Section 1 Flashcards
You have been asked to review a 36-year-old man who has fallen
against a radiator and sustained a penetrating injury to his right eye.
He has a past medical history of learning difficulties and poorly controlled epilepsy with one to two fits per week, on average. He has also recently been referred to a sleep studies clinic.
He is conscious in A&E and responding to questions appropriately, despite being clearly distressed. The caregiver who is with him did not witness the fall but says
that other than his eye injury, he appears to be otherwise acting normally.current medication Carbamazepine 600 mg tds
Levetiracetam 1.5 g bd
Vigabatrin 1g bd
Quetiapine 300 mg od
Lorazepam 2–4 mg PRN
clinical examination Weight 135 kg
Height 175 cm
BMI 44 kg/m2
Heart rate 80/min
Respiratory rate 16/min
BP 165/90 mmHg
Temperature 36.5 °C
He is overweight with a large jaw and thick beard. Airway examination
reveals poor dentition, a large tongue, and a Mallampati score of 3.
Blood investigations Awaited
Arterial blood gas pH 7.38
po2 8.69 kPa
pCo2 6.98 kPa
BE +4.8
HCo3 32 mmol/L
Hb 17 g/dl
sleep studies
done two months ago
The polysomnogram demonstrated an apnoea-hypopnoea index (AHI)
of 15 events/hr and a nadir oxygen saturation of 78%; supine AHI was
44 events/hr. Definitive obstructive events were not observed in the non-
supine position. The total sleep time was 337 minutes, with a sleep time
in the supine position of 113 minutes. A 2-minute epoch from the patient’s
polysomnogram is shown in Figure 1.2.
1. Summarise the case.
• 36-year-old man with penetrating eye injury
• Poorly controlled epilepsy and learning difficulties
• Untreated obstructive sleep apnea (OSA)
• Obese with potentially difficult airway
• Potential liver and renal function impairment due to antiepileptic drugs
comment on the chest X-ray
obvious abnormality is the presence of a vagal nerve stimulator
• Reduced lung volumes
• Lung fields otherwise clear except haziness in left lower border
• Normal heart borders, borderline cardio thoracic ratio
How does a vagal nerve stimulator work?
• Pulse generator/stimulator that sends regular, mild electrical stimuli to the vagus nerve
• Used in drug-resistant epilepsy, particularly partial seizures and treatment-resistant depression
• Often not immediately effective and rarely prevents seizures entirely
• Battery-powered so requires changing every 5–10 years
What are the anaesthetic implications for patients with epilepsy?
• Increased incidence of seizures perioperatively—multifactorial
• Continue anti-epileptic drugs (AEDs) with minimal fasting period (or use parenteral alternative)
• Caution regarding AEDs—hepatic enzyme metabolism and other drug
interactions
correlate and comment on the
ABG and sleep studies result.
Arterial blood gas pH 7.38
po2 8.69 kPa
pCo2 6.98 kPa
BE +4.8
HCo3 32 mmol/L
Hb 17 g/dl
• Hypoxaemia, hypercapnia, and polycythemia, related to OSA
• Metabolic compensation (chronic disease)
• Apnea/hypopnea index indicates severe OSA
What is AHi? How can you classify the severity of osA?
AHi
○ AHI is the number of apneas or hypopneas recorded during the study per
hour of sleep.
○ It is generally expressed as the number of events per hour.
○ Based on the AHI, the severity of OSA is classified as follows:
• None: < 5 per hour
• Mild: 5–14 per hour
• Moderate: 15–29 per hour
• Severe: ≥ 30 per hour
○ Oxygen Desaturation
○ Desaturations are recorded during polysomnography.
○ Although there are no generally accepted classifications for severity of oxygen desaturation, reductions to not less than 90% usually are considered mild.
° Dips into the 80%–89% range can be considered moderate, and those below 80% are severe.
What symptoms suggest a diagnosis of osA?
• Snoring
• Daytime somnolence
• Early morning headaches
• Dry or sore throat upon waking
• Poor concentration and irritability
What scoring systems are used
for screening for osA?
stoP BAnG questionnaire
• Snoring
• Tired—daytime tiredness or fatigue
• Observed apnoea during sleep
• Pressure (blood)—treatment for hypertension
• BMI more than 35 kg/m2
• age over 50 years
• neck circumference greater than 40 cm
• Gender—high prevalence in male gender
○ Epworth sleepiness scale
• The questionnaire looks at the chance of falling asleep on a scale of increasing probability from 0 to 3 for eight regular activities during their daily lives.
• The scores for the eight questions are added together to obtain a single number.
• Normal: 0–9; mild to moderate sleep apnea: 11–15; severe sleep apnea: 16 and above
○ Berlin questionnaire
• Patients can be classified into high or low risk based on their responses to similar questions.
What are the risk factors for osA?
• Obesity
• Male gender
• Age > 40 years
• Neck circumference > 17 inches
• Family history of OSA
What are the complications Or associations of osA?
cardiac
• Treatment-resistant hypertension
• Congestive heart failure
• Ischaemic heart disease
• Atrial fibrillation
• Dysrhythmias
Respiratory
• Asthma
• Pulmonary hypertension
Gi
• Gastro-oesophageal reflux
neurological
• Stroke
Metabolic
• Type II Diabetes Mellitus
• Hypothyroidism
• Morbid obesity
What are the anaesthetic
implications for patients with
osA?
sedative premedication
• Avoid sedating premedication
• Alpha-2 adrenergic agonist (clonidine, dexmedetomidine) may reduce
intraoperative anaesthetic requirements and have an opioid-sparing effect
Difficult airway
• Ramp from scapula to head as patient is obese
• Adequate preoxygenation
• Associated gastro-oesophageal reflux disease—consider proton pump
inhibitors, antacids, rapid sequence induction with cricoid pressure
Analgesia
• Minimise use of opioids for the fear of respiratory depression
• Use short-acting agents (remifentanil)
• Regional and multimodal analgesia (NSAIDs, acetaminophen, tramadol,
ketamine, gabapentin, pregabalin, dexamethasone)
Anaesthetic technique
• Carry-over sedation effects from longer-acting intravenous sedatives and
inhaled anaesthetic agents
• Use propofol/remifentanil for maintenance of anaesthesia
• Use insoluble potent anaesthetic agents (desflurane, sevoflurane)
• Use regional blocks as a sole anaesthetic technique (not in this case!)
Monitoring
• Use intraoperative capnography for monitoring of respiration (mandatory
anyway!)
• Arterial line if OSA associated with cardiac dysfunction
Postoperative period
• Verification of full reversal of neuromuscular blockade
• Ensure patient fully conscious and cooperative prior to extubation
• Non-supine posture for extubation and recovery
• Resume use of positive airway pressure device with close monitoring
post-operatively
• May require HDU/ITU admission
What are your concerns of anaesthetising this patient now?
• Newly diagnosed hypertension
• Urgency of surgery—discuss with surgeons but likely to be urgent rather
than an emergency
• Exclude other trauma, especially neck and intracranial
• Anaesthetic technique in view of potentially difficult airway
• Control of intraocular pressure
• Post-operative care—will need HDU/ITU bed
What would be your induction technique and airway
management plan for this patient?
• Ideally get help—two anaesthetists present
• Awake fibreoptic intubation unlikely to be suitable (coughing, distressed, learning difficulties)
• Allow for adequate starvation time if possible
• Preoxygenate in ramped position
• Modified rapid sequence induction with rocuronium (ensuring sugammadex available) may be most appropriate
• Use of video laryngoscopy may be ideal
The patient is now extubated and in recovery. You are called to review him
because he is agitated
What are the possible causes and how might you manage them?
• Pain: analgesia
• Inadequate reversal of muscle relaxant: check the TOF count and use reversal
• Drug-induced, e.g. atropine, opioids: review anaesthetic chart
• Hypercapnia: treatment of sedative/opioid toxicity, airway manoeuvres, and adjuncts if obstructed
• Hypoxia: O2, airway manoeuvres, and adjuncts if obstructed
• CPAP likely to be contra-indicated due to eye injury
What is your approach to deep vein thrombosis (DVt) prophylaxis in this patient?
• High risk for DVT—obese, polycythaemic
• Mechanical prophylaxis
• Early mobilisation
• Balance risk versus benefit of anticoagulation in eye trauma—get specialist help regarding the plan
An 80-year-old male patient presents to pre-assessment clinic for SCC removal on his forehead. He complains of dizzy spells. The pre-assessment nurse wants to know what to do. See Figure 1.3.
What does the ecG show?
• Regular P waves and QRS complexes are seen but are unrelated to each other
• No QRS widening
• Voltage criteria for LVH
• No obvious features of coronary ischaemia
○ The ECG shows third-degree AV block, with a ventricular rate of 34/min
What are the causes of complete heart block?
Congenital
• With maternal antibodies to SS-A (Ro) and SS-B (La)
Acquired
• Drugs: quinidine, procainamide, disopyramide, amiodarone, β blockers
• Infection: Lyme disease, rheumatic fever, Chagas disease
• Connective tissue disease: ankylosing spondylitis, rheumatoid arthritis, scleroderma
• Infiltrative disease: amyloidosis, sarcoidosis
• Neuromuscular disorders: muscular dystrophy
• Ischaemia: e.g. AV block associated with inferior wall MI
Iatrogenic
• AV block may be associated with aortic valve surgery, PCI
Would you anaesthetise him now? Pacemaker failure symptomatic brady
No. Patient is at high risk of severe peri-operative bradycardia leading to cardiac decompensation, or even cardiac arrest.
• He requires referral to a cardiologist, and probably electrical pacing, ideally with a permanent pacemaker.
• Further cardiac investigations to determine the cause (e.g. angiogram) and to establish his baseline cardiac function (e.g. echocardiogram) would also be helpful.
• If the surgery is deemed too urgent to wait for further investigation and PPM implantation, other options include a temporary pacing wire, or
pharmacological chronotropy via an isoprenaline infusion.
How would you manage pacemaker failure if occurred intraoperatively?
○ Ask surgeons to stop, check correct attachment of monitoring, and feel for a pulse.
○ If there is no pulse palpable, start CPR and then treat the underlying problem.
Pharmacological options
• Trial of antimuscarinic drugs (e.g. atropine or glycopyrollate)
• Carefully titrated adrenaline boluses (10–100 mcg)
• Isoprenaline infusion (β-agonist): 0.02–0.2 mcg/kg/min
Electrical/mechanical options
• Percussion pacing using a clenched fist (rarely achieves electrical capture)
• Transcutaneous external pacing via defibrillator pads; increase current until electrical capture achieved. Set rate at 70–80 bpm
• If pharmacological measures fail to restore an adequate heart rate, a temporary pacing wire (inserted via a central line) will probably be
necessary, but this takes time to organise (and should be done under aseptic conditions by an appropriately trained cardiologist under X-ray
guidance)
• Transoesophageal pacing is also possible but similarly requires specialist equipment and expertise to set up
As for all emergencies, management would also require simultaneous rapid assessment/management of airway and breathing/ventilation
- Is airway patent? Give 100% o2, check ETT/LMA position
- Is oxygenation/ventilation intact? Manually ventilate patient, check for bilateral chest rise, air entry on auscultation, EtCo2, misting of ETT, and saturation
- Remember to maintain anaesthesia while you sort out the new-onset complete heart block!
What are the indications for
insertion of a permanent
pacemaker?
• Any symptomatic bradycardia (i.e. causing collapse/syncope/presyncope)
• Complete heart block
• Mobitz type II block
• Sick sinus syndrome
• Hypersensitive carotid sinus syndrome
• Symptomatic bradycardia in transplanted heart
• Severe heart failure (cardiac resynchronisation therapy)
• Some patients with dilated or hypertrophic cardiomyopathy
Indications for temporary pacing?
• Any symptomatic bradycardia (i.e. causing collapse/syncope/presyncope)
• Complete heart block
• Mobitz type II block
• Sick sinus syndrome
• Hypersensitive carotid sinus syndrome
• Symptomatic bradycardia in transplanted heart
• Severe heart failure (cardiac resynchronisation therapy)
• Some patients with dilated or hypertrophic cardiomyopathy
• Acute myocardial infarction causing asystole/bradyarrhythmia that entails haemodynamic compromise
• Drug overdose (e.g. β-blockers, calcium channel blockers, digoxin)
• Surgery/general anaesthesia for patients with stable heart block not causing haemodynamic compromise but potentially at risk of worsening bradycardia/asystole
• Following cardiac surgery (usually involves placement of epicardial
pacing wires, rather than transvenous pacing wire, at end of surgery by
surgeons)
What features are associated
with a high risk of asystole?
• Pauses of >3 seconds
• Previous asystolic episodes
• Complete heart block with wide QRS complexes
What do you want to know
before anaesthetising a
patient with a PPM?
Preoperative assessment should be aimed at finding answers to the following questions:
• Indication of pacemaker insertion
• Check date (Does it need checking again before theatre?)
• Is the patient pacing dependent?
• Type of PPM (unipolar/bipolar, number of leads, biventricular/univentricular, etc)
• Programmed mode
Investigations/preparation
• All patients should have CXR (to show PPM position and number of leads)
• ECG: look for pacing spikes before each QRS to determine whether pacing-dependent
• Correction of any electrolyte abnormalities (which may cause loss of capture)
• Switched to fixed rate mode if necessary
• PPM check if any doubts re: function/battery life/failure of capture, etc.
• May need to arrange cardiac-monitored bed post-op (plus another PPM check)
What hazards arise in theatre in patients with a PPM?
• Electromagnetic interference (mainly from monopolar diathermy) may reprogram the PPM (usually into a fixed rate back-up mode) or inhibit
pacing inappropriately. To reduce the risk of PPM malfunction, use bipolar diathermy. If monopolar diathermy is unavoidable, the pad should
be placed as far as possible from PPM; diathermy current should flow perpendicular to PPM current.
• Patient shivering, fasciculations following suxamethonium, and sources of vibration may cause inappropriate ‘sensing,’ which will inhibit pacing or rate modulation (if not previously switched to fixed rate mode).
• PPM may be dislodged during patient positioning or CVP line insertion.
• Theoretical risk of microshock via PPM lead, which may induce
arrhythmia.
• All PPM-dependent patients are at risk of asystole or bradyarrhythmias if the PPM fails for any reason. Emergency drugs and pacing facilities (as
discussed above) should therefore be readily available.
other potential questions for this case
Physiology of cardiac conduction
Hazards associated with diathermy
ICD and anaesthesia—NPSA guideline
comment on the most obvious finding in the film.
Nasogastric tube is above the diaphragm and follows the course of the right lower lobe bronchus
Would you authorise the tube
for enteral feeding?
No
How can the NG tube position be confirmed?
National Patient safety Agency alert/nice guideline
• Use pH paper.
° pH < 5.5 indicates gastric placement.
° If > 5.5, or no aspirate, change patient position and check in an hour.
• X-ray is recommended only if the pH test fails.
The position of all nasogastric tubes should be confirmed after placement
and before each use by aspiration and pH graded paper (with X–ray if
necessary) according to the NPSA guideline.
What are the normal nutrition requirements for a healthy person?
○ Measuring energy use requires sophisticated equipment, so nutrition requirements are estimated using formulae.
○ The Harris Benedict Equation estimates basal metabolic rate (BMR) in kcal/day.
• In men: BMR = 13.75 × weight (kg) + 5 × height (cm) − 6.78 × age (years)
+ 66
For women: BMR = 9.56 × weight (kg) + 1.85 × height (cm) − 4.68 × age
(years) + 655
For an afebrile healthy individual, this is around 25 kcal/kg/day.
Conditions such as fever, sepsis, surgery, and burns increase the requirements.
european society of Parenteral and enteral nutrition (esPen)
The total energy requirements of critically ill patients are given in recent guidelines issued by the ESPEN in 2006.
• Acute initial phase of critical illness: 20–25 kcal/kg/day
• Recovery/anabolic phase: 25–30 kcal/kg/day
• Protein around 1.5 g/kg/day (2g/kg/day in severely catabolic patients).
• lipid should be limited to 40% of total calories.
• Carbohydrate makes up the remaining calorie requirements.
○ Glutamine, arginine, fish oils, and ribonucleotides; antioxidants including Vitamins C and E; selenium and other trace elements are considered useful for immunonutrition.
Sodium 1.0–2.0 mmol/kg/day
Potassium 0.7–1.0 mmol/kg/day
Calcium 0.1 mmol/kg/day
Magnesium 0.1 mmol/kg/day
Chloride 1–2 mmol/kg/day
Phosphate 0.4 mmol/kg/day
Define malnutrition.
Malnutrition is the condition that develops when the body does not get the right amount of vitamins, minerals, and other nutrients it needs to maintain
healthy tissues and organ function.
What is he at risk of? Malnourished
Malnutrition is associated with increased morbidity and mortality.
• Increased risk of infection and pulmonary oedema
• Reduced ventilatory drive
• Impaired production of surfactant
• Prolonged weaning due to muscle fatigue
• Impaired wound healing
• Delayed mobilisation resulting from weak muscles
Look at the ecG strip provided and explain the mechanism.
This is because of the autonomic surges that happen at the onset and
maintenance of ECT, which is described below.
only parasympathetic symptoms are shown in the ECG
shown below is the ct of
abdomen at the level of t12.
orientate yourself with the
different organs at this level.
Look at the second ct image
provided in Figure 1.6. What is
your diagnosis?
Diagnosis: Intraperitoneal and retroperitoneal free gas
Tip: Using lung windows makes free gas easier to visualise.
Look at the third ct image in
Figure 1.7. comment on the
liver texture.
Diffuse fatty liver. The liver is of low density in keeping with fatty infiltration.
(Tip: Use the spleen for comparison. The liver density should be equal to or
higher than the spleen.)
What is the significance of various
types of divisions of the liver?
Anatomical division
• Divided into right and left lobes by the falciform ligament, with the
caudate and quadrate lobes arising from the right lobe
• No clinical or surgical significance
Surgical divisions (corinaud’s classification)
• Total of eight independent segments
• Each segment has its own blood supply and biliary drainage, so they can
be resected without damage to the adjacent segments
Functional classification
Liver lobule is the structural unit of liver. See Figure 1.8
• Classic lobule
° Based on direction of blood flow
° Hexagonal structure with the central vein in the middle and portal
triad (branches of portal vein, hepatic artery, and bile duct) in the six
corners. The hepatic arterial and portal venous blood flows from portal
triad to the central vein
• Portal lobule
° Based on direction of bile flow
° The portal triad is in the middle and the central veins form the corners
of the triangle
• Hepatic acinus
° Based on changes in oxygen and nutrient content as blood flows from
the portal triad to the central vein
° It is rhomboid tissue as shown in the image, containing two triangles of
adjacent classic lobule, whose apices are the central veins
° Hepatocytes in the acinus are divided into three zones
° Zone 1 or periportal zone, where the blood supply is the highest.
This zone is susceptible to damage by blood-borne toxins and
infection
° Zone 2 or intermediate zone
° Zone 3 or centrilobular zone is closer to the central vein. This area
is higher in CYP 450 levels but gets the least blood supply and is
susceptible to ischaemia
What is the principle behind the
working of MRi? see Figure 1.9.
• Unpaired protons in the body (mostly H+ atom in water—abundant) align
randomly and act as bar magnets
• When placed in an external static magnetic field (A), the protons align
• When another magnetic field (B) is applied, the protons are turned out of
alignment
• When this magnetic field is intermittently turned off and on, the
radiofrequency energy taken up by the protons are released before the
realignment takes place. Also there is some ‘Precession’—a wobbling
motion that occurs when a spinning object is subject to an external force.
• This energy released is measured by a set of 3-dimensional orthogonal
gradient coils in the MRI machine
• The energy released by protons in different tissues is different, and hence
a 3-dimensional image with varying intensity is formed
some numbers
• Earth’s magnetic field = 0.5–1.0 Gauss
• 10,000 Gauss = 1 Tesla
• MRI requires magnetic fields between 0.2–3 Tesla (30,000 times the
earth’s magnetic field)
• MRI Safe zone < 5 Gauss
• > 5 Gauss—pacemakers will malfunction and all personnel need
screening
• MRI Conditional zone—50 Gauss
• > 50 gauss—ferro magnetic objects become projectiles and monitors
malfunction
