El-Boghdadly - 3 Flashcards
- 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
D
- 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
• Biochemical 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 –
150 mmHg (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.
decreasing potency:
Halothane>
Isoflurane and desflurane >
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.
- 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
C
- 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).
Inflation
After closure of the aortic valve
Mid-point of the T wave
After dicrotic notch
Deflation
Before opening of the aortic valve
Peak of the R wave
Point just before the upstroke of the arterial trace
The inflation of the balloon in diastole causes displacement of blood both proximally (in the direction of the coronary arteries) and distally.
The implication of this is that both coronary flow and distal systemic flow may increase. By inflating during diastole,
aortic diastolic pressure will increase (therefore excluding option C).
Deflation of the balloon during early systole effectively reduces the volume of blood in the aorta – leading to lower aortic systolic pressure (thereby excluding option A) and left
ventricular afterload. As aortic systolic pressure is lowered, the left ventricle (LV) will not have to generate as much pressure to cause opening of the aortic valve. The time
for isovolumetric contraction (IVC) is therefore shorter, and, since IVC accounts for the
majority of myocardial oxygen consumption, oxygen demand is reduced. As the LV
is able to eject blood more effectively, stroke volume increases, end-systolic volume
is reduced (excluding option D) and preload is subsequently reduced (option B).
This leads to lower LV wall tension and option E is therefore correct. The haemodynamic effects of IABP counterpulsation are summarised in Table 3.5 below:
The main indications for IABP counterpulsation are:
• Acute myocardial infarction pending re-vascularisation
• Cardiogenic shock not reversed by pharmacological therapy
• As a bridging therapy in ventricular failure pending definitive treatment
(ventricular assist device or cardiac transplantation)
• Facilitation of weaning from cardiopulmonary bypass
• 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.
- 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 600 mL 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 2 cm
C
- 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.
Options B and D are accepted methods to improve oxygenation in the event of
hypoxaemia that is not due to tube malposition.
- 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
B
- 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.
- 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 53 mmol/
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
B
- 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 12 months > 69 mmol/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.
- 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.
B
- 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 1 mL/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 noncardiogenic
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.
Answers 99
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:
• Recognise this as an anaesthetic emergency and summon help
• 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
- 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
B
- 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).
(1) Co-axial fow:
Gas infow is confined to the centre of the
airway, while gas exits the lung circumferentially along the
periphery
(2) Pendelluft ventilation:
Movement of gas between lung unit
with different time constants.
(3) Cardiogenic mixing:
Cardiogenic oscillations are transmitted
through the lung parenchyma which
augments gas mixing.
(4) Enhanced molecular diffusion:
Enhanced kinetic activity of gas
molecules increase their diffusion across the alveolocapillary
membrane.
- 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
D
- D Epicardial pacing wires
Safety considerations when anaesthetising patients for MRI scans include:
• Remote location
• Limited access to the patient
• The projectile effect of the magnetic field on ferromagnetic equipment
• The heating effect and risk of burns from conductive wires and coils
• Risk of equipment malfunction
• Noise protection
• 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.
- 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
A
- 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:
- 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 0.01–5 mA.
When performing a nerve block, the ideal initial current is 1–2 mA. 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 0.2–0.5 mA 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 0.2 mA because motor response below 0.2 mA may mean the needle is inside the nerve and injecting maybe harmful.
- 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. - Stimulation frequency: This affects the speed of nerve localisation. The ideal
current frequency is 1–2 Hz, where a higher frequency makes nerve detection faster,
but causes more patient discomfort. Therefore, the most common frequency used is
2 Hz. - Pulse duration: This is the time for which the electrical current is applied to the
nerve. A short pulse duration (0.1 ms) ensures motor neurons are stimulated but not
the sensory neurons. - 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.
- You have been called to site an epidural for a 32-year-old term primigravida patient.
She is now 3 cm 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 10 mL of normal saline into the subarachnoid space to prevent postdural 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 10 mL 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
D
- 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 24 hours 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.
- 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
B
- 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:
• Anaesthetists should only act as part of a multidisciplinary response team incorporating mental healthcare professionals including a psychiatrist
• 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
• When rapid tranquillisation is deemed appropriate the minimum intervention possible should be used as guided by the local protocol
• The full range of ventilatory/resuscitation equipment and trained assistance must be immediately available when rapid tranquillisation is administered
• 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 ‘reallife’ 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 of safety 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.
- 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 500 mL/hour
B Compound sodium lactate, at 500 mL/hour
C 0.9% sodium chloride, at 500 mL/hour
D Colloid solution, at 700 mL/hour
E Compound sodium lactate, at 700 mL/hour
E
- E Compound sodium lactate, at 700 mL/hour
Fluid resuscitation after burns injury is widely guided by the Parkland formula:
4 mL/kg/% body surface area burn, where half of this volume is given in the first
8 hours after the burn injury, and the second half over the next 16 hours.
Thus for the above patient:
4 x 60 x 40 = 9600 mL
Therefore this patient requires 4800 mL in the first 8 hours.
Two litres has already been given in the first 4 hours since the burn, and so 2800 mL should be given over the next 4 hours, which is 700 mL/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 0.5 mL/kg/hour is used to guide adequate resuscitation.
Criteria for referral to a specialist burns unit include:
• > 2% TBSA in children or > 3% in adults
• Full thickness burns
• Circumferential burns
• Unhealed burn after 2 weeks
• Any suspicion of non-accidental injury
Discuss with a burns specialist with an opinion to transfer:
• Burns to hands, feet, face, perineum or genitalia
• Chemical, electrical or friction burns
• Cold injuries
• Febrile child with a burn
• 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 24 hours after the burn.
- 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.
E
- 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: 8–16 mmol/L
The causes can be remembered using the acronym ‘MUDPILES’:
• Methanol
• Uraemia
• Diabetic ketoacidosis
• Propylene glycol
• Isoniazid
• Lactic acidosis
• Ethylene glycol
• 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:
• Gastrointestinal; such as diarrhoea, fistulae (pancreatic, ureters, biliary, small bowel, ileostomy)
• Renal such as renal tubular acidosis and Addison’s
• 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.
- 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 55 mmHg.
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:
• Cardiac output index (CI) L/min/m2 (NR 3–5) – 1.94
• Intra-thoracic blood volume index (ITBVI) mL/m2 (NR 850–1000) – 650
• Systemic vascular resistance index (SVRI) (NR 1970–2390 ) – 3854
• Extra-vascular lung water index (EVLWI) (mL/kg) (NR 3–7) – 14
What is the most appropriate next course of action?
A Fluid bolus of 500 mL crystalloid and repeat studies
B Increase the noradrenaline to increase MAP to 70 mmHg
C Add dobutamine at 2.5 μg/kg/min
D Order an urgent transthoracic echo and send cardiac troponin measurement
E Commence urgent haemofiltration aiming to reduce pulmonary interstitial fluid
e
- A Fluid bolus of 500 mL 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:
- 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);
- 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:
• Cardiac output
• 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
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.
- 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 80/43 mmHg 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.
Parameter Result
Fio2 1.0
pH 6.9
Paco2 2.8 kPa
Pao2 18 kPa
Base excess –13.2 mmol/L
Bicarbonate concentration (HCO3
–) 12 mmol/L
Lactate 10.8 mmol/L
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
b
- 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 > 150 mg/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 tachypnoeic 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 150 mg/kg loading over 15 minutes,
followed by 50 mg/kg over the
next 4 hours and 100 mg/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:
• pH < 7.3 (or 7.25 if on NAC)
Or all of the following:
• Prothrombin time (PT) > 100 seconds (INR > 6.5)
• Creatinine > 300 μmol/L
• 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.
