Section 3

Question 1

You are asked to see a 20-year-old female who is 30/40 pregnant. Her past medical history consists of Insulin Dependent Diabetes Mellitus (Type I DM) and asthma.
She has been admitted with an infected hand and a short history of abdominal
pain.
Her current medications are salbutamol inhaler prn, insulin glargine (Lantus) 20 U
nocte and actrapid 6–8units TDS with meals.
Urine dipstix White cells +
Proteins ++
Ketones +++
Glucose +
summarise the case.

Answer 1

A 20-year-old woman with known Type I DM presenting with an infected hand requiring surgical debridement complicated by the fact that she is 30 weeks pregnant and showing signs of diabetic ketoacidosis (raised blood sugar, compensated metabolic acidosis, and abdominal pain).

Question 2

Can you explain the blood results? Which are consistent with pregnancy?

Answer 2

• Most striking abnormality is metabolic acidosis on blood gas with raised blood glucose and ketones in urine consistent with diabetic ketoacidosis (DKA)
• Raised urea consistent with dehydration, bordering on acute renal failure when taken in context with creatinine (GFR is usually much increased in pregnancy ∼ 50% at term; therefore, although creatinine is in range, it is much higher than would be expected for the increase urea and creatinine clearance than one would expect at this stage of pregnancy)
• Raised white cell count with neutrophilia consistent with bacterial infection (infected hand)
• Mild anaemia consistent with physiological anaemia of pregnancy (plasma volume increases by up to 45% with only a 20%–30% increase in red cell mass, hence a ‘physiological’ anaemia)

Question 3

Discuss the management of DKA

Answer 3

General management
• Managed in HDU setting
• Joint care with obstetricians and medical team
○ DKA consists of the biochemical triad of ketonaemia, hyperglycaemia, and acidaemia. ○ Therefore, management is directed at correcting these key issues.
• Full clinical history and examination
• Rapid ABC assessment including a full set of observations and Glasgow coma score
• Large-bore IV access (or central access if this is not possible)
• Consider precipitating causes and treat appropriately
• All patients with DKA need specialist diabetic team input within 24 hours of admission
Initial investigations
• Blood: blood glucose, urea and electrolytes, full blood count, blood cultures, blood gas
• ECG to look for arrhythmias due to associated electrolyte abnormalities
• Chest radiograph if clinically indicated
• Urinalysis and culture to rule out infection
Specific Treatment
• Drugs
° Establish usual medication for diabetes
° Commence a fixed rate insulin infusion (FRII), if weight not available from patient estimate weight in kg (in pregnancy you should use patients current weight)
• Fluids
° Restore circulating volume with boluses of 500 mL–1000 mL 0.9% sodium chloride if systolic blood pressure is < 90 mmHg (may need more depending on response and may need to consider use of vasopressors to maintain BP)
° The suggested regime in a previously healthy 70 kg adult would be:
- 1L 0.9% sodium chloride over first hour
- 1L 0.9% sodium chloride with potassium chloride over next 2 hours
- 1L 0.9% sodium chloride with potassium chloride over next 2 hours
- 1L 0.9% sodium chloride with potassium chloride over next 4 hours
- 1L 0.9% sodium chloride with potassium chloride over next 4 hours
- 1L 0.9% sodium chloride with potassium chloride over next 6 hours
- Mandatory reassessment of cardiovascular status at 12 hours
° once blood glucose is less than 14 mmol/L, then 10% dextrose should be commenced at 125 mL/hr and ran with the normal saline
• Electrolyte replacement
° If potassium is > 5.5 mmol/L, no potassium replacement is given in fluid infusions
° If 3.5–5.5 mmol/L, 40 mmol per litre of saline should be given
° Below 3.5 mmol/L requires senior ITU input as more potassium will need to be given with extra monitoring
• Goals
° Aim is to reduce blood ketones and suppress ketogenesis
° Achieve a fall of ketones of at least 0.5 mmol/L/hr
° Get resolution within 12–24 hours
• The precipitating cause needs to be treated (in this case, the infected
hand)

Question 4

How do you make a sliding scale insulin or Variable Rate intravenous insulin infusion (VRiii)?

Answer 4

• The latest guidelines for the management of DKA no longer recommend the use of a sliding scale insulin
• A fixed rate insulin infusion is made by drawing up 50 units of human soluble insulin (e.g. actrapid) and making it up to 50 mL with 0.9% sodium chloride. This is then run at 0.1 units/kg/hr until the ketone level is less than 0.6 mmol/L

Question 5

Which fluids would you give her and why? DKA

Answer 5

• There are several mechanisms responsible for fluid depletion in DKA
° osmotic diuresis due to hyperglycaemia
° Vomiting—commonly associated with DKA
° Inability to take in fluid due to a diminished level of consciousness
• Electrolyte shifts and depletion are in part related to the osmotic diuresis
• Hyperkalaemia and hypokalaemia need particular attention
○ I would follow the fluid regime above and tailor it to the specific needs of the patient.
○ I would use 0.9% sodium chloride with potassium chloride as required as it is compliant with NPSA safety regulations, but I would be aware of the risk of hyperchloraemic acidosis.

Question 6

the surgeons are keen to debride her hand. Describe how you would anaesthetise her.

Answer 6

At this stage I wouldn’t anaesthetise her; she needs her DKA treated and her fluid status optimised prior to receiving an anaesthetic, be that regional or general

Question 7

You arrange a bed for her on the high-dependency unit, and 18 hours later her DKA has corrected but her hand still requires surgical debridement. What is your anaesthetic choice?

Answer 7

Regional vs. general anaesthesia.
• My preferred method would be regional in view of recent metabolic derangement and pregnancy.
○ Axillary brachial plexus block is the choice for forearm and hand surgery.
• If GA is planned, then this would need to be a rapid sequence induction.
There is a risk of difficult airway and a need for left lateral tilt.
• Ensure well-balanced anaesthetic avoiding hypoxia, hypercarbia, and hypothermia.
• Fetus would require CTG monitoring.

Question 8

Describe the technique for performing an axillary brachial plexus block.

Answer 8

General
• Full anaesthetic history and examination
• Informed consent of the patient
• Trained assistant
• Full monitoring as per AAGBI guidelines
• Ultrasound machine
• IV access
conduct of block
• Aseptic technique
• Ultrasound probe positioned with short axis to arm just distal to pectoralis major insertion
• Aim to achieve local anaesthetic spread around the axillary artery covering median, ulnar, and radial nerve and a separate injection to cover the musculocutaneous nerve
• Total volume of local anaesthetic 20–25 mls of 0.25% L – Bupivacaine (5–7 mL around each nerve)

Question 9

Look at the ultrasound image in Figure 3.1a and name the structures.

Answer 9

○ Median, ulnar, and radial nerves are seen scattered around the axillary artery with the tissue sheath.
○ The musculocutaneous nerve is seen between the biceps and coracobrachialis away from the rest of the brachial plexus.
○ The axillary vein is compressed leading to the possibility of accidental intravascular injection of local anaesthetic

Question 10

As you inject the local anaesthetic for your block, the woman begins to have a seizure. What is your differential diagnosis?

Answer 10

• Non-pregnancy-related: local anaesthetic toxicity, hypoxia, hypoglycaemia, epilepsy, metabolic derangement (e.g. cerebral oedema from DKA)
• Pregnancy-related: Eclampsia

Question 11

Describe how you would manage
the seizures.

Answer 11

• Call for help.
• Give 100% oxygen.
• Maintain an airway, with intubation if necessary.
• Establish IV access.
• Give IV benzodiazepine in incremental doses to terminate the seizure.
• Ensure left lateral position.
• Treat the cause

Question 12

Describe the specific management of seizures related to local anaesthetic toxicity

Answer 12

• Recognise: change in mental status, severe agitation or loss of consciousness with or without seizures, and cardiovascular collapse.
• immediate management:
° Stop injecting local anaesthetic.
° Call for help.
° ABC: Maintain airway (secure with ETT if necessary), give 100% oxygen, confirm and establish IV access.
° Control seizures with incremental doses of benzodiazepine, propofol or thiopental, assess cardiovascular status throughout. Conventional therapies to treat hypotension, bradycardia, and tachyarrhythmia.
• intralipid:
° Initial bolus: 20% lipid emulsion 1.5 ml/kg over 1 min and start an infusion at 15 ml/kg/hr.
○ After 5 min, if cardiovascular stability not restored, give further two boluses.
○ Continue infusion at same rate, but if she remains unstable after 5 min, increase to 30 ml/kg/hr.

Question 13

What may be the causes for difficult ventilator weaning?

Answer 13

Respiratory causes
• Insufficiently treated pulmonary disease
• Auto-PEEP and hyperinflationbcardiac causes
• Concomitant cardiac disease
others
• Poor nutrition
• Electrolyte imbalance
• Critical illness neuropathy/ICU weakness
• Poor technique—inadequate rest following an exhausting spontaneous breathing tria

Question 14

You mentioned icU weakness.
How can you define it?

Answer 14

○ ICU-acquired weakness (ICUAW) is ‘clinically detected weakness in critically ill patients in whom there is no plausible aetiology other than critical illness’.
○ The criteria for diagnosing ICUAW are the presence of most of the following
factors:
• Weakness developing after the onset of critical illness
• Weakness being generalised, symmetrical, flaccid, and generally sparing the cranial nerves (e.g. facial grimace is intact)
• Muscle power assessed by the Medical Research Council (MRC) score of < 48 (or a mean score of < 4 in all testable muscle groups) noted on > 2 occasions separated by > 24 hours
• Dependence on mechanical ventilation
• Other causes of weakness having been excluded

Question 15

can you list the differential
diagnosis for icUAW?

Answer 15

• Spinal cord dysfunction
• Critical illness myopathy
• Guillain-Barre syndrome
• Motor neuron disease
• Preexisting neuropathy
• Myasthenia

Question 16

What can cause icU weakness?

Answer 16

○ ICUAW can be classified into those with critical illness polyneuropathy (CIP), critical illness myopathy (CIM), or critical illness neuromyopathy (CINM).
○ The causes are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome.
○ Risk factors for CIP, CIM and CINM include:
• Severe sepsis/septic shock with multi-organ failure
• Prolonged mechanical ventilation
• Prolonged bed rest
• Glucose and electrolyte abnormalities
• Use of parenteral nutrition, renal replacement therapy, steroids, muscle
relaxants, vasopressors, and aminoglycosides

Question 17

What is the difference between critical illness polyneuropathy and critial illness myopathy?

Answer 17

• Similar symptoms and presentations
• Often distinguished largely on the basis of specialised electrophysiological testing or muscle and nerve biopsy

Question 18

can you tell me the details of the electrophysiological investigations required for diagnosisnof ICUAW?

Answer 18

• Nerve conduction studies to determine nerve conduction velocities and stimulated amplitudes [compound motor action potentials (CMAPs) and sensory nerve action potentials (SNAPs)]
• Electromyography to look at muscle electrical activity [motor unit potential (MUP) amplitudes, durations, and fibre recruitment patterns] both at rest and during activity

Question 19

How may ICUAW be treated?

Answer 19

• No intervention has been shown in prospective study to improve the outcome
• Focus on prevention
• Optimise rehabilitation
Prevention of icUAW
• Minimisation of the risk factors (as above)
• Intensive insulin therapy

Question 20

can you mention a few care bundles you are aware of in the intensive care unit?

Answer 20

Ventilator care Bundle
• Elevation of the head of the bed
• Peptic ulcer disease prophylaxis
• Deep venous thrombosis prophylaxis
• Daily oral care with Chlorhexidine
central Line Bundle
• Appropriate hand hygiene
• Chlorhexidine skin prep
• Maximal barriers for central line insertion
• Subclavian vein placement is preferred site
• Review lines daily and remove unnecessary catheters
sepsis care Bundle
Three-hour bundle
• Measure lactate level
• Obtain blood cultures prior to administration of antibiotics
• Administer broad spectrum antibiotics
• Administer 30 mL/kg crystalloid for hypotension or lactate ≥ 4 mmol/L
six-hour bundle
• Apply vasopressors (for hypotension that does not respond to initial fluid
resuscitation) to maintain a mean arterial pressure (MAP) ≥ 65 mm Hg
• Measure central venous pressure (CVP) and central venous oxygen
saturation (Scvo2) in refractory hypotension
• Remeasure lactate if initial lactate was elevated

Question 21

A 16-year-old girl with learning difficulties is put on the operation list for dental corrective surgery (surgery due to last 1 to 2 hours). You are asked to preassess this patient.
What are the causes of learning difficulties?

Answer 21

○ The underlying problems in these children may include neurological disability,
developmental delay, behavioural disorders, autism, and mental health or personality problems.

Question 22

What are the issues with this case neuro developmental delay?

Answer 22

• Poor dental hygiene.
• Uncooperative and communication may be challenging.
• Higher risk of infection like hepatitis B, especially in institutionalised individuals.
• Other medical conditions and physical abnormalities may co-exist, such as epilepsy, reflux, and cardiac anomalies.
• Consent issues.

Question 23

What is capacity? How will you assess capacity in this patient?

Answer 23

○ A capable (or competent) person is one who has reached 18 years of age and who has the capacity to make decisions on their own behalf regarding treatment.
○ In England and Wales competent young people of 16 or 17 years of age can give consent for any surgical, medical, or dental treatment; it is not necessary to obtain separate consent from the parent or guardian.
○ The Mental Capacity Act 2005 governs the treating of an incapable person.
○ occasionally in some cases the Act permits medical treatment to be given without the patient’s consent, as long as it is in their best interests and has not been refused in a valid and applicable advance directive (living will) or advance decision.
in adult:
○ Every adult is assumed to be capable. The default position, therefore, is that
all adults have capacity until they are proven otherwise. No other person can
consent to treatment on behalf of any adult, including incompetent adults.
Any treatment, investigation, or physical contact with the patient undertaken
without consent may amount to assault.
But treatment may be given if it is in their best interests, as long as the requirements of the Mental Capacity Act 2005 are adhered to.
in children:
only people with ‘parental responsibility’ are entitled to give consent on behalf of their children.
Parental responsibility is defined in the Children Act (1989) as “All the rights, duties, powers, responsibilities, and authority which by law a parent of a child has in relation to a child and his property” (Children Act 1989, section 3).

Question 24

What are the consent and
parent-guardian issues in
adolescents?

Answer 24

‘Consent’ is a patient’s agreement for a health professional to provide care.
Patients may indicate consent nonverbally, orally, or in writing.
Parent-guardian:
The mother has an automatic right to parental responsibility. The father
has an automatic right only if he was married to the mother at the time of
birth, although he can acquire parental responsibility by court order or by
agreement.
In some circumstances, another person may have acquired parental
responsibility (e.g. a legal guardian, adoptive parent, or a social worker).
Age:
• If a person under 18 years of age refuses treatment that is deemed
essential, then the patient can be made a ward of the Court and the
Court may order that an operation may be carried out lawfully.
• If a young person of 16 or 17 years of age is not competent to give
consent, then the consent of a parent should be sought, unless
immediate treatment is required to prevent death or permanent injury.
• If a child under the age of 16 years achieves a sufficient understanding of
what is proposed, he or she may consent to treatment. The child must be
Gillick competent

Question 25

What is Gillick competence?

Answer 25

○ This term is used in medical law to decide whether a child (16 years or younger) who has achieved sufficient understanding of what is being proposed is able to consent to his or her own medical treatment, without the need for parental permission or knowledge. ○ However, in cases where a competent child has refused or resisted medical treatment, the courts have upheld the right of the parents to consent for the child’s treatment up to the age of 18 years.
○ Lord Scarman’s test is generally considered to be the test of ‘Gillick competency’. He required that a child could consent if he or she fully understood the medical treatment that was being proposed.
○ Fraser guidelines are concerned only with contraception and focus on the desirability of parental involvement and the risks of unprotected sex in children younger than 16.

Question 26

Who are iMcAs?

Answer 26

The IMCA service is provided for any person aged 16 years or older, who has no one able to support and represent them, and who lacks capacity to make a decision about either:
1. a long-term care move
2. a serious medical treatment
3. adult protection procedures
4. a care review

Question 27

What are the different types of
consent forms you have come
across?

Answer 27

Form 1: For adults or competent children
Form 2: For parental consent for a child or young person
Form 3: For cases where the patient will remain alert throughout the
procedure and no anaesthetist will be involved in their care
Form 4: For adults who are unable to consent to investigation or treatment

Question 28

What problems might you encounter while anaesthetising her nurodevelopmental delay in the anaesthetic room?

Answer 28

○ Difficult rapport and aggressive and combative behaviour at induction
requiring sedation.
○ Premedicants like midazolam reduce anxiety at induction of anaesthesia and reduce postoperative behavioural disturbances.
○ Parent-guardian presence at induction and in the recovery area is necassary to eliminate separation anxiety.
○ Starvation status may not be adequately followed by the patients

Question 29

What are criteria for offering GA in a day-care dentistry?

Answer 29

○ The General Dental Council and the Royal College of Anaesthetists guidelines state that general anaesthesia for dentistry should only be administered for:
• Situations in which it would be impossible to achieve adequate local anaesthesia and complete treatment without pain
• Patients who, because of problems related to age/maturity or physical/learning disability, are unlikely to allow safe completion of treatment
• Patients in whom long-term dental phobia will be induced or prolonged

Question 30

You are preassessing a 22-year-old female patient for Functional Endoscopic Sinus Surgery (FESS). She gives a history of palpitations for which she was admitted to A&E a year ago.What are the causes of palpitations?

Answer 30

• Anxiety
• Exercise
• Panic attacks
• Caffeine, alcohol
• Drugs: Thyroxine, cocaine, beta 2 agonists
• Cardiac: MI, arrthymias, ectopics, AF, flutter, VT, reentry tachyarrhythmia
• Endocrine: hyperthyroidism, hypoglycaemia, phaeochromocytoma

Question 31

Why do arrthymias occur?

Answer 31

• Reentry circuits
• Enhanced automaticity
• Triggered activity

Question 32

What investigations would you
like her to have?

Answer 32

• History and examination is paramount
• ECG: 12-lead, 24-hour, ambulatory
• Cardiac electrophysiological study
• Bloods, to rule out endocrine causes

Question 33

Figure 3.2 illustrates her ecG.
comment on the positive findings.
What is the diagnosis?

Answer 33

Rate: 75/min
Sinus rhythm
Normal axis
PR interval: 3–4 small squares (not very short)
Initial slow upstroke of QRS but later becomes normal complexes
Presence of delta waves

Question 34

explain to me what
Wolff–Parkinson-White (WPW)
syndrome is.

Answer 34

• Presence of faster accessory pathway (bundle of Kent) between atrium
and ventricle (accessory AV pathway)
• This pathway conducts impulses faster than the normal AV node
• Electrical signals traveling down this abnormal pathway may stimulate
the ventricles to contract prematurely, resulting in a unique type of
supraventricular tachycardia

Question 35

What are the characteristics of
ecG in WPW?

Answer 35

• Sinus, normal axis, short PR interval
• Presence of delta waves

Question 36

What is a delta wave?

Answer 36

• Accessory pathway conducts impulse faster than AV node, resulting in short PR interval
• The initial depolarization takes place in ventricular muscle; hence, the slow and slurred delta wave
• Later, when the impulse arrives at the AV node, bundle of His and Purkinje carries the impulse, which is normal and faster than ventricular wave; hence, the rest of the QRS is normal

Question 37

What are the treatment options for patients with WPW syndrome?

Answer 37

• Risk stratification to exclude patients who are at risk of sudden death.
-This is done with the presenting symptoms of syncope, etc., and with
invasive electrophysiological studies
• Pharmacological therapy for stable tachyarrhythmias and cardioversion for decompensated patients
• Drugs: Commonly used drugs are amiodarone and procainamide.
-Drugs such as adenosine, diltiazem, verapamil, and beta blockers are avoided due to the risk of slowing the heart’s normal conduction and favouring accessory conduction leading to unstable dysrhythmias
• Ablation: Definitive treatment is by radiofrequency ablation of the accessory pathway

Question 38

What are the implications of WPW for anaesthesia?

Answer 38

○ There is a tendency to paroxysmal supraventricular tachycardia in the perioperative period and there may be associated congenital cardiac abnormality.
○ Unmasking of WPW syndrome under either general or regional anaesthesia has been reported, which means the patient was asymptomatic with normal ECG preoperatively and under anaesthesia re-entrant arrhythmia gets unmasked with clinical symptoms.
○ Anaesthetic drugs tend to change the physiology of AV conduction. If the
patient is asymptomatic, then risk of perioperative arrhythmias is much less.
• General anaesthesia
Avoid light planes of anaesthesia and drugs that can precipitate tachycardia (like atropine, glycopyrrolate, ketamine) resulting in paroxysmal supraventricular tachycardia or atrial fibrillation.
- opioids, such as fentanyl, and benzodiazepines, including midazolam, have been found to have no effect on the accessory pathway.
-There are references showing disappearance of delta waves after propofol administration, making it the drug of choice for induction.
-Isoflurane and sevoflurane have been found to have no effect on AV node conduction, making these agents preferable for maintenance of cardiostability
- Short acting nondepolarizing muscle relaxant without histamine release would be an acceptable choice as reversal of neuromuscular blockade using neostigmine and glycopyrrolate is not required.
• Regional anaesthesia
-There is significant advantage over general anaesthesia as multidrug administration, laryngoscopic stimulation, intubation, and light planes leading to sympathetic stimulation are avoided.

Question 39

What are the common types of tachyarrhythmias that can develop in the perioperative
period?

Answer 39

There are two common life-threatening arrhythmias that occur in patients
with WPW.
• Atrial fibrillation leading to ventricular fibrillation
• Circus re-entrant tachycardia causing ventricular or paroxysmal supraventricular tachycardias.
- Ventricular tachycardias are very difficult to treat and may even be life threatening

Question 40

How would you manage intraoperative tachyarrthymias?

Answer 40

○ After taking all precautions, if arrhythmias develop, the patient is treated after a careful ABC assessment.
Atrial fibrillation
• The treatment principle is to prolong the anterograde refractory period of the accessory pathway relative to the AV node.
-This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate.
-This is in direct contradiction to the goal of treatment of non-WPW atrial fibrillation, which is to slow the refractory period of the AV node
Paroxysmal supraventricular tachycardia
• Vagal manoeuvres initially
• Haemodynamically stable: Lignocaine, adenosine, disopyramide, and procainamide can be used.
- These drugs block transmission via the accessory pathway by blocking fast sodium channel
• Haemodynamically unstable: Synchronized DC cardioversion at 25–50 J
may be needed for atrial fibrillation.
- Digitalis and verapamil are strictly contraindicated in patients with pre-excited atrial fibrillation or flutter with rapid conduction over an accessory pathway
-Treat possible triggers: hypoxia, hypercarbia, acidosis, and electrolyte imbalance

Question 41

When would you monitor cranial nerves (cn)?

Answer 41

surgical
• Intraoperatively during a surgical procedure to identify the nerve, preserve function, and prevent intraoperative injury.
-Several neurosurgical procedures warrant routine monitoring of cranial nerves depending on the position and extent of surgery.
-All cranial nerves except CN I can be monitored. As most cranial nerves are motor, placing the EMG electrodes on muscles supplied by the nerve tests their function.
-CN VIII, being a sensory nerve, is tested by brainstem evoked auditory potential
(BAEP). CN II is rarely monitored.
• III, IV, and VI: removal of tumours at clivus or skull base
• V: microvascular decompression for trigeminal neuralgia
• VII: acoustic neuroma and parotid gland surgery
• VIII: cerebello pontine angle tumours
• IX: radical neck dissection
• X: thyroid or vocal cord surgery
• XI and XII: skull base (jugular glomus tumour) surgery neurophysiological
• Intraoperative nerve monitoring to assess the degree of neuromuscular block (commonly used technique is the Train of Four (ToF)).
- Peripheral branches of the facial nerve are used due to their ability to cause visible
muscular contractions and their proximity to the skin.
• Brainstem testing in ITU: to confirm brainstem death.

Question 42

What are the anaesthetic implications of using cn monitoring for neurosurgery?

Answer 42

(The question is not about anaesthetic implications of neurosurgery but of CN monitoring.)
• Choice of anaesthetic—use of inhalational agents and muscle relaxants
• Physiological factors that influence evoked potentials—temperature, acid-base, blood pressure, haematocrit, etc.
• Electrical artefacts—electrical interference can be a problem as SSEP is believed to simulate pacemaker spikes on ECG tracing
-The degree of muscle relaxation is the only anaesthetic factor for concern
when myogenic (EMG) activity is used for monitoring purposes.
- Special anaesthetic consideration is not required with BAEP.
• If MEP is monitored, then use of TIVA with Propofol and Remifentanil
with no muscle relaxation is the anaesthetic of choice (as volatile limited
to ≤ 0.5 MAC)
• With SSEP, a similar technique is used but without the need to restrict the
use of neuromuscular blocker

Question 43

choose a cranial nerve and tell
me about its origin and course.

Answer 43

Choose the nerve with a less confusing anatomy. (…There is no such
nerve!) I would personally choose Trigeminal nerve. It is just that it has a
fairly succinct origin and course and it can lead to further questioning on
trigeminal neuralgia, which is a treat! Vagus nerve has a complex course, and
it seems there is nothing special about Facial nerve.
Trigeminal nerve is the largest cranial nerve.
Function
• Motor: to the muscles of mastication
• Sensory: to the face, orbit, tongue, nose and anterior scalp
nuclei of origin
• One motor: upper pons below the floor of IV ventricle
• Three sensory
° Mesencephalic nucleus (proprioception): midbrain
° Principal sensory nucleus (touch): upper pons
° Nucleus of spinal tract (pain and temperature): pons to spinal cord
course
• The sensory fibres decussate and emerge at the upper pons as a larger
sensory and smaller motor root
• Gasserian (trigeminal or semilunar) ganglion is crescent-shaped swelling
formed by the sensory fibres situated at the apex of the petrous temporal
bone. The ganglion is surrounded superiorly by the temporal lobe,
medially by the internal carotid artery and cavernous sinus, and inferiorly
lies the motor root
• The motor fibres bypass the ganglion and join the mandibular division
Division and distribution
• Ophthalmic (V1): sensory only
° Emerges via superior orbital fissure
° Frontal, lacrimal and nasociliary nerves
• Maxillary (V2): sensory only
° Leaves the base of skull via foramen rotundum
° Gives off branches to supply the pterygopalatine fossa and the face
before it exits through the infraorbital foramen as the infraorbital nerve
• Mandibular (V3): sensory and motor
° Via Foramen ovale
° Sensory: auriculotemporal, buccal, lingual, and inferior alveolar nerves
• Motor: muscles of mastication

Question 44

How is trigeminal nerve tested
to confirm brainstem death?

Answer 44

It is tested by the interrogation of brainstem-mediated V and VII cranial nerve
reflexes.
• Corneal reflex
° Cornea is touched with a wisp of cotton wool. Blinking of the eyelids is
the normal response
° No response should be elicited in brainstem death
° Reflex: Afferent fibres via ophthalmic branch of CN V and efferent
pathway via CN VII
• Deep central somatic stimulation
° Apply deep supraorbital pressure and look for a central motor
response in the distribution of the facial nerve (grimace)
° Reflex: afferent via CN V and efferent via CN VII

Question 45

What are the causes of trigeminal nerve injury?

Answer 45

Mainly surgical; during neurosurgical decompression of trigeminal ganglion,
maxillofacial procedures, and dental injections.

Question 46

When can facial nerve be damaged?

Answer 46

Anaesthetic: compression from facemasks and endotracheal tube ties,
stretching of the nerve because of faulty positioning, direct injury due to
nerve blocks.
Surgical: direct surgical trauma.
The risk factors associated with incidence of nerve injury are diabetes,
intraoperative hypotension, hypoxia, hypothermia, and electrolyte imbalance.

Question 47

What are the preconditions for brainstem testing?

Answer 47

• Identifiable pathology causing irremediable brain damage
• Coma with exclusion of hypothermia, depressant drugs, reversible circulatory, metabolic and endocrine disturbances
• Apnoea, needing mechanical ventilation

Question 48

What is the basic neurological
principle of apnoea test
component of brainstem death
testing?

Answer 48

The intact respiratory centre will initiate breathing if the threshold PaCo2 is
reached, which is usually 6.65 kPa. In brainstem death the respiratory centre
is destroyed and apnoea persists above this threshold

Question 49

How is oxygenation maintained
during the apnoea test?

Answer 49

By apnoeic mass transfer of oxygen.

Question 50

can you explain the physiology of apnoeic oxygenation?

Answer 50

○ The oxygen consumption (Vo2) remains fairly constant at ∼250 mL/min.
○ This is delivered to the tissues by haemoglobin, whose oxygen is then
replenished, on return to the pulmonary circulation.
○ In an apnoeic patient, approximately 250 mL/minute of oxygen will move
from the alveoli into the bloodstream; only 8 to 20 mL/minute of carbon
dioxide moves into the alveoli, with the remainder being buffered in the bloodstream.
○ The end result is that the net pressure in the alveoli becomes slightly subatmospheric, generating a mass flow of gas from pharynx to alveoli.
○ This process where the alveoli continue to take up oxygen even without diaphragmatic movements or lung expansion is called the mass transfer of
oxygen or apnoeic oxygenation.
○ In healthy people under ideal circumstances, Pao2 can be maintained at
> 100 mm Hg for up to 100 minutes without a single breath, although the
lack of ventilation will eventually cause marked hypercapnia and significant
acidosis.
○ Apneic oxygenation with nasal cannulae works because the pharynx is filled with high Fio2 gas and functions as an oxygen reservoir.
○ The discrepancy between the 10 mL Co2 entering the alveolar space and the 250 mL o2 leaving it causes an influx of gas from the airway above the alveolar space. If it is open and filled with 100% o2 (pre-oxygenation and catheter with o2), then 240 mL is drawn into alveolar space.
○ This is only 10 mL o2 less than requirement; therefore, Pao2 falls at 0.5 kPa/min.

Question 51

What are the various factors
that significantly influence the
time period from the onset of
apnoea to critical hypoxia?

Answer 51

• Functional residual capacity (FRC)
° Conditions where there is a decreased FRC such as obesity, lung
disease, kyphoscoliosis, pregnancy, and children, critical hypoxia is
reached more rapidly
• Preoxygenation
° Denitrogenation due to preoxygenation greatly increases the time for
hypoxia after apnoea
• Maintenance of patent airway
° Closed airway: In closed airway, apnoea commences with an
intrathoracic pressure equal to ambient pressure. The extraction of
oxygen results in subatmospheric intrathoracic pressure and alveolar
collapse almost immediately, thereby dangerously reducing the
alveolar partial pressure of oxygen
° Patent airway: An open airway will allow oxygen to diffuse into the
apnoeic lung, which has been shown in animal and simulated human
studies to maintain oxygen saturation for up to 100 min
• Haemoglobin level
° Anaemia will cause a small reduction in the time to critical hypoxia,
although this effect will be more noticeable in patients who also have a
reduced FRC
• Basic metabolic demand (VO2)
The more the demand, the quicker the hypoxia
(This question tests a core knowledge and is fairly difficult to explain well
even if the candidate has read up on it. The values are not important but the
principle is.)

Question 52

What is the volatile agent you
use for inhalational induction
and why?

Answer 52

Sevoflurane
Nonirritant, sweet smelling, and has optimal oil:gas and blood:gas
coefficients

Question 53

compare and contrast the
three commonly used volatiles:
isoflurane, sevoflurane, and
Desflurane.

Answer 53

Question 54

What is Blood:Gas solubility
coefficient? What does it explain?
can you draw a graph to explain?
see Figure 3.3.

Answer 54

Ratio of the amount of anaesthetic in blood and gas when the two phases
are of equal volumes and pressure and in equilibrium at 37°C.
High B:G—The gas is more soluble in the blood, so low partial pressure in
blood leading to low partial pressure in brain; slow onset.
And vice versa

Question 55

What do you understand by
oil:Gas partition coefficient?
Again, draw a graph to show its
importance. see Figure 3.4.

Answer 55

O:G—link between lipid solubility and potency.
High o:G—Higher lipid solubility; more gas reaches brain. Hence, the drug
has got good potency.

Question 56

What factors influence the
speed at which inhaled agents
attain equilibrium?

Answer 56

To achieve equilibrium the gas must be at the same concentration in the brain
as in the delivered gas flow. The rate at which this occurs depends upon:
Drug factors
• Dilution within existing gases
Ventilation factors
• Inhaled concentration
• Alveolar ventilation
• Diffusion
• Blood/gas partition coefficient. A low b/g partition coefficient indicates
low solubility so equilibrium will be reached with relatively small transfers
of gas, and therefore will be rapid
• Pulmonary blood flow
• V/Q matching
• Concentration effect: More of the gas means greater concentration which
equates to a quicker attainment of equilibrium
• Second gas effect: As nitrous is absorbed it increases the concentration
of the volatile
circulation factors
• Cardiac output
• Distribution to other tissues: Uptake in tissues is related to their blood
flow, solubility and arterio-venous difference

Question 57

What are the clinical features
of raised intracranial pressure
(icP)?

Answer 57

• Headache
• Nausea and vomiting
• Confusion
• Personality or behavioural changes
• Visual disturbances due to papilloedema
Headache is worse in the morning as cerebral oedema is worse in the
lying position and there is a relative increase in hypoxia of the brain due to
hypoventilation during sleep. It is also worse when bending down, coughing,
and sneezing.
Acute severe increase in ICP leads to a decrease in GCS, Cushing’s reflex;
as ICP continues to rise, it leads to fixed and dilated pupils, Cheyne Stokes
breathing pattern, and eventually hypotension and death.

Question 58

What are the causes of increased
intracranial pressure?

Answer 58

Raised ICP may be due to an increase in the blood, tissue, or CSF
components of the brain.
• Blood—Increased blood flow or impaired venous drainage (e.g. venous
sinus thrombosis)
• Tissue—Tumour, brain abscess, haematoma, and cerebral oedema
• CSF—Hydrocephalus or increase in CSF production, which happens in
meningitis or choroid plexus tumour

Question 59

What is the Monroe-Kellie
theory?

Answer 59

The cranial cavity is a rigid closed container; thus, any change in intracranial
blood volume is accompanied by the opposite change in CSF volume if ICP
is maintained.

Question 60

can you draw the icP elastance
curve? see Figure 3.5

Answer 60

Stage 1/2 = compensation phase. As the volume of one of the intracranial
constituents increases, the other two constituents decrease in volume in
order to keep the intracranial pressure constant.
Stage 3/4 = decompensated phase. When compensatory mechanisms are
exhausted, small increases in the volumes of intracranial constituents cause
large increases in ICP.
The slope of the curve is dependent on which intracranial constituent
is increasing. The curve is steeper with blood and CSF as they are
incompressible and less steep with brain tissue as it is compressible

Question 61

What is the cushing’s reflex?

Answer 61

A hypothalamic response to brain ischaemia wherein the sympathetic
nervous system is activated, which causes increased peripheral vascular
resistance with a subsequent increase in blood pressure. The increased
BP then activates the parasympathetic nervous system via carotid artery
baroreceptors, resulting in vagal-induced bradycardia.
The brain ischaemia that leads to Cushing’s reflex is usually due to the poor
perfusion that results from increased ICP due to haematomas or mass
lesions.
Cushing’s reflex leads to the clinical manifestation of Cushing’s triad:
hypertension, bradycardia, and irregular respirations (Cheyne-Stokes
breathing).

Question 62

How do you manage raised icP?

Answer 62

This can be described as a reduction in blood, tissue, and CSF.
Blood
• Ventilation
Both hypoxia and hypercapnia can increase cerebral blood flow, and
hypoxia of the brain can increase lactic acid, which further causes
vasodilatation. Hence, to prevent this, mechanical ventilation is preferred.
Hyperventilation can be employed as a method to decrease the PCo2,
and this in turn causes vasoconstriction. This can be used in an acute
setting, but its efficacy is limited. If controlled ventilation is used, adequate
muscle relaxation and sedation should be used
• Positioning: Patients should be nursed in the head-up position, and
jugular compression should be avoided to encourage venous drainage
Hypothermia and barbiturate therapy may be used to decrease cerebral
blood flow.
tissue
• Surgical decompression or removal of tumour and haematoma
• Cerebral oedema can be treated with mannitol/frusemide or hypertonic
saline
• Corticosteroids may be used for oedema secondary to mass lesions
csF
Shunts via the lateral ventricle to drain CSF in hydrocephalus.

Question 63

How do you measure icP?

Answer 63

noninvasive
• From history and symptoms of headache, nausea/vomiting, confusion,
and behavioural changes
• Papilloedema on eye examination
• CT scan or MRI of the head
invasive
• External ventricular drain placement: catheter is placed in the lateral
ventricle at the level of foramen of Munro
• Intraparenchymal fibre optic catheter placement: monitor is placed in the
prefrontal area

Question 64

How do you interpret the icP
waveforms? see Figures 3.6
and 3.7.

Answer 64

There are four kinds of waves.
1. Normal
• Normal waves have a systolic upstroke (P1) and a diastolic
downstroke (P3) with a dicrotic notch (P2)
2. A waves
• Lundberg A waves, ‘or plateau waves’, are steep increases in
ICP lasting for 5 to 10 minutes. They are always pathological and
represent reduced intracranial hypertension indicative of early brain
herniation
3. B waves
• Lundberg B waves are oscillations of ICP at a frequency of 0.5 to
2 waves/min and are associated with an unstable ICP. Lundberg
B waves are possibly the result of cerebral vasospasm
4. C waves
• Lundberg C waves are oscillations with a frequency of 4–8 waves/
min and are probably caused by interaction between the cardiac and
respiratory cycles