

  • assess for raised ICP
  • more sensitive to sedatives and analgesic


  • prone, semiprone, park bench, sitting



  • a line for bp, cpp and paCO2
  • vae is increaed in spontaneous respiration, and hypercapnia, but some argue brainstem manipulation seen better with spontaneous ventilation

Induction and maintenance

  • dealer’s choice
  • adapt according to neuromonitoring needs


  • bradycardia 2/2 brainstem stimulus
  • tx: glycopyrrolate, atropine, ephedrine
  • severe htn from cranial nerve manipulation


  • neuro exam awakening
  • leak test if prone
  • avoid htn p/o as increases edema and p/o hemorrhage
  • incision local reduces need for p/o opiates

Venous Air Embolism

Pathophys: elevated pulmonary vascular pressure -> gas x impair, hypox, hypercap but decrease ETCO2, bronchoconstrict; hemodynamic instability–> MI/CHF/CV Collapse

PFO (25% in adults and tt echo is <50% sensitive, TCD similar

Monitor: precordial doppler 0.25ml air detection; TEE controversial/over the top/side effects from prolonged use, petco2 also decreases

Pre-Op: make sure CVC is 2cm below junction of svc and atrium, with single orifice catheter 3cm above (cxr, biphasic p wave), talk to surgeon in time out

  • Prevent
    • decrease head to heart to surgery gradient
    • normovolemia to hypervolemia
    • apply bone wax
    • avoid PEEP as it increases RA pressure and potentiates risk for PAE)
  • Treatment 
    • stop N2O, give 100% O2
    • compress jugulars
    • aspirate through CVC
    • supportive measures (fluids, pressors, inotropes)

Supratentorial Anesthesia

Anesthesia for Supratentorial Surgery, from Gupta et al, Essentials of neuroanesthesia and neurointensive care, ch 16

Overall Goals
-maintain cpp
-smooth induction and emergence
-immobility and relaxed brain

-60% primary tumors, gliomas most
-benign to GBM
-Glial tumors disrupt BBB
-autoregulation impaired
-htn can worsen blood flow and cause bleeding
-edema responds to steroids
-meningiomas grow slow and vascular, often require multiple operations and embolization
-secondary neoplasms (35%), from lung (50%) adn breast (10%)
local spread from sinus/ear, commin in DM, right-to-left shunts, and IVDA

Patient presentation
-most slow, large, adaptable: patient present with ICP increase, seizures, focal deficits

Surgical Notes
-stereotactic or mini-craniotomy
-debulking usually pterional (through temporal and parietal lobes) or frontral (biftornal crani for bifrontral and midline lesions)
-bone flap held if swollen brain

-note potential for changes in icp, location and access to lesion
-assume raised ICP
-document neurological signs and preop GCS
-c/w anticonvulsants and steroids
-benzo ok for anxiety

-smooth induction/emergence
-hemodynamic stability (hemorrhage vs. ischaemia)
-relaxed brain
-rapid emergence

-smooth IV
-blunt response to DL with bolus induction, short acting opiod or beta blocker, IV lidocaine
-think about set up for doppler, ssep, emg, bis, a line, central line etc.
-Pins, stimulating: blunt response as per DL, consider scalp blocks

-neutral head, elevated 15-30 degree ead good to decrease ICP
-PEEP can increase ICP, but less than 10 is ok and maintains CPP and ICP

-dealers choice if neuromonitoring not an issue, but opiods should be short acting (remi, alfentanil) essential for rapid emergence
-keep muscle relaxed unless cannot d/t monitoring
-normocapnia, normothermia

Fluid management
-glucose free iso-osmolar crystalloid and colloid to prevent hypoosmolality leading to edema
-no glucose (unless needed for metabolic disorder) as gluocse–>ischamia and edema
-no need for “tight” glycemic control

I/O complications
-hemorrhage, edema, air embolism
-goal hct 30, give blood
-thromboplastin release –> DIC, give factors early
-aggressive management of cerebral edema

Cerebral edema management
-check venous head drainage
-reduce CMRO2: deepen, bolu IV induction agents or lidocaine
-Reduce fluid volume: mannitol, hypertonic saline, lasix
-drain CSF
-consider hypocapnia (short acting for only 6 hrs)
-consider anticonvulsants
-icu usually
-preop GCS >12 = extubate
-tx htn, but no vasodilators as they can increase ICP (think bb esmolol, labetolol)
-tx pain p/o, think long acting and adjuncts (apap)