Neuroanaesthesia Quiz

Recently I conducted a neuroanaesthesia test for our DNB students. It was designed to test their depth of understanding of fundamental concepts of anaesthesia for neurosurgery. By the way, Chintan, the topper got a prize from our HOD, Dr. Muralidhar.

If you want the answer key to this quiz, you will have to leave a comment.

NEUROANAESTHESIA QUIZ

Answer all questions. There is no negative marking. MCQs can have more than one correct answer and all the answer should be correct to get a mark.

Time: 45 mins

  Brain represents ___ % of body weight and receives about ____ % of cardiac output. Oxygen consumption of brain is about ___ ml/ 100 gms of brain tissue per minute, so total brain oxygen consumption constitutes about ____ % of total body oxygen utilization.

3. Normal ICP is __________

4. What can you understand by the illustration shown below

5. Two components of cerebral metabolic activity are

6. CMR decreases by _____ per °C of temperature reduction

7. Why isn’t it a good idea to rapidly normalize PaCO2 in a patient who has had a prolonged period of hyperventilation?

8. What do these different waveforms represent?(Name the different waveforms)

9. Main energy substrate used for energy production is ________

10. What is inverse steal phenomenon?

11. Complete the following table which shows the effects of anesthetics on CBF and CMRO2( Increase = ‘+’ , decrease = ‘–‘ and No change = '0' )

	CBF	CMRO2
Halothane
Isoflurane
Sevoflurane
Propofol
Thiopentone
Midazolam
Fentanyl
N20 with IV agents

12. “Pulsatality index” is measured by which monitoring modality _____________

13. What do you know about Near Infrared Spectroscopy?

14. Rationale of using beta blockers as premedication in neuroanaesthesia ____________

15. The following monitoring techniques are used to detect venous air embolism. Arrange them in decreasing order of sensitivity

a. Pulmonary artery catheter

b. ETCO2

c. TEE

d. Precordial Doppler

e. Mass spectrometry of ETN2

16. During preanaesthetic evaluation of a head injury patient you notice that he has flexion withdrawal response and is making some incomprehensible sounds. He doesn’t open his eyes even on painful stimulus. What is his GCS score?

17. Methods to control intracranial hypertension (at least four).

18. All the following are true about GABA except

a. GABA is inhibitory neurotransmitter

b. There are two major types of GABA receptors- GABA_A and GABA_B

c. GABA_A acts by opening chloride channels and GABA_B acts by opening potassium channels

d. Barbiturates and Benzodiazepines act by enhancing action at GABA_B

19. All are true about cerebral autoregulation except

a. It occurs between 50-150 mm Hg

b. It is a Myogenic response

c. Occurs immediately after the pressure change

d. Range of autoregulation is shifted to a higher pressure in hypertensives

e. Abolished by trauma, hypoxia, and inhalational anesthetics

20. All the following are true about CSF except

a. It is formed at a rate of 0.3-0.4ml /min allowing complete replacement 3-4 times a day

b. One of the three major components that occupy the space in skull, with other two being brain(neurons and glia) and Blood perfusing the brain

c. Furosemide and acetazolamide doesn’t decrease CSF production

d. Formed by choroid plexus epithelial cells

e. Has a higher protein concentration than serum

21. When the brain is stiff (low compliance) and enlarged, ICP

a. rises only minimally when the patient coughs

b. rises significantly with a small increase in arterial CO2

c. is unaffected by arterial desaturation (hypoxia)

d. falls if the patient is put in the head-down position

e. rises if the head is twisted to the left or right

22. Cerebral perfusion pressure (CPP)

i. is satisfactory if more than 70 mmHg in a patient with a head injury

ii. is calculated by adding mean arterial pressure (MAP) and ICP

iii. falls if arterial BP falls following induction of anaesthesia

iv. can be calculated by “guessing” ICP to be 20 mmHg after a head injury causing 5 min unconsciousness

b. when low should be treated by infusing dextrose-saline solution

23. All the following processes protect against ischemic damage of brain except,

a. Maintaining normal blood flow

b. Reducing metabolic rate, thereby maintaining ATP levels

c. Scavenging free radicals

d. Increasing intracellular concentration of sodium and calcium

e. Facilitating release of excitatory amino acids

24. Following a severe head injury, ICP will rise to damaging levels if

a. the patient develops airway obstruction

b. the patient becomes severely hypertensive

c. the patient is allowed to breathe halothane spontaneously during an anaesthetic

d. arterial hypoxemia occurs

e. the patient suffers severe pain from other injuries which is not treated

25. All the following are true with respect to focal ischemia of brain tissue except.

a. There are three regions in the ischemic zone

b. “Penumbra” is a region of normal blood flow

c. Inverse steal is beneficial in focal ischemia of brain tissue

d. Apoptosis occurs at less compromised region of ischemia and necrosis occurs at the core of ischemic area

26. All the following are true about effects of inhalational anesthetics on CBF except

a. Isoflurane and sevoflurane are the ideal volatile anesthetics for neurosurgery

b. Desflurane is recommended for space occupying lesions

c. Induction doses of sevoflurane( 1.5-2 MAC) causes epileptiform seizures in some patients

d. Volatile agents abolish PCO2 reactivity of CBF

27. Concerning intravenous agents

a. ketamine has no effect on ICP

b. thiopentone reduces ICP by direct cerebral vasoconstriction

c. a moderate fall in arterial BP following thiopentone in a patient with cerebral decompensation (raised ICP) need not be treated immediately

d. propofol does not effect cerebral metabolic rate

e. the patient will recover rapidly when anaesthesia has been maintained by a thiopentone infusion

28. EEG

a. Generated by pyramidal cells of granular cortex

b. Deep sleep and deep anaesthesia produce delta waves

c. Theta waves are high frequency, low amplitude waves seen in awake adults

d. Indicated intraoperatively in detection of cerebral ischemia, assessment of pharmacologic interventions(burst suppression) and brain death, diagnosis and management of intractable epilepsy

e. Plot of voltage against time

f. Frequency increased by high dose of intravenous agents like thiopentone, propofol, BZDs and etomidate

29. All the following are true about Sensory evoked potentials except,

a. There are three modalities – SSEPs, BAEPs, VEPs

b. Individual peaks are described in terms of amplitude, latency and polarity

c. For SSEP – 50% reduction in amplitude is clinically significant

d. Evoked potential of brainstem origin are more vulnerable anesthetic influence when compared to those of cortical origin

e. VEPs arise from the brain stem

f. Volatile agents cause dose dependent increase in latency and decrease in amplitude of cortical evoked potentials

30. Mannitol

a. Given IV in the dose of 0.25 – 1 gm/kg; action begins within 10-12 minutes and lasts for 2 hours

b. Larger doses produce longer duration of action

c. Is effective only when BBB is intact

d. Should be given rapidly for it to attain its peak onset of action early

e. Can cause a rebound increase of ICP

f. Prolonged use of mannitol may produce dehydration, electrolyte disturbances, hyperosmolality, and impaired renal function

31. About jugular bulb venous oximetry all are true except,

a. Estimates balance between cerebral oxygen demand and supply

b. Normal SjVO2 is 60-70%

c. Changes in oxygenation of systemic blood influences SjVO2

d. SjVO2 increases to >75% during ischemic injury

e. It doesn’t detect focal ischemia

32. Wakeup test

a. Commonly used in scoliosis surgery to identify reversible damage to CNS by spinal distraction

b. Patient is woken up after complete reversal of muscle relaxation

c. Patient “awareness” is one of the adverse effects of the test

d. TIVA is the anesthetic technique of choice

33. In semi sitting position all are true except

a. Reduced venous return to the heart

b. Increased chances of venous air embolism due to sub atmospheric pressures in cerebral veins and dural sinuses

c. Pressure transducer should be kept at the level of external auditory meatus

d. Spontaneous ventilation is better than controlled, since the latter further reduces the venous return

e. Provides very good access to posterior fossa tumors

34. White matter receives more blood than grey matter, since it plays a crucial role in the normal functioning of grey matter – T / F

35. Optimum burst suppression is obtained more commonly by thiopentone when compared to other anaesthetic agents. T / F

36. Cerebral oxygen consumption decreases above 42⁰ C. T/ F and why?

37. The magnitude of CBF reduction with Hypocapnia is greater during volatile anaesthetic. T / F and why?

38. Resting membrane potential of a neuron is nearer to the equilibrium potential of sodium. T/F

39. Children have higher CMRO2 than adults. T/F

40. Muscle relaxant can be given in just adequate doses while monitoring cranial nerves. T/F

41. Mill wheel murmur is one of the very useful early signs of venous air embolism. T/F

Anaesthesia for awake craniotomy

Awake craniotomy is performed for the surgical treatment of intractable seizures and tumors on the eloquent areas of the brain. Mapping of the normal areas of the brain is done to delineate them from the tumor intraoperatively. This involves stimulating the brain with small voltage ad high frequency currents and assessing patients verbal, motor and sensory response. Thus, an awake and alert patient is the fundamental requirement of this procedure. One can easily understand that keeping the patient awake and responding, pain free and comfortable during the surgery is quite a difficult task and  you can say that, awake craniotomy is more of an anaesthetic challenge than surgical. Recently, we performed an awake craniotomy for the first time in our institution for a tumor which was close to the motor areas of right cerebral hemisphere.
Medical literature is replete with numerous original articles and case reports on anaesthesia for awake craniotomy and thank god for that. It was invaluable for us to plan our anaesthetic. When you go through this knowledge bank on awake craniotomy, you will realise that there are mainly two  techniques commonly used for anaesthetizing these patients – conscious sedation with scalp blockade and “asleep-awake-asleep” (general anaesthesia (LMA with or without IPPV) and scalp blockade-awakening- general anaesthesia (LMA with or without IPPV). The latter technique supposedly ensures better patient comfort and outcome. Craniotomy involves performing scalp blockade (multiple injections), stabilizing the patient’s head on sharp-pinned frames (Mayfield, Sugita’s etc), raising the scalp flap, drilling and removing a piece of skull bone and lying down in quite uncomfortable position for a long time. No wonder it can be  quite a traumatic experience for an awake patient to go through all this for the entire duration of the surgery. So, ours was also a version of “asleep-awake-asleep” technique.
Our patient was a 35 year old male(weighing 61 Kgs) with a glioma over the right parietal sub cortical area measuring about 15 x 15 mm. He had presented with seizures and slurring of speech three months before the day of surgery. He did not have any focal neurological deficits and the speech had also normalized. He had developed allergic bronchial asthma two months before the date of operation, which was attributed to exposure to cold and dusty climate. He was being treated with bronchodilators and inhalational steroids for the same and had become asymptomatic at the time surgery. He was a very cooperative and highly motivated gentleman and had fully understood the need for the procedure and various steps involved. A thorough and patient explanation and showing a video of the procedure helped a great deal in preparing the patient for the procedure. During preanaesthetic examination his upper incisors were found to be significantly mobile and were extracted.
I will give our anaesthesia plan now. I hope it will be of use to somebody. I eagerly welcome all kinds of comments.

Premedication

All his medications (anticonvulsants, bronchodilators) were continued till the morning of the surgery.
T. Clonidine 150 mcg, T. Diazepam 10 mg, T. Pantoprazole 40 mg, inj. Dexamethasone 8 mg, T. Ondansetron 4mg – one hour before the surgery
Salbutamol and Ipratropium bromide nebulisations just before shifting him to operation theatre

Monitoring

Pulse oximetry, ECG, Noninvasive Blood Pressure, ETCO2, Bispectral Index monitor, Invasive Blood Pressure and urine output ( both after induction).

Induction

Intravenous line (16 G) was secured in left hand dorsum under local anaesthesia. Preoxygenated with 100% oxygen and induced with inj. Fentanyl 100 mcg, inj. Propofol 100mg. Size 4 Intubating Laryngeal Mask Airway (ILMA) was inserted and patient was allowed to breathe spontaneously. Anaesthesia was maintained with propofol infusion (50 mcg/kg/min) and sevoflurane (End tidal concentration of 1-1.5%) to BIS of about 50.
Right radial artery was cannulated with 20 G catheter to monitor invasive blood pressure.

Scalp Blockade

Total amount of solution used – 80ml
0.5% Bupivacaine – 40ml
2% Lidocaine – 20ml
Adrenaline – 400 mcg(in 4ml saline)
Saline – 16ml

Nerves blocked – supraorbital, supratrochlear, zygomatico temporal, auricuculotemporal, posterior auricular, lesser occipital and greater occipital on both sides with 2-3ml of drug mixture for each nerve.

Landmarks for the nerves-

a. Supraorbial and supratrochear - above eyebrow at the midpoint, needle  inserted perpendicular to the skin. Also at the medial margin of the orbit

b. Auriculotemporal - 1.5cm anterior to the tragus; needle inserted perpendicular to skin.

c. Zygomatico temporal - midway between supraorbital ridge and post margin of Zygoma; deep infiltration with in the temporalis muscle and fascia

d. Post auricular branches( of greater auricular nerve) - 1.5 cm posterior to th ear at the level of tragus between skin and bone

e. Greater and lesser occipital nerves - along the superior nuchal line approximately halfway between occipital protruberance and mastoid process; infiltration done with 22 G spinal needle.( all other blocks done with 23G 4cm needle)

Remaining soultion used to infiltrate over the pin sites(3) and along the line of incision.

Block was done 15 mins before the procedure and we hoped that it would last for atleast 4-5 hours.

Success of the block was noted by observing that there was no hemodynamic response to pin insertion and to the skin incision. Also, patient was completely pain free through out the procedure which lasted for 6 hours. Only 175 mcg of Fentanyl was used through out the procedure.

Draping for the procedure

Draping for this procedure was little different from that for usual craniotomies. A transparent screen separated head end and the operating site from the rest of the body so that we had unhindered access to the same.

Maintenance and awakening

 Anaesthesia was maintained with propofol infusion (50mcg/kg/min) and sevoflurane (end tidal concentration of 1.5-2%). BIS was maintained around 50. Patient received 0.5 gm/kg mannitol before craniotomy along with Furosemide (20 mg). Surgeon infiltrated dura with 6 cc of 1% lidocaine before incising it. Twenty minutes before planned awakening, sevoflurane was discontinued and propofol infusion was decreased to 25 mcg/kg/min. Patient started moving his limbs when the BIS was about 75. Propofol infusion was fully stopped. LMA was removed after suctioning, when the BIS was between 75 – 80 and patient responsive to oral commands. Another 5 mins was allowed for the patient to fully regain consciousness. Patient became fully awake and responsive when the BIS was around 90.

Cortical mapping and tumor excision was done, to which patient cooperated fully. Excision was completed in about 45 minutes. Patient kept complaining about desire to pass urine, in spite of being told that his bladder had been catheterized. Probably, the patient would have been much more comfortable if only we could somehow abolish the sensation of catheter in the urethra.

He also had mild generalized head ache towards the end of excision, which he felt was quite tolerable. There were no complaints from the surgeon about bulging of the brain. Hemodynamics was maintained at patient’s normal levels through out the procedure and they remained stable through out.

 “Asleep” again

 Patient was anaesthetized again with propofol 2mg/kg and fentanyl 75mcg and ILMA was reinserted. There was not much difficulty in accomplishing this. Patient was allowed to breathe spontaneously and anaesthesia was maintained with sevoflurane (2%) and propofol infusion at 50 mcg/kg/min. Surgeon started closing the dura. Patient received Morphine 6 mg for post operative pain relief. Five minutes after this, the breathing became strenuous with reduced rate along with Inspiratory sound similar to stridor. Anaesthesia was deepened further by increasing both propofol infusion and sevoflurane concentration. There was no improvement, rather breathing seemed to worsen, ETCO2 started increasing (to >45 mm Hg) and surgeon complained of bulging of brain out of the craniotomy site. We suspected displacement of LMA and reinserted the same. Meanwhile we reduced the depth of anaesthesia, which increased the respiratory rate with improvement in patient’s breathing. Rest of the surgery was completed uneventfully.

 Post operative period

 Post surgery, we removed the ILMA when patient was fully awake. The post operative period was uneventful. Patient was awake, alert and comfortable through out. There were no neurological deficits. He was kept in neurosurgery intensive care unit overnight and was shifted to the ward the next day. He was discharged from the hospital after two days of surgery.

P S :

This was our first experience with awake craniotomy. It was indeed a very interesting and learning experience. Please leave comments before you surf away from this page..