ICSOL and Posterior Fossa Tumor

Anaesthesia for Remote Location

Kypho-scoliosis
Anaesthetic concern for Intracranial Aneurysm
Depth of Anaethsia
Drugs for Emergency
Neuromonitoring
 Dr Kiran Lata Kiro
Associate Professor
Neuro-anaesthesia Division, Dept of Anaesthesia and Intensive Care
GIPMER, New Delhi
▪ Content of supratentorium- The Cerbral cortex
and Diencephalon

▪ Contents of Infratentorium- Cerebellum and

Brain stem
▪ Vital respiratory and cardiac centres in
medulla
▪ Cranial Nerve- 3rd to 12th
Supratentorial compartment Infratentorial compartment

▪ Lesions -Space occupying lesions (SOL), ▪ Lesions -SOL, vascular abnormalities,

vascular abnormalities, and epileptic Cranial Nerve schwannomas/ vascular
lesions compressions, CSF lesions
▪ SOL-Neoplastic/ non-neoplastic, 60% ▪ 60% of I/C neoplasms of children are
primary brain tumors, MC are gliomas; infratentorial
followed by meningiomas and pituitary
▪ Adults neoplasms are less frequent
tumors
(acoustic neuromas, metastasis,
▪ 35% are secondary neoplasms (lung - meningiomas, hemangioblastomas)
50% and breast -10%).
▪ Other lesions- hematomas, cystic
lesions, CSF collections, and brain
abscesses.
▪ Supratentorial lesions –slow growing tumors allowing adaptive mechanisms to
establish (very large before becoming symptomatic)

▪ Gliomas frequently associated with large areas of edema, particularly around fast
growing tumors. This edema can persist or even rebound after surgical excision of
the tumor

▪ Posterior fossa being a limited & compact space, symptoms set in early with frequent
association of raised ICP, Association of LCr N involvement is frequent with brain
stem lesion

▪ Generalized Symptoms- Raised ICP (headaches, nausea, vomiting, ataxia, visual

disturbances, and cognitive disturbances) often insidious in onset, Focal symptoms
(effects on adjacent functional areas); New onset of seizures in adults (first sign)
▪ Maintain CPP,

▪ Avoid secondary systemic insults (maintain the systemic milieu of the body),

▪ Provide a slack brain,

▪ Institute neuroprotective strategies, and

▪ To facilitate early awakening.

▪ 55 yr old 70 kg male patient presented with c/o
Headache -2 months,

▪ Behavioral disturbance- 1 and half months and GTCS

seizures 3 episodes in last 7 days.

▪ No significant past medical or family history

▪ ASA physical status-I

▪ Diagnosis- Left Frontal Lobe SOL

▪ Surgery proposed- Frontal Craniotomy and tumor

decompression
▪ Assessment of general condition; cardiac and respiratory systems, comorbidities
(diabetes, renal impairment, hematology,and allergies), Malignancy, Airway
assessment.
▪ Medications for CVS, respiratory, GI, endocrine, anticonvulsants, and steroids
▪ Neurosurgical lesion specific assessment –

o Assessment of neurological status- Level of consciousness, GCS, signs of raised ICP,

specific focal neurological signs; seizures, deficits (hemiparesis)

▪ Laboratory- Routine blood work- Hemogram, blood glucose level, liver and kidney
function tests, ECG, C Xray. (Additional investigation depending upon comorbidity)

▪ Radio Image studies-lesion size, edema, vascularity, venous sinus involvement,

hydrocephalus,
▪ Standard preop fasting orders and stress ulcer prophylaxis

▪ Premedication- Avoid sedation in Low GCS, poor preop neurological status, antiseizure

prophylaxis, and dexamethasone to continue.

▪ Arrange crossmatched blood (2 to 4 units),if excessive blood loss is anticipated

▪ Monitoring- ECG, SPO2, BP, ETCO2, temeperature, Input/Output charting, BIS, PPV

Additional- Invasive arterial BP, Blood Gas Analysis, CVP (vascular lesions, cardiac
comorbidity),

▪ IV Access- 2 wide bore peripheral venous access (18 & 16G) , Central venous access

(optional)
▪ Induction of Anesthesia - Thiopnetone/ Propofol, Opioid- fentanyl 2mcg/kg, NMBD-
rocuronium/ vecuronium/ cisatracurium
▪ Maintenance of Anaesthesia –

o TIVA & Inhalational both are in use

o Isoflurane/ sevoflurane (MAC of 0.8–1 )or total intravenous anesthesia (TIVA):

propofol @ 100–150 μg/kg/min

o Continuous Infusion intermediate acting NMBD along with intermittent boluses

fentanyl

o CMV- FiO2 50% oxygen in air/ oxygen with nitrous oxide

▪ Antibiotic- Ceftriaoxone 20mg/kg, Brain edema- Dexamethasone (4-8mg), Seizure

prophylaxis- phenytoin 15mg/kg (slow IV)

▪ Brain relaxation- Mannitol (0.5 to 1.0 g/kg)/ hypertonic saline solutions (3 mL/kg 3%

NaCl) / Furosemide (10 to 20 mg),

Intravenous fluids-

▪ Crystalloids (normal saline with lactated ringers solution).

▪ Avoid hypotonic and dextrose-containing solutions.

▪ Blood and blood products (when required)

▪ Prevent Sympathetic surge and hypertensive response to laryngoscopy, pin fixation

(deepen plane of anaesthesia, bolus of fentanyl/ esmolol, pin site skin infiltration)

▪ DVT prophylaxis- Elastic stockings or sequential pneumatic compression devices

▪ Warm air blankets to prevent hypothermia

▪ Maintain euglycemia (80/150mg%)

▪ Position- supine with head tilt away from surgical site

Prevent extreme head rotation and neck flexion (obstruct internal jugular veins and
affect venous drainage)
▪ Intraoperative tense brain

▪ Risk of massive blood loss leading to coagulopathy

▪ Risk of hemodynamic instability following large fluid shift and blood loss

▪ Risk of venous air embolism

UNDERSTANDING “TENSE BRAIN” ( ICP)
▪ Cerebral blood flow (CBF) = Cerebral perfusion pressure (CPP)/ Cerebral Vascular

Resistance (CVR)

▪ Therefore, factors influencing either CPP or CVR may affect CBF.

▪ CPP = MAP – ICP

▪ Therefore factors affecting MAP or ICP may affect CPP

▪ MAP affected by CO and SVR and fluctuations of preload, cardiac contractility and

vasomotor tone.

▪ ICP is determined by the relative volumes of the contents of the skull: the brain

parenchyma (85%), blood (5%), and CSF (10%)- Monroe Kellie Docterine
▪ The supratentorial compartment follows the Monro–Kellie doctrine

▪ Increase in the volume of one component of cranium will lead to a rise in ICP unless matched
by an equal reduction in the volume of another.
▪ Contribution of various components to I/C hypertension-
▪ Brain parenchyma- accumulation of water- intracellular/ extracellular
▪ Cerebral blood volume- Mismatch between arterial inflow & outflow,
▪ Reduced absorption of CSF in the arachnoid villi or obstruction of CSF flow
Effect of Cerebral Blood Volume-
▪ Mismatch between inflow of arterial
blood and outflow of venous blood
▪ Venous obstruction which reduces
venous outflow - sinus thrombosis,
extreme neck flexion, right heart strain, a
pulmonary embolus and high PEEP.
▪ An increase in arterial inflow- loss of
autoregulation, hypoxia, cortical
spreading depolarizations and seizures.
MANAGEMENT OF INTRAOPERATIVE TENSE BRAIN
▪ Head-up position (15-30degree)

▪ Optimize oxygenation,

▪ Reduce oxygen metabolism: deepen anesthesia, bolus intravenous anesthetic agents,

▪ Hyperventilation to decrease CO2 (temporal measure)

▪ Repeat a bolus of cerebral decongestants: mannitol

▪ Switch over from inhalational to intravenous anesthetic agents

▪ Ventriculostomy and cerebrospinal fluid drainage

Reversal or elective mechanical ventilation
▪ Most patients can be extubated with controlled intraoperative management

▪ Massive intraoperative blood loss and hemodynamic instability- May require

mechanical ventilation

Postoperative analgesia
▪ Paracetamol

▪ Fentanyl may be added if required

▪ Pain and PONV.

▪ Abnormal coagulation profile following major blood loss.

▪ Hemodynamic instability

▪ Pneumocephalus.

▪ Seizures
▪ 45 yr old 65 kg female patient presented with c/o
Headache- 1year,
▪ Giddiness & vertigo- 6 months and

▪ Tintius-3months.

▪ No significant past medical or family history

▪ ASA physical status-I, 7 & 8 Cr Nerve involvement

▪ Diagnosis- R CP Angle Schwannoma

▪ Surgery proposed- Craniotomy and tumor

decompression in sitting Position
▪ General medical assessment, medications- same as supratentorial lesions.

▪ Neurosurgical lesion specific assessment-

o Signs of raised intracranial pressure- Altered state of consciousness; Nausea and

vomiting; Papilloedema; seizures

o Signs of brainstem dysfunction - Altered respiratory pattern; Sleep apnea, arrhythmias

o Signs of cranial nerve dysfunction- Dysphagia ; Absent gag reflex; Changes in

phonation

o Signs of cerebellar dysfunction -Ataxia; Dysmetria

▪ Laboratory Investigations- same as supratentorial lesions

▪ Neuroimaging- lesion size, edema, vascularity, brain stem compression, venous

sinus involvement, hydrocephalus, uncal herniation

▪ Echocardiography to rule out PFO in patients undergoing sitting craniotomies

▪ Preoperative fasting and premedication orders - standard neurosurgical procedure

▪ Monitoring- ECG, SPO2, BP, ETCO2, temeperature, Input/Output charting, BIS, PPV, IBP,

ABGs

▪ Additional Monitoring- CVP, TEE or precordial Doppler, cranial nerve monitoring

(electromyography [EMG]), brain stem auditory evoked responses (BAER),

▪ IV Access- 2 wide bore peripheral venous access (18 & 16G) venous access, Central

venous access (essential)

▪ Arrange Phenylephrine, Nor Epinehrine, Epinephrine, Dopamine, additional infusion

pumps

▪ Postoperative ventilation consent for possible L Cr Nerve involvement/ injury, injury to

brain stem
▪ Anesthesia-No specific anaesthesia technique has been identified as superior and

management protocol similar to any standard neurosurgical procedure

▪ CMV- FiO2 50% oxygen in air, preferably avoid Nitrous oxide in sitting craniotomies

▪ EMG for facial nerve/lower cranial nerves: Infusions of propofol (75–150 μg/kg) with

inhalational agent (0.8–1 MAC sevo/iso/desflu ), avoid muscle relaxants

▪ Antibiotic; Dexamethasone;, Seizure prophylaxis; Prevent Sympathetic surge

▪ Brain relaxation- Diuretic therapy to be avoided in sitting position craniotomy unless

asked by neurosurgeon, (Avoid osmotic diuretics)

▪ Venous air embolism prophylaxis, DVT prophylaxis; Prevent hypothermia; euglycemia;

Intravenous fluids-

▪ Crystalloids (normal saline with lactated ringers solution) to maintain euvolemia or

hypervolemia

▪ Blood and blood products (when required) & Avoid hypotonic and dextrose-
containing solutions
PATIENT POSITIONING RELATED CONCERNS

▪ Positioning - Lateral: CP angle tumors; Prone: midline posterior fossa tumors & Sitting

- brain stem tumors and pineal gland tumors.

▪ Prevent extreme head rotation and neck flexion, neck traction in sitting and lateral

position(cervical cord injury), extreme arm abduction (brachial plexus injury),

padding of bony prominences

▪ Careful securing of ETT, antisialogouge, bite block

▪ Care to prevent abdominal and chest compression in lateral and prone position

▪ Securing foley’s catheter on thigh to prevent accidental removal and kinking in prone

and lateral position

▪ Intraoperative tense brain

▪ Dysrhythmias, hypertension, hypotension- manipulation of brainstem

▪ Risk of massive blood loss leading to coagulopathy

▪ Risk of hemodynamic instability following large fluid shift and blood loss

▪ Risk of venous air embolism

▪ Cause of VAE in posterior fossa surgery-

o Elevated position (wound higher than heart)

o Numerous non compressed venous channels

▪ Pathophysiology- Air lock causes obstruction to pulmonary blood flow, and intense

pulmonary vasoconstriction leading to a rapid increase in right ventricular afterload,

increase in right ventricular oxygen consumption, and ultimately failure.

▪ Clinical symptoms- depend on patient position, speed and dose of air entrainment

o Diffuse pulmonary wheezes, cyanosis, hypotension, arrhythmias, a mill wheel

murmur, and cardiac arrest
Four grades of intensity of venous air embolus (VAE)
Grade I Characteristic changes in Doppler sounds
Grade II Changes in the Doppler sound, fall of EtCO2 > 0.4%
Grade III Changes in Doppler sounds, fall of EtCO2
concentration, plus aspiration of air through the atrial
catheter
Grade IV Combination of above signs with arterial hypotension
over 20% and/or arrhythmia or other pathologic ECG
changes

Complications associated with VAE-

Sympathetic reflex vasoconstriction
Hypoxia due to increase in physiologic dead space
Release of endothelial/humoral mediators
Air lock Right ventricular failure
Thrombocytopenia
Cerebral ischemia/embolization
▪ Notify the surgeon & ask for flooding of surgical site/ closure of air entrainment source

▪ Stop N2O administration if used & give 100% O2

▪ Perform aspiration through a central venous line

▪ Consider compression of the jugular veins

▪ Lower the operative site

▪ Partial left lateral positioning with Trendelenburg tilt (Durant maneuver)

▪ Institution of hemodynamic support (fluids, pressors, inotropes)

▪ Hyperbaric oxygen therapy

▪ Decrease the gradient between the heart and the site of surgery

▪ Maintain normovolemia to hypervolemia

▪ Apply bone wax during surgery

▪ Vigilant moniotoring
▪ The aim should be early awakening to allow evaluation of neurological function

whenever preoperative neurological status and intraoperative course permit.

▪ Extubation: Patients with stable hemodynamics and preserved Cr nerve functions.

▪ Elective ventilation: Patients with lower Cr N palsy, prolonged surgery, massive

blood loss, and hypothermia.

▪ Level of consciousness

▪ Airway and gag reflex

▪ Edema of Face, tongue, airway

▪ Respiratory pattern (respiratory rate, tidal volume)

▪ Stable vital parameters (blood pressure, pulse oximetry, core temperature)

▪ Absence of residual neuromuscular blockade

▪ Analgesia-Injection paracetamol, with intermittent boluses of fentanyl

▪ Postoperative concerns-

▪ Long duration of Mechanical ventilation, lower cranial nerve dysfunction leading to

aspiration, exposure keratitis (if facial nerve injury), Quadriplegia, peripheral nerve
injury

▪ Posterior fossa syndrome- Cerebellar mutism and absence of vocalization following

midline posterior fossa tumor surgery

▪ Preoperative assessment in neurosurgical patient extends beyond the patient’s past

medical history.

▪ Anaesthesia technique, patient positioning is influenced by the site, size and

vascularity of the intracranial lesion.

▪ Knowledge of the functional anatomy, encountered complications, pathophysiology of

raised intracranial pressure is essential for successful patient outcome.

▪ A Practical Approach to Neuroanesthesia- Mongan, Paul D.; Soriano III, Sulpicio G.;
Sloan, Tod B
▪ Essentials of Neuroanesthesia by Hemanshu Prabhakar
▪ Cottrell and Patel’s Neuroanesthesia 6th edition by James Cotrell and Piyush Patel
Anaesthesia For
Remote Locations
Amit Kohli
Associate professor, MAMC
New Delhi
APPEC-21, 11-02-2021
Scanning 10 years Q Papers …………
How to answer (Layout):

• What is NORA
• Anesthetic concerns (three step approach)
• PAC
• Monitoring: ASA Standards
• Choice of anesthetic techniques (pros and cons)
• Medications
• Complications and brief management
 NORA
• Nonoperating room anesthesia (NORA) refers to anesthesia
that is provided at any location remote from the traditional
operating room.
• These locations include radiology departments, endoscopy
suites, magnetic resonance imaging (MRI), and computerized
tomography (CT) scanners.
Remote Location??
 Royal College of Anaesthetists:
Definition
any location at which
• An anaesthetist is required to provide general / regional
anaesthesia or sedation away from the main theatre suite
• It cannot be guaranteed that the help of another
anaesthetist will be available.
 AIMS
• Safety of patient
• Standards of care and patient monitoring are the same
regardless of location
• Minimise physical discomfort and pain
• Control anxiety, minimise psychological trauma and maximise
the potential for amnesia.
• Control movement to allow safe completion of procedure
• Return the patient to a state in which safe discharge from
medical supervision is possible
 Pre-anaesthesia check-up
• History
• GPE
• Investigations
• Anaesthesia specific examination- Airway, IV access, Spine.
• Drugs
• NPO status.
• Informed Consent
 Transport of patients
 Should be accompanied by an anesthetist, who evaluates, monitors,
and supports the patient's medical condition.
 Patients maybe on mechanical ventilation and drug infusions for
both sedation and hemodynamic support.
 Portable ventilators -useful for transport which are often oxygen-
powered & adequate supplies of oxygen must be available for
transfer and a AMBU bag to allow hand ventilation in the event of
ventilator failure.
 Ensure infusion pumps and portable monitors have adequate
battery power.
 Spare anesthetic and emergency drugs, equipment for
intubation or reintubation, portable suction, portable
defibrillator.
 Notify persons in the destination area that the patient is
in transit so appropriate preparations to receive the
patient can be made in advance.
 Send personnel ahead to secure the elevators to prevent
delays during transfer.
 Three step approach

A three-step paradigm for nonoperating room anesthesia

 Patient Factors
Children ,especially less than 10 years
Elderly (above 50 years) and in the case of
gastroenterologic, cardiology, and radiologic procedures, of
higher ASA physical status
Claustrophobia, anxiety, panic disorders
Seizures, movement disorders or muscular contractures
Pain, related to procedure or other causes
Acute trauma with unstable CVS, respiratory or neurologic
dysfunction
Significant comorbidity and patient fraility
 Special Problems
Limited working place, limited access to the patient
Electrical interference with monitors and phones, lighting
and temperature inadequacy,
Use of outdated ,old equipment
Less familiar with the management of patients
 Lack of skilled personnel, drugs and supplies
 Procedures
Radiologic imaging- CT/MRI/PET
Interventional Radiology- Vascular imaging, stenting,
embolization, RFA, TIPS
Interventional Cardiology- cardiac catheterisation, PCI,
CAD placement
Interventional Gastroenterology- Endoscopy, ERCP,
Colonoscopy
Psychiatry- ECT
 Environment
• Occupational exposure- Ionising radiation and radiation
safety issues-
- Limiting time of exposure
- Increasing distance from source of radiation
- Using protective shielding ( lead lined
garments, fixed and movable shields)
- Using dosimeters
• Allergic Reactions-Radiologic and MRI contrast agents
• Radiologic agents- Iodinated and Gastrografin contrast - in
CT
• MRI agents- (Gadolinium,iron,manganese-ionic & nonionic)
• Adverse effects- Renal and Hypersensitivity
 Incidence of contrast related adverse
reactions
ADVERSE REACTIONS HIGH-OSMOLARITY LOW-OSMOLARITY
CONTRAST MEDIA (%) CONTRAST MEDIA (%)

Nausea and vomiting 6.0 1.0

Urticaria 6.0 0.5

Hoarseness,sneezing,cough,dyspnea, facial 2.6 0.5

edema
GADOLINIUM CHELATES MILD MODERATE SEVERE

Hypotension 0.1 0.01

Incidence 2 .1 .01
• Pretreatment - oral methylprednisolone prior to intravenous
administration .
• Discontinuing the causative agent.
• O2
• Epinephrine – IM .3-.5mg (1:1,000) x 15-20 min
• IV .1mg (1:10,000) over 5min
• or IV infusion 1-4µg/min
• Aggressive fluid therapy
• Antihistamines – diphenhydramine 25-50 mg IV
• H2 blockers – cimetidine
• Inhaled β agonists for bronchhospasm
• High dose IV corticosteroids
• Atropine
• Glucagon 1-2mg IM/IV x 5 min
Circulation. 2010;112:IV-143-IV-145
 ASA standards for NORA
• Oxygen- Reliable source with backup
• Suction source- Adequate and reliable
• Adequate monitors
• Sufficient safe electrical outlets
• Sufficient space and easy access to patient, machine and
monitoring equipment
• Anaesthesia equipment- Anaesthesia machine & Adequate
drugs
 ASA standards for NORA
• Resuscitation equipment- defibrillator, emergency drugs and
equipment
• Adequate illumination- Patient, machine & battery-powered
backup
• Trained staff for reliable communication
• Postanaesthesia care facilities- staff, safe transport to
main PACU
• Scavenging system
 Monitoring
• Anaesthesia personnel (Standard I)
• Continuous display of ECG ( Standard II)
• NIBP-minimum 5 minutes interval
• Pulse oximetry
• Continuous end-tidal carbon dioxide monitoring
• Mechanical ventilation- disconnection alarm
• Oxygen concentration of inspired gas with low concentration
alarm
 Facilities And Equipment
• Gas pipeline, suction, gas cylinder supply for anaesthesia
machine
• Anaesthesia machine- Essential safety features
• Must be familiar with machine operation
• Must perform machine checks before starting
• Equipments for resuscitation
 Medications
Anaesthesia techniques used in NORA locations:
• No anaesthesia or minimal, moderate or deep
sedation/analgesia- General anaesthesia
Anaesthesia care depends upon:
• Desired level of anaesthesia
• Underlying medical condition of patient
• Procedure to be performed
 Anesthesia Sedation or Analgesia
Maintenance Maintenance
Loading Dose Infusion Loading Dose Infusion Elimination half
Drug (µg/kg) (µg/kg/min) (µg/kg) (µg/kg/min) life
Alfentanil 50–150 0.5–3 10–25 0.25–1 4-17 min

Fentanyl 5–15 0.03–0.1 1–3 0.01–0.03 10-30 min

Sufentanil 1–5 0.01–0.05 0.1–0.5 0.005–0.01 15-20 min

Remifentanil 0.5–1.0 0.1–0.4 † 0.025–0.1 5-8 min

Ketamine 1500–2500 25–75 200–800 10–20 2.5-2.8 hr

Propofol 1000–2000 50–150 250–1000 25-75 4-7 hr

Midazolam 50–150 0.25–1 25–100 0.25–1 1.7-2.6 hr

Diazepam 300-500 100µg/kg prn 200-300 20-50 hr

Methohexital 1000–1500 50–150 250–1000 10–50 2-6 hr

Chloral hydrate 25-50mg/kg 50-75mg/kg 8-12hr-TCE

1-4 months children >4 months children 67hr-TCA
Levels Of Sedation/Analgesia
 Problem For Patient
 Too cold
 Immobility

 Noise

 Anxiety

 Claustrophobia
 Problems For Anesthetist
● Babies virtually disappear
● Unfamiliar / outdated equipments
● Isolated - support services
● No piped gases, suction
● Moving away from pt
● Difficult to resuscitate
● Radiation Hazard
● Reaction to Contrast
 Computed Tomography
Issues
• Airway management and adequate oxygenation
• Inaccessibility of patient
• Monitor disconnection and kinking of tubes
• CECT-Oral contrast- Aspiration
• Resuscitation and stabilization before shifting
 Computed Tomography
Premedication with oral chloral hydrate (50mg/kg) in children
• Oral midazolam( 0.25-0.75mg/kg) at least 30 minutes prior
• Intravenous sedation- Ketamine, propofol,dexmedetomidine
• Another technique for healthy neonates, "Wrap and scan”
 Magnetic Resonance Imaging
• Noninvasive, does not produce ionizing radiation

Hiccups of MRI
• Time consuming
• Motion- Artifacts on image
• High level acoustic noise
• Risk of thermal injury
• Effect of magnet on ferrous objects
Hence patients need anaesthesia
 Zones of MRI Suite
• Zone 1 – public zone with free access
• Zone 2 – interface between public zone and MRI suite
• Zone 3 – Ferromagnetic objects should not be allowed. MRI
personnel control movement
• Zone 4 – Scanner room
 Few indications for Anaesthesia
• Infants and Children
• Patients with Learning difficulties
• Patients with Seizures disorders
• Patients with Claustrophobia
• Critically ill patients
SL CCC - Mnemonic
 Strong Magnetic field - Hazards
• Attraction of ferromagnetic objects to the magnetic field
of an MRI
• Risk of dislodgement of implanted metallic objects
o Pacemaker
o Vascular clips AED
o Mechanical heart valves
o Implanted infusion pumps
• Orthodontic braces and dentures and tattoos can degrade
the image quality significantly
• Injury to patients, personnel and equipment
• Gas cylinders, pens, keys, laryngoscopes, scissors, needles
• Malfunctions of electronic equipment's – monitors and
infusions pumps
 Monitors
• MR compatible pulse oximeters mandatory
• Special ECG electrodes and cables are required
• Due to aortic blood flow results in artefacts in the ST-T regions
• Delay upto 20 sec in capnograph signal due to length of
sampling tube
• Need for acoustic protection during MR imaging will
necessitate the use of ear-plugs or ear defenders
 Separate Anaesthesia Workstation
• A MR compatible anaesthesia machine should be located
within scanning room
• Only MR compatible vaporisers and gas cylinders must be
used on anaesthetic machines
 ANAESTHETIC EQUIPMENT

1. Cylinder- aluminium
2. Machine- stainless steel, brass, aluminium.
3. Vapourizers- Bimetallic strip temperature
compensated vaporiser not compatible.
4. Laryngoscopes- plastic scopes with Al covered Li
batteries.
5. Stylet- copper model
6. ET tubes – spring within valve cuff may distort
images, avoid reinforced tubes.
7. Defibrillator- cathode ray tubes and batteries
malfunction in 20 G line Resuscitation carried
outside magnetic field
8. Infusion pumps may malfunction/ damaged. –
Syringe pump and 3 extension sets (this stays at the
foot of the MRI table, far from the machine)
 MRI room is for Radiologists- not
for Anaesthesiologists
• MRI suites have been designed without the considerations
for anaesthetic needs such as gas pipelines, suction
• Bulkiness of the unit
• The patients is often far from the anaesthesiologist
• Access to the airway is limited
• I/V lines, anaesthesia circuit, oxygen tubings, monitoring
cables must be of sufficient length to reach the patient
deep within the scanner
 MRI – Pre-procedural preparation
• Complete history and examination (esp Airway)
• Investigations
• Patient should be admitted in hospital
• No h/o recent URI
• Adequate NPO as per fasting guidelines
• W/I consent for anaesthesia required for procedure
• A functional i/v cannula
 Anaesthetic Concerns
 Limited patient access and visibility
 Absolute need to exclude ferromagnetic components

 Interference/malfunction of monitoring equipment

 Potential degradation of the imaging caused by the stray RF

currents from monitoring equipment and leads
 The necessity to not move the anesthetic and monitoring
equipment when the examination has started to prevent
degradation of magnetic field homogeneity
 Limited access to the MRI suite for emergency personnel in
accordance with recommended policies
 Anaesthesia technique
1) Sedation in children
Oral midazolam (0.5mg/kg, max 10mg with dextrose or IV(0.05 to 0.15
mg/kg) )
Oral choral hydrate (25-100mg/kg)
Disabled children do not need higher doses of sedatives but are more
prone at risk of hypoxia under sedation
A very safe and simple technique for newborns is the ‘feed and scan’
technique
2) Other sedative techniques
Thiopentone- oral or rectal- 3-6mg/kg
Dosing is 1-2mg/kg when applied i/v or 4-5 mg/kg when injected
i/m. onset time is 1-3 min, and duration is 15-30 min
What is this drug????
KETAMINE
 Propofol
• Propofol seems to be a perfect drug for sedation because it is
effective, has a short recovery time and can easily be titrated to the
required sedation level
• Dosing : 10-mg/kg/h or Bolus with 1-2mg/kg and maintenance 50-
150mcg/kg/min
• With ketamine then 5mg/kg/h infusion
• With midazolam
 Other Sedatives
• Dexmedetomidine: loading dose 0.7-1.0 mcg/kg for 10 min
f/b maintenance 0.2-0.7 mcg/kg/h

When Sedation, When GA??

>3 years, 10 kg, No Comorbidities – consider sedation
<3 years, <10kg, lot of co-illness-- GA
 some may sleep without drugs –
Students!!
Which sedation is better??
 Contraindications For Sedation

• Airway problems – actual/potential obstruction

• Apnoeic spells – related to brain damage / previous drug
treatment
• Respiratory distress- SpO₂ <94% with room air, respiratory
failure % inability to cough and cry
• Raised ICT – drowsiness, headache & vomiting
• Epilepsy
• Full stomach
• Severe metabolic disease
 General Anaesthesia
• DUAL STAGED PROCEDURE
• STAGE 1: Induction outside the shielded MRI room.
• STAGE 2: pt transferred into MRI room.
• It is recommended that anticipated difficult endotracheal
intubations be performed in the operating suite because of its
greater availability of skilled assistants and specialized
equipment.
• As soon as the airway is controlled, the patient can be
transported to the site of the planned procedure, should it be
necessary to perform the procedure outside the operating suite.
• INDUCTION – Thio, Propofol, Ketamine
• INTUBATION – Sch/ Vec
• MAINTAINANCE – Inhalation/Intravenous +/- Muscle
relaxant
• Extra long connections for circuits.
• After the procedure pt shifted to recovery area.
• Children should stay atleast 2hrs after scanning in the
recovery area.
 Recovery
• Once procedure has been
completed, patient should
be remove from the
scanner, and be woken up
and recovered in a suitable
recovery area
• Usually there is no need for
analgesics
• Modified Aldrete Scoring
System
 ICU patients requiring MRI
• Multiple drug infusions
• Extension of adequate length of ventilating circuit
• Higher standard of monitoring
• MR compatible monitors- MUST
• Pulmonary artery catheters with conductive wires in contact
with heart muscles- removal planned
• Many TT/ETT are not MR compatible and need to be
changed prior MRI
• During shifting to MR room – very vigilant about
cylinders/monitors or other ferromagnetic objects
What Happens If Any Ferromagnetic
Object Gets Inside The Field?
They can act as a projectile and cause injury to the patient
as well as any personnel inside the area.
 Eg: O2 cylinders, stretchers, IV poles, keys
Risk for thermal burns from various
equipment/monitors/implanted patient devices
 Eg: ECG electrodes and pulmonary artery catheters, wires,
ICDs/pacemakers, VP shunts
 Other effects--tissue damage, malfunction of the device, image
artifacts, and device displacement

 Nowadays MRI compatible (titanium made) ICDs-safe

What Happens If A Patient Suddenly
Collapses During The Procedure?
 Stop the procedure and MRI machine immediately.
 Any personnel who goes inside the area to revive patient
should not have any ferromagnetic material on them.
 Only BLS in the gantry
 Attempt to bring the patient out and provide ACLS

Requirement to quench magnet

 uses cryogenic gases to dissipate the magnetic field
 This can create a hypoxic environment if the patient is not
retrieved from the room in a timely manner
 Electroconvulsive Therapy
Physiologic response to ECT :
Generalised motor seizures ( >20 seconds) and acute
cardiovascular response ( short duration)
Anaesthetic management Goals
• Amnesia
• Airway management
• Prevention of seizure related injuries
• Control of haemodynamic responses
• Smooth, rapid emergence
 Electroconvulsive Therapy
Preoperative evaluation
• Current medications- Antidepressant medications
Anaesthesia Technique:
• Monitoring
• Pre-oxygenation
• Induction- Propofol (1-1.5mg/kg) or Etomidate
(0.15-0.30mg/kg)
• Muscle relaxation- succinylcholine (0.5-1mg/kg)
• Supplemental oxygen and bite block
 Electroconvulsive Therapy
Post ECT
• Oxygenation
• Recovery position
• Monitored till discharge criteria are met
Recording-
Patient’s condition, responses- extra precautions
can be taken during subsequent treatments
Interventional Cardiology
Anesthesia For Coronary Angiography
• PCI maybe performed as a part of the same procedure
• Usual approach- sedation/analgesia
• Commonly fentanyl & midazolam
• Supplemental O2
• GA
• Sedation failure
• Uncooperative patients
• Airway control to manage respiratory failure
• Standard monitors
 Cardiac Catheterization
• Placement of transvenous & transarterial catheters in the
heart & great vessels to allow determination of
 Cardiac anatomy
 Ventricular function
 Valvular anatomy
 Pulmonary vascular anatomy
 Pressure measurements
 Determination of flow
 Detection of shunts
• Complications
• Related to vascular access
• Catheter related
• Supraventricular & ventricular arrhythmias
• Gold standard for evaluation of complex cardiac anomalies
• For the hemodynamic & shunt calculations to be valid, a
relatively constant CVS & respiratory state is necessary
 Anesthesia For Cardiac
Catheterization

• Mild to moderate sedation/analgesia- usual approach

• Supplemental O2 as needed, careful to maintain normal ABG
values (for the patient) if pulmonary hemodynamics are to
be measured
 Anaesthetic Technique
• Sedation/GA
• Steady state must be maintained
• Even in cyanotic patients oxygen is not administered unless
saturation falls below baseline
• Sedation
• Fentanyl, midazolam, propofol, ketamine.
• GA
• Both inhalational & iv induction
• Controlled ventilation has not been found to effect diagnostic
accuracy
 Pacemaker & ICD Implantation
• Placement of transvenous leads into cardiac chambers with
tunneling of leads to a subcutaneous pocket in which the
device is placed.
• Radial arterial catheter if:
• H/O hemodynamic instability
• EF <20%
• Usual approach- sedation/analgesia
• Brief GA during device testing
 Cardioversion

 Transthoracic DC cardioversion often - used for atrial dysrhythmias

including AF and atrial flutter
 Simple cardioversion is distressing, and sedation is preferable except
in life-threatening situations.
 Complications include -thromboembolic phenomena, pulmonary edema,
aspiration pneumonitis, and bradycardia.
 Anesthesiologists provide sedation in the ICU for urgent
cardioversion in an unstable patient.
 A small bolus IV induction agent -sufficient.
 Etomidate- drug of choice .
 Propofol vs Midazolam
Propofol/remifentanil technique
• TEE done prior to cardioversion recommended to
determine whether patients are at low or high risk of
thromboembolism, takes 15 to 30 mins.
Sedation helps the patient tolerate the procedure.
• Thorough airway evaluation is important prior to TEE, and
occasionally, ET intubation may be useful.
• Before TEE, LA (4% lidocaine/20% benzocaine) is sprayed
into the oropharynx to allow easy passage of the probe.
• A bite block is inserted to prevent the patient from biting
down on the probe.
 Electrophysiologic Studies
• Programmed electrical stimulation at various locations to
reproduce arrhythmias which are then ablated with
electrical energy
• Unique problems
• Multiple catheters
• Time consuming
• Severe pain during ablation
 Anaesthesia For Electrophysiologic
Studies

• Usual approach- sedation/analgesia

• Brief periods of GA during RF ablation
 Endoscopy
Indications
• Diagnostic & Therapeutic
Issues
• Comorbidities
• Risk of GER,hepatic
dysfunction, ascites,
coagulopathy
• Local anaesthetic spray-
Abolish gag reflexaspiration
 Endoscopy
Position- Prone or semi prone
• Hypoxemia-Prevention and Management
Increasing supplemental oxygen,
nasopharyngeal airway, Airway manoeuvers
(chin lift, jaw thrust), endoscope removal,
positive pressure ventilation, LMA or ETT
insertion, if required
• Bite blocks
 Endoscopy
Anaesthesia Technique
• Fentanyl (0.5-1mcg/kg)-Propofol (1-1.5mg/kg)
Propofol infusion ( 120-150mcg/kg/min)-
Nasopharyngeal airway-Endoscope
• Dexmedetomidine infusion (0.5-1mcg/kg)
over 10 min – 0.2-0.7 mcg/kg/h
• Careful titration
 Dental Procedures
• Pediatric Dentistry- fillings, crowns, pulpotomies, tooth
extractions and space maintainers
• Oral and Maxillofacial Surgery- extractions of impacted
teeth, insertion of dental implants, treatment of infections
of the head and neck and facial cosmetics
• Peridontics- surgery of teeth, gingiva, connective tissue,
periodontal ligament and alveolar bone
• Mostly performed in the office with no sedation and only
LA.
• GA- more complicated or prolonged cases, uncooperative
patients, phobic, or mentally challenged.
• Tracheal intubation, often via the nasal route to protect the
airway with throat pack, recently the laryngeal mask airway
also used.
• Maintained with intravenous infusions / inhalation
anesthesia.
• The immediate postoperative complications include bleeding,
airway obstruction, and laryngeal spasm.
• Later complications in ambulatory patients include
drowsiness, nausea and vomiting, and pain
 IVF OT
IVF techniques include:
Ovarian stimulation and monitoring.
Ultrasound-directed oocyte retrieval or transvaginal
follicle aspiration.
Fertilization in the laboratory and transfer of embryos
back into the uterus.
Specific concerns: Coexisting illness- TB, Thyroid, renal cardiac pulmonary
diseases, pts with morbid obesity, anticoagulants,antidepressants.
 Anesthtic Technique
 Brief (20 ± 30 min) outpatient procedure.
 Short-acting anesthetic approach with minimal side effects.

 Anesthetic modalities include

 monitored anesthesia care, conscious sedation, GA, regional
anesthesia, local injection as a paracervical block (PCB), epidural
block, subarachnoid block, total intravenous anesthesia (TIVA),
patient-controlled analgesia (PCA).
 MAC, conscious sedation are the method of choice as they result in
minimum exposure to drugs.
 Drugs To Be Avoided In Ivf
Most of the anesthetic agents being used in GA have
been found in the follicular fluid. The duration of GA
should be kept minimum to avoid detrimental effects
of these drugs on oocytes.
Inhalation agents including N2O, local anesthetics,
etomidate were found to be detrimental
Indian Journal of Anaesthesia | Volume 63 | Issue 9 | September 2019
 Complications in NORA
1) Respiratory complications
Respiratory depression is more frequent during NORA
Non-vigilance, inappropriate anaesthetic technique
Non-anaesthesia staff handling a complex medical cases
Esophageal intubation during resuscitation
Unexplain bradycardia were noted to be associated with respiratory
complications
It is said that about 10% of anaesthesiologists have no backup plan for
unanticipated difficult intubation. It is crucial to be familiar with the
difficult airway algorithm and call for help early.
The most common event in NORA claims was inadequate
oxygenation/ventilation which is preventable with vigilant monitoring, using
pulse oximetry and capnography
Maddirala S, Theagrajan A. Non-operating room anaesthesia in children. Indian J Anaesth 2019;63:754-62
 2) Hypothermia
Children are vulnerable to hypothermia
Hypothermia also delays recovery and increases oxygen consumption
3) Aspiration, postoperative nausea, and vomiting (PONV)
Patients need to be fasted according to the standard guidelines
Administration of sedatives and anaesthetic agents can blunt airway
reflexes and predispose to aspiration
4) Hypovolaemia and hypoglycaemia
Prolonged fasting can predispose to dehydration, hypovolaemia, and
hypoglycaemia
Maintenance of a sufficient volume status before the procedure by
pre-hydration
slow injection of intravenous drugs can prevent adverse haemodynamic
events.

Maddirala S, Theagrajan A. Non-operating room anaesthesia in children. Indian J Anaesth 2019;63:754-62

 Take home message

• You are away from home – so be alert and ready with gadgets

• Be vigilant with sedative doses and its complications

• As airway away from us – always attentive and frequent monitoring

• key to efficient and safe NORA practice in children relies on good

PAC, thorough understanding of the anatomical and physiological
variations in Children
 Take home message

• knowledge of the unique pharmacokinetics and pharmacodynamics

of individual sedation agents

• understanding the requirements of the procedure, and efficient

team communication between the anaesthesiologist and
non-operating room personnel

• Keep your calm, improvise and be the conqueror

BEST OF LUCK
Thanks to Deepak Kumar for helping out with ppt
dramitkohli@yahoo.com
9818073402
 KYPHOSCOLIOSIS

Scoliosis: Complex deformity of the spine resulting in lateral curvature and rotation of the vertebrae
as well as a deformity of the rib cage (scoliosis Research Society)

Kyphosis: Exaggerated curvature of the thoracic region of the spine resulting in a rounded upper
back.
Kyphosis and scoliosis
 Classification

• Cervicothoracic

• Thoracic

• Thoracolumbar

• Lumbar

• Combined double primary

Classification based on etiology Associated Conditions
Idiopathic Infantile (0–3 y)
Juvenile (4–10 y)
Adolescent (>10 y)
Congenital Bony deformity
Neural tube defect

Neuromuscular Cerebral palsy

Poliomyelitis
Muscular dystrophy
Spinal muscular atrophy
Mesenchymal disorders Marfans syndrome
Ehlers-Danlos syndrome

Traumatic Postradiation
Vertebral fracture
Postthoracoplasty

Neurofibromatosis Von Recklinghausen’s disease

 Measuring the severity of the disease: the
radiographic evidence

• It is used to characterize
scoliosis.
• A Cobb angle of 10°or greater is
typically used as the cut-off for
determining scoliosis
• Disadvantage: Measures
deformity in two dimensions
 Severity of Kyphoscoliosis and its clinical correlation

• <10° No symptoms

• >25° Increase in pulmonary artery pressure

• >40° Consider surgical intervention

• >65° Significant decrease in lung volume

• >100° Dyspnea on exertion

• >120° Alveolar hypoventilation, chronic respiratory failure

Anaesthetic considerations
 Preoperative evaluation

RESPIRATORY SYSTEM

EFFECT HISTORY PHYSICAL INVESTIGATION

• Decreased compliance • Functional capacity EXAMNINATI • CXR
• Increase V/Q mismatch by exercise ON • Spirometry
• Increase dead space tolerance/ • Bed side (FEV1 &FVC
• Decrease in lung volumes • breathlessness/ pulmon- ↓
and capacities - dyspnea/ ary FEV1/FVC-N)
Restrictive Lung disease cough/ function • PFT
• Decreased ventilatory wheeze/ tests • ABG
response to CO2 • frequent chest
• Arterial hypoxemia infections
• Hypercapnia
• Respiratory failure –in
untreated patients with
severe Scoliosis
 Preoperative evaluation………

Severity of pulmonary impairment:

• Curve severity (>70)
• Number of vertebra involved (7 or more),

• Cephaled location of the curvature and

• Degree of loss in thoracic kyphosis.

 Preoperative evaluation……..

CARDIOVASCULAR SYSTEM

EFFECT HISTORY PHYSICAL INVESTIGATION

• Pulmonary vascular resistance Functional EXAMINATION • ECG
↑ status/capacity • METS • ECHO –
• Pulmonary hypertension by exercise • BHT evidence of
• Right ventricular hypertrophy tolerance/ PAH
• Mitral Valve Prolapse shortness of
• Congenital Heart disease – breath/ dyspnea
common on
• Cardiomyopathy–Duchenn’s exertion/chest
Muscular Dystrophy pain/palpitation
• Mitral/Aortic Insufficiency – /syncope/orthop
Marfan’s syndrome noea/PND
 Preoperative evaluation…….

SYSTEM EFFECT History PHYSICAL INVESTIGATIO

EAINATION N
Airway • Upper thoracic • Restricted neck Airway and neck Cervical spine
or cervical spine movements examnination x-ray
involvement – • Glossal (cervical
airway hypertrophy scoliosis)
difficulties may (Duchenn’s
be anticipated Muscular
Dystrophy)

Neurologic • Increased risk Rule out Neurological

of developing congenital causes/ assessment
spinal cord preexisting deficit
injury during
scoliosis surgery
• Medicolegal
importance
 Intraoperative Considerations

• Possible injury to integrity of neural structures

• Prone position
• Prolonged surgery
• Blood loss
• Hypothermia
• Controlled hypotension
• Risk of venous air embolism
 Concerns related to the prone position

• Accidental extubation

• Eye complications
†Corneal abrasions
†Conjunctival and periorbital oedema of the dependent eye
†Retinal ischaemia
†Postoperative visual loss because of ischaemic optic neuropathy (ION)

& central rentinal artery oclusion

• Accidental dislodgement of i.v. access and monitoring lines

 Concerns related to the prone position

• Abdominal compression

✓Leading to impaired ventilation

✓Increased bleeding from epidural plexus

✓ Decreased cardiac output

• Improper head and neck positioning leading to venous and lymphatic obstruction

• Possibility of venous air embolus

• Neuropathies
 Strategies to reduce intraoperative blood
loss
• Adequate depth of anaesthesia
• Minimize intraabdominal pressure
• Maintain normothermia
• Hypotensive anaesthesia
• Drugs- antifibrinolytics (tranexamic acid)
• Infiltration with vasoconstrictors
• Local Agents: Bone wax/Gelatin foam/Oxidized cellulose/Microcrystalline collagen/Fibrin
glue
 Autologous blood transfusion

✓Preoperative autologous blood donation

✓Acute normovolemic hemodilution
✓Intraoperative red cell salvage
 Preoperative preparation
• Complete blood count
• Platelet count
• Chest x-ray
• KFT
• Serum electrolytes
• LFT (optional)
• Coagulation profile
• ECG
• ECHO
• PFT for baseline ventilatory function
• ABG
 Preoperative Preparation…….

• Typing and cross matching of blood products

• Explanation of Wake Up test
• Instruction about incentive spirometry
• Consent - Written/ verbal/Informed
• Explanation of:
✓Post operative pulmonary complications
✓Risks of blindness
✓Paraplegia
✓Post op ventilation etc
• Postoperative ICU consent
• NPO & aspiration prophylaxis
 Anaesthetic technique

Premedication: Alprazolam night before and morning of surgery

Glycopyrolate prior to induction
Induction: Opioids (fentanyl) + intravenous induction (propofol)
Muscle relaxant (atracurium)
Avoid succinylcholine
Fiberoptic intubation if indicated
Tube selection according to surgical approach
Maintenance: O2+N2O+Sevoflurane (1 MAC) + fentanyl and atracurium infusion
SSEP/Wake up test: High dose of fentanyl, propofol infusion (TIVA)
 Monitoring

• ASA recommended minimum mandatory monitoring

(ECG, NIBP, SPO2, ETCO2, Temperature monitoring )

• Urine output monitoring

• Consider arterial line

• Consider CVP line

• Neuromuscular monitoring

• Assessment of Blood loss

• Spinal cord monitoring (neuromonitoring)

 Spinal cord monitoring

• Somatosensory evoked potentials

• Motor evoked potentials
• Wake up test
 Evoked potential monitoring
Electrophysiological techniques to assess the integrity of the spinal cord
during surgery to prevent iatrogenic injuries to cord structures

• Function of voltage over time.

• (A) latency in milliseconds from stimulus
onset and (B) peak to-peak amplitude in
microvolts.
 Somatosensory evoked potentials

Monitor functional integrity of sensory pathways of

spinal cord
• Low-intensity electrical stimulation to peripheral
nerves
• Square wave stimulus of 50-250 micro sec duration,
strength 20-50mA, stimulation rate 1-6 Hz is
commonly used
• Sites of stimulation are common peroneal nerve at
knee or posterior tibial nerve at ankle
• Response recorded over cerebral cortex or
subcortical regions using the standard EEG scalp
electrodes.
• SSEP warning criteria are a 10% increase in latency
and a 50% decrease in amplitude.
 Factors affecting somatosensory evoked
potential
Anesthetic Agents/factors Amplitude Latency
Volatile anaesthetic agents ↓ ↑
Barbiturates Minimal effect ↑
N2O ↓ ↔
Midazolam/Diazepam ↓ ↑/minimal effect
Propofol ↔/minimal effeect ↑
Dexmedetomidine ↔/minimal effect ↔/minimal effect
Opioids Minimal effect ↔
Etomidate ↑ ↑
Ketamine ↑ No effect
Hypotension ↓ ↔
Hypothermia/Hyperthermia ↓/↓ (loss of wave at 42° C) ↑/↓
Hypoxia ↓ ↑
Symbols: ↓, decrease; ↑ increase; ↔, no change
 Motor evoked potential monitoring

• Functional integrity of the corticospinal

tract (motor pathways)
• Motor gray matter neurons more
vulnerable to ischemia than axons in the
dorsal column sensory white matter
• Elicited by electrical or magnetic stimulation
of motor cortex using scalp electrodes or
stimulation of anterior columns using
epidural electrodes
• Responses recorded after motor pathway
stimulation
 Factors affecting motor evoked potential

Anesthetic Agents/factors Amplitude Latency

Volatile anaesthetic agents ↓ ↑
N20 Minimal effect Minimal effect
Barbiturates ↓ ↑
Midazolam ↓ ↑
Propofol ↓ ↑
Dexmedetomidine ↔/minimal effect ↔/minimal effect
Opioids No change No change
Etomidate ↑/no change No change
Ketamine ↑ No change
Hypotension ↓ ↔
Hypothermia/Hyperthermia ↓/↓ ↑/↓
Hypoxia ↓ ↑
 Wake Up test

To assess the integrity of spinal motor pathways

Procedure to be explained prior to surgery & induction
Technique: switch off inhalation agent and muscle relaxants
Maintain on opioids or TIVA
First ask the patient to squeeze the hand followed by leg movement
Disadvantage: one time test (not a continuous monitoring)/children/cognitive dysfunction
Complications: dislodgement of equipments/ accidental extubation/venous air
embolism/patient may fall on table/intraoperative recall etc.
 Postoperative Considerations

• Post operative analgesia

✓Opioids – infusion or intermittent boulses
✓NSAIDs
✓Epidural analgesia
✓Intrathecal opioids
• Post operative pulmonary complications
• Post operative ventilation
✓Associated comorbidities
✓Blood loss > 30 ml/kg
✓Nature & duration of surgery
• Bleeding and Coagulation abnormalities
• Post operative vision loss (POVL)
Thankyou
 Anaesthetic Concerns In
Intracranial Aneurysms
Dr Priyanka Khurana,
Assoc. Professor, Neuroanaesthesia Unit,
Deptt of Anaesthesiology and Intensive Care,
GB Pant Hospital (GIPMER)
Case Scenario
◦ Name : Anita Devi
◦ Age : 65 years / female, house wife, right handed
◦ Resident of Bagpat UP
◦ Date of admission : 20/01/2021 (GIPMER)
Chief Complaints:
1. Sudden and severe headache * 10 days back
2. One episode of vomiting * 10 days back
3. Altered mental status since * 2 days
4. Generalized weakness since * 2 days
History of present illness-
◦ History was given by patient’s son
◦ Patient was relatively asymptomatic 10 days back then
◦ C/O severe headache which was sudden in onset, very severe in intensity
and progressive in nature
◦ Headache was holocranial ; associated with one episode of vomiting; not
relieved on taking medication
◦ Altered mental status for last 2 days - confused and disoriented to time
pace and person
Past history:
◦ History of HTN for 20years on amlodipine 5mg od
◦ Asthma for 20 years on inhaler Formetrol/budesonide/ipratropium bromide
OD
Systemic examination
◦ CNS Examination
➢ Pt was conscious but non cooperative
◦ Higher functions
➢ GCS-14/15, confused
➢ Not oriented to time, place and person
➢ Speech-Aphasia
◦ Neck rigidity, kernig’s sign, Brudzinski sign- couldn’t be examined
◦ Cranial Nerves Examination: couldn’t be examined in detail
Provisional diagnosis:

◦ 65 yrs old female patient with h/o sudden and severe headache a/w vomiting,
altered mental status, most probably ruptured Intracranial Aneurysm with Hunt
and Hess grade III and WFNS grade II
Ruptured left MCA aneurysm
 CLINICAL GRADING OF SAH
MODIFIED HUNT & HESS WORLD FEDERATION OF
NEUROSURGEONS
PREVALENCE
◦ Prevalence- 5-10%, with unruptured aneurysms accounting for 50% of all aneurysms
◦ Rate of rebleed in untreated aneurysms – 20-30% in 1st month and 3% per year

CONSEQUENCES
◦ 10% die before reaching medical attention
◦ 25% die within 24 hours
◦ 40-49% die within 3 months.
◦ Mortality- 65%,
PATHOPHYSIOLOGY
Integrity of the internal elastic lamina is compromised
Assoc. elastic defects in the adjacent layers of the tunica media and adventitia.

ETIOLOGY
• Osler-Weber-Rendu syndrome
• Multifactorial - interaction of environmental
factors – atherosclerosis/ HTn & congenital • Coarctation of the aorta
predisposition • Other vascular anomalies
• Autosomal dominant inherited polycystic • Moyamoya syndrome
kidney disease
• Marfan syndrome
• Fibromuscular dysplasia
• Ehlers-Danlos syndrome, type IV
• Arteriovenous malformations
• Other collagen type III disorders
Increased ICP
Causes of increased ICP in SAH
◦ communicating hydrocephalus from arachnoidal adhesions
◦ development of vasospasm can also exacerbate a rise in ICP
◦ intracerebral or intraventricular hematoma
Increased ICP
◦ ICP correlates well with clinical grade.
◦ Impaired intracranial compliance
◦ A cerebral perfusion pressure (CPP) value of 60
to 80mmHg
◦ important not to normalize the ICP too rapidly
->increase the transmural pressure (TMP)
gradient -> hemorrhage.
Impairment of Autoregulation and CO2 Reactivity

◦ impairment of autoregulatory ◦ cerebrovascular response to

capacity hyperventilation is generally
◦ rightward shift in the lower limit of preserved after SAH
autoregulation
Systemic Effects
◦ Intravascular Volume Status
◦ bed rest,
◦ supine diuresis,
◦ negative nitrogen balance,
◦ decreased erythropoiesis,
◦ iatrogenic blood loss
◦ Hyponatremia
◦ syndrome of inappropriate antidiuretic hormone
◦ CSWS
Other significant electrolyte abnormalities are hypokalemia and
hypocalcemia.
Cardiac Effects
◦ alterations in the electrocardiogram,
◦ correlates with the amount of intracranial blood
◦ Potassium and calcium abnormalities
◦ leakage of cardiac troponins
◦ depressed left ventricular function
◦ regional wall motion abnormalities
Respiratory System
◦ Pulmonary edema
◦ pulmonary congestion from myocardial dysfunction
◦ sympathetic mechanism,
◦ inflammatory component
◦ incidence of pulmonary edema correlates with clinical grade.
◦ other potential complications - aspiration and hydrostatic pneumonia
Other Major Medical Problems
◦ systemic hypertension
◦ heart disease
◦ diabetes mellitus
Clipping Vs Coiling
Indication of Surgical Clipping
◦ Young patients
◦ MCA aneurysms
◦ Large or very small and distal aneurysms
Indication of Endovascular coiling
◦ Old patients with comorbidities
◦ High H&H grading
◦ Posterior circulation aneurysms
Timing of Surgery
◦ Tight brain with early surgery
◦ Rebleeding vs vasospasm
◦ best outcomes <3 days and >14 days
◦ Trend towards early surgery
◦ Antifrbrinolytics may be given during waiting period
◦ Increased risk of hydrocephalus, vasospasm, thrombosis and embolism
Preoperative Workup
◦ Assessment of the patient’s neurologic condition and clinical grading of SAH
◦ Review of the patient’s intracranial pathologic - performing CT, CT angiograms
◦ Monitoring of ICP and transcranial Doppler ultrasonography TCD
◦ Evaluation of systemic functions comorbid condition,
◦ Communication with the neurosurgeon regarding positioning, anticipated
difficulty/technique to clip and special monitoring requirements
◦ Optimization of the patient’s condition
Perioperative Concerns
Vasospasm
◦ occurrence as determined by angiography- 40%–60%.
◦ symptomatic vasospasm (20–30%).
◦ Blood in basal cisterns -> oxyHB -> suppress EDRF/NO -> vasoconstriction
Clinical manifestations:
◦ decrease in the level of consciousness,
◦ new onset of focal signs
◦ mutism
Diagnosis
◦ appearance of new focal signs/decrease in level of consciousness
◦ Transcranial Doppler ultrasonography (TCD) – flow velocities increase
◦ Confirmed - CT/MR angiography Digital subtraction angiography (gold standard)
Treatment
◦ Pharmacological
◦ Ca Channel blockers (oral nimodipine)
◦ Mg Sulphate
◦ Clazosentan (ER antagonist)
◦ statins
◦ tirilazad
Nonpharmacologic
◦ Surgical –
◦ early operation with extensive irrigation of the cisterns may lower the incidence or
severity of vasospasm.
◦ Reduction of Intracranial Pressure
◦ Hypervolemic, Hypertensive, and Hemodilution Therapy:
Hypertensive tt – only confirmed evidence
Target SBP –
unsecured aneurysm 120 to 160 mmHg
Secured aneurysm – 160 to 180 mmHg / s&s of vasospasm reversed
Euvolemia
Haematocrit – 33% optimal (25% to 30% acceptable)
◦ Transluminal angioplasty
Rebleeding
◦ Incidence peaks at end of first week
◦ overall incidence is 11% which accounts for 8% of the mortality and disability
◦ incidence is lower in patients receiving antifibrinolytic agents.
◦ A/E - greater incidence of vasospasm and hydrocephalus, and have a higher
incidence of venous thrombosis and pulmonary embolism
Anesthetic Technique
Anaesthetic Goals:
◦ Absolute avoidance of acute hypertension - risk of rerupture.
◦ Achievement of intraoperative brain relaxation to facilitate surgical access
◦ Maintenance of a high-normal MAP to prevent critical reduction of CBF.
◦ Preparedness to perform precise manipulations of MAP
Premedication
◦ preoperative medications usually omitted
◦ Narcotics preferred over benzodiazepines
 Induction
◦ vigilant monitoring of blood pressure is required,
◦ Propofol (1.5–2mg/kg) or thiopental (3–5mg/kg) with fentanyl (3–5μg/kg) or
sufentanil (0.3–0.5μg/kg) is suitable
◦ Prophylaxis against rise in Blood Pressure during Laryngoscopy
◦ Anesthetic adjuncts
◦ use of high-dose narcotics (e.g., fentanyl, sufentanil, or remifentanil)
◦ β-adrenergic antagonists (e.g., esmolol, 0.5mg/kg), labetalol (10–20mg),
◦ intravenous or topical lidocaine (1.5–2.0mg/kg),
◦ second dose of propofol (0.5–1mg/kg),
◦ deep level of an inhalation anesthetic such as isoflurane or sevoflurane
Monitoring
◦ standard ASA monitors(ECG, NIBP, SpO2, EtCO2, NMT, urinary catheter,temp)
◦ Direct intra-arterial blood pressure preferably before laryngoscopy or induction
(arterial transducer at the level of the base of the skull)
◦ one 16-G or well running 18-G peripheral catheter
◦ Intermittent blood sampling for Hct, blood gas, glucose, osmolarity & electrolyte
◦ central venous access in select patients:
◦ prevalence of preexisting hypovolemia,
◦ large intraoperative fluid shift with the use of osmotic and loop diuretics
◦ potential risk of aneurysm rupture, necessitating blood and fluid resuscitation
◦ possible presence of myocardial dysfunction
◦ need to administer vasoactive medication via a central route
Maintenance
◦ insertion of the pins - Infiltration with local anesthesia and administration of additional
propofol, or narcotics; esmolol (0.5mg/kg) or labetalol (10 to 20mg)
◦ N2O – may cause vasodilation with inhaled anesthetics, can be used with TIVA
◦ Intermittent bolus/ infusion of fentanyl; remifentanil infusion
◦ Iso/sevo at (0.5 – 1 MAC); des (4 – 6 MAC)
◦ Sevoflurane maintains autoregulation at higher doses also

◦
 Temporary Clipping
◦ limit inflow to aneurysm during application of the
permanent clip- temporary clip proximally on the
feeding vessel.
◦ giant aneurysms in vicinity of the carotid siphon- the
inferior occlusion ICA via separate incision in the neck
◦ Upto 14 minutes tolerated; 7-minute rule with 3 min
reperfusion
◦ MAP should be sustained at high-normal levels during
periods of occlusion to facilitate collateral CBF.
◦ Brain Protection - ischemic hazard first confirmed by
observation of EEG response to a temporary occlusion
Brain Protection
◦ Maintenance of MAP to ensure collateral flow and perfusion under retractors,
◦ efficient brain relaxation to facilitate surgical access and reduce retractor
pressures,
◦ limitation of the duration of episodes of temporary occlusion,
◦ mild hypothermia
◦ bolus of thiopental, etomidate, and propofol to achieve burst suppression
(currently pharmacologic neuroprotection does not have sufficient evidence)
Electrophysiologic Monitoring

1. EEG - indicator of cerebral hypoxia when blood pressure is deliberately lowered

2. SSEP and MEP - Clipping of an intracerebral aneurysm - impede blood flow to
vital cerebral structures

◦ EEG has been used to determine the lowest blood pressure tolerable
◦ SSEP monitoring - anterior and posterior circulation aneurysms
◦ SSEP and MEP together improve both the sensitivity and specificity for ischemia
resulting in postoperative deficit,
Fluid and Electrolyte Balance
◦ Fluid should be administered - patient’s need and guided by intraoperative blood
loss, UO, CVP / other dynamic index of volume status
◦ I.v fluid should not be withheld if induced hypotension is planned (hypovolemic
hypotension is detrimental to organ perfusion)
◦ Electrolytes should be replaced as needed.
◦ Glucose-containing solutions should not be given
◦ Lactated Ringer’s solution is relatively hypo-osmolar
◦ A more physiologic solution, such as Plasma-Lyte or normal saline, is preferred
 Emergence and Recovery
◦ Communication between the surgeon and the anesthesiologist is essential
◦ SAH gr I or II - If surgical procedure uneventful, allowed to awaken, and tracheas
extubated in the OR
◦ minimize coughing intravenous lidocaine, 1.5mg/kg,,
◦ hypertensive tt -> reversing DCI from vasospasm modest levels of postop HTn
◦ SBP < 180mmHg allowed
◦ Extreme HTn - Labetalol 5–10-mg increments & esmolol in 0.1–0.5-mg/kg
◦ SAH grade III may or may not undergo tracheal extubation in the operating room
◦ SAH grade IV or V require postop ventilatory support and continuous neurointensive care
 Endovascular Management Of Aneurysm

◦ Endovascular treatment obliteration of the

aneurysmal sac using coils with or without stents
◦ Transfemoral arterial approach - insertion of a
femoral sheath – catheter - navigated into the
carotid or vertebral artery - micro-catheter is
introduced - detachable platinum coils are
advanced into position - coils deployed into sac
of the aneurysm - occlusion
◦ Manipulation of aneurysm sac may cause distal thromboembolism and rupture
◦ In elective treatment of unruptured aneurysms :
◦ coiling; at least one dose of aspirin 1 day before
◦ stent-assisted coiling : aspirin and clopidogrel should be given 3–5 days before
◦ Post-procedure with stent aspirin 75 mg daily for life; clopidogrel 75 mg daily for
3 mths
Endovascular Management: Specific considerations
Contrast and flush –
◦ Up to 2 litres of flush, and up to 300 ml of contrast used.
◦ at risk for acute CI nephropathy ( limit dose of contrast and good hydration)
◦ renal function monitored for 72 h post-procedure
Anticoagulation –
◦ i.v. heparin to minimize thromboembolic complications prevent vessel occlusion
◦ Baseline ACT -> 70–100 units/kg of heparin – >ACT (target of 2–3 times baseline)
Patient positioning
◦ patient’s head is at the opposite end to the anaesthetist and anaesthetic machine.
◦ requires secure extensions to anaesthetic tubing and lines .

Extubation
◦ Smooth emergence is important to avoid coughing - increases in ICP, re-bleeding
d/t rupture of unprotected or partially protected aneurysm
Post- operative Complications and Management
1. Vasospasm - i.v. nimodipine followed by oral nimodipine
2. Re-bleeds- neurological examination and post op ct
3. Infarction(stroke)- either due to clip /thrombosis/ vasospasm
4. Cerebral edema- mannitol
5. Seizures- antiepileptics
6. Hydrocephalus- External Ventricular Drain/ VP shunt
7. Electrolyte imbalance- check sr electrolytes
8. Contrast nephropathy
9. Pulmonary edema
10. Infection/ meningitis- fever and neck rigidity, meningismus sign
◦ Hydrocephalus is a common sequela of subarachnoid hemorrhage. Blood in the
subarachnoid space may not only fill the basal cisterns
◦ impairment of CSF flow is temporary and transient and does not require
treatment. If it results in significant elevation in ICP preoperatively affecting
neurologic function, w
 Depth of Anaesthesia

Dr Dheeraj Kapoor
MD, FCCP, FACEE, EDAIC
Professor,
Department of Anaesthesia and Intensive Care,
GMCH, Chandigarh
 Dr John Snow (1813-1858)
History
•  First documented a7empt
to assess anaesthe:c depth
in 1845
•  Described 5 levels
(etheriza:on) of
anaesthesia with
progressive impairment of
mental func:on and
voluntary movement
History Dr Arthur E. Guedel
(1883-1956)
•  1937: developed a chart
classifica:on of ether
anaesthesia
•  4 levels based on
–  lacrima:on
–  pupil size and posi:on
–  respiratory pa7ern
–  peripheral movement
 •  Stage 1: Analgesia and
Guedel classificaKon amnesia: from induc:on of
general anaesthesia to loss of
consciousness
•  Stage 2: Delirium and
unconsciousness: from loss of
consciousness to onset of
automa:c breathing
•  Stage 3: Surgical anaesthesia:
from automa:c respira:on to
respiratory paralysis. (four
planes of depth)
•  Stage 4: from apnoea (stoppage
of breathing) to death

JF Artusio (1954) further divided stage 1 into an addiKonal 3 planes of depth

Depth of Anaesthesia:
•  Defined as the drug-induced probability of
non-response to s:mula:on, calibrated
against the strength of the s:mulus,
•  The “depth” of anesthesia is determined by:
–  applied s:mulus,
–  observed response,
–  drug concentra:on at the site of ac:on that
blunts responsiveness

Role of opioid and hypnoKcs in sKmulus-response
relaKonship
•  AnestheKc depth ranges from
–  100% probability of an easily suppressed response
(verbal answer) to a mild s:mulus (e.g., calling
name) and readily suppressed responses (e.g.,
verbal answer),
To
–  100% probability of non-response to profoundly
noxious s:muli (e.g., intuba:on) and responses
that are difficult to suppress (e.g., tachycardia)

Effect of noxious sKmuli
Matrix of relevant sKmuli and responses
 Amnesia

•  Amnesia is the absence of recall

•  Anterograde amnesia: impaired capacity for new learning
–  intended when a drug with amnes:c proper:es is administered
before induc:on of anaesthesia
•  Retrograde amnesia: loss of informa:on that was acquired
before the onset of amnesia
–  intended when a drug (BZD) is administered aQer an event that
may have caused or been associated with intraopera:ve
consciousness in the hope that it will suppress memory
forma:on and “rescue” from recall
 Awareness

•  Explicit memory: inten:onal or conscious recollec:on
of prior experiences as assessed by tests or recall or
recogni:on, which are also called direct memory test

•  Implicit memory: percep:on without conscious recall.

The pa:ent denies recall, but may remember
“something” under hypnosis.

•  Deliberate memory:
–  surgery conducted under local or regional anaesthesia.
–  during some neurosurgical procedures, the pa:ent is
woken upto assess whether surgery has affected, or will
affect, important areas.

Stages of awareness

Five stages of percep:on with memory of intra-
opera:ve events under GA
1.  Conscious percep:on with explicit memory;
2.  Conscious percep:on without explicit
memory;
3.  Dreaming;
4.  Subconscious percep:on with implicit
memory;
5.  No percep:on and no implicit memory
GriffIth et al, BJA 1990
 Clinical Techniques and
ConvenKonal Monitoring

 Clinical Signs: Evans Score (PRST)

•  Autonomic acKvity
related
–  P (systolic blood Pressure)
–  R (heart Rate)
–  S (Swea:ng)
–  T (Tears)
•  Score range: 0-8
•  Score > 2 response to
verbal command or strong
reflex ac:vity is indica:ve
of light anaesthesia Evans JM Clin Anesth 1984
 Clinical Eye Signs
EvoluKon of loss of consciousness under GA:
•  Decrease in lateral excursions of the eyes
•  Nystagmus appear
•  Blinking increases
•  Eyes fix abruptly in the midline
•  ‘Oculocephalic reflex’(CN III, IV, VI, VIII) and the
‘Corneal reflex’(CN V-a, VII-e) are lost [with intact
pupillary response to light]
•  Pa:ent becomes apneic (dorsal and ventral
respiratory groups in the medulla and pons), atonic
(pon:ne and medullary re:cular nuclei), and
unresponsive
Factors masking clinical signs
 Skin Conductance
•  Quan:fica:on of the clinical sign of sweat
produc:on
•  Skin transiently becomes a be7er conductor
of electricity when either external or internal
s:muli occur that are physiologically arousing
•  Factors affec:ng swea:ng can reduce
accuracy: atropine, autonomic neuropathy

Isolated forearm technique

•  Described by Tunstall in obstetric anaesthesia (CS under GA).
• 

Tourniquet is applied to the pa:ent's upper arm and inflated
above SBP, before the administra:on of muscle relaxants
•  Movement of the arm, either spontaneously or to command,
indicated wakefulness, although not necessarily explicit awareness
•  LimitaKon:
–  limited :me available before pa:ents are unable to move their
arm due to tourniquet induced ischemia
–  Recall not seen in all responding pa:ents


 Frontalis (scalp) electromyogram
(FEMG)

•  The frontalis muscle receives both visceral and soma:c fibres from
the facial nerve.
–  dual nerve supply means that this muscle can be influenced by
autonomic ac:vity
•  2 surface electrodes record compound ac:on poten:als from this
muscle
•  The amplitude of the EMG decreases with increasing depth of
anaesthesia
•  Advantages: non-invasive , convenient, easy to apply the
electrodes
•  Disadvantages:
–  technical problems due to low amplitude and interference
–  wide inter-individual variability
–  cannot be used in the paralyzed pa:ent

Lower oesophageal contracKlity

Two types of smooth muscle contrac:on detectable in the lower
oesophagus



•  Improved version: combining the measurement
of SLOC frequency with PLOC amplitude, to
derive oesophageal contracKlity index (OCI): OCI
= 70 x (SLOC rate + PLOC amplitude)

•  The OCI is easy to interpret and can be used in
the presence of muscle relaxants
–  consensus opinion is against this method being a
reliable measure of anaesthe:c depth

Heart rate variability (HRV)


•  Some monitors use HRV at respiratory
frequency or respiratory sinus arrhythmia
(RSA) as a method of assessing anaesthe:c
depth
•  Objec:ve measurement of brain stem-
mediated autonomic tone
 Analysis of HRV: 3 components

1.  Low frequency fluctua:ons (circadian)

2.  Medium frequency fluctua:ons (baroreceptor
reflex)
3.  High frequency fluctua:ons in HRV coinciding
with the frequency of ven:la:on: RSA
•  RSA is easily visible on an ECG monitor that is
:me locked to an ECG R-wave peak
 RSA

•  HR increases during inspira:on and decreases during expira:on

•  Predominantly parasympathe:c reflex connec:ng stretch receptors in the
lungs and aorta to vagal motor neurons innerva:ng the heart
•  Characterized by greater than 10% varia:on in the ECG P-wave interval over
5 minutes
LimitaKons:
•  Requires intact autonomic nervous system
and healthy myocardial conduc:ng system
•  Erra:c results due to beta-blockers,
conduc:on abnormali:es, autonomic
neuropathy and sepsis
Spontaneous EEG acKvity monitors
and Derived Indices
 Electroencephalogram (EEG)

•  Can be obtained using the standard 19-electrode method
–  :me-consuming and imprac:cal
–  requires expert interpreta:on
•  Automated analysis of various EEG components (processed
EEG)
•  Generic problems with processed EEG technologies
–  dissimilar anaesthe:c agents generate different EEG pa7erns/
signatures
–  various pathophysiological events affect the EEG: hypotension,
hypoxia, hypercarbia

 Awake EEG pacern with eyes open

State of paradoxical excitaKon

Beta (13-25 Hz) oscillaKons frequently associated with an arousable state of sedaKon

Slow (0.1-1 Hz), delta (1-4 Hz), and alpha (8-12 Hz) oscillaKons: unconsciousness at
surgical planes

Slow oscillaKons typically recorded during propofol inducKon/

dexmedetomidine sedaKon

Burst suppression: state of profound anestheKc-induced brain inacKvaKon

Isoelectric EEG : brief periods during normal maintenance, anestheKc

induced coma, profound hypothermia
Fourier Analysis: mathemaKcal analysis of waves

Frequency Domain Analysis

•  Raw EEG can be processed by fast Fourier

analysis into its component sine waves
•  These can be further analyzed with respect to
3 features:
–  Frequency distribu:on
–  Power contained within different frequencies (a
func:on of wave amplitude)
–  Phase rela:onships between waves of different
frequencies
 Spectral Array

•  Tradi:onal power spectral analysis inves:gates

the rela:onship between power and frequency
over a short :me period (epoch)
•  Graph of power versus frequency forms a density
spectral array (2D)
•  Effec:vely display raw EEG data that have been
transformed with minimal loss of informa:on
 Compressed Spectral Array (CSA)

•  Obtained by superimposing
linear plots of successive
epochs of :me on each
other
•  Generates 3D ‘hill and
valley’ display
–  power amplitude ver:cally (y-
axis)
–  frequency horizontally (x-axis)
–  :me (z-axis)
•  Reflects purely cerebral electrical ac:vity
•  Anaesthesia causes a reduc:on in high-frequency
and an increase in low-frequency amplitudes,
which is easier to interpret than raw EEG
•  Real :me monitoring (adults, paediatric, neonates)
•  LimitaKons:
–  Inter pa:ent and agent variability
–  Confounding factors: hypoxia, hypotension and
hypercarbia
–  Not reliable monitor of the depth of anaesthesia, but
can provide a trend

Cerebral funcKon monitor (CFM)
• 
Modified from the conven:onal EEG for use during
anaesthesia
•  Uses a single biparietal or bitemporal lead (three wires) to
obtain an EEG signal
•  Signal is filtered, semi-logarithmically compressed, and
rec:fied
•  Output is displayed as a trace (1 mm/min)
•  Represent electro-corKcal acKvity of the brain
•  Used in cardiac, neuro- and vascular surgery: trends reflect
changes in cerebral perfusion
LimitaKons:
•  Unreliable and biphasic response with inhalaKonal
anaestheKc agents
–  Similar values in awake and anaesthe:zed pa:ents
–  recovery from anaesthesia may not occur near
baseline values
•  At deep levels of anaesthesia: Burst suppression by
periods of normal or high-voltage ac:vity alterna:ng
with periods of low or no ac:vity
•  Early burst suppression ar:ficially elevates the reading,
producing an apparent, paradoxical rise in ‘cerebral
funcKon’
 Cerebral funcKon analysis monitor
(CFAM)
•  Produces a con:nuous display of an analyzed
EEG signal from two symmetrical pairs of scalp
electrodes
–  Top trace displayed shows the mean amplitude of
the signal plo7ed in :me
–  Bo7om trace shows the power amplitude in the
frequency band
•  Same limita:ons as CFM

Bispectral index (BIS)

•  Displays a real-:me EEG
trace from fronto-temporal
montage
•  Generates a dimensionless
number: 0-100 [100- normal
cor:cal electrical ac:vity; 0-
cor:cal electrical silence]
•  Display also shows a signal
quality index (SQI) and an
indicator of EMG
interference
•  Proprietary (Medtronic)
 Signal Quality Index (SQI)
•  SQI measures the quality of the acquired EEG signal
•  Calcula:on is based on a number of ar:fact during the
last minute
•  Electrode-to-skin impedance is included in the
calcula:on
•  Higher electrode-to-skin impedances reduce the SQI
•  This quan:ty is displayed numerically as a percentage
–  0-100%, [100%-best SQI]
 BIS derivaKon?
•  BIS analysis combines tradi:onal power spectral analysis with
interroga:on of these phase rela:onships
•  Developed by recording EEG data from healthy adults, who
underwent repeated transi:ons between consciousness and
unconsciousness, using several different anaesthe:c regimens
•  Raw EEG data were :me stamped at various clinical end-points
•  MulKvariate logisKc regression was used in offline analysis
–  EEG correla:ng with clinical depth of seda:on/anaesthesia, and
these were then fi7ed to a model
•  Resul:ng algorithm generates the BIS
 BIS and AnaestheKc Agents
BIS and HypnoKcs:
•  Monitor the depth of the hypno:c component of
anaesthesia or seda:on
–  low-frequency, higher-amplitude oscilla:ons in deeper states of
unconsciousness
•  Track the effect-site concentra:on of hypno:c drugs and
their effect on the cor:cal EEG
•  Demonstrates the dose-response rela:onship with
hypno:cs (inhala:onal, IV)
–  independent of the agent used
–  ExcepKons: ketamine, N2O, dexmedetomidine

BIS and Ketamine:
–  causes EEG ac:va:on
–  produce high frequency oscilla:ons
–  pa:ents can be unconscious but have high index
values
BIS and Nitrous oxide:
–  increases the amplitude of high-frequency and
decreases the amplitude of low-frequency
–  BIS values not reduced upto 50% N2O concentra:on
–  During surgery: decrease in BIS due to an:-
nocicep:ve effects of N2O

BIS and Dexmedetomidine
–  slow oscilla:ons and an appreciable decrease in
beta oscilla:on power during seda:on
–  most likely lead to BIS values that are typically in
the unconscious range, even though the pa:ent
can be aroused by verbal commands or light
shaking
BIS and Opioids:
•  No direct correla:on
–  opioid induced depth of seda:on/anaesthesia not
reflected by decrease in BIS
•  Indirect correla:on
–  synergis:c effect of opioids with hypno:cs
–  due to counterac:on of arousal of pain
 BIS: LimitaKons
•  Variability within adult study popula:ons
•  No specific sensi:ve and specific threshold value
•  No clear transi:on between awake and asleep
states
•  Not able to predict movement in response to
surgical s:mula:on (at spinal level movement)
•  BIS not extrapolated in paediatric (<5 years)
•  BIS work poorly in older adults (>60)
–  lower amplitude oscilla:ons, which the BIS algorithm
can interpret as an awake state or state of
unconsciousness
 BIS use in ICU
•  Con:nuous monitor of seda:on in ICU
•  Useful reflector of the great inter-individual
varia:ons in pharmaco-kine:cs/dynamics of
seda:ves
LimitaKons:
•  Unimpressive correla:on sta:s:cs with
seda:on scores
•  Limited correla:on of BIS in paediatric ICU
 Entropy

•  Entropy measures the degree of disorder or the
lack of synchrony or consistency in a system
•  Measures the regularity of EEG and FEMG
signals (cor:cal electrical ac:vity)
•  Entropy of the signal:
–  drops when a pa:ent falls asleep
–  increase again when the pa:ent wakes up
•  Algorithm uses frequency domain
analysis, combined with burst
suppression to measure the entropy in
pa:ents receiving anesthe:c drugs (GE
device)
•  Monitor reports two entropy numbers
to aid in interpreta:on
–  Response entropy (RE): tracks the changes
in the EEG power in the higher frequency
range 0.8 to 47 Hz
–  State entropy (SE): tracks the changes in the
EEG power in the lower frequency range of
0.8 to 32 Hz
•  Rela:ve changes in the RE and SE
dis:nguish between real brain state
changes versus those that are due to
muscle ac:vity on the EMG
•  Pa:ent becomes more profoundly
unconscious;
–  the RE declines faster than the SE
–  possible to dis:nguish unconsciousness from
movement ar:facts
•  Monitoring entropy is consistent with changes
with the BIS
•  Not useful with certain drugs: ketamine,
nitrous oxide, dexmedetomidine
 NORMALIZED SYMBOLIC TRANSFER ENTROPY
(NSTE)
•  Measure this loss of func:onal connec:vity
between frontal and parietal areas
•  EEG recorded from a montage from frontal
and parietal electrodes
–  Feed-forward funcKonal connecKvity: parietal to
frontal
–  Feed-back funcKonal connecKvity: frontal to
parietal
•  Unconsciousness induced by propofol,
sevoflurane, or ketamine has been associated with
loss of feedback func:onal connec:vity leading to
loss of consciousness
•  Mechanism of feedback loss is related to
‘anterioriza:on’
•  AnteriorizaKon: differences in the
electrophysiologic proper:es (res:ng membrane
poten:als and ionic currents) in the frontal and
posterior thalamocor:cal connec:ons (Vijayan
model*)
Vijayan S et al. J Neurosci. 2013
LimitaKons of NSTE:
•  Does not dis:nguish among the mechanisms
of ac:ons of various anesthe:cs
•  Not possible to compute these mutual
informa:on measures in real :me in OR
sewngs
•  Requires an EEG montage with both frontal
and parietal electrodes
 NARCOTREND

•  Proprietary
algorithm converts
EEG into different
states-A to F
(MonitorTechnik)
•  Performance has
been variable
 PATIENT SAFETY INDEX (PSI)
•  Proprietary algorithm (Masimo) that assesses
anesthe:c state based on EEG
•  Scaled between 0 and 100 (pa:ent is
unconscious between 25 and 50)
•  PSI originally used an electrode montage that
included occipital and frontal EEG leads
•  Current formula:on of the PSI uses a four-lead
frontal EEG montage
–  monitor the phenomenon of “anterioriza:on” as a
marker of change in anesthe:c state
 SNAP index
•  Samples raw EEG signals and uses its own
unique algorithm, analyses both high- (80-420
Hz) and low- (0-20 Hz) frequency components
of the signal
•  First commercial EEG-monitoring tool to use
Personal Digital Assistant computer
•  May be more sensi:ve to uninten:onal
awareness
 Cerebral State Monitor/Cerebral State Index
(CSI)
•  Handheld device that analyzes a single channel EEG
•  Provides EEG suppression percentage and a measure
of EMG ac:vity
•  EEG waveform is derived from the signal recorded
between the frontal and mastoid electrodes
•  Based on the analysis of the frequency content (shiQ)
of the EEG signal
•  Also evaluates the amount of instantaneous burst
suppression (BS) in each 30 s period of the EEG
•  Monitor incorporates an EMG filter that removes most
of the poten:al interfering EMG ac:vity
 •  AddiKonal display of:
–  Real :me unprocessed EEG and its spectrogram
from leQ and right sides of the head
–  EMG ac:vity
–  Ar:fact index
–  Suppression ra:o* (0-100)
•  PSI strongly correlates with BIS
•  Limita:ons same as that with BIS

Suppression RaKo: measures the fracKon of Kme the EEG is in burst

suppression
CLOSED-LOOP ANESTHETIC DELIVERY SYSTEMS
[CLADS]
•  Work by using an EEG marker (BIS) of anesthe:c
state to define a desired state for maintenance
during surgery
•  EEG is monitored, the marker is computed from
the EEG, and a computer-controlled infusion
delivering the anesthe:c drug is automa:cally
changed based on the difference between the
targeted level of the EEG marker and the actual
level of the marker computed from the EEG
analysis
Evoked Brain Electrical AcKvity
Monitors
(Evoked PotenKals)
Somatosensory evoked potenKals (SSEP)
•  Supramaximal s:mulus is applied to
peripheral nerves while a recording scalp
electrode is placed over the appropriate
sensory area.
•  Most anaesthe:c agents increase the latency
and decrease the amplitude in dose-
dependent manner
–  Etomidate consistently increases the amplitude
Visual evoked potenKals (VEP)
•  Light-emiwng diodes are incorporated into
specialized goggles and the op:c nerve is
s:mulated at 2 Hz
•  EEG electrodes take recordings from the occiput
•  Most anaesthe:c agents increase the latency and
decrease the amplitude in dose-dependent
manner.
•  VEP are considered less reliable than AEP
•  They have been used to monitor func:on during
surgery for lesions involving the pituitary gland,
op:c nerve and chiasma
Auditory evoked potenKal(AEP)
•  Defined as the passage of electrical ac:vity
from the cochlea to the cortex, which
produces a waveform consis:ng of 15 waves
(VIII CN s:mula:on)
•  AEP is a composite waveform that can be
plo7ed against :me
Early or mid-cor:cal AEP does (MCAEP 10-50 ms
latency) correspond with depth of anaesthesia

The mid-latency of the Pa and Nb components is
analyzed

Anaesthe:c agents decrease the amplitude and
increase the latency of the MCAEP in a dose-
dependent, but agent-independent, manner
 AEP Index
•  Parameter derived by summing the square
root of the difference in amplitude between
successive 0.56 ms segments of the MCAEP
•  Calculated online and presented as a running
average that can be updated approximately
every 30 seconds.
•  A rough guide to the AEP index
–  >80 in the awake pa:ent
–  <50 in anaesthe:zed pa:ents
 Pharmacological methods of
measuring Depth of Anaesthesia
 END-TIDAL ANESTHETIC CONCENTRATION
(ETAC)
•  Vola:le agent monitoring, linked to MAC,
currently as a reliable measurement for rou:ne
use for intraopera:ve awareness
•  ETAC: related to brain ac:vity through the
concentra:on of inhaled anesthe:c expired in
the lungs
•  Indirect measure of anesthe:c state
•  Supported by: B-Unaware, BAG-RECALL, MACS
trial
•  LimitaKons: cannot be used with TIVA

 Minimum Alveolar ConcentraKon (MAC)
DefiniKon: concentra:on of inhala:on agent required to
prevent 50% of subjects from responding to painful
noxious s:muli
•  MAC-intubaKon: that would inhibit movement and
coughing during endotracheal intuba:on
•  MAC-incision: To prevent movement during ini:al
surgical incision
•  MAC-BAR: To prevent adrenergic response to skin
incision, as measured by the venous concentra:on of
catecholamine
•  MAC-awake: that would allow opening of the eyes on
verbal command during emergence from anaesthesia
ConcentraKon of anaestheKc agent and the probability of response
MAC-awake < MAC-incision < MAC-intubaKon < MAC-BAR
Focused on
•  maintenance of unconsciousness,
–  with an:-nocicep:on
–  with volume status

Recent models (experimental/animals model)
•  Track the burst suppression and burst
suppression probability (instantaneous
probability that the brain is suppressed)
Risk factors of intraoperaKve awareness
Brice Structured Interview
(Suspected Awareness)
 Awareness Trials
•  AIM Trial [Anesth.Analg 2004]
–  mul:-center US study
–  awareness with recall occurs @1-2 cases/1000 pa:ents
receiving GA
•  B-AWARE Trial [Lancet 2004; 363: 1757-63]
–  high awareness-risk pa:ents
–  BIS-guided anaesthesia reduced the incidence of awareness
with recall by approximately 82%
•  B-UNAWARE Trial [N Engl J Med 2008]
–  high awareness-risk pa:ents
–  comparing structured protocols based on the BIS (target, 40–
60) and ETAC (0.7–1.3)
–  restricted to those receiving potent vola:le anesthe:cs alone
–  No difference between 2 groups, incidence of awareness
with recall was 0.21% in each group

•  Safe-1 Trial [Lancet 2000; 355: 707-11]
–  incidence of awareness was 0.18% in those given
neuromuscular blocking drugs (NMBs) and 0.10% in
the absence of NMBs
•  Safe-2 Trial [Acta Anaesthesiol Scand 2004]
–  rou:ne use of BIS monitoring reduced the incidence
of awareness in the general pa:ent popula:on by
77%
•  BAG-RECALL TRIAL [N Engl J Med 2011]
–  3-centric trial
–  BIS protocol not superior than ETAC protocol in high
risk pa:ents
–  sugges:ng that both protocols were likely to have had
efficacy

•  MACS (Michigan Awareness Control Study)
Trial [Anesthesiology 2012]
–  unselected surgical patients
–  algorithms based on either BIS values or
anesthe:c concentra:ons: no difference between
two
–  BIS monitor may play a role in reducing
intraopera:ve awareness compared to no
interven:on (post hoc analysis]
•  TIVA Trial [Chin Med J 2011]
–  BIS-guided TIVA (40-60) decrease the incidence of
awareness compared with rou:ne TIVA
Evidence based decision protocol to prevent
awareness and recall

Avidan et al, Anesthesiology 2013

Comprehensive list of 64 recommendaKons
 Incidence of AAGA
•  The es:mated incidence of pa:ent reports of
AAGA was ~1:19,000 anaestheKcs
–  With NMB,S: ~1:8,000
–  Without NMB’ ~1:136,000
•  Two high risk surgical specialKes:
–  Cardiothoracic anaesthesia (1:8,600)
–  Caesarean sec:on (~1:670)
 Key RecommendaKons
1.  All pa:ents should be informed of the risks
of GA, including the possibility of AAGA,
before their surgery
2.  When consenKng paKents, prac::oners
should use a form of words that
propor:onately conveys the risks of AAGA
3.  Consent for sedaKon should emphasize that
the pa:ent will be awake and therefore may
have recall for at least parts of the procedure
4.  Prac::oners should idenKfy certain situaKons or
certain paKent factors as consKtuKng a higher risk
for AAGA and highlight these at the WHO pre-meet/
team brief
5.  During inducKon of anaesthesia, prac::oners should
adhere to suitable dosing of IV agent, check
anaesthe:c effect before paralysis or instrumenta:on
of the airway and maintain anaesthe:c
administra:on, including during transfer of pa:ents
(which is facilitated by a simple ABCDE checklist)
6.  If AAGA is suspected during maintenance, prompt
a7en:on should be paid to giving verbal reassurance
to the pa:ent, increasing analgesia, and deepening
the level of anaesthesia
7.  For cases requiring paralysis, the minimum dose
NMBDs that achieves sufficient neuromuscular
blockade for surgery should be used, and the nerve
sKmulator is an essen:al monitor to :trate the
dosing of NMBDs to this minimum
8.  Where TIVA is used, prac::oners should adhere to
the relevant recently published SIVA guidelines
9.  At emergence, prac::oners should first confirm
that surgery is complete, then ensure NMBDs
are adequately reversed before allowing the
pa:ent to regain consciousness.
–  Prac::oners should then manage the pa:ent
experience, par:cularly during awake extuba:on, by
speaking to the pa:ent
10. Cases of AAGA should be managed using the
NAP5 pathway as a guide
Suggested Reading:
Miller 9 edi:on (Chapter 40)
Anaesthesia UK (frca.co.uk)
Cook TM et al. Anaesthesia. 2014;69:1102-16.
Pandit JJ, et al. Br J Anaesth. 2014 ;113:549-59.
NAP 5 Handbook, 2019
Rani DD et al. IJA. 2012 ;56:437.
Sinha et al, IJA. 2007; 51 : 365-381.

Drugs for Emergency
Dr. Tina Khurana
Associate Professor
ABVIMS & Dr. RML Hospital
 ADRENALINE/EPINEPHRINE

Adrenaline bitartrate/HCl
1ml ampoule/30 ml vial--1mg/ml (1:1000)
Ampoule constituents –epinephrine, sodium chloride, sodium metabisulfite, Hcl, water
Not compatible with alkaline solution
Natural catecholamine secreted from Adrenal Medulla
Onset-1-2 min
Duration-2-10 min
ROUTES: IV/IM/SC/IO/Nebulization/Endotracheal
Low doses –increase SBP, decrease DBP
Higher doses- increase in both SBP , DBP, MBP
RESP- Bronchodilation, inhibits histamine release
METABOLIC- Increase glycogenolysis, increased lipolysis
Increased blood glucose, free fatty acids, cholesterol, LDL
Inhibition of insulin secretion
Hypokalemia

USES
• CPR-1.0 mg IV/IO every 3-5 mins --- ventricular fibrillation, ventricular tachycardia, asystole, PEA
Dose in children -- 0.01 mg/kg every 3-5 mins; max dose 1mg
• Hemodynamic instability to increase myocardial contractility and vascular resistance
• Bradycardia-- 2-10 micrograms/min as an equal alternative to dopamine when atropine is not effective.
• Sepsis-increases cardiac output and oxygen delivery—vasoconstrictor action
• Anaphylactic shock - 0.5 ml of 1/1000 IM- first line ; 0.5 ml of 1/10000 IV for Adults
• Racemic epinephrine(2.25%) nebulization ---- treatment of severe croup/post extubation/ traumatic
airway edema—0.05 ml/kg(1/1000)per dose to a max of 0.5 ml diluted in NS to 5 ml
Onset- 30 mins; Duration- 2 hrs.
L-epinephrine-0.5 ml/kg per dose-max 5ml
• Severe asthma and bronchospasm
• Weaning from cardiopulmonary bypass
ADVERSE EFFECTS
• Cardiac arrhythmias
• Cerebral hemorrhage, pulmonary oedema
• Local ischemic necrosis
 NOREPINEPHRINE
• Noradrenaline bitartrate; 2ml ampoule-2mg/ml
• 2mg of NE bitartrate is equivalent to 1 mg of NE base/ml
• Diluted in 5D
• Sodium metabisulphite-antioxidant
• Incompatible with alkaline solution
• Endogenous catecholamine
• Immediate precursor of epinephrine
• Alpha and beta1 agonist with minimal effect at beta2 receptors
• Alpha1--Vasoconstriction in all vascular beds except for coronary arteries
• Increases SBP,DBP, SVR
• Vagal mediated HR decrease
• So CO not changed
• Pulmonary vasoconstriction
• Blood flow to kidney & skeletal muscle decreased
• Beta 1receptor effects less than epinephrine
• Metabolic effects-less than epinephrine
• Lactic acidosis
• USES
• As a first line vasopressor to treat Septic shock -2-16 mcg/ min
• 2nd line vasopressor after dopamine to treat other shocks
• After cardiopulmonary bypass pts.

ADVERSE EFFECTS
• Severe hypertension
• Local necrosis at injection site
• Renal failure due to decreased blood flow to the kidneys
• End organ hypoperfusion and ischemia
• To be used cautiously in Right heart failure pts—increased venous return ; Raised PA pressure
COMPARISON: Epinephrine Norepinephrine

Heart rate + -

Stroke volume ++ ++
Cardiac output +++ 0/-
Arrhythmias ++++ ++++
Coronary blood flow ++ ++
Systolic BP +++ +++
MAP + ++
Diastolic BP +/0/- ++
TPR -/+ ++
Cerebral blood flow ++ 0/-
Muscle blood flow +++ 0/-
Renal blood flow - -
Oxygen demand ++ 0/-
Blood glucose +++ 0/-
 DOPAMINE HYDROCHLORIDE

200 mg in 5 ml(40 mg /ml)

Infusion rate- 0.3×weight/4--(5mcg/kg/min)

Should be dissolved in 5D to avoid inactivation in alkaline solutions

Elimination half life-1-2 mins
Naturally occurring endogenous catecholamine
Immediate precursor of norepinephrine
Unique among catecholamines to increase myocardial contractility, RBF, GFR, excretion of sodium and
urine output
Dose dependent effects:
<3 mcg/kg/min: stimulates DA1 and DA2 receptors
in renal, mesenteric and coronary beds— vasodilatation
Diuresis and natriuretic
Decrease in DBP
Reflex increase in HR

3-10 mcg/kg/min : beta 1 and alpha receptor effects predominate Increases HR ,SV,CO,SBP,SVR

>10mcg/kg/min: alpha 1 effects predominate arterial and venous vasoconstriction

increase BP
Increased SVR
Reflex bradycardia
No further increase in CO
Renal dose dopamine/low dose dopamine

Continuous infusion of small doses 1-3 mcg/kg/min to promote RBF

healthy individuals –increased RBF, natriuresis, diuresis
MOA
• D1 Receptors in renal vasculature-proximal tubule, thick ascending loop of Henle and cortical collecting
ducts –inhibits Na K ATPase activity
• D2 Receptors via inhibition of NE release ; stimulates PGE2 production In inner medullary collecting
ducts—antagonizes effect of ADH resulting in free water clearance & enhances blood flow in inner
medulla
• Direct effect on tubular cell function
• Inhibition of aldosterone increases sodium excretion and diuresis
• Higher dose – increase CO(Beta) ,perfusion pressure(Alpha)
Before renal insult—diuretic effect present but no reports of improved creatinine clearance or decreased
need for hemodialysis
After renal insult—no improvement in GFR
DOPAMINE does not prevent or reverse ARF or improve outcome in at risk population

Renal dose Dopamine is not recommended

USES

• Used in chronic heart failure patients to increase CO

• Used in combination with Dobutamine to increase CO &Coronary perfusion while
decreasing afterload
• Bradycardia—5-20 mcg/kg/min—if atropine is ineffective
• Post cardiac arrest care — hemodynamic stability
• After cardiopulmonary bypass
ADVERSE EFFECTS

• Extravasation of DA infusion — ischemic necrosis and sloughing

• Gangrene of the fingers or toes
• avoided/ dose adjustment — patient — MAO inhibitors, tricyclic antidepressants
• Increases PVR — not preferred in pulmonary HTN or right ventricular failure
 DOBUTAMINE HYDROCHLORIDE
• Ampoule-250 mg/5ml; vial-250 mg/20 ml
• Dissolve in 5D
• Incompatible with alkaline solution
• Half life-2 min
• Synthetic catecholamine; derived from isoproterenol
• Racemic mixture

• (--)enantiomer ---potent alpha 1 agonist , weak Beta 1&2 agonist

• (+) enantiomer---alpha 1 receptor antagonist , potent Beta 1&2 agonist

• Dobutamine has potent Beta 1, weaker Beta 2 activity

• Alpha receptor activity increases at higher doses

• Positive inotropic agent—increase in SV, CO, Contractility

• Peripheral vasodilation

• Minimal effect on MAP

• HR-Minimal increase at low doses; Tachycardia, dysrhythmias at higher doses > 10 mcg/kg/min IV
USES
• Congestive heart failure
• MI complicated by low cardiac output
• Does not significantly elevate oxygen demands of the myocardium
• An infusion of dobutamine used in stress Echo
ADVERSE EFFECTS

• Patients with atrial fibrillation are at risk of marked increases in ventricular response rates due to
facilitatory AV conduction
• Tachydysrhythmias, severe hypotension
• Development of ventricular ectopic activity
• Tolerance may develop
 FUROSEMIDE

• Loop Diuretic
sulphamoyl derivative
• Routes-oral/IV/IM
Mech. of action
It inhibits NA-K-2CL-co transport at medullary thick ascending loop of Henle.
The corticomedullary osmotic –gradient is abolished and positive as well as
negative free water clearance is blocked.
• Onset of action – 5-10 mins, peak-30 mins, duration- 2-6 hrs.
• Dose-I.V. 5-40 mg (adults)
• Dose can be increased in Chronic renal insufficiency-max 160-200 mg
• Partly conjugated with glucuronic acid
• Excreted unchanged by kidney

-
CLINICAL USES
•Edema– rapid mobilization of edema fluid irrespective of etiology of edema-cardiac, hepatic, renal. They
are preferred in CHF
•Acute pulmonary edema –they decrease blood volume and venous return
•Hypertension
•First line diuretic in renal impairment
•Cerebral edema-may be combined with osmotic diuretics to lower ICP
Along with blood transfusion in severe anemia to prevent overload
•Forced diuresis in barbiturate poisoning
SIDE EFFECTS- alkalosis, Hypokalemia, ototoxicity
 NITROGLYCERIN

• Mech of action-Nitric Oxide generation, stimulates cGMP production in vascular smooth

muscle

• NTG principally acts on venous capacitance vessels and large coronary arteries

• Peripheral pooling of blood & decreased cardiac ventricular wall tension

• At higher doses-relaxation of arterial vascular smooth muscle cell

• Pulmonary vasodilation is equivalent to systemic arterial vasodilation

• SNP spontaneously produces Nitric Oxide whereas NTG requires presence of thio
containing compounds

• Nitrate group of NTG is bio transformed to NO through a glutathione dependent

pathway
USES
suspected MI NTG -1 TABLET SUBLINGUAL/SPRAY-every 3-5 mins. for ongoing symptoms-total 3
doses
Administer NTG only if SBP>90 mm Hg & HR is 50-100/min
volume overload in heart failure patients-preload reduction
•treatment of hypertensive emergencies
•treatment of pulmonary oedema
• controlled hypotension
•uterine relaxation
Available as
• oral tablet-inactive as extensive first- pass metabolism
•Buccal/transmucosal tablet
•Sublingual spray, Intra nasal spray
• Transdermal patch
• IV
• NTG most frequently administered by sublingual route Peak plasma conc. – within 4 mins.
Transdermal absorption-5-10 mg over 24 hrs provides sustained protection against MI
Tolerance develops if patch left for>24 hrs.
• Drug free interval of 12-14 hrs is recommended
• Elimination half time-1.5 min

NTG should not be used or used cautiously in

• Inferior wall MI & RV infarction—patients are dependant on RV filling pressures to maintain cardiac
output & BP
• Recent phosphodiesterase inhibitor use– cause severe hypotension refractory to vasopressor agents
• (Sildenafil, vardenafil)

• Nitrite metabolite of NTG –oxidizes ferrous ion in hemoglobin to ferric form--

METHEMOGLOBINEMIA
 LIGNOCAINE HYDROCHLORIDE

Amide type local anesthetic

Mech. of action- stabilizes neuronal membranes by inhibiting sodium flux

Class 1B antiarrhythmic –shortens ventricular depolarization

ROUTES--Oral/IV/intratracheal/topical/epidural/nebulization/intraosseous/IM

• Onset: 45-90secs (I.V), Duration:10-20 mins.(IV) 90 mins.(IM)

• CPR-first dose 1-1.5 mg/kg; second dose- 0.5-0.75mg/kg IV/IO over 5-10 min intervals to a
maximum of 3 doses or 3mg/kg. If IV/IO access not available dose for ET administration is 2-4mg/kg
diluted in 5-10 ml of water or normal saline

• Treatment of ventricular arrhythmia 1-1.5 mg/kg body weight; repeat dose 0.5-0.75 mg/Kg (max
cumulative dose 3mg/kg) Follow with continuous infusion (1-4mg/min)

• Side effects: Hypotension, bradycardia, heart block, seizures, CCF

 AMIODARONE
50 mg/mL injection

Mech. of action-Class III anti arrhythmic; weak sodium channel blocker(class I) effect;

noncompetitive alpha & beta blocker(Class II) effect; mild vagolytic & calcium blocking properties.

Onset-immediate, Duration: 4 hrs., half life-long(40 days)

• Indication: CPR --300 mg IV/IO bolus in VF/VT which is resistant to electrical defibrillation

and epinephrine ; Second dose—150 mg IV/IO

First line antiarrhythmic drug because it improves rate of ROSC & Hospital admissions in adults with refractory

VF/pulseless VT

• Life threatening arrhythmias-Rapid infusion-150 mg IV over first 10 mins; repeat every 10 mins as needed

slow iv infusion—360 mg IV over 6 hrs.(1mg/min )for next 6 hours,

maintenance infusion of 540 mg IV over next 18 hrs. ( 0.5 mg/min )

Maximum cumulative dose: 2.2g IV over 24 hours

• suppression & prevention of refractory AF & PSVT; WPW syndrome

Adverse effects: heart block, altered thyroid function, hypotension. Don`t give with QT prolonging(procainamide)

drug
 SODIUM BICARBONATE

• Oral/IV
• 8.4%(1meq/ml), 7.5%(0.9meq/ml) for adults & 4.2%(0.5meq/ml) for children
• Onset 2-10 mins., Duration 30-60 mins
• Renal elimination
• Mech. Of action-Sodium bicarbonate dissociates to provide HCO3 ion which neutralizes H ion
concentration and raises blood & urinary pH
• USES
• Correction of metabolic acidosis-0.3 × weight (kg) × base deficit. Give half of corrected dose initially ,
rest in 24hrs after assessing ABG
• Treatment of hyperkalemia-intracellular shift
• Urinary alkalinization for poisonings (barbiturates, salicylates)
• CPR - PEA management- for treatment of acidosis and Hyperkalemia

It can cause hypercarbia , hypernatremia

Alternate to soda bicarbonate is THAM ,carb/bicarb as it does not increase sodium load
ADVERSE EFFECTS:

• Hypokalemia, hypernatremia

• alkalosis

• hypercarbia

• CCF

• raised ICT

• paradoxical acidosis

• pulmonary edema esp in renal failure patients

• necrosis with extravasation

 MAGNESIUM SULPHATE

Magnesium
Intracellular cation
Normal plasma levels -- 1.7-2.4 mg/dl,(1.4 - 2.2 mEq/l), (0.7-1.1mmol/l )
Therapeutic plasma level: 4.8-8.4 mg/dl, (4-7mEq/l),(2.0-3.5 mmol/l)
Supplied as 10%,12.5%, 50% inj.
Onset: Immediate (IV); Duration: 30mins (IV)
Renal elimination
USES
• Cardiac arrest due to Torsades de pointes/ Hypomagnesemia—1-2 gm IV/IO diluted in 10ml over 5-20
minutes
• Torsades de pointes with a pulse or AMI with hypomagnesemia-Loading dose 1-2 gm mixed in 50-100
ml diluent over 5-60 mins f/b 0.5-1 g/hr. IV(titrate to control torsades)
• Preeclampsia--- improves symptoms of preeclampsia by systemic, vertebral, uterine vasodilation
4 g IV loading dose over 10-15 minutes followed by infusion of 1g per hour for 24 hrs.
4g IV loading dose with10 g IM followed by 5gm IM every 4 hrs. Discontinued 24 hrs. after delivery
Monitor---Urine output, respiratory rate, deep tendon reflexes, serum magnesium levels

Treatment of magnesium toxicity

• Discontinue infusion
• IV calcium gluconate1gm/10 min
• Oxygen, Mech ventilation if required

• Tocolytic therapy
• Analgesia—IV/ Intrathecal route(50-100 mg)/local anesthetic block(50-250mg)-– inhibition of calcium
influx, antagonism of NMDA receptors
• Asthma—bronchodilation-IV route- inhibition of-- calcium mediated smooth muscle contraction,
histamine release, nicotinic acetylcholine release
• Cardiopulmonary bypass– to decrease AF
• During hypokalemia correction
• Hypomagnesemia correction
• Arrhythmias associated with hypomagnesemia are often associated with hypokalemia---Normalization
of both is recommended
• IV Magnesium enhances Nondepolarizing blockers, attenuates fasciculations, K release with scoline
ADVERSE EFFECT
• Magnesium crosses the placenta--- neonatal lethargy, hypotension, resp depression if given for >48
hrs.
• Excess magnesium—decreased SA node activity, prolonged AV node conduction & refractoriness
• IV—pain on inj., muscle weakness, hypotension , bradycardia
• Use with caution if renal failure is present
 CALCIUM
serum calcium concentrations —8.5-10mg/dl; 50% in ionized(active) form
SOLUTION ELEMENTAL Ca UNIT VOLUME OSMOLARITY

10% Calcium chloride 27mg/ml 10ml ampule 2000mosm/l

10% calcium gluconate 9mg/ml 10ml ampule 680 mosm/l

Both calcium solutions are hyperosmolar ---- via large central vein
Onset: <30secs IV; Duration: 10-20mins
●To be used only slow IV, not for IM/SC use
Dose: 500-2000mg I.V.(10% solution), not to exceed rate of 1ml/min (ADULTS)
Indications:
• Treatment of hyperkalemia
• Hypermagnesemia
• CCB overdose
• Hypocalcemia
• Massive blood transfusion
• positive inotrope
.
 POTASSIUM CHLORIDE
Normal serum conc: 3.5-5.5mEq/L
Major cation of ICF
Dextrose & Insulin facilitate intracellular movement
Supplied as: 20mEq/10ml, 40mEq/10ml, 60mEq/10ml inj
Onset: Immediate (IV route)
Dose: 10-20mEq/hr; Max. concentration – 40mEq/L of i.v fluid
● Max. 24hr dose: 200-400mEq
● Peripheral line – 10 mEq/hr, central line – 20-40 mEq/hr
● Always use cardiac monitor (ECG) during infusion
Indications:
Treatment of hypokalemia
electrolyte replacement
treatment of arrythmias associated with digitalis toxicity
● Adverse effects:
Hyperkalemia & its complications Cardiac arrest
Bowel ulceration
Phlebitis
Coma
Nausea
● Use with caution in patients with renal
disease
● digoxin therapy
● metabolic acidosis
● Addison's disease
● myotonias
● dehydration
 METOPROLOL TARTRATE

Cardio selective beta1 blocker

Indication: antihypertensive
SVT & Ventricular arrythmias
Antianginal
thyrotoxic crisis

Dose: 5 – 15 mg IV followed by oral dose 50 mg every 6 – 8 hours for 48 hours.

Toxicity:
Hypotension
Bronchospasm
CNS depression
Arthralgia
Bradycardia
 ESMOLOL HYDROCHLORIDE
• Ultra short acting selective Beta1 blocker

• ROUTE- only IV-10 mg/ml

• USES Antiarrhythmic-Class II-Decreases rate of depolarization-used in supraventricular arrhythmias

• Perioperative MI- 1-1.5 mg/kg IV followed by continuous infusion-50-300microgram/kg/minute
• Attenuation of stress response to laryngoscopy and intubation
150 mg iv-administered 2 mins before- HR and SBP both are decreased
• Perioperative tachycardia and hypertension
• Thyrotoxicosis, preparation of hyperthyroid patients
• PIH
• TOF- hypercynotic spells
 ADENOSINE
Endogenous nucleoside
MOA-Slows conduction through A-V node
interrupt re-entry pathways
decreases peripheral resistance & arterial pressure
● Onset: 10secs; Peak effect: 30 secs
● USE-Treatment of acute PSVT, WPW syndrome
Dose: Rapid i.v. bolus 6-12mg, may be repeated within 1-2 mins, f/b 20ml rapid saline flush.
Side effects: Heart blocks, bronchoconstriction, chest pain, dyspnea, headache, nausea, flushing

ADULT TACHYCARDIA
WITH A PULSE
ALGORITHM—2020
AHA
 ATROPINE SULPHATE

anticholinergic drug, tertiary amine- tropic acid & tropine

Routes – Orally ,IV,IM, SC, Topical, Endotracheally

0.5mg/ml ,0.6mg/ml and 1mg/ml inj

1ml ampoule/ 50 ml vial available.

• Mech. Of Action – muscarinic receptor antagonist.

.Lipid soluble, crosses BBB.

• Onset- 45-60 sec, IV, peak effect 2 min. IM-5-40 min, intratracheal- 10-20 sec.

• Duration of action- vagal blockade-30 – 60 min, antisialagogue – 4 hrs.

• USES & DOSES
• Vagolytic, treatment of bradycardia – 1 mg bolus IV, repeat can be given 3-5 min, max 3 mg.

• Bronchodilator-ipratropium bromide(derivative of atropine)-MDI/Nebulizer-bronchospasm

treatment in combination with beta 2 agonists
• Organophosphate poisoning– 2mg IV every 5-10 mins.as needed until ventilation improves

ADVERSE EFFECTS
• tachyarrhythmias
• Central Anticholinergic Syndrome(Restlessness ,Irritability, Disorientation, Hallucinations
atropine fever, dry mouth, tachycardia, impaired vision) in elderly patients
• Use cautiously in narrow angle glaucoma patients, prostatic hypertrophy, bladder neck
obstruction
 NALOXONE HYDROCHLORIDE

• 0.4 mg/ml

• Competitive Opioid antagonist --both endogenous and exogenous

• Affinity for mu receptors >>kappa /sigma receptors.

• Routes- IV/IM/IN/SC/Nebulization/ETT.

• Onset of action-1-2 min.

• Duration-30-45 min.

• USES

• Restores spontaneous ventilation in opioid overdose.

• Dose- 1-2 micrograms/kg. Cont. infusion dose 4-5 micrograms/kg/hr. for adults.
• AHA 2020 guidelines
Suspected opioid overdose patients without a pulse, CPR is of the utmost priority
• Naloxone can be administered along with standard ACLS care if it does not delay components of high-
quality CPR.
• Dose- 0.4 mg IM or 2mg intranasal; May repeat after 4 mins
• 2mg diluted in 3 ml normal saline for nebulization
• Appropriate dose and concentrations differ by route.

• Dose for neonatal resp depression d/t maternal opioid administration--10 mcg/kg, repeated in 2 min, if
necessary.

Side effects- increase in BP, heart rate ,pulmonary oedema, ventricular irritability, precipitate morphine
withdrawal
 SALBUTAMOL SULPHATE
• First line drug for STATUS ASTHMATICUS
• Several doses are given every 15-20 mins by metered dose inhaler with spacer or
• by continuous nebulization
• Onset- few minutes; Duration 4-6 hrs.
• Mech. Of Action-They stimulate Beta2 receptors of tracheobronchial tree.
Stimulatory G protein activates adenylate cyclase converting ATP into cAMP– reduces intracellular calcium
release & alters membrane potential--smooth muscle relaxation
Routes-oral/nebulization/IV/SC
No advantage of giving systemic Beta 2 agonists

SIDE EFFECTS
Tremors
Tachycardia
Hypokalemia ,Hypomagnesemia
Hyperglycemia
Transient decrease in oxygen tension
Tolerance
 PHENYTOIN SODIUM
• Indicated in STATUS EPILEPTICUS
• diphenyl substituted hydantoin
• Route I.V.,oral
• bradycardia, hypotension if injected fast
• Metabolized in liver

Mech. Of Action
•prevents repetitive detonation of normal brain cells during depolarization shift that occurs in epileptic
patients.
•prolongs the inactivated state of voltage sensitive neuronal Na Channel
At higher doses ——it reduces Calcium influx
inhibits glutamate and facilitate GABA

IN STATUS EPILEPTICUS(ADULT) DOSAGE• I.V –20 mg/kg in combination with a parenteral

benzodiazepine; additional dose of 5-10 mg/kg if required
Max loading dose 30 mg/kg
High therapeutic index
ADVERSE EFFECTS

At therapeutic levels

• Gum hypertrophy (commonest)

• Hirsutism
• Hypersensitivity reactions
• Megaloblastic anemia: it decreases folate absorption and increases its excretion
• Osteomalacia :it interferes with metabolic activation of vit D and with calcium absorption.
• Hyperglycemia by inhibiting insulin
• Fetal hydantoin syndrome- in pregnancy

Dose related toxicity

• Ataxia, vertigo, diplopia, nystagmus- characteristic features

• Drowsiness, hallucinations , behavioral alterations
• Epigastric pain , nausea, vomiting
• Fall in BP and cardiac arrhythmias
• I.V injection causes local vascular injury, edema and discolouration of injected limb
 DRUG DESCRIPTION

• Identify the drug • Uses

• Composition • Contraindications

• Physical properties • Adverse reactions, precautions

• Storage • Toxicity and management

• Dosage and administration • Drug interactions

• Pharmacokinetics

• Pharmacodynamics- system wise

Thank you
NEUROMONITORING
PRESENTER- Dr. Sandeep Kumar
Associate Professor Anaesthesiology
ABVIMS & Dr. Ram Manohar Lohia Hospital New Delhi
 INTRODUCTION

• Brain and spinal cord are a very complex organs to monitor

• Surgical patients are at risk of ischemic/hypoxic injury

• If we have to ensure the correct functioning of these structures we

have to monitor them separately and continuously
 MONITORING OF CNS FUNCTION
• Electroencephalogram ( EEG)

• Bispectral Index (BIS)

• Evoked Potential Monitoring (SSEP, Auditory, Visual &MEP)

• Electromyography (cranial nerves V, VII, IX, X, XI,XII)

• Brain Oxygen monitoring

• Brain metabolism monitoring

• Depth of anaesthesia - Bispectral Index & Entropy

 MONITORING OF CBF & ICP
CEREBRAL BLOOD FLOW (CBF)
• Laser doppler flowmetry
• Transcranial doppler sonography (TCD)

INTRACRANIAL PRESSURE (ICP)

• Intraventricular catheter
• Intraparenchymal catheter
• Epidural, subdural catheters
 Intracranial Pressure ( ICP)
• It is defined as the pressure within cranial cavity relative to the atmospheric pressure

• Normal: 5–15mmHg (healthy adults, supine)

• 3–7 mmHg (children)

• 1–5 mmHg (infants)

✓ Cut off values for treating ICP depends on the intracranial pathology

✓ For head injury treatment is initiated when the ICP exceeds 20–25mmHg

✓ High ICP is an indicator of brain injury and also results in secondary brain injury by reducing
cerebral blood flow (CBF)
 Indications for Intracranial Pressure
Monitoring
• Severe head injury with abnormal CT head scan

• Severe head injury with normal head CT with any of the two - age
>40years, systolic blood pressure < 90 mm Hg & abnormal motor
positioning

• Systemic diseases causing raised ICP, e.g., Reye’s syndrome & hepatic
failure
 Indications for ICP Cont..

• Head injury where clinical neurological examination is not possible for prolonged periods
of time (e.g., patients undergoing long duration under general anesthesia)

• Intra cerebral and subarachnoid haemorrhage (SAH)

• Cerebral infarction

• Hydrocephalus

• Meningitis

• Encephalitis
 Intra Cranial Pressure Monitoring
1. Invasive

A) Fluid-filled external pressure transducer: A catheter is inserted in to the

lateral ventricle and is connected to the transducer through fluid-filled tubing

B) Miniature strain gauge transducer (Codman): In this, the sensor is placed in

the tip of the catheter. Changes in ICP cause change in resistance of the circuit
within the sensor and is interpreted as waveform. Zeroing can not be done in vivo
(Zeroing drifting)
 ICP Monitoring Cont….
C) Fiberoptic (Camino): The sensor at the catheter tip uses a light source.
Pressure changes cause change in the light reflection and this is recorded as
pressure change (can”t zeroed in vivo)

D) Spielberg ICP system: In this system, a fluid-filled catheter has an air

balloon pouch at the tip of the catheter, any fluctuation in balloon pressure is
interpreted as ICP change
 ICP Monitoring Cont….

2. Non invasive

A) Transcranial doppler (TCD)

B) Optic nerve sheath diameter

C) Tympanic membrane displacement

 ICP monitoring cont..

• The catheter can be placed in the epidural/subdural/ intraparenchymal

or ventricular space

• Ventricular measurement is considered as gold standard

• Epidural and subdural sites are less commonly used (less accuracy)

• For intraparenchymal monitoring (Codman, Camino) a burr hole is

placed into the nondominant frontal region (white matter)
• External ventricular drains are considered the gold standard of ICP
monitoring

• In addition to measuring ICP, they can be used therapeutically to drain

CSF (i.e., CSF diversion) to treat increased ICP
• Micro transducer devices measure localized ICP, and their
measurements correlate well with those of EVDs

• They lack therapeutic potential but compared to EVDs because they

have lower rates of complications such as intracranial hemorrhage,
seizures, and catheter associated infections
 ICP waveform
• They may be used to evaluate intracranial compliance
• ICP waveform has three components under normal conditions:

a) P1 (percussion wave) represents arterial pulsation

b) P2 (tidal wave) represents the overall intracranial compliance and
c) P3 (dicrotic wave) represents the venous pulsations

❖When intracranial compliance diminishes, the P2 wave will increase

in amplitude and may exceed the P1 wave’s amplitude
ICP Waveform Comparison

Y
• Pathological ICP waveforms known as Lundberg A and B waves,
occur during sustained intracranial hypertension and represent a state
of reduced compliance
• Lundberg A waves last several minutes and represent sustained ICP
elevation to greater than 50 mmHg and concomitant reduction in CPP;
they indicate evolving brain injury

• Lundberg B waves last only 1–3 minutes and represent an elevation of

ICP that is less than the 50 mmHg range
• Lundberg C waves- represent ICP elevation <20 mmHg; 4-8 min,
clinically normal

• Lundberg B waves may indicate a compromise in the intracranial

compliance and may precede the development of A waves

• Lundberg A waveforms are always pathological, but B waveforms

vary in their clinical significance
 Laser Doppler Flowmetry

• Measures cortical blood flow in a small region of the brain adjacent to

the placement of the device

• Its utility is limited

• Requires a burr hole for placement

• It measures blood flow only in a small area of the brain

 TRANSCRANIAL DOPPLER (TCD)
• Primary modality for non invasive measurement of ICP

• It emits ultrasound waves that travel through various layers of tissue

until they encounter red blood cells (RBCs) in blood vessels

• After contacting the RBCs, the ultrasound waves are reflected back
and the frequency of the returning ultrasound waves indicates the
direction and velocity of blood flow in the large arteries of the brain,
most commonly the middle cerebral artery (MCA)
 TCD Cont…
• TCD can be used to calculate the pulsatile index (PI), which is the difference between systolic and
diastolic blood flow velocities divided by the mean blood flow velocity

• The PI correlates with invasively measured ICP

• Pulsatile index > 1.4 are indicative of elevated ICP and are associated with worse clinical
outcomes (sensitivity 88%, specificity 97%)

• TCD does not have the risks of invasive methods, but its main disadvantage is that it also does not
provide continuous data
 Trans ocular ultrasound of the optic nerve
sheath diameter
Increased optic nerve sheath diameter correlates with increased ICP,
because in between the optic nerve sheath and the nerve itself, there is
subarachnoid space which is in communication with the subarachnoid
space of the brain
Trans ocular ultrasound of the optic nerve
sheath diameter
• Optic nerve sheath diameter greater than 5 mm is pathological

• This noninvasive method of ICP monitoring can be easily performed at the

bedside

• Its accuracy is inferior to invasive ICP measurement and

• It does not provide continuous data

 Cerebral Blood Flow Monitoring
• CBF is normally maintained within a wide range of MAPs (50–150 mmHg)
by adjusting blood vessel diameter, so that CPP is maintained between 50
and 70 mmHg

• Impaired autoregulation, increased ICP, or decreased MAP may reduce CBF

and result in brain injury

• Cerebral blood flow monitoring may detect changes before they lead to
injury and it is used to guide preventive measures
 Invasive Cerebral Blood Flow Monitoring
• Thermal diffusion flowmetry (TDF) is an invasive technique that provides quantitative
assessments of regional CBF (rCBF)

• The TDF catheter utilizes a distal thermistor heated to a few degrees above the regional
tissue temperature, and a second more proximal temperature probe

• The difference in temperature between the two probes reflects the absolute blood flow
between them and is expressed in mL/ 100g/min
 Thermal diffusion flowmetry Cont..
• Thermal diffusion flowmetry can provide continuous CBF

• Normal rCBF values range between 40 and 70 mL/100g/min

• rCBF values less than 20 mL/100g/min will result in cerebral ischemia

without a concomitant reduction in metabolic demand (e.g., hypothermia,
drug-induced coma)
 Noninvasive Cerebral Blood Flow Monitoring
• Trans cranial doppler (TCD) also used for non invasive monitoring of CBF (ml/
gm/min)

• A blood flow velocity (BFV) in the middle cerebral artery (MCA) greater than 120
cm/sec is considered pathological and correlates with cerebral vasospasm
(sensitivity 73%, specificity 80%)

• Patients with SAH should have periodic TCD assessments for early diagnosis of
cerebral vasospasm
 Noninvasive Cerebral Blood Flow Monitoring
Lindegaard Ratio

• The severity of vasospasm can be graded using the Lindegaard ratio (LR), which
is the ratio of the MCA BFV to the BFV of extracranial internal carotid artery
(ICA)

• LR less than 3 is considered normal, whereas

• LR 3–6 is associated with mild to moderate vasospasm and LR greater than 6 with
severe vasospasm
• Although cerebral vasospasm is the most common cause of elevated CBF, it is
not the only pathologic cause

• Common conditions such as fever and increased cardiac output due to any cause
(e.g., peripheral shunting, hyperthyroidism, catecholamine administration) will
increase BFV

• Therefore, BFV should be interpreted in the context of the patient’s condition

• Another limitation is that TCD is not a continuous monitoring technique, and there
is risk of missing significant CBF changes between assessment
 Brain Oxygen Monitoring

• Critically ill patients recovering from neurologic injury are vulnerable

to decreased brain oxygenation

• There are several invasive and noninvasive methods of monitoring

brain oxygenation which are used to guide therapy
 Brain Tissue PO2 (PbtO2)
• Its an invasive probe inserted through burr hole into the brain parenchyma

• It measures oxygen tension in the surrounding brain

• A low PbtO2 is indicative of inadequate O2 delivery to that area of brain only

• Normal PbtO2 values range from 25 to 35 mmHg

• PbtO2 Values < 20 mmHg are suggestive of cerebral ischemia

• A level of less than 15mm Hg is concerning of cerebral hypoxia & warrants

intervention in TBI
 PbtO2

• It reflects oxygenation at the local area only- around the probe

• This may not guarantee oxygenation delivery to other regions of the

brain

• Treating anemia & increase in FiO2 can improve oxygen delivery

• Metabolic suppression with propofol or barbiturate as well as treating

hyperthermia can decrease the oxygen requirements
 Invasive Brain Oxygen Monitoring

• Jugular venous oxygen saturation (SjvO2) can be measured

intermittently by sampling blood from the jugular venous bulb from a
catheter placed in a retrograde direction, or continuously using a fiber
optic catheter similarly placed

• It is used to assess oxygen demand–supply mismatch

• In TBI and SAH, PbtO2 monitoring should always be used in
conjunction with ICP monitoring because

• Cerebral hypoxia may occur even when ICP and CPP are normal and
would otherwise go undetected and be potentially injurious
Jugular venous oxygen saturation (SjvO2)

• PbtO2 gives a local view of the balance of oxygen supply & demand SjvO2
provides same information for a larger portion of brain

• Catheter is inserted into the internal jugular vein in a retrograde fashion

• Catheter tip sits at the base of the skull in the jugular bulb

• It allows continuous as well as intermittent withdrawal of blood sample for

gas analysis
Jugular venous oxygen saturation (SjvO2)

• Confirmation of catheter tip by lateral cervical spine X ray

• Best dominant IJV most commonly right side is chosen

• Side dominance- via USG

• The SjvO2 values whether CBF is sufficient to meet the cerebral

metabolic rate of oxygen (CMRO2) of the brain

• Normal value is between 65-75%

Jugular venous oxygen saturation (SjvO2)
• In TBI SjvO2 < 50% has poor outcome
• It is reasonable to guide intraoperative hyperventilation by maintaining an
SjvO2 >50%
• The blood samples from the retrograde catheter be drawn very slowly to
avoid contamination from non cerebral venous blood
• SjvO2 is a global monitor that could easily miss small areas of regional
ischemia
Jugular venous oxygen saturation (SjvO2)
Noninvasive Brain Oxygen Monitoring Near-
infrared spectroscopy (NIRS)
• Primary non invasive method of measuring cerebral oxygenation

• It provides an indication of the balance between flow & metabolism

• Typically a senor is applied to the forehead

• A light signal is transmitted through the skin

skull & meninges into the cerebral cortex

 Near-infrared spectroscopy (NIRS)

• A complex analysis of the reflected light allows calculation of the

oxygenation of blood in the cortex which is a mix of venous & arterial
blood

• Values for cerebral oxyhemoglobin less than 60% are considered

pathologic and are associated with cerebral hypoxia
 Brain Metabolism Monitoring
Cerebral micro dialysis (MD)

• Allows direct assessment of the brain’s extracellular biochemical milieu by a fine-

tipped double-lumen probe with a semipermeable membrane inserted into the
subcortical white matter

• The fundamental principle of MD is the same as that of hemodialysis; substances

will cross a semipermeable membrane along their concentration gradient
 Cerebral micro dialysis cont..

• Perfusate, a fluid isotonic to the ECF, is introduced into the catheter and molecules

at high concentration in the ECF equilibrate through the semipermeable membrane

• The resulting micro dialysate can then be analyzed

• Microdialysis can be used to detect early signs of secondary neurological insult

 Cerebral micro dialysis cont..

• Glutamate (an excitatory neurotransmitter associated with the inflammatory

cascade), and glycerol (a marker of neuronal cell breakdown associated with
irreversible cell injury), can be measured at the bedside

• Several substances, including glucose, lactate, pyruvate etc can also be

measured
 Cerebral micro dialysis cont..
• Lactate-to-pyruvate ratio (LPR) LPR greater than 40 represent cerebral “metabolic
distress,”

• The combination of LPR greater than 40 and brain glucose levels less than 0.7
mmol/L represents brain “metabolic crisis.”

• These abnormalities have been associated with poor outcomes in TBI patients

• Detected metabolic changes can predict vasospasm in patients with high grade
SAH and may be used to guide timely treatment
 Electroencephalography (EEG)
• Summation of the excitatory postsynaptic potential generated by pyramidal cells
of cerebral cortex

• EEG is recorded from the cup electrodes or needle electrodes from the scalp

• It is a continuous, noninvasive indicator of cerebral function

• In helps in diagnosing non-convulsive seizures

 EEG

• EEG is used in titration of sedatives and antiepileptics in status

epilepticus, minimizing deleterious side effects

• EEG is a plot of voltage versus time of 1–35Hz frequency

• Based on the frequency, the waveforms are classified into different

bands

• Normally higher is the frequency, lower is the amplitude

EEG
• EEG is recommended in patients with an unexplained persistently altered
mental status or whose mental status does not recover following a clinical
seizure

• In comatose patients, it is estimated that 30% have a EEG-detected seizure

after 24 hours of monitoring that would have gone undiagnosed in the
absence of monitoring
• Prompt recognition and treatment of seizures prevents resistance to
antiepileptic therapy

• Continuous EEG also has been used to detect vasospasm and increased
ICP as a component of multimodal prognostication in cardiac arrest
 Indications Of EEG

• Carotid endarterectomy

• Cardiopulmonary bypass

• Aneurysm surgery , vascular bypass procedure

• If burst suppression is desired for cerebral protection

• ICU- Barbiturate coma (TBI)

Subclinical seizures
ELECTROCORTICOGRAM

• Recording of the spontaneous electrical activity of the brain from the

cortical surface or depth of the brain

• The waveforms are better localized and better delineated with

electrocorticogram

• It is recorded intraoperatively to delineate the seizure focus and area of

surgical resection
 Bispectral Index (BIS)

• Most commonly used and extensively studied monitor to assess depth

of anesthesia (degree of hypnosis)

• BIS is derived from raw EEG

• The monitor utilizes various sub parameters in time domain, frequency

domain, and bispectral domain
 BIS Cont..

• The values range from 100 (awake) to 0 (isoelectric EEG)

• As the patient is sedated the BIS value drops to <90

• The values of 60 to 40 are considered adequate hypnosis component of

general anesthesia

• A value of less than 40 is considered as deeply anesthetized

 ENTROPY
• Entropy means randomness
• The principle in measuring entropy is that as the depth of anesthesia
increases with the randomness in the EEG comes down
• The EEG and EMG are recorded from the sensor attached to forehead
• It calculates two parameters: state entropy (SE) and response entropy (RE)
• SE is calculated from the 0.8 to 32Hz frequency and RE is calculated from
0.8 to 47Hz
 SPECTRAL ENTROPY
• SE is a more stable number and ranges from 0 to 91 (isoelectric EEG to awake

state)

• For the calculation of RE, the EMG activity is also taken into calculation

• The RE ranges from 0 to 100 and for anesthesia, the recommended range for both

is 40–60

• The entropies are similar to BIS monitoring, although few studies suggest that

response to pain is better detected by entropy (RE) as the EMG is also included
 Evoked Potentials
• Somatosensory evoked potentials (SSEPs) are electrical signals emitted
from the cerebral cortex in response to a sensory stimulus delivered at the
periphery

• Used in combination with motor evoked potentials (MEPs) which are

electrical signals emitted from muscles in response to stimulation of the
motor cortex via scalp electrodes
• SSEP signals serve as an important noninvasive method of assessing
subcortical structures

• They are less subject to interference by intravenous hypnotics or sedatives

• SSEP & MEP requires specialized equipment and onsite interpretation by a

technician and in communication with a neurologist
 EVOKED POTENTIAL

• Helps to evaluate the integrity of the ascending somatosensory and

descending motor pathways

• It is an important component of intra-operative monitoring for surgical

complications during spine and brain surgery

• It is important to understand the effects of certain medications on EP and

select an proper anesthetic regimen that facilitates reliable monitoring
 Somatosensory Evoked Potentials (SSEP)
• Following peripheral stimulation, electrical activity travels along the posterior column
(proprioception, mechanoception) and spinothalamic pathways (nociception, thermal)

• The pathways are supplied by the posterior spinal artery

• At the level of brain stem, it is supplied by the vertebral arteries and perforators of the
basilar artery

• At the level of sensory cortex, vascular supply is from ACA (lower limb) and MCA
(upper limb, face and trunk)
 SSEP

• The stimulation site should be below the area at risk of ischemia from
surgery and the recording site should be above, so that the neuronal
pathway should travel through the area at risk from surgery

• Changes are considered significant if latency: prolongation by ≥10%

amplitude: decrease by ≥50%
Somatosensory Evoked Potentials (SSEP)
EVOKED POTENTIAL
 Variables Affecting SSEP

• Volatile halogenated- dose-dependent increase in latency and decrease in

amplitude. This effect is pronounced with the addition of nitrous oxide

• Intravenous: At low doses, barbiturates and propofol cause minimal changes

in SSEP. At higher doses, they cause delayed latency and suppressed

amplitude

• Etomidate and ketamine augment amplitude of SSEP

 Variables Affecting SSEP

• Opioids- bolus cause depression, low-dose minimal changes

• Alpha agonists- are compatible with intraoperative SSEP recordings

• Benzodiazepines have minimal depressant effects

• Neuromuscular blocking agents directly do not affect SSEP

 Variables Affecting SSEP
• Temperature: Hypothermia produces increased latency of cortical SSEP

• Hemodynamics: Ischemia can result in prolonged latency and reduced amplitude. Severe anemia
can affect cortical latency and amplitude

• Increased ICP can reduce amplitude and prolong latency of cortical SSEP

• Ventilation: Severe hypoxemia results in changes in amplitude of cortical SSEP

• Hypercapnia has no effect on SSEP. Though hypocapnia augments amplitude and reduce latency
of SSEP in awake volunteers, these effects are not seen in anesthetized patients
 USES OF EVOKED POTENTIAL
•Spinal procedures: intramedullary tumors, scoliosis surgery, spine
stabilization

• Cerebral vascular surgeries where the specific pathways are affected by

ischemia

• Intracranial aneurysm (median/ulnar nerve for MCA territory; posterior

tibial nerve for ACA territory)

• Carotid end arterectomy (CEA)

 LIMITATIONS OF SSEP

• Does not monitor spinal cord supplied by the anterior spinal artery

• A normal intraoperative SSEP does not rule out occurrence of

postoperative paraplegia

• Artifacts by OT table, cautery machine, convection warmer, anesthesia

machine, drill, CUSA, etc. can pose problems in SSEP recording

 MOTOR EVOKED POTENTIALS (MEP)

• MEP is an electromyographic potential recorded over muscles in the hand or foot in

response to depolarization of the motor cortex

• Depolarization can be achieved using electrical stimulation

• MEP is used in addition to SSEP

• Best recorded in absence of neuromuscular blockade

MOTOR EVOKED POTENTIALS (MEP)
 SPONTANEOUS ELECTROMYOGRAPHY (EMG)
• EMG signal is not intentionally generated through the stimulation in the
neural pathway

• It’s the continuous recording in the muscle regions innervated by nerve

roots around which surgeons work

• Its purpose is to detect damage to the those nerve roots during surgery
which allows to modify the surgical technique

• Muscle relaxants should be avoided

 CRANIAL NERVE MONITORING

• Indications are – Posterior cranial fossa & brain stem surgeries

• Cranial nerves with the motor components can be detected either

through spontaneous EMG or through EMG evoked by local electric
stimulation

• These include cranial nerves V, VII,IX,XI & XII

 Auditory Brain Stem Response (ABRs)
• This is also known as brain stem auditory evoked potential (BAEP) or brain stem
auditory response (BAER)

• It’s a specialized form of SSEP

• It is elicited by transient acoustic click stimulation to the eighth cranial nerve via
auditory apparatus

• Decrease in amplitude of BAEP >50% and prolongation of latency of more

than 10% is used as a warning criteria
Auditory Brain Stem Response (ABRs)

• A series of seven wave peaks are generated with this technique

• Latency of each peak has significance with respect to the integrity of

various parts of the auditory pathway

• Useful in acoustic neuromas surgery

• Can be used during surgery around the brain stem to infer its integrity
Auditory Brain Stem Response (ABRs)
 Auditory Brain Stem Response (ABRs)

• Anesthetic agents have only a minor effect on ABRs , and

neuromuscular blockade does not affect therefore anesthetic regimen
is not restricted by the use of ABR monitoring

• The body temperature decrease produces an increase in component

latencies of about 7% for each 1 °C
 VISUAL EVOKED POTENTIAL
• Surgeries involving the optic chiasma for pituitary adenomas,
craniopharyngiomas, tuberculum sellae meningiomas, or other tumors from the
optic pathway can pose a risk of visual impairment

• Internal carotid artery aneurysm clipping, which poses a risk of impeding the
blood flow to the ophthalmic artery
 VISUAL EVOKED POTENTIAL

• In this method, a flash stimulation device is placed over both eyelids

while the patient’s eyes are closed

• Flash stimulation can be performed at a frequency of < 4 Hz but is

generally performed at a frequency of around 1 Hz
 VISUAL EVOKED POTENTIAL
• When flash-stimulating the retina, it is necessary to confirm that the flash stimulus has
reached the retina by taking electroretinogram (ERG)

• Recording electrodes are placed 4 cm above the external occipital protuberance (Oz) and
4 cm to the left and right of Oz (O1 and O2, respectively; International 10–20 System)

• VEP is processed by averaging because they are extremely small potentials

 VISUAL EVOKED POTENTIAL

• A reduction in VEP amplitude is considered to be significant

(more than 50% compared with the baseline)

• Among intravenous anesthetic agents, only propofol has a small

suppressive effect on VEP, while other intravenous anesthetic agents
markedly suppress VEP
 Take Home Message….
• The risk imposed to CNS by neurosurgery warrants more extensive
monitoring

• For many procedures adequate oxygenation, ventilation & systemic blood

pressure do not ensure the well being of brain & spinal cord

• The integrity of CNS needs to be evaluated intraoperatively with monitors

that specifically detect CNS function, perfusion or metabolism

• At times monitoring modalities can be combined for better outcome

THANK YOU