El-Boghdadly - 6 Flashcards
- A 44-year-old woman is on the intensive care unit having had a grade 3 subarachnoid haemorrhage secondary to an anterior communicating artery aneurysm one day ago. She is currently stable neurologically. Her past medical history comprises of hypercholesterolaemia, hypertension and smoking. She has a
drug history of simvastatin and lisinopril.
Which of the following would most likely prevent the development of delayed cerebral ischaemia in this patient?
A ‘Triple H therapy’
B Magnesium administration
C Statin administration
D Nimodipine administration
E Antiplatelet therapy
D
- D Nimodipine administration
Delayed cerebral ischaemia describes neurological deterioration that occurs
secondary to ischaemia alone (i.e. not hydrocephalus or seizure activity) and persists for greater than 1 hour. It develops in more than 60% of subarachnoid haemorrhage (SAH) patients and confers a less favourable outcome.
Patients are at greatest risk of ischaemia from day 3 to day 10 post-SAH. Their risk is also augmented by a poor
grade of SAH (Table 6.2), a large volume haemorrhage within the subarachnoid space or extending to the ventricles and a smoking history. Delayed ischaemia is frequently labelled as intracranial vasospasm, but until confirmed by investigation the two terms should be separately defined. They are treated in an identical fashion.
The use of triple H therapy (hypertension, hypervolaemia and haemodilution) is
now controversial. Those who advocate it do so in order to improve cerebral blood
flow by increasing cerebral perfusion pressure (CPP), volume status and blood
rheology. Targets for each are CPP > 70 mmHg, CVP 12–15 mmHg and haematocrit
0.3 respectively. More recent studies have failed to show conclusive benefits from
any element but it is widely accepted that hypovolaemia and hypotension are
deleterious. The patient’s premorbid blood pressure must also be acknowledged
when calculating a suitable target.
Table 6.2 Grade of SAH as classified by the World Federation of Neurosurgical Societies
(WFNS)
Grade WFNS classification
1 No motor deficit + GCS 15
2 No motor deficit +
GCS 13–14
3 Motor deficit +
GCS 13–14
4 GCS 7–12
(motor testing irrelevant for score)
5 GCS 3–6
(motor testing irrelevant for score)
In addition to treating hypercholesterolaemia, statins have been found to modulate the cytokine response. They also reduce the quantity of reactive oxygen molecules produced in brain injury. Overall, the subsequent inflammatory response is minimised and they have therefore been suggested as part of the treatment for SAH to prevent vasospasm and delayed ischaemic injury. However, data from
the international, multicentre, randomised controlled STASH trial (Simvastatin in
Aneurysmal Subarachnoid Haemorrhage) published in 2014 suggests that there is
no short-term or long-term benefit to using statins in these patients, despite earlier
enthusiasm with the idea.
In 2007, a Cochrane review noted that antiplatelet therapy was associated with a
non-significant trend indicating a benefit to outcome in patients at risk of delayed
cerebral ischaemia. Unsurprisingly, this trend was counteracted by a parallel increase
in haemorrhage. Therefore antiplatelet agents, in this setting, are restricted to use
following endovascular stenting for SAH management.
The only proven effective treatment in the prevention of delayed cerebral ischaemia
is nimodipine. As a calcium antagonist it is thought to protect against vasospasm
and there is level 1 evidence that it improves outcome. Every patient with a
diagnosis of SAH should be started on nimodipine (60 mg every 4 hours) for a course
of 21 days. A side-effect can be systemic hypotension which can be avoided by the
more frequent administration of half doses. If this does not remedy the situation, the
blood pressure should take precedence.
All of these treatments have been considered in the prevention of delayed cerebral
ischaemia. Nimodipine is the only one to have withstood repeated testing with
consistent results.
- A 29-year-old woman who suffered a blow to the left side of her skull vault with a resulting depressed fracture is awaiting transfer to a tertiary centre. She lost consciousness for approximately 1 minute after the incident. Her GCS is currently
14/15 (E4 V4 M6). Which of the following, in isolation, indicates that intubation is essential before transfer?
A Pao₂ of 13 kPa an Fio₂ of 0.6
B A discrete and short-lived seizure en route to your hospital
C Drop in GCS from E4 V4 M6 to E3 V4 M5 in the emergency department
D An increase in respiratory rate leading to a Paco₂ of 4.0kPa
E Blood in the oropharynx
c
- B A discrete and short-lived seizure en-route to your
hospital
This patient has suffered a head injury by a mechanism significant enough to cause a depressed skull fracture. This will most probably lead to an evolving brain injury secondary to underlying contusions. It is important that she is managed in an
appropriate environment, to expedite swift treatment of any complications, and is likely to involve further transfer to a tertiary hospital with on-site neurosurgical care.
Prior to transfer it is imperative to assess her ability to maintain her physiology such that secondary brain injury is avoided as much as possible. This includes adequate ventilation via a patent airway, preservation of an appropriate blood pressure [cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) - intracranal pressure (ICP)] and optimisation of cerebral metabolism.
The aim is to minimise further rises in ICP and secure brain tissue perfusion following the suspected injury.
The following are suggested targets during transfer:
• Pao₂ > 13 kPa
• Paco₂ 4.5–5.0 kPa
• MAP > 80 mmHg
• Adequate analgesia
• Sufficient sedation (and therefore intubation) if agitated
• Treatment of any seizures
• Normothermia
• Blood glucose 6–10 mmol
• Optimal cerebral venous drainage – head-up, avoidance of neck ties
In the scenario given you are asked to choose an instance that would obligate
you intubate the patient in order to maintain each target en route. The AAGBI has
published guidelines for the safe transfer of head injured patients and they include
indications that should initiate intubation and ventilation before any journey:
• Glasgow coma score < 8/15
• Glasgow coma score drop of 2 points in the motor score
• Pao₂ < 13kPa with oxygen administration
• Paco₂ < 4.0 or > 6.0 kPa
• Concern regarding laryngeal reflexes
• Seizure(s) since the injury
• Bilaterally fractured mandible
• Significant bleeding threatening the airway
A drop in GCS from E4 V4 M6 to E3 V4 M5 is a drop of 2 points and significant
enough to warrant consideration of intubation prior to transfer but guidelines allow
for individual clinical decision making. Intubation is regarded as essential if 2 points
are dropped within the motor score.
An increased respiratory rate leading to hypocapnia in this patient could be as a
result of pain. If, despite treatment, this continues and reduces further to jeopardise
cerebral circulation then control of ventilation may be warranted.
Blood in the oropharynx may be small and resolved or ongoing, potentially
interfering with ventilation. Clinical examination and judgement are required to
assess whether this, in isolation, would necessitate intubation.
Seizures in the period following head trauma imply increased severity of the injury
and may recur to further increase intracranial pressure and cerebral metabolic
requirements. All of the options could trigger a decision to secure the airway before
transfer, but seizure activity makes it essential.
- A 65-year-old man presents to the emergency department with acute central
chest pain radiating to the back. He has a history of hypertension and smoking.
The ECG shows evidence of left ventricular hypertrophy and his blood pressure is
190/100 mmHg, heart rate 105 beats per minute. There is a collapsing pulse and an
early diastolic murmur.
What is the next most appropriate management step?
A Commencement of sodium nitroprusside infusion
B Site an arterial line
C Arrange urgent aortography
D Titrate intravenous morphine
E Arrange transfer to a cardiothoracic centre
A
- D Titrate intravenous morphine
The history and clinical signs are suggestive of aortic dissection with aortic
regurgitation. Other clinical signs relate to the area of the aorta involved and are
summarised in Table 6.3.
Table 6.3 Features associated with vascular anatomical areas involved
Anatomical area involved Clinical feature
Aortic valve Aortic regurgitation, cardiac failure
Coronary ostia Coronary ischaemia
Carotid/brachiocephalic artery Stroke, syncope, seizure
Subclavian artery Limb ischaemia
Intercostal arteries (spinal arteries) Lower limb weakness
Coeliac trunk, mesenteric arteries Abdominal pain, bowel ischaemia
Renal arteries Flank pain, renal failure
There are a number of risk factors for aortic dissection, including:
• Hypertension (72% of patients)
• Smoking
• Trauma – deceleration and falls from height
• Aortic surgery/cannulation
• Vasculitis
• Collagen disorders
There are two different classification systems of which the Stanford system is most
widely used. It denotes that dissections involving the ascending aorta are Type A
with all others as Type B.
The priorities are to make an accurate diagnosis, limit the stress on the aortic lumen
(by lowering systolic blood pressure and left ventricular contractility) and forming
a definitive treatment plan, which may include urgent transfer to a cardiothoracic
centre.
It is particularly important to diagnose Type A dissections (i.e. those involving
the ascending aorta) as these are considered surgical emergencies. Non-invasive
diagnostic methods have superseded traditional aortography (option C) with CT,
transthoracic and transoesophageal echo being the most common modalities
employed. Transthoracic echocardiography can be performed at the bedside but is
not able visualise the distal ascending and descending aorta reliably.
The management steps outlined by the European Society of Cardiology guidance
are shown below:
• Detailed medical history and physical examination
• Intravenous line, blood samples, cardiac enzymes
• ECG, heart rate and blood pressure monitoring (both sides)
• Pain relief
• Reduction of systolic blood pressure using beta-blockers/calcium channel
blockers + additional vasodilators if needed
• Diagnostic imaging
• Intensive care level monitoring – right radial arterial line as standard
Although pharmacological control of systolic hypertension may be required, a large
proportion of patients will have pain which may of course exacerbate hypertension.
Titrated morphine is therefore the most appropriate first step in this scenario. If
further blood pressure control is required, beta-blockers are recommended before
pure vasodilators such as sodium nitroprusside. Attainment of clinical stability and
institution of invasive blood pressure monitoring would usually be obtained before
transfer to a surgical centre, however planning for this possible eventuality early will
ensure timely subsequent management.
Survival after surgical repair of Type A dissection is 96% and 91% at 1 and 3 years
respectively. Complicated Type B aortic dissections may be amenable to treatment
with endovascular stents, although some centres are also treating Type A dissections
in this manner as well.
Poor prognostic factors at presentation include:
• Age > 70 years
• Hypotension, shock or tamponade at presentation
• Preoperative renal failure
• Preoperative bleeding/massive transfusion
• Prior myocardial infarction
• Abnormal ECG
- A 65-year-old woman is recovering from an uneventful total thyroidectomy as treatment for a large substernal goitre. On the third postoperative day, she becomes progressively more stridulous and wheezy. She is tachypnoeic, confused
and complaining of circumoral paraesthesia. There is no obvious neck swelling or pain.
What is the most likely cause of her symptoms?
A Bilateral vocal cord paralysis
B Tracheomalacia
C Haematoma
D Tracheal necrosis
E Hypocalcaemia
E
- E Hypocalcaemia
It is important to remain vigilant for any signs of respiratory distress after head and
neck surgery since progression can be rapid with catastrophic consequences. After
thyroid surgery, there are a number of complications which can cause respiratory
difficulties and an appreciation of the associated signs can help identify them.
Iatrogenic injury to the recurrent laryngeal nerve resulting in vocal cord damage
is a recognised complication following thyroid surgery. Post-operative symptoms
depend on whether both the left and right recurrent laryngeal nerves are involved.
Unilateral injury manifests as a hoarse voice, difficulties phonating and aspiration
on swallowing whereas bilateral injuries present acutely following extubation with
stridor necessitating reintubation and tracheostomy formation. Bilateral vocal
cord paralysis is not the most likely cause in the above scenario, as the stridor only
presents after four days. Furthermore, bilateral vocal cord paralysis does not directly
cause circumoral paraesthesia or confusion
Tracheomalacia is believed to occur as a result of longstanding extrinsic tracheal
compression causing a loss of tracheal cartilage rigidity. Removal of this compressive
source (thyroidectomy) may then precipitate life threatening dynamic airway
collapse. It is a very rare complication and does not explain the confusion and
paraesthesia in the above scenario.
Post-operative haemorrhage is a well recognised complication following thyroid
surgery and can result in a rapidly expanding haematoma compromising airway
patency. The haematoma usually presents as a large, tense and immobile swelling
under the wound, which will have to be re-opened at the bedside if there is
impending airway obstruction. The majority of bleeds occur within 24 hours and
presenting symptoms can include stridor, dyspnoea, neck pain, dysphagia and
confusion. Although an important differential to consider, it is not the most likely
diagnosis in the above case due to the normal neck examination and lack of pain.
Symptom occurrence on day four postoperatively and the presence of circumoral
paraesthesia is also not typical.
The blood supply to the upper trachea is primarily from small branches of the
inferior thyroid artery and life threatening tracheal necrosis due to excessive cautery
near the trachea has been described. Tracheal disruption is unlikely to be causing
the symptoms in the case described since there is no subcutaneous emphysema
(formed from the tracheal air leak). Furthermore, stridor, confusion and paraesthesia
are not usually associated with this very rare complication.
Hypocalcaemia is the most common complication following thyroidectomy and
the most likely cause of the clinical picture described. Since the parathyroid glands
are located on the posterior surface of the thyroid gland, these can be damaged
or devascularised following surgery to this area. The fall in calcium levels generally
occurs within 24–48 hours post-operatively and can be sufficient to produce
symptoms. Hypocalcaemia directly increases neuromuscular excitability and
many of the clinical manifestations stem from this underlying problem. The stridor
described in the above case is due to laryngospasm which is an exaggeration of the
normal glottic closure reflex. Circumoral paraesthesia and bronchospasm also arise
as a consequence of neuromuscular irritability.
- A 36-year-old woman with an impacted food bolus needs to go to theatre imminently. She has been unable to swallow her saliva for 24 hours. On inquiring about her anaesthetic history she reports collapsing due to a severe allergic
reaction under anaesthesia, but she is unsure which agent was responsible. There
are no notes available, nor relatives to elaborate on the history.
Which of the following should you avoid as the most likely causative agent?
A Rocuronium
B Latex
C Morphine
D Chlorhexidine
E Gelofusine
A
- A Rocuronium
This patient’s limited anaesthetic history raises the suspicion of a previous episode of
anaphylaxis. Without prior records available it is prudent to avoid agents most likely
to cause such a reaction.
Anaphylaxis is an immune reaction that is triggered by hypersensitivity to an
antigen, e.g. the β lactam ring found in some antibiotics. It results in IgE antibody
production and a subsequent IgE-antigen mediated cascade of events. This leads to
the widespread release of inflammatory mediators such as histamine, leukotrienes
and prostaglandins. The reaction results in an increase in vascular permeability,
bronchial hyper-reactivity and subsequent circulatory compromise that can be fatal
(10% of those reported to the UK Medicines Control Agency).
Similar, and often indistinguishable, reactions may occur that do not involve IgE
release in response to an antigen. They manifest secondary to direct histamine
release or activation of the complement pathway by other means. They are known as
anaphylactoid reactions. An example of which could be initiated by morphine which
acts directly on mast cells to cause histamine release.
The culture of reporting anaphylactic reactions is variable between countries
and thus the frequency of its occurrence (based on information from Australia
and France) ranges from 1 in 10 000 to 1 in 20 000. The 6th National Audit Project
(Perioperative Anaphylaxis) may help determine the incidence of anaphylaxis in the
UK, which is currently unknown.
The following table (Table 6.4) lists the most commonly known triggers for
anaphylaxis and their proposed incidence when associated with anaesthesia.
Agent Incidence
Muscle relaxants 60–70%
Latex 12–20%
Antibiotics 2–15%
Colloids 4%
Induction agents rare
Opioids 1.7%
Local anaesthetics rare
Disinfectant and antiseptic agents Unknown but increasing
As muscle relaxants are reported to be the agents with the highest risk of triggering
anaphylaxis, rocuronium should be avoided in this scenario if at all possible. If the
use of a muscle relaxant is necessary, using a benzyl-isoquinolinium instead of an
aminosteroid may reduce the risk as they are less associated with such a reaction.
To further avoid histamine release, and therefore the possibility of an anaphylactoid
reaction, cisatracurium may be the best option.
The remaining agents can also be associated with anaphylaxis. Further modifications to
the anaesthetic, such as fentanyl instead of histamine-producing morphine or iodine in
place of chlorhexidine and avoidance of all colloids, can be simple enough to make. The
majority of theatres are now run as ‘latex-free’ or can easily be made so these days
- A 34-year-old man presents for laparoscopic excision of his left adrenal gland for phaeochromocytoma. During your preoperative assessment, he tells you that he
has been taking medication for blood pressure for about a month.
Which of the following is most likely to indicate that he is prepared for surgery?
A Good exercise tolerance, but a history of dizziness on standing
B Lack of a history of palpitations, and a normal ECG
C A normal echocardiogram, and chest X-ray
D History of dizziness on standing, a 5-minute ECG with no premature
ventricular complexes, and nasal congestion
E Several blood pressure recordings of < 160/90 mmHg
A
- D History of dizziness on standing, a 5-minute ECG with
no premature ventricular complexes (PVCs), and nasal
congestion
Phaechromocytomas, although rare in clinical practice are more common in
exams. This secreting tumour is named a chromaffinoma, because of its derivation
from chromaffin cells which evolve from the neural crest to make up the normal
sympathetic system. The classical clinical syndrome of severe hypertensive crises
accompanied by headache, sweating, palpitations and anxiety, with resolution
afterwards, is variable and depends mainly on the secretory properties of the
tumour. Most secrete noradrenaline; with some producing both noradrenaline and
adrenaline and a few may also secrete active peptides such as adrenocorticotrophic
hormone (ACTH), calcitonin, vasoactive intestinal peptide (VIP) and somatostatin
also. Tumours are 90% adrenal and 10% extra-adrenal, known as paragangliomas.
The full range of imaging techniques is used for their identification, with functional
PET scanning in some centres. M-iodobenzylguanidine (MIBG) isotope uptake scans
are useful to identify tumour foci and locate extra-adrenal or secondary deposits.
Preoperative assessment and preparation is of paramount importance, and
focuses on assessment for pathology associated with the tumour, namely endorgan
damage caused by hypertension, and pharmacological suppression. With
pharmacological suppression the classic target criteria are:
• Blood pressure < 160/90 mmHg
• Postural hypotension, but not severe (< 80/45 mmHg)
• ECG free from ST/T wave changes for 7 days
• No greater than one premature ventricular contraction on ECG every 5 minutes
• Nasal congestion
Agents used include the non-specific α-blocker phenoxybenzamine (which due to
α2 blockade also causes tachycardia, and therefore must be given with a β-blocker).
Selective α1 blockers, such as doxazosin can now be used alone. If β-blockade
is required, a stable a block has to be established first to prevent the loss of β2
vasodilatation, and therefore increased hypertension.
Some of the stems in this question look for signs of α blockade. These may include
postural hypotension, and nasal congestion. Lack of cardiac irritability feature in
B and D, and are also reassuring, but the normal ECG reading in B cannot exclude
ectopic beats. The normal chest X-ray and echocardiogram in C are reassuring, but
cannot exclude acute physiological changes seen with this condition. Repeated
blood pressure readings <160/90 mmHg (E) are also reassuring about good blood
pressure control, but the stem with both reassuring symptoms and physiological
investigations is option D.
- A 45-year-old man is admitted to the surgical ward with a fever, toothache and neck discomfort. Whilst waiting for surgery you are called to his bedside as he is more breathless and complaining of substernal pain. On examination he is
hypotensive and there is tender, ’woody‘ induration of his neck. On auscultation you hear a pericardial rub.
Which investigation is most appropriate to guide management in this scenario?
A Cervical and chest ultrasound
B Cervical and chest computed tomography
C Cervical and chest magnetic resonance imaging
D Cervical and chest radiograph
E Echocardiogram
B
- B Cervical and chest computed tomography
The above case describes Ludwig’s angina which is an aggressive, rapidly spreading
“woody” cellulitis of the submandibular space, commonly arising from an infected
molar tooth. There is a lack of lymphadenopathy since the typically polymicrobial
infection spreads along fascial planes as opposed to the lymphatic system. Two
life-threatening complications of Ludwig’s angina are upper airway obstruction and
descending necrotising mediastinitis. Sufferers are at risk of airway obstruction due
to posterior infective extension and tongue distension with posterior displacement.
Descending necrotising mediastinitis describes the spread of infection from neck
to mediastinum via contiguous fascial planes which is promoted by gravity and the
negative intrathoracic pressure. Since the disease is rare and early symptoms often
nebulous, diagnosis and treatment can be delayed with fatal consequences.
Computed tomography is the imaging modality of choice for acute deep-seated
neck infections and the correct answer to the above scenario. Imaging the neck
allows a rapid assessment of the depth of involvement as well as the presence of
abscesses which may be amenable to surgical drainage. Chest imaging provides
confirmation and allows an assessment of the extent of mediastinal involvement
which is important for surgical planning. Since a pericardial rub was heard in the
above scenario, computed tomography will also be useful in assessing for secondary
pericardial involvement and the presence of an effusion.
Magnetic resonance imaging does provide excellent soft tissue resolution and
diffusion weighted imaging can help delineate complex fluid collections. This
imaging modality is particularly useful for infections involving the retropharyngeal
space where extension into the spinal column is suspected. However, it is more
time consuming than computed tomography and patients may feel claustrophobic
during scanning. Patient compatibility also needs to be assessed. In the above
scenario where the airway patency can deteriorate rapidly and an early diagnosis
and treatment plan is needed, computed tomography is more appropriate.
Cervical ultrasound can be useful in characterising soft tissue masses and collections
but is unable to penetrate bone or air filled structures. It is also operator dependent
and not as accurate as computed tomography in assessing the extent of mediastinal
involvement.
Plain radiography is easily accessible but is of little value in planning the
management of descending necrotising fasciitis complicating Ludwig’s angina. A
lateral cervical radiograph can highlight pretracheal gas bubbles and a loss of the
normal lordosis, whereas a chest radiograph may show a widened mediastinum
and an enlarged cardiac silhouette if there is mediastinitis or a pericardial effusion
respectively. Computed tomography however provides a much more accurate
picture of the severity of the infection.
An echocardiogram can provide information regarding the extent of the pericardial
effusion and whether it is affecting cardiac function. Echocardiography is not
the most appropriate investigation to plan management since it provides no
information on the degree of cervical involvement or whether there are any
collections amenable to drainage.
- A 35-year-old cyclist suffered a severe traumatic brain injury with a large subdural haematoma and an associated C2–C3 cervical spine fracture. He is comatose and
apnoeic, with neurosurgeons confirming that he is not a candidate for surgery due to poor prognosis. Confirmation of brainstem death is underway, with examination of cranial nerves just being completed. What is the next most appropriate test that will support the neurological diagnosis of death?
A Apnoea testing
B Somatosensory evoked potentials
C No further tests necessary
D A second neurological examination of the cranial nerves
E Electroencephalogram
A
- E Electroencephalogram
The patient fulfils the prerequisites for brainstem testing because he has suffered
irreversible brain injury and he is in an apnoeic coma. The neurological confirmation
of death consists of cranial nerve II – XI examination and apnoea testing performed
by two doctors at two different times. At the end of each set of cranial nerves
examinations an apnoea test occurs. In a patient with a high cervical spine injury,
apnoea might not be due to a central cause but due to spinal cord injury, therefore
ancillary tests are employed to confirm de the diagnosis. Electroencephalogram
(EEG) is the most widely used and validated assessment in this circumstance.
The second battery of brainstem tests cannot be performed in isolation without the
apnoea testing; therefore an EEG is the next most appropriate step to support the
diagnosis of death by neurological criteria. Somatosensory evoked potentials are
used for monitoring of depth of anaesthesia and play no part in the diagnosis of
death.
- An 84-year-old woman with an extracapsular hip fracture is scheduled for a dynamic hip screw on your morning trauma list. On examination she has an ejection systolic murmur in the aortic area and anaemia with a haemoglobin
of of 90 g/L. She has previously had a coronary stent and is on both aspirin and clopidogrel. Your hospital’s echocardiogram technician is unavailable. How do you proceed?
A Postpone the surgery until an echocardiogram can be performed urgently
B Proceed with the case under general anaesthesia and invasive blood pressure
monitoring, with one unit of packed red blood cells
C Perform a spinal anaesthetic after administration of one pool of platelets
D Insert a lumbar epidural and use small volume incremental top-ups to achieve
a surgical block
E Proceed with the case under general anaesthesia and an ultrasound-guided
fascia iliaca block with invasive blood pressure monitoring
E
- E Proceed with the case under general anaesthesia and a
ultrasound-guided fascia iliaca block with invasive blood
pressure monitoring
The management of patients presenting for operative fixation of proximal femoral
fractures is clinically and politically of huge importance, the examiners recognise
this. Therefore it is essential to be familiar with at least one of the national or
international consensus guidelines on the issue. The key elements of these
guidelines are as follows:
Timing of surgery and delays
The Department of Health (UK) guidance recommends surgery within 36 hours
of admission, and evidence clearly shows adverse outcomes in terms of mortality,
complications and stay length if fixation is delayed past 48 hours. Nevertheless, this cannot override the obvious sensibility of stabilisation and resuscitation of an unstable patient. The AAGBI lists several situations in which an operative delay may be acceptable to allow for interim treatment. This list includes reversible
coagulopathic states, severe glucose or electrolyte disorders, uncontrolled
arrhythmias with heart rates above 120 beats per minute, overt heart failure, and chest sepsis
Echocardiography
The presence of a murmur may indicate serious valvular heart disease, and indeed aortic stenosis (AS) is more common in hip fracture patients occurring in 20-40%, ten times the rate of the general elderly population. That said, some studies demonstrate similar early postoperative mortality in patients with AS and those without. One could argue also that an echo demonstrating AS will not change management, in that surgery is still required and that therefore the best way to proceed in these
patients is to treat as if moderate AS were present. Guidelines do support a request
for an echo if no recent study is available, but not at the cost of timely surgery.
Anaemia and transfusion
Anaemia is common in this group, affecting about 40% of patients, and a fall
in haemoglobin around the time of surgery is inevitable. As with many other
patient groups the trigger for transfusion should be tailored to the individual
patient taking account of specific cardiorespiratory and neurological risk factors.
The large hip fracture transfusion (FOCUS) study seems to show little difference in mortality of a trigger of 80 vs 100 g/L. However, given that the haemoglobin concentration is likely to fall, the AAGBI recommend the routine point-of-care testing in recovery as a means to avoid missing dangerously anaemic patients postoperatively.
This is a perennial clinical conundrum facing any anaesthetist covering the
trauma list. The first issue relates to lack of echo, which is listed by the AAGBI as an ‘unacceptable reason to delay hip fracture surgery’. One has to assume a moderate degree of AS, and proceed accordingly with invasive blood pressure monitoring and adequate provision to treat sudden changes promptly. The next problem relates to the dual antiplatelet therapy, of which details are sparse. Here the assumption has to be that the patient has a drug-eluting stent and as such the main risk is of antiplatelet reversal or cessation is in-stent thrombosis leading to major cardiac adversity, as opposed to bleeding. Thus central neuraxial blocks are contraindicated, whereas the use of peripheral nerve blocks is more judged
on risk versus benefit for every case. In this case, the proposed fascia iliaca block is
one with a relatively low risk of bleeding, as with ultrasound it can be reliably sited
without immediate needle proximity to the femoral artery. Therefore, the most
appropriate course of action in this patient would be to proceed with the operation
under general anaesthesia and a ultrasound-guided fascia iliaca block with invasive
blood pressure monitoring.
- A 35-year old man for elective ankle surgery is to have an ultrasound guided popliteal nerve block.
What is the most frequently used combination of ultrasound view and needle visualisation for this nerve block?
A Short-axis view with in-plane needle approach
B Long-axis view with out-of-plane needle approach
C Short-axis view with out-of-plane needle approach
D Long-axis view with in-plane needle approach
E Any of the above combinations
E
- A Short-axis view with in-plane needle approach
The use of ultrasound (US) in regional anaesthesia has significantly increased in the
recent years. Choosing the correct US view and needle orientation is essential for
successful and safe nerve block. When scanning nerves the structures viewed by US
beam will either be in a short-axis view or long-axis view.
In the short-axis view, the nerves and the blood vessels are visualised in section
(sliced across their diameter), nerves are easier to find, and the US image is relatively
stable making this view ideal for introducing a needle.
In the long-axis view, however, the nerves and blood vessels are visualised
longitudinally along their length (demonstrating a tube like structure) making the
US image produced unstable and not ideal for needle insertion.
When introducing the needle, it can be passed either along the long-axis of the US
beam (in-plane) or across the short-axis of the beam (out-of-plane). With an in-plane
approach, the needle is visualised entirely throughout the block and produces good
views of needle-nerve proximity. Therefore this is the safest approach.
With an out-of-plane technique, the needle crosses the US beam as a bright dot
and the accurate location of the needle tip is uncertain and it could be advanced
in unwanted tissue, making this approach less safe for needle insertion. However,
anaesthetists the out-of-plane approach is ideal when inserting catheters as it allows
parallel advancement of the catheter along the long-axis of the nerve as it exits the
tip of the needle (Figure 6.1).
In this example, the combination of short-axis view and in-plane needle visualisation
is the safest approach for the above reasons.
- You are called to the emergency department to assess a young woman that was rescued from a house fire following a gas leak after being trapped confined in a room.
She is awake, with normal observations but suffered 10% body surface area (BS) partial thickness burns over her arms and face. You are asked to transfer her to the nearest burns unit that is 2 hours away.
On examination she has singed nasal
hair, a normal airway and no change in voice. Burns resuscitation is underway with
intravenous fluids and analgesia.
What is the next step in ensuring her safe transfer?
A Add the operating department practitioner to your transfer team
B Full monitoring including invasive blood pressure measurement
C Prepare difficult airway equipment for the transfer
D Prepare Intubating equipment and drugs
E Elective intubation of the patient
D
- E Elective intubation of the patient
Inhalational injury is the aspiration of heated gases, hot liquids, steam, or noxious
substances of incomplete combustion. It can be categorised as:
• Upper airway thermal injury – supraglottic burns causing stridor, a change in
voice quality or uvular oedema
• Lower airway thermal injury – infraglottic burns most commonly by noxious byproducts
of incomplete combustion leading to dyspnoea, wheeze and secretions
• Noxious gases injury – including inhalation of carbon monoxide and cyanide
This patient has a high risk of inhalation injury due to an enclosed space fire with
significant burns to the face. The onset of airway oedema is often unpredictable, but
fluid resuscitation is likely to worsen any impending oedema, while the relatively
long duration of transfer indicates the need to have a secure airway during transfer.
Therefore it is appropriate to plan elective intubation of the patient in controlled
circumstances with senior support, a difficult airway trolley and skilled assistance.
Adding a competent team member to the transfer is reassuring and can help
should complications arise during transfer, but it is often impractical. All transfers
should have full monitoring, including ECG, pulse oximetry and non-invasive blood
pressures, but invasive blood pressure monitoring is only indicated if you anticipate
cardiovascular instability or it is required to guide ongoing therapy. Availability of
difficult airway equipment is necessary once elective intubation has been decided,
and devices such as video laryngoscopes are useful to have when a patient is being
transferred. However, the most appropriate approach would be to ensure a secure
airway prior to transfer.
- A 72-year-old man has been on the intensive care unit after being treated for an infective exacerbation of his chronic obstructive pulmonary disease.
He has been mechanically ventilated for 5 days and has acceptable gas exchange. He has been weaned to pressure support ventilation requiring 12 cmH2O inspiratory support and 5 cmH2O of positive end-expiratory pressure (PEEP) with an inspired oxygen
concentration of 0.35. He is currently obeying commends.
How would you best assess his suitability for extubation?
A Change the patient to continuous positive airway pressure (CPAP) and assess ventilation and cardiovascular parameters for 30 minutes
B Reduce the pressure support gradually over the next 48 hours by 2 cmH2O per 12 hours and assess ventilation and cardiovascular parameters
C Reduce the inspired oxygen fraction to 0.25 and repeat an arterial blood gas 30 minutes later
D Repeat a chest radiograph to ensure resolution of his consolidative process
E Assess the patient’s sputum production and send a repeat sample for microscopy to ensure clearance of the infective process
a
- A Change the patient to continuous positive airway
pressure (CPAP) and assess ventilation and cardiovascular
parameters for 30 minutes
The majority of patients who receive mechanical ventilation have acute respiratory
failure in the postoperative period, pneumonia, congestive heart failure, sepsis,
trauma or acute respiratory distress syndrome (ARDS). Respiratory muscle
weakness may not be a contributing factor to their respiratory failure and once
the acute pathophysiological problem is resolved, invasive ventilation may be
downgraded and patients extubated. The duration of mechanical ventilation is
often unnecessarily prolonged in the setting of a short period of ventilator support
(less than 7 days) with the weaning process accounting for up to 50% of the total
ventilation time. A delay of 48 hours in extubation results in an increased risk of
extubation failure, ventilator acquired pneumonia, thromboembolic disease, longer
intensive care and hospital stay and increased mortality.
Weaning involves progression from a controlled mode of ventilation to a support
mode and then reduction of support delivered until a trial of readiness for
extubation. This trial is termed a spontaneous breathing trial (SBT).
Typical readiness criteria for attempted weaning include:
• Improvement in the underlying condition that caused the respiratory failure
• Pulmonary: fractional inspired oxygen Ratio (PFR) of more than 200 with a
positive end-expiratory pressure (PEEP) of 5 cmH2O
• Haemodynamic stability
• No electrolyte, metabolic, haematological or nutritional deficits
• Neurologically appropriate with cough and gag reflexes present
Once deemed suitable, a SBT may be initiated with minimal pressure support such
as 5 cmH2O, CPAP or a T-piece or tracheostomy mask (no PEEP). A SBT should be
attempted for a minimum of 30 minutes but should be terminated and deemed
unsuccessful if:
• The respiratory rate remains above 35 breathes per minute for 5 minutes
• Oxygen saturations of less than 90%
• Heart rate increases to over 140 beats per minute
• Systolic blood pressure > 180 mmHg or < 90 mmHg
• Panic or diaphoresis
The following classification of the results of the spontaneous breathing trial may be
applied:
• Simple: successful first trial followed by extubation
• Difficult: up to three spontaneous trials but discontinuation of ventilation within
7 days
• Prolonged: more than three unsuccessful trials or more than 7 days of mechanical
ventilation
10–20% of ventilated patients may have prolonged weaning and in-hospital
mortality is increased in this group. In patients who fail a SBT, the strategy is to
reduce the support the patient is receiving and try again. A period of rest between SBTs is advocated of 24–48 hours. Gradual reductions in the pressure support by 2–4 cmH2O per 24 hours or a short SBT period every hour with increasing the duration are both advocated.
Even assessing in a careful manner such as described above, 10–15% of extubations fail, necessitating re-intubation. If this occurs the mortality rate in this group is increased.
In the patient above, the criteria for initiating a SBT is met and if successful, a trial of extubation is warranted. In this patient with COPD, a greater-than-average sputum production and poorer gas-exchange may have been present prior to the acute infection and must be accepted in order to avoid the complications of on-going mechanical ventilation.
- You are asked to review a 72-year-old man who was admitted to your intensive care unit 6 hours ago following elective coronary artery bypass grafts. He is haemodynamically stable with no evidence of end organ hypoperfusion. The concern is that he has been slowly bleeding into his drains (total 570 mL since theatre) and has slow oozing through his sternotomy wound and around his lines and drains.
His core temperature is 36.2°C and pH 7.32. An urgent full blood count and clotting tests were sent 30 minutes ago and the results have just come back
and show:
Haemoglobin concentration 78 g/L;
platelet count 102 ×109/L;
INR 1.4; aPTTr 1.6;
fibrinogen 1.8 g/L;
and ionised calcium 0.9 mmol/L. The patient is
on long-term aspirin 75 mg daily (not stopped for surgery). He received heparin in theatre that was reversed with protamine. He also received a single dose of 1 g tranexamic acid.
Given this information the most appropriate treatment strategy is:
A 1 unit packed red blood cells (pRBC) + 1 pool of platelets + 15 mL/kg fresh frozen plasma (FFP) + 1 dose of cryoprecipitate
B 20 mmol of calcium chloride + protamine + 1 pool of platelets + tranexamic acid
C 2 units packed red blood cells (pRBC)
D 20 mmol of calcium chloride + 1 pool of platelets + 15 mL/kg fresh frozen plasma (FFP)
E Perform a thromboelastogram
A
- D 20 mmol of calcium chloride + 1 pool of platelets +
15 mL/kg fresh frozen plasma (FFP)
In order to form effective blood clots a patient needs an adequate number of
functioning platelets, adequate levels of all the clotting factors, an adequate
haematocrit, an adequate level of ionised calcium, a relatively normal pH and an absence of significant hypothermia. The critical levels of these variables cannot be defined and are mutually dependent. The clinical scenario described suggests that there is ongoing bleeding due to a coagulopathy rather than a failure of surgical haemostasis. The temperature, pH, haematocrit and platelet count are acceptable.
However, the patient has been receiving long term antiplatelet therapy and has been on cardiopulmonary bypass, thus, in the absence of a platelet function test it is reasonable to deduce that platelet transfusion is warranted to correct the coagulopathy.
The clotting tests suggest there is a consumptive and /or dilutional component to this coagulopathy. Given the degree of abnormality, a dose of FFP should elevate the levels of all factors, including fibrinogen, without the need to give
additional cryoprecipitate. Administration of FFP and platelets is likely to result in
a further drop in ionised calcium, it would be prudent to administer a replacement
dose. Given the scenario and timings, a further dose of protamine is likely to result
in an anti-coagulant effect. In the absence of evidence for hyperfibrinolysis, a
second dose of tranexamic acid is not indicated at this stage. The threshold for
pRBC transfusion in this context is <70g/L. A thromboelastogram would refine the
diagnosis further and repetition after intervention guide further therapy. This is a
common practice in many centres but not universal.
- A 60 kg, 55-year-old woman has been admitted to the intensive care unit with severe community acquired pneumonia. Two days later she develops worsening hypoxaemia with new bilateral infiltrates on chest radiography. She is currently
ventilated with the following settings:
• Fio2 1.0
• Inspiratory pressure (Pinsp) 35 cmH2O
• Positive end expiratory pressure (PEEP) 12 cmH2O
• Inspiratory:expiratory (I:E) ratio 1:1
• Tidal volume (Vt) 250 mL
An arterial blood gas reveals results shown in Table 6.1.
Based on current evidence, which of the following would be an appropriate next step to improve her oxygenation and reduce mortality?
Table 6.1 Arterial blood gas test results
Parameter Result
pH 7.28
Paco2 8.6 kPa
Pao2 7.1 kPa
Base excess –3.4 mmol/L
Bicarbonate concentration (HCO3
–) 21.4 mmol/L
Lactate 2.3 mmol/L
Haemoglobin concentration (Hb) 96 g/L
Glucose concentration 6.7 mmol/L
A Extracorporeal membrane oxygenation
B Prone positioning
C Inhaled nitric oxide
D High frequency oscillation ventilation
E Increase Pinsp
B
- B Prone positioning
The worsening hypoxaemia, new bilateral radiology infiltrates and low Pao2:Fio2 (P:F ratio) within one week of the onset of severe pneumonia suggests acute respiratory distress syndrome (ARDS).
ARDS is an acute, diffuse inflammatory lung syndrome that results in respiratory failure. The 1994 American-European Consensus Conference definition of ARDS has now been superseded by the 2012 Berlin Definition (Table 6.5).
The cause of ARDS in this patient is severe pneumonia, which is a direct (or
pulmonary) cause. Other direct causes of ARDS include aspiration, lung contusions and inhalational injury. Indirect (non-pulmonary) causes include sepsis, trauma, pancreatitis and burns.
The pathophysiology of ARDS is complex and involves the interplay of various body systems. A simplified view of this pathogenesis is presented here but this is an area of ongoing exploration.
- Exudative phase: Alveolar capillary membrane disruption resulting in leakage
of protein rich fluid. Inflammatory cells (e.g. neutrophils) infiltration forming
exudate. - Proliferative phase: Proliferation of abnormal type II alveolar cells and
inflammatory cells. There is a resultant dysfunction in surfactant with decreased
pulmonary compliance. - Fibrotic phase: Infiltration with fibroblasts replacing alveolar cells and ducts
resulting in marked reduction in pulmonary compliance. - Restorative phase: Slow and incomplete repair of pulmonary architecture.
The management of ARDS can be subdivided as below:
‘Rescue’ therapies for refractory hypoxaemia
Prone positioning
Prone positioning is based on the theory of recruiting areas of lung that are
non-dependent in the supine position, leading to reduced ventilation-perfusion
mismatching. There are additional benefits of improved secretion clearance
and increased homogeneity of ventilation due to decreased lung deformation
by mediastinal structures. There are potential adverse effects such as line or
endotracheal tube displacement, reduced preload and functional restriction in
cardiac contraction, pancreatitis, raised intracranial pressure and pressure related
nerve damage. The process itself needs to be meticulously performed with adequate
numbers of staff.
PROSEVA (2013) was a landmark prospective, multicenter randomised control
trial investigating early prone positioning in moderate to severe ARDS. It suggests
230 Chapter 6
benefit in terms of oxygenation and mortality. Previous studies appeared to show
improved oxygenation, but no clear mortality benefit.
Inhaled nitric oxide
Nitric oxide (NO) is known to cause pulmonary vasodilatation and hence improve
pulmonary blood flow. The inhaled route delivers NO selectively to ventilated lung
units and hence improves oxygenation. Although inhaled nitric oxide improves
oxygenation, there does not appear to be a mortality benefit.
Extracoporeal membrane oxygenation (ECMO)
ECMO involves insertion of large cannulae into central vessels. It is similar to a simple
cardiopulmonary bypass circuit. Blood leaves a central vessel and is pumped around
a circuit through a membrane oxygenator to allow gas exchange, then returned
to the patient via a central vessel. As oxygenation is predominantly achieved
through the extracorporeal circuit, ultra low tidal volumes can be used to ventilate
the patient minimising ventilator associated lung injury. ECMO requires systemic
anticoagulation, carrying a risk of bleeding.
The CESAR trial (2009) was a multicentre randomised control trial investigating conventional management or referral to consideration for treatment by ECMO in severe potentially reversible respiratory failure. It concluded that referral to a tertiary respiratory centre for consideration of ECMO resulted in improved survival.
It is unclear what proportion of this benefit is attributed to optimum conventional ventilation in a tertiary referral centre.
- A 58-year-old man is brought in by ambulance following a house fire in an enclosed area. He is confused with a GCS 14/15. On examination he has singed facial hair with voice changes. He is noted to have partial thickness burns to the front of his torso, bilateral palms and palmar aspect
of upper limbs. His body weight is 70 kg.
According to the Parkland formula his estimated fluid requirement in the first 8
hours following his burn is:
A 7560 mL
B 4850 mL
C 4620 mL
D 3910 mL
E. 3780 mL
- E 3780 mL
This patient has sustained a significant thermal injury with evidence of inhalational
injury. Significant burns cause a profound systemic inflammatory response
syndrome and early aggressive management is paramount. Mortality from major
burns is in the order of 10–20% with multiorgan failure and sepsis being leading
causes.
Management should follow ALTS guidelines, especially where the mechanism is
unknown. During the primary survey, early intubation is advised where airway
compromise or significant inhalational injury is suspected. A rapid sequence
induction is advised and intubation performed with an uncut cuffed endotracheal
tube; ideally size 8 or larger to aid assessment of the airway via bronchoscopy.
Suxamethonium is considered safe in the first 24 hours following injury, an
exaggerated hyperkalaemic response may occur after this time frame.
As part of the ‘Breathing’ assessment, carbon monoxide poisoning should be
excluded. In this case the confusion at presentation may be an early sign and an
arterial blood gas should be done urgently. Normal carbon monoxide levels can be
up to 10% in smokers and a level greater than 20% raises the suspicion of significant
inhalation injury and carbon monoxide poisoning. It is important to note that pulse
oximetry overestimates Spo2 in the presence of carbon monoxide. Therefore the
saturations of 100% in this case should be corroborated with arterial gas analysis via
co-oximetry. High-flow oxygen decreases the half-life of carbon monoxide from 4 to
1 hours, and should be administered empirically until carboxyhaemoglobin (HbCO)
levels are attained.
Another point of concern in this patient as part of the ‘Breathing’ assessment
is the anterior torso burn. The chest wall should be examined for evidence of
circumferential burn which may require early escharotomies. There is evidence to
support that, where possible, these should be done in specialist burns centres
The focus of this question is on the assessment of circulation. As the burns surface
area affects the management of fluid resuscitation, this must be calculated at this
stage. The body surface area (BSA) takes into account partial and full thickness burns
and can be calculated using the ‘rule of 9s’. In this patient the burn to the anterior
torso represents 18% BSA and bilateral palmar surfaces of upper limbs represent a
further 9% (i.e. 2 x 4.5%); the total BSA is 27% (Figure 6.2).
Age (years) ≤ 5 or ≥ 60
Site Face, hands, feet, perineum, circumferential
BSA (%) ≥ 10% in adults, ≥ 5% in children
Injury Inhalational, chemical, electrical or complex trauma
Comorbidities Significant cardiorespiratory disease, diabetes
