ICP monitoring and management of raised ICP

(a) Which patients with severe head injury should have intracranial pressure
(ICP) monitoring? (20%)
(b) List the methods by which the intracranial pressure (ICP) can be measured
in intensive care. (15%)
(c) Describe two of these in greater detail (30%)
(d) What methods are used to manage or prevent acute rises in the ICP? (20%)
(e) Describe the mechanism of action of mannitol in head injury (15%)

Click for model answer by Dr Najmiah Ahmad

(a)
severe head injury GCS 3-8 with abnormal admission CT (ie haematoma, contusion, oedema, or
compressed basal cisterns)
severe head injury and normal CT but 2 of:
age > 40 yrs,
unilateral or
bilateral motor posturing,
systolic BP < 90 mm Hg
at risk of raised ICP requiring general analgesia
not routinely indicated in patients with mild/moderate head injury however may be appropriate
in certain conscious patients with traumatic mass lesions

(b)
Intraventricular
Intraparenchymal
Subarachnoid, subdural, epidural

(c)

Intraventricular

Gold standard. Catheter inserted into the ventricle connected to a column of fluid and a pressure
transducer. Wheatstone bridge principle. Change in pressure causing change in the resistance of
the transducer system, causing change in electrical current translates to change in intracranial
pressure. Can be used for therapeutic CSF drainage. High risk of infection, can be used for
administration of antibiotics. Can get blocked.

Intraparenchymal
Camino transducer uses fibreoptic able with displaceable mirror at the catheter tip, placed in the
brain tissue. Change in ICP distorts the mirror and reflected light intensity transduced into
pressure. No saline filled column of fluid and manometer in needed.
Accuracy comparable to intraventricular catheter but may only reflect local change in ICP.
Cannot be calibrated in vivo. Prone to drift over time. Cannot be used for therapeutic CSF
drainage.

(d)
 Physiological
Head up > 30 degrees, avoid excessive rotation of head
Loose collar/ ET tube neck tie
Avoid hypoxaemia, hypercarbia, hyperthermia, vasodilatory drugs, hypotension
Avoid PEEP, avoid central line in neck.
Pharmacological
Hypertonic saline 30% up to 20 ml
Mannitol 1g/kg
Barbiturate coma
Hypothermic therapy
Hyperventilation
Steroid
Surgical
Decompressive craniectomy
Insertion of external ventricular drain or ventriculoperitoneal shunt

(e)

Immediate
Osmotically active sugar alcohol, expands intravascular volume, increase flow, reduces viscosity,
increase cardiac output, increase cerebral perfusion, increase microvascular oxygenation.
Compensatory regional vasoconstriction where autoregulation is intact causing reduction ICP.

Delayed
Establish osmotic gradient between plasma and brain cells. Draws out extracellular water into
vascular compartment provided blood brain barrier is intact. Reducing oedema.

Acromegaly and pituitary surgery

(a) What challenges does a patient with acromegaly present to the

anaesthetist? (25%)
(b) What are the advantages and disadvantages of the transphenoidal
approach to the pituitary gland? (35%)
(c) Why might the surgeon request a lumbar drain insertion? (15%)
(d) Describe the possible complications of pituitary surgery (25%)

Click for model answer by Dr Ciara O'Donnell

(a)
-Airway:
* nasal polyps, magroglossia, madibular hypertrophy, difficult BMV, hypertrophy of aryepiglottic
folds, soft palate and epiglottis, difficult intubation; tracheal compression (1/3)secondary to
enlarged thryroid, subglottic stenosis , recurrent laryngeal nerve palsy. May need AFOI.

- Respiratory:
OSA, nasal CPAP impossible as nose packs will be in post op.

- Cardiac
May have cor-pulmonale; refractory HTN, cardiomyopathy and IHD bi-ventricular dysfunction
heart block

- Endocrine:
25% are diabetics. Secretion of ACTH, TSH also (as well as GH) or alternatively compression of
tissue and reduced hormone secretion; hypoadrenalism results in that situation -hormonal and
antihypertensive therapy should be continued pre-op

- Other
Excess peripheral soft tissue deposition may make venous cannulation difficult and increases the
risk -nerve entrapment syndromes; meticulous attention to theatre positioning is therefore
required

-HDU care post op

-Short acting agents such as remifentanil are ideal, allowing intraoperative haemodynamic
control and facilitating rapid recovery; enables neurological assessment
-NSAIDs linked with post op haematoma
-N+V prophylaxis
-Steroid replacement therapy needed

(b)
Advantages (extracranial approach)
Safest approach
Shorter hospital stay
Macro and microadenoma
minimal surgical trauma
minimal blood loss
direct access to the gland
avoidance of the generic hazards of a craniotomy

Disadvantages
Bifrontal craniotomy needed for giant pituitary tumours or failed transphenoidal approach
persistent CSF rhinorrhoea and the associated risk of postoperative meningitis,
panhypopituitarism,
transient DI
vascular damage
cranial nerve injury
cerebral ischaemia, and stroke as a result of vasospasm or thromboembolism.
Deliberate nasal septum fracture is required for transsphenoidal transnasal approach; to
minimize nasal bleeding, mucosal vasoconstriction is achieved by using a topical anaesthetic and
a vasoconstrictor.
co-phenylcaine (5% lidocaine 0.5% phenylephrine) causes less of a hypertensive response than
adrenaline in pts with Cushings.

(c)
To allow descent of tumour into surgical field by injecting small amounts of saline into
subarachnoid space
The same effect can also be achieved by controlled hypercapnoea.
To control post op CSF leak

(d)
Complications:
Venous or arterial bleeding esp larger tumours
 CSF leak, menigitis
Airway obstruction
CN11-V1 damage as close proximity to surgical site
Postoperative neuroendocrine abnormalities can occur afterpituitary surgery. DI (50%) usually
develops within the first 24 h, and resolves spontaneously in about a week. (Polyuria with a urine
specific gravity of < 1.005 and low osmolarity of < 300 mosm)
Hyponatremia can be caused by excess desmopressin admin
SIADH (20% occurs 1/52 post op); fluid restriction to 5001000 ml/ day
HRT will be required in all patients after operation e.g. steroids
VAE 10%

A 54 year-old patient is admitted to the Emergency Department following a

traumatic brain injury. A CT scan reveals only cerebral oedema.
a) What is secondary brain injury and when is it likely to occur? (2 marks)
b) Outline the main physiological and cellular changes associated with
secondary brain injury. (7 marks)
c) How can secondary brain injury be minimised in this patient? (11 marks)

Click for model answer by Dr Emma Murray

A 54 year-old patient is admitted to the Emergency Department following a traumatic brain

injury. A CT scan reveals only cerebral oedema.
What is secondary brain injury and when is it likely to occur? (2 marks)
Inflammation and release of neurochemical mediators result in vasogenic oedema, contributing
to raised ICP, hypoperfusion and ischaemia. It occurs over hours to days from the initial brain
injury.

Outline the main physiological and cellular changes associated with secondary brain injury.
(7 marks)
Physiological
Vasogenic oedema causes ongoing hypoperfusion and ischaemia
Disruption of blood-brain barrier with impaired vasomotor autoregulation leading to dilation of
cerebral blood vessels
Hydrocephalus due to obstruction in flow and absorption of CSF due to blood in subarachnoid
space
Cellular
Excitatory amino acids e.g. glutamate are significantly elevated post TBI
Cause cell swelling and neuronal death
Cause influx of sodium and chloride into the cell, causing acute neuronal swelling
Increased metabolism in injured brain stimulated by increase in circulating catecholamines
TBI induced stimulation of sympathoadrenomedullary axis and serotonergic system
Increase in extracellular potassium leading to oedema
Increase cytokines contributing to inflammation
Decrease in intracellular magnesium contributing to calcium influx
Linked to delayed damage

How can secondary brain injury be minimised in this patient? (11 marks)
Targeted resuscitation and early specialist management beginning in the pre hospital setting and
continuing in tertiary hospital.
 Prehospital
Avoid hypotension and hypoxia
Airway
Early tracheal intubation if GCS <8, hypoxic on supplementary oxygen, hypo/hypercarbic
Respiratory
Avoid hypoxia pO2> 11kPa
Maintain pCO2 4.5-5.0kPa
Hyperventilation 4-4.5kPa for impeding herniation- short term option due to normalisation of pH
through bicarbonate buffering
CVS
Avoid hypotension- maintain MAP >90mmHg
Replace intravascular volume- avoiding hypotonic and glucose containing solution
Use blood products as necessary- reverse existing coagulopathy
Vasopressors to maintain CPP > 60mmHg
Neuro
ICP monitoring- aim <20mmHg
Maintain CPP>60 mmHg
Adequate sedation, analgesia and muscle relaxation
Propofol, midazolam
Opioid infusion
Cisatracurium infusion refractory increased ICP
Hyperosmolar therapy- keep Na<155mmmol-1
Mannitol/hypertonic saline
Posm<320mmol-1
CSF drainage (Extraventricular drainage)
Treatment of seizures e.g. Phenytoin
Barbituate coma- refractory raised ICP
Associated with cardiovascular instability
Head of bed elevated to improve venous drainage
Endotracheal tube taped, to limit venous congestion
Metabolic
Strict blood glucose control 6-10 mmol-1
Avoid hyperthermia, hypothermia for refractory raised ICP
DVT prophylaxis
Surgical
Decompressive craniectomy

One lung anaesthesia and management of hypoxaemia

Hypoxaemia during one-lung ventilation may be a major problem during

thoracic operations.

(a) What are the indications for one lung anaesthesia? (30%)
(b) What are the physiological changes associated with one lung ventilation?
(30%)
(c) How could you manage the development of hypoxaemia during one lung
anaesthesia (40%)

Click for model answer by Dr Anna Laird

(a)
Absolute indications

- Isolation of one lung from the other to avoid spoilage in unilateral infection or massive
haemorrhage
- Control of distribution of ventilation-
- Giant unilateral lung cyst or bulla
- Bronchopleural fistula, bronchopleural cutaneous fistula
- Open surgery on main bronchus
- Life threatening hypoxia due unilateral lung disease
- Tracheobronchial tree disruption
- Bronchoalveolar lavage- risk contamination to other lung

Relative

- Surgical access- pneumonectomy, lobectomy, oesophagectomy, VATS, mediastinal exposure,

Spinal surgery, Thoracic aneurysm repair

- Post cardiac bypass after removal of totally concluding chronic unilateral PE.

(b)
Depending on position of patient:
- ICU pts remain supine however most surgical operations the pt is in the decubitus position with
surgical side upper most therefore non- ventilated.

- The blood flow to the non-dependent lung does not take part in gas exchange and this shunt
causes hypoxia.

- The (lower) dependent lung - has increased perfusion compared non dependant lung due
gravity and surgical compression and lung retraction on the non-dependent lung therefore
receives a greater percentage of CO this therefore decreases shunt.
If pneumonectomy and vessels are ligated entirely then this will decrease shunt further.

- Hypoxic pulmonary vasoconstriction diverts blood flow from the non-ventilated to the
ventilated lung, thereby reducing venous admixture and ameliorating the decrease in PaO2.
It involves the constriction of small arterioles (and to a lesser degree, venules and capillaries) in
response to alveolar hypoxia.

- Expansion of the dependent lung is restricted by the weight of the mediastinum, the cephalad
displacement of the diaphragm and abdominal organs, and non compliance of the hemi thoracic
chest wall.

- The alveolar compliance curve is shifted down and to the left in the dependent lung. This leads
to atelectasis of the dependent lung, decreasing the ventilated lung surface. This causes HPV,
increased resistance to flow in the dependent pulmonary artery, and diversion of flow to the
non-dependent lung, increasing the shunt fraction further.

- PaCO2 can rise with lower volumes, can increase respiratory rate to increase minute volume.

- Secretions can pool in dependent lung, difficult to remove through DLT.

CVS
 - Arrhythmia especially AF can develop
- Reduced venous return and CO if significant peep given to dependant lung

(c)
- Recognise hypoxaemia
- ABC approach
- Place FIo2 1.0
- Check tube disconnection / ventilator working
- Check ventilator settings
- Check DLT movement with fibre optic scope
- Check secretions/ debris - suction
- Maintain PaCO2 5.3kpa as lower can decrease HPV
- Place oxygen flow into dependant lung
- Place CPAP to dependant lung - tell surgeon
- Add peep 5cmh2o to non dependant lung
- Tell surgeon need to reinflate lung
- Clamp pulmonary artery

Check other observations - haemodynamically HR , BP if unstable - need fluid or vasopressors to

ensure adequate CO

Double lumen tubes and tracheal anatomy

(a) Describe the anatomy of the trachea and main bronchi (25%)
(b) List the methods of providing one lung ventilation (30%)
(c) How is the correct size of double lumen tube selected? (10%)
(d) Describe the correct positioning of a double lumen tube (35%)

Click for model answer by Dr Katie Megaw

(a)
- The trachea is a tubular structure composed of C-shaped cartilaginous rings anterolaterally.

- Extends downwards from cricoid cartilage at level of C6 vertebra in the midline to the level of
T5-6 vertebrae.

- 10-11cm in length and 20mm in diameter.

- The trachea bifurcates into the right and left main bronchi.

- The right main bronchus is positioned more vertically than the left main. The right main
bronchus is shorter and wider than the left main bronchus, 3cm v 5cm. At 2.5cm along the right
main bronchus arises the right upper lobe bronchus. At 3 cm the right main bronchus bifurcates
into the right middle and lower lobe bronchi.

- The bronchopulmonary segments of the right main bronchus:

- Right upper lobe bronchus apical, posterior and anterior segments
-Right middle lobe bronchus lateral and medial segments
- Right lower lobe bronchus apical, medial basal, anterior basal, lateral basal and posterior
basal segments.

- The left main bronchus divides into the left upper lobe bronchus and left lower lobe bronchus.
The left upper lobe bronchus bifurcates into the superior division and lingular bronchus.
The bronchopulmonary segments of the left main bronchus:
Superior division of the left upper lobe bronchus apical, posterior and anterior segments
Lingular bronchus superior and inferior segments
Left lower lobe bronchus apical, anterior basal (medial basal segment arises from here), lateral
basal, and posterior basal segments.

Thus the right lung has 10 bronchopulmonary segments and the left lung has 9.

(b)
Methods of providing OLV:

- Double lumen tubes

left and right DLTs cannulate the trachea and the appropriate main bronchus. Right sided
bronchial limbs have side hole to ventilate right upper lobe. Inserted via conventional
laryngoscopy. Checked clinically and with fibreoptic bronchoscope (FOB) at insertion and on
turning. Large external diameter, small internal diameter (39FG DLT has external diameter of
13mm and internal diameter of 6mm). Usually left sided tubes selected except when surgery
involves left main bronchus, due to difficulty in ventilation of right upper lobe bronchus. Tube
has 2 lumens allowing lung isolation and collapse of either lung. This is achieved by clamping the
desired lumen and opening to the atmosphere.
Various types of DLT Robsertshaw, Bronchocath, Sheribronch, Carlens (right sided), Whites (left
sided)

- Bronchial blockers

Fine bore catheter with a distal cuff. It is passed down a tracheal tube under FOB and placed in
the main bronchus of the lung to be collapsed. Its cuff is inflated and the lung collapses through
escape of gas through the blockers lumen. Arndt blocker has loop of nylon thread which
ensnares the FOB. Blockade of right main bronchus more problematic than left main bronchus
due to position of right upper lobe bronchus. Selective lobar blockade possible.
Indications:
Isolation of lobar bronchus required
Difficult intubation
Permanent tracheostomy

Various types: Arndt, Cohen, Uniblocker, Coopdech blockers. Univent tube tracheal tube with
small second lumen containing stiff directable bronchus blocker.
Papworth Bivent tube and blocker DLT which rests on the carina, blocker passed blindly down
side to be blocked. Not designed for use with FOB.

Advantages over DLTs:

Useful for lung isolation in difficult intubation
Tube change at end of operation unnecessary in those requiring post op ventilation
Paediatric use possible
Selective lobar collapse possible
Theoretically lower tube resistance for ventilating one lung

Disadvantages over DLTs:

Positioning takes longer
Migrates more easily
Lung deflation slow and limited suction due to small lumen
Lung reinflation requires deflation of cuff with possible cuff movement
Repeated rapid lung deflation and reinflation may be difficult
Stapling of blocker parts into bronchial stump possible during lung resection

Single lumen endobronchial tubes

Intubation of desired bronchus allowing ventilation of that bronchus alone. Rarely used.

(c)
Sizing of DLT

Patient height most accurate reflection of size of tube to be used. General rule is use the largest
tube that will pass, as the internal diameter of DLTs is small. Bear in mind that the left main
bronchus is narrower than the right main. Robsertshaw DTLs come as small, medium and large
tubes. Other DLTs are sized according to French Gauge (FG). In women use a small Robertshaw
tube or 35 or 37 FG tube. In men use a medium or large Robsertshaw, 39 or 41 FG tube.

(d)
Correct positioning of a DLT

- The DLT is inserted via normal laryngoscopy passing the bronchial portion through the cords
with the tip pointing anteriorly. Rotate the tube through 90 to intended side of cannulation.
Advance tube as far as it will go without undue force. Average depth of 29cm in adults has been
estimated.

- Inflate tracheal cuff to achieve a seal.

- Manual ventilation is commenced with the tracheal cuff inflated. Auscultate the chest to
confirm equal air entry on both sides and there should be no leak around the tracheal cuff.

- The tracheal side of the adapter is then clamped and the tracheal port is opened distal to the
clamp. The bronchial cuff is inflated so as to just eliminate air leak from the tracheal lumen - 1ml
at a time until leak stops. If a reasonable seal cannot be achieved with less than 4ml of air the
tube is either too small or incorrectly placed.

- Auscultate the chest - breath sounds should be heard only on the side of endobronchial
intubation. Look for unilateral chest expansion. Assess compliance via manual ventilation. Also
note a change in airway pressure on tracheal clamping.
The tracheal limb is then unclamped, the tracheal port closed and the bronchial limb of the
adapter is clamped and the bronchial port opened to air. Breath sounds should only be heard on
the contralateral side with unilateral chest expansion seen. Assess compliance via manual
ventilation.

- Fibreoptic bronchoscopy down the tracheal lumen should reveal the carina. The top edge of the
blue bronchial cuff should be just visible in the intended main stem bronchus. When a right-sided
tube is used, the fibrescope should be used to visualise the orifice of the right upper lobe
bronchus.

- Repeat checks after positioning in the lateral decubitus position.

Anaesthesia for bronchoscopy

(a) What are the diagnostic and therapeutic indications for bronchoscopy?
(40%)
(b) List the major contraindications for bronchoscopy. (15%)
(c) How is a fibre optic flexible bronchoscope processed after use? (20%)
(d) How may anaesthesia be maintained during bronchoscopy? (25%)

Click for model answer by Dr Najmiah Ahmad

(a) What are the diagnostic and therapeutic indications for bronchoscopy? (40%)
- Diagnostic
* Assess patency of upper airway
* Localizing lesion of unknown etiology on CXR
* Localizing/assess extent of toxic inhalation/ aspiration
* Assess/ check placement of airway stent
* Recurrent pneumonia/atelectasis/infiltrate
* Investigation of haemoptysis/persistent cough/dyspnoea/localized wheeze/stridor
* Obtain washings/biopsy for cytologic/histologic/microbiology
* Suspicious sputum cytology result
* Problems with endotracheal tube or tracheostomy.

- Therapeutic
* Aid tracheostomy procedure and difficult intubation/difficult airway
* Retrieval of foreign body from airway
* LASER tissue removal/basket/forceps
* Endobronchial toilet in VAP
* Aid in placement of DLT and bronchial blocker in selective intubation of bronchus
* Airway balloon dilatation in tracheobronchial stenosis

(b) List the major contraindications for bronchoscopy. (15%)

- Absolute
Patient refusal
Inexperienced operator
Lack of emergency setup for CPR and management of pneumothorax/bleeding
Patient cannot adequately be oxygenated

- Relative
Coagulopathy
Refractory hypoxaemia
Unstable haemodynamics/Dysarrythmias/recent MI/CCF
Pulmonary hypertension

(c) How is a fibre optic flexible bronchoscope processed after use? (20%)
* Inspect all parts for damage, perform leak test
* All parts/channels/lumens thoroughly cleaned/brushed with soap and water immediately after
use to prevent drying of secretions
* Thoroughly dry
* Soaked with high level disinfectant for 20 mins.
 * Gluteraldehyde/peracetic acid/hydrogen peroxide
10 hrs for sterility
* Rinse 3 times with sterile water/ bacteriological filtered water (water filtered through 0.1-0.2
micron filters)
* Dry internal channels of reprocessed bronchoscope using 70% alcohol followed by forced air
treatment
* All heat stable parts/ accessories e.g biopsy forceps reprocess by ultrasonics followed by
autoclave/ sterilization
* Hang up to dry and not placed in a case.

(d) How may anaesthesia be maintained during bronchoscopy? (25%)

* Flexible bronchoscopy can be done under sedation and local anaesthesia to mucosa.
* Rigid bronchoscopy requires GA induction with IV propofol or gas induction.
* Short acting opiate to obtund profound pressor response, fentanyl/ remifentanil infusion
* Muscle relaxant suxomethonium or rocuronium with suggamaddex reversal
* Anaesthesia is maintained by either intermittent blouses of propofol, TIVA or TCI when using
jet ventilation.
* Volatile agents can be used when using ventilating bronchoscope

The laryngeal mask airway

(a) What are the indications for the use of a laryngeal mask airway?
(b) What are the pros and cons of an LMA as a primary airway device?
(c) How does the design of the LMA protect against aspiration?
(d) What are the modifications of the ProSeal that make it different from the
classic LMA?
(e) What are the modifications of the iGel that make it different from the classic
LMA?

Click for model answer by Dr Charlene McDonnell

(a) What are the indications for the use of a laryngeal mask airway?

Indications for use of a laryngeal mask airway include:

Elective ventilation: During anaesthesia for short surgical procedures. Suitable for both
spontaneous and positive pressure ventilation in both paediatric and adult patients

Difficult airway: Following failed intubation as part of plan C in the difficult airway
society algorithm (DAS) to maintain oxygenation

Cardiac arrest: An acceptable alternative to intubation to maintain ventilation during

CPR

Conduit for intubation: An aid to intubation when direct laryngoscopy fails In patients
at low risk of aspiration it is part of plan B in the DAS algorithm
Prehospital Medicine: As an alternative to intubation where intubation is not safely
possible for example due to patient positioning

(b) What are the pros and cons of an LMA as a primary airway device?

(c) How does the design of the LMA protect against aspiration?

Design features of the LMA that reduce the risk of aspiration include:

High pharyngeal seal of 20cm H20 to prevent gastric distension

High oesophageal seal to stop gastric fluid entering the pharynx and stop vented gas
entering the oesophagus causing distension

Cuff made of soft material to ensure no folds or channels, thereby creating a good seal
and no conduits for passage of the gastric fluid

Large pharyngeal volume which fills the pharynx and reduces the amount of space for
gastric fluid to pool

Drainage tube allows leaked gas to vent from the oesphagus and reduces distension. It
also allows regurgitant fluid to be suctioned up from the pharynx rather than being
aspirated and it alerts the anaesthetist to the presence of regurgitation in the airway. The
classic LMA does not have this drainage tube
 (d) What are the modifications of the ProSeal that make it different from the classic
LMA?

Compared to the classic LMA the ProSeal has 6 modifications:

Oesophageal drain tube

Posterior inflatable cuff and larger softer cuff
Reinforced airway tube
Integrated bite block
Introducer
No epiglottic lifting bar

These modification mainly reduce the risk of regurgitation and subsequent aspiration. The
oesophagus and airway are effectively isolated. The oesophageal seal is higher and there
is access to the stomach via the drainage tube to allow drainage of gastric fluid and
venting of leaked gas. The pharyngeal seal is improved, enabling ventilation with higher
pressures of up to 40cmH20 reducing gastric distension. The bulkier size reduces the
space for gastric fluid to pool.

(e) What are the modifications of the iGel that make it different from the classic
LMA?

Compared to the classic LMA the iGel has 5 modifications :

Single use only

Fewer sizes available
Soft solid thermoplastic elastomer mask rather than an inflatable cuff that alters its shape
with body heat to allow a patient specific fit
Wide short airway tube with an integrated bite block that allows easier passage of fibre-
optic scopes
Gastric channel to allow suctioning of gastric fluid

Asthma and anaesthesia

a) List the factors that may have contributed to an increase in the prevalence
of asthma in developed countries in the last 20 years. (5 marks)
b) What are the possible causes of acute bronchospasm during general
anaesthesia in a patient with mild asthma? (5 marks)
c) Outline the immediate management of acute severe bronchospasm in an
intubated patient during general anaesthesia. (10 marks)

Click for model answer by Dr Rebecca Gibson

Asthma and anaesthesia

a) List the factors that may have contributed to an increase in the prevalence
of asthma in developed countries in the last 20 years. (5 marks)
b) What are the possible causes of acute bronchospasm during general
anaesthesia in a patient with mild asthma? (5 marks)
c) Outline the immediate management of acute severe bronchospasm in an
intubated patient during general anaesthesia. (10 marks)

Click for model answer by Dr Rebecca Gibson

List the factors that may have contributed to an increase in the

prevalence of asthma in developed countries in the last 20 years. (5
marks)
Environment
Hygiene hypothesis
Pollution
Smoking (direct/passive)
Diet
Maternal diet in pregnancy
Lack of breast-feeding
Vitamin D deficiency
Obesity
Infective
Antibiotic overuse
Genetic
Inheritance
Allergy
Other
C-section
What are the possible causes of acute bronchospasm during general
anaesthesia in a patient with mild asthma? (5 marks)
Patient factors
Anxiety
Smoking
Poorly-controlled asthma/lack of compliance
Concurrent infection
Allergy
Anaesthetic factors
Inadequate depth of anaesthesia
Airway manoeuvres/instrumentation
Aspiration of gastric contents/secretions/blood
Drugs
B-blockers
Muscle relaxants (atracurium/mivacurium)
NSAIDs
Morphine
Antibiotics
Ester local anaesthetics
Outline the immediate management of acute severe bronchospasm in an
intubated patient during general anaesthesia. (10 marks)
Stop precipitating factor
Call for help
100% oxygen
Confirm tube position
Check circuit for kink/obstruction
Manually bag/auscultate
Confirm diagnosis of bronchospasm and exclude complications eg
pneumothorax
Suction if required
Consider curarisation
Consider intubation if LMA in situ
Maintain/deepen anaesthesia with volatile
Ventilation
low respiratory rate 8-10/min
tidal volumes 6-8ml/kg
peak pressures <35cmH2O
minimal PEEP
lengthen expiratory time
permissive hypercarbia
intermittent ventilator disconnection/manual chest decompression
Pharmacological
Initial management
Salbutamol
Inhaled 6-8 puffs via ETT adaptor/50ml syringe, repeated as necessary
Nebulised 5mg, repeated as necessary
Ipratropium
Nebulised 500 micrograms
Hydrocortisone
IV 200mg
Magnesium:
IV 2-5g slowly
Refractory
Salbutamol
IV 250 micrograms slowly
IV infusion 5-20 micrograms/min
Adrenaline
Nebulised 5ml 1:1,000
IV 10 micrograms boluses
IV infusion 1-20 micrograms/min
Ketamine
IV 0.2mg/kg
IV infusion 0.5-2mg/kg/hr for 3 hours
Heliox
70:30 He:O2
(Aminophylline
IV 5mg/kg
IV infusion)
Stop/expedite surgery
Consider ICU referral
Obstructive sleep apnoea

You are asked to assess a patient in the recovery room who is particularly
drowsy post anaesthetic. Her BMI is 50 kg/m2.
(a) What are the potential causes of drowsiness or difficulty rousing a patient
in the recovery room? (20%)
(b) What features in a PRE-ANAESTHETIC history and examination might you
make you suspicious of obstructive sleep apnoea (OSA)? What is the
STOPBANG questionnaire? (20%)
(c) What are the physiological consequences of OSA? (20%)
(d) What factors increase the risk of complications arising in the postoperative
period with OSA? (10%)
(e) What are the features of a postoperative care plan designed to minimise the
risk of these complications? (30%)

Click for model answer by Dr Grainne Fitzpatrick

What are the potential causes of drowsiness or difficulty rousing a patient in the recovery
room? (20%)
Causes can be divided into pharmacological, metabolic, patient factors
Pharmacological:
Use of Benzodiazepines and opioids can cause prolonged unconsciousness especially when
combined
Residual neuromuscular blockade, which can be prolonged by a number of drug interactions and
metabolic causes
Residual IV anaesthetic agents which has not yet been metabolised
Residual volatile agents
Unrecognised LA toxicity

Metabolic:
Hypo/hyper- glycaemia
Hypo/hyper- natraemia
Hypothermia
Uraemia

Patient:
Respiratory failure causing hypoxaemia/hypercapnia.
Loss of central respiratory drive: Intracranial pathology/OSA/Drug overdosing
Ventilation is affected by primary muscle disease/metabolic imbalance/obesity/residual
neuromuscular blockade
Unrecognised post-ictal

Surgery:
Carotid surgery or surgery in the sitting position: risk of cerebral hypoperfusion
Surgery with haemodynamic instability e.g. AAA repair can also cause cerebral hypoperfusion
Perioperative thrombotic event

(b) What features in a PRE-ANAESTHETIC history and examination might you make you
suspicious of obstructive sleep apnoea (OSA)? What is the STOPBANG questionnaire?
(20%)
History:
Snoring
Restless sleep
Witnessed apnoea
Day time sleeping
Headaches
Reduced libido
Smoking
Alcohol excess
History of associated insulin resistance/diabetes, hyperlipideamiea, hypertension

Examination:
Age: >40 years old usually
Obese
Male
Neck Circumference >40cm
Craniofacial abnormalities
Neuromuscular Disease
Tonsillar hypertrophy- risk factor for kids
CPAP machine at bedside

STOP-BANG Questionnaire
ASA recommend patients are screened for OSA prior to surgery.
Number of screening tool, STOP-BANG one of them.
Easy to use 8 questions.
High risk for OSA if > 3 criteria
Good sensitivity but low specificity i.e. will miss a significant proportion of patients with OSA.
S- Do you snore loudly?
T- Do you feel Tired during the day most days?
O- Has anyone Observed that you stop breathing during your sleep?
P- History of High Blood Pressure
B- BMI > 35
A- Age over 50 years
N- Neck circumference >40 cm
G- Male Gender

(c) What are the physiological consequences of OSA? (20%)

There is a number of wide ranging physiological changes from repetitive airway obstruction
Arterial hypoxaemia
Arterial hypercarbia
Polycythaemia
Systemic hypertension
Pulmonary hypertension
Cardiac rhythm disturbances
Right ventricular failure
Metabolic syndrome- insulin resistence/hypertension/hyperlipidaemia
Increased incidence of heart disease /CVA/Death
Poor sleep- increased risk of accidents during the day
Diminished quality of life

(d) What factors increase the risk of complications arising in the postoperative period with
OSA? (10%)
 Increased risk of Complications:
More likely to be a complicated period if the patients has a high apnoea/hypopnea index.
Increased severity of sleep apnoea based on sleep studies
Invasive surgery with GA (i.e. Greater risk than minor procedures under LA)
If post- operative opioids are required
(e) What are the features of a postoperative care plan designed to minimise the risk of these
complications? (30%)

Planning should begin prior to the patient arriving into hospital

Pre surgery advice on weight loss if possible, cessation of smoking, reducing alcohol intake
Well thought out anaesthetic plan
- Risk of airway difficulty greater AFOI may be needed
- LA intra op to avoid opioids
- Regional technique is possible as it reduces opioids/sedatives in the post op period
Avoiding pre- meds as a risk of hangover effects, especially if surgery shorter than expected
Extubate fully awake and sitting upright
Patients CPAP machine in recovery immediately ready for use by trained staff
Fully monitoring in recovery
Instruct recovery staff patients is not to be left unattended
Recovery staff should be trained in airway support as near to 20% of patients will need re-
intubated
HUD/ICU care may be needed depending on severity of OSA and surgery type.
Supplementary oxygen until the patient maintains their baseline saturations on RA
Analgesia
- Regional anaesthesia as mentioned above.
- Otherwise multimodal approach using paracetamol, NSAIDs, ketamine, clonidine, gabapentin.
- If opioids must be used, use short acting opioids e.g. Fentanyl PCA with saturation monitoring

Keep for > 3 hours longer in recovery than patients without OSA (as per ASA association
guidance)
Keep for at least 7 hours after last airway obstruction/hypoxaemic episode

Smoking and anaesthesia

(a) What are the physiological changes of significance in cigarette smokers?

(20%)
(b) What are the pathological systemic effects of cigarette smoking? (30%)
(c) What perioperative negative outcomes are more likely in smokers? (25%)
(d) Describe the time course of beneficial effects of smoking cessation (10%)
(e) What is the role of the anaesthetist in a preoperative setting in encouraging
smoking cessation? (15%)

Click for model answer by Dr Chris Wasson

a) What are the physiological changes of significance in cigarette smokers? (20%)

increased circulating catecholamines
SVR increased
aortic and carotid baroreceptors reset
HR and contractility increased
increased closing volume
decrease fev1
reduced compliance of lungs
cilia dysfunction
increased mucous production
airway epithelial damage
increased COhb
oxygen dissociation curve shifted to left
cytochrome oxidase induction
cytochrome p450 induction
increased platelet, white cell, red cell counts
plasma volume reduction
increase blood viscosity

(b) What are the pathological systemic effects of cigarette smoking? (30%)
addiction
hypertension
ischaemic heart disease
increased risk arterial thrombosis
peripheral vascular disease
cerebrovascular disease
renovascular disease
chronic tissue hypoxia
obstructive lung disease
restrictive lung disease
atelectasis
peptic ulcer disease
reflux
crohns disease

(c) What perioperative negative outcomes are more likely in smokers? (25%)
nicotine withdrawal, agitation
bronchospasm, laryngospasm, aspiration, post operative pneumonia, atelectasis, hypoxia,
reintubation, prolonged ventilation, hypoventilation, plugging off bronchial tree.
myocardial ischaemia, myocardial infarction, arrythmia, heart failure.
cva.
critical care admission
increased opiod requirements
acute kidney injury

(d) Describe the time course of beneficial effects of smoking cessation. (10%)
12-24 hours - CO and nicotine levels reduced
2-10 days - upper airways less reactive, decreased sputum production
4-6 weeks - ciliary function returns, improvement in pfts
2 months - immune function improves
3-6 months - reduced rate post operative complications
years - reduced risk, cold, lung cancer, IHD

(e) What is the role of the anaesthetist in a preoperative setting in encouraging smoking
cessation? (15%)
development of pre assessment pathway
education on importance of cessation, informed consent
referral to smoking cessation service early
encourage abstinence for 12-24 hours in those who continue to smoke
Chronic renal failure

(a) List the physiological functions of the normal kidney

(b) What are the systemic manifestations of chronic renal failure?
(c) What are the pathophysiological mechanisms of the common electrolyte
derangements in renal failure?
(d) What is the mechanism behind coagulopathy in patients with chronic renal
failure?
(e) What are the principles of intraoperative management in a patient with renal
failure?

Click for model answer by Dr Emma Murray

(a)
Regulation of sodium and water balance
Excretion of nitrogenous waste products, drug metabolites and other toxins
Regulation of blood pressure via rennin-angiotensin-aldosterone axis
Regulation of electrolytes e.g. potassium, calcium and phosphate
Acid-base balance
Secretion of erythropoietin
Metabolism of Vitamin D

(b)
Cardiovascular
Hypertension
Ischaemic heart disease
Gastrointestinal
Malnourishment
Peptic ulcer disease
Delayed gastric emptying
Musculoskeletal
Abnormal calcium metabolism leading to renal osteodystrophy
Haematological
Anaemia
Abnormal platelet function

(c)
Hypernatraemia
Increased loss of free water (acquired nephrogenic diabetes insipidus) or decreased intake due
to nausea and vomiting or excessive restriction

Hyponatraemia
Loss of kidneys reabsorptive ability without hypovolaemia
Diarrhoea and vomiting
Diuretic use
Dilutional hyponatraemia in anuric patients

Magnesium
Actively excreted by kidneys
Calcium and phosphate
Plasma calcium levels frequently reduced in renal failure- reduced production of active vitamin D
results in reduced absorption of calcium from the guy.
Phosphate actively excreted from the kidneys and will therefore accumulate in renal failure

Potassium
Severe renal dysfunction will cause potassium retention
Acidosis in renal failure results in a potassium shift out of the cells

Chloride
Can accumulate in renal failure causing a reduced strong ion difference and metabolic acidosis

Hydrogen and bicarbonate

Acid-base homeostasis is maintained by renal excretion of organic acids and hydrogen ions and
the production and reabsorption of bicarbonate
Patients with renal failure will develop acidosis as a result of hydrogen retention and reduced
bicarbonate production.
Excessive loss of bicarbonate from the kidney in renal tubular acidosis

(d)
Platelet activity is deranged with decreased adhesiveness and aggregation despite platelet count
being within normal limits
Likely caused by inadequate vascular endothelial release of von Willebrand factor/factor VIII
complex which binds to and activates platelets
Increased platelet release of beta- thromboglobulin and vascular production of PGI2 also
contribute to coagulopathy
Standard tests of coagulation are usually normal (i.e. prothrombin time, activated partial
thromboplatin time and INR) however bleeding time may be prolonged beyond 10 seconds

(e)
Preoperative Assessment
Details of dialysis, with bloods taken most dialysis, weights pre and post most recent dialysis and
quantity of fluids removed
Details of anticoagulant used for dialysis
Urine output
Induction
Full monitoring in place- invasive depending on surgery (awareness to possible fistula sites)
Vasopressors prepared prior to induction of anaesthesia
Anaesthesia
Careful induction of anaesthesia as compliance of circulation in renal failure patients can be
highly abnormal
Impaired gastric emptying and reduced gastric pH may necessitate endotracheal intubation
Recent serum potassium should be known before administration of suxamethonium and high
dose rocuronium substituted if a rapid sequence induction is indicated
Maintainence: Volatile agents- new volatile agents e.g. sevoflurane and enflurane are associated
with an increase in plasma fluoride concentration, however this increase does not cause any
detectable change in renal function
Muscle relaxants that do not rely on renal excretion should be utilised over those dependent of
renal metabolism and excretion. Atracurium or cisatracurium undergo Hoffman degradation.
The patients blood pressure should be maintained as close to normal for that patient
Postoperative
Analgesia
Regional anaesthesia/analgesia may be suitable for procedures such as fistula formation;
however poor platelet function can limit this practice.
Opioids rely on renal excretion, therefore in renal failure these drugs can accumulate and result
in respiratory depression. Short acting opioids such as fentanyl, alfentanil are acceptable, longer
 acting opioids such as morphine should be used cautiously with smaller titrated doses and longer
dosing intervals

Liver Failure

(a) What are the different functions of the liver?

(b) Describe the different tests of liver function - how can these help identify
causes of liver failure?
(c) What are the physiological changes induced by liver failure?
(d) What are the pharmacological considerations in anaesthesia in liver
failure?
(e) What are the serious complications of chronic liver failure - how may these
be managed?

Click for model answer by Dr Grainne Fitzpatrick

What are the different functions of the liver?

The liver has a number of functions, broadly divided into synthetic and non-synthetic functions.
Synthetic functions:
Amino acid synthesis
Gluconeogenesis/glycogenolysis/glycogenesis
Synthesis of vitamin K dependant clotting factors- II, VII, IX, X
Bile production and excretion
IGF-1 and thrombopoietin production
Synthesis of hormones
Production of albumin
Lipoprotein production

Non-synthetic:
Drug metabolism via phase I and phase II reaction
Protein and lipid metabolism
Storage: glycogen, vitamin A, D, B12, iron and copper.

Describe the different tests of liver function - how can these help identify causes of liver
failure?
Tests can be divided into those looking for biliary obstruction, liver function and cell injury
Tests of synthetic liver function
Prothrombin time (PT)
Measure of the extrinsic pathway of coagulation.
Prolongation can reflect deficiencies of vitamin K relating to impaired absorption from poor
quality bile production or abnormalities in factor VII synthesis, both relating to liver dysfunction
Albumin
Synthesised in the liver
Low level may reflect liver dysfunction.
Hypoalbuminaemia also occurs in malnutrition, nephrotic syndrome, malabsorptive states and
pregnancy
Dynamic Tests of liver function
- (looking at the livers ability to clear or metabolise a substance)
Formation of monoethyleneglycine (MEGX)
Lidocaine metabolite can be measured 1530 min after injection of Lidocaine, 1 mg/kg.
Used to quantify the hepatic cytochrome P450 family metabolism

Indocyanine green (ICG) clearance:

Elimination of injected ICG.
Can be carried out at the bedside.
ICG has a high hepatic extraction ratio and measurements reflect changes in liver blood flow

Cell Injury
Alanine Amino Transferase (ALT) and Aspartate Amino Transferase (AST)
Used to detect liver cell damage- no correlation between level and degree of injury
ALT and AST out of proportion with ALP and GGT suggests an intra-hepatic problem.

Tests of Biliary Obstruction

Bilirubin
Elevated by any of the following: haemolysis, biliary stricture, hepatitis, cirrhosis, drugs, Gilberts
syndrome.
Jaundice of the sclera becomes noticeable when serum levels 2-3 mg/dl

Alkaline Phosphatase (ALP)

Present in all tissues throughout the body
Elevated in biliary obstruction, pregnancy and as a by-product of osteoblast activity e.g. Pagets
disease.

Gamma Glutamyl Transpeptidase (GGT)

Present in the cell membrane of many tissues.
Elevation is seen in liver, biliary system and pancreatic disease.
Isolated elevation may also suggest significant alcohol ingestion, congestive cardiac failure and
certain drugs.

What are the physiological changes induced by liver failure?

Impairment of liver function has consequences directly attributable to the failing liver and also
indirect effects expressed via other organ systems.
Multi-organ dysfunction results due to:
- Impairment of hormone modulation
- Activation of cytokines
- Release of vasoactive substances
- The uncleared byproducts of metabolism by the damaged liver

Cardiovascular/haemodynamic changes
Advanced liver disease- hyper-dynamic circulation.
Low SVR due to peripheral vasodilatation
CO increases in an attempt to compensate
Often leads to hypotension.
Adrenal insufficiency is common and contributes to haemodynamic compromise.
Possible associated cardiomyopathy- low SVR may mask underlying cardiomyopathy/CAD by
limiting ventricular workload
Respiratory
Impairment of FRC, increased hypoxia and atelectasis due to
Ascites leads to diaphragmatic splinting
Pleural effusions
Intrapulmonary A-V shunting
Impaired hypoxic vasoconstriction and
V/Q mismatching
-ARDS may occur with or without sepsis in patients with advanced liver disease
-Some have porto-pulmonary hypertension: portal hypertension is accompanied by pulmonary
hypertension and increased pulmonary vascular resistance
Renal
Renal dysfunction secondary to hypo-perfusion.
Use of diuretics/nephrotoxic agents/paracentesis/sepsis/blood loss further increases this risk.
Renal failure also common in acute liver failure
Hepato-renal syndrome- reduced GFR and decline in renal function due to advanced liver
disease.
Hepato-renal syndrome can be defined as: Creatinine>133 mmol/l in patient with cirrhosis and
ascites
diagnosis of exclusion
It is a consequence of the physiological changes that take place, generalised vasodilatation and
altered RAAS and ADH release.
Haematology
Anaemia-
due to blood loss/haemolysis from hypersplensim/anaemia of chronic illness/bone marrow
depression/nutritional deficiency.
Coagulopathy
reflects failure of hepatic synthetic function
Hepatocellular necrosis produces a prolongation in Prothrombin time (PT)
Dysfibrinogenaemia and fibrinolysis may occur
Portal hypertension leads to splenomegaly
resultant platelet sequestration and thrombocytopenia.
Changes in drug handling
Derangement in drug handling.
Hepatocellular damage can alter drug metabolism.
Cholestasis reduces the absorption of fat-soluble drugs after oral administration.
Reduced hepatic extraction can lead to high peak plasma concentrations.
Compartment changes and altered protein binding affect the volume of distribution, clearance
and redistribution.
Infection risk
Acute liver failure patients often fulfil criteria for SIRS
Increase risk of sepsis- impaired opsonisation/chemotaxis/intracellular killing.
Gram-positive organisms and fungal sepsis are common.
Metabolic dysfunction
Secondary hyper-aldosteronism- water retention and hyponatraemia
Loop diuretics used to treat ascites and oedema can cause: hypovolaemia/hypokalaemia.
Spironolactone may lead to hyperkalaemia.
Hypomagnesaemia/hypophosphataemia/metabolic alkalosis are often present.
Rapid correction of hyponatraemia- osmotic demyelination and central pontine myelinosis.
Increase in circulating levels of hormones- insulin, thyroxine, aldosterone and oestrogen.
Hypoglycaemia may be present due to both hyperinsulinaemia + depleted hepatic glycogen
stores. Lactic acidosis especially in paracetamol OD

What are the pharmacological considerations in anaesthesia in liver failure?

- Derangement in drug handling and metabolism due to hepatocellular damage.
- Reduced hepatic extraction can lead to high peak plasma concentrations.
- Compartment changes and altered protein binding affect the volume of distribution, clearance
and redistribution.
Choice of anaesthetic agents
Absorption, distribution, metabolism and excretion of all anaesthetic drugs are likely to be
affected.
IV Induction Agents
Propofol
- Good choice as it undergoes considerable extra-hepatic metabolism.
- Sedative and haemodynamic effects of Propofol increased in liver failure therefore dose should
be reduced.
Thiopentone
Reduced dose as reduction in plasma proteins causes an increased unbound fraction of the drug.
The distribution half life and duration of action are also prolonged.
Chronic alcohol use may increase IV anaesthetic requirements

Muscle Relaxants
Suxamethonium
- prolonged duration of action because reduced pseudocholinesterase concentrations slowing its
metabolism
Vecuronium/Rocuronium
- prolonged elimination phase in severe disease.
Atracurium/Cisatarcurium
- better options as not reliant on hepatic excretion.

Opioids
Morphine
Elimination- delayed in cirrhotic patients due to reduced hepatic bl flow and extraction ratio.
Associated renal failure- accumulation of the active metabolite morphine-6-glucuronide
Morphine may therefore precipitate encephalopathy

Fentanyl
May be better option as it is renally excreted
Will accumulate in larger doses.

Alfentanil
Elimination reduced but volume of distribution is increased.
Deficiency in alpha-1-acid glycoprotein results in reduced protein binding.
Overall dose should be reduced

Remifentanil
Commonly used intra-operatively
Metabolism not liver dependant

Volatile anaesthetic agents

All reduce CO and MAP
Risk of reduced hepatic blood flow, thereby increasing the risk of exacerbating liver dysfunction.
Isoflurane/sevoflurane/desflurane
-all undergo minimal hepatic metabolism.
Desflurane
- Least metabolised
it also has minimal effect on the hepatic arterial buffer response
relatively preserves hepatic blood flow

What are the serious complications of chronic liver failure - how may these be managed?
- Coagulopathy
Vitamin K and FFP administration may in part correct the coagulation defect
Cryoprecipitate if the PT remains prolonged.
Prolonged bleeding time may need prophylactic DDAVP
Tranexamic acid may also be helpful.

- Encephalopathy
Identify and correct the precipitating causes:
Assess vital signs and volume status.
Evaluate for GI bleeding.
Eliminate sedatives or tranquilizers.
Screen for hypoxia, hypoglycaemia, anaemia, hypokalaemia, metabolic alkalosis, and other
potential metabolic or endocrine factors- correct as indicated.
Initiate ammonia-lowering therapy:
Use nasogastric lavage, lactulose to remove source of ammonia from colon.
Initiate treatment with lactulose to produce two to four bowel movements per day.
Consider oral nonabsorbable antibiotics to reduce intestinal bacterial counts.
Consider treatment with flumazenil
(Minimize potential complications of cirrhosis and depressed consciousness)
Provide supportive care with attention to airway, hemodynamic, and metabolic statuses.

- Ascites
Sodium restriction
Diuretic therapy
Fluid restriction
Paracentesis with albumin cover
TIPS procedure

- Spontaneous Bacterial Peritonitis

Empirical antibiotic therapy
Albumin cover

- Portal Hypertension
Propranolol
ISMN
TIPS

- Variceal Bleeding
British Society of Gastroenterology recommend patients with cirrhosis who present with
evidence of upper GI bleeding undergo an urgent upper endoscopic evaluation
Haemodynamic resuscitation
Band ligation
Sclerotherapy
Sengstaken-Blakemore tube insertion
TIPS

- Hepatorenal Syndrome
Discuss suitability of dialysis
Consider Octreotide and oral midodrine
Avoid nephrotoxics

- Malnutrition
Dietetic input and vitamin supplementation should occur as early as possible
Myasthenia gravis and anaesthesia

a) What is the pathophysiology of myasthenia gravis?

(b) How might you distinguish between a myasthenic and cholinergic crisis?
(c) Describe the management of a myasthenic crisis
(d) What would be the key features of your pre-anaesthetic assessment?
(e) Describe the your intraoperative management of a myasthenia patient
presenting for emergency surgery specifically relating to the condition.

Click for model answer by Dr Matthew Grimes

(a) What is the pathophysiology of myasthenia gravis?

Autoantibodies develop against nicotinic ACh receptors on post synaptic membrane
Nerve conduction to muscle is impaired by blockage of binding site by antibodies and destruction
of receptors
Decreased capacity of motor end plate to generate action potential
Characterised by weakness and fatiguability

(b) How might you distinguish between a myasthenic and cholinergic crisis?
Tensilon challenge test: up to 10mg edrophonium IV given
If MG: improvement of symptoms within 1 minute, effect short lived
Patients with cholinergic crisis respond with increased salivation, secretions, diaphosesis, gastric
motility (SLUDGE syndrome)

(c) Describe the management of a myasthenic crisis

1) Anticholinesterase therapy: to enhance NM transmission by slowing down breakdown of ACh.
Pyridostigmine commonly used
2) Immunosuporessants: prednisolone/azathioprine/cyclosporin
3) Thymectomy: for patients up to age 60 with thymoma
4) Plasma exchange/IvIg

(d) What would be the key features of your pre-anaesthetic assessment?

Admit 48hrs prior to surgery to allow assessment and monitoring of resp/bulbar function
Adjustment of steroid/Anticholinesterase therapy
Chest physiotherapy
May need plasma exchange/IvIg
PFTs: FVC measurement. Worrying if less than 2.9litres
Airway assessment: ?co-existant RA
Symptoms of airway obstruction secondary to large thymoma
CXR/CT neck/chest
Exclude other autoimmune diseases
Avoid premedication sedatives
Continue steroids and additional intra-op steroid
Anticholinesterase therapy withheld on morning of surgery

(e) Describe the your intraoperative management of a myasthenia patient presenting for
emergency surgery specifically relating to the condition
Regional anaesthesia where possible
Routine monitoring
Invasive BP
NM function monitoring
Intubation achieved by deepening anaesthesia with anaesthetic vapour
 If using suxamethonium, higher doses required because of reduced number of functional NM
post synaptic ACh receptors
MG patients are extremely sensitive to NDNMB, much reduced dose required (varies according
to agent)
Use of Anticholinesterase often unnecessary, can precipitate cholinergic crises
Most patients can be extubated successfully post op
Few may require HDU care/mechanical ventilation in ICU
Anticholinesterase restarted at reduced dose post-op and up-titrated

Porphyria and anaesthesia

A patient with a family history of porphyria presents to you for a minor
procedure. It will be his first anaesthetic.

(a) What is the biochemical abnormality causing the acute porphyrias? (15%)
(b) What are the symptoms and signs of an acute porphyric crisis? (20%)
(c) How should an acute crisis be managed? (20%)
(d) What are the implications for general (30%) and regional (15%) anaesthesia
of a patient with porphyria?

Click for model answer by Dr Ciara O'Donnell

(a)
- Haem is an iron containing porphyrin ring (an organic cyclical compound)
- A genetic defect causes deficiency of intermediary enzymes in the pathway of haem synthesis
- Pathway begins with glycine and succinyl coenzyme A which is converted to ALA and
subsequently leads to porphyrin production
- Most active in the liver and bone marrow
- All enzyme defects lead to an accumulation of 5-aminolaevulinic acid (ALA)
- Porphobilinogen (PBG) is also elevated in the majority of cases of acute porphyria including
hereditary coproporphyria, variegate porphyria and acute intermittent porphyria

(b)
- Abdominal pain, nausea and vomiting
- Cardiovascular changes including tachycardia, hypertension and arrhythmias
- Neurological including psychosis, confusion, seizures
- Peripheral neuropathy; proximal > distal
- Autonomic neuropathy; gastroparesis, postural hypotension and constipation
- Bulbar paresis; respiratory failure
- Electrolyte disturbance ; hyponatraemia and hypomagnesaeamia
- Skin rash and photosensitivity

(c)
- Have a high index of suspicion if unexplained abdominal pain or precipitating drug
taken/alcohol
- Remove triggering agent
- Send urine protected from light for Porphobilinogen (PBG) assay
- Give 3mg/kg IV haem arginate early
- Avoid catabolic state by giving NG/IV
- Treat any infection
- Supportive management;
Morphine for analgesia,
B blockers for haaemodynamics,
benzodiazepines, vigabatrin, gabapentin, mgSo4 and levetiracetam safe for seizures,
correct hyponatraemia,
ventilator support for respiratory compromise - consider that hood may not be a safe option in
the context of gastroparesis

(d)
- General: Full medical history and family history
- Knowledge of prevalence (higher in S Africa, Sweden)
- Team awareness of the diagnosis and input from a specialist in the field
- Examination; look for signs of peripheral neuropathy, autonomic instability which could indicate
active disease/ risk crisis
- Minimise fasting period/avoid catabolic state: IV dextrose/saline infusion
- Preop anxiolysis and adequate post op analgesia to minimise stress response; diclofenac should
be avoided
- Knowledge of drug database guiding safety of agents in porphyria; inhalationals (with the
exception of sevoflurane) morphine and propofol all safe; avoid barbiturates, etomidate and
sulponamides
- Awareness of clinical features of an attack and method of treatment is important
- IABP monitoring
- Consideration of CVP monitoring depending on nature of surgery
- Patient not suitable for day case surgery; monitoring required post op for urine PBG levels and
CV monitoring; crises can be delayed up to 5 days post op

- Regional: thorough neurological and cardiovascular examination must be carried out to identify
neurological deficits/autonomic neuropathy
- Invasive BP monitoring should be considered
- CV instability may result from dehydration and autonomic neuropathy coupled with a
neruraxial block, ephedrine is unsafe for management of hypotension in porphyria
- Local anaesthetics are safe in porphyria