Anesthesia & Critical Incidents 73

Anaesthesia & Intensive Care
Part 11: Critical Incidents for FCAI, FRCA and EDAIC

‫بسم الله الرحمن الرحيم‬
For Original Materials and Editors, Please refer to:
North Ireland School of Anaesthesia Website

http://www.nischoolofanaesthesia-finalfrca.org.uk/SAQs/criticalincidents/
‫عيداروس‬ CRITICAL INCIDENTS 2
1- Fat Embolism Syndrome
a) What is fat embolism syndrome and what is its clinical presentation? (10 marks)
b) What factors may increase the likelihood of intraoperative awareness? (11 marks)
c) What monitoring techniques can be employed to reduce the risk of awareness during general
anaesthesia? (5 marks)
 What is fat embolism syndrome and what is its clinical presentation? (10 marks)
Fat embolism syndrome; is the embolization of fat globules into the circulation as a result of long bone
fracture or major trauma. The fat globules then travel to the lung parenchyma and peripheral circulation.
Clinical Presentation: -
Typically presents 24-72 hours after initial injury, although can range from 12 hours to 2 weeks.
Typical Triad Presentation
1- Respiratory Changes; respiratory distress with hypoxaemia
2- Neurological Dysfunction; ranging from mild confusion to seizures including focal neurological defects
due to cerebral emboli
3- Petechial Rash; Due to embolization of small dermal capillaries and leakage of erythrocytes from them,
present in 60%. Typically found in oral mucosa, conjunctiva and skin folds of upper body.
There may be a number of minor features present; Tachycardia, Myocardial Depression, Coagulation
abnormalities, Oliguria.
List the clinical conditions that may predispose to fat embolism. (5 marks)
2 main classifications:
- Trauma (95% of causes of fat embolism) and
- Non-Trauma
Trauma:
-Long Bone Fractures
-Pelvic Fractures
-Fractures of other marrow containing bone
-Orthopaedic procedures
-Soft Tissue injury e.g. chest compression with or without rib fractures
-Burns
-Liposuction
-Bone marrow harvesting & transplantation
Non-Trauma:
-Pancreatitis
-Diabetes Mellitus
-Bone Tumour Lyses
-Osteomyelitis and panniculitis
-Steroid Therapy
-Alcoholic (Fatty) liver disease
-Lipid Infusion
-Sickle Cell Haemoglobinopathies

 What measures may be used to minimise and treat fat embolism? (5 marks)
- Measures to minimise fat embolism include; early fracture fixation, operative rather than conservative
fixation, limiting intraosseous pressure during orthopaedic procedures, use cement-less hip prosthesis,
unreamed intramedullary femoral nailing. Prophylactic use of Intravenous corticosteroids (Although
evidence is limited)
- Measures to treat fat embolism are mainly supportive for the respiratory and neurological compromise.
Supportive measures include maintenance of oxygenation, hydration, maintenance of cardiovascular
stability, prevention of DVT & stress ulcers, nutrition and correction of any coagulopathy. HDU or ICU
level care may be necessary. Aspirin may also be of use in patients with fat embolism syndrome.

2-Awareness
a) Define the types of unintentional awareness that may occur during general anaesthesia? (4 marks)
b) What factors may increase the likelihood of intraoperative awareness? (11 marks)
c) What monitoring techniques can be employed to reduce the risk of awareness during general anaesthesia? (5
marks)
 Explicit Awareness – spontaneously recalled intraoperative events with or without pain
Implicit Awareness – patient develops subconscious memory during anaesthesia that they do not later
recall. Memory may be retrieved by hypnosis
 Surgery
Emergency surgery
Cardiac
Obstetric
Paediatric
Rigid bronchoscopy
Trauma
Patient factors
Chronic use of alcohol/benzodiazepines
Smoking
Pyrexia
Anxiety
Masking of sympathetic signs- complete heart block, beta blockers, hypothyroidism, autonomic
neuropathy
Anaesthesia
TIVA
Use of muscle relaxants
Equipment failure
Reduced practitioner vigilance
Poor technique – under dosing for LSCS, unexpected difficult intubation, choice of agent
During transfer of anaesthetised patient
 Gold standard is the isolated forearm technique

Clinical observation for sympathetic activity
Oesophageal motility
ET anaesthetic gas
Forehead galvanometer
EEG techniques such as BIS, narcotrend, M-entropy
Evoked potential techniques such as aepEX

3- Anaphylaxis
a) What is anaphylaxis and how may it present? (5 marks)
b) List three common types of precipitant in an anaesthetic setting. (3 marks)
c) Describe your initial management (including relevant drug doses) in an adult patient. (5 marks)
d) Outline your secondary management (including relevant drug doses) after immediate resuscitation.
 Severe, life-threatening generalised or systemic hypersensitivity reaction.

Sub-divided into:
- Allergic- anaphylaxis mediated by an immunological mechanism usually IgE. (Type 1 hypersensitivity
reaction)
- Non Allergic- non IgE mediated reaction
Clinical Signs:
Cardiovascular
Tachycardia & Hypotension
Bradycardia/Cardiac arrest
Oedema
Cardiovascular collapse
Respiratory
Bronchospasm
Cutaneous
Erythema
Urticaria
 Common Precipitants
- NMBDs (70%)
- Latex (13%)
- Colloids (5%)
- Induction agents (3%)
- Antibiotics (3%)
- Contrast/Dye (2%)
- Benzodiazepines (2%)
- Opioids (<2%)
 Immediate Management
- Stop administration of agents
- Maintain airway & 100% O2
- Call for help
- Elevate feet
- Adrenaline IV 0.5ml of 1:10,000 (May require several doses: consider adrenaline infusion)

- IV fluid bolus 500-1000ml Crystalloid
- If cardiac arrest CPR as per ALS guidlines
- Transfer to appropriate critical care area
 Secondary Management
- IV Chlorphenamine 10mg
- IV Hydrocortisone 200mg
- If ongoing hypotension despite adrenaline consider another vasopressor
- Persistant bronchospasm: IV Salbutamol 250 mcg bolus or 10mg Salbutamol neb, IV aminophylline or
magnesium IV 2-5g slowly
- Send mast cell tryptase: at 0, 2 and 24 hours
- Refer for further investigations to identify causative agent.

4- Local Anaesthetic Toxicity (LAST)
a) List the possible causes of sudden collapse in this patient. (4 marks)
b) What symptoms and signs suggest local anaesthetic toxicity? (4 marks)
c) Briefly explain the pharmacological basis of severe local anaesthetic toxicity. (4 marks)
d) What is the immediate treatment of local anaesthetic toxicity? (6 marks)
e) What follow up is required for this lady? (2 marks)
 List the possible causes of sudden collapse in this patient. (4 marks)

Causes of sudden collapse in this patient include
• Local anaesthetic toxicity
o Seizure
o Arrhythmia
• Intrathecal injection of local anaesthetic and total spinal
• Tension pneumothorax
• Anaphylaxis
 Symptoms and Signs suggest local anaesthetic toxicity:
Symptoms include
• Perioral tingling
• Tinnitus
• Light headed ness / giddiness
• Agitation
• Tremor
Signs
• Confusion
• Tremor
• Decreased conscious level
• Arrhythmia
o Varying degrees of heart block
o Ventricular tachyarrythmias
o Asystole
• Hypotension
• Cardiovascular collapse
 Briefly explain the pharmacological basis of severe local anaesthetic toxicity. (4 marks)
Local anaesthetics enter the systemic circulation through inadvertent intra vascular injection or
absorption.
LA work by inhibition of fast inward sodium channels preventing the depolarisation of nervous tissue and

propagation of action potentials.
In the CNS, LAs disrupt the balance between inhibitory and excitatory neurones leading to seizures and
coma.
In the CVS there is inhibition of action potential generation and propagation in the heart leading to
varying degrees of heart block.
The toxicity of LAs is determined in part by how avidly they bind to sodium channels, those that bind
strongly (bupivicaine) are more cardiotoxic than those that demonstrate weaker binding (lidocaine)
 What is the immediate treatment of local anaesthetic toxicity? (6 marks)

Stop injecting local anaesthetic
Call for help
Establish if in cardiac arrest
• Begin CPR and life support if in cardiac arrest
If not in cardiac arrest give high flow oxygen and maintain the airway
Establish IV access if not already in situ
Control seizures with benzodiazepines, thiopental, propofol
If in cardiac arrest, treat as per ALS guidelines I.e DC shock for ventricular tachyarrythmias, adrenaline /
amiodarone after 3rd shock.
If in PEA then adrenaline every 3-5 minutes
If in cardiac arrest give lipid emulsion, 1.5ml/kg and begin infusion at 15ml/kg/hr
If no return of spontaneous circulation, bolus can be repeated a further twice every 5 minutes and
infusion rate doubled to 30ml/kg/hr
If not in cardiac arrest the convention treatment to manage hypotension – fluids and vasopressors. Raise
legs to increase blood pressure
Treat arrythmias with non sodium channels blocking agents
Seizures should not be treated with phenytoin
Consider the use of lipid emulsion.
e) What follow up is required for this lady? (2 marks)
This lady should be referred to intensive care and monitored for pancreatitis if lipid emulsion has been
given
All cases of lipid emulsion should be referred to the lipid rescue registry
The lady should also be given the chance to be followed up at an anaesthetic clinic to discuss the events
and future anaesthesia.

ASRA guidelines (2018)

5- Inadvertent Intra-arterial Injection
a) What factors predispose to inadvertent intra-arterial (IA) drug injection that could lead to severeextremity injury?
(7 marks)
b) Outline the possible intravascular mechanisms of injury. (3 marks)
c) What are the acute clinical features of inadvertent IA injection? (4 marks)
d) What is the early management of an acute IA injection injury? (6 marks)
 Factors predispose to inadvertent intra-arterial (IA) drug injection:

Patient Factors
-Unable to Report/communicate pain following injection etc – unconscious/sedated, distracting injuries in
trauma, infants/neonates
-Difficult to Cannulate – obese, oedematous tissues, chronic IV therapy, IVDUs, darkly pigmented skin
-Reduced evidence of Inadvertent Arterial Cannulation – hypotensive (lack of pulsatile flashback),
hypoxaemic (darker 'venous' appearance to arterial blood)
-Anatomical Anomalies/factors – eg. 'high rising' radial artery, antebrachialis superficialis dorsalis artery,
proximity of veins/arteries at antecubital fossa and groin
Environmental Factors
-ICU – high arterial line prevalence, multiple infusions ongoing with multiple injection ports (potential for
wrong connection/injection)
- emergency situations - need for rapid cannulation/injection of medications, multiple tasks and
distractions
Medications Injected (most likely to cause severe injury)

-barbiturates
-non- polarising NMBAs
-ketamine
-phenytoin, amiodarone
 The Intravascular Mechanisms of Injury:

-direct tissue damage
-arterial spasm secondary to drug or local norepinephrine release
-precipitation/crystallisation and subsequent thrombosis/ischaemia in microcirculation
-local factor release eg thomboxane
-chemical arteritis
 The acute clinical features of inadvertent IA injection:

-Lack of expected drug effect
-Immediate Pain/discomfort on injection, distal to injection site
- Distal blanching/erythema/hyperaemia/cyanosis/pallor/parasthesia
-Development of Oedema/Gangrene

 The early management of an acute IA injection injury:
No universally accepted treatment protocol, but general measures include:
-Recognise possibility of IA injection
-Immediately discontinue injection/infusion
-Ensure stabilisation of patient from A,B,C approach if necessary (eg if mid-RSI) – call for help
-Elevate limb to maximise venous and lymphatic drainage
-Prompt and adequate Analgesia
-Rapidly assess likelihood for medication involved to cause significant injury
-Assess extent of injury evident – mark area involved
-Early advice/referral to plastic surgery
Consider the following:
-Anticoagulation with heparin to reduce thrombotic complications,
-IA injection of lidocaine to reduce vasospasm (although could damage artery),
-Regional sympathetic block eg. Stellate ganglion block – maximise veno- and arterial dilatation – weigh
benefit against risks,
-Calcium Channel Blockers,
-Aspirin (counteracts Thomboxane),
-IA Papaverine – promotes vasodilation

6- Cardiac Tamponade
(a) Detail the anatomy of the pericardium.
(b) What is the definition of tamponade?
(c) Describe the clinical features of pericardial tamponade
(d) Describe the pathophysiology in early and late stages of tamponade
(e) What are the causes of cardiac tamponade?
(f) Describe (i) non surgical (ii) surgical management of life-threatening tamponade
 Anatomy of the Pericardium:

Pericardium is a two layered
structure surrounding the heart
Fibrous and serous layers
Fibrous layer is a stiff, inelastic
structure, which has little ability
to accommodate fluid
accumulation over a short time
course
Serous layer consists of two
layers, the parietal and visceral
pericardium
Parietal layer is adherent to the
fibrous pericardium
Visceral layer is part of the
epicardium or external layer of the heart wall.
Pericardial effusion is normally between the parietal and visceral layers of the serous pericardium
The pericardial space normally holds 15 to 50 mL of an ultrafiltrate of plasma.
Pericardial fluid is being produced by visceral mesothelium cells and drained from the pericardium by the
lymphatic system into the mediastinum and right side of the heart
The pericardial sac is attached anteriorly to the sternum, posteriorly to the vertebral column, and
inferiorly to the diaphragm
Pericardial sac layers and fluid function to buffer the heart from external impact, to reduce resistance
during motion of heart and to provide a barrier against infection traversing from surrounding structures,
particularly the lungs
 Tamponade:
Pericardial tamponade is an accumulation of fluid (blood or serous fluid) in the pericardial sac. It is a life
threatening emergency creating an increased pressure within the pericardial space that impairs the ability
of the heart to fill and to pump. It is different to pericardial effusion which accumulates over time; in
contrast cardiac tamponade is a physiological diagnosis in which the pericardial effusion must be
accompanied by evidence of obstructive shock.

 The Clinical features of Pericardial Tamponade:
Beck’s triad which consists of hypotension, elevated systemic central venous pressure (CVP) and quiet
muffled heart sounds
Kussmaul sign is a paradoxical increase in CVP with
inspiration
Dyspnoea, tachycardia and hypotension
Pulsus paradoxus on arterial line trace (dramatic
respiratory variation in the systolic pressure)
Equalization of diastolic pressures on PA catheter
monitoring
Pulseless electric activity (PEA) cardiac arrest can
follow
Sinus tachycardia
Chest pain and features of cerebral hypoperfusion
eg confusion, anxiety
ECG may demonstrate electrical alternans or sinus
tachycardia with low-voltage QRS complexes,
atrial arrhythmias
Chest radiograph may show an enlarged cardiac silhouette with a globular heart shape
Echocardiography is very useful, single most important investigation
Diastolic collapse of the anterior right ventricular free wall, right atrium, left atrium
Increased left ventricular diastolic wall thickness, described as “pseudohypertrophy”
Inferior vena cava dilatation, without respiratory variation in size, suggesting raised right atrial pressure
M-mode echo to identify large respiratory fluctuations in mitral and tricuspid flows
TTE is more limited post cardiac surgery and may need TOE to identify retroatrial haematoma
 The Pathophysiology in Early and Late stages of Tamponade:

Tamponade will only be maintained if a sustained increase in pericardial pressure is generated.
Requirements for sustained pericardial hypertension are an effusion volume that exceeds the pericardial
reserve volume and for the rate of fluid accumulation to exceed the rate of pericardial stretch.
Early
Fluid fills the pericardial reserve volume and the pericardial pressure begins to rise
Filling pressures within the right side of the heart are lower than within the left side of the heart and are
the first to be equalled then exceeded by a rising pericardial pressure
The cardiac chamber filling pressure gradient is reduced and there is a massive reduction in venous return
to the heart
The right atrium and right ventricle become compressed causing impaired diastolic filling
Right sided pressures are lowest in diastole
As less venous blood returns to the right atrium the central venous pressure rises

Impaired right ventricular filling results in an under-loaded ventricle, which operates at the low end of the
Frank-Starling curve
Underfilling and limited contractility result in a low stroke volume
Late
Pericardial pressure rises sufficiently to overcome the left atrial and higher left ventricular filling pressures
then a dramatic decrease in cardiac output occurs
Reduction in coronary blood flow occurs, in tamponade this is accompanied by limited cardiac work and
the myocardium is usually not ischaemic
A cycle of exhausted physiological compensation measures follows, with increased fluid retention,
decreased cardiac output and venous return
Leads to a state of obstructive shock and eventually cardiac arrest (PEA)
Increase in sympathetic tone is a compensatory physiological response
Tachycardia and sympathetic-mediated vasoconstriction cause an increase in systemic vascular resistance
in a bid to maintain mean arterial pressure
The renin-angiotensin system is activated causing increased fluid retention. Elevated central venous
pressures improves diastolic filling against intrapericardial pressure, but this has a limited effect
 The Causes of Cardiac Tamponade:

Bleeding after cardiac surgery
Blunt or penetrating mediastinal trauma (especially stab wounds)
Acute myocardial infarction with free wall rupture
Aortic dissection
Malignancy/infection/idiopathic/massive pleural effusion (likely to be more chronic onset)
Endovascular catheterization (including aortograms and carotid arteriograms) with perforation
Central venous catheter placement is uncommon (due to erosion of the catheter through a vessel wall)
 Non-surgical Management of life-threatening Tamponade:
Resuscitation to include principles of airway, breathing and circulation, taking into account the specific
pathophysiology of cardiac tamponade
Intubation and mechanical ventilation should be avoided unless strictly necessary, as this will tend to
exacerbate cardiac failure in tamponade
Ventilated patients should have PEEP minimised to avoid limiting venous return
Adequate fluids to ensure preload, allow tachycardia
The haemodynamic goals in tamponade are to increase cardiac output by augmented chronotropy, to
decrease afterload and decrease right atrial pressures
Isoprenaline, dopamine and dobutamine are all appropriate first choice inotropes and have been shown
to increase cardiac output in tamponade however they increase risk of MI

Small studies have shown vasopressors such as noradrenaline improve mean arterial pressure with
minimal myocardial strain and no change in cardiac index
Bedside needle cardiocentesis
Placement of a catheter percutaneously into the pericardial sac in order to externally drain the effusion
Procedure can be performed using anatomical landmarks alone, or under echocardiographic or
fluoroscopic guidance
Pericardiocentesis is contraindicated in aortic dissection and relatively contraindicated in severe
coagulopathy
Reverse any coagulopathy which is present especially after cardiac surgery
Surgical Management of life-threatening Tamponade:

Pericardotomy (pericardial window) a video-assisted thoracoscopic approach is less invasive, creating a
drainage window between pericardium and pleura
Sternotomy
Percutaneous balloon pericardiotomy can be performed under local anaesthesia in the cardiac
catheterisation laboratory and involves insertion of a valvuloplasty balloon into the parietal pericardium
via a subxiphoid approach under radiological guidance

7- Iatrogenic Pneumothorax
(a) What are the possible causes of iatrogenic pneumothorax?
(b) What are the ventilatory parameters which minimise the risk of pneumothorax on mechanical ventilation?
(c) What signs or symptoms may indicate the development of a pneumothorax in an intubated and ventilated
patient?
(d) Describe the management of recurrent pneumothoraces.
(e) What is re-expansion pulmonary oedema? How can this risk be minimised?
 Causes of Iatrogenic Pneumothorax:

- Transthoracic Needle Biopsy
- Central venous Catheterization, particularly Subclavian
- Thoracocentesis
- Transbronchial Lung Biopsy
- Pleural biopsy
- Positive pressure ventilation
- Tracheostomy
- Pericardiocentisis
- Bronchoscopy
- Nasogastric Tube Insertion
- Cardiopulmonary Resuscitation
 The ventilatory parameters which minimise the risk of pneumothorax on MV:

- Plateau Pressure <35cmH2O
- Minimise PEEP and auto-PEEP
- High Inspiratory Flow Rates
- Reduced tidal volumes eg. 6ml/kg
- Permissive Hypercapnia
 Signs or Symptoms may Indicate the development of a Pneumothorax in an Intubated

and Ventilated Patient:
Signs
Sudden desaturation
Sudden rise in peak airway pressures
Hypotension
Cardiovascular collapse
Pulseless electrical activity
Symptoms
Patient-ventilatory dysynchrony
Respiratory distress
agitation
 Management of Recurrent Pneumothoraces:

Indications for management include:
Recurrent pneumothorax
Patients with chronic air leak
Patients with large bullae
Patients who live in remote areas
Patients in whom a recurrence could prove hazardous, eg airline personnel, deep sea diver
Methods of preventing recurrence include:

- Chemical pleurodesis – injection of sclerosing agent between the parietal and visceral pleura via a chest
tube. Agents used include doxycycline and talc slurry
- Video-Assisted Thoracoscopy – can be used to resect pleural blebs or bullae or for pleurodesis
chemically, mechanically via pleurectomy or laser ablation of the parietal pleura
- Thoracotomy – largely superseded by VATS procedure.

Remains indicated in cases of:
persistent air leak from a large fistula requiring surgical closure
frank haemothorax requiring surgical control of bleeding
decortication of trapped lung that fails to expand
 Rre-expansion Pulmonary Oedema:
Re-expansion pulmonary oedema occurs after rapid re-expansion of a collapsed lung:
Typically unilateral.
Pathophysiology is unknown
Believed to be related to duration of pneumothorax and the magnitude of negative pressure applied to
the pleural space to re-expand the lung
Re-expansion pulmonary oedema can be minimised by:

Withholding pleural suction in managing pneumothoraces of unknown duration or greater than 3 days
Applying low levels of negative pressure (<20cmH2O) to the pleural space.

8- Medication Errors
a) What are medication errors? How do these differ from adverse drug events? (25%)
b) Which human factors contribute to intravenous drug administration errors in theatre-based anaesthetic practice?
(25%)
c) Outline the organisational strategies that might minimize intravenous drug administration errors. (25%)
d) Outline a system for reporting medication errors (25%)
 Medication Errors: A medication error is any error that occurs in the medication process e.g. from
prescribing it, administering it, omitting it etc.
An Adverse Drug Event: is an adverse outcome that can be attributed, with some degree of likelihood, to
be due an action of a drug. An adverse drug event may or may not be due to a medication error.
 Human Factors contribute to IV drug Administration Errors in Theatre-based Anaesthetic Practice:

Human factors are those factors that encompass all those factors that influence people and their
behavior.
Mis-labelling of syringes, failure to mix iv drugs, syringe swaps, wrong or inadequate dose, change in drug
packaging which is misread, tiredness, distraction by colleagues when preparing or administering drugs,
distraction by unexpected difficulty, lack of clarity of roles especially when a number of anaesthetists are
present.
 The Organisational strategies that might minimize IV drug administration Errors: Ensuring that
theatre lists are confirmed prior to starting to to administer correct drugs to correct patient, confirming
which patient has attended theatre, use of the WHO surgery checklist, ensuring a nationally recognized
syringe labeling system is in place and stickers available to ensure that all anaesthetists recognize the
contents of a syringe and there is no inter-hospital variation, communication of any change in ampules,
doses or packaging for drugs or change in supplier, encourage a culture of drawing up drugs in silence
without disturbances, ensure staff have proper periods of rest, encourage culture of one person being
responsible of iv drugs and who can administer the drugs to ensure the correct drug is given and in a
timely manner.
 System for Reporting Medication Errors:

Medication errors should be reported through local incident reporting systems. They should also be
reported nationally to the National Patient Safety Agency, NPSA, through the yellow card scheme, which
is available at the back of the BNF. NPSA recognize which reported errors are due to adverse drug effects
and those that are due to medication error.

9- Critical Incident Reporting (OVR)
a) What do you understand by the term critical incident? (15%)
b) How does the RCOA recommend that incidents are graded? (25%)
c) How are critical incidents reported? (15%)
d) What are the factors considered in the analysis of critical incidents? (30%)
e) What is The Bolam Principle? What is the Bolitho amendment? (15%)
 Critical Incident:
- ‘An event which led to harm or could have led to harm if it had been allowed to progress’. It should be
preventable by a change of practice.
 The RCOA recommendation:

Two types based on the outcome or preventability.
Outcome
❚ No effect.
❚ Transient abnormality unnoticed by the patient, e.g. laryngospasm.
❚ Transient abnormality with full recovery, e.g. headache.
❚ Potentially permanent but not disabling damage, e.g. chipped tooth.
❚ Potentially permanent disabling damage, e.g. stroke.
❚ Death.
Preventability
❚ Probably preventable within current resources, e.g. failure to perform a preoperative machine check.
❚ Probably preventable with reasonable extra resources, e.g. failure to detect oesophageal intubation
(which could be obviated by capnography).
❚ Possibly preventable within current resources, e.g. pneumothorax during insertion of a central venous
line, which might be prevented by better teaching/ super vision.
❚ Possibly preventable with reasonable extra resources, e.g. inability to replace unwell anaesthetist
because of inadequate staffing which might be prevented by more cover.
❚ Not obviously preventable by any change in practice,e.g.idiosyncratic drug reaction.
 Critical Incidents Reported:

Trust reporting system which should be used for events which have caused harm to the patient, staff or
to the reputation of the Trust - Voluntary reporting ie 1R1 forms
National reporting systems ie; NPSA

 The Factors considered in the Analysis of Critical Incidents:
Experts from the speciality use a standardised methodology to interrogate data and generate meaningful
learning outcomes.
They should have a detailed list of the chain of events that lead to the incident to consider what
interventions, and at what level in the chain, can prevent the incident from occurring again.
Use root cause analysis.
They must pay attention to psychological and human factors in the nature, mechanisms, and causes of
the error.
National reporting systems work alongside the local risk management structures for comprehensive
analyses and cross-learning from the incidents.
Areas for improvement must be high lighted (e.g. medication errors, retained throat packs), and further
focus by national organizations to trigger further actions such as raising awareness, research, audits,
training initiatives, curriculum, and specific guidelines.
Local safety initiatives of investigating and analysing incidents are extremely important to get into the
root cause of the incidents and how these can be prevented in the future.
Learn from near misses, or where an incident was effectively managed without actual harm
 The Bolam principle: The doctor is not liable for his diagnosis, treatment, or refusal to give information
to the patient, if he follows a responsible body of medical opinion.
Bolitho amendment:court should not accept a defence argument as being ‘reasonable’ ‘respectable’ or
‘responsible’ without first assessing whether this opinion is susceptible to logical analysis

10- Aspiration under Anaesthesia
(a) What is Aspiration? What clinical syndromes may result? (3 marks)
(b) What are the risk factors for aspiration while undergoing anaesthesia? (4 marks)
(c) Describe the physiological sequelae of aspiration (4 marks)
(d) Describe the precautions to prevent aspiration and the actions to modify the consequences (5 marks)
(e) Describe the management of pulmonary aspiration (peri- and post-aspiration) (4 marks)
 Aspiration:
Aspiration is the inhalation of oropharyngeal or gastric contents below the level of the vocal cords.
Clinical syndromes range from asymptomatic to death. Include:
- Chemical pneumonitis/ aspiration pneumonitis (Mendelson’ syndrome)
- Bacterial pneumonia
- ARDS
 The Risk factors for Aspiration while undergoing Anaesthesia:

Risk factors can be patient, surgery and anaesthetic related:
Patient Related
Impaired laryngeal reflexes – low GCS, intoxication
Full stomach – emergency surgery, inadequate fasting time, gastrointestinal obstruction
Decrease in barrier pressure – pregnancy, obesity
Relaxation oesophageal sphincter – hiatus hernia, pregnancy, achalasia
Reduction in gastric emptying – mechanical obstruction, gastroparesis, CKD, trauma, opioids, raised ICP,
previous GI surgery, pain
Oesophageal disease – previous surgery
Surgical Factors
Type: upper GI surgery, cholecystectomy.
Position: lithotomy, head down.
Increase intra-abdominal pressure: laparoscopy.
Duration: more than 2hrs.
Anaesthetic Factors
Airway: difficult airway, SGA, gas insufflation abdomen.
Light plane anaesthesia
Positive pressure ventilation
 The Physiological Sequelae of Aspiration:

The physiological consequences of aspiration depend on the particle size, acidity, volume and bacterial
composition.
- Particle size – large particles can result in complete airway obstruction or distal airway obstruction with
post obstruction collapse and atelectasis.
- Acidity – particularly severe if pH <2.5.

According to Mendelson:
Phase One-
Immediate chemical burns of the airway occur.
Destruction of alveolar pneumocytes and ciliated cells occurs within 6 hours.
Alveolar permeability increases.
Increased lung water and interstitial oedema
Decreased lung compliance, increased A-a gradient and VQ mismatch occurs.
Cells regenerate over 3-7 days
Phase Two-
Inflammatory response secondary to cytokine release, production of oxygen free radicals and proteases
Acute lung injury, acute respiratory distress syndrome and multiple organ failure ensue
Volume – worsened if >0.3ml/kg aspirated
Bacteria – gastric juices and oropharyngeal secretions contain bacteria
Acid damaged lungs prime breading ground for superimposed bacterial infection.
 The Precautions to Prevent Aspiration and the Actions to Modify the Consequences:
A number of strategies to prevent aspiration:

- Avoidance of GA – regional anaesthesia
- Decrease Gastric Volume
Adequate fasting times
NG tube aspiration
Prokinetic medication
- Increase Gastric Emptying

Prokinetic medication
Airway protection
Endotracheal intubation
Awake intubation
Second generation SGA
- Prevent Regurgitation
Rapid sequence induction
Cricoid pressure
Extubation
NG placement and suction prior to extubation
Awake
Position – lateral, head down, upright

Actions to Modify Consequences Include
- Neutralise gastric contents
- Antacids
- H2 receptor antagonists
- Proton pump inhibitors
- Sodium citrate
- Decrease gastric volume
- Adequate fasting times
- NG tube aspiration
- Prokinetic medication
- No evidence for early antibiotics or for steroid therapy.
 Management of Pulmonary Aspiration (Peri- and Post-aspiration):

Peri-aspiration
Inform the surgeon and theatre team
Place patient head down and in left lateral position
Suction oropharynx and apply 100% oxygen
Perform rapid sequence induction with cricoid pressure if regurgitation and not active vomiting
Suction airway post intubation and prior to ventilation to prevent oropharyngeal contents being further
propelled into lungs. (Only if feasible – may require ventilation prior to intubation if desaturated – if so
ventilate with cricoid pressure on)
Post aspiration
Keep intubated and ventilated if respiratory failure and transfer to intensive care unit
Apply lung protective ventilatory strategies to prevent further lung damage
CXR, ABG and sputum samples.
Nurse in head up position
If obstruction consider bronchodilators or bronchoscopy to retrieve particulate
Provide supportive therapy and organ support
Antibiotics if evidence of bacterial pneumonia
Document in the notes, discuss with patient and family, inform consultant.

11- Propofol Related Infusion Syndrome
(a) What is propofol related infusion syndrome and what are its clinical effects ( 7 marks)
(b) List the risk factors for PRIS ( 5 marks)
(c) What specific laboratory findings might be expected in a case of PRIS? (3 marks)
(d) How may PRIS be prevented (3 marks) and managed (2 marks)?
 Propofol Related Infusion Syndrome and what are its clinical effects:
Propofol related infusion syndrome (PRIS) was originally proposed by Bray to describe the adverse effects
associated with propofol infusion in the paediatric population. It has subsequently been described in the
adult intensive care population.
The clinical effects are refractory bradycardia leading to asystole associated with any one of the following:
- metabolic acidaemia with base deficit < -10mmol/l due to lactate acidaemia
- rhabdomyolisis due to myocyte necrosis leading to myoglobinuria and renal failure
- hyperkalaemia
- lipaemic plasma due to hypertriglyceridaemia
- enlarged or fatty liver
- progressive myocardial collapse
 The Risk Factors for PRIS:

- Prolonged propofol infusion >48 hours, particularly when >4mg/kg/hr (although some studies have
shown it to occur at doses of <2mg/kr/hr)
- Severe head injuries
- Sepsis
- High endogenous or exogenous catecholamines or glucorticoid levels
- Low carbohydrate supply leading to increased lipolysis during times of starvation
- Inborn errors of fatty acid oxidation
 Laboratory findings might be expected in a case of PRIS:

- lactate acidaemia
- elevated CK with no other explicable cause
- myoglobinuria
- hyperkalaemia
- hypertriglyceridaemia
How may PRIS be prevented (3 marks) and managed (2 marks)?

PRIS may be prevented by:
- providing an adequate carbohydrate intake
- keeping propofol infusions to <4mg/kg/hr

- minimizing duration of propofol infusion to < 48 hours
PRIS is managed by supportive measures:

- Ceasing Propofol infusion and switching to alternative Sedation
- Inotropic or vasopressor support
- Cardiac Pacing for refractory Bradycardia
- Haemodialysis to resolve Acidaemia
- ECMO has been used for combined respiratory and cardiovascular support

12- Malignant Hyperthermia
(a) What is malignant hyperthermia? Describe the defect resulting in the presention of MH. (3 marks)
(b) Describe the cellular events, presentation and metabolic abnormalities associated with the disease. (c) Describe
your management of an MH crisis (including post-recovery) (4 marks)
(d) How does dantrolene work? How is it prepared? (3 marks)
(e) Describe how you would prepare for an anaesthetic in a patient with known malignant hyperthermia
susceptibility. (3 marks)
(f) Compare and contrast MH with malignant neuroleptic syndrome (NMS). (3 marks)
 Malignant Hyperthermia:
- Malignant hyperthermia is a pharmacogenetic disorder, which produces hypermetabolism, muscle
rigidity and muscle injury.
- It is caused by exposure to trigger agents, either suxamethonium or volatile anaesthetic agents.
- It is a Genetic defect:
Inherited Autosomal Dominant disorder.
Abnormality along excitation-contraction coupling process.
Abnormal dihydropyridine receptor in T-tubule.
OR abnormal Ryanodine Receptor isoform, responsible for calcium efflux.
 The Cellular Events, Presentation and Metabolic abnormalities:
- Cellular Events:
Uncontrolled release of free calcium from the sarcoplasmic reticiulum
Hypermetabolism of skeletal muscle occurs

Hydrolysis of ATP, glycogenolysis and glycolysis, increased O2 consumption and heat production
- Presentation:
Unexplained Tachycardia
Rise in etCO2
Muscular Rigidity despite NDMR
- Metabolic Abnormalities:
Acidaemia with Respiratory and Metabolic Components
Hypoxaemia
Hyperthermia
Rhabdomyolysis
Hyperkalaemia and Hypercalcaemia
Acute Kidney Injury
 Management of an MH crisis (including post-recovery):
- Call for help
- To halt the MH process:
- Remove triggers; turn off vaporisers; ventilate with 100% O2; switch to IVI propofol
- Dantrolene 2-3mg/kg IV followed by 1mg/kg PRN
- Active Cooling; Cold IVFs; Cold Peritoneal Lavage
To treat the effects of MH:

- Hypoxaemia and Acidaemia – 100% O2;Hyperventilate; Sodium Bicarbonate
- Hyperkalaemia – Sodium Bicarbonate; 10 units Actrapid with 50mls 50% Glucose; 10mls 10% Calcium
Gluconate
- Myoglobinaemia – forced alkaline diuresis; urine output >3ml/kg/hr
- DIC – FFP; cryoprecipitate; platelets
- Cardiac arrhythmias – amiodarone; magnesium; avoid calcium channel blockers
- ICU Care:
- Ongoing Monitoring – SpO2, ECG, ABP, etCO2, temperature, ABGs
- Assess Renal Function
- Further Dantrolene as Necessary
- Consider Alternative Diagnosis eg. Sepsis, Myopathy, Phaeochromocytoma
- Late Management:
- Counsel patient and family
- Refer to MH unit
 Dantrolene:
- Mode of Action:
- acts within muscle to reduce calcium release by the sarcoplasmic
reticulum, reducing intracellular calcium levels
- Preparation:
- Each vial dissolves in 60mls of water for injection.

- Dissolution can be accelerated by warming dilutent and using large volumes of dilutent.
 Anaesthetic Management of a patient with Malignant Hyperthermia susceptibility.

- Pre-operatively:
- Take time to counsel the patient regarding the implications of MH, the necessary monitoring and any
treatment required.
- Consider Regional Anaesthesia if appropriate
- Intra-operatively:
- Avoid Triggers ie; Suxamethonium and all Volatile Agents.
- Prepare anaesthetic machine by changing vaporizer and CO2 absorber and blowing O2 at 10L/min for 30
minutes.
- Use new breathing circuit, ETTs and LMAs.
- Ensure Dantrolene is readily available.
- Communicate Risk to all theatre staff.
- etCO2 and Body Core Temperature Monitoring throughout.
Post-operatively:
- ICU/HDU post-operatively if suspected/confirmed MH reaction.
 Malignant Neuroleptic Syndrome (NMS):

Like MH, NMS may present with:
 Hyperthermia.
 Tachycardia.
 Muscle Rigidity.
 Cyanosis.
NMS can be differentiated by:

 Akinesis
 Sensory abnormalities
 Autonomic Dysfunction (Tachy/Bradycardia,
Hyper/Hypotension)
 Elevated CK levels.
Causes:
 Administration/Ingestion of Psychotropic Agents eg. Haloperidol
 NMS affects are initiated within the CNS, and not in the Muscle as in MH:
excess dopamine release in the Hypothalamus and Basal Ganglia.
Treatement:
 Dantrolene can be used.
 Bromocriptine, which acts as a Dopamine Receptor Antagonist.

13- Suxamethonium Apnoea
You are pre-assessing a ten year old for their first anaesthetic for an appendectomy. His mother tells you
there’s a history of a reaction to an anaesthetic agent in the family, that an uncle “didn’t wake up” for
hours after their last anaesthetic. You begin to suspect Suxamethonium Apnoea.
(a) What are the indications for suxamethonium? What is the mechanism of action? (20%)
(b) What are the side-effects of suxamethonium? (10%)
(c) Describe the genetic enzymatic variations that can result inprolonged activity of suxamethonium (20%)
(d) What are the causes of acquired plasma cholinesterase deficiency? (20%)
(e) What are the effects of suxamethonum apnoea? (10%)
(f) What is the management of suxamethonium apnoea? (20%)
 The indications for Suxamethonium:

Rapid sequence induction
Presumed full stomach
Treatment of laryngospasm
Anticipated difficult airway
Mechanism of Action:
Two nitrogen contain groups bind
to alpha subunit of post synaptic
acetylcholine receptor at NMJ
(Neuromuscular Junction)
Causes ion channel to open in the
post synaptic membrane and
depolarisation of the muscle
(Fasciculations)
Molecule stays bound to
membrane, causing it to stay
depolaroised, further action
potentials cannot propagate and
muscles become flaccid, allowing
intubation.
 The side-effects of
Suxamethonium:
Bradycardia
Malignant hyperpyrexia
Increase in intraocular
pressure
Decrease in lower oesophageal sphincter tone
Hyperkalaemia
Myalgia
Anaphylaxis
Prolonged neuromuscular blockade due to inherited or acquired suxamethonium apnoea
 The Genetic Enzymatic Variations:
Single amino acid substitution in coding for plasma cholinesterase resulting in altered activity of
enzyme- four alleles make up 10 genotypes
Usual (normal)
Atypical
Silent
Fluoride-resistant
95% of population are homozygous for the normal gene
4% of population possess one normal gene and one of the three abnormal genes. This results in a
prolonged block of typically 10-20 minutes
>0.01% of the population are homozygous with 2 abnormal genes, this results in a prolonged block
that can last several hours until excreted by the kidney
 Causes of Acquired Plasma Cholinesterase Deficiency:

Hepatic failure
Pregnancy
Renal failure
Malignancy
Burns
Malnutrition
Hypo-proteinaemia
Drugs : ketamine, OCP, lithium
 The Effects Of Suxamethonium Apnoea:

Absence of muscle function after effects of anaesthesia have worn off i.e. inability to breathe
Risk of awareness at end of procedure- anaesthesia worn off but inability to breathe- presenting as
tachycardia, tearing of eyes etc
Depending on patients genotype patient may only have slightly prolonged muscle paralysis, but
homozygotes for one of the 3 abnormal alleles may have a prolonged block requiring repeat anaesthesia,
prolonged ventilation and monitoring.
 Management of Suxamethonium Apnoea:

Primarily supportive
Management depends when prolonged block becomes apparent- either during a failed intubation or at
the end of a procedure.
If during a failed intubation, follow failed intubation algorithm
If at end of procedure
Maintain anaesthesia with volatile or IV agent
Monitor neuromuscular function with peripheral nerve stimulator
Consider ICU for continued sedation and ventilation
Fresh frozen plasma (FFP) can be considered to provide a source of plasma cholinesterase
Refer for investigation after recovery
Full explanation to patient/guardian/parent. Referral for other family members and letter for general
practioner

14- Electrical Injury
Electrical injury occurs when the body forms part of an electrical circuit.
(a) What are the two main methods by which this can occur?
(b) What factors affect the degree of injury that occurs? What are the physiological effects of electrocution as the
current increases?
(c) Describe the general and specific measures taken to prevent electrical injury in theatre
(d) Describe how equipment is designed to  chance of electrical activity according to safety standard
(e) What is Microshock?
(f) What are the Late Complications of Electrocution?
 Methods by which Electrical Injury can Occur:

The body forms part of a circuit through:
- Resistive Coupling: This occurs when the body comes in direct contact with a source of electricity and
earth.
- Capacitive Coupling: This occurs when the body forms a connection between an electrical source and
earth by acting as one plate of a capacitor (i.e. direct contact is not needed). A capacitor consists of two
parallel conductors separated by an insulator. AC current can pass through a capacitor and induce current
flow in a patient.
Electricity can cause morbidity or mortality through electrocution, burns, or ignition of a flammable
material (causing a fire or explosion).
 Factors affect the Degree of Injury :
- Tissue damage is proportional to: the amount of electricity that flows (current), the current path, the
current density (the amount of current flowing per unit area), the type of current (AC or DC; AC at lower
frequencies is the most dangerous, especially 50Hz; at >1kHz the myocardium is much less susceptible to
arrhythmia), and the duration of exposure.
- 1mA: tingling pain
- 5mA: pain
- 15mA: tonic muscle contraction (“can’t let go”). May cause fracture of long bones and vertebrae. May
cause rhabdomyolysis.
- 50mA: tonic contraction of respiratory muscles, respiratory arrest
- 100mA: VF
- >1A: sufficient heat generated to burn skin and internal organs (especially nerve tissue and blood
vessels)
- >5A: Asystole
 Measures to Prevent Electrical Injury in Theatre:

General Measures: Regular maintenance of electrical equipment; Preventing patient contact with
earthed objects; Antistatic footwear
- Antistatic footwear has a resistance (75kOhm – 10MOhm) which is low enough for the safe dissipation
of electrostatic charges, thus preventing the build-up of static charges, but high enough to stop passage

of a dangerous current.
Specific Measures:
Maintenance of equipotentiality – If equipment in close proximity have different potentials, then current
can flow between them if something (e.g. patient or staff) makes contact between them and completes
the circuit. To prevent this, different equipment are connected to each other to bring them to the same
earth potential.
Isolated or Floating Circuits – Patients are not connected directly to earth via plates or electrodes, so
current cannot flow through the patient to earth should contact with a live supply occur. This is achieved
through the use of an isolating transformer, which operates on the principle of capacitive coupling.
Circuit breakers – In this device the supply live and neutral wires are coiled around the core of a
transformer. A third winding connects these to the coil of a relay that operates the circuit breaker. If the
current in the live and neutral conductors are the same, then the magnetic fluxes cancel each other out. If
they are different (due to current leakage), then the magnetic flux will induce a current in the third
winding, which will cause the relay to break the circuit.
 The Equipment Design to  chance of Electrical Activity according to Safety Standard:

- The International Electrotechnical Commission publishes and regularly updates the IEC 60601, a series of
technical standards for the safety and effectiveness of medical electrical equipment. The general standard
(IEC 60601-1 – Medical Electrical Equipment – Part 1: General Requirements for basic safety and essential
performance) gives general requirements of the series of standards.
- Equipment is Classified according to the Means of Protection:
Class 1: Any conducting part of the equipment which may contact the patient is connected to earth by the
earth wire. Contains a fuse in the mains plug and also in the live and neutral conductors.
Class 2: Equipment protected by double or reinforced insulation
Class 3: Battery-powered equipment with Safety Extra Low Voltage (SELV). SELV – voltage not exceeding
25V AC or 60V DC.
Type B: May be Class 1, 2 or 3, but the maximum leakage current must not exceed 100 microamps. Not
suitable for direct connection to the heart.
Type BF: As for Type B, but uses an isolated (floating) circuit.
Type CF: Use isolated circuits and have a maximum leakage current of <10 microamps. These provide the
highest degree of protection. Are suitable for direct cardiac connection e.g. ECG leads, pressure
transducers, thermodilution devices.
Types B, BF and CF may also be designed with defibrillator protection.
 Microshock:
- Small currents (50 microamps at 50 Hz), if applied directly to or near the heart, can cause VF. This is
termed microshock. This can happen via equipment such as central venous catheters, PA catheters, or
transvenous pacing wires. This is because of the increased current density for any given current when it is
applied directly to the heart.
 The Late Complications of Electrocution:

Muscle fibrosis; Tissue loss from debridement; Peripheral neuropathies; Joint stiffness; Reflex
sympathetic dystrophy (i.e. CRPS); Cataracts; Paraplegia; Quadriplegia; Mental/personality changes

15- Residual Neuromuscular Blockade
Residual neuromuscular blockade is a common and under diagnosed problem in patients post-
anaesthesia.
(a) Describe the mechanism of action of (i) depolarising muscle relaxants (ii) non-depolarising muscle relaxants (iii)
neuromuscular blockade antagonists
(b) What is the definition of residual neuromuscular blockade? What are some of the adverse effects?
(c) What are the factors which contribute to residual neuromuscular blockade?
(d) What are the clinical criteria for evaluating adequacy of muscle function?
(e) Describe the train of four method of peripheral nerve stimulation - how does it guide your management with
regards to reversal agents?
(f) What methods of neuromuscular monitoring exist that do not require subjective assessment?
 The Mechanism of Action of Depolarising Muscle Relaxants:

DMRs act by attaching to the nicotinic Ach receptor and causing membrane depolarisation. As its
hydrolysing enzyme (plasma cholinesterase) is not present at the NMJ its duration of action is longer than
Ach. Persistent depolarisation produced render the voltage sensitive sodium channels inactive. This
electrical inexcitability prevents transmission of further action potentials resulting in muscle relaxation.
The Mechanism of Action of Non-depolarising Muscle Relaxants:
NDMRs inhibit the action of Ach by binding competitively to the alpha subunit of the nicotinic Ach
receptor.
The Mechanism of Action of Neuromuscular Blockade Antagonists:

Neuromuscular blockade antagonists work in different ways:
Anticholineserases antagonise Ach so more is available at the NMJ - 2 main groups used clinically:
Easily reversible inhibition e.g. edrophonium - Hydroxyl group of edrophonium forms hydrogen bond at
esteratic site of AchE that stabilises the complex so Ach cannot reach active site
Formation of a carbamylated enzyme complex e.g. neostigmine - Ach acetylates AchE while neostigmine
produces a carbamylated enzyme which has a slower rate of hydrolysis and so is unable to work for
longer hence stopping AchE hydrolyzing Ach.
Sugammadex encapsulates steroidal NMDAs effectively removing them from the plasma and allowing
further drug diffusion away from the NMJ so reversing the effect
 Residual Neuromuscular Blockade:

Residual neuromuscular blockade is a term used to describe residual paralysis after anaesthesia in which
neuromuscular blocking agents have been used. It has been defined as inadequate neuromuscular
recovery as measured by objective neuromuscular monitoring. Recent opinion suggests a definition of
inadequate train of four recovery of less than 0.9.
Adverse Effects; include increased risk of aspiration and airway obstruction, post-operative hypoxaemia,
difficulty speaking and patient distress
 The factors which contribute to Residual Neuromuscular Blockade:
Factors which lead to residual neuromuscular blockade include:
Use of NMBs - only use when indicated

Dose - high doses used for RSI will prolong blockade
Type - use of long acting NMBs e.g. pancuronium - intermediate acting NMB should be used when
possible
Depth - routine maintenance of deep intra-operative paralysis (TOF count 0)
 The Clinical Criteria for Evaluating Adequacy of Muscle Function:

Clinical criteria include assessment of patient’s ability to sustain head lift, jaw clench, grip strength and
tidal volume. These are unreliable predictors of recovery.
 The Train of Four:

Train of four ratio (TOF) is when assessment is made for fade in T4 compared to T1. Tactile evaluation is
more reliable than visual assessment but most assessors cannot detect fade when TOF >0.4. Therefore
objective measurement using techniques below are more accurate.
TOF 1 or zero - delay reversal

TOF 2 or 3 - give reversal
TOF 4 with fade - give reversal
TOF 4 with no perceived fade - give reversal - consider low dose neostigmine
TOF 4 and greater than 0.9 - withhold reversal
 Methods of Neuromuscular Monitoring exist that Do Not Require Subjective Assessment:

 Mechanomyography measures force of contraction
 Electromyography measures amplitude of muscle action potential
 Kinemyography measures movement of muscle
 Acceleromyography measures acceleration of muscle

16- Post-operative Cognitive Decline and Age
(a) List the physiological consequences of ageing by body system (25%)
(b) What intra-operative concerns are there for the elderly patient undergoing surgery?
(c) Classify the changes in cognition that may occur following anaesthesia and surgery (10%) How may cognitive
function be assessed? (10%)
(d) What are the risk factors for postoperative cognitive change? (10%)
 The Physiological Consequences of Ageing by Body System:
-CVS
CO reduces, reduction in HR and SV and contractility.
Reduced sensitivity to catecholamines, reduced adrenoreceptor density
increased SVR, fibrosis of conducting system
Increased risk of DVT/PE
Anaemia is common
- Respiratory:
Reduced FRC, increased closing capacity, reduced TLCO, increased V/Q mismatch, widened Aa gradient,
reduced sensitivity to hypoxia and hypercapnia, reduced compliance
- GIT
Increased reflux, reduced LOS tone, increased bowel transit time, reduced hepatic reserve
- Renal
Reduced renal clearance, reduced GFR, reduced concentrating function, preop dehydration more
common
- Neuro
General cognitive decline, cerebral atrophy, reduction in neurotransmitter concentration, reduced CBF
and o2 consumption, MAC reduced, BMR is reduced
- ANS
Gradual decline leading to orthostatic hypotension, less subcut fat for insulation
- Airway
Edentulous, osteoporotic, arthritic
Co morbidities affecting all systems are common
 Intra-operative Concerns are there for the Elderly Patient undergoing Surgery:
 Higher mortality
 Hypothermia more likely
 IV access may be more difficult
 Pre-oxygenation is a must due to CC encroaching on FRC
 Arm-brain circulation time is increased
 Airway maintenance may be more difficult due to loose/damaged teeth, edentulous, arthritic spine
 Increased sensitivity to some agents eg volatiles, benozs, opioids
 Reduced sensitivity to inotropes

 Fluid management may be difficult and may necessitate invasive devices
 Pressure sores more likely
 DVT/PE more likely
 Sepsis more likely
 Post-operative cognitive decline
 Cognition changes that may occur following Anaesthesia and Surgery:

1) Delirium: acute onset, reversible alteration in mental state with increased or decreaed psychomotor
function, confusion, reduced cognitive dysfunction and alteration of sleep-wake cycle
2) Dementia: series of chronic organic brain syndromes with irreversible pathology. Presents as a global
deterioration of cognitive ability in the absence of clouding of consciousness
3) Post-operative cognitive dysfunction: a deterioration in performance in a battery of
neuropsychological tests that would be expected in <3.5% of controls ie a catashrophic loss of cognitive
ability. A long term, possibly permanent, disabling deterioration in cognitive function following surgery.
Assessment of cognitive function
 MMSE is a test of global cognitive function
 Scored out of 30. A score <23 is not indicative of dementia but is supportive of a diagnosis. Scores of 26-
29 imply a degree of cognitive deficit, which may have implications for postopertive management. In the
absence of dementia scores of 28 or less are associated with >2x risk of postoperative delirium
 The Risk Factors for Postoperative Cognitive Change:

 Increasing age, General Anaesthesia rather than regional, increasing duration of anaesthesia, respiratory
complication, lower level of education, re-operation, postopertive infection
 Identify High Risk Patients Pre-operatively.

 Avoid Causative Drugs as much as possible ie Benzos, Long Acting Opioids.
 Continue drugs Perioperatively that are for cognitive function (if patient already on these).
 Minimise duration of Anaesthesia.
 Correct Electrolyes.
 Careful Fluid Balance.
 Regional over General.

17- Bone Cement Implantation Syndrome
(a) What is the composition of bone cement? (10%)
(b) What are the advantages and disadvantages of antibiotic loaded cement? (10%)
(c) What is bone cement implantation syndrome (BCIS)? (20%) How is it graded? (20%)
(d) What are the risk factors for BCIS development? (20%)
(e) What is the Pathophysiology of BCIS? (20%)
 Composition of Bone Cement:

1. Polymethyl methacrylate (PMMA) (90%)
Powder polymer: pre-polymerized PMMA
Initiator: dibenzoylperoxide
Liquid monomer (MMA)
Activator: N,N-dimethyl-p-toluidine
Powder polymer + liquid monomer = initiator/activator = Bone cement
2. Antibiotics can be incorporated within the polymerized matrix as a soluble powder that is released into
the joint cavity: gentamicin, tobramycin, clindamycin
3. Radiographic contrast material (10%) Zirconium dioxide or barium sulphate
 Advantages of Antibiotic Loaded Cement:
Treatment of infected joint arthroplasties (high dose)
Prophlyaxis of periprosthetic infection (low dose) – evidence less clear
Disadvantages:
Alteration in the mechanical and structural properties of the bone cement
Antibiotic resistance
Allergic reactions
Systemic toxicity e.g. case reports of renal failure
Cost implications
 Bone Cement Implantation Syndrome:

No agreed definition
Important cause of intraoperative mortality and morbidity
Most commonly associated with cemented hip arthroplasty
Clinical features typically occur at time of cementation, prosthesis insertion, reduction in the joint or
deflation of tourniquet
Spectrum of clinical features from transient desaturation and hypotension to cardiac arrhythmias and
cardiac arrest
Increase in PA pressure causes RV failure, dilation and shift of interventricular septum → immediate
decrease in LV compliance, reduced ventricular filling and CO
Transpulmonary passage of emboli or passage through patent foramen ovale into left heart may cause
post op delirium

Classification according to severity:
Grade 1: Moderate Hypoxia (SpO2 <94%) or decrease in systolic arterial pressure >20%.
Grade 2: Severe Hypoxia (SpO2 <88%) or hypotension (decrease in SAP >40%) or unexpected loss of
consciousness.
Grade 3: Cardiovascular Collapse requiring CPR.
 The Risk Factors for BCIS development:

Patient factors:
ASA III–IV, pre-existing pulmonary hypertension, significant cardiac disease, osteoporosis
Surgical factors:
Pathological fracture, intertrochanteric fracture, long-stem arthroplasty
 The Pathophysiology of BCIS:

Monomer mediated model – toxicity from systemic absorption of monomer. In vitro evidence but not in
vivo
Embolus mediated model (in vitro and in vivo evidence):

Mechanical – debris (marrow, fat, cement particles, air, bone, aggregates of platelets and fibrin) embolize
to the RA, RV and PA intraoperatively. High intramedullary pressure is main causative factor.
Mediator release
Cement emboli cause:

Release of vasoactive or pro-inflammatory substances, causing increased thrombin and tissue
thromboplastin which directly increase PVR
Endothelial damage and subsequent release endothelial mediators cause reflex vasoconstriction
Raised C3a, C5a and histamine
Increase in PVR causes V/Q mismatch and hypoxia.

18- Nerve Injury During Anaesthesia
(a) What are the symptoms and signs of postoperative nerve injury? (30%)
(b) How may postoperative nerve injury be classified? (30%)
(c) What risk factors exist for intraoperative nerve injury? (30%)
(d) What are the commonly injured nerves? (10%)
 Symptoms and Signs of Postoperative Nerve Injury:

Symptoms
Partial/complete sensory and/or motor loss
Onset can occur rapidly (hrs) or be delayed (weeks)
Anaesthesia, paresthesia, hypaesthesia and pain
Autonomic dysfunction
Chronic regional pain syndrome
Severe cases – muscle wasting, joint dysfunction and bone weakness
Signs
Decreased/absent power in a muscle group
Decreased sensation to light touch, pinprick, two-point discrimination, vibration or proprioception.
The presence of Tinel's sign.
Decreased sweating.
Reflex changes.
 Post-operative Nerve Injury Classification:

There are 2 methods of classifying nerve injury.
Seedon’s Classification divides nerve injury into three groups based on the nerve pathology:
Neuropraxia: damaged myelin with intact axon.
Axonotemesis: axonal disruption.
Neurotmesis: nerve is completely severed.
Sunderland’s Classification is based on which connective tissue components are disrupted.

Type 1: Local myelin injury
Type 2: Disruption of axonal continuity.
Type 3: Disruption of axonal continuity and endoneurial tubes. Perineurium and epineurium.
Type 4: Disruption of axonal continuity, endoneurial tubes and perineurium damaged. Epineurium intact
Type 5: Nerve entirely severed.
 Risk Factors exist for Intraoperative Nerve Injury:

Surgical Factors
Type of surgery (highest risk with neurosurgery, cardiac surgery, general surgery and orthopaedic surgery)
e.g. rib retraction in cardiac surgery may stretch the brachial plexus.
Position for surgery
Tourniquet
Plaster casts

Anaesthetic Factors and Positioning
Direct needle damage during regional anaesthesia
Inadequate padding
Poor positioning
 Commonly Injured Nerves Include:

Ulnar nerve (28%)
Brachial Plexus (20%)
Lumbosacral Root (16%)
Less commonly the common peroneal, sciatic, tibial, saphenous, lateral cutaneous nerve of the thigh,
supraorbital, facial, median, radial, and femoral nerves.

19- Throat Packs and Anaesthesia
a) List the indications for using a throat pack during general anaesthesia (25%)
b) What are the complications of using a throat pack (30%)
c) Describe the strategies that may be adopted to minimise the potential for postoperative complications associated
with the use of throat packs? (35%)
 The Indications for using a Throat Pack during General Anaesthesia:

As highlighted in the 2009 NPSA report
- Absorb material & prevent entry to lungs or oesophagus during oral surgery
- Seal a tracheal tube and reduce gas leak
- Stabilise the airway device and prevent displacement
 Complications of using a Throat Pack:

- May cause sore throat and result in intraoral damage (tongue, frenulum and uvula) during insertion.
- More serious complication of retention may cause air way obstruction with subsequent pulmonary
oedema, re-intubation and fatality.
- 2009 NPSA report looked at 38 incidents of throat pack retention over a 24 month period, beginning in
2006, of which 14 related to tissue damage and 24 related to retention of a throat pack.
 The strategies to minimise the potential for postoperative complications associated with the use of
throat packs:
- The NPSA advocate a dual strategy employing procedures involving least one visual check and one
documentation check to avoid retention of a throat pack.
- Visual checks include labelling the patient or airway device, attaching the throat pack to the airway
device or leaving part of the pack clearly protruding.
- Documentary checks include a formalised two person record of insertion and removal of the throat pack
or inclusion of the throat pack as part of the swab count.
- It would also be possible to include the throat pack check as part of the WHO surgical safety checklist.
- All personnel involved in the immediate perioperative care should be made aware of the insertion and
removal of a throat pack.

20- Wrong Sided Peripheral Nerve Block - 'Stop Before You Block' Campaign
a) List the implications for the patient of a inadvertent wrong-sided peripheral nerve block
b) Summarise the recommendations of the "stop before you block" campaign and list factors that have been
identified as contributing to performance of wrong sided block
c) Define the term "Never Event" as described by the NPSA and list three never events of relevance to anaesthetic or
intensive care practice (30%)
 Complications from the unnecessary block:

Local anaesthetic toxicity
Nerve damage/damage to structures/bleeding
Prolonged immobility and dexterity
Delay discharge
Surgical start delay
Patient dissatisfaction/reduced trust
 Recommendations of “stop before you block”:
WHO check list sign in as usual to confirm correct

patient, correct operation, correct site/side, against a
consent form
A stop moment immediately before the needle is
inserted for a block.
Confirm correct side/site, surgical marking by the
anaesthetist and assistant.
Particular attention when:

Time delay occurs between ‘sign in’ and nerve block being performed
The patient has been turned and the site to be blocked has moved side
Lower limb nerve block- surgical marking might be obscured
Obvious distractions in the anaesthetic room since ‘sign in’
Personnel performing the block does not routinely do it e.g trainee/locum
Factors Contributing to Wrong Sided Block

Increased activity in anaesthetic room
Teaching/demonstration new technique/equipment
Distractions in anaesthetic room/referral/discussions of other cases
Delay between doing block and WHO checklist sign in
Covering surgical mark in attempt to keep patient warm
 Never Event:
Never Events Are Serious, Largely Preventable Patient Safety Incidents That Should Not Occur If The
Available Preventative Measures Have Been Implemented.

Never Events relevant to Anaesthetic and Intensive Care:
 Retained foreign object post op e.g Throat Swabs/Instruments.
 Overdose of Midazolam in Conscious Sedation.
 IV administration of Epidural Solution.
 Opioid overdose in Opioid Naïve Patients.
 Wrong Gas Administration.
 Failure to Monitor and respond to Oxygen Saturation.
 Air Embolism.
 Maternal Death due to Post partum Haemorrhage in an Elective C-section.
 Transfusion of ABO –incompatible Blood Components.
 Wrongly Prepared High Risk Injectable Medications.
 Maladministration of Potassium Containing Solution.
 Maladministration of Insulin.
 Misplaced Naso/Orogastric Tube.

21- Death while under Anaesthesia
Death on the operating table is a thankfully rare event in anaesthesia but one which will occur to most
anaesthetists at least once over their career.
a) What immediate actions should be taken in the hours following a death under anaesthesia? (30%)
b) What later actions should be taken? (20%)
c) What is the role of the clinical director in this instance? (20%)
d) Describe the medicolegal issues faced by the anaesthetist involved in an anaesthetic-related death
 Immediate Actions should be taken in the Hours following a Death under Anaesthesia:
- Accurate and contemporaneous records should be kept
- The consultant should be informed if they are not already present
- The patients family need to be informed
The consultant anaesthetist should be present for this
The discussion should not take place by telephone
Other team members may be part of the discussion with family e.g. surgeons or nursing staff
Give an open and honest explanation of what happened- do not use medical jargon
If the cause of death is unclear do not speculate
Apologise
Give the family an opportunity to ask questions
- It should be decided if it is appropriate for the anaesthetist involved to continue the list or on-call
- Do not remove any lines or tubes from the patients body
- If there is any doubt about ETT position this should be checked by an independent anaesthetist
- Telephone the coronor’s office
- Telephone the patient’s GP
- The consultant or clinical director should initiate moving the equipment and drugs to a secure
storeroom as they may need to be investigated later
 Later Actions should be Taken:

Inform the patient’s GP
Inform the clinical director
Complete an incident report form
Team debriefing- with trained facilitators and further psychological support if necessary
Once the cause of death has been investigated the case can be discussed at a departmental morbidity
and mortality meeting
 The Role of the Clinical Director (CD) in this Instance:

The CD should ensure that departmental procedures are in place for dealing with these incidents
The CD should review the clinical commitments of the anaesthetist involved
The CD has a responsibility to secure the equipment and drugs used
The CD should ensure that the coroner has been identified
The CD should identify staff involved and collect statements from them and ensure they have received

psychological support
The CD should ascertain if there is any evidence of poor staff performance or systems failure
The CD should liaise with the medical director
The CD should appoint a mentor for the anaesthetist involved
The CD should keep a record of all the actions taken
 The Medicolegal Issues faced by the Anaesthetist involved in an Anaesthetic-related Death:

The anaesthetist involved should keep accurate and contemporaneous records of the incident
The anaesthetist will be required to prepare a statement for the coroner and may have to give evidence
at the inquest
There may be civil legal proceedings
There may be criminal charges against the anaesthetist or the trust
The police may investigate the case
A complaint about the anaesthetist may be made to the GMC
The anaesthetist will be very stressed during the investigation and will require support from their
colleagues and psychological support
Medical defense organizations (e.g. MPS, MDU) can provide useful advice

22- Needlestick Injury
While suturing a chest drain in a conscious adult patient in the Emergency Department you sustain a
needlestick injury to your hand.
a) What immediate actions should be undertaken? (15%)
b) After the immediate management, what further steps should be undertaken? (20%)
c) What steps may be necessary if exposure to one of the blood borne viruses is suspected or confirmed?
d) What standard precautions exist to avoid needlestick injury? (20%)
e) What are the arguments for and against nonconsensual testing of patients in the event of a needlestick injury to a
health care professional? (20%)
 Immediate Action:
- Call for help so some one can take over the case and
relieve you
- Encourage bleeding from the wound; wash the wound
with soap and water
- Follow local policy: Inform occupational health, Critical
Incident form; seek further advice (A&E if out of hours)
 Immediate Management:
- Establish if patient is high risk, and whether you need to
take Post Exposure Prophylaxis
- Risk assessment by
A) History
1- HBV, HIV, HCV status
2- Tattoos, Use of IV drugs, sharing needles
3-Sexuality
4-Hx of blood transfusion abroad, Hx of jaundice and
vaccination history
B) Examination
C) Pt’s consent to take blood from patient - for HIV,
HCV, HBV testing following appropriate counselling
D) Establish your Hep B status, last booster.
 Necessary Steps if Exposure to Blood Borne Viruses is

Suspected or Confirmed:

A) Blood test shortly after exposure to confirm your
current status.
B) Commence post exposure Prophylaxis, ideally should be
started within an hour of exposure, triple therapy regime
(Zidovudine, Lamivudine, Indinavir), side effects are
profound fatigue, Diabetes, nausea and vomiting and
jaundice.
C) Establish your Hep B status, all HCW sould be vaccinated
against HBV.
D) Inform your clinical lead, Airway manipulation using
glove is not exposure prone procedure but as a suspected
exposure to BBV there will be restriction for exposure
prone procedures.
E) Counselling and Critical incident form.
 The Standard Precautions exist to avoid Needlestick Injury:

1- Universal precautions when performing exposure prone procedures; mask glove and goggles
2-Avoid re sheathing needled and use sharps bin to dispose equipment promptly.
3- Wash your hand between patients or after contact with blood or body fluids
4-Do not over fill sharp bins
5-cover abrasions and cuts with water proof
plasters
 Non-consensual testing of patients in the

event of a Needlestick injury to a HCP:
Non consensual testing in against the law in
England and Wales if it’s not in patient’s best
interest.
Arguments in Favour of Testing
Social, clinical and psychological effect on
health care worker
This option emphasises on the HCW welfare
May boost the recruitment to high risk specialities, boosts stuff morale and
reduce the burn out
In case of unconscious patient, they might have no objections against blood
testing if they were awake.
Reciprocity: one may argue that patients have duty towards HCW that put
them selves at risk to look after them.
The colleagues of the injured worker who are working in a team may be
reassured by: a)knowing the status of their colleague, b)the lawful testing is
reassuring for them if the sustain a needle stick injury,

Against:
1- Non consensual testing may violate patients autonomy if patient is explicitly refusing the test or in
unconscious patient.
2- practicallity of testing when patient is refusing.
3- If testing is compulsory; patient may be reluctant to seek treatment for fear of being tested against
their will. This could have adverse effect on patient’s health and negative cost implications on NHS.

23- Dental Trauma and the Anaesthetist
A 22 y/o man anaesthetised by a colleague awakens following tonsillectomy and complains that an upper
incisor tooth has broken off during the operation.
a) List the anaesthetic/surgical factors that predispose to perioperative dental damage
b) List the patient related factors that predispose to perioperative dental damage (25%)
c) How might you minimise the risk of dental trauma? (25%)
d) What is your management of the described situation? (25%)
The Anaesthetic/Surgical factors that predispose to Peri-operative Dental Damage:
Dental trauma occurs in 1:4500 operations. Most occur at intubation in patients over 50 with limited
mouth opening. Two main reasons:
Direct trauma
Damage due to biting
20 times more common to cause direct trauma in a ‘difficult airway’
a high Mallampati score (3 or 4)
poor mandibular subluxation
limited head and neck movement
limited inter-incisor gap (<5 cm)
 The Patient Related Factors that Predispose to Peri-operative Dental damage:
Dental factors that render teeth more susceptible to injury

Children in the mixed dentition phase
Carious teeth
Periodontal or gum disease
Large anterior restorations
Veneers, crowns, bridgework and implants
Protruding upper incisors
Extensive tooth surface loss
Endodontically or root-treated teeth
Isolated teeth
Structural abnormalities (such as enamel (amelogenesis imperfecta) or dentine (dentinogenesis
imperfecta) abnormalities)
Previously traumatized teeth
 The Risk of Dental Trauma can be Minimized by:
Pre-operative assessment:
Ask patients about loose teeth/dental fixtures
Feel teeth for looseness

Warn patients of the risks
Record dialogue in patient notes
Refer high risk patients to a dentist pre-procedure
Use a bite block on solid back teeth or for patients with poor mouth access
 Management of the Described Situation:

Anaesthetic departments should have a protocol for this, which should include the following points:
All dental fragments need to be accounted for (may require CXR)
Although most dental fragments will pass though the gastrointestinal tract without causing harm but
surgical or endoscopic removal may be required in some cases.
In children, the loss of a primary tooth does not require treatment. If a permanent tooth is displaced from
its socket, push into socket and hold for several minutes or if you are not happy with this procedure, it
should be stored in cool, fresh milk or normal saline until it can be splinted or fixed back in place.
When the patient is sufficiently awake, a full explanation must be given. This should include a clear
apology and a description of the events that led up to the damage and the efforts made to minimize
complications.
All actions and discussions should be clearly documented in the patient’s records.
It is the responsibility of the anaesthetist to organize an urgent dental assessment and arrange
subsequent treatment.

24- Inadvertent Perioperative Hypothermia
a) Define the term "inadvertent perioperative hypothermia". (10%)
b) What are the physical mechanisms by which heat is lost from a patient in an operating theatre? (20%)
c) Why does anaesthesia produce hypothermia? (10%)
d) List clinical complications of hypothermia in perioperative period (20%)
e) Outline the current recommendations in UK for prevention of perioperative hypothermia. (40%)
 Inadvertent Perioperative Hypothermia:

Unintentional fall in core body temperature to under 36oC, in and around the operative period (defined as
1hour pre induction to 24 hours after entry into recovery (including time on ward)).
 Mechanisms of Heat Loss:

- Radiation 40%
- Convection 30%
- Evaporation 15%
- Respiration 10%
- Conduction 5%
 Mechanisms by which Anaesthesia Produce Hypothermia:

Loss of normal behavioural response to low temperature
Loss of ability to shiver
Resetting of thermoregulatory range
Reduction of BMR so less heat production
Vasodilatation
Cold fluids/gases
Environmental exposure
 Complications of Hypothermia in Perioperative Period:

Coagulopathy and increased blood loss
Arrhthymias
Post operative shivering and increased oxygen consumption
Increased infection
Reduced wound healing
Increased mortality
Thermal discomfort for patient
Prolonged hospital stay
Altered drug metabolism
 NICE Recommendations for Prevention of Perioperative Hypothermia:
Pre-operative:

information for patients and carers on appropriate clothing for hospital and importance of keeping warm.
Training of staff on use of thermometers. Pre-op identification of high risk patients (ASA2-5, kids, elderly,
those at risk of cardiovascular complications, long surgery, intermediate/major surgery)
Patients’ temp should be >36oC prior to induction and if not then active warming should follow (unless
surgery must be expediated)
Intra-operative
If surgery >30mins then actively warm patient with forced air warmer
If surgery <30mins but patient has 2 or more of above risk factors then actively warm patient with forced
air warmer
Monitor temp pre induction and then half hourly
Induction should not begin unless temp >36oC (unless surgery must be expediated)
IV fluids (>500ml) should be warmed to 37oC
Post- operative:
Cannot leave recovery until core temp >30oC
If temp <30oC then actively warm with forced air warmer

25- Prions and Creutzfeldt-Jakob Disease
(a) What are prions? How are anaesthetic devices cleaned after possible contamination with prions?
(b) What patients are identified as being at high risk of CJD?
(c) What are the implications for patients with CJD and anaesthesia.
(d) Describe the practical steps and measures for patient with CJD undergoing surgery
(e) What factors should be taken into account in deciding whether instruments should be disposable?
 The Prions:
Prions are small particles of infectious proteins that cause Transmissible Spongiform Encephalopathies
(TSEs)
TSEs are a group of progressive, neurodegenerative conditions that are ultimately fatal
Characteristic pathological changes
Only definitive method for diagnosis is biopsy and examination of affected tissue
Human prion disease can be either sporadic (commonest), inherited or acquired (variant)
Creutzfeldt-Jakob Disease (CJD) vCJD is a TSE caused by the same prion protein that causes Bovine
Spongiform Encephalopathy (BSE) in cattle
De-contamination and Sterilization:

Prions are resistant to all methods of sterilization including subclaving, ionizing radiation and ultraviolet
radiation
However standard washing and decontamination techniques reduce the concentration of prions
exponentially so after 10-20 cycles infectivity is negligible
The only safe method of preventing transmission is to use disposable items
 What patients are identified as being at high risk of CJD preoperatively?

Related to previous blood transfusion- patients who received blood products from a donor who later
developed CJD, anyone who received blood components from UK donors between 1980-2001
Related to previous surgery- those who have undergone surgery where surgical instruments have
previously been used on a patient who later developed CJD; those who had a dural graft inserted during
intracranial or intradural spinal surgery before August 1992; patients who have received an organ or
tissue from a donor who later developed CJD
Related to medical issues- patients treated with growth hormone sourced from humans before 1985,
gonadotrophin sourced from humans before 1973
Take an accurate history pre-operatively
At the end of the procedure WHO checklist asks if patient at high risk of CJD transmission
 The implications for patients with CJD and Anaesthesia:

Potential for CJD to be transmitted to other patients
Sporadic CJD prion protein found in brain, spinal cord and posterior eye; Variant CJD can also be found in
lymph nodes, tonsils and appendix
Implications for anaesthesia in these patients include cost, resources sourcing equipment and it poses a

risk to the public
In a patient with CJD, even if tonsils have previously been removed, laryngoscope blades have become
contaminated with lymphoid tissue- therefore should be disposed off, including bougies, Magill’s forceps
and LMAs
Endoscopes and fibreoptic equipment must be recorded at each use and permit contact tracing
Guidelines have been published for safe use and decontamination of endoscopic equipment; Fibreoptic
equipment for tracheal intubation and GI endoscopy in patients with confirmed variant or sporadic CJD is
available from the National Creutzfeldt-Jakob Surveillance Unit in Edinburgh
Individuals who have received a blood transfusion after 1980 are no longer accepted as donors; since
1998 all blood donated has been leukodepleted
 Steps and Measures for a patient with CJD undergoing Surgery:

Anaesthetizing these patients is essentially the similar to routine practice; routine contact does not pose a
risk/isolation is not needed
Comply with local theatre infection control policies
Preoperative assessment should include neurological impairment, swallowing abnormalities and
aspiration risk
As for any surgical case all instruments should be traceable
Blood and other samples/specimens should be labelled ‘biohazard’
Invasive procedures, e/g CVL insertion, spinal anaesthetic mandate full asepsis including mask and eye
protection
Safe disposal of sharps
Inhalational and IV techniques both acceptable
Anaesthetic machine does not need quarantined
High infectivity tissue (brain, spinal cord, posterior eye); medium (anterior eye, olfactory epithelium); low
(CSF, urine, blood and bone marrow, peripheral nerves); any needles used by anaesthetists near these
tissues are disposable
Any instrument that contacts the brain or spinal cord must be destroyed after use
Laryngoscopes for tonsillectomies or bronchoscopes should be considered potentially contaminated-
should either be destroyed or quarantined
Routine management post-operatively
 Factors should be taken into account in deciding whether instruments should be disposable or
reusable if used in a high risk patient:
Depends on infectivity risk
Lymphoid tissue, e.g. adenoids, tonsils are ‘high infectivity’ for vCJD so surgeons use reusable instruments
(single use associated with excessive bleeding); RCOA and AAGBI advise against reusable devices,
however guidance is confusing as an exception is use of a reusable LMA if it has been sterilized many
times (>35)
Any instrument that contacts the brain or spinal cord must be destroyed after use
Any instruments used on patients who may have vCJD or be at risk must be destroyed or quarantined

26- Ionising Radiation and the Anaesthetist
(a) Describe the action of ionising radiation on tissues. Which tissues are most affected?
(b) What are the physical sequelae of acute and chronic high dose radiation exposure?
(c) What types of procedures expose the anaesthetist to ionising radiation?
(d) What types of procedures expose the anaesthetist to non-ionising radiation?
(e) How does current legislation seek to reduce the exposure to radiation by healthcare workers?
(f) What are the responsibilities of the (i) employer (ii) individual worker?
 Action of Ionising Radiation on Tissues:
Direct - transfer of linear energy causing excitation of atoms and a chemicophysical cascade resulting in
damage to exposed tissues
Indirect - energy causes production of free radicals dirupting DNA causing cell; apoptosis, mutation,
delayed division
Rapidly dividing cells e.g. haemopoetic, reproductive, gastrointestinal
 The physical sequelae of acute and chronic high dose radiation exposure:
acute - nausea, vomiting, fatigue, loss of appetite, cataracts, hair loss, burns, change in blood count,
immunosupression, haemorraghe, marrow failure, GI failure, CNS failure
chronic - inflammation, fibrosis, ulceration, atrophy, stenosis. Cancer; blood cancer, solid tumour
 Procedures expose the Anaesthetist To Ionising Radiation:

X-ray exposure; image intensifier in theatre, portable x-ray ICU, image guided pain procedures (plain and
fluroscopic), anaesthesia in radiology suite e.g. neuroradiology, EVAR. Transferring unwell patient to CT
scanner.
 What types of procedures expose the anaesthetist to non-ionising radiation?

Laser - urology, ent, colorectal, hpb, neurosurgical, opthamology, gynaecology, plastic surgery.
 How does current legislation seek to reduce the exposure to radiation by healthcare workers?
As low as reasonably practicable (ALARP), health and safety act, IRR99, IRMER;
referrer - provides information about request
practioner - authorises request
operator - performs procedure
Risk vs benefit assessed
responsibilities of employer and individual to limit exposure outlined
 The Responsibilities of the Employer:

- Restrict exposure to employees, provide appropriate personal protective equipment and ensure it's
appropriate use, maintenance and storage. Ensure exposure of pregnant and breast feeding mothers is
limited

The Responsibilities of the Individual Worker:
- Employee not knowlingly expose oneself or others unnnecessarily, use and store ppe appropriately,
inform employer if pregnant immediately, be aware and use techniques to limit dose when performing
fluroscopic techniques.

27- Major Hemorhage
A 35-year-old woman has a Major Haemorrhage following significant Trauma and is admitted to your
Emergency Department. She does Not have a head injury.
a) Give one definition of major haemorrhage. [1 mark]
b) What are the principles of management of major haemorrhage in this patient? [12 marks]
c) What complications might follow a massive blood transfusion? [8 marks]
d) List the transfusion targets that you would aim for in major haemorrhage [4 mark]
 Major Hemorrhage :
• Loss of > one blood volume within 24 hours (approx 70ml/kg, >5L in 70 kg adult)
• 50% of total blood volume lost in less than 3 hours.
• Bleeding in excess of 150 ml/minute.
• Bleeding leading to a systolic blood pressure of <90mmHg and pulse of >110 bpm.
 Management of Major Haemorrhage:

• Ensure appropriate team members are contacted (not just “call for help”).
• Activation of Major Haemorrhage Protocol.
• Identification of Source of Bleeding.
• Control/Prevention of further Blood Loss.
• High flow Oxygen/Airway Control.
• Establish IV or IO access.
• Baseline Bloods.
• Frequent measurement of Hb & coagulation using point-of-care tests – TEG / ROTEM / Haemocue / ABG
to direct transfusion (must mention POC tests).
• Frequent measurement and correction of Electrolytes Abnormalities.
• Transfusion of Blood and Coagulation products to restore organ perfusion.
• Strict compliance with patient identification procedures, product handling & traceability.
• Measures to maintain/achieve Normothermia.
• Consider imaging and/or damage control surgery.
• Consider the use of Anti-fibrinolytics eg: Tranexamic Acid.
 Complications of a Massive Blood Transfusion:

• Coagulopathy.
• Acid base abnormalities.
• Hypothermia.
• Circulatory overload.
• Electrolyte abnormalities: Hypocalcaemia, Hyperkalaemia/Hypokalaemia Hypomagnesaemia, Citrate
Toxicity (give 3 to get the mark)
• Transfusion Related Lung Injury (TRALI).
• Immediate haemolytic transfusion reactions and non-haemolytic febrile reactions.
• Allergic reactions.
• Transfusion related infections.
• Transfusion related graft-vs-host disease.
• Immuno*modulation.

 Transfusion Targets:
• Hb 70-90 g/L.
• Platelets > 75 x 109/L.
• PT/PTT < 1.5 x normal.
• Fibrinogen > 1.5-2.0 g/L..

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Anaesthesia & Intensive Care

Part 11: Critical Incidents for FCAI, FRCA and EDAIC

For Original Materials and Editors, Please refer to:

North Ireland School of Anaesthesia Website

‫عيداروس‬ CRITICAL INCIDENTS 3

‫عيداروس‬ CRITICAL INCIDENTS 4

 Explicit Awareness – spontaneously recalled intraoperative events with or without pain

 Gold standard is the isolated forearm technique

‫عيداروس‬ CRITICAL INCIDENTS 5

 Severe, life-threatening generalised or systemic hypersensitivity reaction.

‫عيداروس‬ CRITICAL INCIDENTS 6

‫عيداروس‬ CRITICAL INCIDENTS 7

 List the possible causes of sudden collapse in this patient. (4 marks)

 Symptoms and Signs suggest local anaesthetic toxicity:

‫عيداروس‬ CRITICAL INCIDENTS 11

 What is the immediate treatment of local anaesthetic toxicity? (6 marks)

e) What follow up is required for this lady? (2 marks)

‫عيداروس‬ CRITICAL INCIDENTS 12

‫عيداروس‬ CRITICAL INCIDENTS 15

 Factors predispose to inadvertent intra-arterial (IA) drug injection:

Medications Injected (most likely to cause severe injury)

 The Intravascular Mechanisms of Injury:

 The acute clinical features of inadvertent IA injection:

‫عيداروس‬ CRITICAL INCIDENTS 17

‫عيداروس‬ CRITICAL INCIDENTS 18

 Anatomy of the Pericardium:

‫عيداروس‬ CRITICAL INCIDENTS 19

 The Pathophysiology in Early and Late stages of Tamponade:

‫عيداروس‬ CRITICAL INCIDENTS 21

 The Causes of Cardiac Tamponade:

 Non-surgical Management of life-threatening Tamponade:

‫عيداروس‬ CRITICAL INCIDENTS 22

Surgical Management of life-threatening Tamponade:

‫عيداروس‬ CRITICAL INCIDENTS 23

 Causes of Iatrogenic Pneumothorax:

 The ventilatory parameters which minimise the risk of pneumothorax on MV:

 Signs or Symptoms may Indicate the development of a Pneumothorax in an Intubated

 Management of Recurrent Pneumothoraces:

Methods of preventing recurrence include:

- Thoracotomy – largely superseded by VATS procedure.

Re-expansion pulmonary oedema can be minimised by:

‫عيداروس‬ CRITICAL INCIDENTS 26

 Human Factors contribute to IV drug Administration Errors in Theatre-based Anaesthetic Practice:

 System for Reporting Medication Errors:

‫عيداروس‬ CRITICAL INCIDENTS 28

 The RCOA recommendation:

 Critical Incidents Reported:

National reporting systems ie; NPSA

‫عيداروس‬ CRITICAL INCIDENTS 29

‫عيداروس‬ CRITICAL INCIDENTS 30

 The Risk factors for Aspiration while undergoing Anaesthesia:

 The Physiological Sequelae of Aspiration:

‫عيداروس‬ CRITICAL INCIDENTS 31

A number of strategies to prevent aspiration:

- Increase Gastric Emptying

‫عيداروس‬ CRITICAL INCIDENTS 32

 Management of Pulmonary Aspiration (Peri- and Post-aspiration):

‫عيداروس‬ CRITICAL INCIDENTS 33

 The Risk Factors for PRIS:

 Laboratory findings might be expected in a case of PRIS:

How may PRIS be prevented (3 marks) and managed (2 marks)?

‫عيداروس‬ CRITICAL INCIDENTS 34

PRIS is managed by supportive measures: