Volume 1 Corrected

HUNDRED QUESTIONS & HUNDRED ANSWERS
Question No. 1
You are asked to anaesthetize a 70 years old man with bronchiectasis for a
trabeculectomy. The patient is concerned about the risk of general
anaesthesia & wants local anaesthesia
1. Define bronchiectasis?
2. How would you optimize the patient’s medical condition
preoperatively?
3. What factors would you consider when assessing this patient’s
suitability for local anaesthesia?
4. Outline the role of anaesthetist during operation?
5. List the advantages of local anaesthesia for trabeculectomy.
Answer: -
1. Bronchiectasis is an abnormal and irreversible dilatation of the bronchi, which may
be localized or widespread, and is caused by destruction of the elastic and muscular
layers of the bronchial walls.
2. Treatment is symptomatic as specific therapy directed at the underlying
pathophysiologic mechanisms is not available.
Regular chest physiotherapy with percussion and postural drainage of excessive
bronchial secretions is of value in reducing cough and sputum and in preventing
recurrent infection.
Antibiotics to control infection: Haemophilus influenza and Pseudomonas aeruginosa
are common infections. Continuous antibiotic therapy may be necessary if recurrences
are frequent.
Bronchodilator drugs (methylxanthines, β2 agonists and anticholinergics) to reduce
airway tone. In this context, anti-inflammatory drugs may also prove to be beneficial.
Controlled oxygen therapy may be required to treat hypoxemia.
General measures should include cessation of smoking and adequate hydration to
mobilize secretions. There is no evidence for the efficacy of nebulized saline, mucolytic
or enzymes.
3. The treatment of the bronchiectasis must be optimized and any acute exacerbations
dealt with effectively prior to surgery. For trabeculectomy to be performed under
local anaesthesia the patient should be able to lie flat with 1-2 pillows and remain
still for 20-30 minutes. Dyspnoea at rest or uncontrolled coughing would preclude
local anaesthesia. The ability to lie flat comfortably for period up to 30 min must be
assessed pre-operatively, in the ward. Other contraindications to local anaesthesia
include lack of comprehension or co-operation, severe anxiety or claustrophobia and
involuntary movements.
4. A full clinical pre-operative evaluation must be carried out and special investigations
(e.g. ECG, chest X-ray) requested when indicated, irrespective of whether local or
general anaesthesia is to be used. Patients presenting for eye surgery are often
elderly and treatment of co-existing medical conditions must be optimized.
Following full explanation and informed consent, either the surgeon or the
anaesthetist may institute LA of eye. Intravenous access must be established (for
Vol. I 1
resuscitation/sedation/rapid lowering of IOP) and supplementary oxygen is

provided underneath the drapes. Verbal contact should be maintained throughout
and monitoring should include blood pressure measurement, ECG and pulse
oximetry.
Sedation with its potential for respiratory depression is best avoided in this patient.
It also decreases patient co-operation during surgery and is unnecessary when
painless local anaesthetic techniques are used. It is useful to hold the patient’s hand
during the procedure so that the patient can indicate the need to speak or cough by
squeezing the anesthetist’s/nurse’s hand. The surgeon can then be forewarned of
imminent movement. The anaesthetist should also be responsible for supervision of
post-operative recovery.
Safety and simplicity of providing anaesthesia, akinesia and low IOP necessary for the
procedure. LA avoids interference with the respiratory system and possible exacerbation
of symptoms. Endocrine and metabolic responses are attenuated and elderly patients
tolerate surgery under LA very well. The shortening of hospital stay is economically
advantageous.
Vol. I 2
Question No. 2
A 59 years old man with long standing chest disease is scheduled for an
elective inguinal hernia repair.
Vol/L 2
0 1 2 3 4
Time (sec)
1. What is this graph? What pattern does it shows & why?

2. List for types of drugs that might help optimize this patient’s
respiratory condition?
3. List three non-pharmacological methods that may optimize his
respiratory condition?
4. Which of the following is appropriate for this patient’s intra-
operative management: -
a. Low inspiratory oxygen concentration.
b. Short inspiratory phase
c. Ventilation to normocapnia i.e. PaCO2 of 40mmHg (5.3 Kpa)
Answer: -
1. Spirogram. An obstructive pattern of lung disease as FEV 1/FVC is less than 70 %.
This patient’s FEV1, the forced expiratory volume in the first second of expiration, is
1 L and the FVC, the forced vital capacity is 2 L. a restrictive pattern has an FVC
lower than predicted and a ratio of FEV 1 to FVC > 70 %. The FVC in a normal pattern
is within normal predicted limits for that population’s age, sex and size and the ratio
FEV1/FVC is greater than 75 %.
2. Patients with Chronic Obstructive Airways Disease (COAD) are twice as likely to
suffer post-operative respiratory problems as a normal patient. The key to pre-
operative management is accurate assessment allowing appropriate optimization of
the patient’s condition. The effect of drugs should be monitored, as it is difficult to
predict how much benefit each will have. The following may be used: -
 Β2 –agonists (e.g. salbutamol) should be given even if initial spirometry does not
show benefit, as this can occur later.
 Anticholinergic drugs, e.g. ipratropium bromide, have a more prolonged duration
of action than the Β2 –agonists.
 Aminophylline has a narrow therapeutic window. Blood levels are affected by
many drugs and diseases and so must be monitored. It may also improve
pulmonary function by inotropy of the diaphragm.
Vol. I 3
 Inhaled corticosteroids (e.g. beclomethasone dipropionate) work by decreasing

bronchial mucosal inflammation, so reducing bronchial oedema and secretions.
 Disodium cromoglycate is a mast cell stabilizer and is used for asthma
prophylaxis.
 Diuretics may improve right ventricular failure but thicker secretions may impair
expectoration.
 Antibiotics are only indicated when an acute respiratory infection is diagnosed.
Specific therapy is guided by sputum cultures.
3. Physiotherapy, including deep breathing exercises to prevent basal atelectasis and
postural drainage and percussion to facilitate coughing of trapped secretions.
Nutrition is important if a patient is debilitated. Delaying a case from winter to
summer may be appropriate for a patient with chronic bronchitis. If obese, reducing
weight will: -
 Increase FRC so reducing basal atelectasis;
 Reduce the work of breathing
 Reduce the risk of upper airway obstruction.
Stopping smoking will decrease carboxy-haemoglobin levels within 24 hours.
Improvement in ciliary function excessive mucus production takes six weeks. Raised
pulmonary and systemic vascular resistance due to nicotine may improve on
withdrawal.
4. Intra-operative management of ventilation includes: -

 A high inspired oxygen concentration to maintain a PaO2 of >75 mmHg (10 kPa);
 A long inspiratory time allowing adequate ventilation of underventilated alveoli;
 A long expiratory phase to prevent gas trapping by the obstructed airways;
 A minute volume that maintains the pre-operative PaCO 2 level without
barotraumas;
 Aspiration of sputum.
Inevitably, one must use a low respiratory rate and a tidal volume, which produces peak
airway pressures unlikely to cause a pneumothorax.
Vol. I 4
Question No.3
You are called to a casualty to see a cyanosed, Apnoeic patient with known
history of asthma. You immediately intubate the patient but are unable to
produce chest movement despite applying high pressure to the breathing
center: -
1. Give three possible causes of this inability to ventilate.
2. List three things you could do to help differentiate these causes?
3. Why may aminophylline be dangerous drug to use in this patient?
4. On ventilation, the abdomen moves but the chest is motionless.
Does this guarantee that the trachea tube is misplaced?
Answer: -
1. Causes of difficult ventilation include: -
 Blocked tracheal tube lumen by blood, tissue, tumor, secretions or foreign
body;
 Kinking or external pressure on the tracheal tube, e.g. teeth biting;
 Cuff herniation;
 Blocked breathing circuit;
 Pneumothorax;
 Bronchospasm;
 Pulmonary oedema.
2. The golden rule when ventilation is difficult following intubation is ‘if in doubt, take
it out’, i.e. remove the tracheal tube.
Methods for the differentiation of causes of difficult ventilation include:
 Disconnect the taper mount from the breathing circuit and check the
pressure of gas at the patient end of the breathing circuit. If there is no gas
pressure at the circuit end, change the circuit. Remove the tracheal tube
and ventilate by mask. If ventilation using a mask is easy the tracheal tube
is at fault.
 Auscultate the lungs. Breath sounds may be absent in severe
bronchospasm. Unilateral breath sounds suggest endobronchial
intubation or pneumothorax. Spontaneous pneumothorax is more
common in asthmatic patients. If there is a release of air under pressure
your diagnosis is confirmed and ventilation should improve. Leave the
cannula in place and site a chest drain.
 Pass in endobronchial sucker down the tracheal tube. If it does not pass
easily suspect kinking, external compression or blockage of the lumen.
Deflate the cuff and if the sucker suddenly passes through, the diagnosis is
herniation of the cuff. Examine the tracheal tube in the oropharynx to
exclude kinking. The commonest misdiagnosis of an obstructed tracheal
tube is bronchospasm.
 Aspirate the endobronchial sucker. Frothy pink secretions suggest
pulmonary oedema, purulent secretions suggest a chest infection and a dry
aspirate suggests bronchospasm. In practice, the diagnosis by tracheal
aspiration may not be clear-cut.
Vol. I 5
 Fibreoptic examination through the tracheal tube may show malposition,

deformation due to external pressure, cuff herniation, intraluminal
obstructions and the presence of secretions.
3. The difference between therapeutic and toxic levels of aminophylline is small. If the
patient has taken aminophylline recently any further administration may lead to
toxic levels. This may manifest as vomiting, haematemesis, sinus tachycardia,
ventricular or supraventricular arrhythmias, profound hypokalaemia, or
convulsions. The usual treatment for aminophylline toxicity is a β-blocker but this is
contraindicated in asthmatic patients.
No. Abdominal movement without chest movement can occur when the tracheal tube is
correctly placed and the lungs are being ventilated normally. This happens if the chest
wall is fixed because expansion of the lungs is then solely dependent on diaphragmatic
movement, e.g. in ankylosing spondylitis. It is therefore mandatory in such
circumstances to be absolutely certain of the tracheal tube position.
Vol. I 6
Question No. 4
You are asked to see a 60-year-old male in the pre-operative assessment
clinic. He smokes 40 cigarettes a day and is awaiting elective
cholecystectomy.
1. List the health risks of tobacco smoking.
2. Outline the effects of smoking on the cardiovascular system.
3. Outline the effects of smoking on the respiratory system.
4. What are the peri-operative benefits of abstinence from smoking
prior to surgery?
5. List your considerations when selection a technique of general
anaesthesia for this patient.
Answer: -
1. Cancer: lip, mouth, pharynx, oesophagus, larynx, lung, bladder. There is a clear dose
response relationship between the number of cigarettes smoked and lung cancer
mortality.
CVS: ischemic heart disease and peripheral vascular disease.
Other risks: gastric and duodenal ulcers, induction of hepatic microsomal enzymes,
polycythemia and hyperviscosity, alterations in macrophage and T-lymphocyte
function, abnormalities of spermatozoa, psychological effects.
2. Decreased myocardial oxygen supply: Carbon monoxide decreases O2 bound to

haemoglobin, causes a left shift of the O 2 dissociation curve and inactivates
cytochrome oxidase in myocardium with a consequent decrease in intracellular O 2
transport. Polycythemia, increased platelet count and aggregation, and
hyperfibrinogenaemia increase blood viscosity and risk of thrombosis.
Increased Myocardial O2 demand: Nicotine increases heart rate, systolic and
diastolic pressure and peripheral and coronary vascular resistance. Atherosclerosis
and the reduction in the oxygen supply/demand ratio increase the risk of ischemic
heart disease.
3. Cigarette smoke is irritant to the respiratory tract, induces epithelial change and
increases production of hyperviscous mucus. This, coupled with inactivation of cilia,
reduces clearance of particulate matter by the mucociliary escalator. There is an
increase in laryngeal and tracheobronchial reactivity. Alveolar macrophages lose
their immunoregulatory function, and release reactive metabolites (e.g. superoxide),
elastase loss of elastic recoil together with increased small airway narrowing are
reflected in an increased closing capacity which, coupled with a reduced FRC,
increases P(A-a)O2. Epithelial permeability is increased.
4. Cessation of smoking for even 1 week will reverse the effects of nicotine and carbon
monoxide, improve ciliary function, reduce laryngeal reactivity and restore platelet
function. With abstinence up to 8 weeks there is continued improvement in ciliary
function with reduction in sputum production. Small airway function improves and
there is a reduction in post-operative pulmonary morbidity (bronchospasm, purulent
sputum and pyrexia, segmental pulmonary collapse, pneumonia necessitating
antibiotic therapy). Normal immune function is restored.
Vol. I 7
Emphasize the benefits of abstinence from smoking for several weeks pre-operatively.
Treat respiratory tract infections, and consider chest physiotherapy and bronchodilators
to correct reversible airway narrowing. Anticholinergic drugs (glycopyrolate,
pirenzepine, ipratropium) are useful in premedication, as they will influence both
airway tone and secretions. Benzodiazepines may be used to produce sedation with
minimal cardiovascular and respiratory depression. A smooth induction technique is
more important than choice of induction agent. Airway manipulation at light planes of
anaesthesia may cause coughing, breath holding, laryngospasm and desaturation.
Opioids and neuromuscular blockers that cause minimal histamine release may be
advantageous. The commonly used inhalational agents have bronchodilator properties
and may be used safely for maintenance of anaesthesia. Total intravenous anaesthesia
and central neural blockade may be useful alternatives.
Vol. I 8
Question No. 5
A 59-year-old man with long-standing chest disease is scheduled for an
elective inguinal hernia repair. These are the blood results on air: -
Hb 18 g/100 ml
WCC 15 000/mm3
pH 7.28
PaCO2 12.2 kPa
PaO2 5.0 kPa
Standard bicarbonate 42.0 mmol/l
Base excess 15.2 mmol/L
1. Comment on the haemoglobin and white cell count.

2. Comment on the arterial blood gases.
3. What will happen if he is given a high-inspired oxygen
concentration?
4. What other tests would you require when assessing this man?
Answer: -
1. He is polycythemia, probably secondary to long-standing hypoxemia. His white cell
count is raised so it is important to exclude or treat any chest infection.
2. He has a type B pattern of chronic respiratory failure. He is acidaemic. There is a
primary respiratory acidosis that is partially compensated by a metabolic alkalosis.
He is hypoxemic with a PaO2 of less than 8 kPa.
3. He may stop breathing as he has a hypoxemic respiratory drive. Normally, central
chemoreceptors respond to PaCO2 stimulating the respiratory center in order to
control body pH within narrow limits. This ensures enzymes (which are proteins)
work in optimal conditions. If central chemoreceptors become insensitive to
increases in PaCO2 then the primary drive to ventilation becomes hypoxemia. A PaO 2
below 8 kPa stimulates mainly the carotid body but also the aortic chemoreceptors,
causing hyperventilation via the respiratory center. This raises the PaO 2 as per the
Ideal Alveolar Gas Equation: -
PaO2 = PiO2 – PaCO2 + F
R
PaO2 = partial pressure of oxygen in an ideal alveolus
PiO2 = partial inspired pressure of oxygen
PaCO2 = partial pressure of carbon dioxide in an ideal alveolus
R = Respiratory quotient
F = Small correction factor
This patient is retaining carbon dioxide. This is long-standing as there is a

compensatory metabolic alkalosis shown by a raised standard bicarbonate and base
excess. Renal compensation occurs slowly over days and respiratory compensation
over minutes. The CSF will have normalized and the central chemoreceptors will
have reset to a high PaCO 2. Increasing this patient’s inspired O 2 concentration will
reduce his hypoxemic drive and the hypoventilation will cause further hypercapnia
and acidosis and may result in cardiac arrest. Volatile agents cause a dose dependent
Vol. I 9
decrease in the ventilatory response to carbon dioxide but as little as 0.1 MAC will
ablate the hypoxemic ventilatory response. It is important to ensure adequate post-
operative washout of volatiles. The administration of oxygen post-operatively should
be by a fixed performance device such as a Venturi type mask.
4. Blood urea, glucose and electrolytes, ECG and chest X-ray would be appropriate.
Chronic obstructive airways disease usually co-exists with ischemic heart disease as
smoking is the primary etiology in both. Right ventricular failure may occur as
chronic hypoxemia leads to pulmonary hypertension.
Notes on chronic obstructive airways disease

COAD describes a group of lung diseases that often co-exist:
Chronic bronchitis is defined symptomatically by a productive cough on most days for
three months of the year for two consecutive years. Classically this is the blue bloater
who is obese, hypercapnia and hypoxic with compensatory bicarbonate retention and
polycythemia (type B respiratory failure). They are prone to RVF, have a decreased
ventilatory sensitivity to carbon dioxide and may have a hypoxic respiratory drive.
Emphysema is defined histopathologically as dilatation of those parts of the lung distal
to the terminal bronchioles. Classically this is the pink puffer who is thin and may have
normal arterial gases of a low PaCO 2 (type A respiratory failure). They have a normal
ventilatory response to carbon dioxide but a low transfer factor.
Asthma is defined functionally by reversible episodic airway obstruction.
Vol. I 10
Question No. 6
The medical houseman asks you to ventilate a 40 year old man who has
suspected pneumonia and the following arterial blood gas values: -
pH 7.54
PaCO2 28 mmHg (3.7 kPa)
PaO2 60 mmHg (8.0 kPa)
Standard bicarbonate 26 mmol/L
Base excess 3 mmol/L
1. What other information would you like to have before you

comment on the result?
2. Briefly comment on the blood gases despite this lack of
information and give two possible causes other than pneumonia.
3. The houseman has arranged for the nurse to monitor the oxygen
saturation overnight and increase the concentration of inspired
oxygen to keep saturation levels ≥ 94 %. Why is this management
dangerous? When you go to assess him the nurses say he is
sleeping and his respiratory rate is down to 10/min. Is this a good
sign?
4. What graph helps you predict the inspired oxygen concentration
required to maintain a normal arterial oxygenation? Give one
other use for this graph.
Answer: -
1. Arterial blood gases can only be fully assessed with the clinical condition of the
patient. Specific treatment depends on the reversibility and nature of the disease and
whether it is improving or deteriorating. Specific information required in this patient
would be his age, clinical condition and his inspired oxygen concentration (FIO 2).
2. This patient is alkalaemic with a primary respiratory alkalosis. At a PaO 2 of 60
mmHg (8 kPa) the chemoreceptors are stimulated and hyperventilation occurs
which reduces the PaCO2. This offsets the hypoxia as described by the alveolar gas
equation. The hypoxia will also directly depress the respiratory center. There is no
renal compensation so the diagnosis is acute respiratory failure. Causes of
hypoxemia with Hypocapnia include chest infection, pulmonary oedema and
pulmonary embolus, pneumothorax and venous admixture (shunt).
3. The low PaCO2 implies hyperventilation and an increased work of breathing.
Normally, the work of breathing is only 2 % of the energy consumption of the body.
If lung compliance decreases, as in pneumonia, this proportion may increase to 20
%. Also, infection increases the CO2 production (increasing the respiratory workload)
and O2 consumption (which reduces respiratory muscle oxygenation). When the
respiratory workload exceeds his capacity for respiratory work the PaCO 2 will rise.
The pulse oximeter gives the arterial oxygen saturation, which depends on the PaO 2
and the position of the oxyhaemoglobin dissociation curve. It does not reflect PaCO 2
levels. A relatively small increase in FIO2 can compensate for the hypoxia caused by
hypoventilation so this management may allow the patient to become grossly
hypercapnia and acidaemic. He may then become more settled but this is CO 2
Vol. I 11
narcosis and he is about to become apnoeic, hypoxic and arrest. He should be

monitored clinically for his ability to perform the work of breathing as reflected by
his respiratory rate, use of accessory muscles of respiration and general condition. If
an FIO2 > 60 % is required to maintain oxygenation (equivalent to a 20 % shunt on
the iso-shunt diagram given below) there should be a low threshold for intubation
and IPPV.
MmHg
Assumptions:
A –v O2 content diff. 5 ml/dl
400 - PaCO2 25 – 40 mmHg
Hb 10 – 14 g/dl
Arterial PO2
15%
300 - 20%
25%
30%
200 -
50%
100 - 20 30 40 50 60 70 80
90 100
The iso-shunt diagram. Redrawn from benatar SR, Hewlett AM and Nunn JF. The use of
iso-shunt lines for control of oxygen therapy. BJA 19973; 45:711
0-
4. The shunt can be conveniently calculated by plotting the initial FIO 2 and PaO2
values. Assuming the shunt remains constant; the FIO 2 that will give a normal PaO2
can be predicted. This graph explains why an FIO2 of 30 % is used.
During general anaesthesia: following induction, shunt increases from the
physiological (< 5 %) up 15 or 20 % and it requires an FIO 2 of 30 % to counteract
this. Changes in respiratory function can be monitored. This helps predict successful
weaning from mechanical ventilation (which is unlikely if shunt > 20 %).
Vol. I 12
Question No. 7
Write short notes on the causes, diagnosis, and treatment of a
pneumothorax occurring during anaesthesia.
Answer: -
Causes
 Injury by needle: injuries to pleura and lungs with needles such as during insertion
of a central venous cannula, supraclavicular brachial plexus block, intercostals nerve
block or intrapleural block and rarely thoracic epidural block.
 Anaesthetic machine: barotraumas, as a result of pressure transmitted from the gas
supply, cylinders or oxygen flush system; also high inflation pressure during IPPV, or
accidental occlusion of expiratory limb or a pressure relief valve in the patient’s
circuit.
 Trauma to the airway: injuries to the larynx, trachea, and carina during
instrumentation of the airway, for example during induction of anaesthesia and
especially in a difficult intubation situation.
 Patient factors: some patients are more prone to developing a pneumothorax.
Asthmatic patients and patients with chronic obstructive airway disease requires
high inflation pressure during IPPV and have high alveolar trapping volumes;
patients with congenital lung bullae and patients with previous trauma to the chest
may develop pneumothorax after IPPV.
 Surgical factors: some surgical procedures such as nephrectomy, operations on the
thoracic spine, operations on the larynx, and obviously cardiac and thoracic
operations, are associated with high risk of pneumothorax.
Diagnosis
 Diminished air entry on the affected side.
 Resonance to percussion on the affected side.
 Diminished expansion of the affected side.
 Diminished auscultation sounds on the affected side.
 Shift of trachea, only if tension pneumothorax, to the opposite side.
 Surgical emphysema, felt, as crepitus under the skin and soft tissues when palpated
against bone such as a clavicle, is characteristic of trauma-related pneumothorax
with injuries to the chest wall. It may also occur with tension pneumothorax.
 High airway ventilatory pressures.
 Drop in SpO2 is a late sign especially during anaesthesia with FiO2 of ≥ 0.3.
 Hypotension, especially in tension pneumothorax, from increased intrathoracic
pressure and reduced venous return.
 Chest X-ray will confirm the diagnosis but this should not delay treatment if tension
pneumothorax is suspected.
Treatment
 Insertion of a chest drain in the 4 th – 5th Intercostal space in the mid-axillary line,
with connection to underwater seal drainage.
Vol. I 13
 In the case of tension pneumothorax, immediate action is necessary. Drainage of the

air may be achieved quickly by inserting a wide bore needle in the 2 nd Intercostal
space in the mid-clavicular line.
Vol. I 14
Question No. 8
Describe how would you diagnose and manage a patient with massive
pulmonary embolism.
Answer: -
Massive pulmonary embolism when 50 % or more of the pulmonary circulation is
obstructed.
Diagnosis
Relevant history, examination, and investigations should be made with special attention
to the points below: -
 Risk factors include heart failure, cancer, hip fracture, prolonged bed rest, obesity,
estrogen therapy, and age over 65 years, antithrombin III deficiency.
 Symptoms include sudden onset of dyspnoea, chest pain (sunbsternal or pleuritic),
and possibly haemoptysis if pulmonary infarction ensues.
 Physical signs include tachypnea, cyanosis, tachycardia, and systemic hypotension,
raised CVP. The rise in pulmonary artery pressure may be associated with splitting of
the second heart sound and a loud pulmonary component, right ventricular heave
and a gallop rhythm. There may be clinical evidence of deep vein thrombosis and a
slight fever.
 ECG: sinus tachycardia and signs of right ventricular strain are common findings. P
pulmonale, right bundle branch block and atrial arrhythmias may also be seen. The
classic pattern of S1, Q3, and T3 is unusual.
 CXR: may show large pulmonary arteries, pulmonary oligaemia, pleural effusion,
and raised hemidiaphragm.
 Arterial blood gases show hypoxemia, metabolic and respiratory acidosis.
Ventilation/perfusion isotope scanning and pulmonary angiography confirm the
diagnosis but often-clinical judgment must be relied upon in patients with massive
pulmonary embolism.
Management
 Resuscitation: includes oxygenation and maintenance of the airway, mechanical
ventilation, expansion of circulating volume, and inotropic support to maintain right
ventricular perfusion.
 Definitive treatment: direct towards preventing further thrombus formation and
proximal embolism: -
o Thrombolytic therapy such as streptokinase 250,000 unit’s i.v. Over 30 minutes,
followed by infusion of 100,000 units/h for 24 h; streptokinase is pyrogenic,
antigenic, and poses a significant hemorrhagic risk;
o Pulmonary embolectomy may be indicated in a profoundly shocked patient when
streptokinase is contraindicated or fails.
o Role of heparin.
Vol. I 15
Question No. 9
Define the acute respiratory distress syndrome, and describe what methods
can be used to improve oxygenation in this condition.
Answer: -
The acute respiratory distress syndrome (ARDS) is defined as a clinical condition in
which the patient has hypoxia, poorly compliant lungs, and high airway pressure. This is
ascertained with characteristic chest X-ray findings of diffuse pulmonary infiltrates
combined with a normal or low pulmonary artery wedge pressure. There is an
underlying pathology from a recognized list that leads to ARDS. The most common
causes are trauma and sepsis.
The following methods have been used to improve oxygenation: -
 Raising inspired oxygen concentration (Fi O2). It is desired to keep the Fi O2 below 60
%. This is often not possible and the patient may require 100 % Fi O2
 Ventilation with PEEP. The patient is ventilated often with up to 15cm H 2O of PEEP.
High airway pressures are often encountered and the patient is at risk of
barotrauma.
 Reverse I:E ratio. Allowing a longer time in the inspiratory phase of the respiratory
cycle often provides enough time for more efficient ventilation of the relatively stiff
lung.
 Pressure controlled ventilation. With this technique the lungs are inflated to a pre-
set pressure. The tidal volume is therefore determined by the compliance of the lung.
The upper pressure limit can be increased to recruit previously collapsed sections of
lungs and maximize the amount of lung available for ventilation. It is often necessary
to paralyze patients in addition to their sedation to perform adequate pressure-
controlled ventilation.
 Prone position. Postural change has often been observed to temporarily improve
oxygenation in ARDS. This is probably due to a favorable V/Q mismatch. Prone
ventilation is, however, not without risk, and meticulous attention to airway
management must be observed.
 Extracorporeal membrane oxygenation (ECMO). Although ECMO has always
seemed to be a good idea in ARDS, it has not been found to be of value in improving
outcome in adults.
 Nitric oxide (nebulised prostacycline)
 Permissive hypercapnia
 Liquid ventilation
 IVOX
Vol. I 16
Question No. 10
What are the causes of stridor in a child? List the symptoms and signs of
upper airway obstruction.
Answer: -
Causes
The common causes of upper airway obstruction are:
I. Congenital
II. Acquired
 Infective
Epiglottitis
Laryngotracheobronchitis (croup)
 Traumatic
Laryngospasm
Post-intubation oedema
Foreign body inhalation
Smoke inhalation
 Neoplasm
The most common cause seen by anaesthetist is laryngospasm, but upper airway
obstruction from infection is perhaps the most demanding in the emergency situation.
The incidence of infective causes has decreased recently because of the introduction of
Haemophilus vaccination and there has subsequently been a drop in cases of epiglottitis.
Symptoms and signs

The symptoms and signs of upper airway obstruction include:
 Barking cough
 Nature of stridor-inspiratory/expiratory
 Chest recession
 Accessory muscle usage
 Hoarseness
 Nasal flaring
 Drooling
 Sitting upright
 Tachycardia
 Tachypnea
 Cyanosis
 Drowsiness
In the most acute situation these symptoms can lead to complete upper airway
obstruction. Anaesthesia is directed towards treating the cause and bypassing any upper
airway obstruction.
Vol. I 17
Question No. 11
Describe your management of a 38-year old HIV-positive male suffering
from atypical pneumonia and respiratory failure.
Answer: -
 Does the patient require ventilation?
 Does the patient fulfill local criteria for intensive care admission?
 What is the causative agent?
The first two questions need to be dealt with rapidly and are usually easy to answer. If
the patient is looking exhausted or has worsening blood gases, and other forms of
respiratory support, including pharmacotherapy, have failed, then he will require
ventilation. As the patient is defined as being HIV-positive and not as having AIDS, this
is the first AIDS-defining illness. Under these circumstances, he would generally fulfill
the local criteria for admission to most units. Once an AIDS patient presents with a
further atypical pneumonia, having already been fully treated for a previous pneumonia,
admission criteria become more complicated.
Contact with the patient should be performed observing “universal precautions”.
This involves the wearing of gloves for all contact with body fluids, goggles and masks if
fluids may become airborne, and gowns if there is a risk of being splashed.
If ventilation is indicated, the patient is induced in a standard way, for example
pre-oxygenation, propofol and suxamethonium and the airway secured. Initially, simple
ventilator settings such as SIMV may be adequate. This may have to be adjusted, for
example using high Fio2 levels, PEEP, inverse I:E ratio, or more sophisticated ventilator
modes, in order to ventilate the patient satisfactorily. The aim is to support the patient
through the acute phase of the illness, while the antimicrobial agents start to work.
There are usually special protocols for management of blood samples, including blood
gases. These are usually kept to the minimum and sent to the laboratory, rather than
analyzed on bench top equipment in the intensive care unit. Continual oximetry is very
useful in these circumstances.
A wide range of pathogens cause atypical pneumonia in patients infected with the
HIV virus: 50 % are caused by Pneumocystis carinii, and 50 % are caused by fungi,
viruses (such as cytomegalovirus), mycobacterium, and pyrogenic bacteria such as
streptococci and staphylococci. Making the correct diagnosis can have in important
bearing on the success of treatment. Pneumocystis is characterized by dyspnoea, little in
the way of clinical signs and a chest X-ray that may be anything from normal to showing
diffuse alveolar infiltrates. The patient’s general condition may look much worse than
the chest X-ray. This diagnosis is confirmed by positive identification in sputum, or
bronchoalveolar lavage, or brushings. It is preferable to take brushings or samples for
culture for culture before starting empirical, antimicrobial therapy. If the patient’s
condition allows, it is also better to wait for results and treat specific, identified
pathogens. Often this is not possible and an empirical approach to treatment is
required. It is typically treated with high doses of methylprednisolone and high doses of
co-trimoxazole.
Vol. I 18
Question No. 12
A 50 years old man had a resection of abdominal aortic aneurysm as an
emergency. Following this the wound edges oozed & the abdominal drain
showed a continuing bleeding. A coagulation screen showed: -
APTT. 100 sec (control 40 sec)
Prothrombin Time 25 sec (control 15 sec)
Thrombin Time 50 sec (control 15 sec)
Reptilase Time Normal
1. Comment briefly on these results. Why might this result not reflect
the coagulation of the patient’s blood? What advantages does the
activated clotting time have over the standard coagulation time?
2. State what drug would you give to correct this coagulopathy, give
two side effects it may produces?
3. What conditions would you suspect if the reptilase test was
prolonged & the thrombin time was greater than twice normal?
How could you confirm this.
Answer: -
1. This shows a heparin effect. Table 1 summarizes the basic coagulation tests and
Table 2 the results in some coagulopathies. Heparin potentiates (X 2000)
antithrombin III, which neutralizes the activated factors XIIa, XIa, IXa, Xa, IIa and
XIIIa. It causes an increase in the prothrombin time (PT) and larger increases in the
activated partial thromboplastin time (APTT) and the thrombin time (TT). The
reptilase test is similar to the TT but is not affected by heparin and this supports a
diagnosis of heparin coagulopathy. The blood sample may have been contaminated
by the coagulant effect of heparin is dose dependent but 100 mg/kg has a half-life of
1 h. if the dose and timing of heparin given intra-operatively correlate with the
coagulation result, it should be treated but if not, suspect contamination and send
another sample. The activated clotting time can be performed in theatre or at the
bedside: 3 ml of blood is agitated with 12 mg of diatomaceous earth in a tube which
is rotated at 370 C. A metal bar in the tube rotates with the tube and a magnetic
sensor stops the timer. It reflects the intrinsic system and is normally <135 s.
2. Protamine is a basic protein, which reacts with heparin to form a stable compound
with no anticoagulant effect. It is produced from salmon and may cause systemic
hypotension, pulmonary hypertension, bronchospasm, bradycardia and anaphylaxis,
especially in patients who are allergic to fish. It should be given slowly. By itself it
can cause bleeding by an effect on platelets and fibrinogen.
3. Disseminated intravascular coagulopathy (DIC): a pathological condition involving
increased coagulation causing microvascular ischemia and consumption of
coagulation factors and platelets leading to increased bleeding.
Vol. I 19
Table 1: Coagulation tests
Name Pathways tested Factors tested

PT Extrinsic and common VII, X, V, II and I
APPT Intrinsic and common VIII, IX, XI, XII, X, V, II and I
TT Common X, V, II and I
Table 2: Some examples of coagulopathy
PT APTT TT
Normal (s) 10-14 30-40 10-12
Warfarin +++ + Normal
Heparin + +++ ++
Dilution + + Normal
Acute DIC + + > 2 x Normal
+ = Prolonged
DIC = Disseminated intravascular coagulopathy
The diagnosis would be supported by platelet count of < 150 000/µL with a prolonged
APTT and PT and fibrinogen levels <1.6 g/L (normal 2-4 g/L). DIC would be confirmed
by fibrinolysis tests, e.g.
 Increased fibrinogen (and fibrin) degradation products (FDPs), which reflect
plasmin activity. Dilutions of serum are added to a combination of fibrinogen-coated
latex particles and antifibrinogen antibodies. FDPs inhibit the agglutination. The
highest dilution at which agglutination occurs is reported: more dilute than 1 in 16
suggests DIC.
 Euglobulin lysis time <120 minutes.
The FDP titre and the TT are both affected by heparin but the reptilase test is then
normal. The treatment of DIC is that of the underlying cause and replacement of
coagulation factors and platelets. Cryoprecipitate is given to replace factors VIII and I.
The use of heparin is controversial and a hematologist should be consulted.
Vol. I 20
Question No. 13
Briefly outline your plan of management for anaesthetizing a patient with a
permanent pacemaker.
Answer: -
Pre-operative assessment: This includes identification of the primary pathology, the
indication for the pacemaker and the pacemaker and the pacemaker type and generic
code, as shown below (these details may be found in the patient’s pacemaker card).
Pacing Sensing Response

O O O
A A I
V V T
D D D
NB: O = none; A = atrium; V = ventricle; D = dual; T = trigger and I = inhibit.
VVI is the commonest mode. It represents ventricular pacing, ventricular sensing, with
inhibition of pacing when a ventricular beat is sensed.
Preoperative assessment also includes a chest X-ray to identify the site of the pacemaker
unit and its leads, and an ECG to check the pacing spikes and the intrinsic cardiac
rhythm. The heart rate is pacemaker dependent if spikes present before most of the
beats.
Intra-operative Management: Preparation in theatre should include ensuring a magnet

is available in case a change to VOO pacing is required. This change renders the pacing
less susceptible to interference but makes some pacemaker more vulnerable to
reprogramming by external stimuli. Resuscitation drugs such as atropine and
isoprenaline should be prepared and the defibrillator checked. ECG monitoring is
essential peri-operatively.
During the operation the risk of microshock/burn must be minimized. It should be
remembered that pacemaker leads provide direct access to the electrical current.
Arrhythmias may be induced, the pacemaker may be damaged, pacemaker sensing may
be triggered with resultant inappropriate inhibition, or the pacemaker may be
reprogrammed to a different mode. Diathermy should ideally be avoided, or if necessary
bipolar diathermy used. If unipolar diathermy is deemed necessary a minimum duration
and intensity may be allowed. The diathermy lead and plate should be positioned away
from the chest to ensure the current between the two does not traverse the chest.
Post-operative: the function of the pacemaker should be checked. This should include a
12-lead ECG and if necessary a check at the pacemaker clinic. This is especially
important if the anaesthetist suspects that the pacemaker was reprogrammed or showed
any significant change in function from its pre-operative status. Ideally, the patient’s
regular pacemaker clinic should be informed of any procedure the patient undergoes
involving diathermy.
Vol. I 21
Question No. 14
List the causes of abnormal cardiac rhythms arising during anaesthesia.
Answer: -
Patient factors
 Pre-existing cardiac disease – ischemia, re-entrant circuits
 Undiagnosed disease – phaeochromocytoma, carcinoid
 Electrolyte imbalance – potassium, magnesium
 Acid-base imbalance.
Anaesthetic factors
 Hypoxia
 Hypercapnia
 Response to laryngoscopy and intubation
 Pain
 Awareness
 Drugs – wrong dose, interactions
 Hypothermia
 Malignant hyperthermia
 Central line irritation.
Surgical factors
 Reflex responses – eye and dental surgery, visceral manipulation
 Retractors incorrectly sited
 Exogenous adrenaline.
Arrhythmias during surgery are not uncommon and are usually benign. The most
common arrhythmias arising during surgery are nodal rhythm and sinus bradycardia.
Vol. I 22
Question No. 15
Describe the techniques that are available for acute pacing of a patient in
complete heart block immediately post-cardiac arrest.
Answer: -
Repeated Precordial Thump
This is the least satisfactory option. If other equipment is not immediately to hand,
repeated rhythmic striking of the precordium with the fist may produce enough
electrical activity in the myocardium to produce depolarization and contraction. This
technique is traumatic and may be ineffective.
External pacemaker
This is available in some hospitals and has the advantage that it can be rapidly applied
to the patient and does not require central venous access or radiographic imaging. It
involves two pads coated with adhesive electrically conductive gel, connected to a special
unit that allows for adjustment of the energy delivered to the pads. In this way, the
energy is increased until capture occurs and the patient is successfully paced. Energy is
then turned down to threshold as in temporary pacing.
Disadvantages of this technique include: -
 Discomfort if the patient is conscious
 Skin burns from the pads
 Usefulness for a short period of time only
 Not always effective
Temporary transvenous pacing wire

In this technique a thin, bipolar pacing wire is connected to the myocardium. The wire is
initially passed through the subclavian or internal jugular vein and then manipulated
into the right ventricular apex with cardiac fluoroscopy. The energy required for pacing
is then established by turning the energy down initially until the unit is no longer pacing
(the pacing threshold). The unit is usually then set to three times the threshold and put
on a demand mode of 60-80 beats per minute.
The disadvantages of this technique are that: -
 It requires skill and significant technical support
 It carries all the risks of central venous cannulation such as pneumothorax or
inadvertent arterial puncture
 The pacing wire may become detached from the myocardium and fail to capture
 Risk of microshock
 The patient has to be as stable as possible before being taken to the pacing room,
which may be an isolated site
The advantages of this technique are that: -

 It is generally the most reliable of the acute pacing techniques
 It can be left in situ for a long period of time (days) until the patient recovers or a
permanent pacemaker can be fitted.
Vol. I 23
Question No. 16
Outline the special anaesthetic problems encountered in a patient with a
prosthetic heart valve.
Answer: -
There are two fundamental questions with respect to artificial heart valves: -
 Is the valve functioning well?
 What is the nature of the valve-mechanical or tissue?
Mechanical valves
 Valve failure is rare; if failure occurs, it is generally sudden and frequently results in
the death of the patient.
 Incidence of thromboembolism is high and patients require long-term
anticoagulation with the INR maintained between 3-4.5. The risk is greatest with
mitral valve.
Tissue valve
 Failure is common, but gradual in onset. A recurrence of cardiac symptoms and
signs would suggest that the valve is not functioning adequately, and
echocardiography is indicated prior to anaesthesia.
 Thromboembolic complication rate is low and there is no requirement for long-term
anticoagulation.
Anticoagulation
The management of anticoagulation prior to surgery demands careful consideration of
the clinical risk of bleeding versus the risk of thrombosis. For elective surgery: -
 Stop warfarin 3 days preoperatively and start heparin infusion 24 hours later
(approx 15,000 units/12 hours), maintaining APTT at 2-3 times normal.
 Stop heparin 6 hours preoperatively and check INR and APTT 1 hour preoperatively.
 Restart heparin infusion 6-12 hours postoperatively and continue until the patient is
able to take warfarin.
In the emergency situation fresh frozen plasma may be necessary. For optimal
management of such patients advice from hematologists is often required.
Antibiotic prophylaxis
This is essential because prosthetic valves are very prone to endocarditis, which
frequently results in the development of a paraprosthetic leak, with consequent
haemodynamic deterioration. Intravenous amoxycillin 1 g must be given at induction
and continued postoperatively; if the patient is penicillin-allergic, then intravenous
vancomycin 1 g or teicoplanin 400 mg should be substituted for amoxycillin.
Intravenous gentamicin 120 mg must be added when sepsis and contamination are
likely complications of surgery (dental, genitourinary, obstetric, gynecological, and
gastrointestinal surgery).
Vol. I 24
Question No. 17
Outline the management of ventricular tachycardia arising during
induction of anaesthesia.
Answer: -
Is there cardiac output?
Check the central pulses. If absent treat as cardiac arrest with cardiopulmonary
resuscitation, cycles of DC defibrillation, and administration of adrenaline. If central
pulses are present, assess circulation and cardiac output by checking colour, capillary
filling, peripheral pulses, and measurement of arterial pressure.
What is the cause?

Check and reverse any secondary causes for ventricular tachycardia (VT). Check the
patency of airway, position of tracheal tube, and the adequacy of oxygenation and
ventilation. Observe the color of the skin, the Sao 2 reading (if there is adequate pulse
signal!) and the Etco2 if a capnogram is connected. Aim for maintaining a patent airway,
adequate ventilation, oxygenation with Sao2 > 94 %, and normocapnia.
Treat the VT
In unstable VT (low cardiac output judged by hypotension, weak pulses, and poor color
and capillary filling), urgent treatment should be considered with synchronized DC
shock. A low voltage synchronized DC cardioversion should be used and repeated with
stepped increase in energy starting with 25 J, and gradually increasing to 50,100,150
and 200 J until the cardioversion is achieved. In severe resistant cases consider
overdrive cardiac pacing.
In stable VT, one or more of the following medical regimes may be considered;
lignocaine 100 mg (or 1 mg/kg) intravenously, repeated in 10 – 15 minutes and followed
by intravenous fusion 1 –2 mg/kg/h; procainamide 100 mg (or 1 mg/kg) intravenously,
repeated every minute to a maximum of five doses; or amiodarone 500 mg (or 2 mg/kg
in children) intravenously given over 30 minutes through a central venous line.
Vol. I 25
Question No. 18
An eight-year-old black Nigerian boy is admitted following a car crash. He
has an Hb of 7g/dl & requires debridement of an ankle wound.
1. What blood test would you do to exclude which condition? What
definitive blood test may confirm this?
2. If the patient has this disease, list the principles of anaesthetic
management to prevent exacerbation of this disease.
3. List one complication of this disease for each of the following organs:
Lungs, Kidney & Spleen.
Answer: -
1. Sickle cell disease should be excluded. This includes the homozygous (HbSS) sickle
cell anaemia (SCA) and the heterozygous (HbAS) sickle cell trait (SCT). Although
commonest in black Africans this genetically determined haemoglobinopathy can
occur in other ethnic groups and Caucasians. When sickle cell haemoglobin (HbS) is
deoxygenated it starts to polymerize and after a delay forms a gel that is insoluble.
This process is enhanced by acidity, hypothermia, infection, low 2,3-DPG levels, high
% HbS and a high mean corpuscular haemoglobin concentration (MCHC). It is
inhibited by the presence of other haemoglobin e.g. foetal HbF, which is present up
to six months of age. Polymerization occurs at different levels of hypoxia that are
dependent on these factors and causes the red blood cells to become sickle shaped.
The homozygous state, SCA, is symptomatic as sickling starts at a PaO 2 of 40 mmHg,
which occurs, in normal venous blood. The severity of SCA varies from mild rare
crises to those needing 40 admissions a year or childhood death. In the heterozygous
state, SCT, sickling only occurs below a Pao2 of 30 mmHg so symptoms only occur
under severe physiological stress. Sickling causes an increase in blood viscosity
resulting in vessel occlusion and infarction of potentially all tissues. The severe
ischemic pain produced by these vasocclusive crises contrasts with the minimal
clinical findings. HbS releases oxygen to the tissues more easily so between crises
these patients feel well. The life span of sickle cell may be reduced by 85 % (normal is
120 days) due to increased fragility. The haemolytic anaemia that results may cause
hepatomegaly, jaundice or frontal bossing. Outside daytime hours a sickle solubility
test will show the presence of HbS in patients over 2 year of age: a reluctant, e.g.
sodium metabisulphite causes blood with HbS to become turbid or show sickling
under microscopy. This does not distinguish SCA from SCT. In SCA the Hb
concentration is usually 6 – 8 g/dl and the reticulocyte count is 10-20 %. In SCT the
Hb concentration and the film are normal. During daytime hours the definitive
diagnosis can be made by Hb electrophoresis.
2. The aims of anaesthesia in SCA are to prevent sickling and to monitor and treat
complications over the whole peri-operative period. Patients with SCT are less
susceptible to sickling but should be treated similarly:
 Avoid hypoxia, acidosis and hypothermia;
 Ensure hydration as this decreases MCHC; hyponatraemia may reduce sickling;
 Maintain cardiac output and avoid stasis, e.g. due to aortocaval compression or
positioning of the patient; if a tourniquet is absolutely necessary then
exsanguinate the limb fully and minimize the duration;
Vol. I 26
 Peri-operative analgesia and oxygen;

 Consider antibiotic cover and transfusion.
3. Complications of SCA include: -

 Lungs: pulmonary infarcts can result in ARDS or pulmonary hypertension and
cor pulmonale.
 Kidneys: papillary necrosis and tubular acidosis can cause hyposthenuria
(inability to concentrate urine) ; this predisposes to dehydration and impaired
excretion of alkaline compounds, e.g. norpethidine.
Spleen: multiple infarcts cause regression (auto-splenectomy), making these patients

susceptible to streptococcal and Haemophilus influenza infections, so prophylactic
penicillin and vaccines are given. Sequestration of blood in both the spleen and liver can
cause sudden hypovolaemic shock, severe anaemia and possible death.
Vol. I 27
Question No. 19
A 70 kg woman is given 14 units of mainly red cell concentrate during an
emergency laparotomy for a reputed ectopic pregnancy. Post-operatively
she continues to ooze from the wound and venepuncture sites.
1. What blood tests would you do to assess her coagulation? What is
the likeliest cause of her bleeding?
2. Give two advantages of using whole blood rather than red cell
concentrate in this situation.
3. What do the letters SAG-M stand for? Give two advantages and two
disadvantages of SAG-M blood over whole blood.
4. By what amount would you except the platelet count to rise in this
patient if given 1 unit of platelets? What else does a unit of platelets
contain?
Answer: -
1. Platelet count, prothrombin time (PT), activated partial thromboplastin time (APPT)
and thrombin time (TT). If the PT, APTT or TT are abnormal, further tests should be
done. A reptilase test will identify heparin coagulation. Massive blood transfusion is
defined as transfusion of the patient’s total blood volume (70mL/kg in an adult)
within 24 hours. The commonest cause of bleeding following a massive blood
transfusion is dilutional thrombocytopenia. There is a poor correlation between the
degree of bleeding and the platelet count. Spontaneous bleeding is rare if the platelet
count is above 20,000/μL, platelets may still be indicated if there is clinical bleeding
and evidence that the quality of the platelets is poor, e.g. if the patient has been on
aspirin therapy in the last two weeks.
2. Red cell concentrate (RCC) has a haematocrit (packed cell volume, PCV) of0.65 and
is produced by removing plasma from whole blood (PCV 0.4). Therefore it does not
contain as much plasma protein, which are necessary to maintain colloid osmotic
pressure, and dilution of coagulation factors, leading to more haemorrhage.
3. Blood that has been collected normally in standard anticoagulant has plasma
removed to give a PCV of 0.9 and SAG-M is then added until the PCV is 0.6. SAG-M
(optimal additive solution) is an acronym for sodium chloride (140 mmol/L),
adenine (1.5 mmol/L), and glucose (50 mmol/L). M stands for added mannitol.
Standard blood degenerates and the minimum standard for viable blood is a red cell
survival of 70 % at 24 h post-transfusion. The adenine and glucose help maintain the
level of ATP, which is necessary for the sodium/potassium pump, and the
phosphorylation of spectrin protein that maintains the integrity of the cell wall. The
sodium/potassium pump is important, as a rise in intracellular sodium is followed
by water, which causes swelling, and fragility of the cell Mannitol offsets this.
Compared to whole blood SAG-M has: -
 Decrease viscosity due to the absence of plasma proteins so transfusion is quicker
but it does not maintain colloid osmotic pressure and intravascular volume so
well;
 An increase in shelf life from 28 to 35 days;
 No coagulation factors; so dilutional coagulopathy is more common.
Vol. I 28
Whole blood maintains most factors for 21 days but factors V and VIII decrease to 50 %
by day 1 and day 14 respectively. Its platelets do not function after 48 h. Fresh frozen
plasma (FFP) contains all the coagulation factors. Cryo precipitate is prepared from FFP
and has higher concentrations of factors VIII, XIII von Willebrand, fibronectin and I.
7-10,000/μL. Each unit contains 50 ml of plasma including some clotting factors and
this should be taken into account when treating coagulopathy. It will also contain some
red blood cells and these can cause Rhesus sensitization.
Vol. I 29
Question No. 20
What are the additives used in red cell storage? What are the complications
of blood transfusion?
Answer: -
Additives
The additives used to promote red cell storage include: -
 Citrate – chelates calcium
 Phosphate – maintains ATP, decreases hemolysis
 Adenine – maintains ATP, improves cell mobility
 Saline – decreases viscosity
 Glucose – energy
 Mannitol – decreases hemolysis
Complications
The complications of transfusion are listed below: -
 Physical
o Overload
o Hypothermia
o Embolism
 Immunological
o Pyrogenic
o Type I hypersensitivity
o Graft versus host disease
 Infective
o Hepatitis B and C
o Syphilis
o HIV
o Cytomegalovirus
o Malaria
o Epstein – Barr virus
 Haemolytic transfusion reactions
o Human errors
 Biochemical
o Acid/base
o Hyperkalaemia
o Citrate toxicity
 Disseminated intravascular coagulation
The complications of blood transfusion, especially massive transfusion can be serious.

The most important factor in the transfusion of blood is to avoid human errors,
especially giving wrong blood to the wrong patient.
Vol. I 30
Question No. 21
Concerning Brachial plexus Block
1. What two muscles enclose the root & how can these muscles be
demonstrated clinically? If the plexus is blocked at this point is
pneumothorax a common complication & what complication is more
likely if the needle is used in a cephalic direction?
2. What is anatomical marking of a subclavian pulse? If you accidentally
puncture the subclavian artery in which direction will you redirect
the needle in order to approach the plexus?
3. List three end-points that may be used to confirm correct placing of a
needle for Brachial plexus block?
4. What cutaneous nerve is often missed by an axillary approach
resulting in a inadequate block for a Colle’s fracture? What nerve is
this branch of & why may the axillary approach miss it?
Answer: -
Several techniques of brachial plexus block have been described. The choice of which to
use depends on the particular advantages and risks of each block. The key to these, their
performance and their management if not successful is the anatomy. The brachial
plexus consists of roots, trunks, divisions and cords. The five roots are formed by the
anterior primary rami of the C5-8 and T1 nerves. These pass between scalenus anterior
(SA) and scalenus medius and combine to form the trunks as they emerge from behind
SA. The upper (C5,6), middle (C7) and lower (C8 and T1) trunks cross the posterior
triangle of the neck. At the lateral edge of the first rib and just behind the clavicle, each
divides into a posterior and an anterior division. On emerging from behind the clavicle
into the axilla, the three anterior divisions form the medial and lateral cords and the
three posterior divisions form the posterior cord. The subclavian a. is anterior and below
the trunk on the first rib. It becomes the axillary a. at the lateral edge of the first rib. The
axillary a. is divided into three parts by pectoralis minor that crosses its second part. The
cords approach the first part of the axillary a. and are closely applied to its second part,
gaining their titles (lateral, posterior and medial) from this relationship. By the third
part, the cord has produced all their major branches except the musculocutaneous and
axillary branches, which have diverged before this. The whole plexus is enclosed from
the vertebra to the distal axilla by an extension of the prevertebral fascia. Whatever
technique is used, brachial plexus block involves entering this sheath and injecting local
anaesthetic (LA) to fill it. The extent of the block will depend on which part of the sheath
is entered, the volume of LA injected and whether pressure is used to direct the LA. A
volume of > 40 ml is required to block an adult arm effectively.
1. Scalenus anterior and medius bound the interscalene groove. The patient sniffing or
taking a maximal inspiration demonstrates this. It is entered at right angles at the
level of C5,6 above the level of Sibson’s fascia so pneumothorax is rare. The roots
emerge from the intervertebral foramina in a caudal direction. A needle that points
cephalad may enter these and results in a subarachnoid block or vertebral artery
injection.
Vol. I 31
2. The subclavian pulse can be palpated directly under or directly behind the midpoint
of the clavicle. The plexus is at its most compact here and lends itself to an effective
block. Supraclavicular and infraclavicular approaches have been described.
Supraclavicular approach may enter the skin at the inferior part of the interscalene
groove behind the subclavian pulse. The sheath is pierced near the first rib. If the
subclavian a. is entered the needle is withdrawn and then directed posterior to the
artery. Pneumothorax occurs in up to 5 % and phrenic n. block in 50 %.
3. The needle position can be confirmed by arterial puncture, paraesthesiae, peripheral
nerve stimulation (distal muscle contractions at <1 mA), loss of resistance to saline, a
‘pop’ as fascia is pierced or pulsation of the needle. Monitoring nerve potentials
generated at the wrist with the block needle and ultrasound methods have also been
described.
4. The lateral cutaneous n. of the forearm is a branch of the musculocutaneous n.,
which leaves the plexus proximally at the level of the first rib and enters
coracobrachialis. It can be blocked by injecting 10 ml of LA into this muscle just
superior to the plexus in the axilla. The muscle’s fascia limits the spread of the LA.
Vol. I 32
Question No. 22
Immediately following a cholecystectomy, for which you had given a muscle
relaxant, the patient is spontaneously breathing 100 % oxygen through an
endotracheal tube and has oxygen saturation on pulse oximetry of 100 %.
1. If the patient is still anaesthetized give three patterns of ulnar nerve
stimulation that indicated residual paralysis.
2. If the patient is swallowing and maintaining normocapnia does this
indicate that neuromuscular function is adequate for maintenance of
the airway?
3. If the patient is awake what volitional test indicates adequate
neuromuscular function for maintenance of the airway?
4. Give four causes of prolongation of non-depolarizing neuromuscular
blockade.
Answer: -
1. Peripheral nerve stimulation: a train of four (TOF) ratio < 0.7, fade with 50 Hz
tetanus for 5 s and fade with double burst stimulation (DBS 3,3). However, the
absence of fade when sought by sight or touch with these techniques does not
guarantee adequate recovery from neuromuscular blockade. This requires
assessment by mechanomyograph or electromyography.
2. No.
3. Head lift for 5 s. this requires voluntary effort and is not performed well if in pain,
e.g. following an abdominal operation.
4. Neuromuscular blockade (NMB) may be prolonged because of :
 Hypothermia: a reduction of core temperature from 36.5 0 C to 34.50 C doubles
the duration of action of atracurium and vecuronium;
 Myasthenia gravis;
 Renal failure or hepatic failure;
 Respiratory acidosis or metabolic alkalosis;
 Drugs, e.g. volatile agents, gentamicin;
 Electrolyte imbalance, e.g. low potassium, sodium or calcium levels or high
magnesium levels;
 Biological variation.
Notes on NMB and recovery
The duration and intensity of NMB are very variable between patients and with many
factors, as indicated above. Safe recovery from0NMB requires that patients can
maintain their airway, swallow secretions, cough and ventilate so as to maintain normal
blood gases. This is assured by a TOF ratio ≥ 0.7, and the ability to sustain by 50 Hz
tetanus for 5 s or to raise their head for 5 s. the muscles of the upper airway are more
sensitive to NMB than the diaphragm and ventilation can be adequate even though the
patient cannot maintain an airway or swallow their secretions. External appearances of
swallowing do not guarantee the ability to complete this maneuver. 50 Hz tetanus is
painful and only reliable detects fade manually if TOF ration is < 0.3. The detection of
fade of TOF by vision or touch is only reliable if TOF ratio <0.4. This may be due to the
Vol. I 33
middle two responses confusion the comparison of the first and fourth responses. This
led to the development of DBS.
DBS3,3 is two bursts of three stimuli each at 50 Hz and separated by 750 ms. The two
tetanic burst are each perceived as one response. A faster tetanus is painful and above
100 Hz, in the presence of volatile agents, fade can occur painful than TOF stimuli,
which are usually painless. Manual DBS3,3 is more reliable than manual TOF stimuli at
detecting fade and reliably indicates a TOF ratio < 0.5 but does not guarantee a TOF ≥
0.7. Absence of fade as assessed manually or visually be 50 Hz tetanus, DBS or TOF does
not guarantee adequate reversal of NMB. Manual DBS 3, 3 has two stimuli in the second
burst and so has integral fade and will detect a TOF ration < 0.8 reliably. Unfortunately
it will also show fade at levels above 0.7 and may lead to the inappropriate use of
reversal agents.
The ability to reverse NMB adequately is inversely proportional to the value of T 1, the
first response of the TOF, at reversal. Vecuronium and atracurium are rapidly reversed
by 50 µg/kg neostigmine when T1 > 10 % of the pre-relaxant control or when there are
spontaneous movements.
Vol. I 34
Question No. 23
List the indications, contraindications, and complications, of Stellate
ganglion block.
Answer: -
Indications
 Chronic pain states
o Causalgia
o Reflex sympathetic dystrophy
 Peripheral vascular disease
o Acute vascular disorders, for example inadvertent intra-arterial injection of
thiopentone, postembolectomy
o Chronic vasospastic disease, for example Reynolds’s disease
Contraindications
 Anticoagulants and hemorrhagic disorders
 Local infection or neoplasm
 Local anatomical or vascular anomalies
 Patient refusal
Complications
 Systemic toxicity (almost immediate effect if injected into the vertebral arteries)
 Pneumothorax
 Brachial plexus block
 Recurrent laryngeal nerve block (cause temporary hoarseness)
 Phrenic nerve block (cause hemidiaphragmatic paralysis)
 Vagus nerve block (cause tachycardia)
 Cardiac accelerator nerve block (cause bradycardia)
 Subarachnoid injection (if injected into a “dural sleeve”)
Vol. I 35
Question No. 24
Give a brief account on the types of muscular dystrophies and their
anaesthetic problems.
Answer: -
Muscular dystrophies are a group of genetically transmitted disease and are due to an
inborn error of metabolism characterized by progressive atrophy of symmetric groups of
skeletal muscles without evidence of involvement or degeneration of neural tissue. In all
forms of muscular dystrophies there is loss of strength with increasing disability and
deformity, but each type differs in the groups of muscles affected and the degree of their
weakness, the age of onset, the rate of progression, and the mode of genetic inheritance.
Associated medical disorders are respiratory infections, kyphoscoliosis, and cardiac
abnormalities.
Types of muscular dystrophies

 Pseudohypertrophic (or Duchenne) muscular dystrophy is the commonest type. It
starts after the age of two with rapid progression and incapacity in the teenage years,
and early death in the twenties. Cardiac involvement is relatively high.
 Limb- girdle muscular dystrophy less severe than Duchenne dystrophy is a mild
form that occurs later in life with normal life span.
 Myotonic dystrophy starts at about the age of 30 years with death before the age of
60. Associated problems are cardiomyopathy, baldness, testicular atrophy, and
cataract.
 Other rare forms include Becker’s muscular dystrophy, distal muscular dystrophy,
and ocular myopathy.
Anaesthetic problems
 Postoperative pulmonary insufficiency and chest infections are due to muscle
wasting, kyphoscoliosis, and maldevelopment of the respiratory muscle.
Postoperative observation in HDU/ITU is often indicated.
 Cardiac arrhythmias may be due to an associated cardiac lesion such as in
Duchenne’s dystrophy, or an inappropriate release of potassium such as in myotonic
dystrophy. Cardiac arrest has been described during induction of anaesthesia in
patients with myotonia. Acute heart failure due to cardiomyopathy is also a
recognized complication in patients with myotonic dystrophy.
 Abnormal reaction to muscle relaxants: increased sensitivity to the non-depolarizing
muscle relaxants and difficulty in their reversal are known problems. However, some
patients, particularly those with myotonic muscles, may exhibit resistance to
relaxation with anesthetics or muscle relaxants. Suxamethonium can cause an
exaggerated response and excessive release of serum potassium especially in
myotonia.
Vol. I 36
Question No. 25
List the methods of pain relief available to a patient who has multiple rib
fractures. Give the benefits and problems of each of them.
Answer: -
Methods
 Systemic analgesics
 Simple analgesics
 Non-steroidal anti-inflammatory drugs
 Entonox
 Opioids
 Intercostal nerve blocks
 Thoracic epidural analgesia
 Intrapleural analgesia.
Benefits and problems
Systemic analgesia
Benefits
 Non- invasive simple to administer and does not require skilled operator or
anaesthetist.
Problems
 Does not provide effective analgesia. Painful ribs/chest wall due to inadequate
analgesia may lead to further respiratory complications such as hypoventilation,
atelectasis, and retention of secretions,
 Opioids are probably the most effective amongst systemic analgesics but also carry
more side effects, such as respiratory depression, nausea, and vomiting,
Intercostal nerve blocks

Benefits
 Effective analgesia.
 Allows physiotherapy with possible reduction of respiratory complications such as
hypoventilation, atelectasis and retention of secretions.
Problems
 Invasive, requires a skilled and experienced anaesthetist.
 Risk of toxicity of local anesthetics.
 Risk of pneumothorax
 Multiple injections.
 Analgesia is short lived and use of catheter is not possible.
Vol. I 37
Thoracic epidural analgesia

Benefits
 Very effective analgesia.
 Can be used continuously with a catheter.
 Allows physiotherapy with possible reduction of respiratory complication.
Problems
 Invasive, requires a skilled and experienced anaesthetist.
 Complications as for spinal/epidural analgesia, which include dural tap, highblock,
hypotension etc.
Intrapleural analgesia
Benefits
 Effective analgesia.
 Can be use continuously with a catheter
Problems
 Invasive. Requires a skilled and experienced anaesthetist.
 High risk of pneumothorax.
 Risk of phrenic nerve and recurrent laryngeal nerve palsies
Vol. I 38
Question No. 26
Briefly describe the technique of Stellate ganglion block. What are the signs
of a successful block?
Answer: -
The Stellate ganglion is part of the sympathetic chain and is formed from the fusion of
the inferior cervical (C7, C8) and first thoracic sympathetic ganglia. The Stellate
ganglion provides sympathetic innervation to the face, head, neck, and upper extremity.
Technique
(1) Patient supine
(2) Head extended on neck and looking straight ahead
(3) Aseptic technique
(4) Palpate chassaignac’s tubercle (transverse process of C6) at level of cricoid
cartilage.
(5) Retract carotid sheath laterally with fingers and raise a skin wheal over the
tubercle.
(6) Insert a 4 cm 22 G needle directly posteriorly to contact the tubercle, passing
medial to the retracted carotid sheath.
(7) Withdraw the needle 1-2 mm, aspirate, and inject a test dose of 1 ml of local
anaesthetic solution (lignocaine 1 % or bupivacaine 0.5%).
(8) Presuming no untoward effect from the test dose, inject a further 8-9 ml of
solution slowly with regular aspiration.
Bilateral blocks should never be performed.
Successful block signs

The signs of a successful block are ipsilateral
 Dropping of the upper lid (ptosis)
 Papillary constriction (miosis)
 Reduced sweating (anhydrosis)
 Retraction of the eyeball (enophthalmos)
 Conjunctival engorgement and nasal congestion (Guttmann’s sign)
 Increased skin temperature
 Increased lacrimation.
The combination of ptosis, miosis, anhydrosis, and enophthalmos is known as Horner’s

syndrome.
Vol. I 39
Question No. 27
A 40-year-old woman complains of headache, vomits and then collapses. On
admission to hospital she localizes and opens her eyes in response to pain
but does not speak. A lumbar puncture is performed and the sample is
reported as containing 200 RBC/mm3 with no xanthochromia on
centrifugation.
1. How can one differentiate this from a traumatic tap? If this is not
traumatic, what is the diagnosis?
2. What test, if available, should have been done before the lumbar
puncture and why?
3. Was the Glasgow coma score on admission 2, 5, 8 or 10?
4. Give two reasons why a central venous catheter would be
indicated.
5. Twelve hours after admission she suddenly deteriorates. List two
preconditions that must be met before she can be tested for
brainstem death. Which of the following is necessary for diagnosis
of brainstem death: -
a. Core temperature of > 350 C
b. Apnoea with a PaCO2 > 50 mmHg
c. Absence of seizures
Answer: -
1. Take three aliquots of cerebrospinal fluid (CSF) and compare the first and third. If
the lumbar puncture was traumatic the blood content of the third aliquot will be
much less than the first. The composition of normal CSF from lumbar puncture is as
follows: -
Appearance Clear, colorless + no clot

Pressure with patient recumbent 6-18 cmH2O
Cell count ≤ 5 RBC/mm3
≤ 5 lymphocytes/ mm3
No polymorphs
Glucose 50 – 60 % of blood glucose
Protein 0.15 – 0.40 g/L
IgG < 15 % of total CSF protein
Oligoclonal bands None
The presence of > 100 RBC/mm3 and no xanthochromia on centrifugation is diagnostic

of subarachnoid haemorrhage (SAH). The presence of xanthochromia, a yellow
coloration of the CSF, can be due to:
 Hemolysis of blood six hours after a subarachnoid bleed and later from altered
haemoglobin;
 Systemic jaundice due to unconjugated bilirubin;
 Large amounts of pus or tumors, which cause local stasis of CSF. They are
associated with high protein content.
Vol. I 40
2. Computed Tomography (CT) scan. LP is contraindicated if an intracranial mass or

intracranial hypertension is suspected. The change in CSF pressure may cause a shift
of brain tissue. The cerebellar tonsils may come through the foramen magnum. This
results in ischemia of the brainstem and death.
3. The Glasgow Coma Score (GCS) (see table) is an internationally agreed physiological
scoring system for the assessment of neurological status. It is stated as a total score
from 3 to 15 or as the three parts, e.g. 465.
Score
Eyes open:
Spontaneously 4
To speech 3
To pain 2
Nil 1
Best more response:
Obeys commands 6
Localizes pain 5
Flexion withdrawal 4
Decerebrate flexion 3
Decerebrate extension 2
Nil 1
Best verbal response:
Oriented 5
Confused conversation 4
Inappropriate words 3
Incomprehensible sounds 2
Nil 1
Coma is defined as a GCS of <8. On admission this patient had a GCS of 8 or 251
(2+5+1).
4. The reperfusion injury is decreased by the calcium channel blocker nimodipine. This
reacts with PVC and light and must be given via a central vein. Central venous
pressure measurement may help in fluid management. This is important for
maintaining normo-volaemia and cerebral perfusion pressure (CPP) and preventing
cerebral vasospasm.
CPP = MAP – ICP
MAP = mean arterial pressure

ICP = intracranial pressure.
The preconditions are that the patient is in Apnoeic coma and that the cause is
irremediable structural brain damage due to a disorder that can lead to brain death. All
three conditions (a, b and c) are necessary.
Vol. I 41
Q. No. 28
You are asked to anaesthetize a 65-year-old man with endogenous
depression, in whom drug therapy has failed, for a course of
electroconvulsive therapy (ECT).
1. List the reasons for providing general anaesthesia during ECT.
2. List the physiological consequences of ECT.
3. What are the absolute contraindications to ECT?
4. List the important interactions between anti-depressant drugs and
drugs that may be used during anaesthesia.
Answer: -
1. ECT may be used in the treatment of major depressive illness in patients who are
refractory to medical treatment, in patients who are unable to tolerate the side
effects of anti-psychotic medication and in patients with acute deterioration in their
symptoms. A brief pulse of electrical current is applied to the anterior temporal areas
of the scalp. The stimulus is in a square wave form and usually, 80 V is applied for a
duration of 0.1 – 0.3 s to produce a modified grand mal seizure with a tonic phase of
10 – 15 s followed by clonic phase of 30 – 50 s. A series of treatment is usually given
over a 2 – 3 week period. General anaesthesia is provided during ECT: -
 To render the patient unaware of the treatment, which is unpleasant;
 To modify the motor component of the seizures induced by ECT, so that injury to
the patient is prevented(e.g. fractures of bones, biting of tongue).
2. Physiological effects: -
 Cardiovascular system: ECT causes an initial vagal discharge with bradycardia
and hypotension. Intense parasympathetic stimulation upon application of the
current may result in asystole. There follows activation of the sympathetic
nervous system with consequent hypertension and tachycardia, which lasts 5 –
10 minutes. Both cardiac output and myocardial O 2 consumption are increased.
Arterial or ventricular arrhythmias may be precipitated. ECG changes often
occur and include prolongation of the PR and QT intervals and inversion of T
waves.
 Central nervous system: ECT causes increases in cerebral blood flow, cerebral
metabolic rate and intracranial pressure. The intraocular pressure is also raised.
 Other: Intragastric pressure is raised. There is an increase in plasma levels of
ACTH, cortisol and catecholamines.
3. The absolute contraindications to ECT are: -

 Myocardial infarction within 3 months;
 Cerebrovascular accident within 3 months;
 Intracranial surgery within 3 months;
 Intracranial mass lesion;
 Phaeochromocytoma.
4. Tricyclic antidepressants: These drugs (e.g. amitriptyline, imipramine and dexepin)

prevent re-uptake of noradrenaline and serotonin. The use of directly – acting
Vol. I 42
sympathomimetic drugs must be avoided as the interaction may cause intra-

operative hypertensive crises. Anti-cholinergic drugs have additive antimuscrinic
side effects with the tricyclics and can cause post-operative confusion and delirium.
Monoamine oxidase inhibitors: These inhibit the enzymatic breakdown of
noradrenaline, serotonin and dopamine. Interaction with sympathomimetic amines
may cause hypertensive crises. They interact with opioid analgesics and produce
either excitation or depression of the CNS. Phenelzine has been reported to reduce
plasma cholinesterase in 40 % of patients taking it. Both the MAOIs and the
tricyclics augment the effects of barbiturates.
Other drugs: Lithium prolongs the action of pancuronium and suxamethonium. The
newer serotonin uptake inhibitors (e.g. fluvoxamine, fluoxetine, paroxetine and
sertraline) are less sedative, less cardiotoxic and cause fewer anticholinergic side
effects.
Vol. I 43
Question No. 29
What methods are available to measure and reduce intracranial pressure?
Answer: -
Intracranial pressure is measured to give an indication of cerebral perfusion pressure, to
assess the possibility of “coning”, in the monitoring of neurological status in ITU and in
the management of cerebral oedema and hydrocephalus. Normal intraventricular
pressure is < 10 mmHg and a pressure of > 20 mmHg should be a cause for concern.
The methods of measuring intracranial pressure are listed below: -
 Intracranial catheter connected to a transducer-accurate but infection risk.
 Subdural devices
o Bolt (Richmond screw)
o Catheter
 Extradural devices
o Bolt
o Gaeltec – transducer at catheter tip
o Ladd - fibreoptic system with mirrors
Methods to reduce intracranial pressure are listed below: -

 Surgical removal of an intracranial lesion
 Hyperventilation to a PaCO2 of 4.5 kPa
 Drainage of CSF via an intraventricular catheter
 20 % mannitol
 Dexamethasone
 Intravenous induction agents excepts ketamine
 15 degree head up tilt-promotes venous drainage
 Neutral head and neck position with unobstructed venous outflow
Vol. I 44
Question No. 30
Describe the physiological regulation of cerebral blood flow. Outline how
this may be influenced by anaesthesia.
Answer: -
Cerebral Blood Flow (CBF) should be 50-ml/100 g/min or 15 % of cardiac output. It is
regulated by: -
 Arterial pressure
o Autoregulation: normal brain has the ability to maintain a constant cerebral
blood flow despite wide variations in mean arterial pressure (60-130 mmHg).
Two or three minutes are required for autoregulation to take place.
o Mechanisms: myogenic and metabolic; a variety of factors may abolish (ischemia,
trauma, tumors and other intracranial pathology, hypoxia, hypercapnia, volatile
agents) or modify autoregulation (hypertension, sympathetic activation). Under
normal circumstances regional cerebral blood flow and metabolism are tightly
coupled, with an increase in cortical activity leading to a corresponding increase
in cerebral blood flow.
o Cerebral perfusion pressure (CPP): CPP = MAP – ICP; CPP presents the pressure
head available for CBF. Normal is 70 – 80 mmHg; critical level for cerebral
ischemia is 30 – 40 mmHg.
 Venous pressure: any increase (head-down position, coughing, straining) will
decrease CBF.
 CSF pressure: raised ICP reduces CBF.
 PaCO2: Hypocapnia reduces CBF and hypercapnia increases CBF; CO 2 reactivity is
mediated by hydrogen ion concentration in CSF.
 PaO2: less influence on CBF than is the case with PaCO 2; an increase in CBF occurs
when PaO2 falls below 8 kPa.
 Temperature: PaO2 reduction in CBF with hypothermia appears to parallel reduction
in metabolic rate.
The influence of anaesthesia is outlined as follows: -

 Drugs: volatile agents and ketamine increase CBF; thiopentone and propofol cause a
dose-related fall in CBF.
 Disruption of controlling factors: cardiovascular instability raised jugular venous
pressure (coughing, vomiting, fluid loading, intubation, IPPV), hypoxia,
hypercapnia, Hypocapnia, hypothermia.
Vol. I 45
Question No. 31
Describe how brain-stem death is confirmed.
Answer: -
It is essential that certain preconditions and exclusions be fulfilled before a diagnosis of
brain-stem death can be made.
Preconditions
 Apnoeic coma (unresponsive and on a ventilator, with no spontaneous respiratory
efforts).
 Irremediable structural brain damage of known cause.
Exclusions
 Poisons, sedative drugs, and neuromuscular blocking agents.
 Hypothermia (central body temperature should be > 350 C.).
 Metabolic or endocrine disturbances (no profound abnormality of plasma
electrolytes, acid-base balance, or blood glucose levels).
Assessment of brain-stem function

 It is necessary to establish that all brain-stem reflexes are absent: papillary, corneal,
oculocephalic, vestibulo-ocular, gag, and cough.
 There should be no motor response within the cranial nerve territory to painful
stimuli applied centrally or peripherally.
 Spontaneous respiration should be absent. This test is crucial to the diagnosis of
brain-stem death.
In the UK, it is not necessary to perform tests such as ECG and carotid angiography for
confirmation of brain-stem death.
Tests should be performed

 Two doctors once have met the preconditions. Diagnosis should not normally be
considered until at least six hours after the onset of coma or if anoxia or cardiac
arrest was the cause of the coma (particularly in children), until 24 hours after the
circulation has been restored.
 By two medical practitioners of adequate experience. One should be a consultant, the
other another consultant or a doctor registered for more than five years; neither
should be a member of the transplant team.
 On two separate occasions, the interval between the two being agreed by all the staff
involved.
Vol. I 46
Question No. 32
You are asked to anaesthetize a dehydrated seven-week old boy who present
with regurgitation & projectile vomiting. The result of preliminary
investigations is as follow: -
Na + 131 mmol/L
K+ 2.2 mmol/L
Cl - 84 mmol/L
Urea 6 mmol/L
Hb 18 gm/dl
pH 7.2
1. What is likely diagnosis & what operation is a surgeon likely to perform?

2. What positive clinical signs would you look for?
3. What are the metabolic consequences of this condition & does this
constitute a surgical emergency?
4. What pre-operative management would you prescribe?
5. Following resuscitation, how might tracheal intubation be achieved in
this case?
Answer: -
1. (a) Infantile pyloric stenosis.
1. (b) Ramstedt’s operation (pyloromyotomy)
2. Waves of peristalsis can be observed moving across the upper abdomen when the
infant sucks and an olive-shaped mass is palpable in the epigastrium. There usually
is weight loss, and dehydration as evidenced by reduced skin turgor, sunken eyeballs,
depressed fontanelles, dry mucous membranes and a decrease in the urine output.
The blood pressure may be low and the pulse fast and thready. Jaundice is seen in 2
% of the cases.
3.
a. The metabolic consequences include dehydration, hypokalaemia,
hypochloraemia, metabolic alkalaemia and a paradoxical aciduria. The
haemoconcentration reflects dehydration.
b. Emergency resuscitation of the infant is a priority. Surgical treatment is not an
emergency.
4. The volume deficit, metabolic derangements and acid-base imbalance should be

corrected prior to surgery. A bolus of 20 ml/kg of 0.9 % saline can be administered
initially whilst further fluid administration is titrated against the level of hydration,
haemodynamic parameters and urine output. Potassium supplementation (daily
requirement = 3 mmol/kg/day) is usually necessary once urine output is established.
Surgery can be safely undertaken after haemodynamic stability has been restored
and pH = 7.3 – 7.5, Na+ > 135 mmol/L, Cl- >90 mmol/L and HCO3- < 30 mmol/L.
Vol. I 47
5. Ensure that resuscitation is adequate before administering anaesthesia. Monitoring

should include non-invasive blood pressure, electro-cardiograph, pulse oximeter,
precordial stethoscope and a peripheral temperature probe. A nasogastric tube is
usually in place and this should be aspirated. Pre-oxygenation is achieved via a
facemask. Atropine in a dose of 20 µg/kg may be given prior to induction of
anaesthesia. The choices for tracheal intubation in the cesarean controlled rapid
sequence induction with cricoid pressure, gases induction (e.g. oxygen and
halothane) or awake intubation.
Additional Notes
1. Pyloric stenosis results from a combination of hypertrophy of the pyloric smooth
muscle and mucosal oedema. It is seven times commoner in boys, and presentation
is usually between 2 and 6 weeks with regurgitation and nonbilious projectile
vomiting, resulting from gastric dilatation and delayed gastric emptying.
Pyloromyotomy involves dividing the pylori muscle along its entire length until the
mucosa protrudes into the incision.
3. H+, Cl-, Na+ and K+ are lost in considerable amounts during vomiting. Initially serum
pH is defended by excretion of alkaline urine that contains Na + and K+. When Na+
and Cl- are depleted, ECF volume is defended over pH. Thus the kidney retains Na+
and Cl- and H+ is lost resulting in paradoxical aciduria. The worsens the existing
alkalaemia.
5. In addition to the special consideration necessary for neonatal anaesthesia it must be
remembered that there is a potential danger of vomiting and aspiration during
induction of anaesthesia and tracheal intubation.
Vol. I 48
Question No. 33
A 5-year-old boy present for circumcision in the day surgical unit
1. List the local anaesthetic techniques that may be used to provide
postoperative analgesia?
2. Outline the anatomy of caudal canal?
3. Outline the technique for performing a caudal epidural Block?
4. List potential side effects/complications of caudal epidural Block?
5. Give three reasons for failure of caudal anaesthesia for this procedure.
Answer: -
1. Caudal epidural block; dorsal nerve of penis block; subcutaneous ring block; topical
anaesthesia with lignocaine gel, ointment and spray (EMLA cream is not as effective
as dorsal nerve of penis block)
2. The caudal space is a continuation of the spinal canal. The roof is formed by the
fused posterior laminae of the sacral vertebrae. The failure of development and
fusion of the laminae of the S5 vertebra produces the sacral hiatus, marked laterally
by the articular processes. The sacral hiatus extends from the sacrococcygeal joint to
the fused arch of S4 and is covered by the sacrococcygeal membrane, which is the
continuation of the ligamentum flavum. The canal is bounded anteriorly by the
vertebral bodies and laterally by the modified intervertebral foramina through which
the sacral nerve roots emerge. The caudal canal contains the dural sac, nerve roots,
valveless veins, fat and areolar tissue. The dural sac terminates at S2 in adults, but
extends to the S3-S4 vertebral level in children.
3. Preliminaries: Obtain informed consent from parents; observe strict aseptic
precautions.
Position: Prone, knee-chest or lateral positions may be used. The lateral position is
most convenient in a child of this size. Flexing the hips to 900 optimizes access.
Location of sacral hiatus: It is easily felt between the sacral cornua in children. A
triangle, the apices of which are the posterior superior iliac spines and the sacral
hiatus, is usually equilateral.
Needle insertion: A variety of needles, cannulae with hollow stylets, and angles of
entry have been recommended; a 21-gauge needle is a popular choice. Advance
needle at 200 to 300 to skin until a ‘give’ is felt as the sacrococcygeal membrane is
pierced. Entry into the epidural space can be confirmed by negative aspiration tests
for blood and CSF and loss of resistance to saline or air injection (NB: injection of air
has been associated with significant venous air embolism in infants). A test dose may
be used. The needle should not be inserted beyond a depth of 2-3 mm once the
sacrococcygeal membrane is pierced.
Dosage: Various dosage regimens have been suggested. A useful formula is 0.5 ml/kg
of 0.25 % plain bupivacaine, which reliably provides a high sacral block.
4. Accidental intravascular injection: This can be a serious problem because of the

vascularity of the region and the large volumes of local anaesthetic used. The use of
blunt short beveled needles and plastic cannulae will help reduce the incidence.
Motor Blockade: Weakness of the muscle of the legs is minimal when concentrations
< 0.25 % bupivacaine are used.
Vol. I 49
Delayed micturition: True retention is rare.

Nausea and vomiting: An incidence of up to 30 % has been reported after caudal
anaesthesia with local anesthetics.
Other: All of the undermentioned problems are rare: accidental dural puncture and
spinal anaesthesia; intraosseous injection with systemic toxicity; penetration of
pelvic organs, infection (the anus is in close proximity).
5. There is considerable anatomical variation in both the sacral hiatus and the caudal
canal; the sacral hiatus may be difficult to locate. Spread of local anaesthetic may be
uneven or unilateral, particularly in older children, due to dense areolar tissues.
Leakage through the intervertebral foramina may render a predetermined dose
inadequate.
Vol. I 50
Question No. 34
Outline with reasons, your technique for anaesthetizing a 3 year-old child
for removal of a peanut from the right main bronchus.
Answer: -
This is a serious and potentially fatal situation.
Problems
 The distress child may be hypoxic, coughing or have some degree of bronchospasm.
 Peanuts are notoriously difficult to remove bronchoscopically as they are smooth
sided and fit neatly into the bronchus.
 There is a risk of advancing the foreign body down the airway if positive pressure is
applied. This is complicated by the fact that sufficient relaxation of the vocal cords
must be produced in order to pass the bronchoscope.
 All the problems associated with general anaesthesia and bronchoscopy are present,
for example a shared airway.
 Rigid bronchoscopy is required.
Solution
Visit the child and parent preoperatively. A full history and explanation must be given to
the parents. Assess the degree of urgency. Reduce risks of a full stomach by fasting the
child. In the anaesthesia room, having performed all routine checks and preparations,
induce anaesthesia using an inhalational induction with oxygen, nitrous oxide, and
sevoflurane or halothane. Once anaesthesia has been induced establish intravenous
access. The anaesthetic is “deepened” by the use of a volatile agent in oxygen. It is best
to use a more soluble volatile agent at this stage and therefore sevoflurane is not
recommended for maintenance as it wears off too quickly. Anaesthesia is taken to the
deepest level that prudence allows. The mask is then removed and the bronchoscope
passed. The patient breathes spontaneously throughout the procedure. Depending on
the type of the bronchoscope it may be possible to pass oxygen and volatile agent
through a sidearm on the bronchoscope. If this is not possible the child will steadily
lighten as air is breathed down the bronchoscope. As the child lightens, the
bronchoscope is removed and the process of deepening the anaesthetic is repeated.
Vol. I 51
Question No. 35
A lady is admitted to the labour ward in the 29 th week of her first pregnancy
with a blood pressure, which is consistently greater than 160/100mmHg.
1. How would you classify hypertensive disorders of pregnancy?
2. Define pre-eclampsia.
3. Outline how you would manage hypertension in pre-eclampsia.
4. Outline the management of anaesthesia for Caesarean Section in
this patient.
Answer: -
1. International Society for the study of Hypertension in Pregnancy classification: -
 Gestational hypertension and/or proteinuria developing after 20 weeks gestation
in a previously normotensive nonproteinuric woman.
 Chronic hypertension incidentally associated with pregnancy, diagnosed before,
during or persisting after pregnancy.
 Unclassified hypertension, found at the first antenatal visit after 20 weeks
gestation, in a woman who’s past hypertensive history is unknown.
 Eclampsia
2. Pre-eclampsia is defined as a pregnancy complicated by hypertension with either

proteinuria or oedema or both. Hypertension is defined as a diastolic blood pressure
(phase IV) ≥ 90 mmHg on two occasions at least 4 h apart or a single recording ≥ 110
mmHg. Severe hypertension is defined as a diastolic pressure ≥110 mmHg on two
occasions at least 4 h apart or a single recording ≥ 120 mmHg. Proteinuria is defined
as ≥ ++ on reagent dipstick testing of two clean caught midstream samples taken six
hours apart or greater than 0.3 g in a 24-hour collection. Oedema is manifested by
accelerated weight gain in the third trimester.
3. Admission to hospital is essential if the mother is symptomatic or has proteinuria.
Bed rest is not of proven value. It is important to remember that abrupt reductions
in perfusion pressure may adversely affect both mother and child and that volume
expansion may be required before vasodilators are used. A gradual reduction of
blood pressure is favored. Long-term treatment is usually with methyldopa, 1-3 g
daily, in divided doses. It has a good safety record in pregnancy but may cause
sedation and postural hypotension. Sublingual nifedipine (10 mg, repeated at 30
min) is useful in short-term treatment but may cause headaches and palpitations.
Hydralazine is currently popular. It may cause a tachycardia, either resting or reflex,
and may necessitate the addition of a β-blocker. Labetalol in divided doses blunts the
rise in blood pressure without significant effects on the fetus and is therefore safe in
short-term use. Diazoxide, nitroprusside and GTN are not widely used.
4. Well-conducted epidural anaesthesia is safe and probably the method of choice. It
does not have deleterious effects on the cardiac output if the patient is adequately
hydrated and it suppress the vasoactive response to pain. In addition, it reduces
circulating endogenous catecholamines with resultant decrease in LV stroke work.
With adequate intravascular volume expansion epidurals may reduce uterine artery
vasospasm and increase intervillous blood flow, thus benefiting the fetus.
Vol. I 52
The main risk with general anaesthesia at difficulties with airway management and
the exaggerated pressor response to intubation, which may cause rises in ICP,
cerebral haemorrhage and cardiac failure. Drugs used to blunt the pressor response
to tracheal intubation include lignocaine, nifedipine, alfentanil, α and β-blockers and
magnesium sulphate. A combination of these agents may be used. A standard
obstetric general anaesthetic with rapid sequence induction must be carried out.
Careful monitoring of intravascular volume status and provision of adequate post-
operative analgesia are important. Delivery cures the condition. Post-operative
laryngeal oedema may occur.
Vol. I 53
Question No. 36
Define Pregnancy-induced hypertension. List the maternal complications of
the condition.
Answer: -
Pregnancy-induced hypertension (PIH) is difficult to define. The International Society
for the Study of Hypertension in Pregnancy defines PIH as a single diastolic reading
(Phase V) of ≥ 110 mmHg or above, or two reading of ≥ 90 mmHg or greater at least
four hours apart, occurring after the 20 th week of pregnancy in a previously
normotensive women. An American Working Group has defined it as a rise of > 15
mmHg diastolic or > 30 mmHg systolic compared with reading taken earlier in
pregnancy (this definition allows for the identification of women with PIH that is
superimposed on chronic hypertension).
A diastolic pressure of > 90 mmHg before 20 weeks suggests chronic hypertension.
While oedema and proteinuria are not essential for the diagnosis, proteinuria remains a
hallmark of the severity of this disorder. Proteinuria is defined as 2 + strip test on two
occasions four hours apart or a 24-hour collection with a total protein of > 0.3 g.
Eclampsia is an extreme hypertensive disorder of pregnancy and is defined as a
generalized convulsion occurring during pregnancy, labour, or within seven days of
delivery in the absence of epilepsy or any other disorder predisposing to convulsions.
The complications are multisystemic and are listed below: -
 Placenta: abruptio placenta, intrauterine growth retardation
 Cerebral: hyperreflexia/clonus, convulsions, visual disturbances, cerebral
haemorrhage
 Hepatic: liver dysfunction (HELLP – hemolysis, elevated liver enzymes, low
platelets), periportal necrosis, subcapsular haematoma, epigastric pain
 Hematological: thrombocytopenia, hemolysis, disseminated intravascular
coagulation
 Cardiovascular: hypovolaemia, abnormal left ventricular function, pulmonary
oedema.
Vol. I 54
Question No. 37
What are the warning signs of eclampsia? List the benefits and problems of
the available prophylactic anticonvulsant therapies.
Answer: -
Warning signs
Typical warning signs of eclampsia are: -
 Headache
 Nausea
 Epigastric or hypochondrial pain
 Blurring of vision in a patient with proteinuric gestational hypertension.
However, it should be remembered that eclampsia has been described in patients

without the development of these warning signs and even prior to any evidence of
proteinuria or gestational hypertension.
Prophylactic anticonvulsant therapies

These can be categorized into three major types: -
Benzodiazepines
Benefits:
 Effective in treating convulsions. Controversy exists about their role in prophylaxis
(see problems).
Problems:
 High risk of unconsciousness, pulmonary aspiration and respiratory depression.
 Neonatal hypotonia.
Owing to the high risk of complications, diazepam or other benzodiazepines are no

longer recommended for prophylaxis. This has been emphasized in many of the
“Confidential Enquiries into Maternal Deaths” reports.
Phenytoin
Benefits
 Little or no effect on the level of consiousness.
Problems
 Variable effectiveness.
 Narrow therapeutic window with its therapeutic dose very close to the toxic dose.
 Zero order kinetics with a fixed rate of metabolism and elimination.
 ATPase stimulator with risks of arrhythmias, hence the need for ECG monitoring
during the loading dose.
 Other side effects include pain on injection, hypotension, nausea, vomiting, and
nystagmus.
 Requires interval measurements of plasma levels.
Phenytoin is still widely used in the UK and many parts of Europe.
Vol. I 55
Magnesium sulphate
Benefits:
 Probably more effective than phenytoin.
 Little or no effect on the level of consiousness.
Problems:
 Unknown mechanism of action and a potential for drug interaction.
 Requires measurements of plasma levels.
 Reduces the liberation of acetylcholine at the neuromuscular junction, and
depresses the excitability of the endplate, and the muscle membrane. Hence, the
increased sensitivity to both depolarizing and non-depolarizing muscle relaxants.
 Hypotonia in mother and newborn.
Used in North America, widely used in Australia and South Africa, and now increasingly
used in the UK.
Vol. I 56
Question No. 38
Outline the management of Eclampsia.
Answer: -
Eclampsia is a generalized convulsion occurring in pregnancy, labour or within seven
days of delivery in the absence of epilepsy or any other disorder predisposing to
convulsions.
The initial object of treatment is to control the convulsion. Therefore airway control,
oxygen, and left lateral positioning of the pregnant patient, who can be either pre- or
postpartum, must be made. A suitable benzodiazepine such as diazepam should be
administered intravenously in a dose normally of 5-10 mg as a bolus. Diazepam is not
prophylactic in the prevention of further convulsions.
Secondary treatment involves stabilizing the patient because this disease is

multisystemic in its nature. Therefore blood pressure control and monitoring of the
hematological system is mandatory to prevent and treat any clotting abnormalities that
may occur. The renal, cardiovascular, and hepatic systems need monitoring as
multisystem failure can occur. Should oliguria occur central venous pressure monitoring
is advisable.
Attention must be given to the delivery of the fetus and often this is done immediately
with general anaesthesia in the emergency situation.
Care is often best undertaken in the ITU or HDU environment.
The prevention of further convulsion is best undertaken by magnesium sulphate

therapy. This can be given via an intravenous bolus of 4 g followed by a maintenance
infusion of 1 g/h. Neuromuscular, cardiac, and neurological side effects may occur and
the level of consciousness, reflexes, and serum magnesium levels must be monitored
regularly.
Vol. I 57
Question No. 39
Describe the management of a massive postpartum haemorrhage.
Answer: -
{1} Does the patient have a pulse? If not start external cardiac massage.
{2} Ensure adequate venous access. A 14 or 16 G cannula should be sited in each arm.
{3} Give 60 % oxygen via a fixed performance mask.
{4} Connect monitoring NIBP, Sao2, and ECG.
{5} Call for help: obstetricians, senior anaesthetist.
{6} Alert haematology laboratory and send off blood for FBC, clotting screen, fibrin
degradation products/d-dimers and cross-match 10 units.
{7} Record blood loss
{8} Give 10 units syntocinon intravenously
{9} Start syntocinon infusion at 10 U/h. consider intrauterine prostaglandin F 2α.
{10} Review the situation with the obstetrician
 Is there genital tract trauma?
 Is there uterine inversion?
 Is the uterus empty?
 Does the patient require a manual removal of placenta or evacuation or
retained products of conception?
{11} If removal of the placenta is require, give 30 ml of oral 0.3 M sodium citrate. Make
decisions regarding the suitability of general or regional anaesthesia.
 Epidural and spinal anaesthesia may cause vasodilatation and hypotension
superimposed upon hypovolaemia.
 General anaesthesia must be considered with the use of “rapid sequence
induction” technique to reduce the risk of pulmonary aspiration.
{12} Fluid replacement – initially give colloid. Treating haemodynamic values may be
misleading as even moderately severe haemorrhage is sometimes manifested only
as tachycardia. Try to keep up with blood volume lost. If, after 2000 ml of colloid,
further fluid is required urgently and the laboratory has not yet cross – matched
the patient, consider giving type-specific blood or O negative packed red blood
cells. Once blood is available, continue replacing losses with blood. Be aware of all
the problems associated with massive blood transfusion such as hypothermia and
coagulopathy. Repeat the blood tests regularly and correct any abnormalities with
blood products
{13} Once the operation has finished, it may be appropriate to transfer the patient to the
intensive care unit.
Vol. I 58
Question No. 40
You are asked to anaesthetize a full-term parturient for an emergency
Caesarean section for fetal distress. On questioning she says she is allergic
to suxamethonium and can remember waking up in the ITU after her
previous Caesarean section. She thinks her mother is also allergic to
suxamethonium and has had a blood test to prove it. No notes are available.
1. What is the diagnosis?
2. The patient insists on a general anaesthetic. Would you use
suxamethonium?
3. Following the operation the patient’s old notes show the following
blood results:
Dibucaine number (DN) – 60
Fluoride number (FN) – 50
Is the action of suxamethonium likely to be prolonged in this
patient?
4. Give the normal values for DN and FN.
5. Name two alternative methods of anaesthetizing a patient for a
Caesarean section without using suxamethonium.
Answer: -
1. Pseudocholinesterase variant or allergy to suxamethonium.
2. No. If a patient says that they are allergic to drug this must be taken seriously until
the history can be confirmed. A family history suggests a plasma cholinesterase
variant. The reason for the previous admission to ITU may have been either
pathology or unrelated to the use of suxamethonium, e.g. for the stabilization of pre-
eclampsia.
3. And 4. Refer to Table given below: -
Major abnormal Pche genotypes

DN FN Frequency Clinical prolongation
E1 uE1u 80 60 97 % None
E1 uE1a 60 50 3% None/minimal
E1 aE1a 20 20 1:3000 +++
E1 fE1f 65 35 very rare +
E1 sE1s 80 60 very rare +++
5. Alternatives to suxamethonium for anaesthesia for Caesarean section include:

 Regional or infiltration technique. However, this may need to be converted to a
general anaesthetic;
 High dose vecuronium;
 Priming, although the large inter-patient variation means that the priming dose
may fully paralyze some patients while having little effect on others;
 Awake intubation.
Vol. I 59
Notes on plasma cholinesterase (PchE)

PchE is a tetrameric glycoprotein that is synthesized in the liver and found in all tissues
except erythrocytes. It has no proven function but be involved in detoxifying esterase
present in the diet. It hydrolyses suxamethonium, normally terminating its action
within 3-5 minutes. Prolonged action beyond this is diagnosed by peripheral nerve
stimulator (PNS) which may show dual block. Causes include:-
 Pregnancy, maximum on the third day post-partum and lasting up to eight weeks;
 Liver disease, renal disease, bronchial and gastrointestinal carcinoma and burns;
 Inhibition of PchE, e.g. by bambuterol, ecothiopate eye drops and trimetaphan;
 Abnormal PchE gene is on chromosome 3 at location q26 and all relevant variants
are due to mutations at this one gene.
Initial management is maintenance of anaesthesia to prevent awareness and IPPV until

muscle power returns as assessed by PNS. Recovery can be hastened by the
administration of fresh frozen plasma or purified serum cholinesterase but the former
has inappropriate risks for a benign disease and the latter is not readily available in the
UK. Chemical inhibition analysis (above Table) may confirm the result but can miss
rarer variants. If clinical evidence supports a diagnosis of abnormal PchE, chromosomal
studies may be necessary to identify a rare genetic variant. The family should be
appropriately investigated and counseled. The use of suxamethonium in future
anesthetics is not absolutely contraindicated provided that the risks of using
suxamethonium as a long-acting muscle relaxant are taken into account.
Vol. I 60
Question No. 41
An 18-year-old youth has an operation on his fractured femur. Ten minutes
after intubation he has a pulse of 130/min and is starting to breathe
spontaneously despite a relatively large dose of opiate and muscle relaxant.
1. What myopathic condition could account for this? Give three
possible causes for this tachycardia.
2. List three other signs that would support a diagnosis of this
myopathic condition.
If you suspect this myopathic condition:
3. What blood tests should be sent?

4. What drug is given to treat this condition, what are its side effects
and what else is present in each vial?
5. He has had several previously uneventful anaesthetics. For this
operation he has been given total intravenous anaesthesia with no
volatile and no depolarizing muscle relaxant. How does this help
your diagnosis and management?
Answer: -
1. Malignant hyperthermia (MH). Other causes of intra-operative tachycardia include:-
 Light anaesthesia: absence of sweating and dilated pupils are inconclusive but
check presence of volatile in vaporizer and doses of drugs given. Give test dose of
opiate;
 Hypovolaemia: look for hypotension and poor perfusion and give a fluid
challenge.
 Hypercarbia: check the Capnography. Causes include excess CO 2 production in
sepsis and thyrotoxicosis or rebreathing, e.g. due to exhaustion of soda lime or
disconnection of the inner tube of a Bain circuit;
 Thyrotoxicosis.
 Phaeochromocytoma.
2. No. Sign is pathognomonic of MH. The clinical presentation varies from normal to a
fulminant crisis. The clinical and biochemical features can be explained by the
pathophysiology. Following a trigger agent (the disease can be trigged by any volatile
agent or depolarizing muscle relaxant) the skeletal muscle becomes hypermetabolic.
There is a massive increase in O 2 consumption, CO2 and heat production. When the
local energy demand exceeds supply anaerobic metabolism produces a metabolic
acidosis. The actin-myosin coupling requires energy to uncouple so the muscle
becomes rigid. Signs of MH include:
 Difficult intubation due to masseter spasm that is not relieved by muscle
relaxant;
 Flushed skin due to hypercarbia;
 Tachycardia;
 Cyanosis due to increased oxygen consumption despite an increased inspired
oxygen concentration;
Vol. I 61
 Hypercarbia despite increased ventilation: this may present on capnography or as

a hot soda lime canister;
 Arrhythmias due to acidosis and hyperkalaemia;
 Rise of core temperature of > 20 C/h.
3. The following investigations are indicated:

 Arterial blood gases are the most important: hypercarbia, hypoxemia, respiratory
acidosis and metabolic acidosis;
 Full blood count may show a high white cell count (infection), a low haemoglobin
(hypovolaemia) or low platelet count (disseminated intravascular coagulation);
 Electrolytes: hyperkalaemia suggests MH;
 Coagulation: to assess disseminated intravascular coagulation;
 Creatine kinase: raised, but not diagnostic due to wide overlap with normal
values.
4. Dantrolene: is available as vials of 20 g Dantrolene sodium, 3 g mannitol (to

maintain is tonicity), and enough NaOH to produce a solution of pH 9.5 (so that it
dissolves) when reconstituted with 60 ml of sterile water. Extra mannitol for renal
protection is probably unnecessary. Dantrolene has no side effects in the short term
but should be given by CVP, as it is irritant.
5. These do not affect your management. Exposure to known triggering agents does not
always provoke a response so a previous uneventful anaesthetic does not exclude the
diagnosis. Residual volatile agent in the breathing circuit can trigger MH. The initial
management of the patient is clinical; the diagnosis is only confirmed by in vitro
contracture OLU testing of muscle biopsies at a later date. In the future, diagnosis
may be aided by genetic testing of MRI techniques.
Vol. I 62
Question No. 42
A 34-year-old lady presents for a trans-sternal thymectomy. She developed
an autoimmune disease three years previously and is taking
pyridostigmine.
1. What is the disease?
2. List two other non-surgical treatments for this disease.
3. What two crises of muscle weakness can occur and how can you
differentiate them?
4. List two pre-operative abnormalities that increase peri-operative
risk.
5. How may the effects of thiopentone, suxamethonium and
atracurium be abnormal in this patient?
6. List two factors that might help predict the need for post-operative
ventilation?
Answer: -
1. Adult myasthenia gravis (MG), which is a myopathy affecting 1 in 20,000 adults. It is
characterized by muscle weakness that deteriorates with repetitive muscle
contraction. It usually presents with diplopia. 85 % of patients develop involvement
of the laryngeal, pharyngeal, facial, respiratory or limb muscle. The maximum effect
occurs within three years of onset. It is an autoimmune disease associated with SLE,
rheumatoid arthritis and thyroiditis. Antibodies to acetylcholine receptors (Ache)
occur in 90 % of patients. These are mainly IgG and do not occur in any other
disease. Diagnosis is confirmed by giving the patient edrophonium (‘Tensilon’), a
short-acting anticholinesterases (Ache) which causes a dramatic improvement in
muscle power within 30 s.
2. MG is treated by:
 Anticholinesterases: for symptomatic relief of mild MG; pyridostigmine is longer-
acting than neostigmine so gives more stable control; antimuscarinics are often
necessary initially but can often be tapered off.
 Immunosuppression: azathioprine helps in 45 % of patients but takes 3 months
to work; steroids can cause improvement in days in up to 80 % of patients but
have numerous side effects.
 Plasmapheresis helps in 45 % of patients by reducing the concentration of Ache
anti-bodies, but requires access to large veins.
3. Myasthenia (MC) and cholinergic (CC) crises. MC, a worsening of the myasthenia
condition, can be provoked by emotional upset, infection, overexertion, or drugs
(magnesium containing enemas or aminoglycosides). CC (excessive Ache effects)
may present with collapse, confusion, vomiting, sweating and salivation.
Differentiating may be difficult. A test dose of edrophonium (with immediately
available respiratory support) should improve a MC and exacerbate a CC. 70 % of
adult patients with MG have thymic hyperplasia and 10 % have thymomas. 50 % are
improved by thymectomy and a further 46 % develop complete remission. Trans-
sternal surgery gives better results than transcervical as more thymus can be excised
but it is more invasive and often requires post-operative ventilation.
Vol. I 63
4. Pre-operative risk factors include: -

 Respiratory muscle involvement which leads to chest infections and respiratory
failure;
 Bulbar involvement (pharynx and larynx), which predisposes to aspiration
pneumonitis and airway obstruction. It may require a gastrostomy feeding tube.
5. Characteristic drug responses in MG are: -

 A normal response to thiopentone: because of the inherent muscle weakness
(especially if the pre-operative dose of Ache is omitted), intubation may be
possible without a muscle relaxant;
 Resistance to suxamethonium: use 2 –3 times the normal dose for a rapid
sequence induction; there is an increased risk of dual block;
 Increased sensitivity to nondepolarizing muscle relaxants: use 10-20 % of the
normal dose and monitor the result clinically and by peripheral nerve stimulator;
 Reversal agents: risk of cholinergic crisis.
The need for post-operative ventilation is MG patients is difficult to predict but factors
include: the operation, duration of the disease > 6 years, vital capacity of < 2.9 L,
pyridostigmine doses > 750 mg/day, and chronic respiratory disease other than that to
MG.
Vol. I 64
Question No. 43
Write a short account on porphyria. List the drugs used in anaesthetic
practice that may precipitate an acute attack.
Answer: -
The porphyrias are an inherited group of metabolic, autosomally linked genetic
disorders of porphyrin metabolism. They are characterized by lack or partial block of the
functional enzymes in the biosynthetic pathway of haem. This causes an overproduction
of porphyrins. Porphyria is classified into the acute porphyrias, which include
intermittent porphyria and variegate porphyria, and the non-acute porphyrias, which
include porphyria cutanea tarda, and erythropoietic porphyria.
Acute attack of porphyria may be precipitated by triggers such as infection,

administration of drugs (see list below), fasting, or menstruation. These attack usually
present with nausea, vomiting, acute abdominal pain, and variable degrees of
neurological dysfunction. These include lower motor neuron lesions leading to paralysis
and loss of sensation of a limb or bulbar palsy, peripheral neuropathy, and/or
autonomic dysfunction. Mental disturbances, coma, convulsions and cranial nerve
palsies have all been described. During the acute attack, the color or the urine is
typically described as dark brown on standing or red fluorescent under ultraviolet light.
The appearance of aminolaevulinic acid in urine and porphyrins in the faeces are
characteristic of acute intermittent porphyria and acute variegate porphyria
respectively.
Drugs that may precipitate acute attacks of porphyria are listed under the two categories
below:-
1. High-risk precipitants (should never be given)
All barbiturates, especially thiopentone
Chlordiazepoxide
Phenytoin
Meprobamate
Sulfonamides
Chloramphenicol
2. Unpredictable and controversial drugs (should be avoided when possible)

Hyoscine
Metoclopramide
Chloral hydrate
Diazepam, but not temazepam that is known to be safe
Halothane and enflurane
Alcuronium
Lignocaine
Cocaine
Non-steroidal anti-inflammatory drugs, namely diclofenac, mefenamic acid, and
piroxicam
Vol. I 65
Angiotensin - converting enzyme inhibitors such as Captopril, enalapril, and

lisinopril
Clonidine
Hydralazine
Amiodarone
Ergot preparations
NB. Quite modest changes in the chemical structure of drugs of the same group change
their porphyrinogenicity.
Vol. I 66
Question No. 44
Outline the problems associated with anaesthetizing a patient with
rheumatoid arthritis.
Answer: -
Patient with rheumatoid arthritis can present with a number of complex problems
arising as a result of the following: -
Articular consequences of the disease
 Presence of deformities may compromise positioning during surgery as well as effect
the access for regional techniques or venous cannulation.
 Rheumatoid involvement of the head and neck may predispose to difficult airway
management during anaesthesia:
o Cervical spine – instability, anterior subluxation at axial level, fixed flexion
deformities make conventional laryngoscopy difficult, if not possible;
o Temporomandibular joint – disease produces limitation of mouth opening;
o Cricoarytenoid joint – bilateral fixation can cause airway obstruction.
Systemic consequences of the disease

 Heart: pericarditis and effusion, myocarditis, granulomatous disease affecting
conduction pathways and heart valves.
 Lungs: pleural effusion, interstitial lung fibrosis, nodules, Caplan’s syndrome in coal
miners, restrictive lung defect.
 Blood: normocytic, normo – or hypochromic anaemia, felty’s syndrome with
hypersplenism.
 Kidney: function impaired from interstitial nephritis, amyloidosis, drugs.
 Eyes: uveitis, Sjögren’s syndrome.
 Nerves: mononeuritis, peripheral neuropathy.
Adverse effects of concomitant drug therapy

 NSAIDs: deterioration in renal function.
 Gold: nephritic syndrome, immune thrombocytopenia, hepatitis, pneumonitis
 Penicillamine: proteinuria, SLE.
 Corticosteroids: cushingoid features
 Methotrexate: gastrointestinal side effects, bone marrow suppression.
 Cyclosporin: nephrotoxicity.
Vol. I 67
Question No. 45
Write a short account on the intracellular pathophysiology of malignant
hyperpyrexia. How does Dantrolene work?
Answer: -
Malignant hyperpyrexia (MH) is an autosomal dominant subclinical myopathy in which
the muscle fibres show no defect in histology but undergo abnormal contracture
responses after exposure to triggers such as volatile anaesthetics or suxamethonium.
The main feature of the pathophysiology is an inability to control calcium ion
concentrations within the intracellular compartment of the muscle fibre.
Normally depolarization travels from the end-plate through the transverse tubule (TT)
and to the sarcoplasmic reticulum (SR). The SR releases calcium ions, which removes
the troponin complex inhibition of the contractile elements and cause contraction.
Reuptake of calcium is rapidly carried out by intracellular calcium pumps, which
transfer calcium back into the SR, facilitating relaxation.
In MH there seems to be an excitation – contraction coupling defect which initiates an

early surge in free myoplasmic calcium leading to a low threshold and subsequent
increased release of ionized calcium at the SR, the so called “calcium-induced calcium
release”. In the acute attack, the rapid rise of calcium forces the muscle into a
disorganized non-propagated prolonged contracture rather than the normal, reversible
propagated contraction. The rapid rise of aerobic and anaerobic metabolism, glycolysis,
neutralization of hydrogen ions, and hydrolysis of high-energy phosphate compounds,
cause intense heat and carbon dioxide production, lactate accumulation, metabolic
acidosis, and release of potassium, creatinine kinase and myoglobulin. A cascading cycle
of increasing metabolism, heat, and acidosis results in metabolic exhaustion and
breakdown of cellular permeability, leading to muscular and generalized oedema.
The exact etiology of MH is unknown, but close associations with this condition are
specific genetic alterations in two important intracellular receptors: the dihydropyridine
receptors which are located in the TT and control the transfer of depolarization from the
TT to the SR, and, more importantly, the ryanodine receptors which are located in the
SR and are known to control the calcium releasing channels.
Dantrolene
Dantrolene stabilizes the cell membrane and the intracellular excitation-contraction
coupling. It binds to the TT and the sarcoplasmic reticulum and reduces the rate and
amount of release of calcium ions but it does not affect its reuptake. Dantrolene does not
interfere with the transmission at the neuromuscular junction.
Vol. I 68
Question No.46
A new volatile anaesthetic agent has the following properties:
a. Saturated vapor pressure at 20 C=664 mmHg
b. Boiling point = 23.5 C
c. Blood/gas solubility = 0.42
d. MAC = 7.5
1. Define MAC
2. How does blood/gas solubility influence the clinical usefulness of a
volatile agent?
3. How does oil/gas solubility influence the clinical usefulness of a
volatile agent?
4. Outline the attributes of the ideal volatile agents.
5. Based on the physical properties given above what properties
would you predict this new volatile agent to possess?
Answer: -
1. Minimum Alveolar Concentration (MAC) is a standard index of the potency of
volatile anaesthetic agents. MAC is defined as the concentration of volatile
anaesthetic (at 1 atmosphere) measured in end-tidal gas that prevents a response
(gross muscular movement) to a standard painful stimulus (surgical incision) in 50
% of subjects.
MAC95 is the concentration of anaesthetic, which prevents response to a
supramaximal stimulus in 95 % of subjects. MAC 95 is 1.3 – 1.5 times MAC and is
probably more useful in terms of achieving clinical anaesthesia.
MAC awake has been defined as the alveolar anaesthetic concentration at the first
response to command.
MAC awake, which is a measure of awareness, is the alveolar concentration of volatile
anaesthetic at which 50 % of subjects are aware and 50 % are not. MAC awake is
approximately 40 % of the MAC value of an anaesthetic agent.
2. Blood/gas solubility is an important determinant of the rate of rise of alveolar partial

pressure of an anaesthetic agent when the inspired partial pressure is held constant.
With agents with high blood/gas solubility, equilibrium between the inspired and
alveolar partial pressures is reached slowly. The lower the blood/gas solubility of an
agent the more quickly the alveolar-blood-brain equilibrium of volatile agent
concentration will be achieved. The blood/gas solubility, therefore, has an inverse
relationship to the speed of induction.
3. Meyer and Overton found that hypnotic potency of volatile anaesthetic agents is
proportional to their oil/water partition coefficients. Better correlation is found
between hypnotic activity and the oil/gas partition coefficient. The product of the
oil/gas partition coefficient of an anaesthetic agent and its MAC is approximately
constant. The oil/gas partition coefficient reflects the avidity with which a volatile
agent is taken up by neuronal tissue and is directly proportional to the potency of a
volatile anaesthetic agent.
Vol. I 69
4. The attributes of an ‘ideal’ volatile agent are given below: -

 Cheap;
 Chemically stable;
 Nonflammable, not irritant or pungent;
 Minimal autonomic effects;
 Low blood/gas solubility, i.e. low MAC;
 Minimal metabolism;
 Minimal cardiovascular depressant effects;
 Dose dependant/predictable side effects;
 Environment friendly;
 No teratogenicity.
5. This drug has a relatively high MAC, which implies that it is of low potency. Large
quantities of the agent would therefore have to be administered, which could prove
expensive. It has a high-saturated vapor pressure at 20 0 C, i.e. it is almost boiling.
This will result in the production of large volumes of vapor and excessive cooling
unless the vaporizer is provided with an external heat source. The inability to
administer this agent from a standard vaporizer would mean additional capital
expenditure. An advantage of the drug is its low blood/gas solubility. This should
ensure rapid onset of inhalational anaesthesia unless the drug possessed irritant
qualities. The low blood/gas solubility should also facilitate precise control of the
depth of anaesthesia and rapid recovery.
Vol. I 70
Question No. 47
Summarize the advantages and disadvantages of total intravenous
anaesthesia. What do you understand by “target-controlled infusion”?
Answer: -
Total Intravenous Anaesthesia
Advantages: -
 Avoid pollution.
 Avoid the use of N2O. Diffusion of N2O to body gaseous spaces may be harmful, for
example in ear surgery or in patients with pneumothorax. Prolonged anaesthesia
with N2O also carries a risk of bone marrow depression.
 Does not require anaesthetic machines or vaporizers. May be used in field
anaesthesia.
 Fewer incidences of postoperative nausea and vomiting. This applies to total
intravenous anaesthesia with propofol and not ketamine or methohexitone!
 Easy and rapid control of induction of anaesthesia and rapid control on the change of
depth of anaesthesia during the maintenance period.
 Administration of anaesthesia is independent of airway patency and ventilation. For
example, depth of anaesthesia can be maintained during bronchospasm or breath
holding. Another example is the maintenance of anaesthesia during fibreoptic
intubation, laryngoscopy, or bronchoscopy with oxygen insufflations or oxygen jet
ventilation.
 Suitable for certain condition such as malignant hyperpyrexia, especially when a
vapor-free anaesthetic machine is not available, or in patients with latex allergy
where latex material is incorporated in many of the rubber parts of the anaesthesia
machine, circuit, and ventilator.
Disadvantages
 Requires repeated injections or reliable infusion devices.
 Unpredictable dose requirement.
 Body movement during surgery in unanalyzed patients. Doses that are required to
prevent such movements are usually associated with respiratory and cardiovascular
depression.
 Risk of awareness in paralyzed patient. This is due to the complexity of the
pharmacokinetic profile of intravenous anesthetics with the variability of time
constants of distribution and elimination in different individuals.
 Unlike inhalational anesthetics which can be removed from the body by ventilation,
intravenous anesthetics once injected or infused cannot be removed other than by
metabolism or excretion.
 Often more expensive than inhalational anesthetics.
Vol. I 71
Target-controlled Infusion (TCI)

This is an intravenous infusion system which allows the operator to select the desired
target drug concentration in the blood of the patient receiving the infusion. The system,
which incorporates a syringe pump and a computerized controller, delivers the infusion
at a variable rate determined by an electronic algorithm based on a set of validated
pharmacokinetic compartmental-model equations from previous studies with the drug
concerned. In anaesthesia TCI was recently introduced with propofol as the intravenous
anaesthetic agent.
Vol. I 72
Question No. 48
Give details of the current clinical uses of magnesium.
Answer: -
Magnesium is currently used in variety of clinical situations: -
 To treat Hypomagnesaemia: This is a common problem in the intensive care unit
and it has been shown that correction of abnormally low magnesium levels helps in
the process of ventilatory weaning.
 In the management of Tachyarrhythmias: Magnesium is a co-factor for Na + - K+
ATPase. With hypomagnesaemia, intracellular potassium will be depleted.
Magnesium may also have some intrinsic antiarrhythmic action and is particularly
useful in the treatment of torsade des pointes, multifocal atrial tachycardia and the
ventricular arrhythmia seen with digitalis intoxication.
 In the treatment of Eclampsia: Throughout a large part of the western world,
magnesium is now well established as the first-line treatment of Eclampsia. It is
currently gaining in popularity in the UK. Magnesium antagonizes calcium at
membrane channels and reduces cerebral vasospasm. It produces a similar effect on
the systemic vasculature and along its inhibitory action on catecholamine release;
magnesium has a mild antihypertensive action. Magnesium is also a tocolytic agent
and therefore improves uterine blood flow. It is sometimes given to obtund the
hypertensive response to intubation in eclampsia. Investigations into the role of
magnesium in the prophylaxis of eclampsia have failed to show any benefit.
 As a treatment for Constipation: Magnesium is now used less for this condition, as
bulking agents such Fybogel, and suppositories and enemas are becoming more
widely used.
 Possibly in the management of patients following Myocardial Infarction: The LIMIT-
II study showed an improvement in post infarction survival in the group given
magnesium. This was not confirmed by a larger study and, because of side effects,
magnesium is currently not recommended in the management of acute myocardial
infarction.
 In the management of Severe Asthma: Magnesium has been used in the treatment of
severe refractory asthma. It is thought to block calcium channels and to inhibit
parasympathetic acetylcholine release.
 Hypocalcaemia: Hypomagnesaemia may exacerbate hypocalcaemia by inhibiting the
release and action of parathyroid hormone.
 Tetanus: Magnesium has been used as an adjunct to sedation in the treatment of
tetanus.
Vol. I 73
Question No. 49
A 73-year-old woman who is found convulsing in front of her coal fire is
admitted to casualty. She is conscious but confused & vomiting. The pulse
oximeter shows a saturation of 100 % while breathing oxygen via MC mask
at 4L/min.
1. What is the most likely diagnosis & how can it be confirmed?
2. What is your immediate management?
3. What further management may be required?
Answer: -
1. Carbon monoxide (CO) poisoning. The history is strongly suggestive, particularly if
the fire was used continuously for a long period with inadequate ventilation in the
house. Acute CO poisoning may cause convulsions and coma and prove fatal if
resuscitation is not immediate. Pallor of the skin is commoner than the classical
cherry red coloration. Skin necrosis occurs at pressure points. Carboxyhaemoglobin
(COHb) causes overestimation of oxygen saturation by pulse oximetry. A tachycardia
and ECG evidence of myocardial ischemia/infarction may be present. The
measurement of COHb content in a heparinized blood sample may confirm the
diagnosis. Note that blood COHb levels are of limited value in assessing the severity
of exposure, particularly after O2 therapy.
2. 100 % oxygen should be administered via a tight fitting facemask. Variable
performance plastic masks deliver only 60-80 % oxygen even at high flow rates. If
the level of consciousness deteriorates or the patient is uncooperative, tracheal
intubation and positive pressure ventilation with 100 % oxygen must be instituted.
In addition to general supportive measures, specific treatment may be required for
convulsions, cerebral oedema and metabolic acidosis. Useful tests include: arterial
blood gases, electrolytes (hypokalemia), cardiac enzymes and baseline chest X-ray.
3. Of the COHb level is greater than 40 % she should be referred for hyperbaric oxygen
(HBO) therapy. HBO therapy is recommended at this level even when symptoms are
absent. Post-hypoxic diffuse cerebral demyelination warrants long-term follow up.
Neuro-psychiatric sequelae include headaches, irritability, confusion, parkinsonism,
memory loss and personality changes.
Notes: -
1. CO is formed when carbon-containing materials, particularly solid and liquid fuels
undergo incomplete combustion. The poor and elderly are at increased risk in the
winter when fires are used for long periods with poorly maintained flues and
chimneys and inadequate ventilation. Chronic exposure to CO causes non-specific
influenza-like symptoms including fatigue, confusion, nausea, vomiting, dizziness
and abdominal pain.
2. The affinity of CO for Hb is 250 times that of oxygen. CO binds avidly to Hb resulting
in decreased O2 carriage. Shift of the oxyhaemoglobin dissociation curve to the left
inhibits O2 release from Hb. Tissue hypoxia is made worse by inhibition of cellular
respiration due to CO binding to haem-containing enzymes cytochrome oxidase and
P450 . It also binds to myoglobin. COHb concentration correlates poorly with clinical
symptoms and has little prognostic significance. The elimination half time of CO
Vol. I 74
from COHb is 2-5 h when breathing air, 80min when breathing 100 % O 2 at 3 bar.
100 % O2 at 3 bar optimizes CO release from Hb and provide enough dissolved O 2 to
meet tissues needs. HBO is used at 2-3 bar for the treatment of CO poisoning and the
duration of treatment varies with the severity of symptoms and response to
treatment. HBO also minimizes cerebral oedema that may result from cerebral
hypoxia.
3. Others who should be considered for HBO therapy include those who have been
unconscious, pregnant women (fetus has increased risk) and those with cardiac,
neurological and psychiatric complications.
Vol. I 75
Question No. 50
A 40 years old man is admitted to casualty having been rescued from a fire
at the plastic factory. He is conscious pulse oximeter-Oxygen saturation
reading is 97 %
1. Having initially assessed his airways, breathing & circulation, what
are the next two things you will do to him?
2. List three signs that would make you suspect an inhalation injury.
3. List three advantages that may be gained from intubating this
patient.
4. List two advantages of using a fibreoptic bronchoscope in this
scenario.
5. List two things that would make you suspect cyanide poisoning in
this patient. List two drugs that may be used to treat cyanide
poisoning.
Answer: -
2. A pulse oximeter reading of 97 % and consciousness does not exclude cyanide (CN)
or carbon monoxide (CO) poisoning. Give 100 % oxygen until these are excluded.
Remove clothing and contaminated material as hot plastic may continue to burn the
skin.
3. Inhalation injury is clinically significant damage to the airway or lungs caused by hot
or noxious gases or smoke. This may include direct thermal damage; smoke
inhalation or systemic CO or CN toxicity. Thermal damage is supraglottic as the
upper airway is designed for heating inspired air and dissipated the heat efficiently.
The exception is pressurized steam as this has the thermal capacity to transmit heat
distal to the cords. The first clinical examination, chest X-ray and arterial blood
gases may be normal. Clinical demise may occur more than 24 hours later when
airway oedema becomes maximal. If there is CO or CN poisoning tachypnea may not
occur as the carotid bodies respond more to the PaO 2 than the arterial oxygen
content. If any of these signs are initially abnormal it suggests significant
inhalational injury. There should be a high index of suspicion if there: -
 Is a history of impaired consciousness or the fire was in an enclosed space;
 Are oropharyngeal inflammation or deposits of soot or carbonaceous sputum;
 Is burnt nasal hair and eye brows;
 Are facial burns especially lips and nose;
 Is stridor or clinical signs of respiratory distress?
Initial management is chiefly supportive and should be proactive and

comprehensive. The need to intubate is a clinical decision based on the initial
assessment of the respiratory status, the damage to the airway and the likelihood of
further deterioration. Some patients will die at the scene. 50 % of those reaching
hospital with inhalation injury will require intubation and the rest careful
monitoring for 48 hours.
Vol. I 76
4. Endotracheal intubation ensures a safe airway. If delayed, it may be more difficult

due to increasing airway oedema. It facilitates the basic treatment of inhalational
injury by: -
 Warmed, humidified, 100 % oxygen with IPPV and PEEP to minimize atelectasis;
 Physiotherapy with tracheobronchial toilet;
 Desloughing of dead bronchial mucosa.
Other injuries, burns and sepsis predispose to ARDS and should be treated
aggressively. CO and CN poisoning should be treated. Routine antibiotics and
steroids are not indicated.
5. Beneficial uses of the fibreoptic bronchoscope in inhalational injury include the
assessment of the extent and severity of the airway and lung injury, the therapeutic
desloughing of dead bronchial mucosa and the facilitation of a difficult intubation.
6. Cyanide causes non-specific symptoms and signs due to tissue hypoxia. Serum
analysis of cyanide levels is slow. The following should make one suspicious of
cyanide poisoning: -
 Normal PaO2, metabolic acidosis, high blood lactate and mixed venous oxygen
saturation > 75 %;
 Decrease in the pulse oximeter saturation reading due to cyanohaemoglobin;
 Anion gap > 12 μmol/L.
Drug treatment of cyanide poisoning includes amyl nitrite, sodium nitrite and sodium
thiosulphate. Dicobalt edetate is toxic and only recommended in severe poisoning.
Vol. I 77
Question No. 51
A 28-year-old insulin dependent diabetic with a two-day history of having
been “unwell” is admitted to hospital with Glasgow coma score of 10. On
examination he is hyperventilating, dehydrated and has an infected ulcer
on his left foot: -
1. What is the most likely diagnosis?
2. Outline your initial management?
3. What other types of coma may be encountered in patients with
diabetes?
4. Define anion gap & how would you calculate plasma osmolarity?
Answer: -
1. Diabetic ketoacidosis.
The history is strongly suggestive; he may also not have taken his insulin as
prescribed. The diagnosis is confirmed by demonstrating hyperglycemia and
ketonaemia/ketonuria together with acidosis shown by arterial blood gas analysis.
2. Initial management includes: -

 Replacement of fluid and electrolyte losses: Give consecutive 1 L bags of 0.9%
NaCl over 30 min, 60 min, 1,2,4, and 6-hours periods. Add 20 mmol KCl to each
bag. CVP monitoring is useful to monitor the haemodynamic effects.
 Replacement of insulin: Give insulin 6 units i.v. stat followed by 6 u/hour by i.v.
Infusion.
 Restore acid-base and electrolyte balance: Monitor blood glucose and electrolytes
hourly. Adjust K+ replacement according to results. Bicarbonate should not be
given to correct acidosis unless the pH is < 7.0. when blood glucose falls to 12
mmol/L replace saline infusion with 5 % dextrose infusion with K + (1L six-hourly)
and change insulin dosage to sliding scale regimen.
Other investigations should include FBS, ECG, chest X-ray, and blood and urine
cultures. Catheterize if urine output is poor and pass nasogastric tube to prevent
acute gastric dilation. Intravenous fluids and insulin are continued until the patient
is able to eat and drink. The maintenance regimen of subcutaneous insulin can be
restored.
3. Other types of coma in diabetes include: -

 Hyperosmolar non-ketoacidotic coma: This accounts for 5-15 % of diabetic
hyperglycemic emergencies. The patient is usually elderly, often with previously
undiagnosed diabetes. There is usually a long history, and profound dehydration,
with plasma glucose > 35 mmol/L and osmolality > 340 mmol/kg. Focal
neurological signs and disseminated intravascular coagulation may be present.
Common precipitating factors are intercurrent illness and consumption of
glucose rich drinks. Treatment is as for ketoacidosis. Use 0.45 % NaCl if serum
Na > 150 mmol/L. Anticoagulate as risk of DVT is high.
Vol. I 78
 Hypoglycemic coma: Usually a consequence of inadequate calorie intake or

insulin overdose. Presents with behavioral change, sweating, tachycardia, fits and
coma of rapid onset. A rapid response is usually seen when 50 ml of 50 %
dextrose is given i.v. If i.v. Access is difficult; 1-2 mg of glucagon may be given
i.m.
4. (a) The anion gap is calculated as (NA ++K+) minus (Cl- + HCO3-). The normal anion
gap is <17. The anion gap is helpful in the differential diagnosis of metabolic
acidosis. If the anion gap is normal in the presence of acidosis, it is likely that
H+ and Cl- is being retained or NaHCO 3 is being lost. An increased anion gap
reflects an increase in unmeasured anion, which could be endogenous or
exogenous. Causes of metabolic acidosis with an increased anion gap include
lactic acidosis, ketoacidosis and salicylate toxicity.
4. (b) The osmolarity of a solution is the number of osmoles of solute per litre of a
solution and is therefore dependent on temperature. Approximate plasma
osmolarity can be calculated as 2[Na+] + [urea] + [glucose] mosmol/L. This
may be taken to reflect osmotic pressure (usually measured by depression of
freezing point of solution) and will be increased in dehydration and decreased
in fluid overload.
Vol. I 79
Question No. 52
You are called to the recovery ward by junior anaesthetist to asses a patient
who at the end of a general anesthesia is making no respiratory effort.
1. What is the first thing you would do on arriving in the recovery
ward?
2. List three pharmacological and three physiological causes for post-
operative apnoea.
3. List three monitoring devices and three blood tests that you would
use to diagnose the cause of apnoea.
4. List two pharmacological antagonists that may be useful. What is
important about their duration of action?
Answer: -
1. A good general principle is that when you are called to assess a patient who may be
in a life-threatening situation your first priority is to ensure that the patient is safe.
Therefore, on arrival in the recovery ward you should assess the patient’s airway,
breathing and circulation before progressing to the specific diagnosis and treatment.
2. Causes of post-operative apnoea include: -
 Prolonged effect of drugs used during the anaesthesia, including premedication,
e.g. opiates, volatile agents, benzodiazepines and muscle relaxants;
 Hypocapnia, acidosis;
 Intra-operative cerebral insult, e.g. surgery, hypoxia, hypotension or fat emboli;
 Hypoglycemia and hyperglycemia;
 Hypothermia
 Incidental pathology, e.g. head injury, drug intoxication, dystrophia myotonica or
hypothyroidism.
These factors may also interact; e.g. hypothermia and acidosis can increase the duration
of action of muscle relaxants and cause cerebral depression.
3. The patient’s medical history should be assessed for diabetes, respiratory, hepatic
and renal disease, Pseudocholinesterase deficiency and medications. The anaesthetic
including premedication, should be reviewed, especially the drugs used, their doses
with respect to the patient’s size and any periods of hypoxia or hypotension. After
ensuring that the patient is being ventilated with 100 % oxygen and no anaesthetic,
further assessment includes: -
 Clinical examination of the patient: miosis suggests narcosis but also occurs in
pontine haemorrhage; an upgoing plantar reflex suggests a cerebrovascular
accident but can occur in many causes of deep coma, e.g. hyperglycemia.
Spontaneous movement of limbs excludes neuromuscular blockade (NMB) as a
cause of post-operative apnoea.
 A peripheral nerve stimulator: absence of fade visually or manually with a train-
of-four or double burst stimulation does not guarantee a safe airway but does rule
out residual NMB as a cause of post-operative apnoea. Painful stimuli should not
be used to assess the patient’s condition until NMB is excluded lest pain in
inflicted on a paralyzed and awake patient.
Vol. I 80
 Pulse oximeter and capnographic: to assess the adequacy of oxygenation and

ventilation and to ensure that the PaCO 2 is high enough to stimulate the
respiratory center.
 A thermometer: to assess core temperature.
 Arterial blood gases: to assess blood pH and confirm the Capnography and
oximetry.
 BM-stix testing and blood glucose: to exclude hypo and hyperglycemia.
 Blood-urea: uremia can cause coma and renal failure can delay excretion of
drugs.
4. The following drugs may be useful: -

 Naloxone: a specific opioid antagonist which will reverse respiratory depression
and sedation but also analgesia.
 Flumazenil: a specific benzodiazepine antagonist that will reverse their sedative
and respiratory depressant effects.
Both these drugs act within a minute but their duration of action is much less than that
of the drugs they are reversing. So respiratory depression may re-occur 20 minutes later
and further doses of the antagonist or a continuous infusion may be necessary.
Vol. I 81
Question No. 53
You are called to the Casualty department to assess a 4-year-old boy who is
thought to have accidentally swallowed some aspirin tablets.
1. Briefly list two abnormalities you may find on arterial blood gas
measurement.
2. List three abnormalities you may find on clinical examination.
3. List three causes of dehydration in this patient.
4. List three general contraindications for the use of ipecacuanah
syrup.
5. Should gastric lavage be used 12 hours after ingestion of aspirin?
List two methods that may be used to eliminate aspirin from this
patient.
Answer: -
1. Acute aspirin poisoning may result in a compensated or uncompensated respiratory
alkalosis or a metabolic acidosis or a combination of these. Following absorption it is
hydrolyzed to salicylate which has multiple effects. It causes a respiratory alkalosis
by direct stimulation of the respiratory center. Renal compensation then occurs with
urinary loss of sodium, bicarbonate, potassium and water. The plasma bicarbonate
falls and the PaCO2 and pH return toward normal. The salicylate then causes a
metabolic acidosis by:
 Uncoupling oxidative phosphorylation in skeletal muscle, increasing the oxygen
consumption and CO2 and heat production;
 Derangement of carbohydrate metabolism resulting in accumulation of organic
acids;
 Renal impairment due to poor perfusion causing accumulation of inorganic
acids;
 Accumulation of its acidic metabolites.
The result is a picture of uncompensated respiratory acidosis with a high PaCO 2 and low
pH and plasma bicarbonate. This is exacerbated by higher toxic doses, which directly
depress the respiratory and vasomotor centers. Cardio-respiratory collapse results.
2. Serum levels may be deceptively low as salicylate is taken up by tissue. Clinical

findings are more important and include: -
 Initially tinnitus, nausea, vomiting;
 Hyperventilation (tetany is unusual and hypoventilation is a late ominous sign);
 Restlessness that may progress to coma;
 Dehydration (poor perfusion, tachycardia);
 Vasodilatation, fever and sweating (unless too dehydrated);
 Arrhythmias due to acidosis, hypokalemia;
 Cerebral oedema with fits, a late sign;
 Coagulopathy due to platelet effects, rare in acute aspirin intoxication.
3. Dehydration occurs due to hyperventilation and renal losses in response to the

respiratory alkalosis, sweating and vomiting. Hypernatraemia occurs as water loss
Vol. I 82
exceeds sodium loss. Hypo- and hyperglycemia can occur. Fluid is replaced by
dextrose with potassium, as the total body potassium is low.
4. Ipecacuanha causes vomiting by gastric irritation and stimulation of the
chemoreceptor trigger zone. Vomiting may not occur, especially if the patient has
taken an antiemetic or been given charcoal which absorbs the ipecacuanha. The dose
may be repeated or gastric lavage instituted. Contraindications to the use of
ipecacuanha include: -
 Ingestion of corrosive poisons, e.g. alkalis;
 Patients who, by the time they vomit, may be comatose and not protect their
airway;
 Ingestion of hydrocarbons (turpentine, furniture polish) as these can cause a
hemorrhagic aspiration pneumonitis if inhaled;
 Ingestion of a central stimulant as it may provoke a fit.
5. Gastric lavage is done with the largest possible tube, i.e. about 36 FG in an adult and
24 FG in a child. It is unlikely to be of use > 4 hours after ingestion unless an
antiemetic is ingested, e.g. opioids, aspirin (up to 24 h) or a tricyclic antidepressant
(up to 8 h). a safe airway is a prerequisite, i.e. the presence or a cough reflex or an
tracheal tube. Gastric lavage also allows installation of charcoal, desferrioxamine (for
iron poisoning) and Fuller’s earth (for paraquat poisoning). Other methods of
eliminating aspirin include forced alkaline diuresis and multiple dosing of activated
charcoal. Haemodialysis is effective and allows correction of altered biochemistry.
Vol. I 83
Question No. 54
Outline the causes of immediate postoperative hypoxemia.
Answer: -
The causes of early postoperative hypoxemia include diffusion hypoxia as a result of
nitrous oxide anaesthesia. The commonest categories are listed and discussed below.
 Hypoventilation
This commonly arises from upper airway obstruction in the unconscious patient, central
respiratory depression which is usually caused by opiates, or respiratory muscle
weakness which can result from inadequate reversal of muscle relaxants.
 Ventilation/perfusion abnormalities
This arises from prolonged anaesthesia in patients with other systemic disease such as
chronic bronchitis. Abnormal surgery can exacerbate this cause.
 Increased oxygen consumption

This can occur in the patient who is cold and is often made worse by shivering.
 Impaired response to hypoxemia

Anaesthesia especially with the volatile anaesthetic agents can impair the normal
response to hypoxia and therefore hypoxemia can occur.
 Decreased oxygen content

This can occur after major surgery that has especially been complicated by
haemorrhage. A low cardiac output and low haemoglobin will account for this cause.
For the above reasons, 40 % oxygen is routinely given to patients immediately after
anaesthesia.
Vol. I 84
Question No. 55
A 45 year-old man has been rescued with extensive burns from a house fire.
Outline your management of the problems that may be encountered in the
first 24 hours.
Answer: -
Immediate
The immediate problems from a severe burn are: -
 Hypovolaemia from loss of plasma.
 Airway oedema and respiratory complications from inhalation of poisonous or hot
gases.
 Difficulty with tracheal intubation in the presence of facial or airway burns.
 Pain.
 Metabolic effects from a high catabolic state.
 Infection risks from loss of skin barrier, dead tissue, and immunodeficiency.
As many of the above are life-threatening complications, it is appropriate that

experienced personnel are involved in the patient’s management from the outset.
Following resuscitation and stabilization, arrangements must be made to transfer him to
a specialist burns unit.
Management
Management includes: -
1. Initial treatment
 Assessment of airway, breathing, circulation, and conscious level.
 100 % oxygen via a tight-fitting mask connected to an anaesthetic machine.
 Intubation and ventilation if unconscious or if evidence of smoke inhalation.
Intubation can prove to be difficult or even impossible by conventional methods.
Suxamethonium is considered safe in the first 24 hours following a burn injury.
 Intravenous access – may be difficult.
 Blood for FBC, Urea & Electrolytes, Blood grouping and cross-matching, ABGs,
and carboxyhaemoglobin.
 Secondary survey to exclude other injuries he may have sustained in an attempt
to escape.
 Assessment of the extent of burn (rule of nine) – depth, surface area.
 Intravenous opioid analgesia.
 Urinary catheter.
 Nasogastric tube (to prevent acute dilatation of the stomach).
2. Fluid replacement
 Various formulae; colloid/crystalloid (colloid favored in the UK).
 Type and amount depend on pulse, BP, urine, haematocrit, CVP.
 Frequent reassessments crucial to guide therapy.
Vol. I 85
3. Inhalational injury
Indicators: fire in an enclosed space; stridor/wheeze; burns to the head and neck
and/or circumferential burns; coughing of soot-stained sputum; burnt nasal hair and
eyebrows; impaired consciousness. Fibreoptic bronchoscopy is useful to assess the
extent and severity of the airway and lung injury. Direct thermal injury, toxic gases
and smoke inhalation cause: -
 Supraglottic oedema
 Damage to distal airways and lungs parenchyma
 Carbon monoxide poisoning: suspect clinically and confirmed by oximetry.
Treatment: administer 100 % oxygen which reduces the half-life of

carboxyhaemoglobin from 4 hours to < 1 hour; intubate and ventilate if unconscious;
hyperbaric oxygen therapy for severe cases (COHb level > 40 %)
 Cyanide poisoning – suspect if metabolic acidosis, high blood lactate;
Treatment –amyl nitrite, sodium thiosulphate.
4. Hypothermia: nurse in warm environment.

5. Nutrition: early enteral feeding because of high catabolic state.
6. Stress ulcer prophylaxis.
7. Definitive treatment:
 Infection – isolation, topical antibiotics, tetanus toxoid.
 Surgery – escharotomy, dressing, early grafts.
Vol. I 86
Question No. 56
List, with examples when appropriate, the possible causes of air embolism
during surgery and the methods of diagnosis and treatment.
Answer: -
Causes
 Inadvertent intravascular injection of air into vein or artery (iatrogenic).
 Suction of air into open veins or sinuses under low hydrostatic pressures, for
example cannulation of central veins especially when the Trendelenberg position is
not used; open cerebral sinuses during an operation in the sitting or head up
position; open veins and sinuses of the uterus when it is elevated or inverted such as
during a caesarean section.
 Entrainment of air with rapid transfusion of blood or infusion of intravenous fluids
especially with the use of rotary pumps or pressure bags.
 Reuse of disconnected plastic intravenous fluid bags or use of air vents with
intravenous fluid bags.
 The use of extracorporeal circulation such as during cardiac surgery.
 Use of air for the loss of resistance technique in insertion of the epidural needle may
be a potential risk for air embolism in small children.
Diagnosis
 Loss or dramatic fall in the end-tidal CO2 trace of the capnograph.
 Drop in the cardiac output, manifesting as low arterial pressure, weak pulses and
poor color and capillary filling.
 Elevation in central venous pressure with dramatic fall in arterial pressure.
 ECG changes, mainly signs of right-sided strain.
 Mill-wheel murmur heard more clearly when an oesophageal stethoscope is used.
 Precordial Doppler ultrasound.
 Transoesophageal echocardiography.
Treatment
 Prevent further air entrainment by treating the cause, for example: -
o Stop intravenous fluid if air is seen in the intravenous fluid system.
o Ask the surgeon to cover open veins or sinuses with saline.
o Reverse sitting or head-up positions. Level (make horizontal) the patient or even
make dependent the part of the body where open veins are suspected, for
example head-up position when the uterine veins and sinuses are opened or
head-down position during insertion of a central venous line.
 Supportive measures, for example increase FiO2.
 Aspirate air through the central venous catheter.
 Consider the left lateral head-down position if ventricular flow obstruction is
suspected. This may also help aspiration of the air from the central venous catheter.
 In extreme situation, a cannula may be inserted percutaneously into the right
ventricle for aspiration of air.
Vol. I 87
Question No. 57
Briefly list factors involved in the pathophysiology of septic shock resulting
from Gram-negative bacterial infections.
Answer: -
Gram-negative infections often lead to rapid onset, life-threatening situations.
Endotoxins are released and these cause: -
 Factor XII activation
o Thrombin
o Fibrin
o Clot formation
o Fibrinolysis, which ultimately can lead to, disseminated intravascular
coagulation.
 Complement and mast cell activation
o Histamine release and production of kinins
o Reduction in systemic resistance and leakage of capillaries
o Hypotension
o Reduced renal blood flow leading to oliguria and renal failure.
 Release of myocardial depressant factors leading to high output cardiac failure
causing tissue hypoxia and lactic acidosis.
 Endothelial damage resulting in capillary leakage and acute respiratory distress
syndrome.
 Monocyte activation causing fever, and a hypermetabolic state.
 White blood cell activation.
 Free oxygen radical release.
 Arachidonic acid metabolites.
More recently the following substances have been implicated: -

 Cytokines
 Tumor necrosis factor
 Interleukins
Vol. I 88
Question No. 58
A 30 year-old man is admitted to the casualty department with acute head
injury. List the indications for intubation, ventilation, and referral to a
neurosurgical unit
Answer: -
Indications for intubation and ventilation after head injury *
 Immediate:
o Coma – not obeying commands, not speaking, not eye opening
o Loss of protective laryngeal reflexes
o Ventilatory insufficiency as judged by blood gases: hypoxemia (PaO 2<9kPa on
air, or < 13 kPa on oxygen); hypercarbia (PaCO2>6kPa)
o Spontaneous hyperventilation causing PaCO2<3.5 kPa
o Respiratory arrhythmia
 Before the start of the journey:
o Significantly deteriorating conscious level, even if not in coma
o Bilateral fractured mandible
o Copious bleeding into the mouth (example from a skull fracture)
o Seizures.
Criteria for neurosurgical referral of head-injured patients

 Without preliminary head CT:
o Coma persisting after resuscitation even without a skull fracture
o Deterioration in the level of consciousness of more than 2 Glasgow Coma Scale
points, or progressive neurological deficit
o Open or penetrating injury, depressed or basal skull fractures
o Tense fontanellae in a child
o If a CT is indicated but cannot be performed within a reasonable time (3 – 4
hours) in the general hospital
 After CT scan in a general hospital:
o Abnormal CT Scan (preferably after neurological opinion on electronically
transferred images)
o CT Scan normal, but patient’s progress unsatisfactory
* From the recommendations for the transfer of patients with acute head injuries to neurosurgical units. Association of Anaesthetist
of Great Britain and Ireland, December 1996.
Vol. I 89
Question No. 59
What is PEEP? Outline the indications for and list the complications of its
use.
Answer: -
PEEP stands for positive end expiratory pressure and is the application of a positive
airway pressure in the expiratory phase of ventilation. It is given in pressures of 2.5-20
cm H2O. Above this level it is called “Super PEEP”.
It minimizes airway and alveolar collapse and increases compliance by increasing

functional residual capacity. The net result, which is the indication for PEEP, is an
increase in patient oxygenation and a decrease in lung ventilation/perfusion mismatch.
It helps to provide increasing oxygenation of the patient without having to increase the
FiO2 and therapy runs the risk to the patient of oxygen toxicity. Therefore it is used
when the FiO2 is maximal to facilitate adequate oxygenation in a ventilated patient.
It has been suggested that PEEP can prevent air embolism and decrease blood loss but
these tenets are unproven.
Complications:
 Decreased cardiac output
 Oliguria
 Raised intracranial pressure
 Increased VD/VT (dead space to tidal volume ratio)
 Reversal of pulmonary hypoxic vasoconstriction
 Barotraumas (increased risk of pneumothorax)
Vol. I 90
Question No. 60
List the anaesthetic problems of severe, intractable epistaxis in elderly
patients.
Answer: -
Problems of anaesthetizing elderly patients_
 Altered volumes of distribution
 Lower minimum alveolar concentration (MAC) values
 Pre-existing disease
Problems relating to the pathophysiology of hypovolaemic shock in the

elderly
 Cardiovascular: the elderly tolerate hypovolaemia poorly. They are less able to vary
peripheral vascular resistance to maintain blood pressure. They need careful, expert
intravascular fluid replacement and probably central venous pressure monitoring.
They should be fully resuscitated prior to anaesthesia. Hypotension may exacerbate
angina. Care needs to be taken with intravascular fluid replacement as the elderly
patient can easily be tipped into left ventricular failure.
 Respiratory: the patient may have poor pulmonary reserve and decompensate in
response to V/Q mismatch due to hypovolaemia.
 Renal: the elderly patient may have poor reserve function, and acute tubular necrosis
after hypovolaemia can occur.
 Cerebral: confusion may be apparent.
 Hematological: the elderly may develop a transfusion coagulopathy or disseminated
intravascular coagulopathy (DIC), and require fresh frozen plasma, platelets, or
cryoprecipitate.
Problems relating to the epistaxis

 It is difficult to assess total blood loss since blood can be swallowed.
 Blood in the upper airway and stomach carries the risk of pulmonary aspiration. An
anaesthetic technique involving a rapid sequence induction is used.
 If packing and cauterizing the nose has failed, maxillary artery ligation may be
needed.
 Postoperative problems, depending on the size of blood loss, the frailty of the
patient, and the operation performed, may include high dependency care.
Vol. I 91
Question No. 61
What are the problems with monitoring a critically ill patient during an
ambulance journey to a neurosurgical unit? How may these problems be
overcome?
Answer: -
Problems
 Vehicle movement:
o Affects NIBP, ECG and Sao2
o May affect zeroing
o May dislodge monitoring devices
o Makes clinical assessment difficult and hazardous.
 Moving patient in an out of ambulance may require interruption of monitoring.
 Light may interfere with Sao2 problem or make screen difficult to view.
 Noise may obscure the noise of monitors or alarms.
 Limited space may make it difficult to see all the monitors together.
 Monitoring less sophisticated.
 Length of journey may be considerably longer than expected.
 Battery life.
Solutions
 Arrange for minimal monitoring requirements to be met-clinical observation and
technical monitoring includes NIBP, ECG, oximetry, and capnography.
 Check your equipment and monitors for life of batteries and spare batteries.
 Ensure that you are happy with the “set up” on your unit before leaving. Your
equipment should be attached and working and you should have formulated a plan
for all stages of the transfer.
 Transfer into the ambulance check the patient’s condition, do baseline observations
and ensure monitoring is functioning properly. Find out where you sitting and check
that you can see all the monitors from that position. It is preferable to insist on a seat
where you can easily reach your patient’s body and giving sets. Pull all window blinds
down to minimize external light. Tape Sao 2 probes to the finger and try to keep NIBP
cuffs isolated from any potentially vibration solid objects, such as cot sides, that may
create artifact.
 Negotiate with your ambulance driver the optimum speed for the transfer._
 Be vigilant throughout the journey. Observe the patient’s clinical condition and
regularly record the observations on a chart. Monitor the state of your monitors – do
they need a battery change?
 At the receiving hospital the same rules apply. Check that your monitoring is
functioning properly before leaving the ambulance.
Vol. I 92
Question No. 62
Describe the precautions you would take when inserting a chest drain for a
non-tension pneumothorax into a 40 year-old female patient known to
hepatitis B carrier e-antigen positive.
Answer: -
This patient has high concentration of virus in her blood. Anaesthetist and other
healthcare workers are therefore at risk of occupational infection through contact with
infected blood and bloodstained fluids. This may occur through needle stick and other
sharps injury, or through cuts and abrasions in the skin of these individuals.
Precautions must be taken to protect not only staff, but also other patients.
 Anyone undertaking or assisting at an exposure-prone procedure must be
immunized against hepatitis B virus and known their immune status.
 The procedure must be undertaken in disposable gowns, gloves, masks, visors and
overshoes.
 Equipment in the room must be kept to bare minimum.
 Disposable equipment must be used where possible.
 Needles, which have been in contact with the patient, should not be resheathed or
handed to another person. They should be placed either in a tray or directly into a
sharps bin.
 All sharps and other equipment must be carefully disposed of in appropriate bins.
 Contaminated material including clothing should be sealed in bags and labeled as
infective.
 All non-disposable contaminated equipment should be autoclaved. Where this is not
possible the equipment should be thoroughly washed with detergent and water and
left to soak in fresh 2 % glutaraldehyde solution or hypochlorite.
 Floors and surfaces contaminated with blood should be washed with a solution of
hypochlorite and then with detergent and water.
Vol. I 93
Question No. 63
List the benefits and problems of the drugs available for sedation of
patients on the intensive care unit. What are the indications for muscle
relaxation in this setting?
Answer: -
Sedatives
The five commonly used sedative drugs are analyzed below: -
Propofol
 Benefits: short half-life, no accumulation.
 Problems: hypotension, hyperlipidaemia (pediatrics), and product license, cost.
Midazolam
 Benefits: rapid onset of action, short half-life of the drug and its α-hydroxyl
metabolite, reversal agent available (flumazenil), cheap.
 Problems: cardiovascular depression, action may be prolonged in the critically ill.
Morphine
 Benefits: cheap, antitussive, reversal agent (naloxone) available, analgesia.
 Problems: slow onset of action, accumulation of morphine and morphine-6-
glucuronide (a high active metabolite) if renal function is impaired, antitussive,
delayed gastric emptying and reduced intestinal motility, tolerance.
Alfentanil
 Benefits: reversal agent (naloxone) available
 Problems: accumulation may occur if hepatic function is impaired.
Ketamine
 Benefits: raised arterial blood pressure, bronchodilator, and analgesia.
 Problems: raises intracranial and intraocular pressure, may produce hallucinations.
Indications for the use of muscle relaxants

The routine use of muscle relaxants is not advocated because of awareness and the
obvious dangers of airway disconnection. The indications include: -
 To facilitate intubation
 To aid ventilation in, for example fighting the ventilator which causes complications
such as pneumothorax
 To allow the use of certain modes of ventilation, for example pressure controlled
ventilation
 In severe hypoxia or hypercapnia
 Raised ICP
 Tetanus
Vol. I 94
Question No. 64
Outline the causes of hypoxemia in the first 24 hours following surgery.
How may its occurrence be minimized?
Answer: -
Causes of hypoxemia
 Low inspired oxygen concentration
o Depleted oxygen supply; delivery system disconnection.
 Hypoventilation
o Airway obstruction; central depression from anaesthetic drugs and opioids;
residual neuromuscular blockade; sleep apnoea; lack of respiratory drive; pain;
diaphragmatic splinting; pneumothorax.
 Diffusion hypoxia
o Usually observed as the patient is emerging from an anaesthetic where nitrous
oxide is a component; rapid outpouring of insoluble nitrous oxide can displace
alveolar oxygen, resulting in hypoxia.
 Ventilation/perfusion mis-match and shunt
o Atelectasis; bronchial intubation; pneumonia; bronchospasm; mucus plugging;
pulmonary oedema; pulmonary aspiration; pulmonary embolism.
 Reduction in cardiac output/oxygen carrying capacity
 Increased oxygen consumption – shivering
 Diffusion impairment
o Pulmonary fibrosis, pulmonary oedema; ARDS.
Prevention
Direct prevention at the cause.
 Give chest physiotherapy for at risk groups, for example elderly, obese, bronchitis
patients, smokers.
 Administer 100 % oxygen on cessation of anaesthesia
 Optimize oxygen delivery – treat anaemia; improve cardiac output.
 Provide adequate pain control
 Optimize ventilation – perfusion relationships (CPAP, PEEP, IPPV).
Describe oxygen consumption from shivering.
Vol. I 95
Question No. 65
Describe the different waves that can be seen in a central venous pressure
trace. Give examples of disease that can alter these waves.
Answer: -
A typical central venous pressure (CVP) waveform in health would appear like this: -
c
v
a
Y descent
X descent
Diastole Systole Diastole
The “a” wave is a positive deflection caused by arterial contraction.
The “c” wave represents the initial bulging of the tricuspid valve into the atrium with the
onset of ventricular contraction and the sharp increase in ventricular pressure. The
adjacent pulse of the carotid artery also makes a contribution, hence the name “c” wave.
The “x” descent follows as the atrium relaxes and the tricuspid valve is pulled downward
during ventricular contraction.
The “v” wave is a positive deflection that occurs as blood accumulates in the vena cava
and right atrium whilst the tricuspid valve is closed.
The “y” descent results from opening of the tricuspid valve and the start of right
ventricular filling.
The waves of the CVP trace may alter in disease as follows: -

 The “a” wave is absent from CVP traces in patients with atrial fibrillation. This is due
to ineffective atrial contraction.
 Large “a” wave amplitude is seen when the atrium contracts against an increased
resistance. This occurs in tricuspid stenosis, decreased right ventricular compliance,
and increased right ventricular pressure from an increased afterload, such as in
pulmonary valve stenosis or pulmonary hypertension.
Vol. I 96
 Giant “a” waves or “cannon” waves occur when the atrium contracts against a closed
tricuspid valve. This occurs with cardiac dysrhythmias when the atrial and
ventricular contractions are not synchronous, such as with nodal or ventricular
arrhythmia or complete heart block.
 Absence of an “x” descent with a large c-v wave is seen in tricuspid regurgitation
from valve incompetence. This is caused by pressure in the right atrium rising
caused by regurgitation of the blood during ventricular contraction.
 Hypovolaemia may change mean CVP measurement and dampen its trace, but does
not specifically alter the shape of its waveforms.
Vol. I 97
Question No. 66
Briefly describe the physical principles involved in pulse oximetry.
Answer: -
Oximetry utilizes the different absorption coefficients of different wavelengths of light
by oxyhaemoglobin (oxy-Hb) and reduced-haemoglobin (reduced-Hb) to measure
oxygen saturation, as in the figure below.
Absorption coefficient
10.00
(long scale)
1.00
Oxy-Hb
0.10
Reduced-Hb
0.01
600 660 805 940 1000
Wavelength (nm)
At 660 nm wavelength (red light) reduced-Hb exhibits absorption approximately 10

times that of oxy-Hb while at 940 nm wavelength (near infrared light) oxy-Hb exhibits
the higher absorption. At 805 nm wavelength both reduced-Hb and oxy-Hb have similar
absorption coefficients. Pulse oximetery operates with two alternating light-emitting
diodes and one sensing photodiode placed on opposite sides of a digit or any other
suitable part of the body. It uses the isolation and processing of the pulsatile part of the
signal of light absorption to verify the arterial component of oxygen saturation, as in the
figure below.
Vol. I 98
Pulsatile
Arterial
Light absorption
Venous
Non-pulsatile
Tissue
The electric algorithm used in the substantial sophisticated signal processing is

simplified by the equation: -
X = (P660 / P940) / (NP660 / NP940)
Where X is the arterial oxygen saturation, P is the pulsatile component of the absorption
coefficient, and NP is the non-pulsatile component of the coefficient.
Vol. I 99
Question No. 67
List the complications that may be encountered when a pulmonary artery
flotation catheter is inserted into the left subclavian vein via the
infraclavicular route. Choose two complications and describe what
precautions you would take to minimize their risk.
Answer: -
1. Complications associated with cannulating the left subclavian vein are: -
 Pneumothorax
 Subclavian artery puncture with possible haemothorax
 Misplaced catheter
 Damage to the thoracic duct with possible chylothorax
 Air embolism
 Infection
2. Complications associated with insertion of a pulmonary artery flotation catheter

(PAFC) are: -
 Arrhythmias
 Knots in the catheter
 Pulmonary artery rupture
 Pulmonary infarction.
Precautions for two complications are outlined below.

 Air embolism can be avoided. A sufficient degree of head-down, Trendelenberg
position should ensure filling of the subclavian vein with blood. All lines and
connections should be flushed with normal saline and any ports should have bungs
attached. The PAFC balloon should be checked to see that it is intact before the
catheter is inserted. The 2 ml of air are unimportant in most adults but may be
significant if the patient bas an undetected right-to-left cardiac shunt.
 Optimizing medication and electrolyte balance before the procedure is begun can
minimize arrhythmias. Through out PAFC insertion, one person should watch the
ECG monitor. Certain points along the catheter’s journey may be particularly
arrhythmogenic. If these areas are encountered it is usually prudent to withdraw the
catheter and try again once the arrhythmia has resolved. It may be possible to pass
quickly through the arrhythmogenic area. Either way, it is inadvisable to leave the
catheter tip sited at the arrhythmogenic area itself.
Vol. I 100
Question No. 68
Briefly describe the physical principles involved in Capnography.
Answer: -
Capnography is the continuous measurement of carbon dioxide concentration in the
expired gases. The widely used method of measurement in clinical Capnography is
absorption spectrophotometry with infrared light and operates on the principle that the
concentration of CO2 can be determined by passing infrared light of a particular
wavelength (approximately 4.3 micrometre) through a very small amount of expired
gas. The CO2 then absorbs the infrared light in proportion to its concentration. The
figure below shows the set-up:
Sample
Detectors s
Light
Infrared filter Beam splitter Control
The absorption of infrared light is dependent upon the molecules of the gas being
polyatomic and asymmetric, therefore N 2O and water vapor are two examples of gases
that can interfere with the meaurement of CO2 as in the figure overleaf:
Corrections for N2O interference can be programmed into the capnogram by
incorporating an additional wave length of light to measure the concentration of N 2O
independently. Single- atom gases such as H2 H, and Ar, or gases with symmetric
molecules like N2and O2 do not absorb infrared light and therefore do not interfere with
this measurement.
CO2(4.3μm)
N2O
H2O
Absorption
Vol. I 101
. . .
3 4 5
Wavelength (μm)
Question No. 69
A 50-year-old man with symptomatic esophageal reflux presents for an
elective incisional hernia repair. You decide to do a rapid sequence
induction with pre-oxygenation & cricoid pressure:-
1. List three pre-operative methods to reduce the acid content of his
stomach. List two factors that may delay empting of the stomach?
2. What decision concerning laryngoscopy should you make before
starting induction?
3. At laryngoscopy you cannot see the epiglottis. What Cormack &
Lehan grade of laryngoscopy is this? If you do not manage to
intubate the trachea list briefly the first four stages of your failed
intubation drill?
4. If you have managed to intubate the trachea, list three features
during the operation that make you suspect the patient had
aspirated gastric contents?
Answer: -
1. “The minimum gastric content in humans that may result in aspiration pneumonitis
is 25 ml (0.4 ml/kg) of pH < 2.5” provide the basis for prophylaxis for aspiration
pneumonitis. The pH value bears scrutiny but the volume value is overcautious.
These levels are exceeded by up to 60 % of all patients. The incidence of aspiration
pneumonitis is of the order 0.1-0.01 %. Food can cause airway obstruction and
should be restricted for 6 h pre-operatively do not increase gastric content.
Cisapride, metoclopramide and nasogastric aspiration reduce gastric volume. Gastric
acid production is normally 1 ml/kg/h. Production is reduced by omeprazole, which
inhibits the hydrogen-potassium-ATP pump (proton pump) and H 2 receptor
antagonists, e.g. ranitidine or cimetidine. These should be given from 6 h pre-
operatively as they only stop production of acid and time must be allowed for
emptying of any acid already present. Mist.Mag.Trilil. is not used as it particulate
and can itself cause aspiration pneumonitis. Causes of delayed stomach emptying
include trauma, pain, autonomic neuropathy (e.g. diabetes mellitus), labour, opiates,
achalasia, pyloric stenosis, small bowel obstruction, ileus and peritonitis. No method
reduces the gastric acidity and volume to a level that guarantees 100 % safety from
aspiration pneumonitis.
2. You should have already decided what management you would take if you could not
intubate the trachea. If you are suddenly in a situation of a failed intubation you will
not have the time to ponder over what to do next. You should have a management
scheme already decided; e.g. for a Caesarean section whether you will wake up the
mother and do a regional technique or an awake fibreoptic intubation, or continue
the anaesthetic with a mask and spontaneous breathing.
3. Cormack and Lahane Grade 4. The first part of the failed intubation drill is to make
the conscious decision that you cannot intubate the patient. The following steps
should then be taken: -
 Give 100 % oxygen and call for help;
 Maintain cricoid pressure and turn the patient head down into the lateral
position;
Vol. I 102
 Maintain airway patency (+_ oropharyngeal airway) and apply gentle IPPV to
maintain oxygen saturation;
 Allow the patient to wake up and breathe spontaneously.
The problems and controversy occur when one cannot maintain the airway and the
patient becomes cyanosed. Alternatives then include: -
 Removing cricoid pressure;
 Nasopharyngeal or laryngeal mask airway;
 Turning the patient supine which may make airway control more familiar and
easier;
 Cricothyroid puncture, cricothyrotomy;
 Oesophageal obturator airway.
4. Features which suggest aspiration include: -

 Visual presence of acid in the pharynx or on suction of the endotracheal tube
(use litmus paper to check pH);
 Difficulty in ventilation if solids aspirated;
 Presence of shunt, recognized by decreased saturations or PaO 2 despite an
increased inspired oxygen concentration;
 Presence of wheezes or coarse crepitations generally localized to the right
lower lobe (may present as bronchospasm).
Vol. I 103
Question No. 70
A patient who is 1.7 m tall and weighs 130 kg presents for elective open
cholecystectomy.
1. (a) Define body mass index.
1. (b) What is this patient’s body mass index?
1. (c) Classify obesity based on body mass indeed?
2. What are the medical complications of severe obesity?

3. List the causes for pulmonary dysfunction in the severely obese
patient.
4. List the problems the anaesthetist may encounter when
administering general anaesthesia to this patient.
Answer: -
1. (a) Body Mass Index = Weight [kg] divided by Height2 [m2].
(b) This patient’s BMI = 44.98
(c) Obesity can be classified on the basis of Body Mass Index as follows: -
Underweight < 20
Normal 20 – 25
Overweight 25 – 30
Obese 30 – 40
Severely obese > 40
2. Medical complications include: -

 Sudden death;
 Pickwickian syndrome comprising hyper-somnolence, daytime hypoventilation,
hypercapnia, hypoxia, polycythemia and corpulmonale;
 Congestive cardiac failure;
 Association with hypertension/diabetes mellitus/hyperlipidaemia;
 Nephritic syndrome/renal vein thrombosis;
 Obstructive sleep apnoea;
 Immobility which restricts normal daily activities/psychosocial problems.
3. Functional residual capacity (FRC) is decreased due to the decrease in chest wall
compliance caused by truncal obesity. The reduced FRC may fall within the closing
capacity range in the upright position resulting in ventilation perfusion mismatching
or right-to-left shunting, both of which will result in arterial hypoxemia. The
decreased chest wall compliance, in conjunction with the need to increase minute
ventilation in order to maintain normocapnia, increases the work and oxygen cost of
breathing. The increase in BMI also increases oxygen consumption.
Despite a low PaO2 many obese patients can sustain an adequate minute ventilation
which maintains normocapnia. With increasing obesity and age, some patients
become unable to maintain normocapnia. As the PCO 2 rises, they become reliant on
the hypoxic ventilatory drive.
Vol. I 104
4. Transporting and positioning of patient on operating table: For elective procedures it

is probably easier for the patient to walk to theatre than be transported on a trolley;
it may be necessary to use two tables. Asking the patient to position himself on the
table minimizes the need for lifting. Appropriate padding and protection of pressure
points is important; both tables must be adjusted simultaneously when changing
table position.
Induction: Venous access may be difficult. Gastro-oesophageal reflux is common, so

premedication with H2-blockers is prudent. Awake intubation or a controlled rapid
sequence induction may be necessary. Airway control and tracheal intubation may
be difficult.
Maintenance: Direct blood pressure measurement may be preferred (a cuff of

appropriate size is needed for NIBP measurement). Serial arterial blood gases,
airway pressure and end tidal CO2 measurement will yield useful information intra-
operatively. Intra-operative hypoxia is not uncommon and a minimum FIO 2 of 0.5
must be used. Haemodynamic swings are poorly tolerated and PCWP monitoring
may be necessary, particularly in patients with the Pickwickian syndrome.
Pneumatic compression leggings will minimize the risk of DVT.
Recovery: May be prolonged due to altered drug handling, increased sequestering of

lipid soluble agents and residual neuromuscular blockade. Post-operative respiratory
depression and hypoxia are common and severely obese patients are best managed
in an ITU/HDU after surgery.
Vol. I 105
Question No. 71
You are asked to anaesthetize a 5-year-old boy who is still bleeding on the
ward following a tonsillectomy three hours earlier.
1. Estimate his weight, blood volume and likely blood loss.
2. List three signs in this patient that may suggest hypovolaemia.
Why may this assessment by difficult?
3. List two problems complicating induction.
4. List two methods of induction of anaesthesia and a disadvantage of
each.
Answer: -
1. Rules of thumb regarding children include: -
 Birth weight (3.5 kg) doubles by 5 months (7 kg) and trebles (10.5 kg) by a year;
 1 – 10 years: weight (kg) = 2 (age + 4);
 Estimated blood volume is:
80 – 90 ml/kg from 0 to 3 months;
75 – 80 ml/kg from 3 to 12 months;
70 – 75 ml/kg from 12 months;
i.e. an estimated weight of 18 - 20 kg and a blood volume of 1.3 to 1.5 L. up to 40% of
children having tonsillectomies lose 10 % of their estimated blood volume. If the
child is still bleeding three hours later he will have lost more than this 10 % (130 ml)
and will need a blood transfusion. He should be given oxygen and one unit of blood
should be cross-matched urgently. He should be resuscitated fully before the
induction of anaesthesia.
2. Children tend to swallow the blood so the amount visible is not a good indicator of
the total amount lost. Initially they compensate well and changes in blood pressure
and heart rate may be small. The average systolic blood pressure in children is about
80 + (2 x age) in mmHg. Poor perfusion is indicated by cold, pale, cyanosed or
mottled peripheries with constricted veins and no return of capillary flush within two
seconds. Tachypnea may occur due to increasing catecholamines. The maximum
respiratory rate per minute is 40 at 1 month, 25 at 1 year and 20 at 5 years. Agitation
or drowsiness may occur but the effects of the previous anaesthetic may mask all
these signs.
3. There are three main problems at induction: hypovolaemia, a full stomach and
difficult intubation. Hypovolaemia causes difficulty with venous access and
cardiovascular instability on induction. This is complicated by the presence of
residual anaesthetic so no premedication is given and the induction dose should be
reduced. Swallowed blood in the stomach may be aspirated or complicate intubation.
Intubation may be difficult in the presence of blood clots in the pharynx and a
swollen laryngopharynx from the previous surgery and intubation.
4. An experienced anaesthetist should be present due to the risks mentioned and the
quick onset of cyanosis in children. Included in the standard equipment are two
large bore suckers, two laryngoscopes and a range of tracheal tubes. The two main
methods of induction are:
Vol. I 106
a. Pre-oxygenation and a rapid sequence intravenous induction using cricoid

pressure and suxamethonium. The advantages include familiarity with the
technique and rapid securing the airway. The disadvantage is the potential for
losing the airway when the child is not breathing spontaneously. If the
anaesthetist is unable to intubate the child, ventilation by a mask may be difficult
due to the presence of airway oedema and clot.
b. A gaseous induction with halothane and oxygen in the left lateral head down
position. When anaesthesia is deep enough to allow suction of blood the airway is
assessed by laryngoscopy. The child may be intubated on its side or cricoid
pressure applied, the patient turned supine and then intubated. The main
advantage is maintenance of the airway at all times. Disadvantages include the
cardiovascular depression with halothane (more common than when this
technique was used with ether), the slow induction if the airway is narrowed, the
risk of laryngospasm if intubated too early and the difficulty of intubating the
child in the left lateral position which is not a technique familiar to many
anaesthetist.
After securing the airway a wide bore gastric tube should be placed and aspirated.
Awake extubation should be performed in the left lateral head down position.
Vol. I 107
Question No. 72
You are called to the recovery ward to see a cyanosed patient. She has a
thyroidectomy incision and is starting to twitch.
1. What is the first thing you would do?
2. List four causes specific to this patient which could account for her
cyanosis.
3. Why may she be twitching?
4. What two signs would you look for to confirm this?
5. What is the treatment?
Answer: -
1. Clear the airway and give 100 % oxygen.
2. Methylene blue is used to identify the parathyroid glands at surgery and will cause
cyanosis but no dyspnoea or agitation. Haemorrhage into the wound is a medical
emergency-causing blockage of the airway and needs to be recognized and dealt with
immediately. The wound sutures or clips are removed and the clot evacuated.
Damage to the recurrent or superior laryngeal nerves can occur during surgery and
post-operatively the presence of damaged tissue and locally released potassium can
impair their function. Unilateral recurrent laryngeal nerve palsy cause stridor but
bilateral damage leads to complete airway obstruction. Partial obstruction can occur
due to laryngeal mucosal oedema secondary to venous congestion but this usually
presents the following day. Very rarely, tracheal collapse occurs due to removal of
supporting tissue during the thyroidectomy. Removal of thyroid tissue may result in
hypocalcaemia and tetany. Excess thyroxine causes osteoporosis and the sudden
reduction in thyroxine may cause a massive uptake of calcium into the skeletal
system. If parathyroidectomy is carried out or the parathyroid glands are damaged
during thyroidectomy may also cause tetany but this usually occurs two or three days
later. Tetany of the vocal cords can cause obstruction. Thyroid storm is discussed
below and can cause cyanosis due to the high oxygen utilization. Thyrotoxicosis may
present as cardiac failure although this should have been controlled before surgery.
3. Hypocalcaemic tetany.
4. Trousseau’s sign: a blood pressure cuff inflated above systolic blood pressure for two
minutes will exacerbate latent tetany and produce carpopedal spasm.
Chvostek’s sign: tapping the facial nerve at the facial notch in the mandible
precipitates. The QT interval may be prolonged.
5. Intravenous calcium gluconate.
Notes on thyrotoxic crisis (thyroid storm)
This is caused by an excessive release of thyroid hormones into the circulation resulting
in sudden increase in metabolic rate. It may be precipitated by any acute medical or
surgical event or trauma. It has a mortality of 20 %. It may present as pyrexia,
tachypnea, tachycardia, arrhythmias, nausea, vomiting, delirium or coma. Oxygen
consumption rises and pulmonary oedema can occur so the patient may be cyanosed
despite oxygen therapy. The differential diagnosis includes sepsis, phaeochromocytoma
Vol. I 108
and malignant hyperthermia. The diagnosis is clinical as thyroid function tests are too
slow and will not distinguish between thyroid storm and thyrotoxicosis. The initial
management is treatment of the initial cause and oxygen, intravenous fluids and drugs.
β-blockers will reduce the catecholamine-mediated symptoms but should be used
carefully if there is cardiac failure or asthma. Thiouracils will decrease the synthesis of
thyroxine in the thyroid gland and can be given orally or by nasogastric tube. Iodine will
inhibit the release of thyroid hormones and steroids will stop the peripheral
transformation of thyroxine to tri-iodothyronine. Tepid sponging and antipyretics may
be necessary if the pyrexia does not settle. Dantrolene has been used.
Vol. I 109
Question No. 73
Discuss the problems of general anaesthesia in a morbidly obese patient.
Answer: -
The problems of general anaesthesia in such a patient are the result of: -
 Pathophysiological changes
 Concurrent disorders
 Alterations in drug metabolism
 Physical effects of morbid obesity
Preparative problems
 Cardiovascular derangements: cardiac output and blood volume are increased;
systemic hypertension is common; pulmonary hypertension is present in
Pickwickian patients; left and right ventricular hypertrophy and biventricular failure;
higher incidence of ischemic heart disease.
 Respiratory changes: obesity is accompanied by hypoxemia due to increased oxygen
consumption, reduced pulmonary compliance, increased work of breathing,
decreased FRC, ventilation-perfusion mismatch.
 Gastrointestinal derangements: higher incidence of gastro-oesophageal reflux and
hiatus hernia; increased risk of pulmonary aspiration.
 Associated conditions: endocrine disorders, obstructive sleep apnoea, Pickwickian
syndrome.
Intraoperative problems
The following are often difficult: -
 Veins to find and cannulate.
 Airway maintenance with facemask; tracheal intubation – short neck, large breasts,
rapid sequence induction.
 Blood pressure measurement.
 Lifting and positioning.
 Surgical access.
 Regional techniques
 Drugs: lipophylic drugs such as opioids, benzodiazepines, and barbiturate have an
increased volume of distribution and decreased elimination half-life (exception
fentanyl); obesity increases the biotransformation rate of enflurane and halothane
resulting in increased serum levels of fluoride ions; neuromuscular blocking agents
should be given according to lean body weight.
Postoperative problems
 Atelectasis and hypoventilation are common with increased risk of hypoxemia,
infection and respiratory failure; elective IPPV may be required.
 Increased incidence of DVT: subcutaneous heparin and early ambulation required.
 Good pain control important for both improved pulmonary function and early
ambulation.
 Wound dehiscence.
Vol. I 110
Question No. 74
What are the main objectives of care in the recovery unit? List the main
criteria for discharge of a patient from the recovery unit.
Answer: -
Specialized recovery staff care for the patient ideally on a one-to-one basis after
anaesthesia but the overall responsibility of patient care remains with the anaesthetist.
The objectives of care are as follows: -
 Management of the airway.
 Assessment and management of the unconscious patient.
 Pain relief management, including the management of epidural devices.
 Observation of the patient.
 Clinical and technical monitoring as indicated – non-invasive blood pressure
measurement, pulse, temperature, and oximetry are mandatory; however, in more
complex cases, invasive monitoring is necessary.
 Management of shivering.
 Management of hypothermia.
 Management of nausea and vomiting.
 Care of intravenous infusions.
 Oxygen therapy.
 Observation of urine output.
 Observation of surgical wounds.
The discharge criteria include: -

 Awake patient.
 Patient responds appropriately to commands.
 Patent upper airway.
 Airway reflexes present.
 Satisfactory respiration.
 Cardiovascular stability.
 Control of vomiting.
 Adequate pain control.
Vol. I 111
Question No. 75
Outline the advantages and disadvantages of performing a transurethral
resection of the prostate (TURP) using regional anaesthesia rather than
general anaesthesia.
Answer: -
Advantages of regional anaesthesia
 Allows early warning of acute H2O intoxication (TUR syndrome).
 Reduced blood loss.
 Good postoperative analgesia.
 No mental confusion and earlier recovery.
 Avoidance of respiratory failure in patients with chronic obstructive airways disease.
 Avoidance of pulmonary complications in patients with chronic pulmonary
disorders.
 Reduced incidence of deep vein thrombosis.
Disadvantages of regional anaesthesia

 Not all patients accept being awake during surgery.
 Patient co-operation is important for success and therefore not suitable if patient is
unable to lie still.
 Contraindications exist-absolute and relative:
o Local sepsis
o Disorders of haemostasis
o Fixed cardiac output
o Gross spinal deformities
 Complications may occur:
o Immediate: hypotension, bradycardia, total spinal, intravascular injection of local
anaesthetic
o Late: arachnoiditis, meningitis, epidural haematoma, epidural abscess, spinal
artery syndrome.
Vol. I 112
Question No. 76
Write notes on the prophylactic measures that may be used to prevent
stress ulcers in patients on the ITU. What are the advantages and
disadvantages of these methods?
Answer: -
Feeding
Controversy exists as to how feeding helps to reduce stress ulcers. Intra-luminal feeding
may act as a buffer or provide nutrients to the mucosal wall and therefore help it to
function more effectively as a barrier. Cannot always be used as there may be a
contraindication to feeding.
Sucralfate
An aluminium salt of sucrose sulphate that acts as a cytoprotective agent probably by a
local action that improves mucosal blood flow. The integrity of the mucosal barrier is
maintained without altering pH. It is cheap and has a very low toxicity. May produce
hypophosphataemia as the aluminium chelates phosphate in the gut.
Antacids
Often very difficult to titrate the amount of antacid required to produce the desired rise
in pH. Stops the antimicrobial action of low gastric pH.
H2-antagonists
More effective at consistently raising gastric pH than antacids. Stops the antimicrobial
action of low gastric pH. Relatively expensive. Cimetidine is not commonly used because
of its action as a hepatic enzyme inhibitor and its tendency to accumulate if renal
function is impaired.
Optimize splanchnic perfusion

Ensuring optimal perfusion pressures and oxygen delivery to the splanchnic bed is very
important in the prevention of mucosal injury. Most attempts at monitoring perfusion,
such as tonometFVGry, are as yet of unproven value.
Vol. I 113
Question No. 77
Briefly describe the possible techniques of anaesthetizing the larynx for
awake fibreoptic intubation.
Answer: -
There are 3 different techniques: -
1. Transtracheal injection of local anaesthetic: Draw 3 ml of lignocaine 4 % in a 5 ml
syringe and attach to a 22 G hypodermic needle. Wipe the area of the cricothyroid
membrane with antiseptic. Feel the gap between the thyroid and cricoid cartilages
and insert the needle in the mid-line and perpendicular to the skin. A sudden give
way (pop) at a depth of 1 – 2 cm with aspiration of air confirms the placement of the
needle in the trachea. Inject and pull the needle out rapidly as this is followed
immediately by a violent cough. The cough is useful in spreading the local
anaesthetic in the trachea and up to the larynx.
2. Superior laryngeal nerve block: Draw 5 ml of lignocaine 1 % in a 5 ml syringe. Clean
with antiseptic the skin overlaying the hyoid bone on each side of the neck. Start on
one side. Insert a 22 G needle perpendicular to the skin and 0.5 cm caudad to the
cornu of the hyoid bone. Advance 0.5 – 1 cm, aspirate to exclude intravascular
placement of the needle, and infiltrate 2.5 ml. Repeat the same technique on the
other side injecting the other 2.5 ml.
3. Topical anaesthesia or “spray as you go” technique: A minimum of 4 ml anhydrous
lignocaine 4 % solution or 10 doses from the 10 % lignocaine spray pump may be
used to spray the larynx. Alternatively, 2 – 4 ml of 4 % lignocaine may be injected
through the suction channel of the fibrescope as soon as the glottis comes to view
and before entering the larynx.
Vol. I 114
Question No. 78
What factors should be considered in the pre-operative preparation of a 4
year-old child presenting for correction of a squint?
Answer: -
Considerations for squint correction
 Possible association with other conditions, for example Cruzan’s and Apert’s
syndromes or malignant hyperthermia.
 Need for psychological preparation. Addressing and allaying parental concerns are
important in establishing the trust and confidence of the concerns are important in
establishing the trust and confidence of the child. Contact between the child and
anaesthetist before anaesthesia positively effects the quality of induction and overall
experience of the child.
 Need for pharmacological premedication.
 Parental presence at induction.
 Suitability of procedure and child for day-case surgery. Several factors have allowed
day-case squint correction to be performed with a very low incidence of
postoperative morbidity-availability of EMLA cream, propofol, and the reinforced
laryngeal mask airway, which alleviates the need for endotracheal intubation and
muscle relaxation. Suitability for day surgery depends on ASA status (1 or 2), home,
and social circumstances. The preoperative preparation should include the
following:-
o A written and verbal explanation to the parents about the surgical procedure,
preparations to be made, the postoperative course and their involvement in the
care of the child;
o An explanation to the child appropriate to child’s ability to understand;
o A pre-admission programme using play simulation, photographs, videos etc;
o Information about fasting requirements.
 Possible intra-operative problems in relation to this operation. Oculocardiac reflex-

elicited by surgeon when applying traction to the extraocular muscles especially the
medial rectus and lateral rectus. Usually causes bradycardia but occasionally other
arrhythmias. Prophylactic measures such as intravenous atropine 20 micrograms/kg
or glycopyrrolate 10 micrograms/kg are required at induction.
Vol. I 115
Question No. 79
Outline the preoperative assessment of a patient who requires a partial
thyroidectomy. What early complications may result from this operation?
Answer: -
General assessment
The same as for any patient having general anaesthesia.
Specific assessment
To elucidate thyroid status and possible upper airway obstruction: -
 Thyroid function: assessed clinically and by laboratory investigations. If patient has
hyperthyroidism check cardiovascular and neurological aspects; tachycardia, atrial
fibrillation and congestive cardiac failure will need controlling in order to prevent
thyroid crisis. Other features to look for are exophthalmos, myopathy, and diabetes
mellitus. Investigations include plasma thyroxine and tri-iodothyronine, TSH, ECG,
Hb.
 Airway:
o Clinical evidence of upper airway obstruction.
o Chest X-ray including thoracic inlet views to assess tracheal compression,
deviation and retrosternal extension.
o Indirect laryngoscopy to assess vocal cords function in case of pre-existing
damage to laryngeal nerves.
 Presence of other autoimmune disease: for example myasthenia gravis.
 Presence of superior vena caval obstruction: from a retrosternal goiter.
 Mediation: what drug?
o Antithyroid drugs: for example carbimazole; this increases the vascularity of the
gland and needs to be stopped two weeks before surgery.
o Iodine: this is sometimes given two weeks before surgery to reduce glandular
vascularity.
o Beta: adrenergic receptor antagonists.
Complications
 Intraoperatively
o Tracheal intubation may be difficult
o Arrhythmias may occur from stimulation of carotid sinus
o Air embolism
o Pneumothorax.
 Postoperatively
o Bleeding
o Airway obstruction from expanding haematoma tracheomalacia, damage to
laryngeal nerves
o Hypocalcaemia and tetany
o Thyroid crisis
Vol. I 116
Question No. 80
Outline the methods of providing postoperative analgesia for a patient who
has had a thoracotomy.
Answer: -
Postoperative pain is influenced by many factors including age, sex, social class, anxiety,
attitudes of staff, and other patients, and includes the nature of the surgery and the type
of anaesthesia. It is imperative in surgery such as a thoracotomy to minimize potentially
fatal chest complications by providing excellent postoperative analgesia.
The preoperative visit, explanation and discussion of the techniques available is
invaluable in terms of future management.
Premedication with opiates and non-steroidal anti-inflammatory drugs may provide
some postoperative analgesia.
Systemic drugs similar to those used in the premedication can be given via the oral,
intramuscular, intravenous, subcutaneous, or the rectal routes. The mode of
administration can be patient – or medical staff – controlled, and the drugs can be given
via intermittent or continuous methods. Intravenous morphine PCA pumps or
subcutaneous morphine infusions have been used successfully using these techniques.
Regional anaesthetic technique using “low dose local anaesthetic and opiate” epidural
techniques especially in the thoracic region are now successfully employed. Intercostal
nerve blocks and wound infiltration have also been used. Intrapleural nerve blocks are
also being evaluated as a method of analgesia after this type of surgery.
Miscellaneous techniques with cryotherapy, Entonox, acupuncture, and transcutaneous

nerve stimulators have also been tried but have not been found to enhance analgesia in
the immediate postoperative period.
The benefits and the side effects of the techniques must be considered. The most
common technique in current practice is thoracic epidural analgesia but this has side
effects including technical difficulties and drug administration problems, such as
hypotension, high block, drowsiness, respiratory depression, and itch. However, this
technique provides excellent analgesia, which allows for the provision of good
postoperative physiotherapy.
Follow-up and constant evaluation of the chosen technique must occur.
Vol. I 117
Question No. 81
List all the possible factors that may contribute to postoperative nausea and
vomiting.
Answer: -
The factors contributing to postoperative nausea and vomiting (PONV) may be classified
as relating to the patient, the anaesthetic technique, or the type of surgery.
Patient
 History of previous PONV
 History of motion sickness
 Female – particularly when the surgery is during the ovulation phase of the
menstrual cycle
 Pregnant women
 Lower in infants and small children and lower in elderly patients.
Anaesthesia
 Fasting. Infusion of intravenous fluids reduces the incidence of PONV.
 Inflation of stomach with air such as during incorrect or difficult mask ventilation.
 Choice of intravenous anaesthetic. Etomidate and ketamine are known to cause
PONV. Propofol causes the least PONV. It has been suggested that it has antiemetic
effects.
 Choice of inhalation anaesthetic. Ether, which is not used today in the developed
countries, is very emetic. The currently used inhalational anesthetics are not
particularly emetic, but when compared to total intravenous anaesthesia they do
have a higher incidence or PONV. The use of N 2O is thought to be associated with an
increase in the incidence of PONV.
 The use of opioid analgesics is known to be associated with higher PONV. Simple
analgesics and non-steroidal anti-inflammatory drugs have no effect on PONV but
their use has a sparing effect on the requirement of opioids and may reduce PONV.
 Inadequate analgesia.
 Premedication with metoclopramide, droperidol, or ondansetron, or inclusion of
these drugs in the anaesthetic technique may reduce the incidence of PONV.
 The effect of anticholinergic drugs is controversial.
 Anticholinesterases drugs such as neostigmine are known to increase the incidence
of PONV.
 PONV is also associated with deranged physiology such as in hypotension, hypoxia
and hypercapnia.
 Local and regional anaesthesia donot cause PONV themselves, but secondary
hypotension/hypoxia or inadequate analgesia may be contributing factors.
Vol. I 118
Surgery
 Laparoscopy procedures
 ENT operations – PONV is especially high with middle ear surgery.
 Abdominal (intraperitoneal and visceral) operations.
 Ophthalmic surgery, especially with strabismus operation.
 Orchidopexy
 Ambulatory surgery.
Vol. I 119
Question No. 82
Discuss the causes of heat loss during general anaesthesia. What are the
physiological effects of hypothermia in the anaesthetized patient?
Answer: -
Hypothermia is a consequence of anaesthesia and surgery. Heat is lost by radiation,
convection, evaporation and conduction. There is also decreased heat production. The
physiological mechanisms for conserving heat are also affected by anaesthesia. For
example, behavioral techniques and the ability to vasoconstrict are lost and shivering is
prevented by muscle relaxants. The main causes of heat loss are radiation and
evaporation.
Factors contributing to heat loss

 Cold operation theatre environment
 Prolonged surgery
 Infusion of cold intravenous fluids
 Breathing cool dry anaesthetic gases
 Use of cold antiseptic solutions and cold irrigation solutions
 Exposure of abdominal and thoracic contents
 Patient factors
o Extremes of age
o Associated endocrine disorders
o Severe illness
Effects of hypothermia
 Cardiovascular: vasoconstriction, reduced cardiac output, J waves on ECG at 30 0C,
ventricular arrhythmias at 300C, ventricular fibrillation at 28 0C, increased blood
viscosity, increased haematocrit, thrombocytopenia.
 Respiratory: decreased O2 delivery, increased O2 requirement, and apnoea at 240C.
 Neurological: confusion below 350C, unconsciousness at 300C, reduction in MAC of
volatile agents, cessation of all cerebral electrical activity below 180C.
 Metabolic: reduced basal metabolism, hyperglycemia, increased fat mobilization,
decreased drug metabolism.
 Renal: GFR reduced by 50 % at 300C.
Vol. I 120
Question No. 83
Outline the management of a “failed intubation” in an emergency caesarean
section.
Answer: -
This is a difficult and potentially fatal situation. Before emergency caesarean
section is decided under GA, a plan for failed intubation management must be made.
The anaesthetist must know the degree of urgency of the caesarean section. A caesarean
section for “severe fetal bradycardia” cannot be delayed where as “failure to progress”
allows the anaesthetist more time to make further decisions. In other words, the
decisions as to whether a general anaesthetic should be continued or regional
anaesthesia be employed should be made prior to commencing the general anaesthetic.
The mother’s safety is paramount. General anaesthesia can be continued with either a
suitable volatile anaesthetic agent or 100% oxygen. Opiates can supplement the
anaesthesia after delivery of the baby. Alternatively the mother can be awakened. After
consideration, anaesthesia may be recommended with senior help and with advanced
intubation devices such as a fibreoptic laryngoscope. “In extreme cases” cricothyroid
puncture has been successfully used to secure the airway.
If regional anaesthesia is not contraindicated and can be performed, the mother should
be woken up, and spinal or epidural anaesthesia commenced. There are potential
problems in this situation as high/total spinal blockade will be particularly dangerous
because resuscitation is difficult owing to the potentially fatal airway problem.
Specific points of care include: -

 Help should be called for early.
 Ideally, cricoid pressure should be maintained
 Hypoxia must be avoided.
 A second dose of suxamethonium should only be given if intubation is deemed
absolutely possible and there is no hypoxia.
 Left lateral tilt should be maintained.
Vol. I 121
Question No. 84
Summarize the problems associated with anaesthetizing patients with
transplanted organs.
Answer: -
An allograft that is functioning well presents few problems. The anaesthetist must
however, be aware of the patient’s altered physiology and have some understanding of
post-transplant complications.
General peri-anaesthetic considerations

 Effect of immunosuppression
o Infectious complications – early nosocomial and late opportunistic infections
(CMV, HSV, PCP, Legionella commonly)
o Associated neoplasia – especially lymphoma
 Rejection
The transplanted organs are most at risk of rejection within the first three months,
but rejection can occur at any time. If rejection is suspected, the operation should be
cancelled if feasible and the patient referred back to the transplant unit.
 Adverse effects of immunosuppressant therapy

o Cyclosporine – renal dysfunction, hypertension, gingival hyperplasia
o Azathioprine – hepatic dysfunction, bone marrow depression
o corticosteroids – pathological fractures, aseptic necrosis of hip joint, diabetes
 Altered physiology and pharmacology of transplanted organs

o Drug metabolism and elimination by renal allografts
o Drug biotransformation and metabolism by hepatic allografts
o Denervated cardiac allografts
 Transfusion and transplantation

o Immune sensitive, blood-borne infectious disease
Specific peri-anaesthetic considerations

Two examples of specific consideration are listed below: -
 Orthotopic cardiac allograft recipients – denervated heart. Preload dependence; no
response to indirectly acting drugs such as atropine, glycopyrrolate, neostigmine;
delayed heart rate responses to hypoxia, hypovolaemia; normal intrinsic Frank –
starling response; accelerated coronary atherosclerosis and silent ischemia.
 Heart – lung allograft recipient. Loss of cough reflex – can cough to command, but
able to protect airway only when fully awake.
Vol. I 122
Management
Transplant recipients are very well acquainted with hospital procedures; special care
and understanding are required when managing these patients.
 Avoid unnecessary invasive monitoring.
 Avoid enthusiastic barrier nursing
 Maintain strict asepsis and antibiotic prophylaxis – flucloxacillin, cefotaxime
 Maintain immunosuppression.
 Maintain renal function and fluid balance.
Vol. I 123
Question No. 85
Outline the methods for producing deliberate hypotensive anaesthesia.
Answer: -
Hypotensive anaesthesia is indicated to improve surgical visual field access and to
minimize surgical blood loss. It can be provided by both general or regional anaesthesia.
The methods available to assist with these aims include: -
(1) Posture: gravitational effects from raising the head of the patient assist with better
visual access, for example, in the ENT patient. Each 1 cm height above the
horizontal lowers the blood pressure in that area by 0.7 mm Hg.
(2) General anaesthetic technique: a “smooth” anaesthetic without a tachycardia,
coughing, straining, or bucking stops any rise in venous and arterial pressures. To
this end premedication with a sedative is often helpful and anticholinergics should
be avoided as they can cause tachycardia. A technique involving intermittent
positive pressure ventilation decreases cardiac output and can lower blood
pressure and this may stop straining in a spontaneously breathing patient. Some
muscle relaxants, such as tubocurarine, have ganglion blocking actions and lower
blood pressure themselves. Inhalational volatile anaesthetic agents are useful as
many have both cardiac depressant and peripheral vasodilator effects.
(3) Specific drugs: many drugs are available. Labetalol, and α and β blocking agent is
commonly used and this can cause postural hypotension. Other direct vasodilating
agents such as infusions of nitroglycerine can also be used as supplements to
general anaesthesia.
(4) Regional anaesthesia: is often used facilitate surgery such as total hip replacement
or transurethral resection of the prostate because of redistribution of blood away
from the operative site. This is due to symptomatic blockade with resultant
vasodilatation.
An intriguing problem is how low the blood pressure should be allowed to fall. It is
sufficient to state it must not fall below the appropriate pressure required for
autoregulatory processes to function, especially those of the brain and kidneys. This
depends on many factors including age and previous medical health.
Vol. I 124
Question No. 86
Describe the intraoperative anaesthetic management of a 3 year-old child
with a penetrating eye injury.
Answer: -
Anaesthetic considerations
 Need for rapid intubation and airway protection due to potential full stomach.
 Need for protect the eye from a rise in intraocular pressure.
 Need for urgent operation – to assess damage, remove foreign bodies, restore
integrity of the globe, and reduce the risks of infection and sympathetic ophthalmia.
 Possibility of associated injuries – face, head, chest, abdomen, limbs (especially
following explosions).
 Possibility of hypovolaemic shock from associated injuries.
 The pediatric patient
Intraoperative management
Aim to protect airway and eye.
 Assess the balance of relative risks in consultation with the surgeons. Can surgery be
deferred for sufficient time to reduce the risks of aspiration and enable intubation
with a non-depolarizing relaxant?
 Ensure presence of experience senior anaesthetist.
 Ensure smooth induction, maintenance and recovery – avoid coughing, straining,
struggling, vomiting.
 Avoid drugs that are known to increase intraocular pressure – ketamine,
suxamethonium.
 Adopt measures to minimize the rise of intraocular pressure with laryngoscopy and
intubation – intravenous lignocaine, alfentanil, or fentanyl.
Use a technique that has been shown to provide good early intubation conditions
without raising intraocular pressure – a described technique is to give fentanyl 2
micrograms/kg followed by vecuronium 0.15 mg/kg; at the first sign of muscle weakness
give thiopentone 5 mg/kg and apply cricoid pressure. Intubation can be performed 90
seconds following vecuronium, approximately 60 seconds after loss of consciousness.
The stomach should be emptied as much as possible before the end of anaesthesia.
Vol. I 125
Question No. 87
A 50-year-old man is admitted at 14:00 for exploration of a forearm wound.
He denies any alcohol intake in the previous six months. He had previously
been admitted many times for haematemesis but no cause was found. He
has the following blood results:
Hb 11 g/dl
MCV 110 fL
WBC 3600/mm3
Platelets 50000/mm3
Alcohol 200 mg/dL
1. Briefly comment on these results.

2. List two tests that may help confirm the chronicity of this
condition.
3. List five associated complications that increase peri-operative risk,
if these tests are positive.
4. Why may he be confused post-operatively? Name one drug that
may be used in the management.
Answer: -
1. There is a macrocytosis (normal mean corpuscular volume is 80 – 96 fL), leucopenia
and thrombocytopenia. General cause of a macrocytosis include: -
 Megaloblastic anaemia due to vitamin B12 or folate deficiency;
 Haemorrhage or hemolysis, which also cause a reticulocytosis;
 Alcoholism and cirrhosis;
 Marrow aplasia or leukaemia;
 Myxoedema.
Macrocytosis occurs in 60 % of those with a current alcohol problem but usually

resolves with 2 to 3 months abstinence. The legal blood alcohol limit for driving a car
in the United Kingdom is 80 mg/dL. This patient has therefore been drinking heavily
toxic to the bone marrow and alcoholism results in malnutrition and vitamin
deficiencies. Hence megaloblastic anaemia, macrocytosis, leucopenia and
thrombocytopenia can all occur.
2. The following strongly suggest a chronic alcohol problem: -

 Urinary alcohol > 120 mg/dL (> 200 mg/dL is diagnostic);
 Raised gamma glutamyl transferase with a normal alkaline phosphatase;
 Macrocytosis
3. A blood alcohol > 250 mg/dL is associated with an increased surgical risk. This must
be balanced against the urgency of surgery. Problems of acute alcoholic intake
include: -
 Reduce sensitivity to anaesthetic agents;
 Full stomach, as alcohol delays emptying;
 Hypoglycemia and hypokalemia;
Vol. I 126
 Hypothermia;
 Dehydration: alcohol inhibits ADH release.
Complications of chronic alcohol intake include psychosocial problems and : -

 CVS: cardiomyopathy, cardiac beriberi and recurrent arrhythmia;
 RS: 20 % have chronic bronchitis;
 Liver dysfunction: cirrhosis, coagulopathy, low albumin and oesophageal varices;
 GIT: gastritis; pancreatitis causes further malnutrition and steatorrhoe;
 Hematological disorders;
 CNS: seizures, Korsakoff’s psychosis and Wernicke’s encephalopathy. The history
from the patient may not be accurate due to memory loss or confabulation;
 Skeletal: osteoporosis and myopathy;
 Autonomic and peripheral neuropathy due to B12, folate, B6 and B1 deficiencies.
4. Delirium tremens (DTs) due to acute alcohol withdrawal usually occurs within 48
hours of stopping alcohol. It may be preceded by coarse generalized tremor,
disorientation, agitation, auditory and visual hallucinations or seizures. It presents
signs of an overactive sympathetic system with hyperthermia, hypertension,
tachycardia, sweating and dilated pupils. The differential diagnosis includes
malignant hyperthermia, sepsis and other causes of delirium e.g. withdrawal from
benzodiazepines. Management is supportive and sedative. Assessment should
include a septic screen as DTs may be precipitated by sepsis. Treatment is supportive
and includes the following: -
 Correction of hypoglycemia, dehydration, and malnutrition with i.v. Dextrose,
trace elements and multivitamins;
 Alcohol, chlormethiazole or benzodiazipines may be used for sedation but all
cause both hypotension and respiratory depression and so should be closely
monitored.
Vol. I 127
Question No. 88
You are asked to see a lady who has developed a headache 24 hours after
having had a lumbar epidural catheter inserted for the provision of
analgesia during labour.
1. What questions would you ask her?
2. How would you manage her?
3. Describe how you would perform an epidural blood patch.
Answer: -
1. Questions should be directed at eliciting the following information: time of onset
with respect to timing of procedure, nature of headache, severity, radiation, effect of
posture, other aggravating or relieving factors, presence of nausea, vomiting, visual
and auditory disturbances.
2. Post-dural puncture headache (PDPH) may be severe, and interfere with parent –
child bonding; the patient may display a wide range of emotions. A full explanation
of the reason for the PDPH, reassurance that it is often self-limiting, discussion of
the management options and regular assessment are important. Breast-feeding
should be encouraged and psychological support provided as necessary. A horizontal
position will be the most comfortable (mobilize whenever possible) and it is prudent
to maintain adequate oral/intravenous hydration (although there is no evidence that
it relieves headache). Simple analgesics will treat mild to moderate pain effectively.
Limited evidence suggests that caffeine (oral or i.v.) and DDAVP may be useful
adjunct. If initial conservative management fails, epidural blood patching, which is
safe and effective for the treatment of PDPH, must be offered.
3. Two-experienced anaesthetist is required. Strict asepsis must be maintained. The
epidural space is identified in an adjacent space and the second operator withdraws
30 mL of autologous blood from an arm vein. 10 mL are sent for blood culture and
20 mL are injected into the epidural space over 20 minutes. Injection should be
stopped for 30s if the patient experiences discomfort or parasthesiae and then
resumed. The patient must remain supine during the injection and for 30 min after.
The patient should be advised not to strain or lift heavy objects for a week
afterwards.
1. PDPH commonly occurs within 48 hours of dural puncture. It is throbbing in nature,

on varying severity, aggravated by the upright position and relieved when
recumbent, typically fronto-occipital and may radiate to the neck and shoulders.
Neck stiffness, nausea, vomiting visual and auditory disturbances (diplopia tinnitus
etc.) may be present.
PDPH is thought to be caused by a combination of ongoing CSF leakage and reflex
cerebrovascular dilatation. Relief of the low-pressure headache by manual
abdominal compression is a useful diagnostic test. Spontaneous resolution is not
uncommon. Rarely it causes cranial nerve palsies, subdural haematoma and may be
incapacitating. The onset of PDPH may sometimes be delayed and rarely it may
persist for one week or longer.
Vol. I 128
Headache unrelated to anaesthesia is common following delivery (39 %). Important

but rare causes that need exclusion are paranasal sinusitis, cortical vein thrombosis
(1:3000 – 1:6000 deliveries) and intracranial tumors, haemorrhage and vascular
malformations.
2. Abdominal binders and the prone position have been shown to raise pressure in the
epidural space but are uncomfortable and unpopular.
3. A success rate of 89 % with epidural blood patching has been reported, whilst a
second blood patch was successful in 97.5 %. Blood should not be injected epidurally
in the presence of systemic infection. Epidural patching with Dextran 40 has also
been successful.
Vol. I 129
Question No. 89
Write notes on the techniques available for decontamination, disinfection
and sterilization of solid theatre equipment.
Answer: -
Decontamination
This is defined as the removal of organic matter from equipment. It does not involve the
killing of either bacteria or spores. It has a decreasing role in the modern medical
environment with increased concern about cross-infection and the rise in use of
disposable equipment.
Disinfection
Disinfection involves the killing of vegetative organisms, but does not effect all bacterial
or fungal spores or viruses. Various methods are used to disinfect equipment: -
 Pasteurization: this involves heating in hot, but not boiling; water (usually 80 0C for
10 minutes).
 Boiling: this is a more efficient technique and requires less time than pasteurization.
It is important to monitor the temperature to ensure high enough temperatures.
 Chlorhexidine: this is a non-detergent disinfectant that is mixed with aqueous or
alcoholic solutions of different concentrations. It does not damage rubber.
 Gluteraldehyde: this is an expensive disinfectant, which, if used for extended periods
of time, also has some antispore activity. It is mixed with an activator and then has to
be used within 14 days. Residual gluteraldehyde can cause pulmonary oedema. It is
therefore important that it is washed off after use. Gluteraldehyde is commonly used
in the disinfection of endoscopic equipment.
 Sodium hypochlorite: this has good activity against viruses but corrodes metal. It is
generally used as a surface disinfectant to clean floors and walls in theatre.
 70 % Alcohol.
 Phenolic compounds.
Sterilization
Sterilization implies the killing of all microorganisms, including spores and viruses.
 Autoclaving: this is a term used to define the application of steam and pressure to
equipment. It is suitable for a wide range of equipment, including metal, cloth, glass,
and some thermoresistant plastics. It may cause some plastics to degrade with
repeated use.
 Ethylene oxide: gaseous ethylene oxide at a humidity of 30-40 % acts as an
alkylating agent to kill microorganisms. It is a useful technique for the sterilization of
anaesthetic machines and electronic equipment. At the end of the sterilization phase,
an aeration phase is required to remove toxic residues from the equipment. This can
make this technique time-consuming.
 Formaldehyde sterilization.
 Radiosterilisation.
Vol. I 130
Question No. 90
Outline the problems of anaesthesia for a 20 year-old heroin addict
requiring drainage of an arm abscess.
Answer: -
This problem needs to be assessed firstly from the point of view of the addiction:
 Heroin addicts can be unreliable when giving a clinical history and may not give
accurate history of operations and previous medical illness.
 Venous access which is mandatory prior to anaesthesia can be impossible and
occasionally surgical cut-down is necessary.
 Acute intoxication may be apparent and the co-operation of the patient may be
difficult.
 Drug withdrawal can occur in hospital and must be managed by appropriate
professionals including social workers and psychiatrists.
 Associated addictions can occur which may have physical consequences for the
patient. These include alcohol and tobacco abuse; when these patients are examined
care must be taken to ensure that associated diseases such as cardiomyopathy do not
exist.
 Intercurrent infections can co-exist, especially septicemia and endocarditis.
 Associated infections can influence the anaesthetist in the management of this case.
There is an increased risk of hepatitis and HIV infections and it is the duty of the
anaesthetist to prevent personnel, theatre staff, and equipment transmission of these
infections. Universal sterility precautions must be undertaken.
 Thrombosis and embolism are greater risks in this patient.
 Multisystem investigations are needed, as conditions such as thrombocytopenia can
occur in this group of patients and may preclude regional anaesthesia.
 Enzyme induction may influence anaesthetic requirements in general anaesthesia.
 Postoperative analgesia is often difficult to manage.
Secondly the type of anaesthesia needs to be considered. This operation can be

performed under regional anaesthesia with a brachial plexus block. This, whilst having
potential complications such as pneumothorax may be the best technique if there is no
infection locally or clotting problems. General anaesthesia may be chosen and in an
emergency would necessitate a “rapid sequence induction” technique.
Vol. I 131
Question No. 91
Outline the physiological changes that occur during laparoscopy.
Answer: -
The physiological effects during laparoscopy are associated with changes in patient
position and the creation of a pneumoperitoneum.
Position (Trendelenberg/Reverse Trendelenberg)

 Respiratory effects: in the head-down position the weight of the abdominal viscera
causes cephalad shift of the diaphragm with a decrease in functional residual
capacity, total lung volume, pulmonary compliance; these pulmonary function
changes depend on the patient’s age, weight, preoperative lung function, degree of
tilt and the intraoperative ventilatory technique.
 Cardiovascular effects: the head-down position favors venous return and therefore
improves cardiac output; the reverse position causes pooling of blood in legs with
reduction in venous return and cardiac output.
 Central nervous system effect: the head-down position increases both intra-cranial
and intravascular pressures.
 Gastrointestinal effect: the head-down position increases the risk of passive
regurgitation.
Creation of pneumoperitoneum
This results in the following: -
 Raised intra-abdominal pressure and its consequences.
o A cephalad shift of the diaphragm, ventilation – perfusion mismatch and carinal
displacement with potential for inadvertent right bronchial intubation
o Reduction in cardiac output
o Reduced blood flow to intra-abdominal organs
o Increased risk of gastric regurgitation
 Systemic absorption of insufflated carbon dioxide causing hypercarbia and possible

gas embolism
 Vagal reflexes causing bradycardia and cardiac arrest
In summary, the extent of cardiovascular changes depends on the intra-abdominal

pressure attained, the volume of carbon dioxide absorbed, changes in intravascular
volume, patient position, and the ventilatory technique and anaesthetic agents
employed.
Vol. I 132
Question No. 92
Summarize the problems relating to perioperative management of HIV
positive patients.
Answer: -
General health
Poor health, poor nutrition, generalized lymphadenopathy, diarrhea, fever, malaise, and
weight loss are common problems.
Associated diseases
Secondary infections such as respiratory and CNS infections. Secondary malignancies.
HIV drugs
Drugs used to interfere with viral DNA replication have severe side effects such as
anaemia, thrombocytopenia, neutropenia, nausea and vomiting, and peripheral
neuropathy.
Psychological problems
Emotional, mental, and psychological disturbances are common. Attention should be
paid also to other possible but less common neurological problems such as psychosis,
dementia, and encephalitis.
Isolation
HIV patients should be isolated if contamination from their body fluids is likely, for
example when there is bleeding or an open wound. Immunosuppressed patients should
also be isolated if there is an infection risk to themselves.
Aseptic procedures
Strict asepsis is required to prevent opportunistic infections. the need for using invasive
monitoring should be balanced against the risk of sepsis.
Precautions for staff

As it is unethical to test all patients for HIV prior to surgery, it is recommended that
universal precautions are applied on every patient as routine.
Simple hygiene: cover wounds and avoid body fluids.
Use gloves, masks and overshoes. Use protective glasses (goggles) and protective
clothing if there is a risk of splashing.
Disposal of sharps, avoid use of needles, needle resheathing, or passing needles from
one person to another.
Policy for needle-stick injuries must be in place.
Precautions for other patients

Cleaning of theatres is required after treatment of HIV patients. This includes floors,
walls and furniture.
Vol. I 133
Equipment used in contact with body fluids should be sterilized. Disposables should be
used when possible, and filters should be used on the breathing circles. Minimum
equipment and spaces should be used with induction and recovery in the same
operation theatre.
ICU admission
HIV patients requiring critical care are usually managed in an HDU bed with the
isolation criteria observed as discussed above. ICU admission may be considered if there
is a strong definite indication with a clearly curable condition.
Vol. I 134
Question No. 93
Identify the patient groups who are at a high risk of, or conditions that
predispose to postoperative deep venous thrombosis. Write short notes on
the currently available prophylactic measures.
Answer: -
Patients at risk, or conditions predisposing to deep venous thrombosis (DVT) are: -
 Obesity
 Age over 40 year-risk increases almost linearly with further advancement of age
 Previous history of DVT or pulmonary embolism
 Malignancy
 Major trauma and immobility
 Major operations and length of operation
 Abdominal operations, especially in the pelvic region
 Orthopaedic (hip and knee) operations
 Pregnancy and caesarean delivery
 Gynecological operations
 Combined contraceptive pills and other estrogen drugs
 Smoking
 Polycythemia
 Dehydration
 Diabetes mellitus
 Varicose veins
Prophylactic measures: a combination of more than one measure is usually used:

 Correct any of the reversible conditions above when appropriate, for example stop
the contraceptive pill 4 weeks before major surgery and start after 2 weeks if the
patient is mobile again. Progesterone-only pill does not require to be discontinued
 Prophylactic anticoagulation
o Subcutaneous heparin in a dose of 5000 units, two to three times per day is
commonly used;
o Fractionated low molecular weight heparin has a longer duration of action and is
thought to be more effective in preventing DVT; it is also more convenient to use
as a once-daily subcutaneous dosage.
 Mechanical measures
o Elastic compression stockings;
o Leg padding and elevation;
o Manual massage of calf muscle and intermittent pneumatic-pump compression
during surgery.
 Regional anaesthesia. The sympathetic denervation, vasodilatation and improved
peripheral circulation in the legs may reduce the incidence of DVT.
 Early mobilization after surgery
 Early screening of high-risk patients with the non-invasive duplex Doppler (> 50 %
of cases are detected in preclinical stage).
 IVC filters.
Vol. I 135
Question No. 94
Write brief notes on the specific problems encountered when
anaesthetizing for MRI scan.
Answer: -
Problems
 MRI scanners tend to be in the basement of the hospital, isolated from other
anaesthetic sites.
 Full independent sets of anaesthetic equipment, monitoring and drugs have to be
available in the MRI suite.
 The anaesthetic machine has to be separated from the magnetic field.
 The strong magnetic field will affect pacemakers and may dislodge metal cerebral
aneurysm clips or metal foreign bodies.
 There are individual problems with monitoring: -
o ECG in general, cannot be used because of interference, artifact and metal
components; if definitely required, ECG can be used with electronic filters and
the electrodes placed on the peripheries as far out of the scanner as possible
o SaO2 poor signal, artifact, and the presence of metal components again make
oximetry difficult in the MRI scanner; if it is definitely required the probe can be
placed as far out of the scanner as possible;
o NIBP safe to use but requires a long hose and the monitor box needs to be away
from the magnetic field
o Invasive BP can not be used because of the effect of the magnetic field on the
transducer
o Capnography can be used, but the main monitor box has to be outside the
magnetic field; this may necessitate a long piece of tubing, which will provide
resistance and time lag.
 Infusion pumps should not be allowed within the magnetic field.

 The MRI scanner is very noisy and claustrophobic. It is very frightening for young
children, and they often require general anaesthesia to allow a scan. The noise also
creates a problem with hearing monitor signals and alarms.
Solutions
 The patient should be assessed in the ward as normal. The patient should be directly
questioned about the presence of pacemakers, previous neurosurgery, and metal
foreign bodies or prostheses. A final decision should be made as to whether the scan
with general anaesthesia is indicated.
 All equipment should be available and checked before the patient is taken to the
scanner.
 The whereabouts of the resuscitation drugs and defibrillator should be known.
 Skilled anaesthetic assistance should be present.
Vol. I 136
 The anaesthetic machine and monitors should be placed outside the main scanning
room, and the NIBP cuff and the Capnography monitor should be connected to the
patient.
 Infusion pumps should be placed outside the magnetic field and long manometer
tubing used.
 Anaesthesia should be induced outside the magnetic field and the patient then
transferred into the MRI on a trolley that can enter the magnetic field.
 A long Bain’s system is the breathing system of choice.
 The anaesthetist should keep in constant eye contact with the patient and the
monitors.
 At the end of the scan, the patient should be extubated outside the magnetic field
and recovered in standard recovery room conditions.
Vol. I 137
Question No. 95
A 40 year-old ASA-1 patient is admitted as a day case for an inguinal
herniorrhaphy under general anaesthesia. When would you consider him
ready for discharge from the day surgery unit?
Answer: -
The prompt and safe discharge of patients from a day surgery unit helps in improving
efficiency and reducing costs. The use of discharge criteria and discharge scoring
systems ensure safe discharge after anaesthesia. A set of day surgery discharge criteria is
described below.
 The patient’s vital signs should have been stable for at least one hour.
 The patient must be: -
o Oriented to person, place, and time, or returned to preoperative mental status
o Able to maintain oral fluids
o Able to void urine
o Able to dress himself (consistent with preoperative state)
o Able to walk without assistance (consistent with preoperative state)
 The patient must not have: -
o More than minimal nausea or vomiting
o Excessive pain
o Bleeding
 A responsible fit adult should escort the patient home and stay for at least 24 hours.
Discharge scoring systems have been evaluated. A common system in use is the
modified post-anaesthesia Discharge Scoring System (PADSS). This is based on: -
o Vital signs
o Ambulation and mental status
o Pain
o Nausea/vomiting
o Surgical bleeding
The patient is considered “home ready” when the required numerical score is achieved
on two occasions at 30-minute intervals. Any discharge criteria/scoring system must be
used with common sense and clinical judgment, and the patient must feel well enough
to go home.
Psychomotor tests and driving simulators can be used to assess a patient’s overall
recovery. However, these tests are complex, require skilled operators take considerable
time to perform and are generally not useful in a clinical setting.
Vol. I 138
Question No. 96
Outline the management of a brain-dead patient before organ donation.
Answer: -
For all potential donors assiduous supportive treatment is essential to prevent
deterioration of organs-this will both increase donation rates and improve graft survival
and function. Potential donors should be carefully monitored and corrective measures
instituted early. Maintenance of tissue oxygenation, organ function, and metabolic and
cardiovascular stability should be pursued as for critically ill patients, until and during
organ removal.
The local transplant co-coordinator should be contacted early for advice on donor organ
suitability. Blood samples should be obtained for screening for hepatitis antigen and
HIV, blood group determination, and tissue typing. For heart and heart-lung donors,
chest X-ray and 12-lead ECG should be obtained.
Haemodynamic support
Hypotension is a frequent complication of brain-stem death. This should be treated with
aggressive fluid resuscitation and inotropic support, guided by measurement of
haemodynamic variables.
Endocrine disorders
Brain-stem death can precipitate a variety of endocrine disturbances. Antidiuretic
hormone, thyroid hormones such as tri-iodothyronine, cortisol, and insulin levels are all
reduced. The ensuing diabetes insipidus and hyperglycemia need appropriate treatment.
Temperature control
Temperature regulation is markedly impaired after brain-stem death because of a
reduction in heat production secondary to a fall in metabolic rate, loss of muscular
activity, and peripheral vasodilatation. Insulation and active warming should maintain
body temperature.
Vol. I 139
Question No. 97
Describe the systems you know for quantifying obesity. Why are the obese
unsuitable for day-care surgery?
Answer: -
Quantifying obesity
Obesity can be quantified using a number of different systems: -
 Height/weight nomograms: These allow for differences in sex and build. An ideal
body weight for height is calculated and the subject is said to be morbidly obese if
their weight is > 20 % above the ideal.
 Body mass index (BMI): This is the weight in kilograms/(height in meters) squared.
Normal is 22-28 and morbidly obese is > 35.
 The Broca index: This states that the normal weight (kg) is the height (cm) minus
100 for males and minus 105 for females.
 It has recently been suggested that the distribution of fat should also be considered,
as abdominal obesity is associated with a much higher incidence of cardiovascular
disease than other forms of obesity.
Day-care surgery problems

The obese present a number of different problems to the anaesthetist. Many of these
problems make them unsuitable for day-care surgery.
Pharmacological
 The above have a high percentage of body fat and therefore retain anaesthetic agents
that are redistributed to the fat compartment for longer. This may lead to increase
length of action of anaesthetic agents.
 Doses that are calculated on a mg/kg basis may result in an overdose of drug. This
may cause unwanted side effects or prolong the action of the drug.
 The obese patient with obstructive sleep apnoea may be very sensitive to opioids and
sedatives.
Physiological
 Cardiovascular: increased blood volume and cardiac output that may lead to left
ventricular hypertrophy; hypertension, ischemic heart disease, arrhythmias,
cerebrovascular accidents and deep vein thromboses are all more common in the
obese.
 Respiratory: decreased FRC; low chest wall compliance usually requires ventilation if
patients are to have a general anaesthetic; the obese patient may have obstructive
sleep apnoea, Pickwickian Syndrome or cor pulmonale.
 Alimentary: the obese patient has a high incidence of hiatus hernia and therefore is
prone to impaired gastric emptying and reflux of gastric contents; a rapid sequence
induction with intubation is usually needed if the patient is to have a general
anaesthetic; there is often hepatobiliary disease with abnormal liver function and
frequency type 2 (non-insulin dependent) diabetes mellitus.
Vol. I 140
Technical
The obese are: -
 Often difficult to intubate
 Often difficult to monitor
 Difficult to cannulate
 Difficult to perform local or regional blocks
 Difficult to handle – two theatre tables may be required
Postoperative morbidity
The obese have a high rate of DVT, wound infection/dehiscence, and chest infections.
The problems with opioids and with regional techniques often make the provision of
postoperative analgesia difficult. Postoperative mortality is three times higher than in
the non-obese.
It can be seen from the above lists that anaesthetizing the obese creates a large number
of pre-, peri-, and postoperative problems. Obese patients often require a more invasive
anaesthetic and need to be observed carefully postoperatively. This makes them
unsuitable for day-case surgery.
Vol. I 141
Question No. 98
Briefly outline the necessary safety precautions when a patient is
anaesthetized for laser surgery to the larynx.
Answer: -
Risks
There are risks to both patient and operating room staff when lasers are used. These
include:-
 Explosions and fires following ignition of anaesthetic vapors, tracheal tubes, and
drapes.
 Ocular damage both corneal and retinal.
 Atmospheric contamination – the fumes produced by vaporization of tissues with
lasers may be noxious, potentially infective, and can cause acute bronchial
inflammation.
Safety precautions
 A formal safety programme should be in operation in hospitals undertaking laser
surgery.
 Personnel should be properly trained in the use of the equipment and regular
servicing carried out to ensure its correct function.
 Notices restricting admission should be posted on the doors to the theatre in which
laser is being used.
 Personnel should wear protective goggles to prevent eye damage from deflected laser
beam.
 Measures must be taken to reduce risk of fires.
 Shield endotracheal tubes from the laser beam by wrapping with aluminium foil or
use a flexible metallic tube.
 Use double cuffed tubes, and fill cuffs with saline, which absorbs stray energy more
effectively than air.
 Choose an anaesthetic technique that could avoid the use of tracheal intubation, for
example injector techniques, high frequency ventilation, and cuirass ventilation.
 Use non-explosive mixtures of gases, for example under 30 % oxygen in nitrogen or
helium.
 Limit laser power and duration of bursts.
 Use saline-soaked swabs to protect surrounding tissues from laser.
Vol. I 142
Question No. 99
Write a short account on the nerve supply of the larynx. Give examples
from anaesthetic practice on how this nerve supply may be interrupted
accidentally or intentionally.
Answer: -
The vagus nerve provides the larynx with all of its nerve supply through two branches on
each side, the superior laryngeal nerve and the recurrent laryngeal nerve.
The superior laryngeal nerve travels deep to the internal and external carotid arteries
and divides into two branches: (a) the external motor branch which provides the motor
supply to the cricothyroid muscles, the tensors of the vocal cords, and (b) the internal
sensory branch which carries the sensory fibers from the upper part of the larynx
including the vocal cords.
The recurrent laryngeal nerve originates as the vagus nerve crosses the subclavian artery
on the right side and the aortic arch on the left side. It runs in the groove between the
oesophagus and the trachea on each side of the neck to reach the larynx. It carries both
motor and sensory fibers providing motor supply to all of the larynx (excluding the
cricothyroid muscles) and sensation from the lower part of the larynx below the vocal
cords.
The recurrent laryngeal nerve may be blocked unintentionally by the local anaesthetic
instilled during Stellate ganglion block, or interscalenus or supraclavicular brachial
plexus block. This nerve may also be accidentally cut or injured during thyroid surgery.
The superior laryngeal nerve may be blocked on both sides by local anaesthetic to
facilitate intubation during awake fibroscopy. This is achieved be blocking the sensory
input from the upper part of the larynx including the vocal cords which travels through
the internal branch fibers of the superior laryngeal nerve as explained above.
Vol. I 143
Question No. 100

Draw and label the view of the laryngeal inlet as seen during direct
laryngoscopy. Describe the position that the vocal cords may take up
following damage to the laryngeal nerves.
Answer: -
The figure below shows the laryngeal inlet: -
Epiglottis
Vallecula
Epiglottic tuburcle
Piriform fossa
Vocal cord
Vestibular cord Aryepiglottic fold
Tracheal rings Corniculate cartilage
Cuneiform cartilage
Damage to the laryngeal nerves may lead to the following types of palsies.
Adductor palsy (unilateral or bilateral)

This occurs with partial or incompletes injury of the recurrent laryngeal nerve on the
same side or on both sides of the vocal cords. The affected vocal cord (or cords) assumes
and adducted position instead of the neutral position, as the abductors are more
sensitive to injury than the adductors. During inspiration the normal cord fully abducts
but not the affected cord. During phonation both the cords, the affected and the
unaffected, are able to adduct and meet in the mid-line (see figure below) – the dotted
lines represent normal cord positions.
Vol. I 144
Left
Bilateral
Resting Inspiration Phonation
Adductor palsy
Pure adductor palsy is not known to occur.
Adductor and adductor palsy (unilateral or bilateral)

This occurs with a complete incision of the recurrent laryngeal nerve such as may occur
during thyroid surgery. Both abductors and adductors are affected. The vocal cord rests
in the neutral mid-position. During inspiration the affected cord cannot move in the
mid-line, but in unilateral injury the normal vocal cord may cross the mid-line to meet
the affected cord.
Left
Bilateral
Total paralysis of the cords

This includes paralysis of the cricothyroid muscles (the tensors of the vocal cords) which
are supplied by the external motor branches of the superior laryngeal nerves, as well as
paralysis of the abductors and adductors supplied by the recurrent laryngeal nerves. The
vocal cords assume a midposition with slack untaut appearance and the anterior-
posterior diameter of the glottic opening is reduced. This mimics the cadaveric position
of the vocal cords. It is also very similar to the position assumed by the vocal cords
during complete muscle relaxation.
Vol. I 145

Volume 1 Corrected

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Volume 1 Corrected

Uploaded by

Copyright:

Available Formats

HUNDRED QUESTIONS & HUNDRED ANSWERS

resuscitation/sedation/rapid lowering of IOP) and supplementary oxygen is

1. What is this graph? What pattern does it shows & why?

 Inhaled corticosteroids (e.g. beclomethasone dipropionate) work by decreasing

4. Intra-operative management of ventilation includes: -

 Fibreoptic examination through the tracheal tube may show malposition,

2. Decreased myocardial oxygen supply: Carbon monoxide decreases O2 bound to

1. Comment on the haemoglobin and white cell count.

This patient is retaining carbon dioxide. This is long-standing as there is a

Notes on chronic obstructive airways disease

1. What other information would you like to have before you

narcosis and he is about to become apnoeic, hypoxic and arrest. He should be

 In the case of tension pneumothorax, immediate action is necessary. Drainage of the

Symptoms and signs

Table 1: Coagulation tests

Name Pathways tested Factors tested

Table 2: Some examples of coagulopathy

Pacing Sensing Response

Intra-operative Management: Preparation in theatre should include ensuring a magnet

Temporary transvenous pacing wire

The advantages of this technique are that: -

What is the cause?

 Peri-operative analgesia and oxygen;

3. Complications of SCA include: -

Spleen: multiple infarcts cause regression (auto-splenectomy), making these patients

The complications of blood transfusion, especially massive transfusion can be serious.

Notes on NMB and recovery

Types of muscular dystrophies

Benefits and problems

Intercostal nerve blocks

Thoracic epidural analgesia

Bilateral blocks should never be performed.

Successful block signs

The combination of ptosis, miosis, anhydrosis, and enophthalmos is known as Horner’s

Appearance Clear, colorless + no clot

The presence of > 100 RBC/mm3 and no xanthochromia on centrifugation is diagnostic

2. Computed Tomography (CT) scan. LP is contraindicated if an intracranial mass or

MAP = mean arterial pressure

3. The absolute contraindications to ECT are: -

4. Tricyclic antidepressants: These drugs (e.g. amitriptyline, imipramine and dexepin)

sympathomimetic drugs must be avoided as the interaction may cause intra-

Methods to reduce intracranial pressure are listed below: -

The influence of anaesthesia is outlined as follows: -

Assessment of brain-stem function

Tests should be performed

1. What is likely diagnosis & what operation is a surgeon likely to perform?

4. The volume deficit, metabolic derangements and acid-base imbalance should be

5. Ensure that resuscitation is adequate before administering anaesthesia. Monitoring

4. Accidental intravascular injection: This can be a serious problem because of the

Delayed micturition: True retention is rare.

2. Pre-eclampsia is defined as a pregnancy complicated by hypertension with either

However, it should be remembered that eclampsia has been described in patients

Prophylactic anticonvulsant therapies

Owing to the high risk of complications, diazepam or other benzodiazepines are no

Phenytoin is still widely used in the UK and many parts of Europe.

Secondary treatment involves stabilizing the patient because this disease is

Care is often best undertaken in the ITU or HDU environment.

The prevention of further convulsion is best undertaken by magnesium sulphate

Major abnormal Pche genotypes

5. Alternatives to suxamethonium for anaesthesia for Caesarean section include:

Notes on plasma cholinesterase (PchE)

Initial management is maintenance of anaesthesia to prevent awareness and IPPV until

If you suspect this myopathic condition: