SBA 300 Paper 1 Flashcards
1
Q
- You are called to anaesthetise a claustrophobic patient who requires an MRI scan.
The patient has a cervical fixation device in place to stabilise a recent C-spine
fracture, and the neurosurgeons have requested that it remains in situ until after
the scan results.
Which of the following factors would most likely mean that an MRI scan is
contraindicated?
A The provision of a standard anaesthetic machine in the MRI suite
B The patient having a permanent pacemaker (PPM) in situ
C The patient recalling that he has a foreign body in his eye
D The provision of standard infusion pumps in the MRI suite
E A Halo device for cervical stabilisation
A
- C The patient recalling that he has a foreign
body in his eye
Magnetic resonance imaging (MRI) scans are often utilised for investigating the
central nervous system as they provide images that show improved distinction
between tissue types compared with computed tomography (CT) scans.
MRI scanning takes advantage of the fact that atomic nuclei within tissues naturally
spin, generating their own small magnetic field. By applying a larger external field to
a tissue, these spinning nuclei align with the field which has been applied. A second
external field is then pulsed in a perpendicular fashion causing some nuclei to be
pulled to an angle. This incorporates nuclear energy absorption, and they begin to
wobble or precess – a term used to describe rotation around an axis different to that
of original spin. Precession results in tissues producing rotational magnetic fields,
the amplitude and specific frequency of which can be detected and used to form
an image. As the nuclei return to their previous positions between pulses, they emit
the energy they previously absorbed at the same frequency. The rate of their return
depends on the elemental content of the nucleus (e.g. hydrogen or phosphorous)
in addition to the molecule of which it is a part (e.g. water or fat). Different tissue
types therefore return at different rates. By using a combination of magnetic field
gradients and pulse configurations, detailed cross-sectional views can be obtained.
MRI scanners raise a number of safety concerns with regards to equipment. As the
magnetic field is constantly present, anything containing ferromagnetic material
will be attracted to it, turning them into projectiles. The field strength is measured
in Tesla (T) and Gauss (G). 1T=10,000G. MRI scanners for medical imaging are usually
1.5T but sometimes 3T. The strength declines with distance from the magnet and
contours are marked in Gauss lines on the floor of the MRI suite (Figure 1.2). Beyond the 5G line no ferromagnetic material should ever be taken. This includes
many items of equipment and implanted devices. Another concern with regards to
equipment is the effect of radiofrequency energy resonating with material causing
the dispersion of energy as heat. Patients can therefore suffer burns from any
conductive material with which they are in contactAs a result of the above, all equipment is classified according to the hazard it
poses under certain conditions such as magnetic field strength or in view of
radiofrequency absorption. MR safe equipment can be used in all MR settings,
MR conditional in specified environments, and MR unsafe in none of the
aforementioned situations.
Monitoring in the MRI suite is essential and has evolved accordingly. MR compatible
monitoring is standard, with many units using telemetric equipment to avoid any
induced currents in long cables. MR compatible anaesthetic machines and infusion
pumps are available; however standard equipment can be used with extensions to
beyond the 5G line. The anaesthetic machine must be securely fixed to the wall and
the pumps attached to their extensions through a port into the control room.
Pacemakers and implanted cardiac defibrillators are at risk of malfunctioning or
displacing and so were, until recently, a strict contraindication to having an MRI.
Technology has, however, advanced and there are now some MR-compatible models.
There are also MR strategies and guidelines that have been described to limit risk in
the event that an MRI is absolutely necessary for a patient with a standard device.
Cervical fixators, such as the halo device, vary in their classification. Some are MR
safe and this, or the hazard of any other item, can be easily checked by referring to a
list on www.MRIsafety.com.
Foreign bodies in the eye have the potential to migrate and cause bleeding into the
vitreous, therefore contraindicating an MRI scan.
2
Q
- A 77-year-old man arrived in the intensive care unit 2 hours ago following coronary
artery bypass grafting (CABG). He has a background of interstitial lung disease
and hypertension. He is intubated, ventilated and sedated and on a noradrenaline
infusion at 0.05μg/kg/min. Atrial pacing wires are in situ. You are called to see him
as the nurse looking after him thinks the ECG has changed. His blood pressure is
110/80mmHg and the cardiac index reading on the PiCCO is 1.5L/min/m2. The
readings an hour ago were 130/80 and 2.4L/min/m2 respectively. His 12-lead ECG
is shown in Figure 1.1.
What is the most appropriate course of action?
A 1mg intravenous metoprolol
B 300mg amiodarone over 30 minutes
C Synchronised DC cardioversion with 100J
D Atrial pacing at 100 beats per minute
E 250µg intravenous digoxin
A
- C Synchronised DC cardioversion with 100J
The ECG shows atrial flutter. Up to 40% of coronary artery bypass grafting (CABG) Patients will develop postoperative atrial fibrillation or flutter. The majority of these dysrhythmias occur within 48-hours and may be recurrent. Presence of atrial fibrillation or flutter is associated with an increase in hospital mortality as well as other complications including stroke.
Risk factors for the development of atrial fibrillation or flutter include:
• Atrial injury during cannulation
• Ischaemia
• Prolonged cardiopulmonary bypass time
• Use of post operative catecholamines
• Hypokalaemia and hypomagnesaemia
Although accompanied with reasonable haemodynamics, there is a clear fall in cardiac index (and hence output) as measured by the PiCCO. Atrial flutter may change to atrial fibrillation and rate control is rarely an option. Restoration of sinus rhythm should be the aim in this circumstance and this is best achieved with synchronised DC cardioversion. Although amiodarone is frequently used for atrial flutter, data concerning its use in this setting is surprisingly lacking. When using amiodarone, cardioversion may take hours rather than minutes. Another reason to avoid amiodarone in this
circumstance would be the history of interstitial lung disease, which is a risk factor for exacerbation of any lung fibrosis that may be caused by amiodarone.
Rate controlling agents such as metoprolol and digoxin would not be optimal treatment here.
Atrial pacing is a viable option but would usually be performed at a rate 10–15 bpm higher than the atrial flutter rate. If the ventricular rate rises to match the atrial rate, the pacemaker frequency can then be reduced (i.e. the rhythm is entrained) to an acceptable rate. This may lead to conversion to sinus rhythm (or atrial fibrillation!).
Given this patient is already sedated and ventilated, it is quicker and more effective to perform DC cardioversion.
As well as addressing strategies for cardioversion, it is also imperative that other contributing factors for the development of any dysrhythmias are addressed:
• Hypoxaemia
• Hypercarbia
• Electrolyte disturbances
• Other causes of myocardial ischaemia e.g. graft failure
3
Q
- You are scheduled to anaesthetise an 80 kg man for aortic valve replacement. He is
73 years old and reports a rash upon administration of penicillin. His skin swab is
positive for methicillin-resistant Staphylococcus aureus (MRSA) colonisation.
Which of the following antibiotic regimens is most appropriate for the patient?
A Flucloxacillin 2 g, gentamicin 120mg
B Vancomycin 1.5 g, gentamicin 400mg
C Cefuroxime 1.5g, metronidazole 750mg
D Co-amoxiclav 1.2 g, linezolid 600mg
E Clindamycin 900 mg, ciprofloxacin 400mg
A
- B Vancomycin 1.5g, gentamicin 400mg
Common pathogens in cardiac surgery are Staphylococcus aureus and
Staphylococcus epidermidis. In addition, this man has evidence of methicillin-resistant staphylococcus aureus (MRSA) colonisation, so any prophylactic antibiotics must cover this organism (vancomycin or linezolid). Most centres also administer some gram negative cover such as an aminoglycoside (gentamicin at 5mg/kg) or a fluoroquinolone (ciprofloxacin).
Although the skin reaction reported after penicillin may not be significant, it is prudent to avoid penicillins thus flucloxacillin and co-amoxiclav should be avoided.
Vancomycin 1.5g with gentamicin 400mg provides gram-positive (including MRSA) and gram-negative cover and is the correct regimen for this patient. The dose of vancomycin is 15mg/kg and should be given as an infusion. The combination of cefuroxime and metronidazole does not have MRSA cover and although clindamycin with ciprofloxacin gives good gram positive, gram negative and MRSA cover, the use of untargeted ciprofloxacin is often discouraged due to the speed by which plasmid
mediated resistance can occur.
Other elements of perioperative care that may reduce the incidence of surgical site
infection include patient warming, tight glycaemic control, hair removal and the
sterility of instruments and the surgical field.
4
Q
- A 76 year old woman who is spontaneously breathing through a temporary double lumen cuffed tracheostomy tube following a laryngectomy becomes acutely breathless. Help is on its way but despite application of high-flow oxygen, her oxygen saturations are 82% with a respiratory rate of 40 breaths per minute.
What is the most appropriate next step in her airway management?
A Deflate the tracheostomy tube cuff
B Remove the inner cannula
C Hand ventilate through the tracheostomy tube
D Position the patient upright
E Remove the tracheostomy tube
A
- B Remove the inner cannula
Tracheostomy airway emergencies can lead to significant morbidity and mortality if not managed correctly. Laryngectomy patients do not have an upper airway so crucially cannot be intubated or oxygenated orally. They are unlikely to obstruct when lying flat so sitting them more upright is not the immediate airway priority. In this scenario following a call for help and application of oxygen, the tracheostomy tube patency needs to be assessed as a priority.
With double lumen tracheostomy tubes, the initial step is to remove the inner tube which will clear any secretions if these are causing a blockage. Following inner tube removal, passage of a suction catheter should be attempted to confirm airway patency and also help clear any further secretions within the tracheostomy tube. If the suction catheter fails to pass, deflation of the tracheostomy tube cuff may improve airflow if the tracheostomy tube is partially displaced. If the clinical condition fails to improve following cuff deflation, the tracheostomy tube may be completely blocked or displaced, preventing the patient to breathe around the tube adequately and should therefore be removed. Attempting hand ventilation through a tracheostomy tube to confirm airway patency is hazardous, since significant surgical emphysema can ensue in the presence of tube displacement making
subsequent airway management more difficult. Figure 1.3 provides a graphical suggestion for the steps to be taken in the assessment of tracheostomy tube patency in post-laryngectomy patients.Therefore, this patient requires removal of the inner cannula for further assessment
and management of the cause of her respiratory distress.
5
Q
- A 28-year-old woman has an Achilles tendon repair under general anaesthesia as a day case. She has a BMI of 32kg/m2 and is taking the oral contraceptive pill. She will need a below knee plaster cast for 6–8 weeks postoperatively
What is the best form of venous thromboembolism prophylaxis for her?
A Advice on mobilisation and fluid intake
B Graduated compression stockings and pneumatic compression device on day
of surgery
C Graduated compression stockings post discharge for 7 days
D Single dose low molecular weight heparin on day of surgery
E Extended course of low molecular weight heparin post discharge
A
- E Extended course of low molecular weight
heparin post discharge
The risk of venous thromboembolic disease (VTE) after a day surgery procedure is lower than after in-patient procedures as surgery is generally less invasive and mobilisation is earlier. However, more complex and longer procedures in higher risk patients are increasingly being performed in this setting. The 2010 National Institute for Health and Care Excellence (NICE) guidelines for the prevention of VTE includes day surgery as a specific cohort of patients and recommends that mechanical prophylaxis should be used if one or more risk factors are present. Pharmacological prophylaxis should be added depending on ‘patient factors and clinical judgement’.
• Surgical procedure with a total anaesthetic and surgical time of more than 90 minutes, or 60 minutes if the surgery involves the pelvis or lower limb
• Acute surgical admission with inflammatory or intra-abdominal condition
• Expected significant reduction in mobility
• One or more of the risk factors below:
– Active cancer or cancer treatment
– Age over 60 years
– Critical care admission
– Dehydration
– Known thrombophilia
– Obesity (body mass index [BMI] over 30kg/m2)
– One or more significant medical comorbidities (for example: heart disease,
metabolic, endocrine or respiratory pathologies, acute infectious diseases,
inflammatory conditions)
– Personal history or first-degree relative with a history of VTE
– Use of hormone replacement therapy
– Use of oestrogen-containing contraceptive therapy
– Varicose veins with phlebitis
Pharmacological prophylaxis should be continued for 5–7 days if significantly reduced mobility is expected. This patient has three risk factors and extended pharmacological prophylaxis is indicated. In addition she will have a lower limb plaster cast, where NICE recommends that prophylaxis should be continued until the cast is removed after discussion with the patient and evaluation of risks and benefits.
The exact duration will vary between centres.
6
Q
- A 65-year-old woman is scheduled for an extended abdominal hysterectomy. She is not on any anticoagulants but 2 years ago she developed a blood clot following a total hip replacement. At that time her treatment injections caused a wound haematoma, and she was put on a ‘blood thinning’ infusion for several days. At the end of the treatment she remembers having investigations for low platelets in her blood. These results are unavailable.
For immediate perioperative prophylaxis this time the best treatment would be:
A A heparin infusion started 6 hours following surgery if bleeding is controlled
B Treatment dose low-molecular-weight heparin (LMWH) injection once daily
C Fondaparinux injection once daily
D Low-dose aspirin orally throughout the perioperative period
E A danaparoid infusion
A
- E A danaparoid infusion
Venous thromboembolism (VTE), is of major clinical significance given that up to a quarter of inpatients with risk factors may be affected, albeit subclinically.
Candidates will be familiar with the risk factors for VTE (see above) but also should be comfortable with the drug treatment strategies available and their complications.
Mechanical methods
○ Anti-embolism stockings or thromboembolic deterrent stockings (TEDS), are graded to provide increased compression from distal to proximal. They are effective at promoting venous return and increasing the speed of blood flow, but not suitable for all patients, such as those with arteriopathy. ○ Intermittent calf and thigh compression devices produce pressures of approximately 40mmHg 10 times per minute to emulate the limb muscle pump.
Heparins Unfractionated heparin is a naturally occurring antithrombin binder.
○ This inhibits factor Xa and thrombin and in higher doses also has an antiplatelet function.
○ Low-molecular-weight heparin (LMWH) is more effective than subcutaneous heparin, has a lower risk of bleeding, and less anti-platelet effects. It is more convenient with once daily administration, but is less controllable than a heparin infusion, and accumulates in renal failure. It will not usually affect the activated partial thromboplastin time (aPTT), which is a useful monitor of unfractionated heparinisation.
Warfarin
○Warfarin has the advantage of being given orally, and has similar risks of bleeding as LMWH. It can be monitored using the international normalised ratio (INR).
Fondaparinux
○Fondaparinux is a synthetic saccharide which emulates the structure of the heparin anti-thrombin binding site. It indirectly inhibits factor Xa, and is given by subcutaneous daily injection. It is more effective at preventing VTE than LMWH, but also at producing bleeding. The half-life is long, and the drug-free time before neuraxial block is thus 36 hours. It has a lower incidence of HIT, and has been used as a LMWH substitute in this condition.
Others
○ Lepirudin is a hirudin derivative made as a recombinant protein in yeast, whose main use is in heparin-induced thrombocytopenia (HIT). It directly inhibits thrombin and due to its short half-life is administered by a continuous infusion and is monitored with the aPTT. Due to manufacturer cessation of production in April 2012, lepirudin is no longer
available in the UK. Notably, this withdrawal was not due to any safety concerns.
○ Danaparoid is a heparinoid that inhibits factor Xa, and can be used in patients with HIT. There is a need for close monitoring as some HIT cross reactivity does occur. It has now replaced the use of lepirudin in the management of HIT in the UK due to the aforementioned withdrawal.
○ Dabigatran is an orally administered direct thrombin inhibitor licensed for VTE prophylaxis after surgery. It does not require monitoring but also lacks any method to reverse the anticoagulant effect.
○ Rivaroxaban is a direct oral inhibitor of factor Xa that is becoming more common.
Previously only for postoperative VTE prophylaxis, it is now being used in atrial fibrillation and in Europe as an adjunct to aspirin and clopidogrel in acute coronary syndromes.
The likely diagnosis in the above patient is an episode of heparin-induced
thrombocytopenia (HIT). HIT is an immune-mediated IgG response to an
immunogenic component of heparin, leading to thrombocytopenia. This occurs in around 3% of patients as a consequence of treatment with unfractionated heparin,
and less-so at a rate of 0.1–1% with LMWH preparations. Paradoxically, the risk of thrombosis is increased to 50% at this time, so alternate forms of anticoagulation
are needed. Platelet counts should be monitored from day 4 – 14, which is the risk period for antibody formation.
Although the diagnosis is not absolutely confirmed, the question forces you to respond and treat in the safest way possible. If HIT is a possibility then a heparin infusion should be avoided, as should LMWH, as this can also precipitate the condition. In addition, the dose of LMWH is probably too high, given that she is no longer on anticoagulant treatment. Aspirin may or may not be indicated for this patient in terms of primary cardiovascular prophylaxis, but does not have any role in thromboprophylaxis. Of the two HIT-safe options, fondaparinux and danaparoid, only danaparoid has no association with HIT. Fondaparinux has a very low rate of
giving rise to HIT and is sometimes used off-license as a treatment. However, in this scenario the long half-life makes fondaparinux irreversible and uncontrollable
in the immediate postoperative phase. From day 2 onwards, without bleeding,
fondaparinux would represent a good choice for prophylaxis with adequate
monitoring of platelets.
7
Q
- A 21-year-old woman is undergoing a Le Fort I transverse osteotomy to correct her maxillary retrusion. A nasal tube is used and anaesthesia is maintained by propofol and remifentanil infusions. During the down-fracture, her pulse rate falls to 29 bpm and her blood pressure reads 70/30mmHg. Her oxygen saturation, end tidal CO2 and airway pressures remain unchanged.
What is the most likely cause of her haemodynamic compromise?
A Haemorrhage
B Venous air embolus
C Endotracheal tube damage
D Trigeminocardiac reflex
E Remifentanil
A
- D Trigeminocardiac reflex
The horizontal Le Fort I osteotomy is a common procedure used to correct maxillary deformities and knowledge of the surgical technique and relevant anatomy is useful in recognising and treating complications. Surgery involves an intraoral incision and the formation of a transverse maxillary osteotomy that extends to the pterygomaxillary junction. The maxilla is then separated from the upper face along this osteotomy plane by a down-fracture and fully mobilised to aid surgery.
Bleeding is a recognised complication during the down-fracture since the bony mid-face receives a rich blood supply and is in close proximity to an extensive venous plexus. The blood vessels most likely to be injured during the down-fracture are the pterygoid vessels, palatine and alveolar arteries, or on rare occasions the internal carotid. In order to visualise the source of bleeding and achieve haemostasis, completion of the down-fracture is often required. It is unusual for an acute haemorrhage to present with a severe bradycardia as described in the above case. Venous air emboli can occur during any head and neck surgery where open veins are exposed to the atmosphere. However, end-tidal carbon dioxide levels would be expected to fall as a result of an increase in physiological dead space and intrapulmonary shunting which is not observed in the above case.
A nasal endotracheal tube is usually the airway of choice when correcting for maxillary retrusion, since the jaw is frequently closed and wired to ensure normal alignment of the upper and lower teeth. During the osteotomy and down fracture, the nasal tube may be damaged resulting in impaired gas exchange and secondary haemodynamic compromise. In such a situation, the airway (which is now likely to be difficult) needs to be re-established. This scenario is unlikely in the above case since the oxygen saturations, end tidal carbon dioxide levels and airway pressures remain unchanged.
The Le Fort I osteotomy can also cause nerve damage and pressure effects to cranial nerves II-VII due to their proximity to the surgical field. A recognised complication of the maxillary down-fracture in particular is the generation of the trigeminocardiac reflex. This reflex occurs as a result of pressure on the cranial nerve V(trigeminal nerve) initiating a vagal reflex causing a severe bradycardia which may even progress to asystole. Cessation of the down-fracture and return of the jaw to its original position can increase the heart rate, as can administration of anticholinergic drugs. The isolated bradycardia and hypotension in relation to the down-fracture in
the above scenario makes this reflex the most likely cause.
Remifentanil use in maxillofacial surgery is increasing in popularity due to its
favourable pharmacokinetic profile and its useful contribution to deliberate
hypotension. Severe bradycardia and hypotension are recognised complications of remifentanil use, however the temporal relationship between the down-fracture and the bradycardia in the above case make the trigeminal reflex more likely.
8
Q
- A 64-year-old man with no previous cardiac or respiratory morbidity is attending
for his second treatment of electroconvulsive therapy (ECT). After his previous
treatment, he had a supraventricular tachycardia with a peak blood pressure
of 198/105mmHg, which resolved spontaneously within 5 minutes. For his
anaesthetic he had received propofol 90mg and suxamethonium 40mg.
What is the most appropriate course of action for this second treatment?
A Perform procedure with defibrillation pads on his chest
B Pre-medicate with oral atenolol
C Use intravenous esmolol during procedure
D Use remifentanil infusion during procedure
E Use sublingual nifedipine during procedure
A
- C Use intravenous esmolol during procedure
During electroconvulsive therapy (ECT) an electrical current is applied to the brain via transcutaneous electrodes to induce a generalised therapeutic seizure lasting between 10–120 seconds. There is a biphasic physiological response. The seizure causes an immediate direct stimulation of the vagal parasympathetic outflow, which can lead to transient bradycardia and hypotension, and rarely asystole.
Premedication with an anticholinergic agent is often used to attenuate this effect.
This is followed by a more prominent catecholamine mediated sympathetic
response, which peaks 3–5 minutes after therapy, causing a tachycardia, and hypertension and may give rise to tachyarrhythmias.
This sympathetic response can be attenuated using a variety of agents. Beta blockers have been shown to be the most effective in controlling both heart rate and mean arterial pressure. Due to the risk of initial bradycardia short acting agents such as esmolol or labetalol given just prior or during the procedure may avoid accentuating the parasympathetic response compared to longer acting agents. Esmolol is preferred as it reduces the peak systolic blood pressure more than labetalol while labetalol may be associated with a shorter seizure duration.
Calcium channel blockers can also be effective to control arterial pressures but reflex tachycardia may occur with nifedipine. Remifentanil has been shown to reduce both the heart rate and blood pressure and does not havean effect on seizure duration, though use of an infusion may not be available or suitable for these short procedures
9
Q
- You are called to see a 65-year-old patient in the surgical ward 3 days following an
elective abdominal aortic aneurysm repair. A thoracic epidural catheter is in situ.
He is febrile and complains of back pain and lower limb weakness.
What would be the most appropriate next step?
A Stop the epidural infusion and contact the neurosurgeon
B Stop the epidural infusion, do regular neurological observations and monitor
the epidural catheter site
C Arrange an urgent MRI scan and inform the neurosurgeon
D Stop the epidural infusion and start empirical antibiotics
E Remove the epidural catheter and do a full neurological examination
A
- C Arrange an urgent MRI scan and inform the
neurosurgeon
There are many benefits for neuroaxial drug delivery. However, we need to balance the advantages against the risk of complications such as infection, nerve damage and haematoma.
In the third National Audit Project (NAP 3) report, the incidence of epidural abscess after central neuraxial block (CNB) was quoted as 2.1 in 100,000. Although this is considerably lower than previous studies, epidural abscess is still a very serious complication of CNB and can lead to permanent neurological damage. In the above scenario, the patient has signs and symptoms of an established epidural abscess that needs decompression immediately.
We should recognise patients at increase risk of spinal infection before commencing the CNB, with risk factors including:
• Immune compromised patients
• Patient with local or systemic infection
• Long-term vascular access
• Long duration of epidural catheterisation
• Difficult CNB or a bloody tap after epidural
• Prolonged hospital stay
• Disruption of the spinal column, e.g. surgery or trauma
Following epidural catheter insertion, catheter site checks and regular temperature monitoring are very important to recognise epidural abscess.
The classical presentation of epidural abscess is of pyrexia, back pain and progressive abnormal neurology of the lower half of the body. However, 1 in 4 patients have no back pain. Therefore, a high index of suspicion is required to diagnose epidural abscess.
Advice from neurosurgeons, neurologists, radiologists and microbiologists are needed early in established epidural abscess.
The most important action when we suspect epidural abscess is to organise MRI with gadolinium. This will help to decide whether open or percutaneous drainage should be usedIn this example, arranging an MRI scan and informing the neurosurgeons are the first and most important steps to perform because early diagnosis and surgical decompression is needed. Although option E is correct, it is time consuming and delays the diagnosis. Once muscle weakness is present, only 20% patients regain full
function, even after surgery.
A full infection screen including blood cultures is mandatory if an epidural abscess is suspected. At the same time, it is essential to remove the epidural catheter, as well as stop the epidural infusion, and send the catheter tip for culture and sensitivity.
As solely stopping the infusion is inadequate, options A, B and D are insufficient management options.
The most common microorganism found in spinal infection is Staphylococcus. Initial antibiotic therapy should be empirical and then modified depending on the culture and sensitivity results, while treatment must be guided by microbiological input.
Intravenous antibiotics are required initially for 2–4 weeks, followed by a prolonged course of oral antibiotics. Regularly checking of inflammatory markers, back pain and neurology should be used to monitor the response to antibiotics.
10
Q
- A 70 kg, 36-year-old man is scheduled for foot surgery under a regional anaesthetic
approach.
Which of the following needles would you use to perform a lateral popliteal nerve
block?
A 50mm length, short bevel peripheral nerve block needle
B 50mm length, long bevel peripheral nerve block needle
C 150mm length, short bevel peripheral nerve block needle
D 100mm length, short bevel peripheral nerve block needle
E 100mm length, long bevel peripheral nerve block needle
A
- D 100mm length, short bevel peripheral nerve block
needle
When performing nerve blocks, the length of the block needle is an essential
consideration. Longer needles might have potential tissue damage if advanced
further than needed, while the shorter needle may not be long enough to reach the
nerve.
The ideal needle length for peripheral nerve blocks is:
t 25mm – Interscalene
t 50mm – Cervical plexus, supraclavicular, axillary, femoral and popliteal (‘posterior
approach’)
t 100mm – Infraclavicular, paravertebral, lumbar plexus, sciatic (‘posterior
approach’) and popliteal (‘lateral approach’)
t 150mm – Sciatic (‘anterior approach’)
There are two types of nerve block needles: cutting tip needle and pencil point tip
needle (see Figure 1.4).
Cutting tip needles might be long bevel (15°) or short bevel (30–45°). Long bevel
needles are more likely to cause nerve damage by causing sharp nerve penetration.
Although the nerve damage caused by a short bevel needle is less frequent, the
damage will be more severe. Pencil point needles are believed to penetrate tissue rather than cut through it, thus
providing an improved feel of anatomical layers through which they pass. It is not
clear whether a pencil point needle or a short bevel needle is safer to use.
The most frequently used needle in the current practice is the short bevel one. It
offers more resistance as it passes through the tissue planes, provides better tactile
feedback than long bevel needles and is less likely to cause nerve damage. Thus in
this clinical scenario, the most appropriate needle for a lateral approach popliteal
nerve block is a 100mm, short bevel needle.
11
Q
- A 28-year-old pedestrian struck by a bus presents to the emergency department.
In hospital, he has had a primary survey which reveals an obvious head injury; he
also appears to have a fracture to his right arm. His chest appears clear and a FAST
scan of the abdomen is negative. Because he had been confused, the emergency
medicine registrar has asked you to sedate him for a CT scan of his head. On
examination, he grimaces and groans to a deep painful stimulus, but does not
open his eyes. He flexes his left arm and leg.
The safest option for CT scan would be to:
A Titrate small doses of propofol to effect with continuous monitoring including
waveform capnography
B Refuse to give sedative drugs on account of his depressed conscious state, but
accompany him to the scanner
C Perform a rapid sequence induction (RSI) with propofol and suxamethonium
1.5mg/kg, and transfer with a propofol infusion
D Perform a modified RSI with 1.5mg/kg suxamethonium, after 2µg/kg fentanyl
and propofol and manual in-line stabilisation of the cervical spine
E Fit a Miami J collar and blocks and then perform a modified RSI with 1mg/kg
rocuronium and 3mg/kg ketamine.
A
11 D Perform a modified RSI with 1.5mg/kg
suxamethonium, after 2µg/kg fentanyl and propofol and
manual in-line stabilisation of the cervical spine
This question relates to the management of the patient with traumatic brain
injury (TBI). TBI is a major cause of morbidity and mortality in young patients, with
over 10% of injuries falling in the moderate to severe category. The principles of
management are those relevant to all neurosurgical emergencies and neurotrauma
patients.
Initial assessment and resuscitation
Should be along the familiar treatment algorithm of ABCDE, but with treatment and
stabilisation of each problem simultaneously as the assessment continues. Haemodynamics
Even one episode of hypotension has been shown to double mortality. The aim is to
maintain cerebral perfusion pressure (CPP), in the face of raised intracranial pressure
(ICP) as CPP = MAP – ICP. International targets differ slightly, but a widespread MAP
target is 90mmHg. Fluid resuscitation to normovalaemia would be the logical first
step, with vasopressors following if required. Crystalloid is best, with some evidence
of harm with albumin colloid. Hypotonic dextrose solutions must be avoided (unless
hypoglycaemic), as they contribute to tissue oedema.
Airway/ventilation
Intubation is indicated for a deterioration in Glasgow coma scale (GCS), or a GCS
of <8, or if there is a failure of the patient’s protective reflexes. Any disturbance
in oxygenation or ventilation leading to hypoxia or hypercapnia is likewise a
mandatory indication as hypoxic episodes are shown to worsen prognosis.
Hypercapnia will increase cerebral blood flow (CBF) and thus ICP, so must be
controlled; similarly a patient hyperventilating to hypocapnia must move to
controlled ventilation as they will compromise their cerebral perfusion. Other
indications include those that may compromise the airway if not dealt with, such as
bilateral mandibular fractures, oral bleeding, or seizures. Targets again differ, but a
PaO2 of >10 kPa and a PaCO2 in the normal range of 4.5–5 kPa are assumed to be safe.
Managing ICP
Outside of a neurosurgical centre, intracranial hypertension is either a presumptive
diagnosis, or made when so severe as to bring about herniation and associated
pupillary unresponsiveness. Where facilities exist for monitoring, the level at which
treatment should begin, is >20–25mmHg.
Hyperosomolar fluids such as mannitol and 3% saline draw fluid from the
intracellular space back into the interstitium and vasculature. Fewer complications
are seen with hypertonic saline and doses depend on the concentrations available,
but 3ml/kg of 3% or 2mL/kg of 5% are reasonable, titrated to a serum sodium of
<155mmol/L.
Hyperventilation has been shown to compromise cerebral perfusion, and is thus
reserved for severe cases resistant to other treatments. A temporary course of
hyperventilation titrated to a Paco2 of 4–4.5 kPa may be used.
Hypothermia reduces ICP and cerebral metabolic rate of oxygen (CMRO2), and is
used in neurosurgical centres for this reason. The target temperature, and duration
to achieve benefit are not known, as no benefit has yet been reliably shown. Most
would ensure mild hypothermia (35°C), and ensure prevention of fevers, which are
known to be harmful.
Adequate sedation (reducing CMRO2) and muscle relaxation preventing coughing
and associated rises in ICP is essential. This is extrapolated using barbiturates for
burst suppression in some cases of raised ICP, but is associated with significant
hypotension.
In the above patient, the GCS is E1 V2 M3 = 6/15, and, in the context of a head
injury this represents an indication for intubation. The patient meets the criteria for immediate CT scanning, and the need for imaging in this patient also mandates
securing of the airway prior to the scan.
This is a dangerous mechanism of injury, and the C-spine is compromised until
proven otherwise. Therefore C-spine control is needed for intubation and scanning.
Clearing this clinically is no longer possible due to the conscious level. Even if the
GCS were 15, with a distracting fractured arm, one cannot clear the neck confidently
without imaging.
The final discriminator here is choice of drugs used. The priority is rapid control of
the airway with muscle relaxation, whilst preventing either hypertension, (and raised
CBF and therefore increased ICP), or hypotension (with a fall in cerebral perfusion
pressure). Most would achieve the former by adjunctive use of an opioid, and the
latter with cautious use of induction agent. Ketamine has recently been shown to
have no effect on increasing ICP, contrary to traditional teaching, but the dosing
of 3mg/kg is high, and a dosing of 1.5–2mg/kg is likely sufficient. Similarly, for
muscle relaxation, classical teaching has urged against suxamethonium because of a
transient rise in ICP. However, the rise is small and for the most part offset by the fall
in perfusion pressure caused by co-administration of induction agents. Therefore the
most appropriate course of action in this patient would be to perform an RSI with
fentanyl, suxamethonium and propofol and manual in-line cervical stabilisation.
12
Q
- A 19-year-old man presents to a district general hospital emergency department
8 hours after suffering a penetrating injury to his anterior chest. He has a Glasgow coma scale (GCS) of 15, heart rate of 105 beats per minute, blood pressure of 95/50
(MAP 65)mmHg, saturations of 99% on oxygen and a haemoglobin of 105g/L.
Transthoracic echocardiogram shows a haemopericardium for which he requires
transfer to a nearby cardiothoracic centre for exploration.
What pre-transfer intervention is most appropriate?
A Needle pericardiocentesis
B Intubation and ventilation
C Insertion of a pulmonary artery catheter for cardiac output monitoring
D Insertion of invasive arterial and central venous catheter
E Transfusion of 2 units packed red cells
A
- D Insertion of invasive arterial and central venous
catheter
This patient requires transfer for specialist surgical services. Although not in extremis
his condition may become compromised during transfer and adequate resuscitation
and pre-transfer planning are essential.
Motion artefact may make non-invasive blood pressure (NIBP) readings unreliable
and continuous invasive arterial blood pressure (ABP) monitoring in these situations
is more appropriate. Central venous catheters provide a reliable form of intravenous
access and allows for the use of inotropic or vasopressor support should the need
arise during transfer.
The use of a pulmonary artery catheter and cardiac output measurements by
thermodilution is not practical during transfer and will not contribute to this
patient’s management.
Intubation and ventilation monitored with continuous capnography should occur
pre-transfer in patients in whom the airway or ventilation may be compromised,
neither of which are a concern in this case. Pericardial clots may prevent adequate
pericardial drainage and blood may further accumulate. Pericardiocentesis in a non-
cardiac centre without immediate surgical support should be carefully considered,
and may unnecessarily delay transfer. It is indicated in patients with significant
haemodynamic compromise, although a haemodynamically unstable patient with a
penetrating chest wound likely warrant a thoracotomy. Aggressive fluid resuscitation
in patients with penetrating injuries should be cautious and goals should be to maintain an adequate filling pressure, heart rate and contractility. Blood should
be cross-matched and available to administer in the ambulance if required, and
tranexamic acid would be an appropriate adjunct in this circumstance.
13
Q
- A 62-year-old man who sustained an isolated non-penetrating chest injury resulting in lung contusions and rib fractures is on the intensive care unit
intubated and ventilated. He has deteriorated over the past 72 hours and now has a Po2:Fio2 ratio (PFR) of 50mmHg with a Fio2 of 1.0 and a positive end-expiratory pressure (PEEP) of 5cmH2O. The investigations suggest he has developed Acute Respiratory Distress Syndrome (ARDS).
The most important first intervention is:
A Furosemide bolus of 40mg intravenously and commence an infusion aiming for a negative fluid balance
B Administer a neuromuscular blocking agent
C Perform a recruitment manoeuvre and incrementally increase the PEEP to
above 14cmH2O
D Adjust the ventilator settings to ensure tidal volumes of 6mL/kg and a peak pressure of less than 30 cmH2O
E Prone the patient
A
- C Perform a recruitment manoeuvre and incrementally
increase the PEEP to above 14cmH2O
○ Acute respiratory distress syndrome (ARDS) was first described in 1967 by Ashbaugh et al to describe tachypnoea, pulmonary infiltrates, decreased pulmonary compliance, atelectatic lungs with alveolar oedema and hyaline membranes on pathological examination.
○ The first formalised diagnostic criteria were created by the American-European Consensus Conference (AECC) in 1994 and have since evolved. This included:
• An acute clinical course
• Bilateral infiltrates on the chest radiograph
• No atrial enlargement or left ventricular failure
• A severity classification dependent on the PaO2/FIO2 ratio (PFR)
– ARDS was classified as a PFR <200mmHg
– Acute lung injury (ALI) was classified as a PFR of >200 <300mmHg
○ In 2012 the Berlin definition by the AECC superseded the original classification:
° Respiratory failure now needs to occur within a week of a known initiating process.
° Heart failure no longer needs to be excluded but must not fully explain the patients respiratory failure.
° Acute lung injury no longer exists, and grades of severity of ARDS
has replaced the older classification (Table 1.2).
○ The new definition offers better predictive information for duration of treatment and the mortality.
○ This patient has severe ARDS as defined by his PFR and is at risk of dying from hypoxia. There is an escalation protocol on how to manage such a patient, starting with simple manoeuvres and ending with desperate measures: - Recruitment manoeuvres to improve oxygenation. There are several methods, which are detailed by Lapinsk and Mehta. Most involve a transient increase in PEEP and peak ventilator pressures, which can be performed using a manual technique or the ventilator.
- ARDSNet ventilator strategy which includes an appropriately high maintenance LEEP >14mmHg with tidal volumes of less than 6mL/kg and peak pressures of less than 30cmH2O.
- Other ventilator settings such as reverse inspiratory: expiratory (I:E) time ratios may be beneficial.
- Fluid balance management is key for more long-term management. Recent evidence suggests that avoiding a positive fluid balance increases ventilator-free days and may reduce mortality.
- Prone positioning has recently been shown to improve oxygenation, improve 28-day and 90-day mortality and is not associated with an increase in complications if performed properly. It should be commenced early in the
disease process and for a minimum of 17–24 hours per day. - Extracorporeal membrane oxygenation (ECMO) is becoming increasingly used for refractory respiratory failure in a select cohort of patients with reversible conditions, however caries a significant risk of haemorrhage. It can only be carried out in regional centres.
○ Two therapies investigated previously include steroid administration and oscillation ventilation. Both these interventions do not improve outcome, and in the case of oscillation may infer risk if used by a centre without significant experience. Therefore they are no longer recommended treatment options for ARDS.
○ In summary, at present the only interventions for ARDS that infer a mortality benefit is ARDSNet ventilator strategy, fluid balance managing and most recently prone ventilation.
○ In the above scenario the patient was not on an optimum ventilator
setting. Recruitment manoeuvres would be the most important first intervention followed by maintenance of recruitment with appropriate ventilator settings.
14
Q
- A 26-year-old woman with a past medical history of self-harm was found
unconscious at home with empty alcohol and amitriptyline bottles on the
floor. These had been ingested within half an hour. On arrival to the emergency department her Glasgow coma scale (GCS) was 5 (E1, V1, M3). She was intubated for airway protection. The patient subsequently developed a blood pressure of 80/60 mmHg associated with a heart rate of 150 beats per min, a QRS width of 100 msec and multiple ventricular ectopic beats.
The next most important intervention is:
A Nasogastric tube insertion and administration of activated charcoal
B Intravenous crystalloid bolus of 20mL/kg followed by a noradrenaline infusion to maintain blood pressure
C 500 ml intravenous sodium bicarbonate 1.26% for treatment of a broadened QRS complex
D Lignocaine 2mg/kg for the management of ventricular ectopic beats
E Lipid emulsion 20% 1.5mL/kg for intravascular sequestration of tricyclic drug
A
- B Intravenous crystalloid bolus of 20mL/kg followed by a
noradrenaline infusion to maintain blood pressure
○ Tricyclic antidepressants (TCA) are a class of drug used to treat depression, chronic pain syndromes and attention deficit disorder in children.
○ Amitriptyline is the most commonly used in clinical practice.
○ Overdose occurs at all ages including accidental overdose.
○ TCAs are some of the most frequently overdosed medications and contribute to up to 300 deaths per annum in the UK.
○ Cardiovascular collapse is due to a sodium channel ‘stabilising effect’ due to blockade of fast sodium channels in the myocardial conduction system. ° This leads to an increase in QRS duration initially and may progress to decreased myocardial excitability, bradycardia and asytole.
° In addition a dose-dependent decrease in myocardial contractility occurs due to noradrenaline (NA) and serotonin re-uptake inhibition.
° Alpha-1 adrenergic receptor blockade causes profound vasodilatation,
which leads to distributive shock
° Altered mental state resulting in confusion or agitation may be as a result of central anti-histaminic and anti-cholinergic activity.
° Increasing central nervous system levels of noradrenaline and serotonin reduces the seizure threshold.
○ The management of the patient described above should include an ABC approach to protect the airway.
○ All options are viable: - Once the airway is protected, if ingestion is within an hour of presentation
activated charcoal may be considered but this will only prevent further
gastrointestinal absorption and not impact the current emergent problem of
hypotension and may in fact worsen it. - Fluid and vasopressors are the most important initial management. This will counteract the distributive shock component as described above. This may be sufficient to improve mean arterial pressure resulting in a decrease in heart rate.
- The high sodium load found in sodium bicarbonate stabilises the myocardium and may prevent arrhythmias. It is indicated if the QRS width is over 100 msecs.
○ An alternative treatment is hypertonic saline if no metabolic acidosis is present.
○ Increasing plasma pH also has the effect of increasing drug protein binding, which can be achieved by hyperventilation. - Amiodarone and other class 1a and 1c anti-arrhythmic agents should be avoided as they increase the cardiac action potential.
° Both lignocaine and magnesium have been used for arrhythmia management in TCA overdose. - There are case reports that lipid emulsion has been used successfully in cardiac arrest secondary to TCA overdose by sequestering plasma drug and reducing the active concentration. If used, this should follow the same protocol as for local anaesthetic toxicity.
○ A multi-faceted approach is required however the initial management should focus on airway control, volume expansion and management of vasoplegia before moving onto more complex treatment options.
15
Q
- A 28-year-old woman presents with progressive and ascending motor weakness.
She reports a recent history of coryzal symptoms.
The following would be an early indicator of the requirement for intubation:
A Respiratory rate >35 breaths per minute
B Pao2 <8 kPa
C Paco2 >6.5 kPa
D Vital capacity <15mL/kg
E Absence of bulbar weakness
A
- D Vital capacity <15mL/kg
The symptoms of progressive and ascending motor weakness with the antecedent
history of a viral infection suggest Guillain–Barré syndrome. Guillain–Barré is a
collection of diseases that result from acute inflammatory demyelination leading
to the hallmark signs of ascending muscle weakness and areflexia. Sensory and
autonomic function can also be affected by Guillain–Barré.
The pathophysiology of Guillain–Barré appears to be an immune mediated reaction
to a prior infection, commonly upper respiratory tract infections or Campylobacter
jejuni. Autoantibodies (such as antiganglioside autoantibodies) initiate either a
cascade of myelin destruction or axonal damage; the latter results from C. jejuni
infection with a worse prognosis.
Early detection of the need for intubation is imperative as rapid deterioration
can ensue. Indications for intubation predominantly include respiratory failure secondary to muscle weakness or the presence of bulbar symptoms necessitating
airway protection.
Whilst clinical signs of respiratory failure such as tachypnoea, hypoxia and
hypercapnia will strongly suggest the requirement for intubation, these are relatively
late signs. Serial vital capacity (VC) measurements should be taken and management
in a critical care area should be considered when VC <20mL/kg. Intubation should
be carefully considered when measurements fall below 15mL/kg in the presence
of bulbar symptoms or rapidly progressive disease. Rapid sequence induction is
recommended due to the raised aspiration risk. In addition to full AAGBI monitoring,
invasive arterial blood pressure monitoring should be instituted, particularly in the
presence of autonomic instability. Due to reports of an exaggerated hyperkalaemic
response, depolarising muscle relaxants should be avoided.
Critical care management should include consideration of immunotherapy in liaison
with specialist teams. Intravenous immunoglobulin or plasma exchange is the
mainstay of current management, while steroids do not appear to have a role.
16
Q
- A 70 kg elderly man, awaiting an elective transurethral resection of prostate
(TURP), is admitted to the intensive care unit (ITU) with urosepsis. His average
urine output over 12 hours is 28mL/hour.
His ITU admission and pre-admission clinic biochemistry profile are shown in
Table 1.1.According to the RIFLE criteria, which stage of acute kidney injury does this man
fulfill?
A Risk
B Injury
C Failure
D Loss
E End-stage renal disease
A
- B Injury
Acute kidney injury (AKI) describes an abrupt decline in renal function. A number of
classification systems have been devised to further the definition and staging of AKI.
Three in common use are the RIFLE criteria (2004), AKIN criteria (2009) and KDIGO
(2012). All three rely on a defined creatinine rise with or without criteria for urine
output. There is an increasing recognition that serum creatinine may not detect early
AKI and the role of renal injury biomarkers, such as neutrophil gelatinase-associated
lipocalin (NGAL), is under investigation.
Of the three criteria to describe AKI, none have shown clinical superiority, although
the AKIN criteria are more sensitive. The question uses the RIFLE criteria as this is
commonly referred to in UK practice. According to RIFLE, AKI is subdivided into five
progressive stages based on creatinine rise and urine output. Further information
regarding the AKIN criteria can be found in question 10.13.
The patient described in the question has doubled his creatinine from baseline
and his urine output has been less than 0.5mL/kg/hr (35mL/hour) for 12 hours. He
therefore fulfills the RIFLE ‘injury’ criteria (Table 1.3).The morbidity and associated mortality from AKI is high both within and outside
the critical care environment. Prevention, early recognition (using criteria) and
good adherence to the principles of management should be a part of routine care.
The principles of management include treating the underlying cause, optimising
renal perfusion, withholding nephrotoxic agents and, where appropriate, renal
replacement therapy.
The clinical importance of AKI has lead to a recent National Institute for Health
and Care Excellence (NICE) guideline and the London Acute Kidney Injury Network
releasing an ‘AKI bundle.’
24
Q
- A 46-year-old right-handed violinist presents with a 3-month history of
worsening severe pain in his right wrist, which commenced suddenly after a long performance in a concert. He has noticed the painful wrist going pale and cold at times, and swelling occasionally. Sometimes it sweats, and it has become stiffand difficult to use. It appears smaller than his left hand, and the nails of his right fingers have become brittle and discoloured. He admits to being very distressed and anxious as he is no longer able to perform. Treatment with paracetamol and amitriptyline has been commenced.
The most appropriate next step in his management is:
A Pregabalin 75mg b.d.
B Acupuncture
C Patient education and psychological support
D Application of 5% lignocaine patches
E Mirror therapy
A
- C Patient education and psychological support
○ This patient has developed symptoms and signs of complex regional pain syndrome (CRPS) type 1.
○ CRPS is a chronic, debilitating and painful condition. It is uncommon and usually develops following an injury, but may occur spontaneously. It affects one or more
limbs and typically demonstrates a collection of symptoms and signs described as sensory, vasomotor, sudomotor, trophic and inflammatory.
○ The presentation varies from mild and self-limiting to a chronic and disabling disease process.
○ Diagnosis is clinical.
° In 1994, the International Association for the Study of Pain (IASP)
established a definition, but the latest definition came from Budapest in 2004.
○ The Budapest criteria classify symptoms and signs into four broad categories
(Table 1.4).
○ According to the Budapest criteria, all of the following must be met in order to make a diagnosis of CRPS:
• The patient has continuing pain which is disproportionate to the inciting event
• The patient has at least one sign in two or more categories
• The patient has at least one symptom in three or more categories
• No other diagnosis can better explain the signs and symptoms
○ CRPS can be academically classified as being type 1 (not associated with major nerve damage) or type 2 (associated with major nerve damage), but this does not influence subsequent management or prognosis. Aetiology is uncertain and thought to be multifactorial, as no one single theory
fully explains the condition.
○ Current hypotheses include an inflammatory process, or altered neurological function.
○ There may be an association between the use of angiotensin converting enzyme (ACE) inhibitors and the development of CRPS.
○ Regarding treatment, there is a lack of robust evidence for CRPS and most recommendations are derived and extrapolated from those for other neuropathic pain conditions.
○ Early treatment may help prevent the development of some of the
longer term sequelae of severe CRPS.
○ There are four equally important aspects to treatment (see Table 1.5).
In this scenario, the patient must first be educated about the condition and fully involved in decisions regarding his subsequent management. This will establish whether he will benefit from treatments such as mirror therapy, motor imagery or CBT.
° Physiotherapy and occupational therapy are both recommended early.
° Pharmacologically, there is a lack of evidence for the benefits of anti-neuropathic agents
° Amitriptyline is the first line agent of choice for neuropathic pain in general, followed by pregabalin.
° Additionally, there is still limited evidence to support early use of acupuncture in the treatment of CRPS patients
25
Q
- A 30-year-old woman with chronic lower back pain is assessed in an outpatient
clinic. She tells you that her pain has improved with exercise and local heat
application, but when she thinks about the pain it seems to get worse.
Regarding this gate theory of pain, which of the following is most accurate?
A It applies mostly to nociceptive pain
B It is the basis of how transcutaneous electrical nerve stimulation (TENS)
machines work
C A supraspinal input is required
D Inhibition occurs via AG fibres
E This theory does not apply to children
A
- B It is the basis of how transcutaneous electrical nerve
stimulation (TENS) machines work
The gate theory of pain was proposed by Wall and Melzack in 1967. They stated that
pain synapses are affected by other neural inputs and inhibitory signals may prevent
nociceptive impulses passing to the central nervous system. This applies to all pain
and is the basis of how transcutaneous electrical nerve stimulation (TENS) and spinal
cord stimulation work. It does not explain all pain phenomena, and other theories
such as the neuromatrix theory exist. This hypothesizes that the brain has a map of
the body and disruption of peripheral input may be represented as pain.
Supraspinal input is not always required and an example is the use of localised heat
and light touch causing Aβ fibres impulses to inhibit pain (see Figure 1.5).Aδ have thin, myelinated axons that are responsible for the transmission of thermal
and pressure signals as well as mediating fast pain signals.
The gate theory of pain applies to both adults and children.
26
Q
- A 73-year-old woman with metastatic breast cancer presents with a 4-month
history of severe pain in her back, upper arms and legs. She has been on increasing
doses of modified release oral morphine and paracetamol, and while this
combination provides her some relief, she is troubled by drowsiness, pruritus,
and constipation. At times she feels this is more distressing than her initial pain.
Additionally, she is on warfarin for atrial fibrillation.
The most appropriate next step in her management would be:
A Add diclofenac B Reduce the dose of morphine
C Add naloxone
D Opioid rotation
E Prescribe a laxative
A
- B Reduce the dose of morphine
Pain is a common symptom amongst those suffering with malignant disease, and its
management can be challenging. Aetiology of pain in cancer is multifactorial, and
causes may include: t Mass effect of the tumour
t Effect of treatment, e.g. radiotherapy, chemotherapy
t Paraneoplastic syndromes
t Conditions associated with the disease process, e.g. osteoporosis, hypercalcaemia
t Pre-existing pain from other chronic conditions
t Combination of any of the above
Table 1.6 summarises some of the strategies that may be employed in controlling
pain.
Opioids are very effective in management of cancer-related pain in general. To begin
with, most patients are started on longer acting oral opioids to treat background
pain, supplemented with additional doses to treat breakthrough pain. Oral
morphine is a suitable agent for most patients, but different people may display an
unpredictably different benefit-side-effect profile with different opioids.It is not uncommon to use parenteral routes to administer opioids. In palliative care
settings, opioids are frequently administered subcutaneously by syringe driver.
Those on very large doses of oral morphine (>60mg per 24hours) may benefit from
a fentanyl patch.
Long-term opioid use is associated with significant unwanted effects. These include
dependence, tolerance, drowsiness, constipation, nausea, vomiting, pruritus, urinary
retention and respiratory depression. Sometimes, patients may report a paradoxical
worsening of their pain. This is a phenomenon known as opioid-induced hyperalgesia.
Unwanted side effects will usually settle as tolerance develops. However, at times they
may be more distressing than the pain itself, as in this scenario.
If adverse effects of opioids cause the patient notable distress or discomfort they
warrant specific treatment. The reversal agent naloxone has an extremely short
plasma half-life, and while it is useful for acute opioid poisoning, it has no role in
a chronic setting. In the first instance, the dose of opioid should be reduced, but
other adjuvant analgesia should be prescribed, e.g. paracetamol or ketamine.
Anti-pruritic drugs, laxatives, and other medication for symptom relief may be
considered. Failing this, opioid rotation may be attempted. This is a method by
which one opioid is substituted for an equipotent dose of another (e.g. oxycodone
for morphine).
Prescribing a laxative is not the best option here as it only tackles constipation,
rather than treating the problem of unwanted effects as a whole.
