SBA 300 Paper 4 Flashcards
- A 32-year-old man is admitted to the intensive care unit. 2 weeks ago he suffered a
bout of gastroenteritis, following which he noticed bilateral leg pain and weakness
which then progressed proximally and he soon had difficulty coughing and
swallowing. Since admission he has been persistently tachycardic and sweaty with
episodes of hypertension and hypotension.
Which of the following clinical features is most likely to confirm his diagnosis?
A Progressive areflexic weakness in more than one limb
B Progressive rise in CSF protein levels >0.4 g/L
C Symmetrical weakness
D Autonomic dysfunction
E Bulbar palsy
- B CT angiography
The most likely diagnosis in this clinical scenario is that of a pulmonary embolism
(PE).
The European Society of Cardiology published guidelines in 2014 on the diagnosis
and management of acute PEs. There are a number of prognosticating tests of PE
severity, of which the Pulmonary Embolism Severity Index (PESI) and simplified PESI
(sPESI) are recommended. Due to ease of application and validation, the sPESI is
used most frequently, taking in to account:
t Age >80–1 point
t Cancer–1 point
t Chronic heart failure or pulmonary disease – 1 point
t Pulse rate >110 beats per minute –1 point
t Systolic blood pressure <100mmHg –1 point
t Arterial oxyhaemoglobin saturations <90% – 1 point
0 points gives patients a 30-day mortality of 1.0%, while ≥1 point gives a 30-day
mortality of 10.9%.
Additional markers are also applied to stratify patients:
Clinical: Shock, hypotension
Right ventricular (RV) dysfunction: RV dilatation, hypokinesia or pressure overload
on echocardiogram, RV dilatation on CT or elevated right heart pressure on cardiac
catheterisation.
Cardiac laboratory biomarkers: Cardiac troponin T or I, brain natriuretic peptide
(BNP) elevation
These can then be put together to quantify the risk severity for patients (Table 4.6)It can be seen therefore that a hypotensive or shocked patient will immediately be
classified as high risk. In these patients imaging with transthoracic echocardiography
or CT angiography is recommended. Treatment of the PE must not be delayed for In patients without clinical evidence of shock, such as the patient described in the
scenario above, investigations could be undertaken prior to initiation of treatment
of anticoagulation or thrombolysis. Chest X ray, arterial blood gas analysis and ECG
do not have a high specificity for detecting pulmonary embolism, even though
they may contribute to some extent in confirming diagnosis. Chest X-ray may
demonstrate hypovascularity or peripherally placed wedge shaped consolidation
suggesting infarction. ECG may show a S1Q3T3 pattern suggestive of right heart
strain and arterial blood gases may show hypoxia. It is suggested that in case of a
high clinical probability it is advisable to use a radiological investigation rather than
a non-radiological modality such as a D-dimer test which would in all probability
be high in the majority of in-patient postoperative patients. Transoesophageal
echocardiography is generally reserved for patients that are too unstable to undergo
diagnostic CT angiography, although bedside transthoracic echocardiography is
recommended.
Using CT angiography is most appropriate in this patient as it not only shows the
severity of the embolus but also depicts right heart dysfunction by demonstrating
enlarged size of the right ventricle and a flattened interventricular septum. In
addition, CT angiography may reveal the chronicity and possible clot location.
imaging if there is a high clinical suspicionIn patients without clinical evidence of shock, such as the patient described in the
scenario above, investigations could be undertaken prior to initiation of treatment
of anticoagulation or thrombolysis. Chest X ray, arterial blood gas analysis and ECG
do not have a high specificity for detecting pulmonary embolism, even though
they may contribute to some extent in confirming diagnosis. Chest X-ray may
demonstrate hypovascularity or peripherally placed wedge shaped consolidation
suggesting infarction. ECG may show a S1Q3T3 pattern suggestive of right heart
strain and arterial blood gases may show hypoxia. It is suggested that in case of a
high clinical probability it is advisable to use a radiological investigation rather than
a non-radiological modality such as a D-dimer test which would in all probability
be high in the majority of in-patient postoperative patients. Transoesophageal
echocardiography is generally reserved for patients that are too unstable to undergo
diagnostic CT angiography, although bedside transthoracic echocardiography is
recommended.
Using CT angiography is most appropriate in this patient as it not only shows the
severity of the embolus but also depicts right heart dysfunction by demonstrating
enlarged size of the right ventricle and a flattened interventricular septum. In
addition, CT angiography may reveal the chronicity and possible clot location.
- A 44-year-old woman with a past history of hypothyroidism has suffered a
traumatic brain injury and is on the neurointensive care unit. She had an isolated seizure following a blunt force to her cranium and remains intubated and
ventilated. She is clinically euvolaemic but her investigations reveal the following:
• Serum sodium 122mmol/L (normal range 135–145mmol/L)
• Serum osmolality 270mOsm/kg (normal range 278–305 mOsm/kg)
• Urine osmolality 300mOsm/kg (normal range 500–800 mOsm/kg)
Which of the following is the most likely cause of her biochemical derangement?
A Hypotonic fluid administration
B Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
C Cerebral salt-wasting syndrome (CSWS)
D Phenytoin administration
E Myxoedema
B Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
○ Sodium and water go hand in hand to maintain intravascular homeostasis.
○ Serum osmolality is predominantly dictated by sodium concentration, and the control of sodium is a powerful determinant of water distribution. If the serum osmolality increases, hypothalamic osmoreceptors signal the production of antidiuretic
hormone (ADH, vasopressin) to reduce water excretion and thereby rectify the
imbalance.
○ Total body sodium itself, is controlled by the sympathetic nerves and
natriuretic peptides that govern its renal reabsorption once it has been filtered at the
glomerulus.
○ Hyponatraemia can be classified as a serum concentration <135mmol/L and
may be associated with hyper-, hypo- or euvolaemia.
○ The most common causes
of hyponatraemia in a brain injured patient are syndrome of inappropriate ADH
secretion (SIADH) and cerebral salt-wasting syndrome (CSWS).
○ SIADH leads to unregulated ADH release and lack of feedback response such that
water is indiscriminately reabsorbed. It is characterised by:
1. Serum sodium <135mmol/L
2. Reduced serum osmolality <280mOsm/kg
3. Urine osmolality greater than serum osmolality
4. Low urine output
5. Normovolaemia (occasionally hypervolaemia)
Treatment includes fluid restriction, furosemide (to encourage water excretion) and
demeclocycline (to inhibit renal ADH response, or direct ADH receptor antagonists).
CSWS is not fully understood but is associated with increased natriuretic peptides
and ultimately involves increased renal sodium loss and subsequently, water is lost
in tandem. It is characterised by:
1. Normal or low serum sodium
2. Normal or low serum osmolality
3. Normal or high urine osmolality
4. Normal or high urine output
5. Hypovolaemia
Treatment involves replacement of sodium and water. This is usually commenced
with 0.9%saline solution but hypertonic 1.8%or 3%solutions may be required if the
loss has been acute and the patient is symptomatic.
The negative fluid balance is usually the distinguishing feature between CSWS and
SIADH, but can be hard to assess clinically. Very infrequently CSWS can biochemically
masquerade as SIADH. In this instance the induced hypovolaemia is such that it
results in a consequential rise in ADH.
Iatrogenic hyponatraemia can be seen after hypotonic fluid infusions or as the side
effect of some medications such as anticonvulsants, especially carbamazepine and
phenytoin.
Systemic disease, such as hypothyroidism, can also be associated with
hyponatraemia. Hypothyroid coma or myxoedema is rare but may be triggered by
trauma, particularly in the absence of replacement medication.
SIADH is therefore the most likely cause from the options given.
- You are asked to see a 60-year-old woman with a suspected myocardial infarction.
She is known to have a permanent pacemaker and implantable cardioverter-
defibrillator (ICD). Shortly after arriving she suffers a cardiac arrest. The monitor
shows ventricular fibrillation.
Which of the following best describes the optimum position of the defibrillation
pads?
A Anterior-posterior position
B Directly over the pacemaker
C At least 8 cm from the generator position
D Anterior-lateral position
E No defibrillation pads should be applied
C At least 8cm from the generator position
The patient has a shockable rhythm and requires defibrillation immediately.
In patients with an implantable cardioverter-defibrillator (ICD) or permanent
pacemaker, it is important not to delay defibrillation; the ICD may not be functional
or failed to have detected the dysrhythmia.
Although the strength of evidence is low, the pad should be placed at least 8cm
from the generator; it is possible that automated external defibrillator (AED) devices
may sense pacing spikes and so not detect ventricular fibrillation (VF). The other pad
can then be placed in the lateral position or the posterior position. Placement of
defibrillation pads over the pacemaker/ICD may cause subsequent malfunction of
the device and should be avoided.
- A 7-year-old child is experiencing breathing difficulties. After suffering from
coryza and a 3-day low-grade fever, his parents noticed a rapid deterioration in his
breathing overnight. He is now stridulous with a high-grade fever and is producing
copious secretions. He is lying flat, moving his neck freely and there is no response
to nebulised adrenaline and steroids.
What is the most likely diagnosis?
A Epiglottitis
B Viral croup
C Bronchiolitis
D Retropharyngeal abscess
E Bacterial tracheitis
E Bacterial tracheitis
○ Certain childhood respiratory tract infections have the potential to progress
to life threatening airway obstruction if they are not diagnosed and managed
correctly.
○ Children with acute severe stridor represent an anaesthetic challenge as any agitation from the child might precipitate complete obstruction.
○ Intravenous
cannulation and throat examination in this scenario should therefore not be
attempted.
○ Early, experienced anaesthetic and ENT involvement is recommended
and the priority is to examine and secure the airway under anaesthesia.
○ Bacterial tracheitis is a rare but life threatening condition commonly caused
by Staphylococcus aureus and characterised by subglottic oedema with thick
mucopurulent secretions compromising the airway.
○ Typically, the child experiences
viral upper respiratory tract prodromal symptoms for 2–3days which is followed by a rapid clinical deterioration over 8–10 hours. At this stage the child may appear toxic,
stridulous and have a high fever as described in the above case.
○ A distinguishing feature from epiglottitis is the usual ability of the child to lie flat and the absence of drooling and dysphagia.
○ Croup is the most common cause of acute stridor in children but usually affects
younger age groups (6months to 3years).
○ Commonly caused by the parainfluenza
virus family, sufferers classically display a barking cough preceded by a prodrome of
nasal congestion and rhinorrhea.
○ The deterioration is not as marked as in bacterial tracheitis and copious secretions are not typical features. Furthermore, children often want to sit upright as opposed to lie flat and may show a marked clinical
improvement following nebulized adrenaline and steroids.
○ Since the introduction of the Haemophilus influenzae type b vaccine, epiglottitis
has become rare.
○ Epiglottitis normally affects children aged 2–6years and usually
presents abruptly with a high fever, dysphagia, stridor and drooling. The child may prefer leaning forwards with their mouth open to keep their airway open.
○ The
presence of antecedent viral symptoms, current secretions as well as the child’s
position in the case above makes epiglottitis not the most likely diagnosis.
○ A retropharyngeal abscess arises in the space between the posterior pharyngeal
wall and prevertebral fascia and can cause airway obstruction by physical expansion.
○The abscess can be formed after a penetrating pharyngeal injury or infected lymph nodes associated with an upper respiratory tract infection.
○ Crucially these patients commonly complain of limited neck movement contrary to the above scenario.
○ Bronchiolitis is a common and usually self-limiting lower respiratory tract infection
caused by the respiratory syncytial virus. Children under 2 years old are most
commonly affected and present acutely with rhinorrhea, cough and a low grade
fever preceded by a prodrome of several days. Since it is a lower respiratory tract
infection, stridor is not usually present. Treatment is supportive and includes oxygen and intravenous fluid therapy as needed. Conflicting evidence remains as to the
effectiveness of steroids and nebulised adrenaline in treating this condition
- You are involved in a critical incident in the neuroradiology suite. A patient
undergoing an angiogram received a total of 7mg/kg of plain lignocaine to
anaesthetise the groin for femoral arterial access. The patient then lost cardiac
output which returned following administration of intravenous lipid emulsion, according to national guidelines. They have since been transferred to the intensive
care unit.
Which of the following describes your most appropriate action immediately after
the event?
A Report the case to the NHS Commissioning Board Special Health Authority
B Ensure that you have fully documented the event in the patient records
C Contact your medical indemnity provider
D Organise an ‘after action review’ with all personnel involved
E Instigate the local reporting mechanism for critical incidents
B Ensure that you have fully documented the event in the patient records
Clinical risk management is at the centre of ensuring patient safety and may be
prospective or retrospective. Prospective management can be at an individual level, e.g. planning a patient-specific anaesthetic, or at a department level to comply with
Clinical Negligence Scheme for Trust (CNST) regulations.
In order to manage risk there are five sequential stages of process to be completed.
1. Awareness
2. Identification
3. Assessment
4. Management
5. Re-evaluation
○ Awareness
A critical incident or Patient Safety Incident (PSI) is that which could or did cause
harm, be it unexpected or unintended. It has been reported in the literature that up
to 50% of PSIs are preventable.
○ Identification
Risk is identified in several ways. Local incident reporting mechanisms, by clinical
staff or patients, and national data from the NHS Commissioning Board Special
Health Authority, formerly the National Patient Safety Agency (NPSA), serve to
highlight threats. Case note review is fundamental for recognition and education
regarding events. Root cause analysis (RCA) provides a more formal and structured
investigation to identify failings in a system.
RCA is undertaken by a team of risk managers including clinicians and, on occasion, lay people. RCA aims to analyse each case thoroughly from documented data (from the whole admission), construction of accurate timelines and personnel contribution to an event, and subsequent interrogation of all information collected to identify the cause. It detects barriers to safe practice which are classified as physical, natural
(temporal or distance related), human action and administrative.
○ Assessment
Identified risk can then be scored according to its potential severity and frequency.
This enables a trust to stratify its resources accordingly for the prevention of risk
recurrence.
○ Management
This describes the arrangements implemented to reduce the risk to as low a level as possible. It involves improving those barriers to patient safety identified through
RCA. At a local level it may be prudent to hold an after action review (AAR). This
is an informal discussion between the staff involved in an incident. It is led by an
independent and objective facilitator with the aim of identifying problems and
improvements without the allocation of blame.
○ Re-evaluation
This is essential in order to confirm the absence of renewed risk in light of any
changes made. Although all of the options are applicable to action following a critical incident, full contemporaneous documentation provides the basis of all
further risk analysis
- An 80-year-old man for an open oesophagectomy has a cardiopulmonary exercise test (CPET) as follows:
• Anaerobic threshold (AT) 10mL/kg/min
• Peak oxygen consumption (V
.O2 max) is 75% of that predicted
When describing the results the most correct description includes:
A His AT gives him a higher rate of complications
B His AT gives him a higher risk of death
C His V.O2 max max gives him a low risk of death
D His V.O2 max max is associated with the highest risk of complications
E He should be nursed in intensive care postoperatively
B His AT gives him a higher risk of death
Cardiopulmonary exercise testing (CPET) is no longer the reserve of research labs or
specialist centres, and is now widespread. The detailed physiological data produced
gives a wealth of information, the correct use and interpretation of which takes skill
and experience. Whilst not expecting this standard of candidates, the examiners
have recently demonstrated their willingness to scrutinise candidates on the subject.
Risk stratification is an ever-changing topic, and thus there are several factors
one has to consider in terms of any question on the subject. Firstly a thorough
history and patient examination are a sound foundation, and from there one can
incorporate the information into relevant scoring systems such as the ASA, Goldman,
Lee and Detsky. Frequently, these give a figure based on single organ, especially
cardiac, demise. A detailed history to reveal functional ability is an essential tenet
of any pre-assessment and this can be assimilated into a tool such as the Duke
Activity Index. Unfortunately the revealed levels of activity may not truly reflect
ability and history is subject to bias and recall error. So, in search of more objective
data we arrive in the arena of testing. The traditional tests of function, such as
echocardiography and spirometry give limited data as they are non-dynamic tests
performed at rest.
In addressing this need for another functional test, CPET has evolved into the gold
standard for objective functional assessment and measurement.
● Performing the test
The test requires two staff and special equipment. One member of staff will attend
to and coach the patient whilst the other attends to the data and testing equipment.
The equipment has two parts; a fixed exercise cycle, the resistance of which can
be adjusted by the control computer to increase or decrease the work done by the
patient. The other element is the metabolic cart, which is formed by a facemask
with a gas analyser to measure oxygen use, carbon dioxide evolution, and a
pneumotachograph to quantify gas flows and volumes. A 12-lead ECG is also
connected to the computer of the cart which assimilates all the gas and ECG data to
produce live displays of results alongside a continuous ECG with ST segment analysis.
Pre-test, the exercise bike seat has to be adjusted for height and the facemask straps
adjusted and tested for a good seal. A SpO2 probe is attached and a non-invasive
blood pressure (NIBP) cuff fitted alongside the 12-lead ECG. The patient then enters
the warm up phase, pedalling unloaded at 60 rpm, while baseline spirometry
is performed. This unloaded phase continues into the first 3 minutes of testing,
followed by sequential increased loading to the pre-calculated ramp protocol. At
the end of the test the patient has a cool down period, and remains monitored for a
further 10 minutes to observe recovery.
● Safety
The quoted mortality of the test is in the region of three patients per 100,000 tests,
and full resuscitation facilities must be immediately available. Certain conditions
preclude testing, such as severe or unstable cardiac/respiratory conditions,
thrombosis and dissection and those conditions which may preclude cooperation
such as mental disabilities. Whilst wearing the facemask patients cannot talk, so a set
of previously agreed signals are used to indicate fatigue and chest pain.
● Measurements and results
Gas exchange measurements include oxygen consumption (V.O2), carbon dioxide
production (V.CO2), and the respiratory exchange ratio (RER). Ventilatory measures
of respiratory rate, minute ventilation (VE) and tidal volume (VT) are taken, as are
cardiovascular parameters of NIBP, ECG, heart rate and oxygen pulse (VO2/hour).
Pulmonary exchange calculations can be taken from the ventilatory equivalents for
O2, CO2 and Spo2.
●Cardiac output
The oxygen pulse V.
O2/hour, is an approximation of stroke volume. Increased work
requires more oxygen to fuel energy usage, and so oxygen consumption increases.
Cardiac output is seen to increase in a linear fashion alongside V
.
O2, until a peak
oxygen extraction ratio of 75% is reached. The gradient of the V
.
O2 increase is a
measure of the exercise driven increase in cardiac output.
● Anaerobic threshold/V.O2 max
This oft quoted measure is a marker of the efficiency of the cardiorespiratory system.
It is also largely unchanged with age, and is unaffected by effort or motivation and is
reliable and repeatable for a given patient.
The anaerobic threshold (AT) gives a value for the point at which the oxygen
demand outstrips supply as work increases, and therefore anaerobic respiration is
evoked. The production of lactate generates an extra acid load to the system and
thus increases the production of CO2 (V
.
CO2). Thus the AT is the inflection point of a
graph of V
.
CO2against O2. In other terms, the AT is also the point at which the RER rises
above 1, and is the lowest point on the plot of ventilatory equivalents for oxygen.
Patients can exercise well beyond their AT, and in most tests this represents roughly
the half way mark. V
.
O2 max, is the peak V
.
O2 usually measured at the time the test is
terminated.
It is should be remembered that the variables discussed are part of a whole testing
package and a raft of results which should ideally not be considered in isolation. The
results can be considered to be interlinked in physiological terms and in terms of
complications. For example a complication can give rise to mortality if of sufficient
severity.
The AT is shown to correlate with mortality, and the key ‘cut off’ figure in this
regard is considered to be 11mL/kg/min. Thus he has a higher risk of inpatient
postoperative mortality. V
.
O2 max has more often been shown to correlate with complications, but as alluded to the delineation between morbidity and mortality
is not always established in studies. However, a V
.
O2max of <60%predicted is known
to be associated with both of these bad outcomes. The AT certainly suggests the
patient would benefit from critical care postoperatively, but in most centres this
would be normal for other oesophagectomy patients as well.
- A 76-year-old frail lady is undergoing an awake fibreoptic nasal intubation.
She received intravenous glycopyrrolate as an antisialagogue and midazolam
for anxiolysis. Her nasal mucosa was prepared with co-phenylcaine, and the
anaesthetist is using a “spray as you go” and nebuliser anaesthetic technique
with lignocaine. Remifentanil is used for sedation. She suddenly complains of
lightheadedness, tinnitus, confusion and peri-oral paraesthesia.
Which is the most likely drug responsible for her symptoms?
A Glycopyrrolate
B Midazolam
C Lignocaine
D Phenylephrine
E Remifentanil
- C Lignocaine
Awake fibre-optic intubation is an invaluable anaesthetic tool to help safely manage
patients with difficult airways. Its successful execution requires not only familiarity
with handling of the scope, but also effective sedation and topical anaesthesia.
Multiple agents are frequently given to optimise the intubating conditions and an
awareness of common or serious side effects of these drugs is important.
When anaesthetising the airway, it is important to keep a close track of the amount of local anaesthetic administered to prevent inadvertent drug toxicity. Lignocaine is
fequently given in different concentrations via various routes and is also present in
co-phenylcaine which is sometimes not appreciated. In practice, not all patients are
weighed, and caution should be exercised when administering local anaesthetics
in the elderly. Lignocaine is a sodium channel blocker and during systemic toxicity,
firstly inhibits the inhibitory central nervous system neurons which manifests as
confusion, tinnitus and paraesthesia before culminating in convulsions. As further
toxicity ensues, a more global central inhibition occurs which results in the loss of
consciousness and respiratory depression. Negative inotropy and dysrhythmias
which are difficult to treat may also be seen at this stage. The British Thoracic Society
recommends that the total dose of lignocaine applied during bronchoscopy should
be limited to 8.2mg/kg. Local anaesthetic toxicity is the most likely answer in the
above case in view of the specific excitatory symptoms occurring after multiple
administrations of lignocaine to the elderly patient.
Glycopyrrolate is an anti-cholinergic drug which is frequently used to reduce the
amount of secretions produced in the patient’s upper airway to aid visualisation
during bronchoscopy. Anticholinergics act by competitive antagonism at the
muscarinic acetylcholine receptor and toxic central effects include agitation,
delirium, hallucinations and seizures. Glycopyrrolate however, has a quaternary
ammonium group and therefore does not cross the blood-brain barrier as freely
as other anticholinergics such as atropine or hyoscine. Central effects are therefore
minimal.
Midazolam is a short acting benzodiazepine which produces amnesia, anxiolysis and
sedation. Paradoxical excitement can occur, although this is very rare, and not the
most likely explanation for the above scenario.
Phenylephrine is found in co-phenylcaine and provides vasoconstriction to the
nasal mucous membrane via D1agonism. Absorption across the mucous membrane
can occur which may cause hypertension and reflex bradycardias. Central nervous
system effects are unusual and not the most likely cause for the symptoms in the
above case.Remifentanil is an ultra-short acting synthetic pure μ-receptor opioid agonist
commonly used as a sedative, analgesic and antitussive agent during awake fibre-
optic intubations. Central nervous system effects include respiratory depression,
drowsiness and reduced psychomotor functioning. Excitatory symptoms seen in the
case above are rare.
- A 45-year-old man is brought to the emergency department following a 30 minute
out-of-hospital cardiac arrest. He has a return of spontaneous circulation, is
intubated, has a blood pressure of 110/60mmHg, a heart rate of 80 beats per
minute in sinus rhythm, GCS 3/15, blood glucose 5mmol/L and core temperature
of 34.6°C.
What is the most appropriate step to consider post-cardiac arrest management?
A Transfer the patient to intensive care for further management
B Start surface cooling with ice packs
C Insert an arterial and central line
D Call his family and discuss likelihood of poor prognosis
E Start sedation and muscle relaxation
E Start sedation and muscle relaxation
Therapeutic hypothermia is now recommended by NICE for all patients following a cardiac arrest that resulted in return of spontaneous circulation. This treatment has potential to reduce the burden of neurological disability that is associated with survival post cardiac arrest. However, recent evidence suggests that it is the targeting of temperature management, rather than the specific temperature chosen
that confers neurological benefit. This may begin a new shift in the understanding
and management of therapeutic hypothermia in post-cardiac arrest patients.
Insertion of invasive monitoring and transferring the patient to intensive care are
important steps in the management of this patient. Early discussion with the family
is appropriate but discussing the prognosis might be premature in light of the
circumstances.
The priority at this point would be to commence sedation to reduce his cerebral
metabolic rate (CMRO2) and administer muscle relaxation to minimise rises in
intracranial pressure secondary to shivering, coughing and gagging
- A 76-year-old man has undergone an arthroscopic acromioclavicular joint
decompression. He had an interscalene block and a general anaesthetic. His past
medical history includes obesity, moderate chronic obstructive pulmonary disease
(COPD) and obstructive sleep apnoea (not on CPAP). In the recovery room he is
awake, but struggling to breathe. He has four twitches and no fade to peripheral
nerve stimulation, and saturations are 96% on oxygen via facemask. There is
minimal wheeze on auscultation.
The best treatment is likely to involve:
A Another dose of neostigmine reversal
B Perform an arterial blood gas analysis
C BiPAP until the block wears off
D CPAP until opioid free
E Nebulisers and steroids
C BiPAP until the block wears off
There are a variety of ways to block the brachial plexus principally to facilitate
surgery to the upper limb. The type of block is named in reference to the anatomical
location where the block is performed. Each approach to block the brachial plexus
has its advantages and disadvantages with an associated clinical relevance:
Interscalene – This is the most proximal block of the plexus as it arises between
the scalene muscles of the neck. This block produces good coverage for distal
clavicle, shoulder and proximal upper arm procedures. Interscalene blocks are often
unpredictable for forearm and hand procedures due to common ulnar (C8 & T1)
sparing at this level.
A reliable complication is unilateral phrenic nerve blockade, unless low volumes or
a low neck insertion site are used. The resultant hemidiaphragmatic paralysis can
produce respiratory difficulties in those with airway or chest disease, the obese, or those with contralateral phrenic nerve palsy (which is often asymptomatic).
Other complications include a Horner’s syndrome from sympathetic stellate
ganglion blockade, epidural or spinal spread, laryngeal nerve block, and vertebral
artery injection. The migration of local anaesthetic into cerebrospinal fluid (CSF),
presumably via the dural cuff of a nerve root, can result in a total spinal anaesthetic.
However, at least four cases of direct injection into the cervical spinal cord have also
been documented, associated with devastating permanent neurological damage.
○ Supraclavicular – This is mainly considered as blockade focussed at the brachial
plexus mid-point, as the plexus passes behind the clavicle and in relation to the
subclavian artery in the supraclavicular fossa.
A supraclavicular block will provide coverage for distal humerus, elbow, forearm and
hand procedures. With this approach one is less likely to encounter ulnar sparing,
but it may still occur. Complications more associated with this approach include
pneumothorax, due to the proximity of the pleura. Phrenic nerve involvement is
much reduced from the interscalene approach to about 30% of all blocks.
Infraclavicular and axillary – The infraclavicular block is performed below the
clavicle, but before the axilla while the axillary brachial plexus block is performed, as
the name suggests, in the axilla in direct relation to the axillary artery. These blocks
give good coverage for elbow, forearm and hand surgery. The axillary block can also
cover the medial upper arm, and is used for AV fistula formation in some patients.
From a complication standpoint, these approaches greatly reduce the incidence
of phrenic nerve palsy, and other severe complications. In addition, the use of
ultrasound reduces the possibility of inadvertent vascular puncture, which is the
particular concern at these sites.
This question relates to a perennial exam favourite – the unwell patient in recovery.
The key here is to work through the differential diagnoses to leave the most plausible.
Here the clue relates to the block. The nerve stimulator result indicates no
significant residual curarisation, and clinically there is little wheeze with acceptable
saturations, hinting at a problem more of ventilation than oxygenation. Performing
an arterial blood gas analysis will not be an appropriate treatment for this patient.
○ Continuous positive airway pressure (CPAP) may be a sensible idea in a patient
with obstructive sleep apnoea (OSA) to maintain a patent airway, especially if there
is co-administration of opioids. However the combination of obesity, COPD, and
the inevitable unilateral phrenic nerve blockade from the block can give rise to
respiratory embarrassment. This is often most obvious in the supine position, and
should recede as the block resolves. Therefore the most appropriate management option in this clinical scenario is administration of BiPAP until the block wears off.
- A 70-year-old man is to have a number of tendons repaired in his hand. After
discussion with the patient, a regional anaesthetic technique has been agreed;
your preferred approach is an infraclavicular block under ultrasound guidance. Which part of the brachial plexus is most likely to be blocked by this approach?
A Roots
B Trunks
C Divisions
D Cords
E Branches
- D Cords
A brachial plexus block represents the most common use of nerve blocks in current
regional anaesthetic practice. A good anatomical knowledge is essential for
successful brachial plexus block. The plexus is formed by the anterior primary rami of the lower four cervical nerve
roots (C5-C8) and first thoracic nerve root (T1). The brachial plexus supplies sensory
and motor innervation to the entire upper limb with the exception of the trapezius
muscle (innervated by the spinal accessory nerve) and the cutaneous innervation of
the area of the axilla (supplied by intercostobrachial nerve).
The brachial plexus consists of roots, trunks, divisions, cords and terminal and
collateral branches.
Roots: the ventral rami of C5-T1 spinal nerves form the five roots of the plexus.
An interscalene block mainly targets the upper roots (C5-C7) and, because of the
vertical arrangement of the brachial plexus roots in the interscalene groove, C8 and
T1 are often missed hence the ulnar nerve may not be blocked.
Trunks: shortly after leaving the intervertebral foramina, the roots unify to form
three trunks (upper (C5-C6), middle (C7) and lower (C8-T1) trunks).
Supraclavicular blocks are performed at the level of the brachial plexus trunks so the
entire upper limb is blocked more reliably.
Divisions: each trunk then divides into two divisions to form six divisions in total
(three anterior and three posterior). The divisions generally cannot be blocked
reliably because they lie behind the clavicle.
Cords: The six divisions unite again to form the three cords. The posterior divisions
merge to form the posterior cord (C5-T1). The anterior divisions from the upper and
the middle trunks form the lateral cord (C5-C7). And finally, the anterior division of
the lower trunk will continue to become the medial cord (C8-T1). The brachial plexus
cords are described according to their relation to the axillary artery.
Infraclavicular blocks are performed at the level of the cords of the brachial plexus.
At this level each of the three cords of the brachial plexus are and therefore it may
achieve anaesthesia of the entire arm.
Terminal branches: these are mixed nerves that contain sensory and motor nerve
fibres.
t The ulnar nerve (C8, T1) arises from the medial cord. It provides motor innervation
to the intrinsic muscles of the hand and sensation to the medial one and a half
fingers.
t The musculocutaneous nerve (C5, C6, C7) is derived from the lateral cord. It
provides motor innervation to the flexor muscles (the coracobrachialis, biceps
brachii and the brachialis) and sensory innervation to the lateral surface of the
forearm. The musculocutaneous nerve continues as the lateral cutaneous nerve of
the forearm.
t The median nerve (C5-T1) arises form the both the medial (C5, C6, C7) and the
lateral cords (C8, T1). It provides motor innervation to most of flexor muscles in
the forearm and thenar muscles of the thumb. It provides cutaneous innervation
to the thumb, index finger, middle finger, the lateral half the ring finger, along
with the nail bed of these fingers.
t The radial nerve (C5-T1) is the largest branch of the brachial plexus. It is derived
from the posterior cord, providing motor innervation to the extensor muscles of the elbow, wrist and fingers. It also supplies sensation to the dorsum of the hand.
The radial nerve continues as the posterior cutaneous nerve of the forearm.
t The axillary nerve (C5-C6) also arises from the posterior cord. It supplies the
deltoid and the teres minor muscles. It also provides sensation at the point just
below the shoulder. The axillary nerve continues as the lateral cutaneous nerve of
the arm.
The axillary blocks are performed at the level of the terminal branches of the brachial
plexus and depend on the relationship of nerves to the axillary vessels.
Supraclavicular branches of the BP (Figure 4.1): These nerves are also derived from
the BP but provide innervation above the clavicle.
t The long thoracic nerve (C5, C6, C7) supplies the serratus anterior muscle.
t The dorsal scapular nerve (C5) supplies the rhomboid muscles and the levator
scapulae muscle.
t The nerve to the subclavius (C5, C6) supplies the subclavius muscle.
t The suprascapular nerve (C4, C5, C6) supplies the supraspinatus and the
infraspinatus muscles.
- A 20 kg 5-year-old is admitted to the emergency department with a fractured femur
following a bicycle fall. His leg was splinted prior to arrival and he received two
crystalloid boluses of 400mL. His has a respiratory rate of 40 breaths per minute, a
capillary refill time of 4 seconds and heart rate of 160 beats per minute.
What is the next step in the resuscitation phase while waiting for surgery?
A A further bolus of 200mL of colloid
B 200mL bolus of O negative blood
C Call the transfusion lab and order crossmatched blood, fresh frozen plasma
(FFP) and platelets
D Change the temporary femoral splint to a plaster of paris cast
E Insert an arterial line
- B 200mL bolus of O negative blood
In the management of paediatric trauma, it is crucial to recognise what the normal
physiological parameters are for different aged patients (Table 4.2).It is thus clear that this patient is expressing deranged parameters and has had
significant haemorrhage from the trauma sustained. Fluid resuscitation in paediatric
trauma is similar to adult trauma but with some key differences. If the patient fails
to respond to repeated boluses of crystalloid or colloid up to a maximum of 40mL/
kg, the next most appropriate step is to use blood and blood products. The dose
of packed red cells is 10mL/kg. This patient has already had the allocated 40mL/kg
and still demonstrates instability therefore should be transfused O negative blood. If
the bleeding continues following this, fresh frozen plasma and platelets need to be
administered to avoid the coagulopathy worsening the bleeding.
Changing the temporary splint may result in the bone fragments being disrupted
causing further bleeding, and will not immediately assist in replenishing the
significant blood loss. Insertion of an arterial line will become necessary to monitor
the patient intra-operatively but in the current clinical scenario is unlikely to add
more to the clinical picture
- You are caring for a 35-year-old patient on the neurointensive care unit who has a
serious traumatic brain injury following an assault.
According to the Academy of Medical Royal Colleges 2008 Code of Practice for the
Diagnosis and Confirmation of Death, brainstem death should only be diagnosed
when:
A The blood glucose is 4.0–8.0mmo/L
B Prior to an apnoea test the Paco2 must be 6.0-8.0 kPa and the arterial pH 7.20–
7.40
C Two complete sets of tests have been performed a minimum of 4 hours apart
D The serum sodium is >124mmol/L
E After 5 minutes of observed apnoea the Pao2 is <8 kPa
- B Prior to an apnoea test the PaCO2 must be 6.0–8.0 kPa and the arterial pH 7.20–7.40
The Academy of Medical Royal Colleges 2008 code of practice for the diagnosis and
confirmation of death is the current reference manual for brainstem death (BSD)
testing in the UK.
In order to undertake BSD testing the following preconditions must be fulfilled:
t An unresponsive coma and apnoea with a recognised date and time of onset
t Evidence of irreversible brain damage of known aetiology
You must then exclude potentially reversible causes for the coma and/or apnoea.
These exclusions are:
t The presence or persistence of depressant drugs (or their active metabolites)
t A body temperature ≤34°C
t The presence of a reversible circulatory, metabolic or endocrine disorder
t Respiratory failure due to neuromuscular blocking agents, other drugs
or potentially reversible causes of apnoea (e.g. cervical injury, profound
neuromuscular weakness)
t Sodium levels at time of coma onset must be 115–160mmol/L
t Sodium levels at time of first test. must be 115–160mmol/L and not have
changed by >0.5mmol/L per hour between time of coma onset and first test
t Potassium levels at time of first test must be >2mmol/L
t Phosphate levels at time of first test must be 0.5–3.0mmol/L
t Magnesium levels at time of first test must be 0.5–3.0mmol/L
t Glucose levels at time of first test must be 3.0–20.0mmol/L
To confirm BSD, the following bedside tests must be conducted. (Note, two
complete sets must be performed, however these can be conducted successively
without any fixed interval.):
t Absence of any pupillary reaction to light
t Absence of any eyelid movements when each cornea is touched in turn
t Absence of nystagmus or any eye movement when each ear is instilled with 50mL
ice cold water
t Absence of a gag reflex
t Absence of a cough reflex when a suction catheter is passed down into the
trachea
t Absence of any motor response when supraorbital pressure is applied
t Absence of any spontaneous breathing efforts for 5 minutes
t Preconditions to apnoea test: PaCO2 6.0-8.0kPa and arterial pH 7.20–7.40
t Apnoea test only valid if, after 5 minutes: PaCO2 increases by >0.5kPa; and PaO2
is >5kPa; and the systemic mean arterial pressure is ≥60mmHg throughout.
If one or more of these preconditions are not met or the bedside tests cannot be
performed then ancillary investigations are required to confirm the diagnosis. The
legal time of death is when the first set of tests indicates death due to the absence of
brain-stem reflexes.
- A 47-year-old woman collapsed due to a grade 3 sub-arachnoid haemorrhage. An
extra-ventricular drain was inserted and she is ventilated on the intensive care
unit. On examination the blood pressure is 90/60mmHg, heart rate is 110 beats
per minute and the peripheral capillary refill time is 6 seconds. She has passed
1000mL of urine since catheterisation 4hours ago.
What is the most useful course of action?
A Insert a femoral central line and commence a noradrenaline infusion
B Request urinary and plasma osmolarity measurements
C Administer 20mL/kg intravenous crystalloid
D Request urinary sodium concentration measurement
E Administer intravenous desmopressin (DDAVP) 0.4mg.
- B Request urinary and plasma osmolarity measurements
This question requests the most useful option, not the first action. The most useful
strategy to aid ongoing management would be to work out why the patient is
hypotensive and polyuric so that treatment can be tailored appropriately. The
hypotension and poor peripheral perfusion will most likely respond to intravenous
crystalloid and a noradrenaline infusion but will not aid identification and correction
of the underlying condition which is most likely to be diabetes insipidus given the
clinical history.
Diabetes inspidus (DI)
The clinical manifestations are due to the failure of release of anti-diuretic hormone
(ADH) or reduced activity of ADH on the renal collecting duct. Without ADH there
is no re-absorption of water at the collecting duct of the nephron, resulting in loss
of plasma as urine which results in hypovolaemia. As a result of renal conservation
of sodium, a high plasma sodium concentration and a normal urinary sodium
concentration is seen.
DI is caused by:
t Central nervous system DI
t Traumatic brain injury (35%)
t Sub-arachnoid haemorrhage
t Intra-cerebral haemorrhage
t Pituitary surgery
t End-stage cerebral oedema
t Nephrogenic DI
t Renal DI may be caused by lithium treatment
The differential diagnosis includes:
t Diabetes mellitus
t Osmotic diuretics (which may have been given in this case)
Diagnosis may be made with the following criteria:
• Increased urine volume >3000mL per day or >1000mL in 4 hours
• High serum sodium >145mmol/L
• High serum osmolarity >305mmol/kg
• Low urine osmolarity<350mmol/Kg
A plasma osmolarity measurement would be the most useful intervention out of the
available options to confirm the diagnosis. The diagnosis of DI will enable correction
of her fluid-balance status by administrating exogenous anti-diuretic hormone.
- A 67-year-old woman presents with an acute onset illness and progressive
physiological deterioration. She has a pyrexia of 39.7°C, a heart rate of 135 beats
per minute (in atrial fibrillation), a systemic blood pressure of 85/48mmHg, a
respiratory rate of 28 breaths per minutes, oxygen saturations of 89% on a non-
rebreathe reservoir face mask with oxygen at 15 L/min, is drowsy and has a
capillary blood glucose in 12.2mmol/L.
The best choice of fluid type to bolus as a first step in cardiovascular resuscitation
would be:
A 0.9% sodium chloride
B A balanced crystalloid
C A gelatin solution
D 4.5% human albumin in 0.9% sodium chloride
E A starch solution
- B A balanced crystalloid
The clinical scenario is suggestive of septic shock. Fluid resuscitation is indicated
and should commence with a 10mL/kg bolus of crystalloid. Though controversial, there is a strong theoretical argument, though an absence of definitive evidence
to suggest that balanced solutions are less harmful than the unphysiological 0.9%
sodium chloride. 0.9% sodium chloride is mildly hyperosmotic and contains 50%
more chloride ions per litre than plasma and hence infusion of any significant
volume may result in a hyperchloraemic acidosis. Although the acidosis is
rapidly buffered, the effects of hyperchloraemia are several and include impaired
mental function, nausea, gastrointestinal dysfunction, renal vasoconstriction,
hyperkalaemia, impaired coagulation and a pro-inflammatory response. What is less
clear is whether these effects are clinically important.
Starch solutions have been withdrawn from the UK market due to concerns over
safety and questionable evidence. Albumin has not been demonstrated to confer
any survival benefit in sepsis but carry a more significant risk of reactions.
○ Finally, gelatins are unbalanced solutions, and again have not been demonstrated to be
superior to balanced crystalloid solutions in these circumstances.
Therefore the most appropriate choice of fluid would be a balanced crystalloid
solution.
- A 54-year-old man with known alcoholic liver disease presents to the emergency
department with confusion. On examination he has stigmata of decompensated
liver disease and is oedematous with marked ascites. His respiratory rate is 30
breaths per minute, the oxygen saturations are 94% on air, his blood pressure is
90/60mmHg and his heart rate is 120 beats per minute. After catheterisation he
produces 10mL of urine in the first hour.
What would be the most useful investigation to establish the cause of his
confusion?
A CT head
B Rectal examination
C Arterial blood gas
D Renal function tests
E Amylase
- B Rectal examination
Alcoholic chronic liver disease is a physiological disaster, with some of the clinician’s
concerns being:
t Airway:
t an obtunded patient with a full stomach (possibly blood)
t Breathing:
t Fluid overload results in pulmonary oedema,
t Pleural effusions
t Ascites may splint the diaphragm
t Cardiovascular:
t Myocardial disease (the symptoms of which may be difficult to differentiate
from reflux or pancreatitis) due to:
– Chronic hypervolaemia
– Hypertension
– Alcohol-induced cardiomyopathy
– Pericardial effusion
– Ischaemic myopathy
– Loss of occult blood (chronic or acute) and coagulopathy:
– Gastritis and ulcer disease
– Mallory–Weiss tear
– Varices
t Disability (an acute deterioration in cognition may be multi-factorial):
t Hypoglycaemia
t Intoxication
t Withdrawalt Seizures
t Hyponatraemia
t Delayed presentation of head trauma
t Encephalopathy
t Others:
t Hypothermia
t Infections and sepsis
t Hepatorenal syndrome
t Immuno-suppression
t Pancreatitis
t Diabetes mellitus
t Peripheral neuropathy
t Dementia syndromes
t Malnourishment
t Self-harm and depression
You are presented with such a patient who has an acute change in cognition
associated with hypotension and low urine output. As is often the case you do not
have further detailed information regarding this gentleman’s prior medical history.
Given the complicated picture the appropriate approach is a prioritisation-centred
examination and treatment management pathway (A-B-C-D-E). The most pressing
concern is cardiovascular instability and a rectal examination looking particularly
for occult blood (be it altered or otherwise) is indicated as a matter of urgency.
The finding of rectal blood will focus this scenario from a complicated differential
diagnosis into haemorrhagic shock in a patient with a presumed coagulopathy.
An arterial blood gas does have a haemoglobin measurement, but early on in
haemorrhagic shock the concentration may remain static and chronic anaemia
may complicate the interpretation. The other tests are all important but excluding
immediately life-threatening conditions must be your first priority and a rectal
examination in this group of patients is mandatory
- A 73-year-old man with advanced pancreatic cancer presents with worsening
upper abdominal pain. Despite treatment with opioids and adjuvant medication,
he has no pain relief and is being considered for a procedural intervention.
Which of the following procedures is the most appropriate option for this patient?
A Thoracic epidural injection
B Coeliac plexus block
C Lumbar sympathetic plexus block
D Superior hypogastric plexus block
E Sphenopalatine ganglion block
- B Coeliac plexus block
The pathophysiology of chronic pain is complex and incompletely understood. It is
thought to have a somatic component, but also a contribution from the sympathetic
nervous system (SNS). For this reason, blockade of sympathetic ganglia is widely
used to provide relief to those in whom other forms of analgesia have been
inadequate. Robust evidence for the use of sympathetic blocks is lacking, and often
pain is not completely relieved with these techniques alone, but may be reduced. If
the patient is taking chronic pain medication, this should usually be continued after
the procedure.
The SNS is thought to have a particular role in pain of neuropathic nature, or of
vascular or visceral origin. There may be more than one mechanism. While neurological
sensitisation is suggested in neuropathic pain, sympathetic mediated vasoconstriction
may contribute to chronic vascular pain such as what occurs in Raynaud’s disease.
Indications for a sympathetic block are seen in Table 4.3.Contraindications include patient refusal, bleeding diathesis or coagulopathy, local
infection, local malignancy and hypersensitivity to the drugs used in the block.
There are several types of sympathetic block. These are summarised in Table 4.4Blocks are usually performed under sedation or general anaesthesia in a setting that
has facilities and skills for resuscitation. Image intensifier is used for accurate needle
placement.
In this scenario, the patient has a chronic upper gastrointestinal malignancy,
and a coeliac plexus block would be the most suitable choice for him. A lumbar
sympathetic block is better for lower limb pain (e.g. CRPS or vascular) or rectal
pain. A superior hypogastric plexus block is the best choice for pelvic pain.
Sphenopalatine ganglion blocks are used to treat intractable headaches and facial
pain
