SBA 300 Paper 2 Flashcards
- 5 days ago a 25-year-old woman suffered a traumatic brain injury. Despite a
normal CT, she demonstrated bilateral motor posturing. She therefore had an
intracranial pressure (ICP) bolt inserted shortly after admission in order to
monitor her ICP. You begin your morning review by analysing her ICP waveform.
Which of the following would concern you most acutely?
A Lundberg A waves
B A flat trace
C A baseline value of 20mmHg
D Lundberg B waves
E The most prominent upstroke being the P2 (tidal) wave
A Lundberg A waves
○ An intracranial pressure (ICP) bolt is a solid, intra-parenchymal catheter containing either a fibreoptic sensor or a micro strain gauge in its tip.
○ It can be inserted under local anaesthetic and extends up to 20mm intracranially, thereby allowing the transduction of intracranial pressure in that region of brain tissue.
○ The value is usually displayed as a number but can also be translated into a graphical display of the waveform.
○ The ICP waveform is a reflection of the intracranial arterial pulsation and subsequently has recognisable characteristics (Figure 2.1).
The ICP waveform has 3 identifiable peaks. The first (P1) coincides with the upstroke
of the arterial pressure trace, is a result of choroidal pulsation and is known as the
‘percussive’ wave. It is succeeded by a second ‘tidal’ wave (P2) which ends at the
point of the arterial dicrotic notch, following which, the final or ‘dicrotic’ wave occurs (P3).
**The size of P2 is an inversely proportional reflection of brain compliance. Therefore with decreased compliance its amplitude is increased such that it is more prominent than P1 and P3 (Figure 2.2).
The waveform can also be analysed over a period of time.
○ Lundberg described
trends in waveform analysis and ascribed the letters A, B and C to the trends as
follows.
• Lundberg A waves: Large plateau waves persisting for 5–10 minutes. These are
always pathological and warn of impending herniation
• Lundberg B waves: Fluctuations in ICP that occur with a frequency of 0.5–2
waves per minute. They are thought to be associated with ICP instability and/or vasospasm due to their correlation with increased flow velocity results from
middle cerebral artery transcranial doppler studies
• Lundberg C waves: Fluctuations in ICP at a frequency of 4–8 waves per minute.
These are considered normal in some patients and thought to correspond to the respiratory and cardiac cycles (Figure 2.3)
The advantages of an ICP bolt include ease of insertion, that does not require
transfer to the operating theatre, and output that is neither altered by patient
position nor susceptible to damping.
○ The disadvantages are that it only reflects regional pressure changes and once inserted, cannot be recalibrated. Therefore if the bolt has been in-situ for several days, a degree of drift must be taken into account and subsequently they often need replacing if required for longer than 5days.
The most acutely worrying characteristic in the above scenario would be the
presence of Lundberg A waves. Lundberg B waves would be a matter for concern
but not as pressing. A baseline value of 20mmHg may represent the true ICP
value but at 5 days could also incorporate an element of drift in calibration. When
interpreting a flat trace the possibility of displacement or kinking of the transducer
must be considered in the first instance.
- You are called to the emergency department to assist with a 20-year-old man who presented following a grand-mal seizure. He has begun fitting again and his conscious level has remained below baseline for 30 minutes. He has a history of epilepsy and has not been taking his usual medication since his prescription ran out 1 week ago. He is otherwise well.
Which of the following is the most appropriate immediate action?
A Intubate the patient to protect his airway and optimise ventilation
B Check his blood glucose and treat any hypoglycaemia with intravenous
dextrose
C Take blood for full blood count, electrolytes, urea, creatinine, liver function tests and anti-epileptic medication levels
D Administer his anti-epileptic medication intravenously
E Apply pulse oximetry, blood pressure and ECG monitoring
- E Apply pulse oximetry, blood pressure and ECG monitoring
Seizure activity that persists without return of conscious level to baseline for 30
minutes is defined as status epilepticus and is a medical emergency. Status can occur with any classification of seizure but the generalised form is that which is most commonly observed.
Rapid assessment and swift management is required to minimise the complications of unremitting neuronal discharge.
If status persists,
compensation in blood flow to meet increased metabolic demand begins to fail, leading to insufficient cerebral perfusion. Cerebral tissue damage follows. Cardiac arrhythmias, pulmonary hypertension, pulmonary oedema, global metabolic
disturbances and rhabdomyolysis may also ensue.
All of the options should be performed as soon as possible, and ideally in parallel.
○ National Institute for Health and Care Excellence (NICE) UK guidelines specify that
airway securement should be implemented immediately but in order to perform this
safely, it is mandatory to have standard monitoring in situ.
- You are asked to pre-assess a 68-year-old man for elective open umbilical hernia repair. He suffers from exertional angina (three flights of stairs) and had coronary angiography 6 months ago, which showed right coronary and circumflex artery disease. He had a myocardial infarction 2 years ago. His symptoms have been stable over the past year and he is currently taking bisoprolol 2.5mg once a day (o.d.), aspirin 75mg o.d. and ramipril 2.5mg o.d. His creatinine is 120μmol/L. He is not diabetic and has not had a stroke. He is independent and performs all his own housework.
Which of the following is the most appropriate next step in this patient’s
management?
A Schedule the patient for surgery. Cease the ramipril 24hours preoperatively.
Continue the aspirin
B Schedule the patient for surgery. Cease the bisoprolol 2days preoperatively.
C Obtain non-invasive stress testing
D Refer for repeat coronary angiogram
E Refer for coronary artery bypass surgery
- A Schedule the patient for surgery. Cease the ramipril
24hours preoperatively. Continue the aspirin
○ The European Society of Cardiology (ESC) has produced guidelines and a step-wise pathway for the assessment of cardiac patients for non-cardiac surgery. The patient presented has stable coronary artery disease and scores 2 (for previous myocardial infarction and proposed intraperitoneal surgery) on the revised cardiac risk index (also known as the Lee Index). This gives an approximate risk of cardiac death or non-fatal myocardial infarction of 2.4% (95% CI 1.3–3.5%). The factors included on
this risk index include:
• History of ischaemic heart disease
• History of congestive heart failure
• History of cerebrovascular disease
• History of diabetes requiring preoperative insulin use
• Chronic kidney disease (serum creatinine >170μmol/L)
• Undergoing major surgery (suprainguinal vascular, intraperitoneal or intrathoracic)
The ESC guidelines for non-invasive testing (stress echo, exercise testing) use a
slightly amended version of the above risk scale (with prior myocardial infarction
being assigned a separate point) and recommend that patients with three or more of the clinical factors listed below are referred for further assessment of myocardial
perfusion and function preoperatively.
• Angina
• Prior myocardial infarction
• Heart failure
• Stroke/transient ischaemic attack
• Renal dysfunction with serum creatinine >170μmol/L
• Diabetes requiring insulin therapy
In patients with extensive stress-induced ischaemia, referral for coronary
revascularisation may be indicated. The method of achieving this will depend on the potential benefit of the procedure (percutaneous coronary intervention vs coronary artery bypass grafting) against the risk of the procedure.
Pre-operative diagnostic angiography is indicated in those patients with:
• Acute ST elevation myocardial infarction (STEMI)
• Non-STEMI (NSTEMI) and unstable angina
• Angina not controlled with medical therapy
It may also be considered in stable patients undergoing high-risk surgery. Referral for any procedure must take into account the risk to the patient as well as the potential benefit. In this situation, the patient is relatively low-risk and has had a
reasonably recent angiogram; it is therefore unlikely that a repeat angiography justifies the risk.
In patients already established on beta-blockers, these should be continued
throughout the perioperative period. Although a topic of some debate, usual
practice is to omit ACE-inhibitors 24 hours before surgery due to an increased risk of
intraoperative hypotension. Aspirin should be continued unless there are concerns
regarding haemostasis during surgery (certain neurosurgical procedures, for
example).
The use of biomarkers including Brain Natriuretic Peptide (BNP) is under evaluation and may be of some use in the risk stratification of cardiac patients.
- A healthy 30-year-old man due for an appendicectomy is undergoing a rapid
sequence induction. After full pre-oxygenation and administration of thiopentone
and suxamethonium, three attempts at intubation have failed with an unexpected
grade III Cormack & Lehane laryngoscopy view. His oxygen saturations are 92%
and full cricoid pressure is being applied.
What action is most appropriate in this situation?
A Reattempt intubation using a different laryngoscope
B Reattempt intubation whilst reducing the cricoid pressure
C Attempt insertion of a supraglottic airway device
D Postpone surgery and awaken the patient
C Attempt cannula cricothyroidotomy
laryngoscope can all improve the success rate. However these changes need to be
performed within the allocated initial three attempts.
The use of laryngeal mask airways do have a role during rapid sequence inductions,
but should only be used after a failed initial intubation plan and failed face mask
oxygenation whilst waiting for the patient to awaken. Failure of oxygenation is
defined as oxygen saturations of <90% whilst receiving 100% oxygen.
Only in a ‘cannot intubate and cannot ventilate’ scenario with increasing hypoxemia
should a cannula or surgical cricothyroidotomy be performed (Figure 2.4).
- An 80-year-old woman, admitted with pneumonia 14days ago, suffers an episode of large haematemesis requiring endoscopic investigation. You anaesthetise her and secure her airway uneventfully with a size 7.5 endotracheal tube
(ETT) secured at 24cm to the teeth. Oxygen saturations are 99% (Fio2 0.4). The
gastroenterologist then extends her head. At this point she becomes progressively
hypoxic and chest wall movement becomes limited to the right side.
What is the most likely reason for her desaturation?
A Aspiration of gastric contents
B Bronchospasm
C Sputum plugging of a bronchus
D Pneumothorax
E Endobronchial intubation
- E Endobronchial intubation
When intubating a patient it is imperative that tube position is assessed clinically.
It is important to bear in mind that change in patient position for a procedure may
cause the endotracheal tube (ETT) to migrate. This lady’s ETT is originally placed at a depth most likely to be too great for a female patient. Extending her head probably
resulted in confirming endobronchial intubation.
Aspiration of gastric contents would most likely result in right-sided
decompensation or, in this scenario, be evident from viewing the oral cavity. She
may have plugged off her left bronchus, although her saturations are surprisingly
robust for a patient with the amount of sputum that would be present for such
an event. Bronchospasm and pneumothorax may occur independently or as a consequence of endobronchial intubation.
- A 56-year-old man is taken to the intensive care unit following a laparotomy a week ago for bowel obstruction. He is hypertensive, has a body mass index (BMI) of 42, and has had an ileus for the last 7days. His abdomen is tender and tensely
distended. There are no signs of sepsis, but he has worsening renal function
and a poor urine output, despite a very positive fluid balance. He had become
increasingly breathless with type II respiratory failure, and after a failed trial of non-invasive ventilation, is now mechanically ventilated. His ventilator pressures are worsening and his base excess and lactate are increasing.
Which of the following is the most correct regarding this patient?
A A measurement of intra-abdominal pressure is most safely performed with an intraperitoneal catheter and pressure transducer
B An intravesical measurement is performed at the end of inspiration
C Abdominal compartment syndrome may provoke a cardiac arrest at laparotomy
D An abdominal pressure of 24mmHg can be considered normal
E The only effective treatment is re-laparotomy leaving the abdomen open with a Bogota bag
6 C Abdominal compartment syndrome may provoke a
cardiac arrest at laparotomy
The management of abdominal hypertension and compartment syndrome can
be imagined in a similar way to elevated intracranial pressure. Thus the initial
management relies on the maintenance of abdominal perfusion pressure (APP),
which is mean arterial pressure (MAP) minus intra-abdominal pressure (IAP).
Maintenance of an APP >60mmHg has been shown to improve outcome in a
condition with an untreated mortality otherwise approaching 100%.
Definitions and measurement
Normal IAP is in the region of 5–7mmHg in the critical care setting, and this is
increased by presence of intra-abdominal fluid or collections, upright position, and
mechanical ventilation. Intra-abdominal hypertension is diagnosed with a pressure
persisting above 12mmHg, and this is termed compartment syndrome when the
pressure is consistently above 20mmHg with new organ failure.
Measurement can be direct, using an intraperitoneal needle or catheter and
transducer system, or indirect via intra-vesical, intra-gastric, intrauterine or rectal
routes. The commonest route is the bladder, which can make use of a normal Foley
catheter and gives usable results with lower risk than direct methods. The process
involves connecting a transducer to a three-way tap, which measures the pressure of
25mL of sterile saline instilled into an empty bladder, after the catheter is clamped.
Readings should be taken at end-expiration and one minute following instillation
of the saline to allow for bladder relaxation. The patient should have a relaxed
abdominal wall, and not be coughing straining.
Systemic pathological effects
Elevated intra-abdominal pressure has wide-ranging systemic effects; high
abdominal pressure produces collapsing of the vasculature. On the venous side,
this gives rise to reductions in venous return and reduced stroke volume. Arteriolar
compression gives an increased systemic vascular resistance (SVR) and afterload.
The combined effects are those of reduced cardiac output that can rapidly spiral to
produce gut ischaemia.Respiratory features are those of respiratory failure due to atelectasis, collapse and
shunt. There is a reduction in chest wall compliance and diaphragmatic excursion.
In ventilated patients the increased pressures required to maintain oxygenation and
ventilation can compromise cardiac output further.
Renal function is impaired as a combined result of reduced cardiac output and a
reduction in filtration gradient (FG). The filtration gradient is the pressure difference
across the glomerulus, and is therefore the difference between the perfusion
pressure and the pressure in the proximal tubule. Raised IAP compresses the
collapsible renal outflow tracts and collecting systems, such that tubular pressure
rises, thereby lowering FG. Thus a high IAP both reduces the APP and raises the
tubular pressure all of which reduce the FG required to drive filtration.
High IAPs also increase intracranial pressure (ICP). This occurs by a combination of
high intrathoracic pressure and reduced venous return, and ventilatory difficulties
and the consequences for arterial carbon dioxide tension. The combination of
pre-existing intracranial hypertension and abdominal compartment syndrome is
particularly dangerous and may mandate surgical abdominal decompression to
lower ICP.Management
Non-surgical management is directed toward the joint aims of lowering intra-
abdominal pressure and maintaining APP with careful fluid resuscitation to
normovolaemia followed by vasopressor support if required. Over enthusiastic fluid
therapy may contribute to gut oedema and further compromise tissue perfusion.
Pressure in the abdomen may be lowered by reducing the volumes of the contents,
with nasogastric tubes, endoscopic evacuation or invasive drainage of gas or fluid.
In addition, in the ventilated patient consideration can be given to optimal sedation
and muscle relaxation to reduce straining and asynchrony.
Surgical management involves laparotomy and decompression. The abdomen
is then left open and covered with a temporary closure of a Bogota bag or
vacuum dressing. It remains important to measure abdominal pressure even after
decompression, as 25% of patients with a Bogota bag go on to develop secondary
hypertension. Serious caution should be exercised at laparotomy for raised IAP as
profound haemodynamic instability may ensue as a consequence of abdominal
reperfusion alongside a sudden fall in SVR. This can be massive and of sufficient
magnitude to bring about cardiac arrest.
As described above, indirect methods of measurement reduce the risks of
complications associated with needle or catheter techniques. Measurement
takes place at the end of expiration. A pressure of 24mmHg is more than double
the cut-off for hypertension, and within the range of compartment syndrome, if
sustained. Management strategies are discussed above, with non-surgical options also available. Laparotomy is indeed a risk factor for cardiac arrest given the massive
physiological changes that occur in this situation.
- A 60-year-old man awaiting surgical resection for his tracheal carcinoma presents to the emergency department with worsening dyspnoea. As part of his pulmonary function tests, a bedside flow-volume loop (spirogram) is ordered.
What will be the most likely appearance of his flow-volume loop?
A Flattening of the inspiratory limb only
B Flattening of the expiratory limb only
C Flattening of both the inspiratory and expiratory limbs
D Saw-tooth pattern in both the inspiratory and expiratory limbs
E Normal appearance of both inspiratory and expiratory limbs
- C Flattening of both the inspiratory and expiratory limbs
A flow-volume loop is a plot of flow rate (y-axis) against lung volume (x-axis) during
maximal forced inspiration and expiration. The contour of this loop can aid in
localising upper airway obstructions and assessing their functional impact.
Upper airway obstructions are classified as either intrathoracic or extrathoracic
depending on whether they are present within or outside the thoracic inlet
respectively. In addition, they are also described as either variable or fixed
depending on whether the airway lesion calibre changes during the respiratory
cycle.
For variable extrathoracic obstructions (such as vocal cord paralysis), the flow
volume loop classically displays a flattened inspiratory and normal expiratory limb.
This is because during inspiration, the transmural pressure is negative as a result of
a subatmospheric intraluminal pressure and an atmospheric extraluminal pressure.
Consequently, the extrathoracic portion of the upper airway will have a tendency
to collapse during inspiration resulting in reduced airflow in the presence of an
obstructing lesion. During expiration, the intraluminal pressure surpasses the
pressure surrounding the airway thus reducing the obstruction.
Flow volume loops in the presence of variable intrathoracic obstructions (such as
bronchogenic cysts) classically display a flattened expiratory and normal inspiratory
limb. Flow limitation is encountered during expiration because at this phase of the
respiratory cycle, the pleural pressures exceed the airway pressures exacerbating
the obstruction. During inspiration, the pleural pressures are negative relative to the
intrathoracic airways thereby creating no restriction to airflow.
Fixed upper airway obstructions are characterised by a constant degree of
airflow limitation during the whole respiratory cycle as they limit the influence of
transmural pressures on airway diameter. They can be extrathoracic (large goitres) or
intrathoracic (large tracheal tumours) and their flow loops display flattening of both
the inspiratory and expiratory limbs. The above case is an example of a fixed airway
obstruction.
A saw-tooth pattern describes small oscillations which can be observed
throughout the inspiratory and expiratory limbs of the flow volume loops
as a consequence of either equipment artifact, neuromuscular disease or
pedunculated tumours (Figure 2.5).
- A 32-year-old woman was recently diagnosed with brainstem death following a subarachnoid haemorrhage. She was initially hypertensive, then developed polyuria and gradually became hypotensive. The patient has received 30mL/kg of crystalloid boluses.
What is the next pharmacological intervention needed to restore the patient’s blood pressure?
A Dopamine
B Adrenaline
C Vasopressin
D Noradrenaline
E Further bolus of colloid
C Vasopressin
Brainstem herniation causes relative hypotension and bradycardia after an initial
period of hypertension due to catecholamine release. This is due to loss of autonomic
control of vasomotor tone and loss of vagal tone. Treating episodes of hypotension
with adrenergic vasoactive drugs exacerbates end-organ ischaemia and they are
contraindicated in a potential organ donor. Vasopressin is the agent of choice to
treat hypotension and maintain vascular tone following brainstem herniation as it
improves organ perfusion and corrects the polyuric component of diabetes insipidus caused by hypothalamic ischaemia. Fluid boluses are useful to maintain euvolaemia, but over filling patients also risks detrimental outcomes to organs
- You have been asked to see a 32-year-old patient in recovery following a retrograde intramedullary femoral nailing. He works as a builder and fell from a ladder sustaining bilateral femoral fractures. The plan is to fix the other leg in the next few days. He is desaturating to 88% on oxygen via facemask and is confused, and one of
the recovery staff has also noticed a petechial rash on the patient’s neck.
In diagnosis and treatment of the likely condition, which of the following tests is most important?
A Arterial blood gas analysis
B Bronchoscopic alveolar lavage (BAL) for macrophages
C Trial of methylprednisolone for 48hours
D A CT of the chest
E Urine microscopy for lipid droplets
A An arterial blood gas analysis
Fat embolism indicates the presence of fat within the pulmonary or peripheral
circulation, often without symptoms. Fat embolism syndrome is the clinical
consequences of fat embolism occurring in some patients and has a quoted
mortality of between 5–15%.
The commonest implicated fractures are the closed fractures of the long bones and pelvis. The greater the number of fractures, the higher the incidence. A third of patients with bilateral femoral fractures go on to develop the syndrome.
Presentation and diagnosis
○ The syndrome most often presents at 1–3 days. There are a variety of sets of
published diagnostic criteria, but all have in common either an arterial blood gas (ABG) or clinical features of profound type I respiratory failure. Clinically, the two other major tenets are neurological dysfunction, most commonly acute confusion,
and the classical petechial rash. The rash may be a late sign and only present in 60% of cases.
Blood indices most often reflect a marked anaemia with thrombocytopenia. Other
features such as fat in sputum, urine and alveolar macrophages may support the diagnosis, but equally do not correlate well with the severity of the syndrome.
Pathophysiology
Two main theories exist.
° In the mechanical theory, physical disruption forces adipose
marrow into the venous system and bones with high marrow content are indeed most associated with the syndrome. However, studies have directly demonstrated
embolic load in patients during orthopaedic surgery who have not progressed to develop the clinical syndrome. The mechanical theory also does not explain why,
despite the fact that embolism is greatest around the time of injury, occurrence of the syndrome peaks at 24–72 hours.
° The biochemical theory ascribes toxicity to the hydrolytic degradation of neutral marrow fat to free fatty acids. These free acids are shown to be able to induce acute lung injury in animal models. C-reactive protein may also have a role in abnormal lipid metabolism in these patients.
○ Treatment
The treatment is essentially supportive with good oxygenation and ventilation in an intensive care environment if indicated. Correction of blood indices may be needed.
Prevention is with operative fixation after early immobilisation, and some operative techniques exist to reduce intraosseous pressure during drilling or reaming to reduce the embolic load.
Some advocate steroid prophylaxis with methylprednisolone for those patients at highest risk, with some evidence to support this. There is no evidence to support the use of steroids as a treatment however. Aspirin may speed recovery of platelets and possibly lung injury.
In this question, the stem highlights the diagnosis of fat embolism syndrome, which most candidates are likely to discern. The real question relates to the most helpful test, in both diagnosis and treatment, which requires a more extensive understanding of
the disease. Special investigations which have been used to assist in the diagnosis do include bronchoscopic alveolar lavage (BAL) for lipid-laden macrophages, and urine
microscopy for lipid, but may not add much over clinical examination particularly given that the patient presents with the tell-tale petechial rash. CT and CXR findings
may be variable, and unlike in prevention, there is no beneficial role for steroids in treatment. The ABG will, however both assist in diagnosis (PaO2 is in all diagnostic criteria) and help the clinician decide on level of respiratory support required.
- A 50-year old woman for elective hand surgery is to have an ultrasound guided
axillary brachial plexus block.
Which of the following would be the most appropriate ultrasound probe to use?
A Curved array probe
B Linear array probe
C Low frequency (2–5 MHz) probe
D Phased array probe
E Hockey stick footprint probe
- B Linear array probe
The use of ultrasound is well established in regional anesthesia and pain medicine.
Ultrasound guided nerve blocks offer potential benefits over landmark technique
including reduced complications and increased success rates.
The diagnostic ultrasound in current medical practice is usually in the range of 1–20
megahertz (mHz).
The ultrasound probe contains a large number of transducers in the form of
piezoelectric crystals. The piezoelectric transducer converts an electrical charge into
an ultrasound wave. The produced ultrasound wave then propagates into the tissues
and is either scattered or reflected back onto the probe. The reflected wave the
piezoelectric crystal again, creating an electrical signal that can be processed and
interpreted by the ultrasound machine to produce an image.
The probe transducers are activated in turn so that the probe is always discharging
or receiving signals when operating. Ultrasound probes may have different shapes:
Linear array probes: High frequency (6–13 MHz) probes where the piezoelectric
crystals are arranged in a line along the surface. They provide the best axial
resolution, however the higher the frequency the more attenuation therefore these
probes have poor penetration. A rectangular ultrasound image is produced and they
are best used for performing superficial blocks like interscalene, supraclavicular and
axillary blocks.
⊙ Curved array probes: Low frequency (2–5 MHz) probes where the crystals are
arranged along a curved surface. They provide lower resolution images when
compared with linear probes. However, they have better penetration and allow
visualisation of deeper structures. Curved array probes are best used for performing deep blocks such as sciatic nerve and infraclavicular brachial plexus blocks. These probes produce wide sector-shaped images with a curved upper and lowe edge.
⊙ Phased array probes: Piezoelectric crystals are fired in phases to produce a sector-shaped image on the monitor with an expanding field of view. These probes are mainly used for echocardiography.
⊙ Hockey stick footprint probes: Also called J-shaped probes. These are a type of linear array transducer that are small in size and therefore ideally used in areas where space is limited or in paediatric patients.
As mentioned, higher frequency linear probes are better for more superficial blocks and lower frequency curved probes are better for deeper blocks. Thus in this clinical scenario, the most appropriate ultrasound transducer is the linear high frequency probe.
- A 38-year-old man has sustained a stab wound in the left flank following an
altercation. In the emergency department he is awake and has saturations of 99%
on room air, a respiratory rate of 25 breaths per minute, a heart rate of 110 beats per minute and a blood pressure of 85/40mmHg. Initial resuscitation has started with intravenous access and blood samples taken. Any other injuries have been excluded apart from a dry puncture wound to the left flank associated with mild abdominal tenderness and no peritonism.
What is the next step in the ongoing resuscitation of this patient?
- C No fluid bolus
This patient has sustained a penetrating abdominal trauma and displays signs of at least class 2 haemorrhagic shock according to ATLS guidelines (see Table 2.3). Initial fluid resuscitation uses the principle of permissive hypotension with the emphasis on early surgery in order to stop the bleeding. The debate regarding choice of fluids rages on, but the definitive management of these patients is crucial. It is therefore
currently accepted that the optimal intervention is to refrain from fluid boluses as long as the patient is conscious and thus perfusing his vital organs. Insertion of an
arterial line is not part of the initial resuscitation, but may be required once operative management is to be undertaken. Conservative treatment and observation might be appropriate in certain abdominal injuries, but in a haemodynamically unstable patient early surgery is indicated.
- A 55-year-old woman with a 1-month history of headaches presents with a
severe headache followed by a collapse. In the emergency department of a large
teaching hospital her Glasgow coma scale (GCS) was 3 and she was intubated
and ventilated appropriately. A CT scan demonstrated a large subarachnoid
haemorrhage (SAH) with blood in the intraventricular system and dilated lateral
ventricles. A CT angiogram demonstrated a large posterior communicating artery
aneurysm. Her pupillary response to light is sluggish.
The most beneficial intervention in this patient would be:
A Immediate transfer to neurosurgical theatre for an extraventricular drain
(EVD)
B Immediate transfer to neurosurgical theatre for insertion of an intracranial bolt monitor
C Immediate transfer to the intensive care unit for medical stabilisation before
embolisation of the aneurysm
D Administration of hypertonic saline and mannitol
E Administration of intravenous phenytoin
- A Immediate transfer to neurosurgical theatre for an extra-ventricular drain (EVD)
The normal intracranial pressure (ICP) in the horizontal position is 7–10mmHg and
the normal waveform mirrors the arterial trace but consists of three peaks (P1-3),
which reflect cardiac contraction, brain compliance (the pressure wave reflected
from the rigid skull) and aortic valve closure respectively (Figure 2.6).
° An ICP >15mmHg is considered pathological, and in head injured patients,
levels >20mmHg are usually treated.
° The Brain Trauma Foundation publishes
clinical guidelines regarding ICP monitoring and actively managing intracranial hypertension is associated with improved survival.
° This patient should initially be managed with an ABC approach, controlling the
airway, ventilating appropriately to maintain PaO2>10 kPa and PaCO2 at around 4.5 kPa while maintaining mean arterial blood pressure to optimise cerebral perfusion pressure (CPP). Other key interventions include ensuring cerebral venous drainage (by avoiding internal jugular vein central lines, endotracheal tube ties and
maintaining a 30° head-up position), ensure normoglycaemia, normothermia and avoiding seizure activity.
The important information given to you in the vignette is that she presented to a
teaching hospital (which you may assume has neurosurgical services). Therefore
it suggests that the first 3 options may be most appropriate. The others may be
important if you are awaiting transfer to a neurosurgical centre. In this case a large
subarachnoid haemorrhage (SAH) with dilated ventricles and sluggish pupillary
response to light is suggestive of obstructive hydrocephalus. Thus the intracranial pressure may be assumed to be high and will only increase without intervention.
As you are assuming there is aneurosurgical service in the teaching hospital, your answer will recommend involving the neurosurgeon as soon as possible. Intracranial monitoring will allow you to titrate the therapies to a measured end-point, which reduces mortality. The options are:
• Extra-ventricular drain (EVD): this is the gold standard, which involves a drain
placed directly into the lateral ventricles via the frontal lobe and is therefore
the most invasive. It allows monitoring of the ICP and waveform morphology,
therapeutic draining of CSF to reduce the ICP and administration of intra-thecal
drugs if required. The complications include bleeding into the frontal lobe and
infection (rate 1–5%). Blockage may occur necessitating a revision.
• Intra-parenchymal monitors are almost as accurate with lower complication rates.
However no therapeutic interventions can be performed with it. t
• The sub-dural bolt is least invasive, has the least complications but is also the least accurate and is used for monitoring only, not therapeutic intervention.
Hyper-osmotic treatments are most useful for management of space-occupying
mass lesions including an intra cranial blood clot. It may also be used as a rescue
measure in this scenario to buy time if there is clinical evidence of impending
cerebral herniation.
Phenytoin is usually administered after the second witnessed seizure.
Nimodipine should be given as early as possible via a nasogastric tube to
prevent vasospasm.
Therefore the most important intervention is inserting a device for monitoring and
intervention, which allows you to optimise the medical management appropriately.
Management of the aneurysm is undertaken once the ICP has been controlled and the aneurysm is secured, forced hypertensive treatment can begin to prevent cerebral infarction related to vasospasm.
The other measures may be used to buy
time prior to an EVD insertion if it is not immediately available.
- A 52-year-old man is admitted to the emergency department one hour ago with worsening shortness of breath, fevers and productive sputum. His observations
include a temperature of 38°C, Spo2 95% on high-flow oxygen, blood pressure
88/49mmHg, heart rate 126 beats per minute and respiratory rate 28 breaths per minute. His arterial blood gas is below (Table 2.1):
Blood cultures have been taken and a dose of co-amoxiclav and clarithromycin has
been administered.
The most appropriate next step would be:
A Intubation and ventilation
B Central venous access and noradrenaline
C Central venous access and measurement of SCv–o2
D Non-invasive ventilation
E 30mL/kg crystalloid bolus
- E 30mL/kg crystalloid bolus
Sepsis is the commonest reason for a patient to be admitted to a critical care unit and therefore the 2012 Surviving Sepsis Guidelines is essential revision.
The bundle of care now mandates:
To be completed within 3 hours
1. Measure lactate level
2. Obtain blood cultures prior to administration of antibiotics
3. Administer broad-spectrum antibiotics
4. Administer 30mL/kg crystalloid for hypotension or lactate ≥4mmol/L
To be completed within 6 hours
5. Apply vasopressors (for hypotension that does not respond to initial fluid
resuscitation) to maintain a mean arterial pressure (MAP) ≥65mmHg
6. In the event of persistent arterial hypotension despite volume resuscitation
(septic shock) or initial lactate ≥4mmol/L (36mg/dL):
• Measure central venous pressure (CVP)
• Measure central venous oxygen saturation (Scv–o2)
7. Re-measure lactate if initial lactate was elevated
This patient has recently been admitted to the emergency department with severe
sepsis probably secondary to pneumonia, though the current history is inadequate
to exclude other causes. He has had antibiotics within one hour following blood cultures. This is optimal care as for each hour delay in antibiotic administration there is a 7.6% increase in mortality from sepsis.
This patient has distributive shock based on cardiovascular parameters and a raised lactate, therefore immediate fluid resuscitation should be commenced as per the Surviving Sepsis Guidelines above. 30mL/kg should be given in the next two hours.
If hypotension persists despite this fluid resuscitation, then noradrenaline should beconsidered titrated to Scv–o2, MAP and CVP. The lactate level should be re-evaluated.
This patient has evidence of a raised alveolar-arterial gradient representing a
probable diffusion defect and ventilation/perfusion mismatch with shunting.
However clinically his predominant problem is hypoperfusion and shock so should be fluid resuscitated in the first instance. Currently he does not have an indication for non-invasive ventilation (NIV) or intubation and ventilation.
- An 18-year-old woman presents to the intensive care unit with diabetic
ketoacidosis (DKA) for which she has had multiple admissions in the past. On
examination her heart rate is 110 beats per minute and her blood pressure is
100/60mmHg. Her Glasgow coma scale (GCS) is 14 (E3, V5, M6). Her laboratory
glucose was 39mmol/L and the arterial blood gas demonstrated the following
(Table 2.2):
Current treatment is an insulin infusion of 5 units/hour and 500mL of intravenous
Hartmann’s solution being administered over 4hours.
How would you alter her treatment on admission to the ICU?
A Reduce the rate of insulin when her blood sugar drops below 30mmol/L
B Increase the insulin infusion by 1 unit/hr if the bicarbonate concentration
remains 3mmol/L after 1hour
C Change the intravenous fluid from Hartmann’s solution to 0.9% sodium
chloride and add potassium 20mmol to be given over 4hours
D Give a fluid bolus of 500mL of crystalloid to assess cardiovascular and
metabolic response
E Start an infusion of bicarbonate 1.26% 100mL/hour to correct the acidosis
until the blood ketone level reduces as a result of insulin therapy
- B Increase the insulin infusion by 1 unit/hour if the bicarbonate concentration remains 3mmol/L after 1 hour
Diabetic ketoacidosis (DKA) is an endocrine emergency that presents in diabetic
patients who do not produce endogenous insulin. Relative or absolute lack of insulin
(endogenous or exogenous) results in a triad of hyperglycaemia, a ketotic state and acidaemia. Eleven percent of Type 1 diabetics presented with DKA in 2004–2009.
Mortality is still 2%, most commonly attributable to cerebral oedema.
Glucose forces renal diuresis and results in profound hypovolaemia. The patient
presents with a metabolic acidosis (often partially compensated by a monumental
minute ventilation) with a large anion gap due to unmeasured blood ketones.
Blood ketones can now be measured at the bedside and indicate severity of disease and response to treatment. The patient is often potassium-deplete which may not
e immediately obvious from initial lab results as a high level of acidosis causes
intracellular potassium ions to migrate into the plasma. As acidosis resolves and
potassium once again returns to the intracellular space, the plasma potassium
concentration decreases rapidly.
Management of DKA in critical care areas focuses on the following issues:
• Fluid management including resuscitation and replacement of ongoing losses
• Blood glucose control and providing glucose once the blood glucose drops below 15mmol/L
• Acidosis and electrolyte management (in particular potassium maintained
between 4 and 5mmol/L)
• Insulin administration and titration
• Septic screening and appropriate antibiotics
• Thromboprophylaxis
• Monitoring for complications including cerebral oedema, sepsis, hypokalaemia,
ischaemic cardiac events, acute kidney injury (AKI) and acute respiratory distress
syndrome
• Management of psycho-social issues
• Involving of specialist teams for ongoing management
The management of DKA has undergone a recent change in 2011 and guidelines
have been published by Diabetes UK. The sliding scale is no longer incorporated and titrating insulin to biochemical markers is the primary objective.
To summarise some of the new recommendations:
A ‘fixed rate’ infusion of 0.1 units/kg insulin should be administered. The rate is no
longer adjusted solely according to blood sugar levels, but to blood ketone levels or
bicarbonate levels.
Aims of treatment are:
• A reduction of 0.5mmol/L/hour blood ketone concentration
• An increase of 3mmol/L/hour of venous bicarbonate concentration
• A reduction of 3mmol/L/hour of blood glucose concentration
If this is being met then the current insulin infusion is to be unaltered regardless
of current blood glucose levels. If treatment goals are not being met the infusion should be increased by 1 unit/hour.
1. DKA protocol should be terminated once pH>7.3, venous plasma bicarbonate
above 18mmol/L and blood ketones <0.3mmol/L
2. If the patient is on long-acting insulin this should be continued simultaneously.
In the above clinical scenario, answer B is the most appropriate option that follows
the suggested guidelines. The other options are also viable, but:
• Option A is following the ‘old’ sliding scale regime, which is used on ICUs for
diabetics and non-diabetics alike (the difference between these groups should be distinguished as the pathology and resulting disease is very different);
• Option C may be performed if you wanted to add potassium but that may not be needed yet;
• Option D is possible but the patient is not hypotensive and lactate is not
significantly raised;
• Option E may be indicated in shock unresponsive to inotropes or if the metabolic acidosis is in part caused by AKI, however administrating intravenous bicarbonate masks one of the biological markers of treatment responsiveness.
It is important to be aware of new guidelines and understand the difference
between managing DKA (providing insulin and glucose to reduce ketosis) and
maintaining normoglyaemia in unwell-adults due to a hormonal stress response
- A 76-year-old patient is admitted to the postoperative care unit (POCU) following
a prolonged and difficult laparotomy for ischaemic bowel. She underwent an
extended right hemicolectomy, associated bowel oedema was noted. Her intra-
abdominal pressure (IAP) is monitored due to her risk of abdominal compartment
syndrome (ACS).
Which of the following would define abdominal compartment syndrome in this
patient:
A IAP >12mmHg with new organ dysfunction
B IAP >16mmHg with new organ dysfunction
C IAP >20mmHg with new organ dysfunction
D IAP >25mmHg with new organ dysfunction
E IAP >30mmHg with new organ dysfunction
- C IAP >20mmHg with new organ dysfunction
This elderly patient is at high risk of developing intra-abdominal complications following a complex laparotomy. Monitoring her intra-abdominal pressure (IAP) provides additional information to her clinical status.
IAP can be measured using direct or indirect methods. A direct method would be to leave a catheter or needle within the abdomen at the end of the laparotomy.
Indirect methods are the commonest measurement technique in the UK. This
involves the intravesical method via a bladder catheter; working on the principle that intravesical pressure is a surrogate for intra-abdominal pressure. One technique
involves introducing sterile saline into the bladder and clamping the catheter
distally. A wide bore needle or cannula is introduced into the bladder catheter via
the culture port and connected to a pressure transduction system. The system
is zeroed at the level of the symphysis pubis. In order to provide an accurate measurement, the reading should be taken in the supine patient at the end of
expiration. The measurement should be repeated four hourly.
Normal IAP is 5–7mmHg. The World Society of the Abdominal Compartment
Syndrome (WSACS) classifies intra-abdominal hypertension as a sustained IAP
>12mmHg. Abdominal compartment syndrome is a sustained IAP >20mmHg with
new organ dysfunction, hence making option C correct.
Risk factors can be subdivided into:
t Intraluminal such as gastroparesis, ileus or pseudo-obstruction
• Extraluminal such as ascites or pelvic tumours
• Decreased abdominal wall compliance such as abdominal surgery with fascial closure, obesity, abdominal burns or trauma
• Capillary leak or excessive fluid resuscitation such as pancreatitis, sepsis or
massive transfusion
This patient is at high risk due to the risk of ileus, risk of capillary leak from a systemic inflammatory response syndrome and reduced abdominal wall compliance following a laparotomy.
The principle of management is to optimise abdominal perfusion pressure. The strategies used broadly fall into medical and surgical categories.
Medical management involves:
1. IAP monitoring if risk factors are present
2. Draining abdominal fluid collections such as ascites or abscesses
3. Reducing intraluminal contents; nasogastric and rectal decompression and the
cautious use of prokinetics
• Improving abdominal wall compliance such as sedation and analgesia with possible neuromuscular blockade and removal of constrictive dressings or escharotomy
• Maintain oxygen delivery with the use of fluid challenges and cardiovascular
support. Excessive fluid administration should be avoided and diuretics may have a role
The main surgical option is decompression via a laparostomy with delayed closure.
Close liaison with the surgical team is mandated in the management of high-risk patients, such as this case, and thresholds ascertained which alert the teams to consider a surgical option.
- A 24-year-old asthmatic presents to the emergency department with wheeze,
shortness of breath and a peak flow which is 20% of his usual. He has had two
courses of steroids in the past year and has been hospitalised twice for acute
asthma. The medical team has asked you to review him as they are worried he is
tiring and not responding to initial treatment.
Which feature is most likely to suggest that this is the case?
A pH of 7.32
B Oxygen saturations of 88% on air
C Unable to complete sentences with single breath
D Responding to voice on the AVPU score
E No improvement despite optimum therapy including a salbutamol infusion
- D Responding to voice on the AVPU score
Asthma is characterised by reversible airways obstruction due to bronchial smooth
muscle contraction, airway inflammation and increased airway secretion production.
Chronic management focuses on a step-wise approach to therapy escalation aiming
for minimal requirement for rescue therapy. Around 1400 people a year still die from asthma despite improvements in chronic management.The definition of the severity of an acute attack can be summarised below (Table 2.4):
The first decision as the anesthetist or intensivist is which category your patient
falls into as this dictates immediate management. The time delay from decision-to-
intubate to actually intubating with all the drugs, equipment and help you need may
be significant and thus it is best to prepare early.
The next decision is whether the patient is on optimum therapy, which for life-
threatening asthma should be:
t Oxygen-driven salbutamol nebulisers 5mg continuously (allocate someone to
monitor and change over the nebuliser when finished). Its worth noting however
if there is little respiratory effort the inhaled drug will just move in and out of
conducting airways and not reach the desired site of action
t Magnesium 2g intravenous infusion over 20 minutes
t Steroid therapy: either oral prednisolone 40mg or hydrocortisone 200mg
intravenous
t Intravenous fluids as the patient may become profoundly dehydrated with
a sustained high respiratory rate being treated with non-humidified oxygen
therapy
• Salbutamol infusion 5–20μg/min titrated to effect
• Aminophylline 5mg/kg loading dose over 20 minutes (if not on oral theophylline)
followed by 0.5mg/kg/min
• Adrenaline infusion is an option but the patient is more likely to require an
anaesthetic before this stage is reached
In the case above the most concerning feature is the drowsiness. Patients with
asthma have a high adrenergic response (otherwise known as fear) and should
be alert. You are not told what treatment the patient is on already. A pH of 7.32 is
worrying if it is a respiratory acidosis but both dehydration and salbutamol therapy
can cause metabolic acidosis, which if being appropriately compensated for, is less worrying. Similarly this patient should be on oxygen as part of their treatment and their oxygen saturations should be judged when receiving appropriate therapy. It is helpful to quantify the ability to speak with the number of words used: obviously unable to utter one word is more worrying than reciting the daily adventures of one’s cat and pausing for breath.
Response to treatment is important and if no improvement is being made, a decision to ‘electively’ intubate may be made.
It is therefore crucial to look at the complete clinical picture and use good judgment in the management of acute asthma. Alteration in consciousness is an ominous sign and should be treated very seriously
- A 31-year-old woman with a history of acute intermittent porphyria presents with
severe abdominal pain. She is tachycardic, hypertensive and vomiting. A diagnosis
of small bowel obstruction is made and she is to go to theatre for a laparotomy.
Which of the following is the best option for her postoperative analgesia?
A Epidural with levobupivacaine and fentanyl
B Titrated intravenous ketamine
C Intravenous morphine
D Oxycodone
E Wound infiltration of 0.25% levobupivacaine
- C Intravenous morphine
The expression ‘porphyria’ encompasses a collection of inherited disorders of haem
synthesis. Haem is a key constituent of haemoglobin and an example of a naturally
occurring porphyrin. Its synthetic pathway consists of a series of enzyme-dependent
steps. Genetic mutation causing a deficit of a particular enzyme in this pathway
results in accumulation of the intermediate substrates that rely on it for their
metabolism.
The primary step in the haem synthetic pathway is the combination of glycine and
succinyl CoA to form the compound 5-aminolevulinic acid (5-ALA) by the action of
ALA synthase. Deficiency of any enzyme downstream from this step will cause the
accumulation of 5-ALA. In all acute porphyrias, 5-ALA levels are elevated. Whether
this itself is the cause of the clinical manifestations of acute porphyria is unclear.
In any form of acute porphyria, an acute neurovisceral crisis may be triggered by
anything that increases the demand for haem, including infection, dehydration,
starvation and drugs. The key presenting features are abdominal pain, neurological
symptoms and tachycardia. As these are rather non-specific presentations, diagnosis
is often made late. In this scenario, it is not a surgical condition causing the patient’s
pain, but this may additionally trigger a porphyric crisis. A number of drugs used in common anaesthetic practice may be unsafe for use
in patients with porphyria. The majority are, in fact, safe, and the Table 2.6 below
summarises drugs that are either known to be dangerous or those which are yet
unclassified for use in porphyric patients.Morphine is a safe, effective, titratable drug that can be used in porphyria, and
would be the drug of choice here. The patient is tachycardic with small bowel
obstruction, and likely to be hypovolaemic. This would preclude the use of an
epidural. Levobupivacaine has indeterminate safety profile so should be avoided
and relying on local infiltration of the surgical wound would not provide lasting
analgesia. Oxydone and ketamine are unsafe.
- A 67-year-old man is admitted to the emergency department with a sudden
onset of severe chest pain and breathlessness. His ECG shows ST elevation in the
following leads: I, aVL and V2–V6.
Which of the following is the most likely affected blood vessel?
A Left anterior descending artery
B Right coronary artery
C Left circumflex artery
D Left coronary artery
E Posterior descending artery
- D Left coronary artery
Sudden occlusion of major coronary arteries is the most common cause of
myocardial infarction (MI). The area of myocardial ischaemia depends on the
coronary circulation. Early recognition of acute coronary obstruction and quick
reperfusion is essential for good outcome after MI.
A good anatomical knowledge is essential for successful MI management (Figure 2.7).
The blood to the heart is mainly supplied by two main coronary arteries (CAs), the
right coronary artery (RCA) and the left coronary artery (LCA).
The RCA arises form the right anterior aortic sinus. It mainly supplies blood to the
right side of the heart. However, the RCA also gives twigs to the right atrium and left
ventricle (LV)
The RCA travels along the right atrioventricular (AV) groove on its way to the crux
of the heart. It gives off the right marginal artery, which descends along the acute
margin of the heart and gives off branches to both sides of right ventricle. The RCA
continues on the diaphragmatic surface of the heart along the posterior longitudinal
sulcus to continue to the apex of the heart as the posterior descending artery (PDA).
The PDA supplies the inferior and the posterior walls of the left ventricle (LV), the
ventricular septum and part of the papillary muscles.
The LCA arises from the left anterior aortic sinus. It supplies blood to the left side
of the heart and it is larger than RCA. It usually runs for 1–25mm as the left main
coronary artery before bifurcating into left anterior descending artery (LAD) and left
circumflex artery (LCX).
The LAD runs in the interventricular groove along the anterior surface of the heart.
It gives off diagonal branches (supply the anterolateral surface) and septal branches
(supply the interventricular septum) on its way toward the apex of the heart.
The LCX primarily supplies the lateral wall of the heart. It runs along the left
atrioventricular groove, reaching as far as the posterior longitudinal sulcus. It gives 1
to 3 marginal branches, which supply the lateral free wall of the LV.
The coronary artery dominance is determined by the artery that gives the posterior
descending artery. In most of patient (85%), the RCA gives off the PDA and the
coronary circulation can be identified as right-dominant. In a left-dominant
circulation, the PDA is given off by the LCX (15% of cases).
A 12-lead electrocardiogram (ECG) looks at the heart from different angles.
The changes seen in the ECG leads adjacent to the ischaemic area usually reflect the
areas of the coronary arteries occluded (Table 2.7).
In this clinical scenario, the patient has acute occlusion of the left coronary artery
(anterolateral V2-V6, I and aVL). This lesion results in rapid deterioration of the patient condition because it usually leads to entire LV infarction. These patients have
a poor prognosis if not treated immediately.
