El-Boghdadly - 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
C
- A Progressive areflexic weakness in more than one limb
The history described is classical of the development of Guillain–Barré syndrome.
Guillain-Barré syndrome is a progressive, infective, demyelinating neuropathy.
It has an incidence of 1–2 per 100,000 and usually has a precursor of gastric or respiratory viral illness in its history.
Diagnostic features are progressive weakness accompanied
by areflexia in more than one limb.
Features that support identification of the syndrome include symmetry of limb signs, cranial nerve involvement, respiratory
muscle weakness, autonomic dysfunction, mild sensory symptoms and the investigative findings of increasing cerebrospinal fluid (CSF) protein levels (> 4.0 g/L)
over subsequent days or slowed nerve conduction studies.
Therefore the most relevant diagnostic clinical feature in this patient is progressive areflexia in more than one limb.
- 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 122 mmol/L (normal range 135–145 mmol/L)
• Serum osmolality 270 mOsm/kg (normal range 278–305 mOsm/kg)
• Urine osmolality 300 mOsm/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
C
- 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 < 135 mmol/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 < 135 mmol/L
2. Reduced serum osmolality < 280 mOsm/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:
- Normal or low serum sodium
- Normal or low serum osmolality
- Normal or high urine osmolality
- Normal or high urine output
- 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
D
- C At least 8 cm 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 8 cm 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
A
- 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 2–3 days 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 (6 months to 3 years). 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 2–6 years 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 7 mg/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
- 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.
- Awareness
- Identification
- Assessment
- Management
- 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
- An 80-year-old man for an open oesophagectomy has a cardiopulmonary exercise
test (CPET) as follows:
• Anaerobic threshold (AT) 10 mL/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
A
- 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.co2 against 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 11 mL/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
- 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
frequently 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 8.2 mg/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 α1agonism. 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.
- 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 110/60 mmHg, a heart rate of 80 beats per
minute in sinus rhythm, GCS 3/15, blood glucose 5 mmol/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
C
- 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
- 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,
- 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).
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.
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.
- 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. - The median nerve 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.
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.
* 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
Supraclavicular branches of the BP (Figure 4.1): These nerves are also derived from
the BP but provide innervation above the clavicle.
* The long thoracic nerve (C5, C6, C7) supplies the serratus anterior muscle.
* The dorsal scapular nerve (C5) supplies the rhomboid muscles and the levator
scapulae muscle.
* The nerve to the subclavius (C5, C6) supplies the subclavius muscle.
* The suprascapular nerve (C4, C5, C6) supplies the supraspinatus and the
infraspinatus muscles.
Posterior cord branches ULTRA
Upper subscapular, lower subscapular, thoracodorsal, radial, axillary
Lateral cord branches LLM
Lateral pectoral, lateral root of the median nerve, musculocutaneous
Medial cord branches MMMUM
Medial pectoral, medial cutaneous nerve of arm, medial cutaneous nerve
of forearm, ulnar, medial root of the median nerve
- 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 400 mL.
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 200 mL of colloid
B 200 mL 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
- B 200 mL 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).
Table 4.2 The normal physiological parameters for different aged children
Age RR HR SBP (mmHg)
< 1 / 30–40 / 110–160 / 70–90
1–2 25–35 100 –150 80–90
2–5 25– 30 95–140 80– 105
5–2 20–25 80–120 90– 110
> 12 15–20 60–100 100–120
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 40 mL/ kg, the next most appropriate step is to use blood and blood products.
The dose of packed red cells is 10 mL/kg.
This patient has already had the allocated 40 mL/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 4.0–8.0 mmo/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 > 124 mmol/L
E After 5 minutes of observed apnoea the Pao2 is < 8 kPa
C
- 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:
• An unresponsive coma and apnoea
with a recognised date and time of onset
• Evidence of irreversible brain damage of known aetiology
You must then exclude potentially reversible causes for the coma and/or apnoea.
These exclusions are:
• The presence or persistence of depressant drugs
(or their active metabolites)
• A body temperature ≤ 34°C
• The presence of a reversible circulatory,
metabolic or endocrine disorder
• Respiratory failure due to neuromuscular blocking agents,
other drugs or potentially reversible causes of apnoea (e.g. cervical injury, profound neuromuscular weakness)
• Sodium levels at time of coma onset must be 115–160 mmol/L
• Sodium levels at time of first test. must be 115–160 mmol/L and not have changed by > 0.5 mmol/L per hour between time of coma onset and first test
• Potassium levels at time of first test must be > 2 mmol/L
• Phosphate levels at time of first test must be 0.5–3.0 mmol/L
• Magnesium levels at time of first test must be 0.5–3.0 mmol/L
• Glucose levels at time of first test must be 3.0–20.0 mmol/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.):
• Absence of any pupillary reaction to light
• Absence of any eyelid movements when each
cornea is touched in turn
• Absence of nystagmus or any eye movement when each ear is instilled with 50 mL ice cold water
• Absence of a gag reflex
• Absence of a cough reflex when a suction catheter is passed down into the trachea
• Absence of any motor response when supraorbital pressure is applied
• Absence of any spontaneous breathing efforts for 5 minutes
• Preconditions to apnoea test:
Paco2 6.0-8.0 kPa and arterial pH 7.20–7.40
• Apnoea test only valid if, after 5 minutes:
Paco2 increases by > 0.5 kPa; and Pao2 is > 5 kPa; and the systemic mean arterial pressure is ≥ 60 mmHg 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 90/60 mmHg, heart rate is 110 beats
per minute and the peripheral capillary refill time is 6 seconds.
She has passed 1000 mL of urine since catheterisation 4 hours 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 20 mL/kg intravenous crystalloid
D Request urinary sodium concentration measurement
E Administer intravenous desmopressin (DDAVP) 0.4 mg.
B
- 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:
• Central nervous system DI
• Traumatic brain injury (35%)
• Sub-arachnoid haemorrhage
• Intra-cerebral haemorrhage
• Pituitary surgery
• End-stage cerebral oedema
• Nephrogenic DI
• Renal DI may be caused by lithium treatment
The differential diagnosis includes:
• Diabetes mellitus
• Osmotic diuretics (which may have been given in this case)
Diagnosis may be made with the following criteria:
• Increased urine volume > 3000 mL per day or > 1000 mL in 4 hours
• High serum sodium > 145 mmol/L
• High serum osmolarity > 305 mmol/kg
• Low urine osmolarity < 350 mmol/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 85/48 mmHg, a respiratory rate of 28 breaths per minutes, oxygen saturations of 89% on a non rebreather reservoir face mask with oxygen at 15 L/min, is drowsy and has a
capillary blood glucose in 12.2 mmol/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
- B A balanced crystalloid
The clinical scenario is suggestive of septic shock. Fluid resuscitation is indicated and should commence with a 10 mL/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
90/60 mmHg and his heart rate is 120 beats per minute. After catheterisation he produces 10 mL 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
A
- B Rectal examination
Alcoholic chronic liver disease is a physiological disaster, with some of the clinician’s
concerns being:
• Airway:
• an obtunded patient with a full stomach (possibly blood)
• Breathing:
• Fluid overload results in pulmonary oedema,
• Pleural effusions
• Ascites may splint the diaphragm
• Cardiovascular:
• 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
• Disability
(an acute deterioration in cognition may be multi-factorial):
• Hypoglycaemia
• Intoxication
• Withdrawal
• Seizures
• Hyponatraemia
• Delayed presentation of head trauma
• Encephalopathy
_______________________
• Others:
• Hypothermia
• Infections and sepsis
• Hepatorenal syndrome
• Immuno-suppression
• Pancreatitis
• Diabetes mellitus
• Peripheral neuropathy
• Dementia syndromes
• Malnourishment
• 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.
