SBA 300 Paper 3 Flashcards

1
Q

Questions
1. You are asked to anaesthetise a 40-year-old man for an elective brain tumour resection. He has a Glasgow coma score (GCS) of 15/15 and his CT shows minimal midline shift.
Which volatile-based anaesthetic is least likely to detrimentally affect his
intracranial pressure?
A Desflurane
B Isoflurane
C Nitrous oxide and sevoflurane
D Sevoflurane
E Halothane

A
  1. D Sevoflurane
    All volatile agents have the potential to cause cerebral vasodilation and affect
    cerebral blood flow (CBF) autoregulation. The resulting increased cerebral blood
    volume ultimately leads to an increased intracranial pressure (ICP) – an effect more
    pronounced in cases where the ICP is already raised or there is evidence of midline
    shift.
    Cerebral blood flow is dependent on a number of mechanisms:
    • Autoregulation
    • Cerebral metabolism coupling
    • BBiochemical reactivity
    • The autonomic nervous system
    • Flow dynamics
    All volatile anaesthetics inhibit the autoregulation of cerebral blood flow which is normally maintained over the range of perfusion pressures from approximately 50 – 150mmHg (Figure 3.1).By causing vasodilation, volatile agents obtund the myogenic reaction of the arterial smooth muscle when exposed to increased pressure, thereby preventing the control of blood flow. There is a range of effect across the different agents as listed below.
    Halothane
    Isoflurane and desflurane decreasing potency
    Sevoflurane (minimal effect ≤MAC 1.5)
    Nitrous oxide disturbs autoregulation in a similar fashion when used in isolation
    and with other volatiles. Autoregulation remains intact, however, when it is used
    alongside propofol, but the increased risk of expansion of any air introduced into the
    cranium during surgery, leads most anaesthetists to avoid its use.All volatiles reduce the cerebral metabolic rate as cerebral activity decreases.
    Normally this would be associated with a reduction in blood flow but, if the
    vasodilatory actions of volatiles are taken into account, the balance can be tipped
    towards increased flow. This is known as cerebral flow-metabolism uncoupling and is
    seen at higher concentrations of volatile anaesthetic in the order of potency as seen
    above.
    Biochemical reactivity of cerebral vasculature has been demonstrated with regards
    to the cerebrospinal fluid (CSF) pH, secondary to arterial concentration of carbon
    dioxide (PaCO2), and oxygen (PaO2) (Figure 3.2).Reactivity to carbon dioxide is marginally affected by volatile anaesthetics.
    Subsequently the vasodilation seen in their presence can be opposed by
    hyperventilating the patient to hypocapnia. Clinically, the risk of induced cerebral
    ischaemia with this practice is high enough to render it an emergency manoeuvre in
    the control of a raised ICP.
    Cerebral blood vessels are also responsive to the neurotransmitters released during
    signalling of the autonomic system. It is controversial as to how much this influences
    cerebral blood flow, but theoretically, reduced cardiac output secondary to the
    presence of volatile anaesthetics may play a part.
    The flow dynamics may also be altered by volatiles. Their incurred vasodilation may
    prevent the ordinarily seen vasoconstriction of resistance arterioles. This would
    normally occur when they are exposed to the shear stresses of increased flow.
    No volatile agent is considered fully beneficial to the management of ICP but
    Sevoflurane is accepted as the gold standard in neuroanaesthesia as it is least likely
    to cause a detrimental effect if used appropriately.
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2
Q
  1. A 76-year-old man has been admitted following coronary artery bypass grafting.
    He has severe left ventricular dysfunction postoperatively and failed to wean from
    cardiopulmonary bypass necessitating intra-aortic balloon pump insertion.
    Concerning the expected haemodynamic effects of a correctly sited and timed
    intra-aortic balloon pump, which of the following is the most appropriate answer?
    A Increased aortic systolic pressure, increased left ventricular end-diastolic
    pressure
    B Reduced aortic systolic pressure, increased preload
    C Increased coronary blood flow, reduced aortic diastolic pressure
    D Increased left ventricular volume, increased coronary blood flow
    E Reduced preload, reduced left ventricular wall tension
A
  1. E Reduced preload, reduced left ventricular wall tension
    The aim of Intra-aortic balloon pump (IABP) counterpulsation is to better match
    myocardial oxygen demand and supply and thus improve cardiac function. The
    physical premise is one of ‘counterpulsation’, which in the context of an IABP
    describes balloon inflation in diastole and deflation in early systole.
    Once inserted, the inflation cycle of the balloon needs to be set. This can either be
    achieved with reference to the ECG or arterial pressure (Table 3.4).The main indications for IABP counterpulsation are:
    t Acute myocardial infarction pending re-vascularisation
    t Cardiogenic shock not reversed by pharmacological therapy
    t As a bridging therapy in ventricular failure pending definitive treatment
    (ventricular assist device or cardiac transplantation)
    t Facilitation of weaning from cardiopulmonary bypass
    t Refractory ventricular arrhythmias
    There are a number of contraindications and cautions. Given the propensity for an
    IABP to increase diastolic blood flow, it may worsen aortic regurgitation. It should
    also not be used where there is a suspicion of damage to the aortic wall (dissection/
    arch aneurysm). The device is inserted via the femoral artery and therefore should be
    avoided in patients with severe peripheral vascular disease or bypass grafts.
    The balloon is initially programmed to inflate and deflate with each cardiac cycle, i.e.
    a ratio of 1:1. As the patient improves, weaning can occur in a stepwise manner; from
    1:1, to 1:2 then 1:3–4.
    Complications arising from IABP insertion relate to direct trauma to the femoral artery
    as well as the aorta, thrombosis, infection and balloon rupture leading to gas embolism.
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3
Q
  1. You are anaesthetising a patient for a right pneumonectomy. You have successfully
    inserted a left-sided double lumen tube (DLT) and the patient is taken into the
    operating room and placed in the right lateral position. Initial ventilator settings
    are intermittent positive pressure ventilation (IPPV) with a tidal volume of 600mL
    and Fio2 1.0. Shortly after clamping the catheter mount and deflating the right lung
    the patient rapidly desaturates to 88%. The peak pressure alarm on the ventilator
    sounds.What is the first appropriate course of action?
    A Deflate the bronchial cuff
    B Apply 5 cm H2O CPAP
    C Check the position of the tube with a fibrescope
    D Administer 5 L/minute oxygen to the deflated lung
    E Advance the DLT 2cm
A
  1. A Deflate the bronchial cuff
    Hypoxaemia is an anaesthetic emergency and may occur with the use of double
    lumen tubes (DLTs) and subsequent one-lung ventilation (OLV) because of shunt
    and failure to ventilate. In this scenario, the most likely reason for sudden and serious
    desaturation is misplacement of the DLT following repositioning of the patient.
    Proximal migration of the DLT may lead to obstruction of the trachea by the
    bronchial cuff, whilst distal migration may lead to obstruction to ventilation of one
    or more lobes (Figure 3.3). Other clues to malposition are a decrease in compliance
    (which may manifest as high peak inspiratory pressures).Immediate deflation of the bronchial cuff (option A) may allow two-lung ventilation
    (via the tracheal lumen) if the DLT has migrated proximally or restoration of
    ventilation to the upper lobes in the case of distal migration. This manoeuver may
    restore oxygenation and can then be swiftly followed by definitive repositioning of
    the DLT with a fibrescope (option C). Advancement of the DLT blindly and without
    deflating the bronchial cuff (option E) is not optimal management due to the risk of
    bronchial injury
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4
Q
  1. A 70-year-old woman is receiving laser therapy to vocal cord polyps. Her grade
    1 intubation with a laser-resistant cuffed tube filled with methylene blue was
    uneventful and she is being ventilated with 2% sevoflurane and 50% oxygen.
    Suddenly the surgeon notices flames and methylene blue around the endotracheal
    tube so stops lasering and floods the site with saline.
    What is the most appropriate next step in managing her airway?
    A Reduce the Fio2 and perform bronchoalveolar lavage
    B Stop the flow of all airway gases and remove the endotracheal tube
    C Reduce the Fio2 and pack wet swabs around the endotracheal cuff
    D Reduce the Fio2 and perform a tracheostomy
    E Reduce the Fio2 and inspect the endotracheal tube lumen via fibrescope
A
  1. B Stop the flow of all airway gases and remove the
    endotracheal tube
    Laser technology allows precision microsurgery and improved haemostasis which
    makes it an appealing surgical tool for operating in the airway. However, since lasers
    generate a considerable amount of thermal energy, they also represent a potential
    fire hazard. Fire requires the presence of an oxidiser (oxygen), ignition source (laser)
    and fuel (endotracheal tube), all of which are present within the airway in this
    scenario.
    Although laser-resistant endotracheal tubes offer some protection against airway
    fires, they are still flammable under certain conditions. The endotracheal cuff is
    particularly susceptible to puncture from misdirected laser energy which will lead
    to oxygen enrichment around the surgical site and an increased risk of catastrophic
    airway fire. The most important step after stopping lasering and flooding the
    site with saline is to stop the flow of all airway gases (oxidisers) and remove the
    endotracheal tube (fuel). Wet swabs placed around the surgical site prior to lasering
    can minimise the risk but should not be used to treat an airway fire. In the event
    of an airway fire, all flammable materials should be removed from the airway. The
    patient can subsequently be bag valve mask ventilated with air once the fire is out.
    To assess for airway damage, rigid bronchoscopy is recommended afterwards.
    Gentle bronchoalveolar lavage and fibreoptic assessment of the more distal airways
    is of benefit and if the damage is severe, a tracheostomy may be indicated. Smoke
    inhalation and thermal damage to the lungs may necessitate prolonged intubation
    and mechanical ventilation.
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5
Q
  1. A 27-year-old man with type 1 diabetes is listed for day case shoulder arthroscopy
    under general anaesthesia. He is listed first on an afternoon list and will take an
    early breakfast on the morning of surgery. He takes Novomix 30 twice a day after
    his morning and evening meals. His HbA1c measured last month was 53mmol/
    mol (7%).
    What is the most appropriate advice for his insulin adjustment on the day of
    surgery?
    A Take usual morning dose, and usual insulin with evening meal
    B Halve usual morning dose, take usual insulin with evening meal
    C Omit usual morning dose, take normal insulin with evening meal
    D Halve usual morning dose, halve evening dose
    E Omit usual morning dose, halve evening dose
A
  1. B Halve usual morning dose, take usual insulin with
    evening meal
    Patients with well controlled type 1 diabetes having suitable elective procedures will
    benefit from day surgery as it aims to minimise disruption to their usual routine and
    allows patients to resume self-management of their diabetes.
    Starvation time should be less than 12 hours so that they only miss one meal. They
    should be placed first on a list and anaesthetic techniques that promote early return
    to normal oral intake should be used. The ideal insulin regimens for diabetics can be
    seen in Table 3.6.
    Patients that have an HbA1c in the last 12months >69mmol/mol (8.5%) should be
    considered for referral to their GP or clinic for stabilisation prior to elective surgery. A
    high level of plasma glucose leads to greater amount of glycosylated haemoglobin
    molecules where glucose binds to the globin chain. This persists for the duration
    of the molecule’s lifespan, and so this HbA1c measurement acts as an indicator of
    glucose control over the preceding 8–12 weeks.
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6
Q
  1. A 25-year-old woman is having a hysteroscopic myomectomy for infertility under
    general anaesthesia. The procedure has been prolonged and the irrigation bags
    have been changed several times. On screen you can see some blood and bubbles
    in the uterine cavity. She is positioned in the lithotomy position and is slightly
    head down. You suddenly notice a stepwise decrement in end-tidal waveform
    capnography, the patient desaturates and there is new T wave inversion on her
    ECG.
    Which of the following is the most appropriate immediate management?
    A Call for help, ask the surgeon to stop. Place the patient flat. Give a fluid
    challenge and high-flow oxygen.B Call for help, ask the surgeon to flood the uterus with irrigation. Place the
    patient flat. Give a fluid challenge and high-flow oxygen.
    C Call for help, ask the surgeon to externally compress the uterus. Place the
    patient lateral. Give a fluid challenge and high-flow oxygen.
    D Call for help, ask the surgeon to empty the uterus. Place the patient head up.
    Give a fluid challenge and high-flow oxygen.
    E Call for help. Steepen the head down to insert a central venous line into the right
    internal jugular vein, pass it into the right atrium and attempt to aspirate air.
A
  1. D Call for help, ask the surgeon to empty the uterus. Place
    the patient head up. Give a fluid challenge and high-flow
    oxygen
    Gas embolism can occur either into the venous system or the arterial system, and
    may involve gases other than air e.g. carbon dioxide in the case of laparoscopic
    misadventure. The pathophysiology and principles of management should be clear
    in your mind.
    Incidence
    In the clinical arena, clinically obvious air embolism is thankfully rare; however in
    studies looking for the condition, venous air embolism (VAE) was discovered in 100%
    of seated craniotomies, 40% of Caesarean sections and 30% of hip replacements.
    Dose of air is important, as is the size of the patient and the rate of air ingress. Rapid
    air entry is worst with a lethal dose of around 1mL/kg.
    Pathophysiology
    Gas entering the venous system returns to the right heart and can cause a right
    ventricular outflow obstruction as the air is compressible and causes mechanical
    dysfunction. Distal flow of air causes trapping in the pulmonary vessels and a
    massive increase in pulmonary vascular resistance (PVR) and fulminant right
    heart failure. Some micro-emboli may pass into the distal tree and produce non-
    cardiogenic pulmonary oedema by secondary mechanisms. Air may also pass
    through the lungs and on into the systemic circulation or through a patent foramen
    ovale. Clinically the patient will exhibit tachypnoea, tachycardia and cardiovascular
    collapse if the volume is great enough. Smaller doses may give chest pain, shortness
    of breath and mental disturbance.
    During anaesthesia the end-tidal CO2 falls as shunt increases, and desaturation will
    occur with variable ECG changes and cardiovascular instability. Pulmonary oedema
    may develop as a later sign, and central venous pressure can be elevated.
    Detection
    Clinical suspicion and vigilance are imperative in the detection of VAE. Classically
    described tools for detection such as the precordial and oesophageal stethoscope
    have poor sensitivity and are not often used. Doppler, in transoesophageal or
    transcranial positions are very sensitive detectors of air.
    Treatment
    Immediate treatment is supportive and resuscitative along the ABC algorithm. It
    should then focus on preventing further air entry, reducing the size of the embolus,
    and overcoming the mechanical obstruction in the right side.
    Preventing further air ingress can be achieved surgically at the site of bleeding,
    either by covering or compressing bleeding areas and flooding the area with saline.
    Venous pressure can be increased by positioning the site lower than the heart,
    administering intravenous fluids, performing a Valsalva manoeuvre or increasing
    intrathoracic pressure. Reducing the size of an embolus is achieved by immediate discontinuation of
    nitrous oxide and giving 100% oxygen that promotes nitrogen diffusion out of the
    bubble. Aspiration from the right atrium via a central line may be possible if the
    embolus is large and the patient positioned either lateral or head down position
    to prevent further forward movement of air out of the right ventricle. This would
    depend on the line already having been situated and the tip positioned in the right
    atrium. Hyperbaric oxygen therapy will also promote rapid clearance of emboli.
    Overcoming mechanical obstruction relies on judicious use of fluid and inotropic
    agents to support a right ventricle against the sudden rise in pulmonary vascular
    resistance.
    One may not classically attribute gynaecological surgery with a high risk of venous
    air embolism, but as described hitherto the only requirements are pressurised gas
    and an open vascular system.
    The key elements here in terms of management are:
    t Recognise this as an anaesthetic emergency and summon help
    t Preventing further air ingress
    The aim therefore is to promote higher venous pressure at the site to reduce air
    entrainment. Given the uterine site of bleeding, a head up position will be best.
    Bear in mind the need for resuscitation may necessitate laying the patient flat if
    cardiac arrest ensues. Other measures include compressing the wound edges by
    the surgeon, and flooding with saline. In this case, with a full uterine cavity, external
    compression may increase the pressure gradient and promote residual gas inflow.
    The safest compromise is likely to be to empty the cavity such that the pressure
    driving gas into the venous system is removed.
    Supportive measures
    Increasing the fraction of inspired oxygen to 100% will increase the partial pressure
    of oxygen and favours nitrogen washout from bubbles to the alveoli. This will also
    ensure that, if used, nitrous oxide would also be washed out.
    A fluid bolus will assist in raising the venous pressure, and also assist the right
    ventricle combating elevated pulmonary pressures, as well as support systemic
    perfusion pressure.
    Aspirating the air lock within the right atrium may be possible if there is a central line
    already in situ. However, insertion after diagnosis is likely to distract from immediate
    management and is not recommended
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7
Q
  1. A 68-year-old man undergoing vocal cord surgery is receiving high frequency jet
    ventilation via a subglottic catheter with the following standard settings: Fio2 0.9,
    driving pressure 2 atmospheres, frequency 150 min-1, inspiratory time 50%. Blood
    gas analysis shows a respiratory acidosis and clinically there is no evidence of air
    trapping.
    Which action is most likely to improve the respiratory acidosis?
    A Increasing the driving pressure
    B Increasing the ventilator frequency
    C Increasing the inspiratory time
    D Increasing the Fio2
    E Increasing the expiratory time
A
  1. A Increasing the driving pressure
    High frequency jet ventilation is a specialised ventilation modality designed to
    achieve gas exchange by using high frequency, low tidal volume breaths. It differs
    from conventional ventilation since gas exchange is not primarily dependent on
    bulk flow to the alveoli (as the tidal volumes are often lower than the dead space). Instead, gas exchange is believed to occur due to Pendelluft ventilation, enhanced
    molecular diffusion, cardiogenic mixing and co-axial flow.
    High frequency jet ventilators work by generating high frequency jet streams which
    entrain air at the jet nozzle by the Venturi principle. Adjustable settings include the
    driving pressure, inspiratory time, ventilation frequency and FIO2.
    Responses to adjustments are different when compared to conventional ventilation
    modes and may seem counterintuitive. For example, an increased ventilation
    frequency can worsen CO2 retention by impeding passive exhalation. It is therefore
    recommended to reduce the ventilation rate when treating hypercapnoea if there
    is evidence of air trapping. Increasing the inspiratory time (% ventilator cycle)
    improves oxygenation, but at high values may also impair passive exhalation
    and cause CO2 retention. The action most likely to improve CO2 clearance is to
    increase the driving pressure since this will increase the tidal volumes and alveolar
    ventilation. Increasing the expiratory time (by reducing the inspiratory time) will
    not improve CO2 clearance in this scenario as the tidal volumes will be reduced and
    there is no evidence of air trapping. Increasing the FIO2 will improve oxygenation but
    has no effect on CO2 clearance (Figure 3.4).
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8
Q
  1. A patient 10 days post coronary artery bypass grafting requires an MRI brain scan
    for neurological deterioration.
    Which of the following is most likely to be a safety hazard during the scan?
    A History of a total hip replacement
    B Presence of sternal wires
    C Use of an endotracheal tube with metallic spring in the pilot balloon
    D Epicardial pacing wires
    E Invasive arterial blood pressure transducer
A
  1. D Epicardial pacing wires
    Safety considerations when anaesthetising patients for MRI scans include:
    t Remote location
    t Limited access to the patient
    t The projectile effect of the magnetic field on ferromagnetic equipment
    t The heating effect and risk of burns from conductive wires and coils
    t Risk of equipment malfunction
    t Noise protection
    t Risk of contrast reactions
    MRI scanners operate with magnetic field strengths of 0.5–3 Tesla (T). The strength
    of the field decays exponentially with distance from the magnet, which is always
    kept on. Zones around the magnet are described in terms of Gauss (G), where 1T =
    10,000G. Within 50G zone a significant attractive force will risk ferromagnetic objects
    to act as projectiles potentially causing serious harm or damage, and an area of 5G is
    set where no unscreened personnel should enter (see Figure 1.2). Currents may be
    generated in cables especially in coils causing a local heating effect that may cause
    burns to the patient.
    Special MRI safe anaesthetic machines, ventilators and monitors should be available.
    MRI compatible ECG electrodes, and fibreoptic pulse oximetry should be used
    and all cables should be kept away from the area being imaged, in straight lines
    away from the patient to avoid burns. ST-T wave artefacts may occur due to the
    heating effect of blood around the aortic arch. Blood pressure cuffs without metal
    connectors and invasive pressure transducers may be used. Gas sampling lines
    will be longer, increasing the lag time and dead space. Epicardial pacing wires and
    pulmonary artery catheters containing conductive wires risk myocardial heating and
    burns, and scans cannot be performed in cases where these cannot be removed.
    The spring in an endotracheal tube pilot balloon is safe, however it should be taped
    away from the area being scanned as it may cause image artefact. Only essential
    infusions should be continued and long extensions attached to pass through a wall
    port so that the syringe pumps can stay in the control room.
    Most orthopaedic prostheses, surgical clips and sternal wires are safe, but may
    distort images. Other implanted metallic devices such as pacemakers, cochlear
    implants, intraocular metallic objects and aneurysm clips will cause internal heating,
    malfunction or risk movement and so would contraindicate a scan.
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9
Q
  1. A 27-year-old woman is to have femoral nerve block with the aid of nerve
    stimulator.
    What is the most important feature of an electrical peripheral nerve stimulator?
    A Short pulse duration
    B Stimulation frequency of 2 Hz
    C Constant current generator
    D Negative stimulation polarity
    E Actual current digital display
  2. You have been called to site an epidural
A
  1. C Constant current generator
    The use of a peripheral nerve stimulator to localise nerves is still the commonest
    technique employed worldwide in regional anaesthesia. The method is based on the principle that muscle contraction becomes obvious when enough electrical current
    is applied to the nerve in order to depolarise the nerve fibres.
    The main objective in regional anaesthesia is to stop nerve conduction by infiltrating
    enough local anaesthetic close to the nerve fibres and provide motor and sensory
    block. This goal is possible due to the capability of nerve stimulators to approximate
    the distance between the nerve and the needle tip and hence can localise the
    optimal injection site.
    Nerve fibres differ anatomically according to their thickness and degree of
    myelination. Stimulating motor fibers with nerve stimulator is easier than
    stimulating sensory fibres because Aα motor fibers have the maximal velocity of
    impulse spreading and a relatively low threshold for extrinsic activation because
    of a large diameter and high degree of myelination. In contrast, C-fibres have a
    small diameter and very little or no myelin sheath, hence have a high threshold for
    external stimulation and relatively slow action potential propagation.
    An ideal nerve stimulator should have the following features:
  2. Constant current generator: They must be able to supply a constant electrical
    current between the negative pole and the positive pole irrespective of the
    wide range of impendences encountered by the tissue around the nerve. Nerve
    stimulators provide a current range between 0.01–5mA.
    When performing a nerve block, the ideal initial current is 1–2mA. The needle is then
    inserted until the desired muscle contraction is seen. The stimulating current is then
    gradually decreased until twitches are still seen at a final range of 0.2–0.5mA which
    is the most acceptable current threshold. A current above 0.5 mA may mean the
    needle tip is far from the nerve and the block may not be successful. Twitches should
    not be seen below 0.2mA because motor response below 0.2mA may mean the
    needle is inside the nerve and injecting maybe harmful.
  3. Stimulation polarity: In order to get maximum benefit from the delivered current,
    the needle should be connected to the negative pole (cathode) to depolarise nerve
    fibres. Stimulating nerves with the anode will lead hyperpolarisation of the fibres,
    thus a stronger current will be required to depolarise the nerve. Modern nerve
    stimulators are designed in order to only allow the needle to be connected to the
    cathode electrode.
  4. Stimulation frequency: This affects the speed of nerve localisation. The ideal
    current frequency is 1–2Hz, where a higher frequency makes nerve detection faster,
    but causes more patient discomfort. Therefore, the most common frequency used is
    2Hz.
  5. Pulse duration: This is the time for which the electrical current is applied to the
    nerve. A short pulse duration (0.1ms) ensures motor neurons are stimulated but not
    the sensory neurons.
  6. Accuracy: The current generated by the nerve stimulator must be similar to the
    displaced one on the digital screen. Accurate current generation is mandatory for
    correct needle insertion and successful nerve block.The above features of nerve stimulators are all essential for successful nerve block.
    However, the most important characteristic of peripheral nerve stimulators is the
    constant current generation. This allows the current to remain the same regardless
    of resistance variation encountered by tissue, thus decreases the chance of nerve
    damage or unsuccessful nerve block.
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10
Q
  1. You have been called to site an epidural for a 32-year-old term primigravida
    patient. She is now 3cm dilated with slow progress and very distressed with each
    contraction. While you are placing the Tuohy needle in the epidural space, you see
    an obvious flow of clear fluid through the needle.What would be the most appropriate next course of action?
    A Pull the needle out and arrange alternative analgesia
    B Inject 10mL of normal saline into the subarachnoid space to prevent post-
    dural puncture headache (PDPH) and then re-site the epidural catheter in
    another interspace
    C Remove the needle and re-site the epidural catheter in another interspace. Tell
    the midwife to use 10mL of epidural mixture for each top-up
    D Thread the epidural catheter through the punctured dural hole and use it as
    intrathecal catheter. Make sure only an anaesthetist gives every top-up dose
    E Pull the needle out and call the consultant on call to perform a blood patch to
    prevent PDPH
A
  1. D Thread the epidural catheter through the punctured
    dural hole and use it as intrathecal catheter. Make sure
    only an anaesthetist gives every top-up dose
    Inadvertent dural puncture can occur following many procedures, for example spinal
    surgery. However, in anaesthetic practice it is usually a consequence of epidural
    analgesia and anaesthesia.
    Every year, approximately 140,000 labouring women receive an epidural in the
    UK. 1,400 (1%) will suffer an accidental dural puncture. The commonest reported
    complication is post-dural puncture headache (PDPH), with an incidence varying
    from 60% to 90%. Headache usually develops 12–24 hours following dural puncture.
    PDPH may cause significant morbidity and mothers may be unable to properly care
    for their newborn or themselves for some time.
    Puncturing the dura with a 16G Touhy needle usually results in an obvious
    cerebrospinal fluid (CSF) flow through the epidural needle. The CSF is warm to touch
    and tests positive to glucose with urine dipstick.
    Each obstetric unit should have a plan of action for accidental dural tap.
    At the time of recognised dural puncture, the anaesthetist must decide whether
    to use the catheter for a continuous subarachnoid (intrathecal) technique or
    re-site the epidural in another interspace. Whichever decision is made, only the
    anaesthetist should give every dose of local anaesthetic top-up. Therefore, stem D is
    inappropriate here as the midwife gives the top-up.
    The patient should be informed about the dural puncture and counseled regarding
    potential complications and further management options. A senior anaesthetic
    colleague, the obstetric registrar and the midwife should also be informed, and the
    operator must ensure everything is documented in the patient’s notes.
    If no PDPH is present during labour, pushing at full dilation can be encouraged.
    However, if a headache is present, forceps delivery may be advised.
    After delivery, remove the catheter as usual. There is little evidence that leaving a
    subarachnoid catheter in place for 24hours can reduce PDPH.
    If no headache is present post delivery, do not restrict patient’s mobilisation,
    as immobilisation will not prevent the development PDPH. However, if a PDPH develops, encourage bed rest, regular analgesia, oral fluid and oral caffeine intake,
    and consider epidural blood patch. Epidural blood patch is the gold standard
    therapy for PDPH, however if performed within 24 hours of onset of symptoms there
    is a failure rate of 70%, which reduces to 4% if performed after 24 hours. Therefore, it
    is preferable to perform blood patch more than 24 hours after the dural tap occured.
    Studies investigating the use of epidural saline as a preventative measure against
    PDPH failed to reach statistical significance. In addition, pooled results of the
    four randomised trials failed to show statistical significance for the use of epidural
    blood patch as prophylactic measure to treat PDPH. The use of sumatriptan and
    adrenocorticotrophic hormone (ACTH) has also previously been advocated, but
    again there is a large disparity in the evidence base for their use.
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11
Q
  1. You have been called to an acute medical ward to help manage a man who has
    become distressed and angry with the medical management of a relative, and is
    now behaving violently toward one of the ward staff. When you arrive the situation
    is heated, security and porter staff are already in attendance. The sister tells you
    and the on call psychiatrist that the man is unreasonable and needs to be sedated
    for safety.
    How do you proceed?
    A Offer the man a dose of oral lorazepam
    B Attempt to assess his capacity, and discuss with your consultant. Defer
    immediate management to the security staff and police
    C Give intramuscular lorazepam and haloperidol
    D Give a dose of intramuscular ketamine and transfer to a monitored environment
    E Organise the security staff to restrain the man, and give intramuscular lorazepam
A
  1. B Attempt to assess his capacity, and discuss with your
    consultant. Defer immediate management to the security
    staff and police
    There are multidisciplinary rapid response teams in some hospitals, for the purpose
    of sedating disturbed psychiatric inpatients, which do include anaesthetists. The
    Royal College of Anaesthetists has issued position statement guidance in tandem
    with the Royal College of Psychiatrists, the noteworthy points include:
    t Anaesthetists should only act as part of a multidisciplinary response team
    incorporating mental healthcare professionals including a psychiatrist
    t Trainee anaesthetists should not routinely be involved in initiating
    pharmacological restraint, but if the urgency of the clinical situation dictates they
    must only act within their competence and, whenever possible, after consultation
    with a consultant anaesthetist
    t When rapid tranquillisation is deemed appropriate the minimum intervention
    possible should be used as guided by the local protocol
    t The full range of ventilatory/resuscitation equipment and trained assistance must
    be immediately available when rapid tranquillisation is administered
    t The College does not support under any circumstances the use of rapid
    tranquillisation to manage violence or aggression in visitors or other individuals
    on hospital premises
    This question, like some past exam SBAs, reflects some of the more difficult ‘real-
    life’ clinical situations we can find ourselves in as practising anaesthetists. The
    important points to draw from the stem are the lack of any evidence of confusion
    or signs of organic mental illness. The man is aggressive and violent, but as a visitor
    is not a patient of the hospital. This means that his behaviour should be managed
    by security staff, who have been specially trained to do so, and if necessary by the
    police. If the police after their initial assessment were to believe him to be mentally
    disturbed, they would convey him to the emergency department or other place ofsafety for specialist assessment. This does not remove our responsibility to respond
    to treat visitors in an emergency, such as in the case of a collapse or cardiac arrest.
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12
Q
  1. A 24-year-old 60 kg woman has been injured in a house fire. She has sustained
    40% full thickness lower limb and abdominal burns. Her burns were sustained at
    11 pm. She is intubated in the emergency department for suspected inhalational
    injury and resuscitated with 2 litres of crystalloid in total. At 3 am she is ready for
    transfer to the regional burns unit that is 4 hours away.
    What is the most appropriate fluid regime during transfer?
    A Colloid solution, at 500mL/hour
    B Compound sodium lactate, at 500mL/hour
    C 0.9% sodium chloride, at 500mL/hour
    D Colloid solution, at 700mL/hour
    E Compound sodium lactate, at 700mL/hour
A
  1. E Compound sodium lactate, at 700mL/hour
    Fluid resuscitation after burns injury is widely guided by the Parkland formula:
    4mL/kg/% body surface area burn, where half of this volume is given in the first
    8hours after the burn injury, and the second half over the next 16hours. Thus for the
    above patient:
    4 x 60 x 40 = 9600mL
    Therefore this patient requires 4800mL in the first 8hours.
    Two litres has already been given in the first 4 hours since the burn, and so 2800mL
    should be given over the next 4 hours, which is 700mL/hour.
    Intravenous fluids are given in cases of more than 15% total body surface area
    (TBSA) burns or 10% with smoke inhalation. The fluid of choice is a balanced
    crystalloid solution, and initially a urine output of greater than 0.5mL/kg/hour is
    used to guide adequate resuscitation.
    Criteria for referral to a specialist burns unit include:
    t >2% TBSA in children or >3% in adults
    t Full thickness burns
    t Circumferential burns
    t Unhealed burn after 2weeks
    t Any suspicion of non-accidental injury
    Discuss with a burns specialist with an opinion to transfer:
    t Burns to hands, feet, face, perineum or genitalia
    t Chemical, electrical or friction burns
    t Cold injuries
    t Febrile child with a burn
    t Co-morbidities affecting treatment or healing of the burn
    Intubation for a burn is indicated in the presence of stridor, oropharyngeal oedema,
    deep facial or neck burns, a GCS <8, hypoxia or hypercapnia, or suspicion of
    inhalational injury. Facial oedema can progress rapidly and an early intubation using
    a large uncut endotracheal tube should be performed prior to transfer if there are
    any concerns. A rapid sequence induction using suxamethonium is acceptable if
    within the first 24hours after the burn.
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13
Q
  1. A previously well 28-year-old man presents to the emergency department with
    a 48-hour history of feeling generally unwell and complains of polyuria and
    abdominal pain.
    His arterial blood gas on room air is shown in Table 3.1.
    His biochemistry profile is shown in Table 3.2.
    Which of the following is the most likely diagnosis?
    A Renal tubular acidosis
    B Severe sepsis
    C Pancreatitis
    D Addison’s disease
    E Diabetic ketoacidosis
A
  1. E Diabetic ketoacidosis
    This patient has presented with a raised anion gap metabolic acidosis.
    Causes of raised anion gap metabolic acidosis indicate the presence of an
    unmeasured anion; in this case ketones, the anion gap can be calculated as follows:
    (Na+ + K+) – (HCO3– + Cl–)
    Normal range: 8–16mmol/L
    The causes can be remembered using the acronym ‘MUDPILES’:
    t Methanol
    t Uraemia
    t Diabetic ketoacidosis
    t Propylene glycol
    t Isoniazid
    t Lactic acidosis
    t Ethylene glycol
    t Salicylates
    The abdominal pain and polyuria together with the biochemical profile make
    diabetic ketoacidosis (DKA) a likely diagnosis. DKA is commonly precipitated by
    infection or non-compliance to insulin therapy in the known type 1 diabetic mellitus
    patient. However an increasing proportion occurs in the undiagnosed diabetic
    patient and may indeed be the presenting feature as in this case.
    Severe sepsis would also cause a raised anion gap but is unlikely given the history
    and normal lactate.
    Normal anion gap metabolic acidosis may be due to loss of bicarbonate ions which
    is replaced by chloride ions, a loss of sodium ions or an excess of chloride ions.
    Causes can be classified into:
    t Gastointestinal; such as diarrhoea, fistulae (pancreatic, ureters, biliary, small
    bowel, ileostomy)
    t Renal such as renal tubular acidosis and Addison’s
    t Iatrogenic such as administration of normal saline solution
    Hence option A, C and D would be differential diagnoses if the anion gap was
    normal in this patient.
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14
Q
  1. A 64-year-old man with a background of hypertension and ischaemic heart
    disease is being managed for septic shock. The patient has pyelonephritis
    and gram negative sepsis that is being treated with sensitive antibiotics. The
    management includes a positive fluid balance for the last 24 hours of 5.5 liters and
    a noradrenaline infusion currently administered at 0.8 μg/kg/min maintaining
    a mean arterial blood pressure (MAP) of 55mmHg. The ventilation parameters
    are deteriorating and he is now receiving an Fio2 of 0.6. His latest haemodynamic
    monitoring studies from a minimally invasive device are:
    r Cardiac output index (CI) L/min/m2 (NR 3–5) – 1.94
    r Intra-thoracic blood volume index (ITBVI)mL/m2 (NR 850–1000) – 650
    r Systemic vascular resistance index (SVRI) (NR 1970–2390 ) – 3854
    r Extra-vascular lung water index (EVLWI) (mL/kg) (NR 3–7) – 14What is the most appropriate next course of action?
    A Fluid bolus of 500mL crystalloid and repeat studies
    B Increase the noradrenaline to increase MAP to 70mmHg
    C Add dobutamine at 2.5μg/kg/min
    D Order an urgent transthoracic echo and send cardiac troponin measurement
    E Commence urgent haemofiltration aiming to reduce pulmonary interstitial
    fluid
A
  1. A Fluid bolus of 500mL crystalloid and repeat studies
    Cardiac output monitoring is increasingly more important in the management of
    haemodynamically unstable patients on the intensive care unit. There are many
    different options available including the invasive pulmonary artery catheter (PAC),
    minimally invasive measurements including pulse contour analysis and oesophageal
    doppler techniques and non-invasive methods (such as thoracic bio-impedance).The most popular currently is a minimally invasive technique, requiring arterial
    access for pulse-contour or pulse-power analysis. Two different types exist:
  2. Trans-pulmonary dilution curve for calibration for increased accuracy of analysis
    (e.g. PiCCO uses thermodilution to measure pulse-contour and LiDCO uses
    lithium dilution to measure pulse-power);
  3. No calibration is performed and therefore no central line is required. Analysis
    of the arterial waveform is conducted by proprietary formulae, which are more
    convenient but less accurate (e.g. FloTrac/Vigileo).
    The readings above are from a minimally invasive device using trans-pulmonary
    dilution curve analysis, which offer the advantages of accuracy comparable to a PAC
    in addition to continuous waveform analysis. Cold or lithium injectate is injected
    through the central line and the temperature or lithium concentration is measured
    at an arterial line placed in a large artery (femoral or axillary).
    The injectate mixes with the following before reaching the arterial line (Figure 3.5).From analysis of the dilution curve (Stewart-Hamilton Equation) one can calculate:
    t Cardiac output
    t Detection of volumes:
    – Global end-diastolic volume (GEDV) is a sum of all of the end-diastolic volumes
    – Intra-thoracic blood volume (ITBV) is the GEDV in addition to the pulmonary
    blood volume (PBV)
    – Extra-vascular lung water (EVLW)
    Continuous cardiac output monitoring is displayed after calculation of aortic
    compliance (derived from blood pressure and blood flow recording simultaneously) and is also dependent on heart rate. Systemic vascular resistance index (SVRI) may
    also be calculated using the following equation
    SVRI = 80 × (MAP-RAP)
    CI
    Where:
    MAP is mean arterial pressure
    RAP is right atrial pressure
    CI is cardiac index in dyn·s·cm−5·m−2
    80 is a unit-conversion constant
    ITBV (GEDV + PBV) may be used as a marker of cardiac pre-load, which may guide
    volume therapy. EVLWI reflects the amount of pulmonary interstitial fluid. It does
    not correlate well with oxygenation or chest radiograph lung opacification but does
    reflect severity of illness and length of ventilation. Reducing the ITBV to normal
    levels may reduce the EVLWI.
    Most values are best looked at as a function of patient size and a therefore indexed
    according to body surface area.
    Referring back to our very sick and problematic patient, the decision tree that may
    aid management is summarised in Figure 3.6.
    The patient described above has a low cardiac output, reduced pre-load (ITBVI) and
    is over-vasoconstricted (SVRI). The EVLWI is raised and the ventilation is deteriorating
    muddying the management waters.
    Efforts to exclude an ischaemic cause for shock is warranted and commencing
    haemofiltration is important for modifying fluid balance once the inflammatory
    cascade has settled, but both will help little with the haemodynamic compromise in
    the immediate term.
    The most appropriate intervention given the values above is more intravenous
    volume administration, monitoring for an improvement in the cardiovascular status including a higher MAP and decreasing noradrenaline requirements. If this fails
    or if a further deterioration of the patient’s ventilation occurs, an inotrope such as
    dobutamine would be the next appropriate intervention.including a higher MAP and decreasing noradrenaline requirements. If this fails
    or if a further deterioration of the patient’s ventilation occurs, an inotrope such as
    dobutamine would be the next appropriate intervention.
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15
Q
  1. A 17-year-old man is admitted to the critical care unit having ingested 11 g of
    paracetamol 18 hours ago. An N-acetylcysteine infusion has been started and
    bloods are awaited.
    His blood pressure is 80/43mmHg following one litre of Hartmann’s solution,
    with a heart rate of 118 beats per minute. He is agitated and full neurological
    examination is difficult. On 100% oxygen his Spo2 is 92%, with a respiratory rate of
    42 breaths per minute.
    An arterial blood gas is shown in Table 3.3.The next most appropriate intervention in his management would be:
    A Central venous catheter and start noradrenaline
    B Intubation and ventilation
    C Urgent transfer to a liver specialist intensive care unit
    D CT head
    E Placement of a urinary catheter
A
  1. B Intubation and ventilation
    This is a delayed presentation of paracetamol overdose with evidence consistent
    with fulminant liver failure requiring urgent management. Paracetamol overdose is
    the leading cause of acute fulminant (or hyperacute) liver disease in the UK.
    90% of ingested paracetamol (N-acetyl-p-aminophenol) is metabolised by the
    liver. In non-toxic doses the predominant metabolic pathway is via glucuronidation
    and sulphation, with less than 10% metabolised by an alternative pathway via
    cytochrome P450 to the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI).
    In health, NAPQI is inactivated by glutathione.
    This patient has taken a toxic dose of paracetamol which probably represents
    >150mg/kg. The usual pathway of glucuronidation and sulphation are exhausted
    and the cytochrome P450 represents an increased proportion of the metabolism.
    Once glutathione reserves are depleted, unconjugated NAPQI exerts toxic
    effects through hepatocellular damage. In this patient, the delayed presentation
    has compounded this damage. A staggered overdose may also have a similar
    presentation.
    The management principles of a paracetamol overdose, as with other overdoses, is a
    systematic ‘ABC’ approach with specific management to reduce absorption, increase
    elimination and treat organ failure.
    This patient is tachyponeic due to the profound underlying metabolic acidosis. He is
    likely to tire from the work of breathing and his underlying problems are difficult to
    assess and manage with the agitation, so intubation and ventilation is the next most
    appropriate step.
    Fulminant liver disease is consistent with a high cardiac output and low systemic
    vascular resistance and may require vasopressor support. However, at present he
    is not adequately fluid resuscitated and unlikely to tolerate an awake insertion of a
    central line. Hence option A may become appropriate in his ongoing management
    but not clinically indicated at present.
    Unfortunately he has presented beyond the window for gastric decontamination
    with activated charcoal; this should be considered within two hours of ingestion or
    where a staggered overdose is suspected. He has correctly been started empirically
    on N-acetyl cysteine (NAC), indicated by the severity of his overdose.
    NAC increases glutathione reserves and hence enhances conjugation with NAPQI.
    The dose is 150mg/kg loading over 15 minutes, followed by 50mg/kg over the
    next 4hours and 100mg/kg over the subsequent 16 hours. Where a non-toxic dose
    of paracetamol is suspected, waiting for 4 hours post ingestion paracetamol level
    is appropriate and comparing with the new single line paracetamol treatment
    nomogram. This patient clearly needs to be discussed with the local liver specialist intensive care
    unit as an urgent priority. Once resuscitated, a liver transplant may represent his
    only hope for survival. The King’s College Hospital Criteria for consideration for liver
    transplantation in paracetamol overdose are:
    Either:
    t pH <7.3 (or 7.25 if on NAC)
    Or all of the following:
    t Prothrombin time (PT) >100 seconds (INR >6.5)
    t Creatinine >300μmol/L
    t Grade 3 or above encephalopathy
    He will require a urinary catheter to measure urine output. The cause for his agitation
    is most likely his acidosis and possible encephalopathy. If the circumstances around
    his overdose raised suspicion of trauma or collapse a CT head should be considered,
    however at present is not an immediate action.
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16
Q
  1. A 28-year-old woman presents to the emergency department with pleuritic chest
    pain, shortness of breath and dizziness shortly after disembarking a flight from
    South East Asia. Her respiratory rate is 45 breaths per minute, her blood pressure
    is 70/40mmHg and heart rate is 160 beats per minute. Admission to the high
    dependency unit is requested for cardiovascular support.
    Which piece of information would most influence your choice to administer
    thrombolysis?A Currently on anticoagulation
    B Information from a CT pulmonary angiography
    C Information from a bedside transthoracic echo
    D A history of being 20 weeks pregnant
    E A history of peptic ulcer disease
A
  1. C Information from a bedside transthoracic echo
    The incidence of pulmonary embolism (PE) is around 60–70 per 10,000, and more
    than half occur in hospital. Prompt recognition and consideration of the diagnosis is
    essential to prevent progression of the embolism and death.
    Pulmonary embolism may be categorised into small, non-massive (or sub-massive),
    and massive, the major difference being the degree of cardiac instability:
    t A small PE is an embolism that does not cause hypotension or right ventricular
    dysfunction
    t A non-massive PE is one in which the patient remains normotensive but right
    ventricular dysfunction can be demonstrated
    t A massive PE is onme that causes right ventricular dysfunction and hypotension
    In the majority of patients CT pulmonary angiography (CTPA) is the investigation
    of choice. This is a contrast-enhanced scan, which is conducted rapidly (less than
    one second) to avoid movement artifact due to respiration and cardiac pulsation
    and reduce the radiation exposure, making it safe in pregnancy. A filling defect that
    is seen in the pulmonary vasculature is diagnostic. The problem with this ‘snap-
    shot’ image is that it gives little information over the course of the cardiac cycle. A
    bed-side echo is essential for obtaining detailed information regarding pulmonary
    artery pressures, right ventricular dysfunction and right atrial enlargement when
    considering a potentially life-threatening intervention. In addition if the embolism
    is intra-cardiac or within the proximal pulmonary artery it may be directly visualised
    using this technique.
    Returning to our scenario, the assumption is that this young lady has a massive
    PE and that she is hypotensive as a result. There are relative and absolute
    contraindications for thrombolysis.Absolute contra-indications:
    t Previous intracranial bleeding at any time
    t Stroke within the last 6months
    t Closed head or facial trauma within 3months
    t Suspected aortic dissection
    t Uncontrolled high blood pressure (>180 systolic or >100 diastolic)
    t Known structural cerebral vascular lesion, arteriovenous malformations,
    aneurysm or brain tumors
    t Thrombocytopenia or known coagulation disorders
    t Pericardial effusion
    t Septic emboli
    Relative contra-indications:
    t Current anticoagulant use
    t Invasive or surgical procedure in the last 2weeks
    t Prolonged cardiopulmonary resuscitation
    t Pregnancy
    t Hemorrhagic or diabetic retinopathies
    t Active peptic ulcer
    t Controlled severe hypertension
    This patient has several relative contraindications and in this critical situation these
    factors will not help you make a final decision regarding the need for thrombolysis
    as clearly a young healthy patient has everything to loose from not receiving
    treatment. The CTPA may diagnose a PE (which appears clinically obvious) but the
    patient must undergo a hazardous transfer and the scan takes valuable time to be
    performed and reported. The test that will give most information at this stage is
    the bedside echo which will visualise right ventricular dysfunction. This is seen as a
    dilated ventricle equal or larger in diameter when compared to the left ventricle with
    paradoxical septal movement, which in conjunction with hypotension means the
    diagnosis is massive PE. The treatment is therefore thrombolysis and the sooner it is
    administered the better
17
Q
  1. A 46-year-old man is sedated and intubated for respiratory failure secondary to
    community acquired pneumonia. He is known to have recurrent admissions with
    pneumonia. Your junior colleague sustains a needlestick injury whilst inserting an
    arterial line, is anxious and would like you to test this patient for HIV.
    With regards to HIV testing in this patient, the best course of action is:
    A Request consent from the next of kin
    B Test the patient for HIV
    C Do not test this patient for HIV because you suspect he is low risk
    D Do not test this patient for HIV as it is unethical
    E Wait until the patient has capacity and gain consent from the patient for HIV
    testing
A
  1. B Test the patient for HIV
    HIV testing remains a contentious topic. Recent guidance recommends that, where
    possible, consent from the patient should be sought. However within the intensive
    care environment, valid consent in a patient with capacity is challenging. HIV testing
    can be performed without antecedent consent, where there is reasonable clinical
    suspicion of HIV, and it is in the best interests of the patient. The prognosis following
    a diagnosis of HIV is significantly improved with early diagnosis and treatment.
    This man has recurrent pneumonia and his current episode is severe requiring
    intubation. This should prompt the clinician to consider underlying diagnoses that
    lead to immunosuppression including HIV. A HIV test is indicated in the clinical management of this patient. The result of the HIV test will impact on the length
    of post exposure prophylaxis for the junior colleague, who sustained a needle
    stick injury. However it must be emphasised, this is not the primary indication for
    performing a HIV test in this patient.
    Consent by the next of kin is not valid unless there is a lasting power of attorney
    or advance directive in place. Assent can be gained from the next of kin in certain
    situations such as the decision to perform a percutaneous tracheostomy. Due
    to confidentiality issues surrounding the result of a HIV test, it is not appropriate
    to request assent from the relatives to perform a HIV test. In the sedated patient
    with no prior documented advance directive or lasting power of attorney, it is the
    clinician’s role to act in the best interests of the patient.
    This man has a severe pneumonia and it is currently unclear when he is likely to gain
    capacity. It does not seem appropriate to wait for this, especially as this may delay
    starting treatment in the presence of HIV.
18
Q
  1. A 25-year-old woman is undergoing a category 1 lower segment Caesarean
    section (LSCS) for fetal bradycardia. You perform a rapid sequence induction with
    thiopentone 500mg and suxamethonium 100mg but are unable to intubate after
    three attempts. The patient is desaturating and you are unable to ventilate with
    a face mask and Guedel airway or with a laryngeal mask airway, despite cricoid
    pressure being reduced and then released. You successfully perform a needle
    cricothyroid puncture and an ENT surgeon has been informed and is on their way.
    The fetal heart rate remains at 60 bpm.
    What is the next appropriate step?
    A Continue oxygenation and proceed with emergency LSCS
    B Delay LSCS until ENT have performed surgical tracheostomy
    C Once ENT arrive, perform surgical tracheostomy and LSCS at the same time
    D Abandon LSCS and continue oxygenation until patient wakes up
    E Continue oxygenation until patient wakes up and then perform a spinal
    anaesthetic
A
  1. B Delay LSCS until ENT have performed surgical
    tracheostomy
    In this scenario there is a lot to consider. Your priority as the anaesthetist is the life of
    the mother, even if you are under pressure from the obstetricians to save the baby.
    Airway always comes first!
    Although you have successfully managed to oxygenate the mother, a needle
    cricothyroid puncture is not a definitive airway. Allowing the surgeons to proceed
    with lower segment Caesarean section (LSCS) places the mother at further risk of
    morbidity and mortality, especially if there is excessive bleeding intraoperatively.
    Furthermore, there is still a risk of aspiration and you are not ventilating the mother,
    as carbon dioxide clearance is not effective. There are the added risks of barotrauma
    and surgical emphysema with the high pressures needed to pass gas through the
    cannula, and the LSCS may take longer than expected.
    The LSCS should be delayed until a definitive airway is placed, in this case a surgical
    tracheostomy. As soon as the ENT surgeon has secured the airway, the obstetricians
    should proceed with the Caesarean section. Hence, they should already be prepared
    with the patient cleaned and draped as far as is feasible in this situation.
    Performing a tracheostomy and Caesarean at the same time is not appropriate, as
    it would not be possible to adequately deal with any complications occurring from
    either surgical site without putting the mother in jeopardy. Again, airway always
    comes first!
    Completely abandoning the LSCS and waking the patient up would be correct if this
    was an elective procedure; however, as this is an emergency it needs to go aheadonce the airway is secured. If there was a threat to the mother’s life, then it may be
    necessary to proceed before ENT arrives.
    Performing a spinal anaesthetic at this point would use up even more valuable time,
    considering the tension of the situation.
    There are many newer devices now available for emergency cricothyroidotomy that
    are actually cuffed tubes. Whether it is appropriate to perform emergency surgery
    using any of these is debateable and would very much be a case specific decision.
19
Q
  1. A 30-year-old woman who is 32/40 pregnant is undergoing an open
    appendicectomy under general anaesthesia. She had a rapid sequence induction
    with thiopentone 500mg and suxamethonium 100mg and was maintained on
    sevoflurane in oxygen and air. At the end of the procedure, in the recovery room,
    the patient complains of abdominal discomfort. The midwife from labour ward
    performs a cardiotocograph (CTG), which suggests the patient is going into
    preterm labour.Which of the following is the least likely cause of her preterm labour?
    A Third trimester pregnancy
    B Acute appendicitis
    C Surgical manipulation of the uterus
    D Sevoflurane
    E Maternal pyrexia
A
  1. D Sevoflurane
    Anaesthesia for urgent surgery in the pregnant patient can be a challenge and the
    maternal physiological changes of pregnancy must be considered in these cases.
    Although anaesthetic drugs have not been shown to be teratogenic in clinical
    doses, surgery occurring in the first trimester does have a high miscarriage rate.
    The ideal time to perform urgent surgery is the second trimester, as the risk of
    preterm labour increases as the pregnancy progresses. Elective surgery must be
    postponed until at least six weeks after delivery. Obviously, if emergency surgery is
    needed, it should not be delayed, and a discussion with obstetricians, surgeons and
    paediatricians must take place to decide whether early delivery is necessary before
    surgery.
    The disease process and the associated pyrexia can cause preterm labour due to
    uterine irritability. This risk is very high in both appendicitis and peritonitis. Non-
    intentional surgical interference with the uterus can also lead to preterm labour and
    often laparoscopy may be the preferred technique.
    Volatile agents reduce uterine tone and therefore actually help to reduce uterine
    contractions. Therefore, sevoflurane is the least likely cause of this patient’s preterm
    labour.
20
Q
  1. A 4-month-old 4.5-kg boy is on your elective day case surgical list for bilateral
    inguinal hernia repair. He was born at 27 weeks gestation and his current corrected
    gestational age is 44 weeks. The patient was ventilated for 10 days and was oxygen
    dependent for 6 weeks. He was discharged home 3 weeks previously, but re-
    presented last week with an apparently obstructed hernia that was reduced by the
    on-call surgeon. He is on iron and folic acid for anaemia of prematurity.
    The most appropriate anaesthetic management would be:
    A Proceed with day case surgery under general anaesthesia supplemented with
    regional anaesthesia
    B Proceed with day case surgery under regional anaesthesia supplemented with
    minimal intravenous sedation
    C Postpone surgery until 60 weeks gestational age
    D Postpone surgery until 52 weeks gestational age
    E Proceed with surgery under general anaesthesia supplemented with regional
    anaesthesia and admit postoperatively for apnoea monitoring
A
  1. E Proceed with surgery under general anaesthesia
    supplemented with regional anaesthesia and admit post-
    operatively for apnoea monitoring
    Prematurity, anaemia and gestational age less than 46 weeks are all risk factors for
    postoperative apnoea in this patient. He is at significant risk of postoperative apnoea
    regardless of anaesthetic technique, and should be admitted for postoperative
    apnoea monitoring, making day case surgery inappropriate. The recent history of
    obstructed hernia increases the risk of incarceration; therefore postponing surgery is
    also not appropriate. The most appropriate anaesthetic management of this patient would be to proceed with surgery under general anaesthesia supplemented with
    regional anaesthesia with postoperative apnoea monitoring due to his high risk of
    apnoea.
21
Q
  1. A 16 kg 4-year-old girl with diabetic ketoacidosis (DKA) is given 40mL/kg of
    0.9% saline for resuscitation and 85mL/hour of 0.45% saline with 5% glucose
    as replacement and maintenance fluid. An insulin infusion was commenced at
    0.1unit/kg/hour after an initial bolus dose of 0.1unit/kg.
    2 hours later she has become drowsy with a blood glucose of 11mmol/l. She
    appears lethargic and somnolent, and responds to voice. Her heart rate is 96 beats
    per minute, blood pressure is 128/68mmHg and respiratory rate is 38 breaths per
    minute.
    The most likely cause of her reduced level of consciousness is:
    A Cerebral oedema
    B Meningitis
    C Hypokalaemia
    D Dehydration
    E Exhaustion
A
  1. A Cerebral oedema
    Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in
    children with diabetes. Unlike in the adult diabetic population, the most common
    cause of death in children with DKA is cerebral oedema, and a high index of
    suspicion is always required. Risk factors associated with development of cerebral
    oedema include:
    t Younger age
    t Newly diagnosed diabetes
    t >40mL/kg of fluid given in the first 4 hours
    t Bolus insulin therapy
    t Administration of hypotonic fluid
    t Raised serum urea
    t Initial pH <7.1
    t Hypocapnia
    t Bicarbonate therapy
    Cerebral oedema is a clinical diagnosis with varying signs and symptoms including
    deterioration in neurological status, headache, cranial nerve palsies, bradycardia,
    and hypertension. The patient was afebrile and did not present with headache or
    neck stiffness, making meningitis unlikely. Hypokalaemia does not typically lead to a
    reduced level of consciousness. Dehydration and exhaustion are also unlikely since
    the patient was awake and alert on presentation, and had been fluid resuscitated
    since.
    If cerebral oedema is suspected then treatment should begin immediately using
    either hypertonic saline (saline 3%, 3–5mL/kg) or mannitol (0.5g/kg or 2.5mL/kg of
    20% solution) while arranging for a CT scan. This should be repeated until a clinical
    improvement in neurological status has occurred.
22
Q
  1. A 65-year-old man was scheduled for a below knee amputation for peripheral
    vascular disease. He is currently on 10mg morphine sulphate twice daily for
    analgesia.
    What would be the most appropriate pre-medication to reduce the risk of
    development of chronic pain?
A
  1. B Gabapentin 900mg
    There is now increasing evidence that perioperative gabapentinoids such
    as pregabalin and gabapentin can reduce the incidence of chronic pain
    postoperatively. Moderate evidence exists that shows their effect in acute pain.
    Although ketamine has shown effects in reducing perioperative pain, this is not a
    first line treatment and its evidence so far is less than that of the gabapentinoids.
    Preoperative epidural analgesia was shown in a retrospective study to reduce phantom limb pain but this was disproved by prospective trials. Morphine and
    amitriptyline should only be used for treating pre-existing pain and gabapentin or
    pregabalin are much safer drugs than amitriptyline due to the more tolerable range
    of side effects and reduced incidence of adverse events.
23
Q
  1. A 65-year-old man was scheduled for a below knee amputation for peripheral
    vascular disease. He is currently on 10mg morphine sulphate twice daily for
    analgesia.
    What would be the most appropriate pre-medication to reduce the risk of
    development of chronic pain?
    A Morphine sulphate 15mg
    B Gabapentin 900mg
    C Amitriptyline 25mg
    D Ketamine 20mg
    E Epidural analgesia 24hours preoperatively
A
  1. B Gabapentin 900mg
    There is now increasing evidence that perioperative gabapentinoids such
    as pregabalin and gabapentin can reduce the incidence of chronic pain
    postoperatively. Moderate evidence exists that shows their effect in acute pain.
    Although ketamine has shown effects in reducing perioperative pain, this is not a
    first line treatment and its evidence so far is less than that of the gabapentinoids.
    Preoperative epidural analgesia was shown in a retrospective study to reduce phantom limb pain but this was disproved by prospective trials. Morphine and
    amitriptyline should only be used for treating pre-existing pain and gabapentin or
    pregabalin are much safer drugs than amitriptyline due to the more tolerable range of side effects and reduced incidence of adverse events.
24
Q
  1. A 34-year-old woman presents with a 3-month history of poor sleep, fatigue, and
    worsening widespread muscular pain. On examination, she is extremely tender on
    finger palpation of several muscle groups and a diagnosis of fibromyalgia is made.
    Regarding management of her symptoms, which of the following is the most
    appropriate first step?
    A Trigger point injection
    B Morphine
    C Amitriptyline
    D Ibuprofen
    E Gabapentin
A
  1. C Amitriptyline
    Fibromyalgia is a chronic pain condition that can be very debilitating. Its key features
    are pain of more than 3 months’ duration affecting the trunk and all four limbs (with
    tenderness over at least 11 of 18 defined trigger points), sleep disturbance and
    marked fatigue.
    There is no cure, and treatment is aimed at control of symptoms. Like the
    approach to any chronic pain presentation, the management should be holistic
    and multidisciplinary. General non-pharmacological measures should include
    patient education, support and motivation. They should be encouraged to take a
    proactive role in their own management. Psychological therapies such as cognitive
    behavioural therapy (CBT) and physiotherapy with regular exercise may contribute
    towards overall well-being and hence towards improvement in symptoms.
    Pharmacologically, drugs that affect the reuptake of serotonin and/or noradrenaline
    in the central nervous system seem to be most useful. Of these, tricyclic
    antidepressants (TCAs) such as amitriptyline are first choice. They have been found
    to be effective not only in reducing pain, but also improving sleep, mood, muscle
    stiffness, and fatigue. A suitable starting dose would be 5–10mg at night, and this
    can be increased over time as required. Duloxetine is a suitable alternative.
    Other agents such as gabapentin have been used with mixed success.
    Strong opioids are less effective but tramadol may be helpful. It acts at the spinal
    level and inhibits the reuptake of serotonin and noradrenaline.
    Paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) may help and can
    be used in addition to the agents discussed above, but are usually inadequate if
    used alone.
    Trigger point injections with local anaesthetic ± depot steroids may be of benefit in
    some patients, but those with widespread pain will get short-term relief only in the
    areas injected.
25
Q
  1. A 3-year-old boy presents for circumcision. He is previously fit and well, and
    weighs approximately 10kg. You decide to give him intravenous paracetamol
    intraoperatively.
    Which of the following is the correct dose?
    A 150mg
    B 200mg
    C 75mg
    D 100mg
    E 500mg
A
  1. C 75mg
    Paracetamol is widely used, very effective and safe. The intravenous preparation
    provides greater bioavailability than the oral route and is frequently administered
    intraoperativelyHowever, overdose of intravenous paracetamol is being increasingly reported in
    small children, infants and neonates. This has resulted in one fatality and significant
    morbidity in several children. In most of these cases, there has been a miscalculation,
    and up to ten times the recommended dose had been given.
    In young children, dose miscalculation is an easy error to make and potentially more
    hazardous than in an older child, as drug handling is different with different levels of
    organ maturity.
    In 2013, the MHRA and Royal College of Anaesthetists released dose
    recommendations for paracetamol in children. This is summarised in Table 3.7.
    Hence in a 10 kg patient, the correct dose of intravenous paracetamol would be 75mg.
26
Q
  1. A 49-year-old diabetic man with peripheral vascular disease presents for right
    below knee amputation. He has been in severe pain in his right leg for several
    months and no oral analgesia has provided any relief. An epidural is to be
    commenced preoperatively and continued into the postoperative period.
    Which of the following factors increase his risk of developing chronic post surgical
    pain?
    A Severe preoperative pain
    B Increasing age
    C Male gender
    D Use of an epidural
    E Diabetes mellitus
A
  1. A Severe preoperative pain
    Chronic post surgical pain (CPSP) is a significant complication of surgery, but
    relatively little is known about its precise aetiology, mechanisms, or prevention.
    There is no uniformly agreed definition, and this has led to variable reporting, with
    unreliable figures of incidence or prevalence. Consequently, evidence regarding its
    management and prevention is limited.
    One definition of CPSP is pain of at least 2 months’ duration that develops after a
    surgical procedure, and that cannot be explained by any other cause or pre-existing
    pain problem. Several theories regarding its mechanism have been proposed, one
    of which is of intraoperative nerve damage, leading to central sensitisation, but it
    is acknowledged that not all patients who develop CPSP have had surgical nerve
    damage, and not all those with nerve damage subsequently acquire CPSP.
    Some associations have been found, leading to identification of certain factors that
    may help to predict risk of developing CPSP (see Table 3.8).In this scenario, the nature of the operation, an amputation, and the fact that the
    patient had severe pain preoperatively both put him at increased risk of developing
    CPSP.
    It is unclear what can be done to prevent CPSP. Regional anaesthesia does not
    seem to make a difference, but epidural analgesia commenced pre operatively and
    continued into the post operative period may be a preventive measure. Adjuvant
    agents such as ketamine and clonidine have been investigated, but cannot be
    recommended at present for lack of robust studies. There is an increasing evidence
    base suggesting that gabapentinoids such as gabapentin and pregabalin may
    reduce the progression to postoperative chronic pain states.
27
Q
  1. A 30-year-old man has sustained a partial brachial plexus injury to his left arm.
    He describes constant, sharp pain with spontaneous burning and shock-like
    symptoms. Light touch elicits painful episodes and there are constant tingling
    sensations.Which of these statements about pain classifications would apply?
    A Neuropathic pain requires a disease or lesion of the somatosensory system to
    be present
    B Dysaesthesias are not always unpleasant
    C Paraesthesia is usually painful
    D Complex regional pain syndrome results from serious trauma
    E Hyperalgesia is pain from a non-painful stimuli
A
  1. A Neuropathic pain requires a disease or lesion of the
    somatosensory system to be present
    The International Association for the Study of Pain (IASP) defines pain as “an
    unpleasant sensory and emotional experience associated with actual or potential
    tissue damage or described in terms of such damage.” It serves predominantly as a
    protective function to body tissue. There are some important definitions used in the
    description of pain states.
    t Nociception – The sensation of noxious stimuli in the central nervous system. This
    is different to pain, but is a component of pain symptoms
    t Allodynia – Painful responses to normally painless stimuli
    t Hyperpathia – Increased sensation from a sensory stimulus with a raised
    sensation threshold
    t Hyperalgesia – Exaggerated pain response to normally painful stimuli
    t Dysaesthesia – An unpleasant abnormal sensation
    t Paraesthesia –An abnormal sensation
    t Chronic pain – Pain persisting beyond removal of stimulus and beyond the
    period of time expected for healing and recoveryt Neuropathic pain – Defined by the IASP as pain caused by a lesion or disease of
    the somatosensory nervous system
    t Complex regional pain syndrome – A chronic, painful condition that can
    be either spontaneously occurring or due to nerve injury characterised by a
    collection of sensory, vasomotor, sudomotor and trophic skin changes
28
Q
  1. A 33-year-old man is brought to the emergency department with an 18% body
    surface area (BSA) burn.
    Regarding fluid resuscitation, what is the most appropriate statement?
    A The Parkland formula should not be used as he is an adult with <20% BSA
    burn
    B 4mL/kg/% burn predicts the fluid required in the first 24 hours. Half the fluid
    should be given in the first 8 hours and the remaining half over the next 16
    hours from presentation to hospital
    C Fluid requirement should be calculated as per the Baxter formula: 4mL/kg/%
    burn. Half the fluid should be given in the first 8 hours and the remaining half
    over the next 16 hours from the time of burn
    D Fluid requirement should be calculated as per the modified Brooke formula:
    2mL/kg/% burn
    E Fluid requirement should be calculated as per the Parkland formula. Half
    should be given as colloid and the other half as crystalloid to reduced the
    complications of massive fluid resuscitation
A
  1. C Fluid requirement should be calculated as per the
    Baxter formula: 4mL/kg/% burn. Half the fluid should be
    given in the first 8 hours and the remaining half over the
    next 16 hours from the time of burn
    Major burns cause a systemic inflammatory response syndrome resulting in
    increased capillary permeability and large fluid shifts. It is therefore important to
    maintain intravascular volume to ensure end organ perfusion. However, it should
    be remembered that hypovolaemic shock in the first few hours following a burn is
    never due solely to the burn and an alternative injury/source should be sought.
    Two large bore IV cannulae should be inserted ideally through unburned skin.
    The groins are often spared making femoral CVC access practical. However fluid
    resuscitation should not be delayed if IV access through unburned skin is proving
    difficult.
    IV fluid resuscitation is required in adults if the burn involves more than 15% BSA or
    10% with smoke inhalation.
    There are various formulae that attempt to estimate the fluid deficit but these clearly
    provide no more than a rough guide. The Parkland formula (also known as the Baxter
    formula) is the most widely used. The modified Brooke formula (2mL/kg/% burn in
    the first 24 hours) can also be used but is less well known and was hoping to address
    the issues of ‘fluid creep’.
    Parkland formula: 4mL/kg/% burn in the first 24 hours
    Half of the fluid is given in the first 8 hours and the remaining half is given over the
    next 16 hours.
    The calculation should start from the time of the initial burn and not the time
    of presentation to hospital. It is generally accepted that the fluid of choice is
    Hartmann’s solution. Any pre-hospital fluid administered should be deducted from
    the calculated requirement.
    Given the volume of fluid often administered and the propensity of burns patients to
    hypothermia, the Hartmann’s should be warmed. After the first 24–48 hours capillary
    permeability should have returned to normal and fluid balance is much less of an issue.
29
Q
  1. During the initial surgical dissection of an aortic abdominal aneurysm, the
    surgeon warns you that he needs to apply the aortic cross-clamp above the
    coeliac arteries, following which the patient undergoes significant haemodynamic
    changes.
    What are the changes in left ventricle preload and afterload that are caused by the
    aortic cross-clamp?
    A Increased preload, increased afterload
    B Decrease preload, increased preload
    C No change in preload or afterload
    D No change in preload, increased afterload
    E Increased preload, decreased afterload
A
  1. A Increased preload, increased afterload
    Application of aortic cross-clamp can cause significant rise in systemic blood
    pressure. This is caused by an increase in left ventricular afterload, due to the cross
    clamp. Reflex venoconstriction below the clamp, particularly in the splanchnic
    circulation, causes an increase in the blood volume in the inferior and superior vena
    cavae, hence causing increase in preload.
    The change in afterload is consistent. The change in preload is variable when aortic
    cross clamping is applied infrarenally, but is present in 90% of cases when the clamp
    is applied above the coeliac arteries.
30
Q
  1. A 45-year-old chronic alcoholic in the emergency department was found lying
    unconscious on the floor of his flat amidst claims that he was not contactable for
    almost 48 hours. On arrival his Glasgow coma scale (GCS) is 8, (eyes 1; verbal
    3; motor 4). His has a heart rate of 104 beats per minute and a blood pressure of
    80/60 mmHg. His blood gas shows severe metabolic acidosis and hyperkalaemia.
    His urine output in the last hour has been 5 mL and is brown in colour.The most appropriate investigation would be:
    A Creatinine kinase
    B Urininary haem
    C Myoglobinuria
    D Blood urea
    E Alkaline phosphatase
A
  1. A Creatinine kinase
    This patient has presented with clinical features suggestive of rhabdomyolysis.
    Rhabdomyolysis is a clinical spectrum, which occurs as a result of the breakdown of
    striated muscle. The muscle degradation leads to elevated intracytoplasmic calcium,
    which causes myocyte constituents to be released into blood, eventually leading to
    acute kidney injury and hyperkalaemia.
    The aetiology of rhabdomyolysis can be traumatic, including crush injuries,
    electrocution or blunt trauma, or non-traumatic such as infection (legionella,
    tetanus), drugs (cocaine, alcohol) or immune mediated (polymoyositis,
    dermatomyositis).
    Alcohol is thought to be involved in up to 20% of cases of rhabdomyolysis in the UK.
    Alcohol-induced coma leads to prolonged immobilisation and muscle compression
    with ischaemia. It also leads to myopathy and damages cell sarcolemma, increasing
    sodium permeability. This influx of sodium activates the sodium-calcium exchange
    pump, which increases cytosolic calcium along with direct influx of calcium due to
    cellular damage.
    It presents with a spectrum, from asymptomatic to hypovolaemic shock
    accompanied with life threatening electrolyte imbalance and acute kidney injury.
    Clinically, it is syptomised by malaise, muscle pains, fever and tachycardia.
    Myocyte injury leads to severe hyperkalaemia, hyperuricaemia and
    hyperphosphataemia, while muscle necrosis causes lactic acidosis, further
    exacerbating the hyperkalaemia.
    The most sensitive test for rhabdomyolysis is serum creatinine kinase (CK), an
    enzyme released by striated muscle when damaged. An five-fold increase in serum
    CK is expected in rhabdomyolysis. Serum CK concentrations greater than 5000 units/
    litre are associated with a >50% incidence of acute renal failure.
    High concentrations of myoglobin released can cause myoglobinuria, which is
    responsible for the brown discolouration of urine. Routine dipstick test of urine
    cannot differentiate between haemoglobinuria (haemoglobin in urine), haematuria
    (red blood cells in urine) or myoglobinuria (haem-containing myoglobin in urine) as it detects presence of haem which is positive in all cases. As the liver normally
    metabolises myoglobin rapidly, an absence of it in blood or urine does not eliminate
    the diagnosis of rhabdomyolysis.
    Treatment consists of prompt fluid resuscitation, control of hyperkalaemia and renal
    support with filtration if indicated.
31
Q
  1. A malnourished 93-year-old man with dementia complains of lethargy,
    breathlessness, myalgia and bone pain, and has petechiae, bleeding gums and
    gingivitis.
    Which of the following nutritional deficiencies would most likely be attributed to
    this clinical condition:
    A Ascorbic acid
    B Iron
    C Thiamine
    D Vitamin A
    E Vitamin D
A
  1. A Ascorbic acid
    This patient has clinical features suggestive of scurvy, caused by vitamin C (ascorbic
    acid) deficiency. It is rarely seen in developed countries, except in extremes of age
    most commonly due to malnourishment, but can occur due to dietary vitamin
    C insufficiency. As vitamin C is an essential component for collagen synthesis it’s
    deficiency leads to fragile capillaries, impaired wound healing, poor bone formation
    and muscle symptoms. Administering a diet rich in vitamin C including products
    such as citrus fruits, tomatoes and bell peppers can prevent it.
    Iron deficiency leads to anaemia, which could cause lethargy, breathlessness and
    palpitations.
    Vitamin B1 or thiamine deficiency leads to beriberi, which is characterised, by heart
    failure, oedema (wet) and neuropathies (dry).
    Vitamin A deficiency leads to predominant visual symptoms including xeropthalmos
    and blindness, while vitamin D deficiency leads to osteogenic defects such as rickets
    disease and osteomalacia