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
What are the complications of enteral nutrition?
Mechanical
• Obstruction, discomfort
• Ulceration
Metabolic
• Dehydration or overhydration
• Hyperglycaemia
• Electrolyte imbalance
Gastrointestinal
• Gastric stasis/retention, nausea, vomiting, diarrhoea, bloating
• Aspiration pneumonia due to gastro-oesophageal reflux
What is refeeding syndrome?
○ Group of metabolic disturbances that occur after reinstitution of nutrition in a patient who has been malnourished for a prolonged period.
• Usually starts 4 days after initiating feeding
• Characterised by severe hypophosphataemia and life-threatening complications such as cardiac and respiratory failure, seizures, coma,
rhabdomyolysis, and haematological disturbances
What is the underlying pathology of refeeding syndrome?
• Shift occurs from fat to carbohydrate metabolism
• This causes sudden increase in insulin levels, which in turn increases cellular uptake of phosphate and precipitous fall in extracellular phosphate
• Levels of K, Mg also fall, leading to heart failure
How do you know if the patient is absorbing feeds?
The presence of the following features suggest nonabsorption of feeds:
• Increased aspirate from NG tube
• Nausea and vomiting
• Bloating, abd
What do you do if patient is not absorbing feeds?
• Check correct position of NG tube.
• Ensure 45° head-up position.
• Use prokinetics.
• Institute a high-fibre diet for diarrhoea.
• Start parenteral route.
After your morning list, the duty anaesthetic consultant asks you to cover the afternoon Electroconvulsive Therapy (ECT) list because the usual consultant has to cover emergency theatre. You eventually locate the ECT room in the mental health unit, which you’ve never visited before.
The first patient is a 63-year-old man who is undergoing his second course of
ECT. No previous notes are available, apart from those from his most recent ECT
last week (including the anaesthetic chart).
What is ect, and how does it work?
ECT, having been in clinical use since the late 1930s, is the treatment
for various psychiatric disorders and involves artificially inducing a brief
generalised tonic-clonic seizure. The exact mechanism is still unclear,
although a common (and probably oversimplified) view is that a tonic-clonic
seizure ‘resets’ or ‘jumpstarts’ neuronal transmission (in a similar way DC
cardioversion does for the heart).
What are the indications for ect?
• Depressive illness: failed medical therapy
• Mania: refractory cases
• Schizophrenia
• Parkinson’s disease
• Neuroleptic malignant syndrome
• Delirium
How is it performed?
In the UK, it involves induction of general anaesthesia, and usually partial
muscle relaxation, before inducing a generalised tonic-clonic seizure by
passing a brief current of 30–45 J between two electrodes on either side of the patient’s skull (bilateral ECT), or more commonly over one side only
(unilateral) over 0.5–1.5 seconds
What are the main anaesthetic issues associated with ECT?
Remote site anaesthesia
• Unfamiliar environment and staff
• Potentially old/unfamiliar equipment (which may not have been checked
recently)
• Inconsistent anaesthetic support (ODP)
The overall aims of anaesthesia are
• To induce rapid onset, brief general anaesthesia, with partial muscle
relaxation to reduce the risk of limb injury during convulsions
• To avoid raising the seizure threshold (which may make seizures harder to
induce and/or shorter in duration, which in turn may make the ECT less effective)
• To minimise physiological effects of ECT
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
What are the main physiological
effects of ECT?
cardiac
• Initial parasympathetic discharge, lasting 10–20 seconds; bradycardia,
hypotension, and asystole may occur.
• Followed by sympathetic surge, leading to increased heart rate, blood pressure, and myocardial oxygen demand.
• Potential for myocardial ischaemia or infarction, especially in those with preexisting LV impairment or coronary artery disease.
cerebral
• Increased cerebral O2 consumption, blood flow, and ICP
• Post-procedure cognitive deficits are common: post-ictal confusion,
drowsiness, retrograde and anterograde amnesia commonly occur.
other
• Raised intraocular and intragastric pressure are not thought to be
clinically significant.
• Dental damage, tongue/lip lacerations may occur due to jaw clenching.
• Headache and myalgia.
• Fractures are rare now, due to widespread use of muscle relaxants.
What are the key points in
preoperative patient
assessment for ECT?
• Often poor historians with multiple comorbidities (IHD, COPD, etc)
• No absolute contraindications exist, but most anaesthetists would
consider an MI or CVA within the previous 3 months, or raised ICP, to
place the patient at high risk of further cardiac or cerebral events
• Drug therapy may have anaesthetic implications (lithium, MAOI, etc)
• Patients may not have followed fasting instructions
• All patients should ideally be investigated and optimised as for any procedure; however, if ECT is deemed semi-urgent, the risks of delay must again be balanced against the benefits of optimising comorbidities
How would you conduct your
anaesthetic? ECT
induction
• Check patient, full monitoring, appropriate assistance and equipment as
per AAGBI
• Intravenous access and pre-oxygenation
• Induction agent: ‘minimal sleep dose’, to minimise effects on raising
seizure threshold. Methohexital used to be commonly employed but is no
longer available; propofol is a common choice; etomidate reduces seizure
threshold but affects adrenal hormone synthesis
• Short-acting opioids may allow dose of induction agent to be reduced
and blunt haemodynamic responses
• Muscle relaxants: suxamethonium 0.5 mg/kg commonly used. If
contraindicated, consider mivacurium (or rocuronium followed by
emergence
• Once seizure terminates, ventilation can be supported manually until
anaesthesia and muscle relaxation start to wear off and spontaneous
ventilation resumes
• Keep oxygen applied, and transfer to recovery
• Monitor standards and recovery facilities same as in a normal
postoperative care unit
• Anticipate post-op confusion/agitation
sugammadex if available)
if severe bradycardia occurred,
how would you treat it?
• Check monitoring still attached
• Feel for pulse
• Give atropine 3 mg stat bolus (followed by 10–20 mL flush!)
• Commence CPR and put out crash call if no pulse palpable
• Document on anaesthetic chart and consider prophylactic glycopyrrolate
next time
What drug therapy may
influence your anaesthetic?
Lithium
• Used mainly in bipolar disorder
• Decreases the central and peripheral neurotransmitters and may prolong
depolarising neuromuscular blockade
• May cause nephrogenic diabetes insipidus
• Has a narrow therapeutic index and signs develop at > 2.0 mmol/L.
Signs of toxicity include lethargy or restlessness initially; then tremor,
ataxia, weakness and muscle twitching, hypokalaemia, arrhythmias, renal
failure, convulsions, and coma
ssRis
• May cause SIADH: low [Na+]
MAois
• Potential for hypertensive crisis if used with sympathomimetics (mainly
indirectly acting, i.e. metaraminol, ephedrine)
• Caution with opioids (unpredictable effects with pethidine; morphine and
fentanyl thought to be safe)
• Irreversibly inhibit MAO, so consider stopping 2 to 3 weeks pre-
procedure if concerned about anaesthetic interactions
other potential questions
related to this case
Remote site anaesthesia
What do you understand by
the term t10?
• Vertebral level
Anatomical level of T10 vertebra
• Dermatomal level
° Dermatome is the area of skin whose sensory innervation is derived
from a single spinal nerve (dorsal root)
° Not the same as vertebral body level but refers to the cutaneous area
at the level of umbilicus
• Myotomal level
° Muscle distribution of a single spinal nerve (ventral root)
° T10 myotome includes the abdominal muscles
° Useful in clinical and electromyographic localisation of radicular lesion
causing motor defect
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.
What are the common causes
of pneumoperitoneum?
spontaneous
• Perforated hollow viscus
• Secondary to bowel obstruction
• Secondary to peptic ulcer
iatrogenic
• Endoscopic perforation
• Secondary to mechanical ventilation
• After laparotomy and laparoscopy
Miscellaneous
• In females, the fallopian tube acts as a conduit between the vagina and
the peritoneal cavity
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 are the causes of liver
lesions?
Benign lesions
• Simple cysts
• Abscesses
• Hepatic adenoma
• Focal nodular hyperplasia
Malignant lesions
• Hepatocellular carcinoma
• Cholangiocarcinoma
• Angiosarcoma
Miscellaneous
• Fatty liver
• Cirrhosis
tell me about the liver.
The liver is the second largest organ (second to skin).
Weight is 1500 g, which accounts for 2.5% of body weight.
• Hepatocytes are polyhedral epithelial cells arranged in sheets separated
from each other by spaces filled with hepatic sinusoids
• Hepatic sinusoids are vessels that arise at the portal triad and run
between sheets of hepatocytes receiving blood from the portal triad to
deliver to central vein
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 special about the blood
supply of the liver?
Liver has a dual blood supply.
Total liver blood flow = 1200–1400 mls/min
= 25% of cardiac output
It contains 10%–15% of the total blood volume, thereby acting as a powerful
reservoir.
Hepatic artery
• High-pressure/high-resistance system
• Branch of the coeliac trunk (branch of abdominal aorta)
• Carries oxygenated blood
• 20%–30% of total blood supply
• 40%–50% of total oxygen supply
Portal vein
• Low pressure/low resistance
• Formed by the union of superior mesenteric vein and splenic vein
• Carries oxygen-poor but nutrient-rich blood from the abdominal viscera
• 70%–80% of total blood supply
• 50%–60% of total oxygen supply
Deoxygenated, detoxified blood exits the liver via hepatic veins to join the
inferior vena cava.
What are the factors that
determine the hepatic
blood flow?
Like any other ‘factors affecting blood flow’ question, have a general
classification of factors. (I have listed here the factors in no order of
importance.)
Myogenic autoregulation
• Applicable only to the hepatic arterial system in metabolically active liver
Metabolic/chemical control
• CO2, o2, and pH changes can alter the hepatic blood flow
• Postprandial hyperosmolarity increases the hepatic arterial and portal
venous blood flow
neural control
• Autonomic nervous system via the vagus and splanchnic nerves also
control the hepatic blood flow
• An important example is the stimulation of the sympathetic system in
haemorrhage resulting in constriction of arterioles and expulsion of blood
into the general circulation, thus acting as a major reservoir of blood
Humoral control
• Adrenaline, angiotensin II, and vasopressin are the main constrictors of
the arterial and venous system
Hepatic arterial buffer response (HABR)
• Phenomenon where decrease in portal venous blood flow increases
the hepatic arterial blood flow and vice versa so that a constant oxygen
supply and total blood flow is maintained
• The mechanism of HABR is unknown, but the local production of
adenosine is predicted to be one of the causative factors
What are the functions of the
spleen?
• Immune responses: formation of plasma cells and lymphocytes
• Phagocytosis
• Haematopoiesis: in foetus
• Lymphopoiesis: throughout
• Storage of red cells: 8% of the circulating red cells are present in spleen
What are the causes of
splenomegaly?
• Infection: malaria, infectious mononucleosis
• Malignancy: lymphomas, leukaemia
• Portal hypertension
• Sickle cell disease
• Collagen vascular diseases
• Polycythemia
Indications for splenectomy
• Trauma
° Commonest organ injured in blunt abdominal trauma
° Associated with lower rib fractures
• Hypersplenism
° Hereditary spherocytosis
° Idiopathic thrombocytopenic purpura
• Tumour
° Lymphoma or leukaemia
• Surgical
° Along with gastrectomy, pancreatectomy, etc.
• Others
° Splenic cysts and abscess
° Hydatid cysts
What do you understand by oPsi?
overwhelming post-splenectomy infections (oPSI)
• Infection due to encapsulated bacteria: 50% mortality
• Organisms
° Strep. Pneumoniae
° Haemophilus influenza
° Neisseria meningitides
• Occurs post-splenectomy in 4% patients without prophylaxis
Prevention of oPSI
• Antibiotic prophylaxis
° Penicillin (amoxicillin)
° Lifelong
° Prophylaxis required in children up to 16 years
• Immunisation
° Pneumococcal, haemophilus, and meningococcal
° Perform 2 weeks prior to planned operation
° Immediately post-op for emergency cases
° Repeat every 5 to 10 years
What are the physiological
changes seen after brainstem
death?
The reasons for the altered pathophysiology of the heart-beating brainstem
dead person can be due to
• Primary pathology suffered by the patient
• Complications of ITU treatment (mainly the resuscitation of the injured
brain)
• Specific physiological changes and a systemic inflammatory response
caused by the brainstem death
cardiovascular changes
• Initial changes: The first change to occur is the increase in intracranial
pressure (ICP). Mean arterial pressure increases to maintain cerebral
perfusion in parallel with the increasing ICP. Later brain herniation causes
ischaemic changes in brainstem and a hyper-adrenergic state. This
in turn increases both pulmonary and systemic vascular resistance.
Episodes of ‘sympathetic storm’ of variable duration occur with
tachycardia, vasoconstriction, and hypertension, which can lead to
myocardial ischaemia. Hypertension and bradycardia (Cushing’s reflex)
occur in some patients secondary to reflex baroreceptor activation and
activation of the parasympathetic nervous system
• Subsequent changes: Cerebral herniation leads to loss of spinal cord
sympathetic activity, reducing vasomotor tone, preload, and cardiac
output. This is more consistent and called ‘syndrome with marked
vasodilation and relative hypovolaemia’. Myocardial perfusion can be
affected due to low aortic diastolic pressure
other changes
• Ischaemia to pituitary causes diabetes insipidus, fluid and electrolyte loss,
leading to further cardiovascular instability
• Reduced metabolic rate, loss of hypothalamic control and vasodilatation
results in heat loss and hypothermia
• Coagulation abnormalities can occur due to original pathology and
release of coagulation activators from the necrotic brain tissue and
hypothermia
• Posterior pituitary function is lost, but anterior pituitary function is
preserved. There is reduction in T3 levels with normal TSH levels
What are the contraindications
of organ donation?
In order to ensure that donations are as safe as possible, the donor’s
medical and behavioural history is reviewed to reduce the risk of transmitting
disease to a patient. There are many absolute contraindications for various
tissue donations, but there are only two absolute contraindications for organ
donation along with organ specific contraindications.
Absolute contraindications for organ donation
• Known or suspected new variant CJD and other neurodegenerative
diseases
• Known HIV disease, not HIV infection alone
Relative contraindications for organ donation
• Disseminated malignancy
• Treated malignancy within 3 years (except non-melanoma skin cancer)
• Age >70 years
• Known active TB
• Untreated bacterial sepsis
organ and tissue specific contraindications
Lungs
• Donor age >65
• Previous intra-thoracic malignancy
• Significant, chronic destructive or suppurative lung disease
• Chest X-ray evidence of major pulmonary consolidation
Liver
• Acute hepatitis (AST >1000 IU/L)
• Cirrhosis
• Portal vein thrombosis
Kidney
• Chronic kidney disease (CKD stage 3B and below; eGFR <45)
• Long-term dialysis
• Renal malignancy
• Previous kidney transplant (> 6 months previously)
Pancreas
• Insulin-dependent diabetes (excluding ICU-associated insulin
requirement)
• History of pancreatic malignancy
Heart
• Age >65
• Documented coronary artery disease
• Median sternotomy for cardiac surgery
• LVEF ≤ 30% on more than one occasion
• Massive inotropic or vasopressor support
You have confirmed brainstem
death. How would you proceed
with organ donation?
Referral: Early referral and communication with Donor Team (Specialist
Nurse for organ Donation – SN-oD) should be done once decision is made
to test for brainstem death. Each acute trust in the UK has a nominated
SN-oD. If out of hours, the on-call SN-oD can be contacted.
Patient/relatives: once notified, the SN-oD will collect all the information
about the patient and his or her relatives. The specialist nurse will do a
detailed assessment of the patient for suitability of organ donation. Decision
is made on this assessment and after considering factors such as coroner
and relatives’ views.
Transplant centre: A check on organ donation is then made by contacting
the NHS Blood and Transplant Duty office.
ITU: once decision is made, optimal organ support is continued in the ITU
and specific therapies are initiated to enhance the likelihood of successful
transplantation.
What do you do to preserve organ
function while waiting for organ
retrieval?
General care
Care should always take place in critical care environment. once the brain
death had been confirmed, the care is mainly organ centred rather than
patient centred, as patient is legally dead. Hence, in the brain-dead donor, it
is appropriate to insert new lines for invasive monitoring if indicated for organ
optimisation.
Continue all the basic critical care management including enteral feeding,
essential drugs and antimicrobial therapy, correction of electrolytes,
glucose control with insulin, prevention of hypothermia, and blood product
transfusion to correct significant anaemia and coagulopathy.
organ specific management
Cardiovascular system:
Restoration of circulating volume without overload is essential. Short-acting
drugs are used during the periods of Cushing’s reflux and sympathetic storm
such as esmolol, GTN, and sodium nitroprusside infusions.
Vasopressin is preferred to noradrenaline as this treats diabetes insipidus
and minimises catecholamine requirements. T3 replacement can improve
cardiac function.
Haemodynamic targets include HR of 60–120/min, MAP of > 70 but
< 95 mmHg, CVP of 10–15 mmHg, cardiac index of > 2.1 L/min/m2, and
mixed venous saturation > 60%.
Respiratory system:
Methyl prednisolone 15 mg/kg given intravenously at the earliest opportunity
as this is proven to reduce extra pulmonary lung water.
Use lung protective ventilation with low tidal volumes of 6–8 mL/kg,
inspiratory pressures limited to < 30 cmsH2o, use of PEEP and recruitment
manoeuvres on regular intervals.
Fio2 is adjusted to maintain Spo2 of > 90% or a Pao2 > 8.0 kPa.
Endocrine management:
T3 supplementation is part of many protocols but it is beneficial only in
patients with poor cardiac performance after fluid loading and vasopressin.
Desmopressin is also used if diabetes insipidus persisted.
Insulin may be useful as anti-inflammatory and reduces cytokines in addition
to glycaemic control.
Renal and fluid management:
Early assessment of overall fluid status is vital as hypervolemia is
associated with poor liver graft function. Fluid overload and pulmonary
congestion causes poor oxygenation, which makes the lung unsuitable for
transplantation. Polyuria is common due to diabetes insipidus, diuretics use,
and hypothermia.
Nephrotoxic drugs should be stopped and blood pressure should be
maintained to ensure adequate renal perfusion.
What do you know about
donation after circulatory
death (DcD)?
DBD—Donation after Brainstem Death
DcD—Donation after cardiac Death
DCD refers to the retrieval of organs and tissues for the purposes of
transplantation after death that is confirmed using ‘traditional’ cardio-
respiratory criteria. This pathway refers exclusively to ‘controlled’ DCD; that
is, donation which follows a cardiac death that is the result of the withdrawal
or nonescalation of cardio-respiratory support. Controlled DCD is where
retrieval of organs is planned before death occurs. In uncontrolled DCD,
decision for organ donation is made only after death.
The main difference is in the duration of warm ischaemia time (WIT).
Warm ischaemia starts when perfusion and oxygenation are inadequate
after cardiac arrest or withdrawal of treatment. This period continues until
cold ischaemia starts during organ retrieval. Cold perfusion slows down
metabolism and ischaemic injury to the organs. This can be started earlier to
reduce ischaemic injury.
What organs are available
for DcD?
Kidneys, liver, pancreas, lung, and tissues such as cornea, bone, skin, and
heart valves.
Renal donors are the major group with a WIT of up to 2 hours or sometimes
longer. Liver and pancreas are increasingly used, but WIT is only 30 min.
Lung is an ideal organ as it can tolerate lack of circulation for longer times if
oxygenation is provided.
How is dopamine formed?
Dopamine is a neurotransmitter of the catecholamine family and is formed by
removing a carboxyl group from a molecule of L–DoPA.
Phenylalanine
Phenylalanine hydroxylase
L-Tyrosine
Tyrosine hydroxylase (rate limiting step)
L-DoPA
DoPA decarboxylase
Dopamine
Dopamine β-hydroxylase
Noradrenaline
PNMT (Phenylethanolamine N-methyltransferase)
Adrenaline
How is dopamine broken down?
Dopamine is converted to noradrenaline and adrenaline, which are in turn
metabolised by Catechol-o-methyltransferase (CoMT) and Monoamine
oxidase (MAos)
What is Parkinsonism?
Parkinsonism is characterised by the triad of tremor, rigidity, and
bradykinesia. It has multiple causes, of which 85% is Parkinson’s disease.
other causes of Parkinsonism
Pharmacological:
• Drugs affecting dopamine synthesis, storage, and release; e.g. reserpine
• Drugs blocking dopamine receptor; e.g. prochlorperazine
Vascular: e.g. arteriosclerosis, multi-infarct disease
Infection: e.g. post-encephalitis
Structural lesion: e.g. tumour, trauma (repeated head injury), normal pressure
hydrocephalus
Metabolic: e.g. hypoparathyroidism, Wilson’s disease
Post–trauma: e.g. repeated head injury
What drugs are used to treat
Parkinsons’s disease?
1) Dopamine precursors with peripheral dopa decarboxylase inhibitor (DDI)
Dopamine precursors (e.g. Levodopa) undergo conversion peripherally
and within the CNS. DDI (e.g. benserazide) is administered together
to reduce peripheral dopaminergic side effects (tachycardia, nausea,
vomiting, dysrhythmias).
2) Dopamine agonists
Examples: Ropinirole, Apomorphine. They mimic actions of dopamine at
the dopamine receptors.
3) MAo-B inhibitors
Example: Selegiline. Prevents breakdown of dopamine in CNS by
MAo-B.
4) CoMT inhibitors
Example: Entacapone. Used with Levodopa and DDI in combination to
smooth out end-of-dose ‘off’ periods where symptoms return only a few
hours after the last dose.
5) Anticholinergics
Example: orphenadrine. Antagonises the unopposed excitatory effects of
cholinergic pathways.
6) Atypical agents
Example: Amantadine. Mechanisum of action not fully understood. May
be useful as monotherapy in early Parkinson’s disease.
When should Parkinson’s disease
drugs be stopped preoperatively
and restarted postoperatively?
In general, it is advisable for patients to stop their drugs as late as possible
preoperatively and restart it as soon as possible in the postoperative
period. This is not always possible in patients who are unable to swallow or
maintain enteral feeding (post major abdominal surgery). Levodopa can be
administered via nasogastric or nasojejunal tubes.
Patients can be commenced on apomorphine intravenous infusion and
continue it throughout the operative period. The bolus dose of apomorphine
can be determined by an apomorphine challenge—dose required to
abolish the symptoms and to check that no severe adverse effects occur
(e.g. profound hypotension).
Which drugs are unsafe in this
group of patients?
• Pethidine should be avoided as it can cause hypertension and muscle
rigidity in patients on selegiline
• Antiemetics are of importance as nausea/vomiting can hinder restarting
enteral Parkinson’s disease drugs. Metoclopramide, droperidol, and
prochlorperazine are unsafe as they will worsen the symptoms and cause
extra pyramidal effects. The antiemetic of choice is domperidone as it
does not cross the blood brain barrier and therefore does not cause extra
pyramidal effects
• Antidepressants: tricyclic antidepressants may potentiate Levodopa-
induced arrhythmias
• Antipsychotics (e.g. phenothiazines, butyrophenones, piperazine
derivatives) may worsen symptoms. It is best to use atypical
antipsychotics (e.g. sulpiride, clozapine)
• Antihypertensives may cause severe hypotension (due to postural
hypotension, hypovolaemia)
• Centrally acting anticholinergic drugs can precipitate central
anticholinergic syndrome. Glycopyrrolate is the anticholinergic of choice
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
What do you understand by t1
and t2 weighted images?
• ‘T’ is the relaxation time constant.
• T1 weighted (early image)—few milliseconds after the electro magnetic
field is removed
• T2 weighted (later image)—later than T1
• Protons in hydrogen take a long time to decay to original position, so fluid
will appear dark (minimal signal) in T1 but white (better signal) in T2
can you list the problems posed
to the anaesthetists when taking
an anaesthetised patient to MRi?
• Patient factors
° Patients needing anaesthesia are usually ITU patients, paediatric
patients, patients with learning difficulties, seizures, or movement
disorders
° Pregnancy: Currently recommended that pregnant women should
ideally not be scanned during the first trimester of pregnancy due to
magnetic field problems, noise, and also unscavenged anaesthetic
gas issues
° Patients with implants: Pacemakers, cochlear implants, intraocular
foreign body, and ferromagnetic aneurysm clips are absolute
contraindications. Modern implants such as joint prosthesis, surgical
clips, heart valves, and sternal wires are deemed safe. All patients and
staff need screening
• MRI factors
° Presence of strong magnetic field
- Exert large forces on any ferromagnetic materials in the proximity
- Induce currents in metallic objects and cause local heating
- Interfere with monitoring
- Magnetic field in the vicinity can also derange the quality of images
produced
- < 5 Gauss is the safe zone
° Noise such as that due to the gradient coils switching on and off
- > 85 dB (above safe level)
- Patient and staff should be protected
- Can mask the monitor alarms
° Heat: That produced by the radiofrequency radiation is absorbed by
patient.
• Anaesthetic equipment factors
° MRI safe: Equipment will not pose a danger to patients and staff but
does not guarantee that it will function correctly
° MRI compatible: Equipment is both safe to enter the MR examination
room and will operate normally without interference to the MR scanner
° Anaesthetic machines, cylinders, circuits, ventilators, vapourisers and
scavenging are now available as MRI-compatible
° Infusion pumps fail if field strength is > 50 Gauss
• Anaesthetic monitoring factors
° MRI-compatible short (15 cms) braided ECG leads and insulated pulse
oximetry cables are necessary
° NIBP—plastic connectors; IBP—pressure transducer cabling is
passed through the wave guides or use MRI-compatible pressure
transducers
° Capnography and airway pressure monitoring requires longer sample
lines with a 20-second delay
° Monitoring screens should be in the control room and carbon fibre
cables passed via the wave guide port
• Location factors
° Usually remote
° Difficult to access in case of emergency
What is Faraday’s cage?
Faraday’s cage is a radiofrequency shield built into the fabric of the MR
room. To allow infusion lines or monitoring cables to enter the MR room,
a hollow brass tube or ‘waveguide’ is built into the Faraday cage passing
through into the control room.
Mechanism: An external static electrical field causes the electric charges
within the cage’s conducting material to be distributed such that they cancel
the field’s effect in the cage’s interior.
Examples: Microwave oven, MR room.
What is quenching?
The coils used in MR magnets need to be kept cold (liquid helium) in order to
maintain superconductivity.
Quenching is a process involving the rapid boil-off of the cryogen that causes
an immediate loss of superconductivity. This can happen spontaneously, due
to error or installation, or deliberately such as in order to switch the scanner
off. This produces a large volume of helium gas, which is vented to the
outside atmosphere through a quench pipe. In the event of damage to the
quench pipe, the buildup of helium could potentially lead to asphyxiation.
