Recall Part 2 Flashcards

(438 cards)

1
Q

Prehabilitation domains
Evidence for prehab

A

Physical exercise
Psychological support
Nutrition (malnutrition increases periop wound infections, pressure wounds, LOS, ICU admission and mortality)
Behavioural changes (e.g. alcohol, smoking)
Obesity - unclear role. Bariatric surgery or GLP1 agonists may play part. Obesity obviously worsens all periop outcomes

Evidence for prehab:
- Somewhat lacking. Probably due to large heterogeniety in studies
- Unclear what level of physical exercise needed to attain to reduce risk
- Nutritional support alone may have benefit, meta-analysis in 2020 found nutritional support for abdominal surgery improved post op complications. One RCT found reduced wound infections. Another found better LOS (but heterogeniety still an issue)
- Smoking cessation is beneficial if >8 weeks for morbidity / mortality.
- One study for bariatric surgery found 30 day mortality benefit if weight loss prior to surgery if BMI 35-40
- One meta-analysis of prehab in general, was only able to include 3 RCTs due to heterogeniety. One RCT found improved post op pulmonary complications
- Likely best if multimodal approach

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2
Q

What is patient blood management (PBM)?

A

WHO endorsed, evidenced based approach to care for patients at risk for allogenic blood transfusion.
Reduces transfusion requirements, improved post op infections, reduced LOS, reduced periop mortality at 30d and MACE

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3
Q

Definition of anaemia and causes for anaemia

A

International concensus statement Hb <130g/L for both men and women. WHO has different scores for men and women. Concensus statement suggests same score as if different levels used, women more likely to be transfused

Microcytic anaemic causes (TAILS)
- Thalassaemia
- Anaemia of chronic disease
- Iron deficiency (most common, affects >2 billion people)
- Lead poisoning
- sideroblastic (bone marrow derived)

Normocytic
- acute bleeding
- haemolytic anaemia
- Renal (lack of EPO)

Macrocytic
- B12, folate deficiency
- Alcohol misuse

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4
Q

Signs and symptoms of iron deficiency
Biochemical markers for iron deficiency vs anaemia of chronic inflammation

A

May be from:
- increased iron consumption (bleeding, increased hepcidin from chronic inflammation
- decreased supply (malnutrition, insufficieny dietary intake, absorption abnormalities)

Symptoms: fatigue, brain fog, palpitations, SOB, pallor, hairloss

Iron is transported in blood by transferrin. Stored as haem and ferritin
Microcytic anaemia most commonly from iron deficiency

Ferritin should be >100mcg/L
If ferritin <30mcg/L then iron deficiency present. If Hb <130g/L and microcytoic red cells, then likely iron deficiency anaemia

However, ferritin is also an acute phase reactant. Increases with inflammation. So if ferritin 30-100, check transferrin levels and CRP levels.
If ferritin 30-100mcg/L AND (transferrin <20% or CRP >5mg/L), likely indicates an iron deficiency that is being masked by inflammation. = anaemia of chronic inflammation with iron deficiency

If ferritin >100mcg/L AND CRP >5mg/L, then anaemia of chronic inflammation

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5
Q

PREVENTT trial

A

Patients with iron deficiency anaemia randomised to placebo vs iron infusion preop for major abdo surgery.
No benefit in mortality or reducing blood transfusions.
Reduced rate of readmission to hospital and improved Hb at 6 months time

1g ferric carboxymaltose Iv works faster and more effective than oral iron. Symptoms improve at 3 days, Hb improved around 5 days. Peak at 2 weeks. USeful if <4 weeks until surgery (oral iron takes longer). Hypersensitivity <1: 25,000, if extravasation then skin disclolouration. Can get flushed feeling and SOB

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6
Q

Options to improve anaemia preop

A

Iron tabs (40-60mg daily) - takes at least 2 weeks but usually up to 6 weeks for improvement. Constipating

Iron infusion - faster than tabs. 5 days to improve Hb levels, peak at 2 weeks. hypersensitivty <1:25000, skin discolouration if extravasation. PREVENTT trial found no improvement for mortality or transfusion. But did improve readmission to hospital and Hb at 6 months

EPO - useful in combination with iron often. Can improve Hb within 3 days. Meta-analysis did improve transfusion rates in both orthopaedic and cardiac settings. Costly

Correct other causes: chronic inflammation, alcohol, B12 deficiency, folate deficiency, renal (EPO)

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7
Q

Premedication options and doses for kids?

A

Midazolam - oral 0.5mg/kg up to 20mg
Ketamine - oral or IM 2mg/kg
Clonidine - 4mcg/kg
Dexmeditomidine - 2-4mcg/kg IN

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8
Q

Advantages and disadvantages of premeds

A

ADVANTAGES
Anxiolysis
- decreased SNS
- improves parental satisfaction
- May be only way to get patient to cooperate with GA
- May also provide post op anxiolysis - especially longer acting agents like clonidine

Amnesia
- Especially for children, those having repeat surgeries
- Reduction of awareness under GA or immediately following induction

Analgesia
- especially dexmed, clonidine, ketamine

Sedation
- May allow for monitoring, preoxygenation, IV insertion without need for GA

Anaesthesia sparing
- Less induction dose needed. Faster onset for gas inductions or IV

DISADVANTAGES:
- Slows down lists
- Unnecessary in many situations
- Paradoxical effects (e.g. benzos in elderly)
- Allergy / anaphylaxis exposure
- Airway obstruction, risk of falls while not monitored - need nursing to watch
- Prolonged emergence or prolonged stays in PACU. May delay discharge home for day stay surgery
- Aspiration if unfasted

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9
Q

Risk factors for PONV

A

Patient
- Age 3-50
- Gender - female (this is the biggest risk factor)
- history PONV
- History motion sickness
- Non smoker
- Dehydration

Surgical
- Laparoscopy
- Gynae
- Middle ear
- Eyes (Strabismus)
- Prolonged surgery
- Need for opioids post operatively

Anaesthesia
- N2O
- volatile
- high dose opioids
- Neostigmine use

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10
Q

Definitions for minimal, moderate and deep sedation

A

Covered in PG09 = professional guideline from ANZCA, endorsed by lots of peps including RACS, Australian Denstristy
Only minimal and moderate sedation covered by PG09. Deep sedation and GA is the realm of anaesthetists, ED, ICU only

Minimal = anxiolytic dose only. Includes small dose oral sedation, N2O or methyoxyflurance. Eyes still open. follows commands. Need SPo2 and HR monitoring available but not necessarily on. Doesn’t need fasting unless likely to end up with moderate sedation

Moderate = depressed level of consciousness, eyes may close. But still follows commands, opens eyes when asked. Needs SpO2, Hr and NIBP monitoring at minimum. Similar set up to GA in terms of fasting requirements, informed consent, equipment available (including rescue airways, defib), drugs (O2, adrenaline, atropine, IV fluids), IV access

Deep sedation - only responds to painful stimuli. Similar risks to GA in terms of haemodynamics, airway risks

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11
Q

Requirements for moderate sedation

A

As per PG09 ANZCA document

Moderate sedation = eyes closed, depressed level of consciousness. But responds to commands

Planning
- Sedationists require credentially, CPD (no minimum timeframe stated for training)
- Preop checklist. Informed consent. Fasting status. Allergies. comorbidites (e.g. CVS, OSA). No language barriers
- Targetted plane of sedation discussed with patient
- If paediatric then needs to have appropriate skillset for paeds, equipment for paeds

Equipment
- Airways (OPAs, LMAs), suction, BMV
- defib
- Drugs: O2, adrenaline, atropine, reversal agents (e.g. naloxone if opioids used), IV fluids, dextrose

Monitoring
- Minimum of SpO2, HR, NIBP
- ECG + etCO2 available (unless ASA 3 or 4 then have it on)
- For paeds, RR too

IV access

Personnel
- Ideally 3 people. Proceduralist. Assistant. Sedationist. All need BLS training
- Also 3 people recommended if paeds sedation
- Proceduralist might also be sedationist. Have to delegate sedation and monitoring to another assistant
- If ketamine or propofol used for sedation, need to have a separate sedationist who understands the kinetics of these drugs
- If complex procedure or complex patient, ANZCA suggestion sedationist should be anaesthetist

Post procedure
- PACU style recovery with monitoring, documentation, discharge criteria

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12
Q

Delirium definition and causes for delirium

A

Acute state of confusion, inattention and decreased awareness of environment which is fluctuating and typically associated with precipitating cause

DELIRIUMS as causes:

Drugs (opioids, cholinergics)
Electrolytes, metabolic disturbances (sodium, calcium)
Lack of drugs (withdrawal)
Intracranial disease (meningitis, SDH, stroke)
Reduced sensory input (hearing aids, glasses)
Infection
Urinary retention, constipation
Myocardial disease (MI, arrythmia)
Sleep deprivation

Age >70 and male gender are clear risk factors

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13
Q

What is postoperative neurocognitive disorder?
Ways to reduce POCD?

A

Cognition has multiple domains including:
- Learning and memory
- Language
- Perceptual motor
- Social cognition
- Complex attention
- Executive function

Neurocognitive disorder = decline in any of these domains of cognitive function, beyond expected normal for aging
POCD not defined by DSM5 but often stated as cognitive decline following surgery,
First 7 days after surgery cognitive decline = delirium
7-28 days = delayed neurocongitive recovery
>28 days, within a year of surgery = postoperative cognitive disorder

POCD increases post op mortality. Present in 10% of people at 3 months, 1% at 1 year.

Risk factors:
- Elderly (>60)
- CPB
- Previous stroke with no residual deficit
- Lower education
Other possible ones are repeat surgeries, prolonged GA, post op infections

Reduce by:
- evidence is very uncertain here. Possibly because need to do pre-op and post op cognitive testing which is not frequently done
- Regional - meta-analysis from 2018 found no difference at 7 days comparing GA vs regional
- Propofol vs volatiles - may have benefit. Cochrane review 2018 found TIVA reduced POCD by 0.25. But could be other factors (e.g. EEG)
- EEG is conflicting. One study found if BIS kept 40-60, then slight reduction in delirium and POCD (1000 anaesthetics, would reduce POCD by 23 people). Other studies found no difference
- Dexmed, ketamine, parecoxib potentially. One meta-analysis of 7 dexmed studies found reduced POCD at 7 days. But unclear if opioid sparing vs other effect

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14
Q

Relief trial findings

A

Multicentre, multinational RCT of 3000 patietns for elective major abdo surgery. Not blinded. Adults at risk of fluid complications (ASA 3, 4, over 70, CKD, obesity, heart disease)

Restrictive arm - bolused 5ml/kg for induction. 5ml/kg/hour til end of surgery. Then 0.8ml/kg/hour post op 24 hours. Averaged 3.7L over 24 hours

Liberal arm - 10ml/kg for induction. Maintenance 8ml/kg/hour. Then 1.5ml/kg/hour 24 hours post op. Averaged 6L / 24 hours

Post op 1 year survival the same. No differences in pneumonia, wound infections, anastamotic leaks, ICU, RRT.

Only difference was restrictive group had 1.7x risk of AKI post op (8.6 vs 5.6 % of patients)

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15
Q

Why is CVP a poor indicator for fluid status / responsiveness to fluids?

A

RA pressure (effectively what is measured from CVP) is only one factor that determines preload (=degree of myocardial stretching at end of diastole). Other factors include:
- Mean systemic filling pressure - vascular tone, vascular volume
- Intrathoracic pressure, PEEP
- Abdominal pressure
- Ventricular function
- Ventricle myocte compliance

Frank-Starling curve is non linear. Different for each patient. At any given CVP, could be on flat portion of curve or steep compared to another patient

Marik and Cavallazzi (Chest 2008) meta-analysis of 24 studies. Correlation between CVP and CO change with fluid bolus was very poor (AUROC 0.54, almost as good as random chance)

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16
Q

Uses for CVP (as it is no good for fluid status)

A
  • Confirmation of intravascular puncture (rather than arterial)
  • Sudden changes/ trends more important than raw number. Sudden drop in CVP - hypovolaemia. Sudden increase - right heart strain, pHTN, tamponade
  • Liver resection. Low CVP associated with reduced bleeding (Fan et al, 1999)
  • Waveform analysis. Prominent V wave may indicate TR, if worsening could imply increasing RV systolci pressures
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17
Q

Alpha stat vs pH stat in DHCA for aortic arch surgery

A

Hypothermia increases solubility of gases in blood - both PaO2 and PaCO2 decrease (2-5mmHg per 1c decrease). Causes pH to increase 0.015 per 1c decrease
pH stat uses temperature corrected PaCO2 to determine ventilation. Mean you increase the PaCO2 to achieve pH of 7.4 no matter the temperature (increasing the CO2 in sweep gas for DHCA).
- Get cerebral vasodilation due to increased PaCO2 –> fasting cerebral cooling but also risk of hyperemia.
- pH stat used for infants and neonates as faster cooling (landmark infant trial 1992 by Harvard, demonstrated improved post-arrest EEG and short term neurological outcomes (but not long term).
- Increases risk of emboli to brain as increased CBF (but not an issue in infants). And adults probably don’t get the alpha stat benefit of faster cerebral cooling as larger body surface area so slower thermal equilibrium time

Alpha stat uses non-corrected pH to determine PaCO2. Theory that intracellular protein / enzyme charge state (alpha dissociation) is what is important to maintain enzymatic function (not the raw pH value). Aim for pH 7.4 and PaCO2 40mmHg with no temperature correction.
- Get less cerebral vasodilation than pH stat
- Alpha stat may be useful in paeds for warming phase - less risk of microemobili due to cerebral vasoconstriction + slower warming
- Alpha stat used for cooling and warming in adults. 1987 NEJM trial on hypothermia in CPB found improved neurological recovery if alpha stat used
- Less microvascular emboli with alpha stat in adults (Doppler studies). More atheroscleortic disease in adults hence likely benefit here

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18
Q

Risk factors for AAGA (accidental awareness under GA)

A

Patient
- Obesity
- Previous awareness (5x increased risk)
- higher ASA
- alcohol dependence
- Female
- Younger patients
- Opiod dependence
- BZD dependence

Surgical
-Emergency
- Out of hours surgery
- LSCS
- Cardiac
- Surgery that requires intubation (NDMRs)

Anaesthesia
- Junior practitioner
- TIVA
- NDMR use
- STP
- Anaesthetising patient in one room and transferring them
- Difficult intubation

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19
Q

Four important trials for awareness prevention under GA

A

B-Aware - 2004, Lancet. Multi centre, multi national. High risk for AAGA in non-cardiac surgery
- BIS with targets vs standard care. 40% of patients had propofol infusion, rest were volatile. AAGA reduced by 80% with having routine BIS on (2 vs 11 patients). NNT of 138

B-Unaware 2008, NEJM. n=2000 Randomised to either BIS <60 or MAC >0.7 etVolatile. Single centre RCT. 2 cases of AAGA in each group. No difference
- No propofol, only sevo in this trial

BAG-RECALL 2011. n= 5700. Multi centre, international. Same criteria as B unaware (BIS vs etVolatile). Volatile agents only. No differences

MACS (2012). n=18000. Propofol or volatile. If propofol, then needed to have BIS and EEG targets. If volatile, then could be randomised to either BIS or etVolatile. No difference in AAGA

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20
Q

What particular times did AAGA occur during the anaesthetic?

A

Induction - 50%. PArticularly if an anaesthetic room was used for induction and then transport of patient

Maintenance - 30%. Sometimes from IV tissuing or disconnection

Emergence - 20%. Especially during transfer of patient, off volatile and onto IV infusion

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21
Q

Treatment of PTSD following AAGA

A

40% of patients that had awareness in major trials (e.g. B Unaware) met DSM4 criteria for PTSD.

Initially get acute stress disorder - negative mood, avoidance, intrusive thoughts, sleep deprivation for first 1-28 days. If still persisting after 1 month –> PTSD

Non-pharmacological
- Addressing patient concerns, apologising
- Cognitive behavioural therapy
- Eye movement desensitisation therapy

Pharmacological
- SSRIs often first line

Some evidence suggests combination therapy + pharma best for symptom improvement

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22
Q

Components of the Brice Questionaire

A

Gold standard for detecting AAGA with explicit recall. Used in major awareness studies (B aware, B unaware).
-Typically done 1 day and 30 days post anaesthesia to allow that AAGA not always immediately recalled
- Should be done by anaesthetist / expert not directly invovled in case to reduce bias
- Structured interview with 5 questions:
- What was the last thing you recall before going to sleep?
- What was the first thing you recall when waking up?
- Do you remember anything in between? (clarify if dream or recall)
- Did you dream?
- What was the worst part of the operation?

When Brice questionaire done for all patients, risk of AAGA is around 1:1000 (much higher than the usually quoted 1:19,000 for all comers if anaesthetist-led)

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23
Q

Effects of cannabis perioperatively

A

Contains THC, cannibodial and 60 other cannabinoids. Most evidence is from illicit use from smoking - dose highly variable. As is the effect from other utilisation methods (e.g. edibles). Highly fat soluble so metabolites may appear in urine for 1 month but clinical effects usually <24 hours

CNS
- If used acutely, anaesthesia-sparing. Can cause hallucinations
- May interfere with consent process
- Long term use can cause anxiety, depression, memory impairment, psychosis, hallucinations, cognitive impairment
- There is weak evidence for mild analgesia. But chronic use increases risk of post-op pain

CVS
- Increased coronary disease
- Low doses may get SNS activation - tachycardia, increased CO
- Higher doses - bradycardia, hypotension

Resp
- Highly reactive airways - bronchospasm, laryngospasm
- COPD with chronic smoking use
- High sputum production with impaired mucociliary clearance

GI
- Antiemetic properties

Obstetrics
- Foetal growth resistction, low birth weight child. Infant cognitive impairment

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24
Q

Cocaine use effects on anaesthesia

A

Usually intranasal administration. Can be smoked or injected. Sympathomimetic ester local anaesthetic tropane alkoid from coca plant. Half life of 1 hour. Causes inhibition of pre-synaptic uptake of NA, dopamine, 5HT

CVS
- Hypertension, tachycardia. Risk of myocardial ischaemia, coronary vasospasm or aortic dissection
- Do not give beta blockers. Can give alpha 2 agonists, phentolamine, GTN, hydralazine to reduce BP. Give high dose opioids before laryngoscopy
- Avoid ketamine
- Ephedrine less effective as depletion of NA usually. Give direct acting alpha 1 agonist - phenylephrine, if hypotension

CNS
- Euphoria, dysphoria, addiction, anxiety, confusion
- Risk of stroke

Haem
- Platelet aggregation, thrombocytopenia

Obstetrics
- Placental vasoconstriction - risk placental abruption, IUGR, foetal acidosis, risk of foetal demise

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25
Effects of IV drug use (outside of the drug effect itself)
- Difficult IV access from recurrent use, thrombosis - Thrombosis - arterial and venous. Peripheral ischaemia. DVT. PE - Blood borne infections - HIV, Hep B / C, Syphyllis. Staff hazard - Risk of strep / staph introduction to blood - risk osteomyelitis, endocarditis, epidural abscess - Skin atrophy - Fat necrosis
26
Methamphetamine effects on body systems and anaesthesia
Sympathomimetic, inhibits NET, DAT, SERT to inhibit NA, dopamine and 5HT reuptake. Also inhibits MAOa and MAOb. Neurotoxic to dopamine cells CVS - Autonomic instability possible. Usually hyerptension, tachycardia, tachypnoea, hyperthermia, hypermetabolic - Increased risk of MI, stroke, aortic dissection - Indirect sympathomimetics useless. Use direct - Avoid ketamine - Do not give beta blockers, unopposed alpha blockade. Dexmed or clonidine useful. Or GTN, hydralazine - Long term use --> dilated cardiomyopathy - Arterial line may be of us Resp - Increased airway irritability, bronchospasm and laryngospasm - risk of ARDS, catecholamine induced or heart failure induced APO CNS - Dysphoria, psychosis, aggitation, aggression. - May not be consentable - Addiction - Cooperability may be challenging. May need descalation, sedation (diazepam useful) - Lowered seizure threshold - Risk of serotonin syndrome (possible hyperthermia, rhabdomyolysis, hyperkalaemia) Metabolic - Hyperthermia, may need cooling to avoid rhabdo
27
Benefits and disadvantages of a gas induction
Advantages: - Spont ventilation usually maintained, if stop ventilating, patient lightens and then starts breathing again - Useful for children, highly needlephobic adults for cooperation. Perceived less threatening than IV for lots of parents -Haemodynamically more stable induction generally compared to IV - Sevoflurane bronchodilation - N2O - slightly faster onset gas induction, analgesia for IV insertion (less risk laryngospasm) Disadvantages: - Can take a long time for larger children and adults to get deep enough for an IV. Especially in distressed kids or those with an inhaled foreign body. Onset much less predictable than IV - Aspiration risk until airway is secure, which takes longer with inhalational - Excitation phase can be challenging to manage in adults (need lots of hands on deck to prevent rolling off bed) - No ability to give IV emergency drugs, IV fluids immediately (reliant on IV line access, IM or IO access) - Greenhouse gases - Staff exposure to volatile - MH trigger - Reliant on assistant holding open airway while getting IV access - If N2O, other downsides of increased PVR, increased CBF, expansion of gas filled spaces, nausea
28
Risk factors for incomplete reversal of NDMRs
Surgical - Fast surgeon - Surgery where difficult to know when finishing (FESS, other ENT) - high turnover lists Anaesthesia - Longer acting agents used (not much of an issue now panc isn't used) - Re-dosing NDMRs - Not using quantitative measure of reversal or not measuring twitches at all - Neostigmine instead of sugammadex - Other drugs that augment NDMRs - calcium channel blockers, gentamicin, magnesium, volatiles Patient - Obesity - Hypothermia - Acidosis - Renal / hepatic failure
29
Modes of monitoring NDMR blockade
Train of 4 - 4x maximal stimuli (50mA) at 2Hz. Initially get 1, 2 3 and then 4 twitches returning. Then compare 1st and 4th for the train of four ratio quantitatively. Acceptable target >0.9 for extubation DBS - 2x bursts of 3 x 50Hz stimuli, 750ms apart. Same criteria for extubation as TOFR. but easier to detect fade qualitatively than TOFR (minimal real applications for this, just use quantitative) Post tetanic count = PTC. Tetany at 50Hz for 5s. Then pause. Then 1Hz twitches. Used for assessing deep relaxation. Should get first TOF twitch back around PTC of 9. Sometimes aim for PTC <3 if don't want movement
30
Advantages and disadvantages for quantitative NDMR monitoring:
Induction: - Advantages: As laryngeal muscles paralysed before ABP, if loss of twitches at ABP then almost certainly ready for intubation - Disadvantages: can be long gap of minutes between two muscle groups, may mean waiting long before intubation with unprotected airway Maintenance - Advantages: allows for monitoring of NDMR during case, can keep patient paralysed which will likely improve ventilation, improve surgical conditions - Disadvantages: hand has to be free, ideally visible for quantitative monitoring to be accurate. If tucked hand = inaccurate measure. Keep patient still with high dose remi infusion Emergence - Advantages: gold standard for extubation. >0.9 for TOFR. If reversed at ABP, then most likely reversed at larynx, pharnyx, diaphragm due to these recovering more rapidly than ABP due to higher cardiac output. May be able to give no reversal agent (e.g. TOFR 1.0 due to prolonged case with no repeat NDMR doses) All: Advantages: especially useful in altered physiology / pathology states (e.g. renal failure, hepatic failure, paeds, obstetrics, sepsis) which can make NDMR dosing less predictable Disadvantages: requires hand or foot to be available, not useful if limbs in casts / ex fix / amputees. Sensitive to movement artifacts (need to make sure it is a real detected twitch)
31
Scoring systems for PACU discharge
Aldrete score. Original is out of 10, used for discharging patient to another clinical facility (not home) - Activity (2 = moving all limbs to command) - Respiration (2= breathes deeply, coughs freely) - Circulation (2= BP +/- 20% of pre-anaesthesia numbers) - Consciousness (2= GCS 15) - O2 sats (2= >92% on air) - Modified Aldrete scores often used, incorperate ambulation, nausea, pain, passing urine or bleeding. More appropriate for dsicharge home PADSS score = more used for discharging home. Also out of 10. Includes bleeding, nausea and pain Scoring systems should be: - Generalisable - able to be used for most patients for most surgeries. Ideally for discharge home and ongoing clinical care in another facility - Clear criteria - objective measures, definitive end points - Relevant criteria to patient saftey - Criteria for when to escalate to senior support - Able to be documented There are no perfect scoring systems. Will require modification for safety for certain conditions or surgeries
32
LEMON model for airway assessment
Look - End of bed. Limited mouth opening. C spine collar. Protruding teeth. Obvious facial deformity, halo device Evaluate - Mouth opening (>6cm or 3 fingers is good) - TMD (>6cm is good) - Jaw protrusion Mallampati score (no idea why this isn't just in evaluate but here we are) - PPV for difficult airway is about 10%. Sensitivity 50%. Specificty 75% Obstruction - STOPBANG score - Obvious upper and lower airway obstructions Neck - ROM, circumference
33
Grading systems for video laryngoscopy?
Documentation should include: - Laryngoscope blade size and type (e.g. size 4 Mcgrath or CMAC- D) - Fremantle score - Full view, partial view, no view - Ease of insertion - easy, modified, unable - POGO = percent of glottic opening, as %
34
IRIS study for cricoid pressure
France, 2018, RCT, n=3400. Not obs or paeds. No difference in aspiration or regurgitation events (0.5 vs 0.6%) but did slow time to intubation
35
Purpose of an RSI
To minimise time from an awake patient, protecting their own airway, to an anaesthetised patient with an endotrachael tube protecting their airway. Mainly utilised to reduce risk of aspiration. Aspiration is the leading cause of anaesthesia related death for patients undergoing GA RSI may also be used in cases where patient high risk of hypoxaemia, especially where BMV is either anticipated to be difficult or contraindicated
36
Evidence against using cricoid pressure for an RSI
- Original evidence is shaky to begin with. Sellick 1961, cadaveric studies and then on 26 live patients - Up to 50% of time, cricoid misplaced (based on MRI studies). Incorrect technique, incorrect pressure (30N), oesophagus laterally displaced rather than compressed - IRIS study 2018 France, n=3500, RCT. No difference in aspiration (0.5 vs 0.6%) but did slow time to intubation - Assistant hands freed up for difficult intubation if not used - Both DAS 2025 guideline and PUMA (Project for universal management of airways) suggest optional - Provokes anxiety in patient - Often makes view worse - survey of ANZCA anaesthetists state 75% would use if high risk for aspiration but only 1/3rd actually believed it reduces the risk
37
Nerves that can be injured from SGA insertion?
Lingual (branch of V3 with inputs from facial nerve via chorda tympani) - Cuff vs mandible. - Causes loss of sensation to anterior 2/3rds of tongue. Loss of taste anterior 2/3rds tongue via chorda tympani Hypoglossal (CN 12) - Cuff vs hyoid - Motor to all intrinsic + extrinsic muscles of tongue except palatoglottis. Tongue will point to side of lesion Recurrent laryngeal (branch of vagus) - Cuff at laryngeal inlet - Hoarse voice, stridor Glossopharyngeal (CN 9) - Cuff vs lateral oropharyngeal wall, tonsillar pillars - Posterior 1/3rd of tongue sensation, gag reflex
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As per the ANZCA cognitive aid for supraglottic / infraglottic rescue, what are the criteria where infraglottic rescue should be done?
- 3x attempts ETT - 2x attempts LMA - Unable to B&M = bag and mask - SPO2 <90%
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PUMA criteria for confirmation of ETT placement based on capnography
Project for universal management of airways. 4 criteria - etCO2 rises with expiration, falls with inspiration - consistent or increasing amplitude over 7 breaths - Peak amplitude >1kPa (or >7.5mmHg) above baseline - Reading is clinically appropriate
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Benefits and downsides of a C1CO (cannula first CICO)
Pros - May be less confronting to use needle. Anaesthetists more used to scalpels - Doesnt burn bridges - patient can still be intubated from top end of experienced hands come in - Less bleeding - Can progress to scalpel if unsuccessful, but inverse is not true if scalpel used first - high success rates in simulation. Higher success rates if looking at anaesthetist performed FONA (52% vs 37%) Cons - Possibly less successful than scalpel. NAP4 probably falsely reassuring given most scalpels done by surgeons. Some major guidelines (DAS) suggest scalpel first - Not definitive airway, just rescue. Needs to be converted to Melker kit or intubate from above if wanting to continue - doesnt protect against aspiration - Risks of jet ventilation (pneumothorax, gas trapping, false passage --> subcut emphysema, mucosal necrosis) - Kinking, dislodging of cannula - No etCO2 monitoring, reliant on SpO2 which can be slow to improve
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Jet ventilation technique for once cannula inserted in CICO
- Rapid O2 device. 15L/min flows - Deliver 4s of jet ventilation = 1L O2. Watch for chest rise / fall - Wait 20s. Should get increase in SpO2 in this time. If no increase, give another 2s (500ml of O2). If no increase, then abandon for another technique - Once SpO2 rise confirmed, wait for SpO2 to drop by 5% from peak SpO2. Then give 2s (500ml). Repeat - If unable to record SpO2 (e.g. cardiac arrest), give 500ml every 30 seconds
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Considerations on whether to wake patient or proceed with emLSCS if unable to intubate
Maternal condition - Wake if well, continue surgery if haemodynamic / resp compromise likely to improve with delivery Foetal condition - Wake if well, continue if not good CTG Anaesthetist experience - Wake if junior Airway - Wake if BMV only. Continue if well seated 2nd gen LMA Surgical factors - Wake if highly complex surgery anticipated (e.g. placenta accretia) Alternative anaesthesia available - Wake if neuraxial possible or if AFOI useful Aspiraiton risk - Wake if unfasted + BMV If decision to proceed, minimise risks: - TIVA - Omeprazole - Keep paralysed with roc, reverse wtih sugammadex - Most senior surgeon, minimise operating time
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Difference between a microcuff ETT compared to standard
Higher volume, lower pressure, more distal cuff
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Ayre's T Piece, Jackson Rees modification Mapleson F advantages and disadvantages
Advantages: - Low resistance, valveless - Lightweight, portable. Can be connected onto any O2 source - Allows for CPAP during spontaneous ventilation and IPPV, superior CPAP to self inflating AMBU bag (which only provides positive pressure uring expiration not inspiration if spont venting - Useful for assessing compliance Disadvantages: - Need high FGF if spont ventilating, 3x MV. Less suitable for older children and adults - Less familiar kit for most anaesthetists (unless regular paeds) - Exposure of staff to volatile agents - Greenhouse gas. No scavenging - Less efficient for volatile than circle system - Minimal warming, humidification compared to circle
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How to do an AFOI in a child?
More or less an asleep but spont ventilating bronchoscopic intubation Pre-induction - Consent with parent - Location - theatre most likely - Check list - 2x anaesthetists. consider ENT with rigid bronch or trache kit scrubbed. Trained assistant with paeds and AFOI experience - Calculate maximum LA = 9mg/kg lignocaine. Prepapre 4% and 2% lignocaine - IV inserted beforehand if able - decide if nasal or oral intubation. Ensure correct size ETT and bronchoscope. Slimline bronch = 3.8mm. Olympus smallest bronch = 2.2mm. - 5mcg/kg glyco - Warm nasal tube + lubricate well - Naloxone reversal available Intubation - Monitoring - SpO2, HR, NIBP, etCO2 - Plan B, C prepared (VL, induction drugs (=propofol already attached + 1.2mg/kg rocuronium), rescue LMA) and communicated with team - High flow nasal O2 2L/kg/min - If IV, uptitrate remifentanil TCI to sedation (2ng/ml). Then slow uptration of propofol TCI in 0.2mcg/ml increments. Avoiding apnoea - Cophenylcaine to nostril. Then 4% lignocaine spray to nasal mucosa, nasopharynx, oropharnyx - When view of vocal cords, LA here. Then advance bronchoscope until carina seen - Feed off ETT until visualised in trachea, but before carina Post-intubation - Confirmation placement with etCO2 - Induce with propofol. Consider if NDMR needed - documentation
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Differences between an adult and a paeds needle and scalpel CICO technique?
Based on RCH guidelines Indications - similar to adults, failure to oxygenate despite attempts at intubation, LMA, BMV - RCH also states sats <80% and bradycardia - as per adults, should still be attempting BMV supraglottically while doing eFONA Cannula: - 16g, otherwise insertion technique the same - RapidO2 device connected to O2 at 1L/min/age of child. Minimum of 4L/min - 1 second insufflation at 4L/min = 64ml of O2, 2s = 130ml (both probably acceptable for a 10kg child) - Watch for chest rise and fall, SpO2 rising. Only give subsequent breath when definite chest return to normal + SpO2 starting to decrease again - Melker kit best avoided if possible. ENT trache is better option Scalpel: - If needle failure or child 12 or older - Microcuff ETT. Size 3.0 for neonates and infants with 5Fr bougie - Size 4.0 ETT for children 2-11 with 8Fr introducer - Size 5.0 ETT with 11Fr Airway Exchange catheter for 12 or older
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Indications for gastric ultrasound
Despite fasting guidelines, 4% of patients may have solids or high volume liquids in stomach despite following recommendations - If uncertainty around fasting status (language barriers, cognitive impairment, children) - If suspected delayed gastric emptying (GLP1 agonist, diabetic neuropathy, high dose opioids, pregnancy, obesity, CKD)
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How to do a gastric US?
Goal is to image the gastric antrum - part in between pylorus and body. Most dependent region of stomach. It is posterior and inferior to left lobe of liver. It is anterior to pancreas tail and aorta. Curvilinear probe, low frequency (1-5Hz), deep imaging. Right lateral decubitus positon best to allow gravity to do its thing. May need to do supine though. Place transducer in saggital plane just below xiphisternum. Usually have to sweep to left along costochondral margine. Aim to use liver as acoustic window and line of the gastric antrum (short axis), SMA and aorta (SMA and aorta in longtitudinal cross section). Behind the aorta - vertebrae. Gastric antrum appears different to bowel. Hypoechoic muscular layer. hyperechoic serosal and mucosal layers Quantitative information - Empty, small volume (bullseye appearance) --> low risk aspiration - Volume - clear fluids may appear anechoic or hypoechoic. Measure crosssectional surface area 3x and average this. Then input into formula to get volume. If <1.5ml/kg, lower aspiration risk (1.5ml/kg comes from 95th centile of obs and non obs patients appropriately fasted based on guidelines) Qualitative - Starry night appearance (carbonated drinks) - Frosted glass appearance (solid foods, milk) - Obviously visible solids - All indicative of higher risk for aspiration
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Limitations of gastric ultrasound
- Experience. Misinterpretation / identification of incorrect hollow viscera could lead to dangerous decision making. Usually need 30 supervised US + maintain proficiency - Positioning - may not be possible for patient to get into right lateral decubitus (e.g. ex fix) - Cannot use for hiatus hernia (as most of stomach may not be visible), previous bariatric surgery - More challenging in obesity, pregnancy, children and non-cooperative adults (who are all arguably better candidates for gastric US) - Role in extubation is uncertain
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How and when to use an Aintree Intubating Catheter
Has 4.8mm internal diameter, 6.5mm external diameter. 56cm length Idea is that you have placed an LMA. Then can load an intubation catheter onto a 4.2mm bronchoscope, the last 3cm or so of the bronchoscope should be free so you can still move it up and down as normal. Then pass bronch + intubation catheter through intubating LMA to carina. Then can leave intubating catheter in the trachea and remove bronch + LMA. Then Can railroad an ETT over intubating catheter. Must be at least size 7 ETT (as external diameter is 6.5mm). then remove catheter and leave ETT
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Airway exchange (Cooks) catheter sizing
Smallest = 8Fr = 2.7mm external diameter. 45cm in length. Smaller ETT it can take is a 3.0 Other diameters include 11F, 14Fr and 19Fr. these are all 83cm length. Useful for high risk extubation to facilitate re-intubation DLT airway exchange catheter exists too. This is either 11Fr or 14Fr and 100cm in length
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When using a nerve integrity monitor tube (NIM), what to do if unable to get signal from nerve stimulator
NIM tube relies on EMG activity of intrinsic laryngeal muscles. Surgeon has nerve stimulator for recurrent larnygeal nerve, stimulates nerve action potential, release of ACh at NMJ --> action potential at vocal muscles (EMG) 1) Issues with nerve stimulator - insufficient current for stimulus (increase, or try alternative side). Usually start with 0.5mA and increase to 1 then 2mA. - Incorrectly identified recurrent laryngeal - Scar tissue over RLN. Can stimulate vagus nerve more proximally - Not plugged in or faulty leads 2) Issues at NMJ level - Paralysis. check twitches at APB, give reversal if not or wait - Rarely electrolyte abnormalities 3) NIM tube - Most commonly, tube as moved. Check position at lips. Check position of EMG detector with VL - copious secretions - Occasionally faulty NIM tube or monitoring leads, needing replacement 4) Issues with the nerve - Surgical retraction - Neuropraxia - Surgical transection
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Complications at extubation
NAP4 - 30% of airway complications at extubation Airway - Sore throat, soft tissue injury - Vocal cord trauma (cuff not deflated - Aspiration - Airway obstruction +/- Negative pressure pulmonary oedema - Laryngospasm Breathing - Hypoxaemia. Often multi factorial e.g. hypoventilation, atelectasis (VQ mismatch). Reduce risk with preoxygenation - Bronchospasm CVS - Coughing, straining, inadequate reversal of NDMR --> increased SNS --> hypertension, MI risk Disability - Increased ICP
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Risk factors and Management of an airway fire
Risk factors include: - Laser use - ENT, airway surgery. Surgery above the clavicles - Non-laser tube - High flow O2 - N2O - High FiO2 - inexperienced anaesthetist / surgeon - Poor communication Management: - Recognition and informing entire team. Red bell emergency - Disconnect circuit from patient at ETT. fiO2 down to 21% - Surgical team to stop laser / diathermy. Pour saline onto face / airway to extinguish fire - While fire extinguishing, prepare for re-intubation - drugs, laryngoscope, new ETT, assistant to anaesthesia - Once fire extinguished, remove ETT - Could consider BMV here with 21% O2. But could send charred ETT further down bronchial tree - Inspect airway with laryngoscope for burns, almost certainly re-intubate with new ETT then commence ventilation - Bronchoscope to inspect airway - CXR + ABG to assess for COHb - Finish surgery, admit to ICU most likely - Documentation, Q+A, medicolegal discussion
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Risk factors for aspiration
Occurs around 1:1000 - 1:10000 depending on study. (APRICOT study in kids had 1:1000). Deaths around 1:200,000 (NAP 4 it was 1:350,000). Most common cause of anaesthesia related death (>50%) Patient - Physiological - obesity, pregnancy - Pathological - Renal failure, gastroparesis, diabetic neuropathy, bowel obstruction, ascites - pharmacological - alcohol, GLP1 agonists, opioids, neostigmine - Fasting status - solids, liquids, timing Surgical - Emergency surgery - Trendelenburg - Laparoscopy - Bowel surgery - Airway surgery Anaesthesia - Airway device - ETT vs LMA - RSI - Topicalised airway with LA
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Management of an aspiration event in theatre
Harms from aspiration include: - Mechanical obstruction from foreign body - Chemical pneumonitis - Atelectasis and V/q mismatch Management: - Recognition - Will depend on airway device in situ or if there is one in at all. Ideally intubation of patient to protect airway from further entry into lower airways - FiO2 100% - Suction what is able to be suctioned out. Keep suction available - Prepare for intubation - laryngoscope, ETT, assistant, intubating drugs (1.2mg/kg rocuronium for RSI) - Avoid PPV, bag mask ventilation until airway secure. tolerate SpO2 transiently likely down to 85% briefly to avoid sending regurg contents further into lower airways - Laryngoscopy. Inspect and suction any obvious foreign bodies from airway. Intubate and then PPV, add PEEP (ARDSNET like ventilation) - Consider bronchoscopy if suspect large foreign bodies that could be removed - Empty stomach with NG tube before extubation - Consideration for whether to continue surgery or not - discuss with surgery. Depend on urgency - consideration for whether to extubate patient - depending on O2 requirements, SpO2 and type of surgery. Or send to ICU Post op - Monitor 24 hours overnight - CXR if hypoxia - Antibiotics only if evidence of bacterial pneumonia (e.g. RLL consolidation on CXR, fever, cough, dyspnoea) - Q+A, documentation, inform patient (open disclosure), medicolegal representation
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Management of high airway pressures
Consider context - Sudden increase or gradual creep? - Recent position change or pneumoperitoneum? - Any recent procedures? ?PTX Management - FiO2 100% - Machine to patient approach - Muscle relaxation potentially - consider this. But need to be sure the high airway pressures are not from NDMR anaphylaxis - At any time if concerns (unable to ventilate, desaturation) - call for DA, anaesthetic assistant + inform surgical team. May need to lose pneumoperitoneum or return to supine position if unable to ventilate Machine - Scan monitoring, etCO2 + capnography trace, SpO2, Hr, BP, airway pressures. ?bronchospasm ?able to ventilate ?evidence of anaphylaxis - Determine severity of high airway pressures - Isolate onto manual ventilation, check compliance and feel for obvious secretions. Then likely back onto vent to free up hands Circuit tubing - Any kinks or obvious obstruction in the tubing Airway - Same position from intubation - Assess patency with suction catheter, remove - Always consider that HME filter or other attachments could be cause for obstruction - isolate onto self inflating bag if considering with a new filter - Bronchoscope = gold standard for confirming tube position + if any obstruction - If LMA, intubate the patient Patient - Trachea position ?central - Central cyanosis? - Ausculatate lungs - ?wheeze ? creps ? unilateral (either PTX vs inadvertent OLV) - JVP, neck veins (evidence of obstructive shock) - Lung US may be useful for determining if PTX or not. Or if CXR available If not obvious cause found other than non-modifiable factors (e.g. patient obese + pneumoperitoneum), then can increase RR and decrease TV, increase FiO2, add PEEP, permissive hypercapnia. May have to consider open surgery if unable to ventilate with pneumoperitoneum
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Most common causes of anaphylaxis in the NAP6 study
Antibiotics (47%) NMBAs (33%) Latex (10%) Chlorhexidine (10%) Other - methylene blue, IV contrast 1:10,000 anaesthetics
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Pathophysiology for anaphylaxis including mediators of anaphylaxis and effects on body systems
Type 1 IgE mediated hypersensitivty reaction. 1st exposure antigen, APC presents to T helper, causes production of IgE from B cells (plasma cells) which adhere to surface of basophils and mast cells 2nd exposure, cross linking of IgE --> mast cell degranulation, release of mediators of anaphylaxis Histamine - tachycardia, H1 + H2 mediated decreased SVR, H1 mediated bronchospasm. Mast cell chemotaxis Bradykinin - increases NO, decreased SVR Leukotrienes (C4, D4, E4)- bronchospasm Tryptase - activates compliment and coagulation cascade Serotonin - platelet activiation, vasodilation Prostoglandins (PGD2 PGE2 - vasodilation CVS - Tachycardia, hypotension, arrythmia, arrest. Hypotension most common sign (48%) - Capilliary leak of fluid from intravascular space into interstitial space. Hypovolaemia Resp - Bronchospasm - Airway oedema from capillary leak, stridor, airway obstruction - Desaturation from above. High airway pressures if under GA GI - Nausea, vomting, abdominal pains Haem - Coagulopathy from DIC and / or platelet dysfunction MSK - Rash, urticuria
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IV crystalloid fluid volume for anaphylaxis
Based on ANZAAG guideline 500ml if grade 2 1L if grade 3 2L if grade 4 (cardiac arrest) Consider further 50ml/kg if still hypotension
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Adrenaline IV dosing for anaphylaxis based on severity
Grade 2 = 10-20mcg Q1-2mins Grade 3 = 50-100mcg Q1-2mins. If no response then 200mcg Grade 4 = 1mg After 3 boluses, start adrenaline infusion. 3mg in 50ml NaCl = 60mcg/ml. Start at 3ml/hr = 3mcg/min. Increase up to 40ml/hr
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Drugs other than adrenaline to consider in anaphylaxis
Obvious ones: O2, Iv fluids Hypotension - Noradrenaline - 0.05-0.5mcg/kg/min - Vasopressin - 1-2 unit bolus then 2U/hr - Glucagon 1-2mg IV Q5mins (especially if on beta blocker) Bronchospasm - Salbutamol 100-200mcg bolus or infusion at 5-25mcg/min - Volatiles (sevo) - ketamine - no dose agreed upon Other - Corticosteroids - dexamethasone 8mg IV
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Tryptases for anaphylaxis
Collect at 0, 1, 4 and >24 hours. 24 hour one is the baseline Positive if (1.2x baseline) + 2 Even if -ve tryptases but strong history for anaphylaxis, still refer. Patent blue and IV contrast anaphylaxis less likely to cause tryptase rise
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Decision on whether to carry on or not following an anaphylaxis event
Will depend on patient factors (recovery from event, ongoing support, comorbidities), surgical factors (timing of event, emergency surgery or not, extent of surgery e.g. cardiac). Risk - benefit - increased risks of post op hypotension, AKI, poor wound healing, coagulopathy - MDT discussion with surgeons, anaesthetists, ICU Western Australian paper 2018 with 223 hypersentivity reactions, 104 cases proceeded and 119 abandoned. Of grade 3 anaphylaxis that proceeded (42%), no difference in outcomes
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Doses for paediatric anaphylaxis
Rates of paeds anaphylaxis 1:37,000 (presumably more done on LMAs and masks and less antibiotics given) in NAP6. No mortality - IV fluids - 20ml/kg. Further 20-40ml/kg if resistant hypotension - IV adrenaline. 2mcg/kg (moderate hypotension) 4-10mcg/kg (life threatening) - IM adrenaline. 150mcg if <6, 300mcg if 6-12. Q5 mins - Adrenaline infusion. 20mcg/ml (=1mg in 50ml) then run at 0.1mcg/kg/min (up to 2mcg/kg/min) (less worried about ischaemia and arrythmia in children than adults so smash them with adrenaline / norad) Resistent hypotension - Noradrenaline 0.2-2mcg/kg/min - Glucagon 40mcg/kg - Vasopressin 0.02-0.06U/kg/hr Resistant bronchospasm - Salbutamol (6 puffs if <6, 12 puffs if 6-12) or IV - magnesium 50mg/kg Other - hydrocortisone 2-4mg/kg max 200mg
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Risk factors for latex allergy and prevention precautions for latex allergy
Hev B = haptin protein from latex. Highly immunogenic, antigenic Risk factors: - Female - Chronic exposure (multiple surgeries, healthcare workers, rubber factor workers) - Recurrent catheterisation (spina bifida, neural tube defects). spina bifida have 25-50% rates of latex allergy - Atopy - eczema, asthma, sinusitis - Fruit allergies (cross reactivity with kiwifruit, banana, avocade, passionfruit, peach, cherries and chestnuts) Prevention - If elective surgery, ideally have patient first on list. And all latex items removed from theatre to allow ventilation - Ask all patients about allergies - Assume high risk patients (spina bifida) as latex allergy - Remove all latex products from theatre, tape over latex glove containers - WHO sign in, timeout - signs outside of doors - routine use of non-latex medical equipment - Recognition with routine use of monitoring and index of suspicion. Access to adrenaline. Iv access in patient
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Management of hypoxaemia under GA
Hypoxaemia = PaO2 <60mmHg Temporise with FiO2, consider telling surgeons to stop surgery / pneumoperitoneum and calling for help. -O2 supply - Machine and monitoring - Circuit and tubing - Airway device - ETT, LMA or upper airways if no airway device - Lower airways - Look, listen, feel. Differentials include bronchospasm, aspiration, PTX, foreign body, PE, anaphylaxis, atelectasis, APO. Consider low FiO2, hypoventilation, diffusion issue, V/Q mismatch and shunt - Cardiovascular - Other - methylene blue, methaemaglobinaemia, N2O diffusion hypoxia subsequent management - ABG - CXR - Bronchoscope - CT chest
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Definition for life threatening asthma
Any of the following: - Raised PaCO2 (bad sign, peri arrest) - PEF <33% predicted - SpO2 <92%, PaO2 <8kPa - Silent chest - Cyanosis - Bradycardia, arrythmia - Hypotension - Exhaustion - confusion, reduced GCS All suggest impending resp arrest, need to prepare for intubation
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Management of bronchospasm under GA
FiO2 to 100%, inform surgeons, call for help Confirm diagnosis - fastest way to confirm diagnosis if uncertain is to isolate with a self inflating bag and no HME filter. If still difficult to ventilate, then the issue is the ETT or lower airways. Can pass suction catheter down ETT to rule out this issue -differentials for bronchospasm: anaphylaxis, foreign body, secretions, airway kining, MH, PTX, endobronchial intubation Management - consider intubation if only mask / LMA if unable to ventilate due to high airway pressures - Increase sevoflurane volatile anaesthetic - Salbutamol - 12 puffs via MDI inline with circuit. Or IV 50-100mcg. If awake 2.5-5mg neb - Ketamine - probably a big dose like 1-2mg/kg if needed - Magnesium 2.5g slow push for adult. 40mg/kg in paeds - Adrenaline 10mcg boluses. Or 1mcg/kg in paeds - 8mg dexamethasone - If awake, consider 0.5mg ipratropium neb - Ventilation strategy: fiO2 100% and titrated to SpO2, Peak pressures <40cmH2O, PEEP 0-5cmH2O, RR 8, I:E 1:4, permissive hypercapnia. PCV better than VCV Other - ICU admission - VV ECMO - Consider effects of high dose salbutamol - hypokaelamia, hyperglycaemia - Management of gas trapping - disconnect circuit and push on thorax.
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Management of gas trapping from jet ventillation or severe obstructive airways disease
Recognition - Increasing thorax diameter - Raised JVP, engorged neck vessels - Increasing airway pressures - Reduction in cardiac output (decreased BP) Management: -Inform surgeons - FIO2 100% - Disconnect circuit (if circuit attached), press on thorax to decompress - Back onto circuit if you have one. Allow more time for expiration to avoid gas trapping
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Causes of massive pulmonary haemorrhage?
VITAMIN C (surgical sieve) Vascular - AV malformations, aorta-bronchial fistula Infection (TB, aspergillosis, necrotising abscess) Trauma (blunt, penetrating, high velocity) Autoimmune (SLE, granulomatous with polyangitis, goodpastures) Malignancy (small cell, adeno, mets, radiation) Iatroegnic (PAC, bronchoscopy injury, endotracheal injury) Natural (congenital) - cant think of anything Coagulation (PE, coagulopathy, anticoagulation)
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Management of massive pulmonary haemorrhage
- Call for help, 100% FiO2 - If undifferentiated, PPE as could be TB - Airway. Expect this to be difficult (consider if appropriate if end stage lung cancer). Prepare with 2x suctions, direct + VL. Consider DLT for lung isolation. could use SLT to isolate lung - Breathing 100% FiO2. Most deaths are from asphyxia and V/Q mismatch not haemorrhage. If intubated, consider placing good lung as dependent in lateral position to improve ventilation and perfusion to it, and isolate off bleeding lung - Circulation. large bore Iv access. hypotension very late sign. Give blood products. Prevent coagulopathy. Reverse anticoagulation - Other: bronchoscopy, identify cause (CT A). IR embolisation often preferred treatment Thoracic surgery usually last resort, high risk of death
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Management for a pulmonary embolism
Depends on how big it is. Very small ones may get no treatment (subsegmental) Non-massive / submassive (= some evidence of RHS on echo, CTPA, raised BNP or raised trop but no hypotension) - anticoagulation (usually start enoxaparin 1mg/kg BD or heparin infusion, 10,000U loading then 1500-2000 U per hour based on APTT (aim 1.5-2.5x normal) - Long term anticoagulation Massive PE (hypotension) - Large bore IV access, arterial line, cautious fluid loading - Central line for inotropic support - thrombolysis. Alteplase 10mg over 2 mins then 90mg over 2 hours (relative contraindicated if recent surgery, bleeding. 1-2% risk of intracranial haemorrhage which has 25-50% mortality) - Perc mechanical thrombectomy (especially if available in centre +/- contraindications to thrombolysis) If ongoing anticoagulation contraindicated, IVC filter may be option
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Causes for acute pulmonary oedema
Cardiogenic - MI - Arrythmia - Valvulopathy - Heart failure - catecholamine storm / severe hypertension (pre-eclampsia) Non-cardiogenic - Negative pressure pulmonary oedema / upper airway obstruction - Neurgenic (e.g. SAH) - Aspiration - Sepsis - Impaired lymphatic drainage (e.g. psot lung transplant) - Rapid lung expansion (e.g. post OLV in thoracic surgery)
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4 S's for patients that fail to wake from GA
Sedatives (anaesthetics, opioids, benzos) Strokes Seizures Sudden metabolic disturbances (sodium, calcium, glucose, hypothermia) Also need to consider - non-reversal of muscle relaxant, drug error, poor cerebral perfusion, hypoxaemia, rarely hypothyroid coma Get CT head if no wakeys
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Risk factors for LAST
Patient - Low body weight - Children - Comorbidities - renal, hepatic, cardiovascular, epilepsy - Lignocaine infusion, surgical infiltration of LA on top of regional technique - Malnutrition, low albumin or alpha 1 acid glycoprotein - Acidosis - Sepsis Block factors - Location (trunk has more rapid systemic uptake than peripheral) - US vs landmark (US can often allow less volume) - Plane block (higher volume usually needed) - single shot vs catheter - Not aspirating before injecting (risk intravascular LA) Local anaesthetic factors - Dose - volume and concentration. Exceeding recommended levels - Type of LA - bupivacaine more cardiotoxic than ropivacaine (2mg/kg vs 3). Long acting vs short. Ester vs amide. Isomerism. - Additives (adrenaline for lignocaine)
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Management of LAST
Based on AAGBI (Association of anaeesthetists for GB and Ireland), updated in 2023. ANZCA endorses this - Stop LA infiltration - Call for help - Airway. Consider intubation. Especially if reduced LOC, seizures, cardiovascular instability. Will allow for hyperventilation for impending metabolic acidosis - Breathing. FiO2 100% - Circulation - give 1mcg/kg adrenaline boluses (instead of 1mg) if confident LAST cause of arrest. Animal studies suggest better survival. May be due to lactic and metabolic acidosis from adrenaline (on top of LAST metabolic acidosis). Consider other 4Hs and Ts though (anaphylaxis could present with CVS instability and needs lots of adrenaline) Give metaraminol if hypotension but not collapse Likely prolonged CPR, due to high protein binding (99% for bupivacaine) to myocardial proteins Ensure large bore IV access. Secure arterial access Can give amiodarone (but do not use lignocaine if no amio) VA ECMO if appropriate - Disability. Treat seizures with benzos. Usual 5mg midazolam followed by another 5mg 5 mins after. Consider propofol, thiopentone, (but caution if haemodynamic instability) or rocuronium for refractory seizures. ANZCA APM:SE book suggests getting on top of seizures before intralipid administration -Intralipid 20%. Thought to provide lipid sink for highly lipid soluble LA. Or replace fatty acids as LA inhibits myocardial fatty acid oxidation. Initial dose 1.5ml/kg over 1 minute slow push + start infusion at 15ml/kg/hour (1000ml/hour for 70kg person) Repeat bolus dose 1.5ml/kg every 5 mins until circulation resolved, maximum of 3 boluses total. If not improved at 5 minutes, increase infusion to 30ml/kg/hour (2000ml/hour for 70kg person) Maximum cumulative dose = 12ml/kg = 800ml for a 70kg person Ensure the intralipid is labelled as looks like propofol Post event - ICU admission - Amylase and lipase daily for 2 days (pancreatitis common after high lipid load) - M&M meeting
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Management of a total spinal
= LA at level of brainstem or brain. Impending total spinal when higher cervical nerve roots are being blocked. C8 = 5th digit. C7 = middle finger. C6 = lateral forearm. Shoulder abduction = C3-5 --> impending phrenic nerve block and respiratory arrest - Call for help - Anaesthesia assistant, another anaesthetist if available, obstetrician - Need to consider long list of other causes for maternal collapse: Obstetric causes: haemorrhage, peripartum sepsis, AFE, eclamptic seizure Non-obstetric causes: PE, anaphylaxis, LAST, primary cardiogenic (arrythmia), stroke (especially if preeclampsia), venous sinus thrombosis, other siezure - Ensure 15 degree left tilt to reduce aortocaval compression syndrome - commence ACLS algorithm with chest compressions, early intubation if not breathing and pulseless - Airway - Open airway, if not breathing needs RSI. Give ketamine and rocuronium and intubate immediately. Expect more difficult airway (use VL). Have suction (pregnant). Weight up transfer to theater if able for airway management Head up (reverse trendelenburg) - Breathing - FiO2 100%. Will need ventillation until LA worn off (and don't forget about NDMR either) - Circulation- support with vasopressors, inotropes. Atropine if bradycardia only. If bradycardia + low BP --> adrenaline. Likely to be peripherally vasodilated (low SVR), negative inotropy from LA blocking cardiac accelerator fibres. May be bradycardic (block of T1-T4) but high spinal at brainstem may cause block of vagal tone --> may result in similar HR to that of denervated heart (which tends to be high-normal at 90-100BPM). Likely to have haemodynamic instability. Insert arterial line - Disability - Initially keep anaesthetised with 2mg IV midazolam (amnesia, cardiovascularly stable). Treat seizures with 5mg Iv midazolam. If in theatre, have sevoflurane at MAC 0.3 to start and titrate to MAC 0.7 if haemodynamics allow - Foetal - CTG monitoring, if foetal distress or compromise to mother which could be improved from foetal extraction --> discuss with obstetrician for emLSCS. - Perimortem C section decision by 4 minutes, delivery at 5 minutes if arrest - ICU for ventilation until LA wears off - ABG, FBC, U+Es, LFTs, Coags, TEG - checking for alternative diagnoses (e.g. AFE)
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4Hs and 4Ts for cardiac arrest
Hypoxaemia Hypo / hyper kalaemia Hypothermia Hypovolaemia Thombosis Tension Toxin Tamponade
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Diastolic BP goal during CPR (if arterial line in situ)?
>25mmHg. Coronary circulation
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Post cardiac arrest care
- Repeat A-E assessment. - Often need inotropes, vasopressors - Identify cause (Hs and Ts) if not apparent yet - echo, ABG (electrolytes, Hb) - Decision for continuing vs abandoning surgery - Restart anaesthesia (sevoflurane at 0.3 MAC or 2mg Iv midazolam) - ICU involvement - admission, intubated + ventilated most likely - 12 lead ECG (if evidence ST elevation --> cardiology) - Goals: MAP >65mmHg, urine output >1ml/kg/hr SpO2 94-98% Normocapnia BGL 6-10mmol/L Temp <37.5c for 72 hours - CXR - rib fractures, pneumothorax from this - Prognostication - 72 hours post event neurology - Seizures common (12-24% of patients) - levetiracitam - consider cardiology referral if no obvious cause identified ?primary cardiogenic - Rehabiliation once in ICU, continued on ward
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Dose of dubutamine for cardiogenic shock
Comes in 250mg in 20ml ampoule (12.5mg/ml). Make up to 50ml with saline (5mg/ml) run at 5mcg/kg/min to start. Increase up to 20mcg/kg/min. Often need to give a vasopressor aswell (as also vasodilates)
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Use of SvO2 in shock
True SvO2 needs to be measured from pulmonary artery (PAC). If taken from central line (ScvO2, more likely to represent from SVC (and be lower due to high extraction ratio from brain) SvO2 should reflect O2 supply and demand - If >65% then may indicate high cardiac output state (sepsis, anaphylaxis, neurogenic shock). But could also be from high FiO2 or hyperbaric O2 - If <65% and sepsis, might indicate an inotrope will be helpful - If <65%, typically from low cardiac output states (cardiogenic, hypovolaemic, obstructive shock) Controversial use of ScvO2, Rivers trial lead author had shares in device meaasuring ScvO2. Rivers trial found benefit titrating vasopressors / fluids / inotropes based on ScvO2 ARISE trial in Aus / Nz found no benefit for using Rivers goal directed fluid therapy
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What is base excess? Normal values?
Base excess = amount of acid required to normalise pH to 7.4 with a PaCO2 of 40mmHg at 37c. - More -ve --> more metabolic acidosis Normal between -2 and 2mEq/L
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Causes of hypertension perioperatively
Patient factors - Pre-existing HTN - Endocrine: hyperalodsteronism, hyperthyroidism - Renal + overload - Obstetric - pre-eclampsia - withholding usual antihypertensives - Pain - Medications - vasopressors, serotonin syndrome, neuroleptic malignant syndrome - Phaeochromocytoma - Carcinoid syndrome - Urinary retention - Autonomic dysreflexia - Drugs (methamphetamine, cocaine) - Raised ICP Surgical - Stimulating surgery - Steep head down - Pneumoperitoneum - Aortic cross clamp - LA with adrenaline. Or cocaine use Anaesthetic - Inadequate analgesia / anaesthesia - AAGA - Excess IV fluid administration - Drug error - Measurement error - Intubation, laryngoscopy, extubation
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Causes of a pericardial tamponade? Effects on cardiac output?
Infectious - TB, viral pericarditis, bacterial Inflammatory - autoimmune (SLE, rheumatoid), Dresslers (post MI) Traumatic - blunt, penetrating, type A aortic dissection Iatrogenic - TAVI, PCI Neoplastic Post radiation Pericardium is fibrous, poor compliance. Usually only 20-30ml fluid here. If rapid accumulation fluid --> more dramatic effect on haemodynamics Increased pericardial pressure --> compression of RA, RV. Particularly impaired disatolic filling of RV. With inspiration --> increases bowing of interventricular septum into LV --> drop in BP (exaggerated response, pulsus paradoxus = drop of systolic BP >12mmHg or >9% with inspiration) Eventually tamponade large enough to compress all 4 chambers of heart --> peri arrest
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Echocardiogram for pericardial effusion
eFAST - 89% sensitivity and 99% specificity for tamponade Measurement of effusion during diastole Small <1cm, Moderate - 1-2cm, Large >2cm Usually right heart affected before left. Collapse of RV in diastole. IVC dilation. Excess interventricular septum bowing into LV on inspiration
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Management of a large pericardial effusion + tamponade
- Diagnosis - risk factors, symptoms, exam, US highly sensitive - Need to determine if tamponade and shock features (low BP or evidence reduced end organ perfusion / heart failure). If so, prepare for pericardiocentesis urgently - done with LA. Get cardiologist to do this - Haemodynamic goals "full, fast and tight". Diastolic dysfunction High normal HR High normal SVR Well filled, high preload Sinus rhythm Maintain contracility - If needing GA for surgical window, this is high risk. Ensure large bore IV, arterial line, adrenaline 10mcg/ml drawn up. Often done subxiphoid or VATS access. Prepped and drapped and surgeon ready with sternotomy saw if needing this. Metaraminol infusion running. Preload with 250-500ml IV fluids. Induce with fentanyl (will need if for sternotomy), etomidate or ketamine, rocuronium 1.2mg/kg. ETT. IPPV is high risk as will increase intrathoracic pressure. - Often get rebound hypertension once pericardial effusion drained - turn off pressors, increase anaesthetic
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How to do a pericardiocentesis?
- Consent patient (unless life threatening) - Ideally US guided - 2% chlorhex to skin, lignocaine 1% to skin - 18g pericardicentesis needle - Subxiphoid 1-2cm. Angle 45 degrees from saggital plane and cephalidly. Aim toward left shoulder tip. - Advance and aspirate simulatenously. Ideally watch needle enter pericardial space on ultrasound - Feed of pericardial drain from needle. Remove needle. - Confirm placement, aspirate off pericardial fluid from cannula - Once aspiration of fluid and tamponade resolved (if this was a problem), can place a wire into cannula and then a skin dilator. Then place a pigtail drain
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MHANZ recommendations for amount of dantrolene held at a hospital?
24 vials of 20mg dantrolene at any location where MH triggering could occur (or 2 vials of Ranodex 250mg vials) Larger hospitals should have 36 vials
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Drugs and equipment other than dantrolene should be in an MH box?
Need a warm box and cold box Warm box: Sterile H2O, adrenaline, lignocaine 1%, amiodarone, sodium bicarbonate, 50% dextrose (for insulin-dextrose). 60ml syringes. Large bore filling needles, blood tubes, algorithm / guideline for crisis Cold box (e.g. chilly bin or esky): cold crystalloids for IV + packing, actrapid insulin
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Signs of malignant hyperthermia
In context - exposure to a volatile agent or suxamethonium Early - etCO2 rise, increased HR (initially sinus tachycardia), masseter spasm (won't improve with muscle relaxation), increased RR (if awake) Evolving - Hypotension, body rigidity, hyperthermia >38c, decreased SpO2, arrythmia (tachyarrythmias first then ventricular ectopics), hyperkalaemia (peaked T waves on ECG), oligouria, respiratory then mixed resp + metabolic acidosi Late - Rhabdomyolysis, renal failure / anuria, cardiovascular collapse / arrest
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Management of MH
As per MHANZ guideline = ANZCA endorsed - Call for help - Stop triggering agent - Increase FGF to 15L/min, fiO2 to 100% - Stop surgery as soon as possible (unless absolutely critical e.g. large haemorrhage - get senior surgeon in ASAP) - Start TIVA ASAP - propofol at 30-50ml/hr or TCI at 4mcg/ml or midazolam 2.5-5mg IV -Assume team leader roll, hands off. Assign rolls as people enter. MHANZ recommend at least 9 people (3 on dantrolene). simultaenous treatment with early dantrolene as a high priority - Get MH box (room temp + cold MH box) brought in - Airway - ensure intubated if not already (don't use sux, NDMR may not work) - Breathing - FiO2 100%, hyperventilate with high RR to aim to decrease etCO2 and reduce acidosis. do not change circuit - Cardiovascular - treat arrythmia with amiodarone 3mg/kg or lignocaine 1mg/kg IV. - may need adrenaline / noradrenaline support - arterial line - monitor ECG for signs of hyperkalaemia (e.g. peaked T waves) - Dantrolene - dose = 2.5mg/kg Q10mins based on TBW. No maximum dose. Since each dantrolene vial = 20mg, may be lots of vials. Dissolve in 60ml sterile H2O. 100kg person will need 240mg = 12 vials per dose. Give dantrolene until PaCO2 <6kPa and temp <38c (if Ryanodex available, this is 250mg in one vial and can be dissolved in 5ml H2O) Need to consider where next dose of dantrolene is coming from - especially in smaller centres - may need to be transported - Exposure / electrolytes. Temperature monitoring. Pack axilla and groin with cold saline. If open abdomen --> surgeon can pour in cold saline Give cold IV fluids. Aim temp <38c If no arterial line yet, need to insert one now for checking electrolytes - Treat hyperkalaemia with calcium gluconate 10% 10ml (cardiac stabilisation) then 10u actrapid + 50% dextrose 50ml IV push - Place CVL -Everything else: FBC, U+Es, CK level, TEG (can get DIC), urinary catheter (aim urine output >2ml/kg/hour) Consider sodium bicarbonate if metabolic acidosis (not for respiratory only acidosis) 1ml/kg 8.4% IV push ICU admission - monitor for rebound MH, rhabdomyolysis, hyperkalaemia, renal failure Referral for testing Discuss morbidity / mortality meeting
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Preparing for an MH susceptible patient
Can either purge anaesthetic machine with no vaporiser in for 90 mins on high flows OR Remove vaporiser and flush machine for 90s at 10L/min with 2L test lung. then change breathing circuit and CO2 absorber. Then attach charcoal fitlers to insp + exp limbs. (means can prepare to do anaesthetic on MH susceptible patient in 2 mins) Once charcoal filter on, can do anaesthetist with MH susceptible patient. Keep at 10L/min FGF until 90 mins. then can reduce to 3L/min filters are single use, can be used for 12 hours at 3L/min gas flows
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Neuroleptic malignant syndrome pathophysiology
Life threatening reaction to dopamine antagonists, leading to muscle rigidity, autonomic instability, hyperthermia and possibly rhabdomyolysis. Most commonly due to D2 antagonists (metoclopramide, haloperidol, droperidol), first generation anti-histamines (promethazine, prochlorperizine, levomepromazine), antipsychotics (olanzipine, quetipaine) 10% mortality rate Reduced dopamine effect due to antagonism of D2 receptors at the corpus striatum of basal ganglia --> skeletal muscle spasticity --> hyperthermia, rigidity (like PD on steroids) Risk factors: -Men under 40 (might be just due to high doses of neuroleptics) - Rapid withdrawal of levodopa - Lewy body dementia - Parkinsons disease - Some genetic polymorphisms - High doses of D2 antagonists and use of multiple agents with D2 antagonism
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Signs and symptoms of NMS? Management?
Confusion / aggitaiton (present in 70% of cases, often first symptom) Extrapyramidal symptoms - Rigidity, tremor, occulogyric crisis Autonomic instability - sinus tachycardia (other arrythmia possible), labile hypertension Hyperthermia (80% have temp >38c, 40% will have temp >40c) Other: DIC, rhabdo, respiratory failure, VTE Management: - Generally supportive - Stop dopamine antagonists - Call for help - consider alternative diagnoses (SS, MH, MDMA overdose, thyroid storm, heat stroke, opioid withdrawl) - A-E approach - Airway + breathing - FiO2 100%, consider intubation for hyperventilation (metabolic acidosis) - circulation - 500ml Iv fluids, arterial line - Disability Bromocriptine (=dopamine agonist, oral only) - 2.5mg Q8hrly starting dose Dantrolene for muscle rigidity 2.5mg/kg up to 10mg/kg (only if intubated, severe NMS and using bromocriptine too) Benzos if seizures -Exposure / electrolytes Check ABg, electrolytes, CK - treat hyperkalaemia (insulin dextrose) - Actively cool until temp <38c - Treat rhabdo with IV fluids, consider sodium bicarb (alkalising urine, metabolic acidosis) Other: - ICU - If aggitation, use dexmed (not haloperidol haha)
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Serotonin syndrome pathophysiology
Life threatening excess of serotonin in CNS + peripheries, from medications Causes: confusion, autonomic instability (hypertension, tachycardia, arrythmia), hyperreflexia / clonus, seizures, hyperthermia, rhabdomyolysis, DIC, pupilliary dilation, GI pain / nausea - Often more rapid onset than NMS (with 12-24 hours of drug administration) - Hunter criteria (84% sensitivity, 97% specificity). Clonus or hyperreflexia most important part once confirmed patient on serotonergic drugs Triggers: - Direct agonists - metoclopramide, ergometrine, sumatriptan / rizatriptan - Reuptake inhibition - SSRIs, tramadol, SNRIs, TCAs, pethidine, methadone, antipsychotics, methamphetamine - Block metabolism (MAOi) - meclobemide, slegiline, methylene blue - Interactions (e.g. St Johns Wort + SSRIs) Fentanyl has mild serotonergic effect
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Management of serotonin syndrome
Mainly supportive. ABCs, call for help, usual stuff - Ensure differentials thought about (thyroid storm, NMS, opioid / alcohol withdrawal, encephalitis) - Airway. If intubating, use rocuronium (no sux as fasciculations may worsen metabolic state, hyperkalaemia). No fentanyl. Propofol is good. As are benzos - Breathing - hyperventilation for metabolic acidosis - Circulation - IV fluids for rhabdo, cooling. Arterial line. - Disability Benzos for aggitation, seizures Cyproheptadine = 5HT2a antagonist. Use is off licence but sometimes used. Ensure other supportive agents in place first. Oral only. 12mg loading (NG tube) then 4-8mg Q6hrly -Exposure / electrolyes. Active cooling to 38c Monitor urine output. Iv fluids for rhabdo For severe refractory hyperthermia, rocuronium is drug of choice (mild hyperthermia, give benzos) Other: - ICU admission - Benzos, propofol, dexmed all reasonable for sedation - ABG, electrolyes (K+), CK levels
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Volume / rate of air entrainment needed for clinically significant venous air embolism
Thought to be 3-5ml/kg Rate of 0.5ml/kg/min
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Signs / symptoms / monitoring for detecting venous air embolism
Decreased etCO2, hypoxia, tachycardia, hypotension, arrythmia, bronchoconstriction, cardiovascular collapse EtCO2 = sensitive + readily available Doppler US most sensitive non-invasive monitor (but cant differentiate between clinically insignificant and massive VAE) TOE = most sensitive, can detect as small as 0.002ml/kg air. But invasive and user dependent Least sensitive = windmill swoosh on auscultation
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Management of a massive VAE
Mainly supportive. Usual call for help, ABCs - ACLS algorithm if arrest. CPR may break up air embolism -tell surgeon - they should flood surgical field with saline and bone wax open veins. If laparoscopy, desufflation of abdomen (CO2 absorbed much faster than air. Hyperventilate to remove) -Airway - intubate if not already - Breathing - FiO2 100% will help with hypoxia + decrease size of air emboli. Consider adding PEEP (unless PFO). Ensure no N2O - Circulation - IV fluids to increase CVP. Position surgical site below level of heart Other - If CVL, aspirate to confirm diagnosis + treatment. But unlikely to place CVL unless extra pair of hands - Hyperbaric O2
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Differences between VAE and CO2 embolism?
- CO2 embolism more likely with pneumoperitoneum. Ensure de-sufflate abdomen if suspected. May be from trochar directly in vessel. Or injury to a vessel and CO2 uptake - Like VAE, can get decrease etCO2, tachycardia, hypoxia, arrythmia, RV failure, hypotension or CVS arrest But generally less severe symptoms than VAE. etCO2 may actually increase if small volume emboli reaching pulmonary circulation (and not a large embolism obstructing RV) - CO2 30x more soluble than air, symptoms tend to disapate much faster than VAE - Hyperventilation with 100% FiO2 will aid in clearance of CO2 embolism
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Neurosurgery cardiac arrest consdierations
Causes: VAE, arrythmia from brainstem involvement, raised ICP Positioning - prone, sitting. Mayfield pins. Need to release pins and big team to roll patient. Cover head wound Drugs - Adrenaline smaller dosing (start 100mcg, uptitrate as per UK resus council)
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Management of intraop seizures
- recognise: easier if awake (decreases GCS). Increased etCO2, rigidity, tachycardia, hypertension, dilated pupils. EEG - Cold saline to open craniotomy - Midazolam 5mg IV - Propofol 1mg/kg or thio 3-4mg/kg IV - AEDs - Find cause - electrolytes, glucose, hyperthermia, drugs. CT brain if unsure
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Drugs for status epilepticus
Status epilepticus = >5mins tonic clonic seizure, seizure of any kind >30mins or not recovering between seizures Midaz - IV 0.1mg/kg or 5mg - IM 0.2mg/kg - IN or buccal 0.5mg/kg Levetiracetam - 40mg/kg over 5 mins. Dilute 1:1 saline Valproate - 40mg/kg over 10 mins. Phenytoin - 20mg/kg over 20 mins. Dilute 1:1 saline too Propofol 1-2mg/kg Thiopentone 4mg/kg Treat underlying cause (e.g. glucose if hypoglycaemia) Treat consequence of seizures (e.g. rhabdo with Iv fluids, hyperkalaemia treatment)
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Intrauterine foetal resuscitation
Goal is to improve foetal O2 delivery for foetus that has demonstrated compromise (e.g. foetal heart rate decels on CTG) SPOILT = mneumonic Syntocin (oxytocin) - turn this off, stop uterine contractions Position = left lateral tilt or manual uterine displacement Oxygen - give. Mainly if low SPO2. Routine O2 doesn't improve foetal pH IV fluids - especially if hypotension Low blood pressure - treat with fluids and vasopressors (pressors if recent neuraxial) Terbutiline (or GTN). 250mcg subcut terbutiline tocolysis. or 400mcg GTN SL
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Pathogenesis of an amniotic fluid embolism
Sudden onset hypoxia, hypotension, cardiovascular collapse, right heart failure, seizures or coagulopathy (DIC) peripartum. Between 10-40% mortality Usually get RHF first from pHTN, then LHF with APO Pathogenesis unclear. Not likely mechanical. More likely massive immune response from foetal cells entering into maternal circulation Diagnosis of exclusion basically (try rule out other causes). More likely AFE if a few of the following: - Cardiovascular collapse, severe hypotension. Associated foetal distress - Coagulopathy in 80%, drop in fibrinogen first. Give cryo. DIC. May get concealed bleeding - Seizures (50%), treat as eclamptic in first instance - Hypoxia (80%), acute pulmonary oedema in 90% Risk factors: - advanced maternal age - Multiparous - Obstructed labour - Multiple gestation - LSCS, forceps delivery - Rapid labour progression - Placental abnormalities (praevia, accretia)
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Treatment for an AFE
Mainly supportive -Call for help - anaesthesia assistant, obstetrician (may need urgent delivery), ICU - Airway - intubate early. High aspiration risk. Risk of hypoxia due to increase VO2 - Breathing - 100% O2. Low insp pressures. Avoid hypoxia, hypercapnia (pHTN considerations) - Circulation - CPR if arrested Lateral tilt Perimortum C section Consider neb milrinone for RHF - Disability - treat seizures. Midaz. Magnesium if considering eclamptic seizure Other - TEG. fibrinogen often first to fall. Treat coagulopathy with products / TXA. If not TEG, give prophylactic cryo - ICU post event
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Differences for obestric cardiac arrest compared to general adult
Causes - Obstetric specific: AFE, obstetric haemorrhage, magnesium toxicity, total spinal, LAST, peripartum sepsis (PE and haemorrhagic stroke from PET also increased risk), aortocaval compression Considerations - Foetal wellbeing too. Although priority is maternal survival - Need obstetrician present immediately. Also anaesthesia assistant. Many pairs of hands Prognosis - Worse than general population. Survival 6.9%. Best hope for foetal survival is maternal survival Airway - High priority for intubation over other airway devices - high VO2, high risk of airway obstruction and aspiration, increased insp pressure requirements due to gravid uterus Circulation - Left lateral tilt 15 degrees (aortocaval) - Perimortum c section within 5 mins. Helps both foetus and mother - Compressions - hands higher on sternum (due to diaphragm displacement by uterus) Drugs/ defib - Adrenaline still. More likely to need this as more likely asystole or PEA arrest than VT/ VF - Defib on but less likely to have VT / VF arrest. More likely if structural heart disease Treatment - If magnesium infusion prior, give 10ml bolus of 10% calcium chloride - If considering LAST - intralipid, prolonged cardiac arrest
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Causes of post partum haemorrhage
4 Ts Tone = uterine atony. More likely if prolonged labour, obstructed labour, tocolytic agents, uterine distention (polyhydramnios) Tissue = retained placenta Trauma = cervix, vulva, vaginal, peroneal tears Thrombin = coagulopathy - acquired or congenital. AFE. PET
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Causes of antepartum haemorrhage
- Uterine rupture. Painful. More likely if previous surgery to uterus, LGA baby (1:300 risk if 1 section, 2% risk if 2 or more sections) - Placental abruption. Usually painful. May not bleed (concealed retroplacental). More likely in smokers, meth, cocaine use, older patients - Placenta praevia. Typically painless. Placenta within 2cm of Os. More likely if prev c sections, prev praevia - Vasa praevia = foetal placental vessels over cervix. risk only to foetus but rapid exsanguination (cat 1 section)
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WOMAN and WOMAN 2 trials
WOMAN trial = RCT, n=20000, double blind. Once PPH, then 1g TXA and further 1g at 30mins if bleeding still. Needs to be within 3 hours of delivery. Reduced number of deaths from haemorrhage (not deaths overall). No increase in thrombosis. No changes to hysterectomy rates WOMAN 2. Prophylactic TXA for all women - no improvement
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Options for atonic uterus intraoperatively
Pharmacological - Oxytocin (bolus + infusion) - Ergotmetrine - Carboprost - Stop volatile, start TIVA - Improve coagulation status - avoid acidosis, hypothermia (Active warming), hypocalcaemia. Treat coagulopathy with TEG guided replacement (often cryo) - Reverse any anticoagulation if present Surgical - Uterine massage - Remove retained tissue (will aid in uterine contraction) - B lynch suture - Uterine artery clamping - Bakri balloon - IR uterine artery embolisation - Hysterectomy Cell saver
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Causes of secondary neurological insult after primary spinal cord injury
Ischaemia (hypotension, anaemia, hypoxia, compression) Excitatory neurotoxicity Free radical formation Inflammatory cytokines Oedema
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3 ligamentous structures that provide integrity / stability to c spine
Anterior longtitudinal ligament (along anterior vertebral body) Posterior longtitiduinal ligament (posteroir vertebral body) Posterior ligamentous complex (ligamentum flavum, interspinous and supraspinous ligaments) = strongest Disruption of 2 out of 3 of these --> unstable fracture
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Pathogenesis of neurogenic shock
Higher the lesion, the more likely to happen. Often in initial injury, get massive hypertension (and risk of heart failure, APO) from catecholamines Then get loss of sympathetic tone below level of lesion. Vasodilation --> distributive shock. If above T4 level --> loss of cardiac accelerator fibres. Vagal tone --> bradycardia, decreased inotropy. May last for few hours --> few weeks after injury Differential from sepsis with low HR and cool peripheries Treat with noradrenaline. Atropine may help with bradycardia. MAPs of 85-90mmHg for SCPP of 65mmHg
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ASIA criteria for spinal injury
American Spinal Injury Association. Documentation for spinal injury. Also includes sacral nerves sensation and tone. Done as part of secondary survey and repeated at 48 hours A = absent. Complete sensory and motor loss below level of lesion (chance of ambulating <2.5%) B = sensory preserved below level (but motor gone). 33% chance of ambulating again C = motor incomplete, more than half of muscles have grade 3 or less power. 75% chance of ambulating D = motor incomplete, more than half of muscles have grade 3 or more power below lesion. 100% likelihood of ambulating E = normal
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Nexus criteria for clearing c spine
- No neurology (sensory + motor + reflexes normal) - No distracting injuries - GCS 15 - No sedation / acute intoxication - No midline tenderness Not part of Nexus is FROM neck
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Disadvantages of MILS
- requires person to do it - may already have limited number of people - Person doing it may be in the way (if standing cranial to patient, in the way of airway / intubation. If caudal to patient, then in way of resuscitation / airway assistant) - Already likely difficult airway, may make it more difficult - Makes cricoid difficult (best if another person does this bi-manually - but then very crowded) - Makes jaw thrust difficult - If used for undifferentiated trauma - most of these wont have c spine injuries (1% of comatose patients will have c spine injury. 10% of major traumas). And those that do, only 10% of these are unstable c spine
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Causes and pathophysiology of compartment syndrome
Soft tissue injury - burns / electrocution, blunt trauma, crush injury Vascular - Ischaemia-reperfusion (hypereamia) e.g. prolonged torurniquet, arterial / venous injury, thrombosis (DVT) Iatrogenic - fluid extravasation, surgical positioning (prolonged lithotomy), arterial tourniquet, femoral access (ECMO, IABP) Other - snake envenomation, DIC, infection Most common compartment is the anterior leg and anterior arm compartments. Due to smallest volume to accomodate increased volume Legs up in lithotomy for long time can cause mild ischaemia. Get hyperaemia when legs down. Can become a vicious cycle. Rising pressure in compartment --> reduced venous clearance, reduced arterial perfusion to muscles and nerves --> ischaemia --> tissue damage, capillary and muscle fluid leak --> further increases in pressure. Start to get tissue infarction, necrosis
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Diagnosis and treatment of compartment syndrome
Palor, pulseless, parasthesia, perishingly cold, painful, paralysis Pain usually out of proportion to injury. But can be painless if nerve death Loss of sensation a good indicator Paralysis is a very late sign. As is pulseless (would need to be above arterial pressure) CK is a late sign as marker of tissue necrosis Can place needle or cannula into compartment and attach pressure transducer, zeroed at level of limb. Normal pressure is <12mmHg. If compartment pressure >30mmHg or compartment perfusion pressure <30mmHg (diastolic BP - compartment pressure) then diagnostic for CS Treatment -Need surgical opinion asap, gold standard is fasciotomy decompression as soon as possible - Analgesia - Remove external bandages, casts. - Avoid both elevation and depression of limb - Aim for normotension (avoid hypotension) - If necrotic tissue, this will need debridement at same time as fasciotomy. Stabilise fractures if these are present - Can develop rhabdo, hyperkalaemia and AKI from massive tissue necrosis. Monitor Cr, CK, K+, pH
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What is bone cement syndrome? Risk factors? Pathophysiology?
Bone cement = acrylic polymer (PMMA = polymethyl methacrylate). Provides mechanical interlock between prosthesis and irregular bony structure BCIS = hypoxia, hypotension, right heart failure and/or rhythm changes from cementing of prosthesis. May be from fat emboli, air emobli or directly from PMMA itself Causes acute increase PVR --> Rv dilation, intereventricular septal bulging into LV --> decreased CO. Signs - hyopxia, hypotension, decreased etCO2, bradycardia Late signs = CVS collapse, arrythmia, LOC Grade 1 = mild hypotension 2 = moderte - severe 3 = CVS collapse Risk factors: Male, CVS disease, other severe comorbidity, elderly, malignancy
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Methods for prevention of BCIS?
Prevention: Anaesthesia - Communication with surgical team, acknowledging of surgeon stating cementing about to start - Euvolaemia - well loaded with IV fluids - Increase MAP, ensure +/-10% of normal. Use vasopressors + have vasopressors available - Increase FiO2, 80% - Normocapnia - Attentive more so during cementing process - no distractions, no handovers Surgical - Only cement prostheses that require it. If patient unlikely to ambulate again, no benefit from cement - Communicate 5 mins prior to cementing + when cementing to anaesthetist, theatre team - Lowest possible reaming pressures, intramedullary pressures - retrograde cementing (distal to proximal) - Cement under vaccum (decreases cement porosity)
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Treatment for BCIS
- Inform surgeons, stop operating - Call for help - Consider differentials for collapse in elderly patient - lots. Get TOE in early to help confirm diagnosis (RV failure) - Mainly supportive - If arrest, start CPR. Turn off anaesthetic - Airway - secure with ETT, FiO2 100% - circulation - metaraminol / adrenaline boluses, IV fluid boluses. Insert A line Consider milrinone neb 5mg Typically only lasts minutes - 1 hour. Short lived - Minimise surgical time with senior operator. consider shorter procedure (hemi arthroplasty instead of THJR) - Post event, get ABG, electrolytes - ICU post op
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Considerations for crush syndrome
Physical compression of body - usually limb but can be abdomen, thorax --> systemic effects of crush injury Larger the volume of body crushed + severity of crush + length of time crushed --> greater the effect of crush - Rhabdomyolysis. If CK >5x upper limit of normal (>1000u/L). 50% chance of AKI if CK >5000. AKI from myoglobin. Hyperkalaemia from tissue injury + AKI. Treat hyperkalaemia (insulin-dextrose). IV fluids. Monitor urine output. Consider sodium bicarb. May need RRT - Hyperkalaemia - from tissue damage, acidosis (impairing Na+/K+ ATPase), AKI - Compartment syndrome - ischaemic-reperfusion from hyperaemia. May need fasciotomies - Open fractures - tetanus, antibiotics, washout and repair - May have intraabdominal / intracranial / intrathoracic / c spine injuries having to deal with too - Can get DIC or sepsis from trauma too
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Regional anaesthesia vs compartment syndrome
No good evidence exists. Only case reports. No RCTs In 5/6 cases, CS was recognised promptly despite regional anaesthesia. And 1 delayed diagnosis. Best practice is use regional if benefit likely. Use lowest possible concentration of LA. Ideally have concensus with suregon. But as per AoA report in 2021, regional anaesthesia decision is ultimately the anaesthetists decision
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Pathophysiology, diagnosis of fat embolism syndrome
Fat globules within the circulatory system. Unclear pathophys. - Mechanical theory - macro / microemboli into circulation causing mechanical obstruction (but doesn't explain temporal relationship, often occurs 24-48 hours post injury) - Biochemical - fat metabolised into FFAs by lipase. FFAs toxic to endothelial cells --> inflammatory response, exagerated endothelial dysfunction - Coagulation theory - from inflammatory response + hypovolaemia + traumatic coagulopathy --> mircoemboli formation --> ischaemia. Can get DIC and thrombocytopenia in FES Can be traumatic (most are), usually long bone fractures / pelvic fractures. Atraumatic from pancreatitis, fatty liver disease, liposuction, sickle cell disease. Occurs in 1:100-300 long bone fractures. Diagnosis of exclusion mainly. Based on symptoms + radiology Triad = respiratory distress, neurological symptoms and petchial rash Gurds criteria - need 1 major and 4 minor criteria: Major = axilla / conjunctival ptechia, hypoxaemia + bilateral radiology changes, neurology unrelated to TBI Minor = pyrexia, tachycardia, fat in urine, emboli in retina, fat globules in sputum, sudden decrease in platelets or Hb CXR or CT often shows bilateral infiltration (CT may have ground glass changes) MRI brain may have stairfield appearance of fat globules (consider if neuro symptoms
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Signs and symptoms for fat embolism syndrome
Usually 24-48 hours post fracture of long bone fracture / femur reaming (as opposed to BCIS which is more acute, during surgery) Triad of resp compromise, neurological compromise and petechial rash Resp - Most common symptom + earliest symptom - Emboli / inflammation of pulmonary capillaries --> increased alveolar deadspace - Impaired V/Q matching--> hypoxaemia - Can get ARDS, resp failure. 44% of FES needs mechanical ventilation CNS - Altered mental status, confusion most common - tonic- clonic seizures - Focal neurological deficit CVS - Tachycardia, arrythmia, hypotension - Risk of RV failure Derm - Petchial rash on face, neck acillar, oral mucosa and conjunctiva. All non-dependent regions of circulation, low density fat globules accumulate here Renal - Oligoruia, proteinuria Haem - Thrombocytopenia, DIC, anaemia all possible
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Management for FES
No specific therapy. supportive treatmetn Call for help -Airway / breathing. Intubate if needed. 44% of FES will need mechanical ventilation consider VV ECMO If ARDS - then ARDNET ventilation style. consider prone patient Consider airway pressure release ventilation (APRV) - Circulation - support with inotropes, vasopressors, IV fluids. consider neb milrinone - Disability - treat seizures with midazolam Treat like TBI, keep CPP above 65mmHg Other - Anticoagulation - heparin not shown to be helpful. May be dangerous in trauma. Aspirin useful in animal models - Steroids - one meta analysis from 2009 of 7 RCTs showed benefit using prophylactic steroids. - Early surgical fixation - ex fixing if needed, reduces risk of FES
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APGAR score for new borns
Done at 1 and 5 mins after birth and every 5 mins until normal HR and breathing Appearance (colour). 0 = cyanosis centrally / pallor. 1= peripheral cyanosis. 2 = pink Pulse. 0 = 0. 1= <100BPM, 2 = above 100BPM Grimace. No response = 0. Weak cry = 1. Strong cry = 2 Activity (tone). Floppy = 0. Some flexion = 1. Full flexion, resists extension = 2 Respiration. apnoea = 0. Slow, irregular = 1. Normal = 2 Should be 7 or more at 5 mins. If under 7, will likely need intervention
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When to start CPAP / positive pressure ventilation for a new born?
Should establish breathing within a minute of birth. C section kids may take a bit to establish as no vaginal squeeze to stimulate breathing First few breathes require high negative pressure to overcome surface tension If not established breathing in 1 minute, or HR <100BPM. Start CPAP (with t piece) with air (5cmH2O). If apnoea, start positive pressure ventilation with neopuff (30cmH2O / 5cmH2O). If no resp effort, may need more than 30cmH2O for first few breaths. Watch for chest rise and fall. Down titrate accordingly If premature, then start with 20-25cmH2O Insp pressure Prolonged inspiration and holds (up to 10 seconds) not recommended any more. Not harmful or beneficial at term. But definitely harmful in prematures
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How to assess efficacy of ventilation in neonatal resus?
Chest rise and fall HR increasing to over 100BPM SpO2 improving (should be appropriate for age after delivery. At 0 mins usually at 60-70%, rises to 85-90% at 10 mins There is increased mortality if using 100% FiO2 over 21%. Start with air and titrate to appropriate sats for age. Give 100% FIO2 if CPR Risk of hyperoxia - cataracts, intraventricular haemorrhage, bronchopulmonary dysplasia, retinopathy of prematurity
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ETT sizing for cuffed and uncuffed tubes for newborns
Uncuffed tubes. Gestation in weeks / 10. E.g. for term --> size 4 Cuffed = uncuffed size - 0.5
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Indications for intubation of a newborn in resus
Unable to attain ventilation with no or limited spontaneous effort (particuarly if hypoxia (age adjusted) and/or bradycardic) - Unsuccessful with OPA, LMA Cardiac arrest Diaphragmatic hernia - avoid GI air insuflation. Will need small volumes (may have only one functional lung from compression). Place orogastric tube to decompress stomach
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When to start chest compressions in a newborn resus?
Newborn should have HR >100BPM at 2 mins of life. If after 30 seconds of adequate ventilation, and HR <60BPM then start chest compressions Ventilation is most critical part of newborn resus. If haven't established this, do not start chest compressions Compressions 3:1 - use dual thumb technique. Have separate person for airway and for compressions. Compress at 90BPM. 0.5s pause between compressions to allow ventilation. If intubated, can compress continuously at 120BPM If compressions started, FiO2 to 100% SpO2 on right hand to detect pulse Get umbilical vein access, give adrenaline as soon as possible
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Medications and fluids for new born resus
If CPR started, get umbilical vein access (smiley face, thin walled vessel). Can take cord gas once umbilical vein cannulated Adrenaline as soon as access gained, HR <60BPM and ventilation established. Dose 10-30mcg/kg Q3-5mins. Flush with saline Endotracheal adrenaline can be given if IV access unobtainable. Dose = 50-100mcg/kg If not responding, give 10ml/kg of 0.9% NaCl. Consider blood transfusion if suspect foetal anaemia (4ml/kg)
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Temperature management for a Newborn resus
For non-asphyxiated newborn, should be normothermia 36.5-37.5c Every degree below 36.5c on NICU admission increases mortality by 28% Warming with radiant heater, keep covered with warm towel when able Prem babies more prone to temp loss. Poikilothermic + no fat. Very prem (<28 weeks) cover in polyethelene sheet. Warm theatre to 26c. Cover head with hat If at risk of hypoxic ischaemic encephalopathy (HIE). Target in resus is still normothermia. NICU decision for induced cerebral cooling. Usually if >35 weeks gestation. consider if CPR >10 mins, APGRA <6 at 10 mins, pH <7.0 from cord gas, evidence for neurological sequelae.
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Risk factors for a newborn needing resus
Maternal - Prlonged rupture of membranes (>18 hours) - Maternal sepsis - Antepartum haemorrhage - Diabetes - Hypertension / PET - Substance abuse - cocaine, methamphetamine - Opioid addiction - GA - C section - cardaic disease - previous neonatal or foetal demise Foetal - multiple gestation - <35 weeks pre term - LGA - SGA - allogenic haemolytic disease - intrauterine infection - reduced foetal movements - Oligohydraminos Intrapartum - cord prolapse - concerning CTG - meconium - prolonged labour - narcotics within 4 hours of delivery
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What is laryngospasm? Pathophysiology?
Total or partial occlusion of upper airway from sustained closure of the vocal cords. Can occur in conscious state but typically occurs under GA or sedation Part of reflex to prevent aspiration (glottic closure reflex) - but becomes problematic in light planes of anaesthesia Most commonly, will be physical stimulation on glottis (but could be painful stimuli elsewhere). Vagal nerve mediated, recurrent laryngeal nerve (muscles are cricoaratenoids, thyroaratenoids and lateral cricoaretenoids) Risk factors: Patient - Age (children = 2x risk, if age 0-3 months then 3x risk) - Asthma - COPD - Hypocapnia - Smoker / smoke exposure. 10x increased risk for kids with passive smoke exposure - URTI within 6 weeks - GORD - OSA - hypocalcaemia Surgical - airway surgery, tonsils, dental - Blood in airway - highly stimulating surgery (bum stuff) Anaesthesia - Light planes of anaesthesia - Not using TIVA. Des worse than sevo - For extubation - ETT worse than LMA which is worse than no airway - induction - mask or LMA - inexperienced anaesthetist - Larynscopy, airway suctioning
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Management of laryngospasm
- Prevention is best - Recognition - Call for help - FiO2 100% - CPAP + Larson's manoeuvre (both fingers behind styloid process) - Propofol boluses - 1mg/kg - suxamethonium (give a proper dose as usually desaturating patient if giving it). 1-2mg/kg IV, 4mg/kg IM, 3mg/kg intralingual consider if intubation needed at this stage - Wake on propofol, clear any cause for laryngospasm (e.g. blood on airway) Some rarer things are: chest compressions, magnesium, lignocaine. None are really in standard approach
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Estimated blood volume for children
Prem babies = 100ml/kg Newborns 0-3 months = 90ml/kg >3 months = 80ml/kg (adults = 70ml/kg) Giving a 4ml/kg IV RBC bolus should increase Hb by 10g/L. aim for HCT of 0.25, normalisation of HR and BP for targets of Hb
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Paeds massive haemorrhage protocol dosing
TXA 15mg/kg for all trauma. then further 15mg/kg over 8 hours (extrapolation of CRASH 2 trial) RBCs - typically start with 10ml/kg if <10kg. Then 10ml/kg FFP, cryo and neoplatelets. If >10kg, then typically just give whole units of RBCs, FFP, cry, platelets (still good idea to syringe it in so can keep track of volume) Targets: - Hb >70g/L, HCt 0.25. Normalisation of HR, BP - INR <1.5, APTT <40s (or else give 20ml/kg FFP) - platelets >75, else give 10ml/kg platelets - Fibrinogen >1g/L else give 5ml/kg cryo - Ionised Ca > 1.1mmol/L. Else give 0.3ml/kg calcium gluconate - If hyperkalaemia, give 0.1U/kg actrapid + 5ml/kg 10% dextrose (or 2ml/kg 50% dextrose)
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Differences in airway management for children compared to adults in trauma
Head trauma more common in children (large heads) More likely to require intubation and ventilation to get through a CT / MRI. More likely to become hypoxic with airway obstruction. C spine bony injuries less common than adults (more flexible) but more commonly affect C1-C4 due to large head size. More likely to get SCIWORA (spind cord injury without radiological abnormalities) - get MRI Can still use MILS - but may distress child. If concerns re c spine and unable to sit still --> intubate, ventilate and paralyse
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Definition of a massive transfusion in a child
>50% EBV over 4 hours (40ml/kg) or >100% of EBV over 24 hours (80ml/kg)
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NICE CT head rules for children
Get CT if: - suspicion of NAI - GCS 13 or less - Tense fontanelle - Children under 1 with brusing, swelling or lac >5cm on head Or 2 or more of the following: - LOC >5mins - Abnormally drowsy - 3x episodes of vomiting - dangerous mechanicam - amnesia >5mins
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Analgesia options for trauma in paeds
Pdol Fentanyl 1mcg/kg intranasal Ketamine 0.2-0.3mg/kg IV Morphine 0.1-0.3mg/kg IV
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Complications from massive transfusion
= >50% EBV over 4 hours or >100% EBV over 24 hours transfused (along with usual possible transfusion reactions, these ones are specific to massive transfusion itself) - Hyperkalaemia - storage lesion of blood, longer RBCs are kept in storage, the more K+ that leaks into extracellular fluid compartment (reduced with dextrose and keeping cool). Treat with insulin-dextrose, calcium gluconate. Hyperkalaemia can also be from AKI, rhabdomyolysis - Hypothermia. Storage at 4c. Warm blood products. Monitor temp. Use Belmont rapid infusion device to warm - Hypocalcaemia - citrate used to prevent clotting of RBCs, can sequester calcium once transfused. Replace calcium (as needed for coagulation) - Lack of 2,3 DPG (diminished due to storage) - less effective offloading of O2 to tissues - dilutional coagulopathy. Reduce with TEG guided. Reduce crystalloids. 1:1:1 transfusion. Can lead to DIC
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List causes of adverse reactions to blood transfusion
Immune mediated - Acute haemolytic transfusion reactions (ABO most important) - Delayed haemolytic - TRALI - Anaphylaxis - Non-haemolytic febrile reaction - Graft vs host - post transfusion purpura - Immune suppression Non-immune - TACO - Sepsis - metabolic - hyperkalaemia, hypothermia, hypocalcaemia - iron overload
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Signs and symptoms of acute haemolytic transfusion reaction Management of reaction
Blood transfusion - usually IgM mediated if ABO incompatibility, can occur with only a few ml of blood. ABO will have acute onset of symptoms (where as rhesus D = IgG mediated, typically slower onset over weeks) Incompatibility with host antibodies and transfused antigens leading to antibody-antigen crosslinking. Haemolysis of red cells Symptoms: - If awake - flushing, nausea, urticaria, dyspnoea, chest pain, limb pains, fever, hypotension - If anaesthetised - hypotension, DIC, haemoglobiuria, bronchospasm Diagnosis: - consider anaphylaxis, TRALI - check bloods - haemolysis, raised unconjugated bilirubin Management - Stop transfusion immediately, disconnect. Save blood products to send back to blood bank for testing - Call for help - Check patient labels, group and screen and blood labels for obvious error - Usualy ABC approach. Intubate if needed - Breathing - FiO2 100%. Give salbutamol or neb adrenaline if bronchospasm - Criculation - IV fluids. Aim >1ml/kg/hr urine output. Aim MAP >65mmHg Arterial line. CVL if haemodynamic instability ECG - can get MI, ischaemia If ongoing bleeding (which was why they were getting blood) - contact haematologist for advice. Optimise haemostasis with TXA, surgical haemostasis May need RRT due to microvascular thrombi to kidneys Other - FBC, ABG, coags, TEG. Treat DIC (but caution with blood products so this is tricky. Haem advice is recommended) - Need to repeat group + screen - Documentation, open disclosure, discuss at Q+A meetings - ICU admission
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Pathophysiology of TRALI Management of TRALI
Transfusion Related Acute Lung Injury = immune mediated. Most common cause of death after a transfusion of blood Presents with ARDS within 6 hours of transfusion, most commonly associated with plasma containing products (whole blood, FFP, platelets) 1:5000 transfusions. 5% mortality. Most recovery in 5 days Less likely if male donor for plasma as reduced HLA antibodies 2 hit theory: underlying illness causes neutrophil sequestration at pulmonary endothelium. Then transfusion of plasma containing antibodies causes activation of endogenous neutrophils --> pulmonary endothelium dysfunction, capillary leak --> APO Differentials: TACO (BNP will be raised, overload on echo), sepsis (obviously signs of sepsis), aspiration Signs / symptoms - Dyspnoea, hypoxaemia, cyanosis, fever, tachycardia, non-cardiogenic APO (bilateral) - PaO2 / FiO2 ratio of <300mmHg. With PAWP <18mmHg (non cardiogenic = ARDS) - Bilateral infiltrations on CXR Management - Stop transfusion. Save product - Call for help - FiO2 100% - Intubation, ventilation most likely. Supportive. - Treat as per ARDSNET. Titrate up PEEP - consider VV ECMO
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Risk of sepsis after transfusion
<1:100,000 with red cells 1:10,000 with platelets (as stored at room temp) CLIP-III trial demonstrated frozen platelets inferior). Staphlococcus, yersenia common causes. Gram -ve bacteria may have very high endotoxin levels, sepsis within minutes of transfusion Send to lab for culture + staining Treat with broad spectrum penicillin or cephalosporin (e.g. ceftriaxone) + 5mg/kg gentamicin
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Graft vs host disease after blood transfusion
Almost universally fatal Residual leukocytes in transfusion infiltration host bone marrow, replicate leading to T lymphocytes destroying host cells delayed (1-6 weeks) presentation of fevers, rash, liver failure, pancytopneia, GI failure, diarrhoea Risk factors: immunosuppresion, non-hodkins lymphoma, transfusion of blood from relative, on chemotherapy Reduce risk with irradiation of blood products (25Gy to centre of container, 15Gy to edges) for immunosuppressed people consult haem. Palliation most likely
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Catagorise types of trauma
Trauma = transfer of physical energy to body Can be blunt, penetrating, thermical, chemical, pressure Also can be categorised on high vs low velocity
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7 stages of trauma
Preparation Triage Primary survey Resusciation Secondary survey Continued post-resus evaluation and monitoring Definitive treatment + ongoing care, recovery
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When to activate a trauma call?
May be due to: Mechanism (i.e. dangerous) - >100KPH MVA, >30KPH MBA, car vs paedestrian, fall >5m, fatality at scene Injuries - 2 or more body cavities, TBSA% burns >15%, airway burns, penetrating to chest / neck, penetrating abdominal wound in pregnancy Signs - GCS 13 or less, systolic BP <90mmHg, HR >130BPM
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STEPUP pneumonic in trauma
- Self - identify self, role, rank to team leader (and ensure you are physically ready aka IM SAFE) - Team - have airway, airway assistant, primary survey, drugs, scribe, IV access, hands off team leader. Trauma call. Confirm surgeon. ICU. Blood bank - Equipment + environment - Airway equipment, breathing equipment, circulation (IV, Belmont, IO, IV fluids), drugs (intubation + emergency + TXA) and defibrillator - Primary survey - ABCDE approach - Update - use shared mental model with team (e.g. vortex in airway) - Priorities - identify priorities and desired clinical trajectory (going to OT, CT)
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What is triage?
Utilising the resources available to get the greatest benefit In a mass casualty event, triage may mean not providing care to those with injuries where they are not expected to survive and using limited resources into those that will live Outside of this, usually triage means seeing the patient with the most life threatening illness first
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What is the injury severity score (ISS)?
Score system in trauma, maximum is 75. 6 body parts counted (head, face, torso, abdomen, extremities and external). Each gets a score of 1 (=minor injury) to 6 (=not compatible with life). If any 6, then ISS automatically 75 --> certain death Else, take the 3 highest scores for each of the body parts. And then square those numbers. And then add those 3 together to get total ISS. E.g. if head = 5, abdomen 3 and torso 3. ISS = 25+ 9 + 9 = 43 Main limitation is that there is heavy weighting if one score particularly high (as square of the number) Also can't be used for triage as need CT trauma to know extent of injuries
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ATMIST AMBO handover by paramedics
Age of patient (+identification) Timing of injuries Mechanism Injuries noted Signs (aka vitals + GCS) (not symptoms) Treatment to date Allergies Medications (relevant) Background Other information Ideally everyone should be hands off patient. All listening to paramedic. Only life saving interventions should be done before handover
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Indications for intubation in trauma
- Obstructed airway not response to adjuncts - Hypoxaemia (PaO2 <8kPa) despite supplemental O2 - GCS 8 or less - Aggitated, aggressive and requiring emergency procedure / CT / surgery - Airway trauma - Airway burns - Humanitarean reasons - vast extent of injuries - Damage control surgery / resuscitation - Cardiac arrest - Resuscitive thoracotomy
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What life threatening breathing conditions need to be assessed for and treated as part of "breathing" in primary survey
Things that will cause hypoxaemia: Tension pneumothorax Open pneumothorax Haemothorax Airway disruption Flail chest Cardiac tamponade Inspection, palpation and auscultation. Then US with eFAST
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What is a tension pneumothorax? Signs and symptoms? Treatment?
Air within pleural space, causing obstructive shock. compression of great vessels and airways. Signs and symptoms: - dyspnoea, hypoxaemia, cyanosis - Distended neck vessels - Tracheal deviation away from tPTX - Decreased air entry - Hyperresonance to percusion - Unilateral chest movement US is more sensitive than CXR. Look for lack of lung sliding, no lung pulse, a lung point and barcode sign on M mode Treatment options are either a needle decompression or finger thoracostomy + chest drain Needle - 2nd intercostal space, midclavicular line. 16g. Perpendicular to skin. Remove needle, leave cannula. Now needs chest drain Thoracostomy - in triangle of safety (pec major, lat dorsi, 5th intercostal space. (4th space preferred in pregnancy as diaphragm raised) - 2% chlorhex to skin, surgical drape. Lignocaine with adrenaline if conscious - Scalpel just above rib (avoid bundle) - Blunt dissection with finger to pleura ---> rush of air confirmation in space - 32Fr chest drain, direct apically for PTX - Conenct to UWSD
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Treatment for an open pneumothorax?
Place non-occlusive one way dressing over (e.g. Asherman dressing) Then perform 32Fr chest drain (in separate place to dressing)
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Treatment for a massive haemothorax
Most commonly from intercostal vessels, rarely from mediastinal vessels (but most die pre hospital) Massive haemothorax if >1L in chest May present with hypovolaemic shock and hypoxaemia. US most sensitive to pick up initially (and examination) Treatment - 2x large bore cannula - 100% fIO2 - Blood transfusion - May need Belmont - Chest drain (32Fr at least), direct posterior and inferiorly - If >1.5L or more than 100-200ml/hr after initial dump of blood --> IR or theatre
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Maximum rate of fluid administration via an IO device
Can get 150ml/min with a pressure bag (not great, not terrible)
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What is the shock index?
HR / systolic BP. If >1 then shock is present
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PLACES pneumonic in trauma?
= places people can bleed from Pelvis Long bones Abdomen Chest External Scalp
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TXA trials in trauma
CRASH 2 (2010) = 1g TXA over 15 mins then 1g over next 8 hours. needs to be within 3 hours of trauma. Reduced mortality at 4 weeks (NNT 68, RR 0.91). Harm if after 3 hours. Criticisms included not randomised (phyician decided if indicated) and only 5% of patients died from bleeding CRASH 3 (n=10000). TXA in TBI. If mild - moderate (GCS 9-15), give TXA within 3 hours. Mortality benefit at 28 days for these people. No difference if giving to all patients. Did not increase seizure rates MATTERS trial 2012. N=900. Only 300 got TXA though. Military application, TXA if 1 unit of blood or more. Improved survival (17 vs 24%), even better survival if >10 units RBCs given. 10x increased VTE risk (0.2 --> 2%) PATCH trial (NEJM 2023). N=1200. Nz and Aus and Germany. TXA reduced mortality at 24 hours and 28 days. But same at 6 months. No difference in VTE. TXA group had worse neurological outcomes
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6 views of eFAST?
Enhanced focused assessment with sonography in trauma 2x 2nd intercostal spaces (Left and right), mid clavicular line. Saggital plane --> pneumothorax, haemothorax. Use M mode Subxiphoid view of heart - pericardial effusion RUQ, LUQ and pouch of Douglas. When supine, looking for blood in dependent regions Has good PPV (0.9) --> if fluid present on US, highly likely of fluid actually there NPV less good. If no fluid seen, may still have bleeding
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European trauma guidelines recommendations for lactate and base excess targets for resuscitation?
Aim for lactate <4mmol/L, BE >-6. Use to monitor extent of bleeding / shock and target improvement with resuscitation
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AMPLE history?
Allergies Medications Past medical history (pregnancy if child bearing age female and uncertain status) Last meal Events leading to presentation
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PROPPR trial?
Basically demonstrated improved mortality with 1:1:1 RBCs : FFP : plts transfusion compared to 2:1:1. Also used half the amount of RBCs in the 1:1:1 group too unsurprisingly
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Criteria for a code crimson trauma in NZ?
2 or more of the following: Penetrating injuries +ve eFAST Systolic <90mmHg HR >120BPM
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MHP coagulation targets in adults
INR <1.5, APTT <40s. If not, give 4x FFP Fibrinogen >2g/L, if not give 3x cryo Platelets >75, if not give 1x platelets Ionised Ca >1.1mmol/L, if not give 1g CaCl2
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Transfusion compatibility of FFP and cryoprecipitate?
Both should be ABO compatible. AB = universal donor, O = universal recipient (opposite to RBCs as FFP and cryo have the antibodies not antigens) If no AB available, A is next best does not need to be rhesus compatible as only small amounts of red cell stroma in FFP and cryo. Don't need to give anti-D to women of childbearing age
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Transfusion compatibility of platelets?
Does not need to be ABO or rhesus compatible. Weakly express A and B antigens, so ABO compatible preferred as platelets will last longer O would be universal donor. Next best would be A Rhesus is not present on platelets but small number of RBCs may be in platelet pool. Give anti D if rhesus +ve platelets given to rhesus -ve woman of child bearing age
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Three goals of damage control resuscitation?
1) Permissive hypotension - sys 80-90mmHg unless TBI 2) Damage control surgery - minimal surgery to control bleeding. Restore physiology. Return for definitive surgery later 3) Haemostatic resuscitation - minimise bleeding triad. 1:1:1 transfusion, minimise coagulopathy and minimise crystalloid. TXA. TEG guided should have most senior clinicians available present
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Goals for damage control surgery
Minimal surgery to restore physiology. May need to bypass CT (but ideally getting imaging is useful) Surgeries that may occur - trauma laparotomy, pelvic packing, ex fix of tractures, thoracotomy. IR may count Surgical goals - Stop bleeding - haemostasis with packs, ligation, haemostatic agents, organ removal (splenectomy) - Prevent contamination (stoma formation, washout bowel contents spilled into abdomen) - Protect patient from further injury - Temporary closure Surgery should be <90 mins, patient should go to ICU for resuscitation
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Causes of trauma induced coagulopathy?
Dilutional - haemorrhage (so loss of coagulation factors) + replacement without coagulation factors Consumptive - use of coagulation factors to make clots. Endothelial dysfunction --> further consumption Hypothermia - especially with massive haemorrhage protocols and lack of warming Acidosis - metabolic primarily, usually from tissue ischaemia. Can be respiratory too Hypocalcaemia - citrate sequestering from massive transfusion
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What is REBOA? Where to place it? Evidence for REBOA
Resuscitative Endovascular Balloon Occlusion of Aorta Inserted via a 7Fr sheath in femoral artery, used in trauma and massive haemorrhage to reduce bleeding Temporary measure, as means to allow for survival until damage control surgery can take place Placed in either zone 1 or zone 3 (never zone 2) Zone 1 = between left subclavian artery and coeliac artery. Place here for intraabdominal bleeding (zone 2 we dont talk about but it is between coaelic artery and most caudal renal artery - do not palce here as no benefit) Zone 3 = between most caudal renal artery and iliac bifurcation of aorta. Place here for pelvic haemorrhage or femoral artery bleeding not ammenable to tourniquet Evidence for REBOA is lacking. Hard to do trials on. Only RCT to date is the UK REBOA trial - no mortality benefit. Authors concluded 85% likely REBOA increased mortality compared to standard care. Otherwise, case series and observational studies (which have conflicting results) Contraindications include age >70, significant comorbidities, PEA >10mins, supra-diaphragmatic bleeding, aortic injury
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Signs of airway disruption from airway trauma
Subcut emphysema, dyspnoea, stridor. Orthopnea With mechanism compatible with airway disruption (either blunt to neck / torso or penetrating) CT Nasal endoscopy Bronchoscopy
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Management of an airway trauma for intubation
Goals: - Decide which patients need airway management - Place an ETT distal to the injury - Not worsen the trauma or subcutaenous emphysema Factors to decide where and when airway should be managed: - Patient factors - compliance, aspiration risk - Airway factors - stability (SpO2), pathology of injury - Team factors - skillset, experience - Situation factors - urgency, current location, availability of OT (including staffing, distance from OT) Where Three tiered system: - Crack on. Patient in immediate extremis - complete airway obstruction, hypoxic arrest. Need to immediately manage. Cannot optimise - Stay and play. Too unstable to move. But can optimise (e.g. stridor, cannot lie flat, other injury needing resuscitation) - Head for home - stable enough to get a CT and / or go to theatre Who - Most experienced airway anaethetist available, airway assistant, nurse for drugs, ENT surgeon How - Three approaches to airway management - Awake technique - e.g. bronchoscopic, awake VL, awake trache. Always in green zone. But takes time - Asleep but spont ventilating. Stay in green zone. Might include gas with sevo, ketamine or propofol TCI. Aspiration risk. laryngospasm risk. Bronchoscope to inspect airway is useful - RSI. Enter vortex but reduce aspiration risk. Only option if crack on. Two anaesthetist technique (FARSI) may be prefered here. This is a good option if airway exam is favourable - do not use HFNO if suspected tracheal disruption. Can use NP at 15L/min for apnoeic O2 though - No cricoid If plan fails. May need to place LMA or BMV? may worsen injury. Lower threshold for eFONA by ENT or other anaesthetist
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Risk factors for mortality from burns? Burns scoring systems?
Age (elderly and children) Hypothermia TBSA% Comorbidities Depth of burns Airway burns BEAMS = burns evaluation and mortality score. Used in NZ and Aus Also there is abbreviated burn severity index
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Signs of an airway burn Effects from inhalational burns
Soot around mouth or nostrils Burnt nostril hairs cough Hoarse voice Dysnpea Stridor Airway oedema on nasal endoscopy / bronchoscopy Airway oedema likely to peak at 24-36 hours. If needing intubation, place largest ETT possible to allow for bronoscopy (but may need to place smaller one if lots of oedema) Other than airway injury, can also get: - Carbon monoxide poisoning - Cyanide toxicity - Other poisoning from inhalation
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Parkland formula for burns
4ml/kg/TBSA% burns = 24 hours IV crystalloid for resuscitation (doesn't include maintenance and other losses) First half within 8 hours of burn 2nd half in next 16 hours Titrate to urine output >1ml/kg/hr Balanced crystalloid (e.g. plasmalyte)
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What is a Lund and Browder chart for?
For documentation of burns location and severity. Based on rule of 9s Need to use a paediatric appropriate one for kids, as bigger head and smaller limbs
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Treatment for carbon monoxide poisoning
No symptoms of COHb <15%. Mild confusion if 15-20%. Nausea, fatigue if 20-40%. Coma, seizures 40-60%. Death at 60% or more CO binds to Hb 200x greater affinity than O2. Also binds to other cytochromes. Half life of COHb is 4 hours at room air. Can shorten to 40 mins with 100% FIO2 hyperbaric O2 could shorten to 15-20 mins half life. But hard to get that urgently. Consider if coma, pregnant, ECg changes or cognitive impariment and nearby CO may continue to increase, peak at 24 hours. Due to being released from other cytochromes
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Effects of hydrofluoric acid burns
2% TBSA can be lethal. Used in glass manufacturing. Binds avidly to calcium --> hypocalcaemia Inject calcium gluconate (NOT CHLORIDE) subcut into burn, extend 0.5cm beyond burn edges Rarely might do a Bier's block with calcium gluconate Ca gluconate binds to F- ions
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Treatment for cyanide poisoning
5mg IV hydroxycobalamin (B12)
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Primary vs secondary TBI
Primary = initial insult to brain - parenchymal contusion, axonal shearing, vascular injury. May be diffuse or local. Not modifiable, irreversible Secondary = from initial minutes to days as result of primary injury. It is preventable. Includes oedema, ischaemia, excitatory toxicity, increased CMRO2. Secondary is worsened by: hypoxia, raised ICP, hypotension, anaemia, increased CMRO2, seizures, haemorrhage, hypercapnia
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Goals of management of a TBI
Maintain CPP Minimise ICP increases Maintain oxygen delivery to brain Reduce ongoing injury / bleeding
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BP targets for TBI as per BTF
Brain trauma foundation 2016 guidelines If 15-49 - systolic BP >110mmHg If 50-69 - systolic BP >100mHg If >69, systolic BP >110mmHg
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GCS score
E 1 - closed 2 - opens to pain 3 - opens to voice 4 - open V 1 - none 2 - incomprehensible sounds 3- inappropriate words 4 - confused sentences 5 - normal M 1 - none 2- extension to pain 3 - abnormal flexion to pain 4 - normal flexion withdrawal 5 - localisation to pain 6 - obeys commands
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Evidence for seizure prophylaxis in TBI?
Reasonably little. Meta-analysis from 2024 found prophylactic AED showed small but significant decrease in seizures in mild-moderate TBI (GCS 9-15). Absolute risk reduction of 0.6%. NNT 167
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What was CRASH trial?
High dose methylprednisilone in TBI patietns, worsened mortality. Level 1 evidence. Do not do
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Canadian CT head rules
Cant be used if on anticoagulant, under 16 or had seizure post TBI Any high risk criteria --> CT - GCS <15 for 2 hours post injury - Open or depressed skull fracture - Evidence of base of skull fracture - CSF leak, haemotympanum, Battle's sign, Racoon eyes - 2 or more episodes of vomiting - Age 65 or older Medium risk - Dangerous mechanism - Retrograde amnesia
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Tiered approach to treatment of raised ICPs from a TBI
Tiered approach from Seatle International Brain injury consensus conference SIBICC in 2019. Based on BTF guidelines Start at lowest tier. Do not have to do everything before moving to next tier. If refractory raised ICPs despite maximising tier options --> move on to higher tier Treat ICP if >22mmHg or CPP <60mmHg Tier 0 = basic ICU cares - admit ICU - SPO2 >94% - Head 30 degrees elevation - No neck ties - CPP >60mmHg - arterial line, CVL - analgesia and sedation for comfort - Fever prevention Tier 1 = basic ICP management - EVD for CSF drainage - Mild hyperventilation PaCO2 35-38mmHg - Seizure prophylaxis - Increase sedation and analgesia, decrease CMRO2 - hypertonic saline or mannitol, Aim Na 155mmol/L Tier 2 = more aggressive medical management - Hyperventilate to 32-35mmHg - NDMRs - trial with bolus, if improves then infusion is reasonable - MAP challenge (increase by 10mmHg) Tier 3 - Barbituate coma, isoelectric EEG - Decompressive craniectomy (may improve mortality DECRA and RescueICP studies. But often worse neurological outcomes) Previously hypothermia advocated, but POLAR study suggested increased mortality
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5 mechanisms for injury from an explosion (blast injury)
Explosion = rapidly expanding pressure wave form with exposure to high temperatures. May be supersonic (C4) or subsonic (petrol) Mechanisms - Primary - from initial pressure expansion. Rapid compression and expansion of gas filled spaces (lungs, bowels, eyeballs, tympanic membranes) - Secondary - from flying shrapnel - Tertiary - from victim being flung or thrown into walls, doors, other structures - Quaternary - any other injury from an explosion not from the pressure - thermal, chemical, inhalational - Quinary - tissue contamination post detonation (e.g. radiation from nuclear, biochemical warfare) Blast lung = PTX, pulmonary contusion, air embolism = most common cause for death. V/Q mismatch. Butterfly CXR appearances. OFten need bilateral chest drains Other considerations from blast injury: - If TBI, need to avoid hypercapnia (no permissive hypercapnia for lung protective ventilation. Or monitor ICPs) - PPE if suspecting contamination from blast - traumatic amputation may mean difficult IV access, monitoring - Check tympanic membrane, most sensitive structure to pressure
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Most common causes of death in trauma
1) Haemorrhage (60%) 2) Tension pneumo (30%) 3) Airway obstruction (10%) (above based on military data, civilian data also includes tamponade) 4) Tamponade (10%) I am aware this adds up to 110% Traumatic cardiac arrest survival til discharge from hospital about 5-7% ANZCOR also suggest resus in trauma is reasonable in almost all circumstances (except obvious injuries non-compatible with life). But after 10 mins of arrest, survival universally poor and reasonable to stop
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In traumatic cardiac arrest, when to do bilateral thoracostomies?
MARCH model -Massive haemorrhage - Airway - Respiration Once resuscitation for massive haemorrhage + ideally source control (tourniquet e.g.) underway AND Simple airway techniques instigated If still not responding. And any suspicion chest trauma could be involved, do bilateral finger thoracostomies (ANZCOR). Increased suspicion if tracheal deviation or lack of breath sounds unilaterally - due to 30% chance of traumatic arrest from tension pneumo - Do most likely affected side first - Needs intubation once this is done
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Percentage of traumatic cardiac arrest with VT / VF
7%. More likely if known cardiac disease (could have precipitated trauma) Still good to place def pads on, just in case (might get lucky). But should prioritise massive haemorrhage resuscitation, airway and breathing before this
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When to do a resuscitative thoracotomy? Process of doing it?
Also sometimes called a clamshell thoracotomy, EDRT (ED resuscitative thoracotomy). Need a clear goal in mind. EDRT might treat: - Tension pneumothorax (but idk why you wouldn't just do bilateral finger thoracostomies instead) - Pericardial tamponade (especially useful if penetrating wound to heart) - Clamping of aorta (aortic injury) or other intrathoracic haemorrhage - Internal defibrillation + internal cardiac compressions WHO - need to have airway person (me), trauma surgeon or ED physcian appropriately trained to do it, team leader, nurse for drugs, airway assistant WHAT (better outcomes if): - Periarrest (not yet dead). Do not do it if arrest >15 mins. Or if blunt force trauma and >10 mins arrested - Penetrating injury - especially single stab wound to RV (worse if high velocity e.g. gunshot) - Meta analysis 2015 - 10% survival rate if penetrating injury but 90% favourable neurology. Only 5% survival if blunt trauma with 50% favourable neuro HOW - Stop CPR - Intubate - Bilateral thoracostomies in triangle of safety - Join thoracostomies with heavy duty scissors, cross sternum - Retractors in, open chest - Consider clamping aorta at this stage - Lift pericardium, T incision to avoid phrenic nerves (which run laterally along pericardium) - Suture or staple hole - Can also place vascular access directly into RA now ANZCOR specifically state that practitioners should never be criticised for not doing a procedure that is outside their scope of practice. Aka anaesthetists doing this
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Scoring systems for frailty in trauma
Rockwood clinical frailty score - actually developed for dementia care. But has some applicability in trauma. 1 = very fit. 9 = terminally ill, life expectency <6 months. Others include: - Trauma specific frailty index - Geriatric trauma outcome score
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Risk factors for delirium in the elderly
PInCHME Pain Infection Constipation Hydration Medications Electrolytes (glucose, sodium, calcium, potassium)
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Pathological effects from an intra-arterial injection of medication
Depends on drug, pH, concentration and volume injected - Arterial vasospasm - Precipitation of drug / crystal formation - Chemical arteritis - Thrombosis formation all of the above can lead to reduced perfusion, tissue ischaemia and necrosis
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Management of an inadverent arterial injection of medication
- Stop injection - Attempt to aspirate - Provide analgesia for patient - ensure IV access in alternate limb - Flush with normal saline + slow infusion. Leave cannula in situ (but clearly label as arterial) - May infilitrate lignocaine into art line for analgesia + vasodilation - elevate limb to promote venous drainage - Contact vascular surgeons, seek advice from senior colleagues - Consider heparin infusion (aim APTT 2x normal, bolus 5000IU to start) to reduce thombosis - depend on surgical bleeding risk. May also consider sildenfil or iloprost infusion to vasodilate - Consider regional anaesthesia - ideal for analgesia but also vasodilation may reduce distal ischaemia (peripheral nerve catheter ideal) - Open disclosure with patient. Documentation. Contact with indemnity provider. Treatment injury paperwork for patient - Monitor distal limb over 24-48 hours for evidence of demarkation, skin blistering, necrosis - May need debridement, fasciotomy, amputation in severe cases - Post event hand therapy / PT / rehab - Discuss at Q+A forum
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Considerations for theatre evacuation when taking a patient with you (e.g. large fire)
- Need to determine risk to staff, self and patient - Communicate with theatre coordinator, surgeon. -Need to minimise surgery, cover up and pack wounds - Need plan for route to take, landing destination - Airway - intubate. Ensure take laryngosocpe. Back up LMA, ETTs, SGA - Breathing - ensure O2 cylinders. BMV is fine usually but if mechanical transport vent is available immediately, use this (frees up hands). Use lowest possible fiO2 for sats >94% to conserve O2 - Circulation - need IV access, Iv fluids - Drugs and anaesthesia Anaestheisa - Intermittent propofol / ketamine boluses likely quickest. could give midaz too. Could use pump and start 20-30ml/hr propofol Paralysis + reversal agent (roc patient and take sugammadex with you) Adrenaline always - 10mcg/ml + 100mcg/ml Other things to consider - opioids, atropine, metaraminol, sux - Exposure - warming blankets Transfer with full monitoring on. Including etCO2. Ideally on a patient bed (as OT bed not easy to push) Need enough people to push bed, infusion pumps, open doors
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Management of an operating theatre O2 supply failure
- Anaesthesia machine will temporise with O2 cylinders. Minimise O2 consumption with lowest FiO2, aim sats >92% - Inform theatre team including surgeon - Inform theatre coordinator - determine if theatre specific failure or widespread issue. And likely duration. ?VIE failure - ideally backup cylinder manifold will be able to provide O2 (but smaller regional hospitals may not have VIE) - do not allow for any new cases to be started unless life or limb emergency - If single theatre issue, consider how much longer surgery has to go - potentially better to transfer to another theatre to finish - If numerous theatres affected, need to determine length of surgery remaining. May be appropriate to minimise surgery and come back for completion at later date. If requiring surgery, maintain on lowest O2 possible. - also need to consider other theatres as O2 cylinders could become scarce resource - Have theatre coordiner organise O2 cylinder supply from alternative sites (e.g wards) - Senior surgeon operating to reduce duration - Ensure at least 1 extra cylinder O2 available at all times - TIVA with low FGFs may be best way to decrease O2 use (as not reliant on FGF for anaesthesia delivery. Circle system Post op - Need to consider recovery location - may not have O2 in PACU. Could be best to recover in OT
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RACE pneumonic for fire
Remove - staff and patients from immediate danger. Includes removing drapes from patient that is on fire if safe to do so Alert - emergency services, fire warden, theatre coordinator Contain - close doors adjacent to fire, windows Extinguish - if safe to do so - CO2 extinguisher
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Risk factors for operating room fire
Consider fire triad of fuel, oxidiser and ignition source Surgical - Surgery above xiphisternum. Airway, plastics, vascular, cardiology (PPM insertion) - Monopolar diathermy most common ignition source. ignition source should be >10cm from O2 source if >4L/min used - LASER - Alcohol based prep Patient - Facial hair / eyebrows Anaesthesia - N2O - HFNO - flows above 3L/min - open airways - FiO2 >0.3 Other: poor communications, human factors Christiana scoring system for risk: - Surgery above xiphisternum - Open O2 source - any ignition source If 1 then low risk, 2 then moderate, 3 = high risk
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Methods for prevention of an operating room fire
Institutional level - Fire drills, scenario training. Ensure all individuals in theatre are aware of process and able to extinguish small fire - Fire alarm testing, connection of alarm to emergency services - Fire warden preappointed - Fire resistant intercompartmental walls (30mins) - Culture of safety - where brief of fire risks occurs for any high risk proceedure - Reporting system in place for incidents / near misses with follow up, root cause analysis, discuss and implementation of ways to mitigate risk - Fire extinguishing capabilities - Water sprinklers / fire blankets - Detailed evacuation plans, locations for evacuation. Building planning to allow easy access out of theatre complex - ideally avoiding lifts. Well lit escape pathways Individual level: - Team brief with critical steps outlined, use of ignition sources, plans to mitigate risk and discussion of process for if fire occurs Surgical team - Non flammable drapes - Saline and wet gauze on surgical scrub trolley - Bipolar diathermy where able rather than monopolar. communicate when using ignition sources e.g. laser - Keeping diathermy in sheath when not in use - Avoiding alcohol based prep or allowing for drying completely + not pooling behind patient or drapes - shave beards / facial hair (with informed patient prior) Anaesthesia team: - Minimise FiO2 (<0.3 if able), especially if using high flows - Ideally using closed airway system, laser resistant ETT if able - Avoid N2O - communicate if need for higher fiO2 temporarily with surgical team to not use ignition source
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Definition of pain
Unpleasant sensory and emotional experience, related to real or potential tissue damage, or described in such terms - International association for the study of pain (IASP)
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Definition of opioid stewardship
Aim to minimise harms to individuals and wider society, and balance of providing adequate analgesia to patients As per appendix 1 of PG41 ANZCA document = acute pain
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Physiological responses to pain
CVS - HTN, tachycardia. Myocardial stress Resp - increased MV. Splinting, ineffective cough --> sputum retention, infection Renal - urinary retention CNS - anxiety, depression, PTSD. delirium (especially in elderly) Immune - possibly delayed wound healing, impaired immunity from cortisol GI - delayed gastric emptying Metabolic - increased BGLs, catecholamines, cortisol levels Haem - Non mobilising --> VTE risk
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Ways to measure pain scores
Numerical - sliding scale. Easy to use. Quantitative so good for research. But poor comparibility with different patients Verbal ratings - mild, moderate, severe. Semi-quantiative so not ideal in research. No good in paeds, non-english speaking. Hard to detect changes if only 3 options Visual analogue scales - useful for paeds and non-english speaking. Can be continuous scale if line used Functional activity score (e.g. Scott and McDonald) - A = non limitations B = mild limitations C = unable to do activity FLACC score (Face, Legs, Activity, Cry, Consolibility) Analgesia consumption (post hoc analysis)
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Oxford league table of analgesic efficacy
= NNT for a 50% reduction in pain score over 4-6 hours for a particular drug e.g. Parecoxib = 2.2 Ibuprofen = 2.5 Paracetamol 1g = 3.8 Morphine 10mg IM = 2.9 Tramadol 100mg = 4.8
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Pain history
SOCRATES = Site Onset Character Radiation Associated symptoms Timing Exaccerbating and allievating factors Severity - functional ideally Other includes - relevant comorbidities (e.g. renal, cardiac), pain meds, psychosocial history, drug history
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Definition of neuropathic pain Diagnosis of neuropathic pain
Pain due to lesion or disease directly related to somatosensory nervous system - may be central or peripheral in origin. And acute or chronic symptoms includes: - burning, shooting, stabbing characteristic - Paroxysmal, spontaenous in nature - Dysthesia, allodynia, hyperalgesia all common - May have regional autonomic dysfunction (sudomotor, temperature, vasomotor) - May have phantom phenomena Leads assessment of Neuropathic Symptoms Score (LANSS) - sensitivity and specificity between 0.8 - 0.9. Maximal score of 24, if >12 then likely neuropathic. - Includes 5 symptoms (describing pain as electrical / burning, sensory changes, skin temperature changes) and 2x clinical examinations (allodynia with cotton wool and pin prick testing) Pathphys involves: - Injury to nervous system - Formation of neuromas, nerve buds --> incresed excitability - Peripheral and central sensitisation - Damage to decending inhibition
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TIME 1 study for pleurodesis
RCT comparing NSAIDs and opioids for pleural effusion pleurodesis. No differences in efficacy of pleurodesis in NSAID group Only animal studies have demonstrated NSAIDs reduce efficacy of pleurodesis. Risk benefit for analgesia
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Gabapentinoids place in practice
Mainly for neuropathic pain - acute and chronic. Pregabalin NNT 4 for post herpatic neuralgia, 7 for post traumatic neuralgia Use in acute neuropathic pain is based on evidence for chronic neuropathic pain Routine use is recommended against otuside of this. Metanalysis from 2020 (200 studies, 25,000 patients). Reduced post op pain vs placebo (NNT = 11) but increased sedation, pre syncope, visual symptoms
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Lignocaine infusion evidence
Level 1 evidence for analgesia in GI surgery - decreased pain scores, less opioids, less side effects (less nausea, less ileus, reduced LOS) In breast surgery, reduced amount of post op opioids. But didn't reduce pain scores Occasionally used in hyperalgesia - may have role in central sensitisation via NMDA inhibition Probably good for laparoscopic GI surgery. But might limit regional anaesthesia use in open
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Requirements for PCA use as per ANZCA PS41 on acute pain
PCA = advanced pain modality, needs oversight by anaesthetist / acute pain service daily - Standardised guidelines - including monitoring of GCS (most sensitive to OIVI), RR, SpO2, Hr, and pain assessment. Frequency of monitoring - Naloxone charted and guideline for when to give - Appropriate opioid for patient (e.g. not morphine in renal failure) - Regular assessment by anaesthetist or delegated authority - Equipment requirements - non reflux giving sets, tamper proof boxes, standardised concentrations and dosing. Ideally only single agent in PCA - Step down plan onto orals, discontinuation of PCA
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How to set up a paediatric PCA
Need to determine if PCA or NCA - PCA probably only if 8 or older I'd guess Morphine as default (slower onset, less likely apnoea compared to fentanyl or oxy) Mix 0.5mg/kg morphine into a 50ml 0.9% NaCl + 5% dextrose bag. 1ml solution = bolus dose For PCA, can be Q5mins. Max 12ml For NCA, Q10mins. Consider 1-2ml/hr continuous infusion (could start this later if needed). Max 8ml in 1 hour Naloxone dose = 0.1mg/kg IM or 10mcg/kg IV Need to ensure appropriate RR, sedation parameters for childs age
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Methods for reducing chronic post surgical pain (CPSP)
Regional. Proven in 3 types of surgeries - Thoracotomy (epidural, NNT = 7) - Mastectomy (PVB, NNT = 11) - CS (neuraxial spinal or epi, NNT = 19) (epidural reduces severity of phantom limb pains after amputations but doesnt reduce long term CPSP) LA infiltration - reduced CPSP in breast surgery and iliac crest bone graft Ketamine - cochrane review showed reduction CPSP at 3 months but only if given >24 hours (mainly benefit for abdominal surgery) - One RCt found no benefit for thoracotomy Lignocaine - reduced CPSP for breast surgery at 3 months Surgical approach - minimally invasive superior to open
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PUMA criteria for sustained CO2
Project for universal manageemnt of airways 1) CO2 rises with expiration, falls with inspiration 2) Increasing or stabilised level of etCO2 (not falling) 3) Reaches peak of at least 1kpa (7.5mmHg) 4) In keeping with clinical context If not achieving this, default should be removal of ETT. If dangerous to remove, then alternative is to look with VL AND use one other method to confirm (bronchoscope, airway US or oesophageal detector) But if never get etCO2 back, or SpO2 starts to fall --> take out ETT
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Risk factors for chronic pain
Patient factors - female - younger adults - anxiety / depression - Pre-existing pain / functional neurological conditions - smoking - Cannabis - Unemployed - genetics Surgical - Surgery type (amputation > thoracotomy > mastectomy > sternotomy > c section) - high impact trauma - surgery involving nerve transection - revision surgery Anaesthesia - pain intensity pre + post op, regional, high dose remifentanil, ketamine
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Pathophysiology of opioid induced hyperalgesia How to avoid?
Not fully understood, seen with high doses of opioid agonists - particularly high potency opioids like remifentanil infusions. first demonstrated in patients on methadone for opioid addiction May be related to NMDA activation, glutamatergic activation, glial cell activation or beta arrestin. Ways to reduce - Not using opioids or minimising use of potent opioids - especially those who might come to more harm from OIH. - Propofol (level 1 evidence) - Ketamine (level 1 evidence) - Tapering remi infusion (level 2 evidence) - Pregabalin (level 2 evidence)
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Management of naltrexone for patient coming in for elective surgery?
Long acting opioid antagnoist. Patient may be on it for opioid addiction or alcohol addiction (usual dose 25-50mg daily). Or may be in combination with bupropion (selective NA and dopamine reuptake inhibitor) for weight loss aka Contrave Chronic naltrexone use --> doubles number of Mu and delta opioid receptors in brain, may cause increased sensitivity to opioids. But continuing naltrexone will cause opioids to be ineffective Withhold naltrexone for 72 hours. Patient may have reduced or increased sensitivity to opioids. Monitor in high dependency area if needing opioids (or use regional and non-opioids)
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Buprenorphine management for elective surgery
Mu partial agonist, kappa antagonist. Usual doses are 8-32mg. Very high affinity for opioid receptor. Use in opioid substitution therapy - less resp depression than methadone. Less neonatal abstinence syndrome too. Also less QT prolonging and less OIH. Often in combination with suboxone - oral naloxone to prevent IV administration Doses >20mg will likely reduce efficacy of full agonists. some centres will consider splitting doses to 2-3 per day for better analgesia leading up to surgery Strategies include: - Continue buprenorphine and accept you'll need to give high doses of opioid agonists + use opioid sparing options (which is what we do at waikato) - convert to methadone (but can be challenging) - Continue buprenorphine and Use buprenorphine as analgesic
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What is complex regional pain syndrome? Pathophysiology? Diagnosis?
Chronic neurological condition following traumatic insult No single linear pathophysiology - Peripheral nerve sensitisation (reduced threshold to firing APs, contributes to hyperalgesia) - Central sensitisation (allodynia, hyperalgesia). Mediated by substance P and glutamate. NMDA. Brain may get reduction in representation of somatosensory cortex --> neglect, motor dysregulation - Autonomic dysregulation - linking of sympathetic fibres to peripheral fibres, upregulation of alpha 1 receptors, altered circulating catecholamines - Immunological - substance P and calcitonin gene related peptides --> TNF alpha, IL1b - Genetics - Psychological stress Diagnosis made using Budapest criteria - 2003. Sensitivity 0.99 and specificity of 0.7 - Pain disproportionate to inciting event - One symptoms from each of the following four categories: Sensory: allodynia, hyperalgesia Vasomotor: temperature asymmetry, skin colour changes Sudomotor: oedema, sweating changes Motor: decreased ROM, nail and ahir changes, motor dysfunction - At least 1 sign at time of examination from: sensory, vasomotor, sudomotor and motor - No other diagnosis that would explain criteria - CRPS1 = no nerve involvement. CRPS2 = nerve involvement
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Risk factors for CRPS?
High velocity trauma Upper extremity injury - especially distal radial # Female Psychological disorders Prolonged time under GA Rheumatoid arthritis
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Treatment for CRPS
1) Physical/ occupational / psychological therapy - Of low quality evidence with high heterogeniety. But is mainstay for recommendations as safe - Cochrane review 2016 - graded motor imagery and mirror therapy 2) Neuropathic drugs - most the evidence is from other neuropathic conditions. But one RCT found improved pain scores at 6 weeks with both gabapentin and amitriptyline 3) Anti-inflamatories. There are a few RCTs demonstrating improvement with steroids - give short course early in diagnosis - NSAIDs are lacking in efficacy 4) Bisphosphonates (alendronate, pamendronate) - Meta-analysis suggests its useful (but unclear how it works, usually used to treat bone pains) 5) Sympathetic nerve blocks (lumbar sympathetic block, stellate ganglion block) 6) Spinal cord stimulation / dorsal root stimulation 7) vitamin C - mainly found to reduce risk of developing CRPS in some studies. But not in others
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Anatomy relevant for a stellate ganglion block
Preganglionic smpathetic fibres for upper limbs, neck and head originate in upper thoracic levels and ascending via sympathetic chain. form the superior, middle and inferior cervical ganglion Stellate ganglion is a fusion of the inferior cervical ganglion and first thoracic ganglion. Sits around C7 just medial to vertebral artery. Anterior to longus colli. Just superior to pleura. Supplies sympathetic innervation to upper limb Block often done at cervical sympathetic trunk at C6 (identify Chassaignac's tubercle) and expect caudal spread. Less risk of pleural puncture, vertebral artery puncture or epidural spread Basically get the same image you would for a CVL insertion. Then lateral to medial approach with sonographic needle in plane. Pass needle directly posterior to IJV and ICA. Sympathetic chain is directly posterior to the carotid artery (outside the carotid sheath) and directly anterior to longus colli. Aim to get through prevertebral fascia and "lift off" longus colli muscle. Usually use 5-8ml LA
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Effects and adverse effects from a stellate ganglion block
As blocking the sympathetic nerves to the upper arm (and also to the neck and face), effects will include: - horners syndrome - Miosis, ptosis and anhydrosis unilaterally - Upper limb vasodilation (warm, flushed, red) complications - Intravascular puncture, haematoma (needle passes directly posterior to IJV and CCA). - Inadvertent LA intravascular injection LAST (siezures, CVS collapse) - Recurrent laryngeal block - hoarse voice, stridor - Pneumothorax - Phrenic nerve block (dyspnoea) - Upper limb weakness, loss of sensation (brachial plexus spread) - Epidural spread, high spinal (haemodynamic instability, bradycardia, hypotension, apnoea, LOC) - Infection
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Diagnosis and management of fibromyalgia
Functional pain syndrome - no obvious organic cause identified. DEscribed as muscle pains. More likely to have other functional pain syndromes as well American college of rheumatology have scoring system - generates a WPI (=widespread pain index, out of 19) and SS (=severity of symptoms, out of 12). If WPI >7 and SS >5 or WPI >3 and SS >9 then diagnostic Unclear pathogenesis. But liekly environmental, patient and genetic. 8x increased chance if first degreee relativ. COMT genes implicated somehow Management: - Rule out other causes - Graded exercise - Pain specialist - Education - TCAs, SNRIs maybe
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Management for post-herpetic neuralgia (Herpes Zoster)
Aka shingles Antivirals commenced within 72 hours of rash accelerate resolute of acute pain. But dont reduce severity, incidence or duration of neuralgia Immunisation reduces incidence of herpes zoster TCAs (low dose, 90 day course) reduces incidence of neuralgia Regional anaesthesia reduces incidence of neuralgia by up to a year Some level 2 evidence for topical lignocaine
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Trigeminal neuralgia Causes Diagnosis
Primary TN - direct compression of trigeminal nerve, often by superior cerebellar artery at root entry. Get focal demyelination and firing of action potentials --> neuropathic pain Secondary - due to AV malformations, tumours, MS, post herpatic neuralgia Neuropathic in nature. Burning, electrical, shooting (Leeds Assessment for Neurpathic Symptoms and Signs (LANSS) - Typcially lasts seconds to minutes, with refractory period - Most commonly V2, can be V1 or V3. Does not cross midline. - Triggers can include brushing teeth, chewing, talking or cold air Risk factors: - Females - >50 years old More likely to be secondary TN if: - bilateral symptoms, headaches, sensory loss, age <40, other cranial nerve signs
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Treatment of trigeminal neuralgia
Medical: - Carbemazepine = gold standard. Most evidence. = sodium channel blocker, stabilises neurons. 80% get initial response to treatment. Reduces both frequency and severity. Keep this going - Gabapentinoids - TCAs - Baclofen (especially if MS too) - Other AEDs - lamotrigine, phenytoin - Tramadol NOT Opioids Non-pharmacological: - Cognitive behaviour therapy - cognitive restructuring, mindfullness based, acceptance therapy - Surgical. - Peripheral - neurolysis with alcohol or surgery (often get 6-12 months benefit) - At trigeminal ganglion - balloon compression, neuolytic agents (phenol, alcohol) or radiofrequency ablation. Generally well tolerated, less invasive than MVD. Can become bradycardic from vagal response to ballooning. 80% patients get improvement. 50% will have recurrence at 5 years - Trigeminal microvascular decompression (V MVD). Posterior fossa crani and separation of trigeminal nerve and blood vessel (usually superior cerebellar artery). Major operation. Gold standard surgery with 80-90% improvement initially and 80% pain free at 5 year mark. Need to be good fit candidate for this
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Things to rattle off quickly for doing any major peripheral regional nerve block
As per PG03 ANZCA document for major regional techniques - Informed consent - Trained assistant (as per PS08) - Appropriate environment (PS55). Need access to intralipid. And US ideally - Infection control (PG28) - asepsis. 0.5% chlorhex. Gloves +/- gown and mask - IV access - Monitoring - during need BP, RR and mental status. SpO2 and ECG need to be immediately available. If any sedation, then SpO2 and O2 given. - Once block done, HR, BP, sedation, pain and motor blocks for 30 mins minimum - block timeout. Confirm side, patient details, allergies, consent - If block for analgesia, then proceduralist should be available until block established. Then can handover to nurse - If block for anaesthesia, then proceduralist must remain with patient until end of surgery then can hand over (PS53) - document block + follow up daily until block worn off
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Definition of non-critical, semi critical and critical equipment when it comes to infection control
PG28 Non-critical = not tocuhing patient or in contact with intact skin only.. Wipe clean after use then alcohol containing disinfectant between patients Semi-critical = mucous membranes or broken skin. Should have sterile cover + sterile gel for use. Disinfect after use Critical = inside patient's vasculature. High level disinfectant (ortho-phthalaldehyde)
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Infection control precautions for a spinal anaesthesic
PG28 = ANZCA document on infection control For neuraxial (or nerve catheter) - full aseptic technique. 0.5% chlorhex. Sterile drape. Gown, sterile gloves, mask, hat But PG28 also suggests could do with sterile gloves and don't necessarily need the sterile gown - only if straightforward single shot spinal. If in training, or anticipated difficulty --> gown up. Also, would only really consider doing this if needing a "rapid sequence spinal" e.g. cat 1 obs but likely difficult GA
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Treatment for methaemoglobinaemia
Can get from prilocaine, much more likely in children (especially if EMLA too) In adults, usually need to give >600mg prilocaine = 30ml of 2% Treatment with methylene blue 1-2mg/kg IV over 5 mins (can cause anaphylaxis)
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Dose of bicarbonate in a regional block
1ml of 8.4% bicarb per 10ml lignocaine or 20ml bupivacaine. Faster onset + less pain on injecting (more unionised drug due to higher pH so more rapidly enters nerve axon)
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Dexamethasone for regional anaesthesia
4mg perineurally will increase block duration about 8 hours (systematic review of 29 RCTs). But is off label use. And precipitates ropivacaine IV dex 8mg almost as long block increase as perineural + systemic benefits such as PONV. IV also prolonged LCSC spinals from 100 ---> 160mins on average. Motor blocks unchanged
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Dexmedetomidine use in regional anaesthesia
0.5 - 1mcg/kg perineural. Increases block duration about 3-6 hours. Speeds up onset by 9 mins. Might provide more sensory than motor block - Also causes sedation, hypotension, bradycardia in higher doses IV dexmed also useful to increase regional duration. 2021 study found increased spinal duration from 180mins --> 300 mins (regression of block to L1). 1mcg/kg loading then 0.5mcg/kg/hour infusion
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How to use a peripheral nerve stimulator for regional anaesthesia
- Negative to needle (black to needle). Red to patient (place an ECG dot at least 20cm from nerve) - Start with 1-2mA and frequency of 2Hz - Insert insulated needle, move in 1-2mm increments - When starting to get motor response, try optimise with 0.2-0.5mA - If getting twitches at <0.2mA, then withdraw needle slightly. Might be intraneural - Aspirate to excluse intravscular - Inject 1ml LA - should abolish twitch - Inject remaining LA
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Benefits of using US for regional blocks
Less LA used - less risk of LAST More successful blocks Faster onset Faster to perform the block Less vascular puncture (don't think it reduces the rates of nerve injury)
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Evidence for doing a peripheral nerve block on anticoagulation / antiplatelets
ASRA have no hard and fast rules for anticoagulation and regional never blocks Review from 2018 of 10,000 patients on anticoagulation / antiplatelets, 60 had bleeding complications (but 90% of these were from one study where femoral nerve catheters done on patients on rivaroxiban) - All case reports neurology fully recovered by 12 months. Bleeding rather than neurology was the main issue If peri-central neuraxial block, should have same standards as neuraxial (e.g. lumbar plexus, paravertebral, deep cervical plexus). Same for nerve catheters Plane blocks and US guided will reduce vascular injury risk Fascia iliaca blocks are frequently done on anticoagulation with low risks demonstrated
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How long to withhold antiplatelets / anticoagulants before a spinal?
Heparin infusion - either normal APTT or 4 hours Enoxaparin. 12H if prophylactic. 24H if treatment dose Warfarin. INR <1.5 (5 days) Rivaroxiban. 3 days if eGFR >50, 4 days if <15 Dabigatran. 3 days if eGFR >50. 5 days if >30 Aspirin. no need Clopidogrel. 7 days Ticagrelor 5 days Tirofiban. 8hours Alteplase. 10 days
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Bleeding drugs that are okay to give with an epidural on board?
Aspirin - yes Heparin infusion - maybe. Risk benefit Enoxaparin. Prophylactic dose only. Risk benefit Everything else - nope
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When can bleeding drugs be given after an epidural catheter has been removed?
Heparin infusion - 1 H Enoxaparin - 4H (both treatment and prophylactic dose) Warfarin, aspirin - immediately Dabi, rivaroxiban, clopidegrel, ticagrelor, tirofiban - 6H Alteplase - 10 days
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Pathophysiology of peripheral nerve injury after regional anaesthesia
Can be from direct needle trauma, compression from LA, LA or additive toxicity or local vasoconstriction causing ischemia 90% resolve by 3 months, 99% by 12 months. Risk of permanent nerve injury around 1:7000. Temporary around 1:10 Risk factors: - Patient: elderly, diabetic, pre-existing neurology conditions (MS). Children and pregnant women lower risk - Block factors: higher concentration LA, more volume, more proximal brachial plexus (interscalene highest risk)
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Methods for reducing risk of peripheral nerve injury during regional?
- US + always visualising tip. Away from nerves - Short, blunt tipped bevel - Compressed air technique or other means to reduce ressure when injecting so not high pressures intraneural - Awake patient, not heavily sedated - Small boluses of LA and visualising spread - Not using excess LA concentration or volume
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Advantages of doing an awake regional anaesthetic?
Can tell you if you're hitting a nerve (but won't always get parasthesia. And can get nerve injury even without nerve contact) Can demonstrate CNS symptoms of LAST (which occur before CVS symptoms) Most patients are fine with awake or mild sedation
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Relevant anatomy for a neuraxial block
Spinal cord terminates at L1 in adults (L3/4 in infants) subarachnoid space extends to S2 in adults, S3 in infants. It is in continuum with spinal nerve roots laterally to dorsal root ganglia Iliac crest line intersects L4. More L3/4 in pregnancy Inferior border of scapula = T7. Spine = T3 Cervical prominens = C7
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Absolute and relative contraindications to spinal anaesthesia
Absolute - patient refusal - Uncorrected coagulopathy - OVerlying infection Relative - Systemic infection - Cardiac outlet obstructions (HCM, AS) or mitral stenosis. Unable to compensate for drop in SVR - Coagulopathy / anticoagulation - Uncorrected hypovolaemia - Raised intracranial pressure (obctructing hydrocephalus)
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Complications from neuraxial anaesthesia
Data from NAP3 mainly Nausea Hypotension (decreased SVR, reduced preload and bradycardia (from Bezold-Jerrish reflex + cardiac accelerator fibre block) Itch (if IT morphine) Urinary retention Motor block PDPH High spinal, total spinal Nerve damage. Permanent 1:50,000. Paralysis 1:200,000 Infection (abscess 1:100,000 and meningitis 1:100,000) Haematoma (1:50,000) For obs specifically - older data with higher concentration epis suggested increased instrumental delivery. But not with current concentrations. No changes to C section or foetal issues.
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Evidence for thoracic epidural in open AAA repair
Level 1 evidence, cochrane review. Less pain intensity Faster time to extubation Less time in ICU Less acute resp failure Less MI Less GI bleeding (but no mortality benefit)
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4 sensory nerves of the cervical plexus
Greater auricular Lesser occipital Transverse cervical Supraclavicular These are from C2-C4. cover the neck and scalp region directly posterior to the ear. These are the 4 nerves blocked in a superficial cervical plexus block (deep cervical plexus is mainly motor nerves to neck and vertebral column, unncessary to block)
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Describe intermediate block to the superficial cervical plexus
Position: supine, head turned outwards US, high frequency, linear probe Locate C4. Can do this by finding C7 (transverse process has no anterior tubercle) and shifting cephalidly. C4 also around level of carotid bifurcation Superficial cervical plexus in betweeb deep border of SCM and prevertebral fascia overlying deep muscles (levator scapulae, middle scalene) Insert sonographic needle from posteriorly, in plane. Into fascial plane. Inject 10-15ml LA (0.375% ropi for carotide surgery) Complications include: - Phrenic nerve palsy - Recurrent laryngeal nerve palsy - Brachial plexus block - Carotid puncture If doing for carotid surgery, won't cover the carotid sheath (CN 9) - best by surgeons. Also wont cover the surgical retractors
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Describe landmark technique for superfical cervical plexus block
Aims to block 4 sensory nerves of superficial cervical plexus: - Transverse cerivcal - Greater auricular - Lesser occipital - Supraclavicular Middle of posterior border of SCM. Fan cranially and then caudally through same injection site. 10-15ml of LA or so. Minimal risks / complications. One RCT found superficial cervical plexus and US guided intermediate approach to cervical plexus had same rates of surgeon LA top ups (about 50% for both which is typical) Also won't cover the carotid sheath (CN 9) - get surgeon to do this
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7 nerves to block for a scalp block
23g needle for all. Landmark based V1 nerves - supratrochlear and supraorbital (both exit via orbital foramen, supratrochlear = most medial). Orbital foramen palpable (medial aspect of superior orbital rim. 1cm cranial and 1cm medial to foramen. Then 1cm more medial to get supratrochlear V2 nerve - zygomaticotemporal. Passes through temporalis muscle so have to do superficial and deep injecting. Start at supraorbital margin (near eyebrow edge), inject 3ml LA until bone contacted. Then redirect towards zygomatic arch- then another 3ml of LA here V3 nerve - auriculotemporal. 1cm LA immediately anterior to auricle at level of TMJ. Ensure palpate superficial temporal artery (which will be deep). Aspirate before injection Cervical plexus nerves (C2-C4) - Greater auricular. 1cm posterior to tragus, contact bone, withdraw slightly. 3ml La here - Lesser occipital. Start at mastoid posterior to auricle. follow superior nuchal line and infiltrate LA along this (will cover both greater and lesser occipital nerves). Follow towards occipital protuberance - Greater occipital - usually about 3-4cm lateral of occipital protuberance. Next to occipital artery so try palpate this. Aspirate before injection
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Complications from scalp block
- High systemic uptake of LA from scalp. Careful with LA doses to avoid LAST - Infection - Bleeding / intraarterial injection - especially nearby 2x arteries. Superficial temporal artery (for auriculotemporal nerve) and occipital artery (for greater occipital nerve) - Facial nerve palsy (especially with auriculotemporal nerve block - facial nerve is deep to this nerve) - Ptosis
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Advantages and disadvantages of a subtenons block?
Adv: - Provides good akinesia and analgesia, equivalent to peribulbar block - Less risk than peribulbar block - less risk of peribulbar haematoma, globe rupture. Study of 180,000 subtenons blocks found only 1 sight threatening complication (ciloretinal artery occlusion) and two life threatening reactions (anaphylaxis and MI). 4% risk of subconjunctival haemorrahge - Can be done on anticoagulated patients / anti plateleted patients - Easy to perform - Less rise of IOP than peribulbar blocks - Can be done in long axial lengths (>26mm) - dont need IV access Disadv: - chemosis - blood shot eyes, can last for days (mainly cosmetic issue) - Repeat subtenons blocks are subsequently more difficult due to scarring, fibrosis. May need to use alternative sites - Cant use in eye trauma - visual impairment post op (unlike topical LA)
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How to perform a subtenons block?
- Consent, positioning (supine), confirm operative side and allergies. Tell them vision will blur, won't be able to move eye - No need for monitoring, IV access - 1% tetracaine drops to eye, allow to work - Iodine to eye (not chlorhex) - get patient to look "out and up" - superior-laterally - Place in eye speculum - Use Morrfield forceps, pick up conjunctiva approx 5mm from limbus in medial-inferior portion covering globe - Make snip with westcott scissors in conjunctiva, should see avascular tenons capsule underlying. Dilate tract with blunt dissection with scissors - Tenons cannula (curved, blunt) on end of 5ml syringe. Advance in tract, following contour of eye until at hilt of needle - Aspirate and infiltrate 3ml 0.5% bupivacaine. Chemosis might suggest wrong plane - Monitor for effects - akinesia + loss of sensation. - Tape eye shut
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How to do a peribulbar block?
- Consent, positioning, monitoring, Iv access, assistant - Can be done with eye open or closed - 1% tetracaine to eye - iodine to skin - 25g 25mm needle on 5ml syringe. - inferior to globe. Junction of medial 2/3rds and lateral third of inferior orbit (inferior-temporal approach). Palpate orbital rim and pass needle so skimming just above this (1mm) - Alternative approach to inferior-temporal is the superior nasal approach - Aim perpendicular to skin, horizontally parallel to globe, to avoid risk globe rupture. If anything, aiming inferiorly is better. If encountering bone early, may need to adjust angle superiorly slightly - Get to 25mm. needle needs to be past the equator of the eye - Aspirate - ensure no blood or CSF - Infiltrate 5-8ml of LA. some people put in hyaluronidase (3-30U / ml) to speed up onset. Warn patient will get full sensation behind eye - Monitor for adverse effects. Cover eye
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Advantages and disadvantages of a peribulbar block (compared to subtenons)
Advantages: - Can be done with eyes open or closed - Less eye chemosis - Get equivalent analgesia, akinesia - May be faster to perform than subtenons - single needle puncture without need to blunt dissect tract Disadvantages: - More risk - retrobulbar LA, haematoma, total spinal, intra-arterial injection (LAST), globe perforation - contraindicated if globe axial length >26mm (risk of globe rupture) - Cannot be done if on DAPT or anticoagulation - Requires IV access, more monitoring due to higher risk - More rise in IOP than subtenons
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Anatomy relevant to an interscalene block
Brachial plexus block targetting nerve roots level. C5, 6, 7. Of brachial plexus blocks, reliably blocks suprascapular nerve so better shoulder joint glenoid coverage and scapula coverage. Sensory and motor block of axillary, radial, musculocutaenous, median nerves (spares pec major motor though) Nerve roots emerge at respective levels. Appear usually as C5 and split C6 in between anterior and middle scalene muscles. Relatievly superficial block Block typically at C7. Can start around level of thyroid cartilarge (C6). Identify as C7 TP doesn't have an anterior tubercle. C6 has a wide TP and prominent anterior tubercle (Chassiagnac's tubercle). Will be able to see both vertebral artery and vein at C7 level as only single tubercle of TP (where as higher up, these run between the TP tubercles so can't see them) Anterior scalene is immediately lateral and posterior to carotid artery. Can either track nerve roots as they exit Often doesn't block C8, T1 so don't get coverage of ulnar distribution (medial hand, medial forearm) and medial upper limb. Not good for tourniquet Risks: - phrenic nerve. Superficial to anterior scalene. 60-90% get phrenic nerve palsy - Recurrent laryngeal block - Horners syndrome, sympathetic block - Long thoracic nerve injury (within middle scalene) - vascular structures. IJV, carotid. Highly vascular area (transverse cervical artery runs through nearby. Use Doppler)
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Anatomy relevant to a supraclavicular brachial plexus block
Brachial plexus at divisions level in the supraclavicular fossa (place US probe parallel to clavicle, appears as "bunch of grapes". Covers all terminal branches reliably - sensory and motor block to axillary, musculocutaenous, ulnar, radial, median nerves. Sensory to upper limb except T2 (intercostobrachial nerve = medial upper limb, won't be covered). also motor block Plexus is just lateral to the subclavian artery. Lies deep to omohyoid muscle It is superior to the pleura - best to line it up so 1st rib directly underneath plexus as hard backstop to reduce pneumothorax risk Does not reliably cover glenoid for shoulder - suprascapular nerve often branched off already within middle scalene. risk of injury. Phrenic nerve still about 30-60% risk of being blocked. Lies anterior to anterior scalene
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Risks of a supraclavicular nerve block
Specific to block - Pneumothorax - Horners syndrome - Phrenic nerve block - Injury to suprascapular nerve Generic regional risks - LAST (but higher risk in general as central so higher cardiac output, more systemic uptake) - Haematoma, intravascular injection (subclavian artery. not easily compressible either) - Infection - Nerve injury
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Anatomy relevant to an infraclav block
Brachial plexus, level of the cords. Sensory and motor block to the arm (except T2 = intercostobrachial nerve). Similar sensory to supraclav block (but no chance of suprascapular nerve being blocked) Axillary artery has lateral, medial and posterior cords surrounding it. In between the artery and vein is the medial cord. Lateral cord is cephalid to artery (you know this) Axillary artery / brachial plexus is deep to pec major, pec minor. Inferior to clavicle. Relatively deep block. Often need to "heel" US probe. Challenging in obesity. Inbetween pec major and minor are the pectoral nerves and thoracoacromial artery / vein. Avoid these. Imaging parasaggital plane. Just medial to coracoid process of scapula Medial to this image will be lung, pleura. do not direct needle medially Less risk of phrenic nerve palsy compared to supraclav and ISB. Also no risk of Horners or recurrent laryngeal block.
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Anatomy relevant to an axillary nerve block
Terminal branches of brachial plexus at this point. Provides sensory and motor to the arm (except T2 = intercostobrachial). compared to infraclav and supreclav, doesn't cover axillary nerve so no deltoid / lateral upper arm coverage either. Useful for anything from the elbow down, Radial, ulnar and median nerves surround the axillary artery (RUM). Deep to this is the conjoint tendon of pec major, teres major. (and deep to CT is triceps). With axillary vein more posterior to artery (but often compressed). Median nerve often has medial cutaenous nerve of forarm with it. Anteriorly, corocobrachialis muscle (with bicepes more anterior to this). Musculocutaenous is within this muscle, must be blocked separately for lateral wrist and forearm coverage - often this nerve is missed in axillary block. Musculocutaenous usually has lateral cutaenous nerve of forearm with it No risk of PTX, phrenic nerve block, recurrent laryngeal block, horners syndrome. Does usually take a few passes with needle to cover all nerves Although block is nearby the axillary artery, this is relatively easily compressible
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Using a PNS while doing a axillary nerve block, what motor movements would you expect for each nerve?
- Radial: wrist extension, finger extension - Ulnar: thumb adduction - Median: finger flexion, wrist flexion, forearm pronation - Musculocutaenous: biceps and brachialis flexion of elbow
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Sensory innervation of median, musculocutaenous, ulnar and radial nerves
Median - hand only. Ventral aspect from 1st - 4th digits (usually only lateral portion of 4th digit) and corresponding ventral aspect of hand proximal to this. Ulnar - also hand only. Ventral + dorsal aspect. Medial aspect of 4th digit and 5th digit and corresponding ventral and dorsal aspect of hand proximal to this Radial - dorsal aspect of the forarm and dorsal hand (1st-4th digits). Lateral aspect of 4th digit only. Also some of the ventral upper arm too. Musculocutaenous - lateral aspect of forearm from elbow to wrist
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Technique for doing an IV regional anaesthesia (IVRA) = Biers block
- Indications: usually upper limb surgery, should be less than 30-40 mins. Fracture reductions - contraindications: sickle cell disease, crush syndrome to arm - Consent, positioning, IV in arm for surgery and then IV in another limb, monitoring - either 0.5% prilocaine or 0.5% lignocaine (lignocaine easier to remember. maximum 3mg/kg or 0.6ml/kg for children. Typically need 40-60ml of LA for adults) - Exsanguinate upper limb with compression bandage or elevation - Double cuff tourniquet. Must be on humerus (not forearm as radius + ulnar splint open blood vessels). Could do intercostobrachial block for this to reduce risk of tourniquet pain. Inflate proximal cuff only to 50-100mmHg above systolic BP. Must not be released for 20 mins minimum. If discomfort, can now inflate distal cuff (as will be blocked by LA). Then can deflate proximal cuff. - IV infiltrate LA. Should get mottled, warm vasodialted appearance of arm within minutes --> test block but should be good to go - IV cannula on surgical side can be removed if in the way of surgery - Monitor post op for risks of LAST (or methaemoglobinaemia if prilocaine)
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Anatomy relevant to a suprainguinal fascia iliaca block
SIFI Aims to block both femoral nerve and lateral cutaenous nerve of thigh Femoral nerve - mixed motor and sensory nerve. L2-L4 of lumbar plexus. It is within the femoral triangle but outside of femoral sheath (which contains the vein and artery) - Sensory - anterior and medial aspect of thigh. Divides a few cm inferior to inguinal ligament into anterior cutaenous branches and saphenous nerve. saphenous nerve supplies medial aspect of lower limb, down to medial malleolus and 1st toe. - Also supplies anterior capsule of hip - Motor - hip flexion (iliacus, sartorius, pectineus) and knee extension (quadraceps) Lateral cutaenous nerve of thigh - from higher in lumbar plexus than femoral nerve. L2-L3. - Sensory only. Supplies lateral thigh cutaenous innervation Locate ASIS and inguinal ligament. US in saggital plane. Follow inguinal ligament medial and inferiorly from ASIS to locate next bony structure (AIIS - same as you would for a PENG block). Should get classic bowtie appearance. With internal oblique cephalidly. Sartorius caudally. Beneath both of these is the fascia iliaca. And deep to this is iliacus muscle. Plane block for spread to femoral nerve and lateral cutaenous nerve (and more reliable spread to LCFN than infrainguinal fascia iliaca block) Often get view of deep circumflex artery and vein deep to internal oblique. Fascia iliaca just deep to this. Often used as landmark for where to palce needle. Deep to IO is also the peritoneal cavity As plane block, need to use higher volume of LA (often 30ml 0.2% ropi for analgesia block) Risks: - usual LAST, infection, bleeding, intraarterial injection, nerve injury (although most of these are reduced as plane block) - Intraperitoneal puncture - Quads weakness - not ideal for ERASing
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Anatomy relevant to a PENG block
PEricapsular Nerve Group block. Aims to block nerves that supply capsule of hip joint - hence quadriceps sparing (as doesn't block motor component of femoral nerve) Hip capsule innervation -Anterior - femoral nerve (L2-4) + obturator nerve +/- accessory obturator nerve capsule branches. These are main branches blocked. Also anterior capsule = main source for pain in hip fracture / hip surgery so most important to block - Medial- Obturator nerve (L2-4) (variably covered) - Posterior - quadratus femoris nerve (usually not blocked) Doesnt cover cutaenous innervation. Need to have something else for covering this (e.g. lateral cutaenous femoral nerve block. Or LA by surgeons) Locate ASIS in transvere. Curvilinear low frequency probe. Then track 2cm medial and inferiorly along inguinal ligament to locate AIIS (next bony landmark). Then rotate probe so medial portion of probe goes 45 degrees towards pubis, keeping view of AIIS laterally. Then angle probe caudally. Should be able to line up so AIIS and iliopubic eminence seen in continuum with each other as continuous hyperechoic line. Between these bony landmarks, should visualise tendon to psoas Needle from lateral to medial. Aim to place needle onto bone directly lateral to psoas tendon. Withdraw couple mm. then infiltrate 20ml LA. Watch spread
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Anatomy relevant to a poplietal sciatic nerve block
Scatic nerve = largest nerve in body. Formed from lumbo-sacral plexus L4-S3. Mixed sensory and motor nerve. Provides motor innervation to hamstrings in thigh (semimembranousis, semitendinonsis, biceps femoris) Provides all motor innervation to lower limb below the knee via the tibial and common peroneal nerves Provides sensory innervation to posterior thigh and posterior femur osteotome Provides sensory innervation to the majority of the lower limb below the knee. Splits into the tibial and common peroneal nerve just proximal to the popliteal fossa (Importantly the medial aspect of the lower limb and forefoot are innervated by the saphenous nerve = sensory branch of femoral nerve) Lateral position is probably best. Place US transducer in popliteal fossa transversely. Locate popliteal artery and vein. Above this will be tibial nerve. Track cranially to watch common peroneal nerve come together with tibial nerve (from laterally) as sciatic nerve. Block here (usually lateral --> medial approach)
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Adductor canal anatomy
Saphenous nerve. Sensory branch of femoral nerve Superior is sartorius muscle Medial is femoral artery (with femoral vein inferior to this). Adductor magnus Lateral is vastus medialis Provides medial knee coverage. Combined with iPACK for more knee coverage If done at mid thigh, it is quads motor sparing. But if you do it above midthigh (more proximal) more likely to get vastus medialis nerve which provides sensory input into the medial capsule of the knee (but at expense of blocking one of the quads muscles)
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Anatomy relevant to iPACK block
iPACK = interspace between popliteal artery and capsule of posterior knee. Basically the space that is between the popliteal artery and the femur. Block is done more distal than popliteal sciatic block so the tibial and common peroneal nerves have separated Used in combination with adductor canal block for analgesia to knee for TKJR (adductor canal provides anterior and medial knee capsule coverage) Specifically, iPACK blocks the posterior capsule branches of the tibial nerve. Quads sparing block
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Innervation of the knee relevant to knee joint replacement
Femoral nerve (L2-4) - Saphenous - anterior capsule + anterior-medial cutaenous (adductor canal blocks this. If high enough, can also block vastus medialis nerve) - Nerves to individual quads muscles - motor but also sensory to anterior capsule of knee Obturator (L2-4) - Medial capsule Sciatic (L4-S3) - tibial. Branches form genicular nerves. Posterior capsule. (iPACK blocks this) - Common peroneal. Lateral capsule
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Nerves that need to be blocked for an ankle block Sensory distribution of these
Saphenous. Sensory branch of femoral nerve. Provides innervation to medial aspect of lower limb from knee, along medial malleolus, to medial forefoot +/- 1st toe. Block this by locating saphenous vein and putting LA near by Tibial. Branch of sciatic nerve. Travels in deep posterior compartment of lower limb. Supplies calcaenous, medial and lateral plantar nerves (so plantar aspect of foot). Motor to gastrocnemius, soleus, posterior tibialis (=plantar flexion). Block this by locating posterior tibial artery (posterior to medial malleolus) and infiltrate posterior to this. Sural. Combination of both the common peroneal nerve (lateral sural nerve) and tibial nerve (medial sural nerve), converge around distal 1/3rd of lower limb. Sensory only. Supplies cutaenous innervation to posterior aspect of lower limb and lateral portion of foot (may include the 5th toe). Landmark technique is 5ml LA from lateral malleolus to achilles tendon. (it also runs next to lesser saphenous vein, share same fascial plane so can use this for US guided) Deep peroneal. From sciatic nerve, branch of common peroneal. Runs in anterior compartment alongside anterior tibial artery, motor innervation to tibilas anterior, extensor digitorum longus, extensor hallicus longus. Sensory innervation only in webspace between 1st and 2nd toes. Locate tibialis anterior before branches to dorsalis pedis and put LA lateral to this Superficial peroneal. From sciatic, branch of common peroneal. runs in lateral compartment. Provides cutaenous innervation to anterior and lateral portion of the lower limb and the majority of the dorsal aspect of the foot. Motor to peroneus longus and peroneus brevis (eversion of foot). Can block by using 10ml LA medial to lateral infiltration 2cm distal to intermalleolar crease along dorsum of foot
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Anatomy relevant for a paravertebral block
Indications: rib fractures, breast surgery, thoracotomy Chest wall supplied by intercostal nerves from thoracic spine. Intercostal nerves are mixed sensory and motor nerves, arise into paravertebral space from intervertebral foramen. Divide in the paraveretebral space into the dorsal and ventral rami. Also have a sympathetic branch to the sympathetic chain along the vertebral body. Dorsal rami supply sensory + motor to dorsal trunk. Ventral rami form intercostal nerves, run in between internal and innermost intercostal muscles. Lateral branch pierces through intercostals around midaxillary line, supplies lateral chest wall. Anterior branch supplies medial aspect of chest (medial breast, sternum) Block performed seated. Parasagital plane with US. Either two or three layers of muscle depending on level (rhomboid from T2-T5). Trapezius, rhomboids, erector spinae. Locate transverse processes of level of block you want. Approx 2cm lateral to midline spinous processes. Square shaped. Further lateral will get rounded ribs. Pass needle in plane, caudal to cranial. Pass through layers of muscle. In between transverse processes. Through costotransverse ligament. Aspirate here (ensure no blood and no air). then infiltrate LA. Watch pleura being depressed. Reliably get a 2 levels up and down from block. Depending on volume. More spread up and down that ESP block with same volume
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Risks for a paravertebral block
Generic: - Infection, bleeding, haematoma, intravascular injection, LAST, nerve damage Specific - Pneumothorax - Epidural / intrathecal infiltration --> hypotension, bradycardia, total spinal, coma, CVS collapse - Epidural haematoma - Sympathetic block, Horner's syndrome
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Describe how to do an interpectoral and pectoserratus plane block?
Interpectoral = plane in between pec major and pec minor (PECS1). Blocks the medial and lateral pectoral nerves. Provides some sensory innervation of lateral chest wall, minor contribution to shoulder joint (medial). Thoracoacromial artery runs in this plane too (you also have to dodge this when doing an infraclav block) Pectoserratus plane block = plane between pec major and serratus anterior. Contains lateral cutaenous branches of intercostal nerves. also long thoracic nerve (for serratus anterior) and intercostobrachial nerve (T2 which covers axilla, medial aspect of upper arm). Provides lateral and anterior chest wall analgesia (useful for breast surgery, rib fractures). does not cover medial cutaenous branches Use linear high frequency US. Place in delto-pectoral groove. Similar to infraclav. Identify pec major, pec minor. Rotate caudal aspect of probe 30 degrees laterally. Then slide inferiorly until at 4th rib. Three layers should be pec major, pec minor and SA.
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Technique for performing a superficial serratus anterior block
Pretty much the same coverage as a pectoserratus plane block (pretty sure they are the same planes). So cover the lateral cutaenous branches of intercostal nerves, long thoracic nerve, thoracodorsal nerve and intercostalbrachial nerve Mainly lateral chest wall coverage. Doesn't cover anterior intercostal branches (so no medial chest wall) and doesn't cover supraclavicular nerve (from cervical plexus) so no superior chest wall Start at midlcavicular line, saggital plane. Identify 5th rib. Follow this around to mid axilliary line. Only muscle overlying ribs here is the serratus anterior. If keep following around, will start to see lat dorsi. Target plane is inbetween lat dorsi and serratus anterior Watch for thoracodorsal artery which can be in this plane
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Anatomy relevant for performing a quadratus lumborum block
QL embedded in thoracolumbar fascia, provides means for spread in fascial plane to ipsilateral paravertebral space (proposed mechanism for how it works). Blocking lower intercostal nerve cutaenous branches (usually blocks T7-L1). As well as ilioinguinal, iliohypogastric nerves (inguinal region). Sympathetic chain blockade from paravertebral spread explains viscera analgesia from QL. May also spread to lumbar plexus, providing analgesia to hip and proximal femur (as well as blockade of motor function here) QL is triangular shaped muscle, imaged with patient in lateral position with curvilinear probe midway between iliac crest and inferior costal margin. Forms part of "3 leafed clover" with transverse process of vertebral as stem. QL = middle leaf. Anterior leaf = psoas. Posterior leaf = erector spinae. Anterior QL block most fashionable these days. LA infiltrated between QL and psoas Anterior to QL and superficial to psoas is paranephric fat. This is inferior to the renal fascia (which contains pernephric fat and kidney)
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Anatomy relevant to a caudal block
Caudal space = space in continuum with epidural space. epidural space contains fat, connective tissue, epidural vessels and nerve roots. Aim of caudal is to spread LA to cover these nerve roots, provide analgesia to sacral, lumbar and or lower thoracic levels. Dural sac terminates around S2/3 in neonates, S2 in older children. Spinal cord terminates around L2/3 in children. Utilises fact that in children, sacral hiatus exists where sacral vertebrae have not yet fused together. Sacral hiatus is located by forming an equilateral triangle between the two posterior superior iliac spines (PSIS) on dorsal aspect of patient. At the sacral hiatus, the sacrococcygeal membrane is located within an equilateral triangle formed between the two sacral cornue and the 4th sacral vertebrae. Use 22g cannula to pass through sacrococcygeal membrane (can be done under US guidance). Dose of 0.2% ropivacaine. Sacral coverage = 0.5ml/kg Lumbar coverage = 1ml/kg Lower thoracic coverage = 1.5ml/kg Can add 1mcg/kg clonidine or use IV dexamethasone to prolong block. Usually get 4-8 hours from block.
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Advantages and disadvantages of caudal anaesthesia
Adv: - Easy to do. Can be done under US and can watch for LA spread. Reliable blockade. One study found after 30 times, trainess could have >80% success rates - Opioid sparing - Useful for neonates with terrible lungs (e.g. premature) - May help reduce anaesthetic dose. Or avoid GA all together (good for not having repeat GAs) - Less haemodynamic drop compared to spinal (although neither is particularly concerning in kids usually). Typically very well tolerated - Can be done on preterm neonates up to 50kg children - Low risk of dural puncture - Low risk of any complications. European trial suggested 0.1% risk for paeds regional Disadvantages: - Motor block - may be distressing for toddlers that are used to running around - Urinary retention - Cant be done if on anticoagulation (rare in children) - Inadvertent dural puncture - Inadvertent intravascular injection - LAST - Other blocks may be more targetted (e.g. ilioinguinal + iliohypogastric for hernia) Contraindications: - Local infection - Pilonidal cyst - tethered spinal cord - Spina bifida / other meningeal abnormalities - Anticoagulation
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Differences for paediatric epidural insertion
Distance to epidural space can be 1cm. Rarely it is more than 1.5cm Thoracic spinous processes less angulated - use more traditional approach Obviously smaller spaces, more challenging insertion Lumbar spinal cord terminates around L2/3 in infants LOR to saline only. There have been deaths from LOR to air from pneumocephalus Ligamentum flavum is less well developed, less convincing LOR Complications from epidurals are lower than adults 18g Touhy needle fine for children. 19g needle for infants and neonates Epidural catheter itself only has a single hole near the tip. Leave a couple cm in epidural space. Dose of epidural mix. Can use 1.25% bupivacaine + 2mcg/ml fentanyl. run at 0.1-0.4ml/kg/hour
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Spinal anaesthesia in paediatrics differences
Spinal cord terminates at L2/3 in most children. Can be as low as L4 in premature neonates. Aim for L4/5 or L5/S1 Shorter distance to dural sac (1.5 - 2cm). Use 2.5cm or 5cm needle. Still often use a 25g needle. do not need introducer Skilled assistant necessary. Place lateral position, curl up legs Challenging insertion due to small spaces. Ultrasound useful as no calcification so readily can see intrathecal space If neonate, can keep still with sucrose on pacifier. Dose - 0.1ml/kg of 0.5% heavy bupivacaine. Have to account for needle deadspace (around 0.06ml) CSF volume in neonate is 2x adult for body size. And higher pia blood flow. Faster onset but faster offset of spinal (reliably only 60 mins). Less hypotension, bradycardia than with adults due to immature autonomic nervous system Higher spread cephalidly with same LA volume due to lack of thoracic kyphosis PDPH in children harder to detect. 10mg caffiene is an option. Epidural blood patch dose is 0.1-0.2ml/kg
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Describe anatomy for penile block
US guided is good Have US on ventral surface of penis (underneath it) so don't compress superficial vessels. can put wheal of LA along ventral surface to cover ventral penis (supplied by pudendal nerves). Also provides acoustic window for US Penis has 3 big circles on US. 2x superior corpus cavernosa (each has internal artery). 1x inferior corpus spongiosum (has urthera) Superior to the corpus cavernosa is the dorsal vein. Either side of dorsal vein like 2x dorsal arteries. And with each artery run the 2x dorsal nerves Overlying the 3 big circles and the dorsal vein + arteries + dorsal nerves is the deep (or Buck's fascia) Then overlying this is the superficial fascia. Can actually just put LA through the superficial fascia (in between the deep and superficial) and it seems to work well enough too
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Anatomical considerations for an ilioinguinal / iliohypogastric nerve block
Inguinal cutaenous innervation, unilateral groin. Mainly only done for inguinal hernia repair, orchidopexy or hydrocoele repair Doesn't provide spermatic cord, penile or ventral peritoneum cover Ilioinguinal = closer to inguinal ligament (so therefore more lateral on US). It is sensory and motor nerve. Branch from L1 nerve root. Motor to oblique + TA muscle. Anterior-medial upper thigh, groin. scrotal / labial areas Iliohypogastric. From higher up in lumbar plexus. T12 (subcostal nerve) and L1. Also sensory and motor. Sensory = abdominal wall. Motor = same as ilioinguinal Nerves tend to run in between fascial plane of internal oblique and transversus abdominus (like doing a TAP block). US guided, IP. Find ASIS and draw line with probe from ASIS to umbilicus. Ilioinguinal nerve tends to be about 1cm medial from ASIS. Iliohypgastric 1-2cm medial from this again. Often has blood vessels in same plane (branches of deep circumflex artery), helps identify plane 1ml/kg of 0.2% ropivacaine
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Advatnages and disadvantages of a ilioinguinal / ilihypogastric nerve block
Adv - Unilateral block, if used for inguinal hernia repair then covers surgical site without unnecessary coverage elsewhere (unlike caudal) - Motor block uncommon (only 10% get unilateral spread to femoral nerve) - Equivalent analgesia to caudal for hernia repair. Superior to LA and TAP blocks - US guided, superficial block Disad - Plane block so need reasonable volume of LA (which can be limited in children) - In same plane as 2 nerves are branches of deep circfumflex arteries - risk arterial puncture, intravascular injection, haematoma - Peritoneal puncture, bowel injury - Usual infection, bleeding, LAST, nerve injury - In neonates, often not done by anaesthetist as can obstruct surgical view - Doesn't cover spermatic cord (for high orchidopexy), penis, ventral peritoneum
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TAP block anatomy
Subcostal TAP blocks seem to be the way to go. Midaxilliary only get a couple of dermatomes. Where as subcostal, tend to get a lot more. spinal nerves T6-L1 supplies anterior abdominal wall travel in transversus abdominus plane As long as you place LA in the fascial layer above the transversus abdominus muscle, it counts as a TAP block. May be: 1) Between rectus abdominus and TA 2) Between linear semilunaris (=conjoined tendon between rectus abdominus and oblique muscles) and TA 3) Between internal oblique and TA
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Cuff and pressure settings for arterial tourniquet Maximum time for tourniquet?
Should be pneumatic (not mechanical) - more even spread and titratable pressure. Cotton wool underneath to reduce pressure injuries Cuff width: 20% greater than diameter of upper limb. Or 40% circumference of thigh (as per AHA) Cuff length: 7-15cm greater than circumference of limb Pressure: 50mmHg above systolic BP for arm 2x systolic BP for leg No known "safe" time. 2 hours should be hard limit. Every 30 mins, 3x increased risk of nerve injury. Should then have at least 15 minute break from tourniquet
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Risks of arterial tourniquet?
Generally, longer the tourniquet time and larger the limb being tourniqueted --> larger effects below. More comorbid patient, more prone to effects Biochemical effects - Reduced perfusion. Decrease PO2, increased PCO2, increased lactic acid production. On release of tourniquet, acidosis, hypercapnia, hypoxia. May get decreased SVR and negative inotropy from acidosis, lactate, K+ --> hypotension - Increased CBF if increased PacO2 (bad if head injury) - hyperkalaemia from acidosis --> arrythmia possible Coagulation effects - Venous stasis. Can get DVT formation --> PEs can occur on release Tourniquet pain - increasing HR, BP, RR due to compression of unmyelinated c fibres. (can abolish this with regional anaesthesia). May need to treat with ketamine, clonidine (but risk over sedating) Neurpraxia / nerve injury - Increased risk after 2 hours, but can occur earlier in vulnerable patients (e.g. diabetes) - Anoxic injury to nerves. Get loss of conduction after around 30 mins of tourniquet - Relatively rare. 60,000 patients having tourniquet in Norway, 15 thought to have injury from tourniquet Ischaemic-reperfusion hyperaemia - Risk of compartment syndrome. Especially if at risk for this already e.g. tibial fractures, crush injuries Peripheral vascular disease - Risk of arterial injury (due to heavy calcification). One study of 5000 knee arthroplasties, 7 had arterial injuries from calcified vessels. 3 of those patients needed amputations Sickle cell disease - Risk of creating sickling crisis. Relative contraindication - Could exsanguinate limb first. But still risk sickling if patient becomes hypoxic or acidotic once arterial tourniquet comes down. Risk benefit whether to use or not
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Advantages and disadvantages of cell saver
Advantages - minimises allogenic transfusion - reducing risk of ABO incompatibility, TRALI, anaphylaxis - No risk of rare antigen sensitisation (kell, duffy, kidd etc) - Minimises storage lesion - no hyperkalaemia, normal 2,3 DPG, no acidosis - don't necessarily have to give blood back - if at risk of overload - safe in c sections, SALVO trial (2018) demonstrated no increased risk of AFE Disadvantages - No coagulation factors, platelets - Slow to centrifuge blood and deliver - especially if using a 40 micro filter or leukodepletion filter (maximum of 100ml/hr). May outpace bleeding - Risk of giving blood to another patient (e.g. if cell saver blood taken into PACU) - Risks of spread of bacteria, endotoxins - Cannot use with fibrin glues, bone cement, antibiotics not intended for IV use, chlorhexidine wash - Use in malignancy is controversial - used in some circumstances e.g. urological malingnacy (NICE guidelines). Manufacturers recommend against use in malignancy - Cost of machines, maintenance - Requires training to set up and run machine - sickle cell disease - Heparin sensitivity (need to use citrate) - Transfusion related hypotension - thought to be bradykinin related
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SALVO (2018) trial
Routine use of cell salvage in c sections. n = 3000. No increased risk of AFE. Also didn't reduce allogenic transfusion rates in routine CS. Best to only use cell saver in high risk of bleeding
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Quantitative measures of systolic function on echo
Fractional shortening. - M Mode. Transgastric mid papillary short axis view. Determinedistance of ventricle cavity in end diastole and end systole - % change = FS. (normal = 26-44%) Fractional area change - Parasternal short axis. Measure area of LV in end diastole and end systole - % change (normal = 36-64%) Ejection fraction - Simpson's biplace commonly used. Uses both 2 chamber and 4 chamber view. Both views so get 90 degree rotation - End diastole (after P wave, before QRS) and end systole (end of QRS, before T wave) - "stacked discs" = volume of LV determined by 20 hypothetical discs. Difference diastole and systole = EF
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How to determine diastole function based on echo?
Use E and A waves during diastole. Measured using apical 4 chamber view, detecting blood flow through the mitral valve. E = early wave = early filling of LV during diastole A = atrial wave = atrial kick at end of diastole e' = septal muscle velocity of ventricle near mitral valve (tissue doppler at septal annulus ventricle muscle), away from probe in diastole. Reduces in diastolic dysfunction Determine ratio of E/A and e' Normal E/A = 0.8 - 1.5. Most blood flow occurs in early diastole. e' >8cm/s Grade 1 = impaired relaxation. E/A <0.8. More filling is occuring due to atrial kick than E wave. e' <8cm/s Grade 2 = pseudonormal. E/A of 0.8-2. Raised LA pressures in early diastole drive more blood into ventricle. And rising LA pressure starting to impair atrial kick. So get normal E/A. Need to look at e'. If <8cm/s, then it is grade 2 diastolic dysfunction. E/e' 8-15. Grade 3 = restrictive. E/A >2. e' will also be <8cm/s. E/e' will be >15. Large LA driving blood into rigid ventricle (large E wave) and reduced efficacy of atrial kick (reduced A wave) Grade 4 = irreversible. Same parameters as grade 3 but doesn't change. Do a valsalva and see if there is any change Limitations: - AF will lose A wave - Prosthetic mitral valves will cause inaccurate readings - Tachycardias may cause fusion of E and A waves - Aortic regurg will cause interferrence
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How to estimate pulmonary pressures with echo?
TR jet peak velocity. Bernoulli equation. Pressure = 4v(squared). Then add on RA pressure (estimated by appearances of IVC compressibility) = RVSP Normal = 15-30mmHg Mild = 30-45mmHg Moderate = 45-60mmHg Severe > 60mmHg
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IVC assessment on echo
Measurement in shortaxis. Subxiphoid view. Find IVC within liver M mode, assess diameter change in respiration CVP 5 or less - IVC <1.5cm and total collapse with inspiration (or if IPPV, total collapse with expiration) CVP 5-10mmHg - IVC 1.5-2.5cm with >50% collapse on inspiration CVP 10-15mmHg - IVC 1.5-2.5cm with <50% collapse CVP >15mmHg - IVC >2.5cm with <50% collapse and minimal variation with respiration CVP can be raised due to: tension PTX, tamponade, heart failure / overload, cardiogenic shock, PE. Only a static measure, doesn't necessarily mean they're fluid responsive or not
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PG 47 on POCUS
Basically states minimum training recommendations for use of point of care ultrasound There is a separate one for comprehensive TTE and TOE (PG46) Might be useful to know that: Gastric POCUS suggestion is for formal image interpretation on 20 cases. 30 studies if basic US competance or 15 if experienced in POCUS Cardiac POCUS - 90 complete studies. 20 directly supervised. Another 20 with review by superviser Also mentions lung US and airway US
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Advantages and disadvantages of 5 lead ECG
Has RA, LA, LL, RL and a precordial lead (usually V5) Advantages - Increased sensitivity to detect myocardial ischaemia. With V5 alone it is 75%. Incombination with II it is >85%. superior to 3 lead ECG for detecting ischaemia - Modern anaesthesia machines can detect changes in ST segments - No additional training needed - all anaesthetists should be able to use - Recommended by both ANZCA and AHA for high risk for MI patients - EAsy to apply Disadvantages: - Has downsides of 3 lead such as interference, ECG dots not sticking, in the way of surgical access - Less able to detect inferior and posterior ischaemia (less sensitive than 12 lead ECG, although not by much) - TOE and RWMA detection will be better at picking up RCA territory ischaemia - Once ischaemia detected, may not be ammenable to treatment
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How does a NIRS work?
Cerebral oximetry, near infrared spectrometry Similar to how saturation probe detects arterial oxygenation. Utilises Hb light absorption characteristics. With 660nm peak for deoxyHb and 940nm peak for oxyHb. Isobestic point at 800nm Cannot detect pulsatile blood so instead detects average Hb absorption in cortical tissue. Due to 70% of blood being in venous state, rScO2 (regional O2 saturation of cerebral tissue) is lower than arterial saturation Reliant on reflection of light back to the sensor 60-80% is normal, but can be 55% and still normal for patient Measures both sides. Need to get baseline before O2 or anaesthesia drugs given. Does not measure posterior circulation oximetry
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Advantages and disadvantages of cerebral oximetry
Advantages: - Able to measure non-invasively, the oxygen saturation of cerebral tissue. - Provides level of monitoring that is suggestive of an intact circle of willis and autoregulation during carotid surgery when there is carotid stenosis and then subsequent clamping of the carotid. Provides warning to anaesthetist to improve rScO2 or inform surgeon to shunt - May also be used in higher risk for ischaemia e.g. beach chair position, especially if known carotid stenosis - Strong correlation between a decline in rScO2 of >20% from baseline, and an increase in worse outcomes such as delirium post op (mainly from cardiac surgery- RCT of 265 CABG patients) - May also be indicator for aortic arch surgery (both endovascular and open), if occlusion by surgical team or atheroma, may cause decline in rScO2, and may be ammenable to immediate resolution Disadvantages - 20% decline is somewhat arbitrarily defined, evidence is uncertain on what a significant decline actually is and what targets to have - There is no evidence that if there is a decline of 20% or more, and then treating this, that there are improved outcomes. NIRS may just provide prognostication rather than provide means to prevent injury. No evidence improves mortality or stroke rates - don't actually tell you why there is a drop in rScO2, need to find this out yourself - Cost - use of NIRS could add up signfiicantly, approximately 70$ per unit - Interference with diathermy, other electrical interference - Need to get baseline level before O2 or anaesthesia or else inaccurate
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What to do if cerebral oximetry drops by >20% of baseline
Inform surgeons but start treatment Goal to increase delivery of oxygen to cerebral - can do this by increase O2 content of arterial blood or increasing cerebral blood flow Arterial content of blood - Increase FiO2 - Correct for anaemia, aim Hb >90g/L - deepen anaesthesia (down to isoelectric) --> decreases CMRO2, decreases O2 consumption. But caution to not drop MAP - Treat hyperthermia or seizures Increase cerebral blood flow - Ensure normal PaCO2 (or high normal PaCO2) - do ABG if etCO2 unlikely to correlate to PaCO2. Hypercapnia may cause cerebral steal syndrome. Hypocapnia will cause vasoconstriction and reduced CBF - Increase MAP - +10% of baseline. Vasopressors - Ensure no causes for raised CVP - neck ties, IJV obstruction If still unsuccessful with above --> surgeon needs to shunt
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Advantages and disadvantages of Belmont Rapid infuser
Advantages - High flow blood and crystalloid delivery - 1L/min for crystalloid, 750ml/min for blood. With roller pump (electrical, not reliant on medical air). Able to detect flow rates, adjust flow rates and alarm when pressure limiting too. - high volume resevoir (either 1.2L or 3L), can have multiple blood products infusing at same time (up to 5x bags spiked. Both FFP and red cells) - Warming - reliable warming. at 40s and 1L/min, warming at 37c (superior to level 1 infusion device). Uses counter current aluminium heat exchanger. Measures temp and turns off if >40c - Air detection - has both input and output air detection systems. Will not infuse if detected air - Battery systems exist - Can be set up within 1-2 minutes with proper experience. Quick to prime - Audible alarms + screen monitor Disadvantages - Costly system, some centres will rarely need or use them - fluid overload - can give 1L/min. Ensure dedicated person using Belmont and titrate to effect. Can slow infusion to minimum of 2ml/min - Compartment syndrome, limb ischaemia if extravasation due to high pressure - Portability is limited - Requires power - Need large bore access without flow restricting bungs for ability to run high flows - can be challenging to acquire in situations where Belmont useful - Cant give platelets or cryo through it - Air embolism possible still - but less likely with detectors - Dilutional coagulopathy - Risks of transfusion (massive transfusion and standard transfusion reactions - amplified risk as can be dozens of units given)
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Requirements for a shock to occur
Current source - Equipment fault / current leak Person to come in contact with current source Person to connect fault to earth, forming lower resistance connection
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How does an RCD work?
Residual current device. Has a toroidal coil = detector coil, determines if difference between active (live) wire and neural wire. In usual circumstances, current in active wire and neutral wire should be equal and opposite. If current leak >5-10mA detected --> trip circuit activated, disconnects power within 10-20ms --> fast enough to prevent shock. Only prevents macroshock though (as microshock can occur at 0.1mA) Also alarms if trip circuit activated
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How does a LIM work?
Line isolation monitor Creates floating circuit using transformer from main circuit. Floating circuit = not earthed. Requires 2x faults to occur before shock can occur. Monitor detects if current leak >5mA between secondary circuit active wire and secondary circuit neutral wire to earth - if there is --> alarms. But requires a 2nd fault before a shock can occur Protects against macroshock (not microshock which can occur at 0.1mA)
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How does equipotential earthing work?
Only method for protecting against microshock - requirement for cardiac protected areas e.g. theatre In normal circumstances, small potential differences can occur between different earthing points - resulting in current leak by induction. By connecting earthing points with a low resistance copper connetor (<0.1Ohms) --> equalisation of earthing potentials
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Equipment design to prevent shock in theatre
- Earthing. Having lower prong on 3 prong connection. If fault occurs where casing becomes in contact with active wire --> current leak to earth --> melting of fuse, disconnects circuit - Double insulated. If single fault occurs, 2nd layer of protection - Low voltage (battery powered instead of AC)
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Management of a mains power failure
- Priority to ensure safety to patient - Ensure oxygen delivery, anaesthesia machine function including ventilation, delivery of anaesthesia. O2 should be separate to electrical supply. If ventilator malfunction, will need to manually ventilate with BMV. If O2 supply failure, need cylinder O2 - Anaesthesia machine should have minimum 30 mins of battery (ANZCA standard) - Lighting - torches, mobile phones if theatre lights not working - but should be connected to essential power supply - UPS = uninteruptable power supply. should immediately kick in with theatre power supply. Battery powered. Ensure only essential items plugged in - Essential power supply (often red) - generator powered. Should kick in within 20s of power failure. Need minimum supply of diesel (24 hours) - Determine extent of supply failure - whole hospital, only single theatre, only theatre complex. And when power likely to return. Phones should also be conencted to essential power supply - Discuss with surgeons whether to proceed with surgery or discontinue. Will depend on urgency of case, likelihood of power returning, need for power in operation (surgical diathermy and haemostatic measures, imaging equipment, lighting, other surgical equipment), duration of surgery - If continuing, need to have most senior operator available. Only essential equipment plugged into essential / UPS sockets - Open blinds for natural light if able - Get patient spont ventilating if concerns for ventilator failure - Post op consider destination - if not power there either, may be best to recover in theatre
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How does ECMO work?
Two main types: VV and VA ECMO VV ECMO most common form - Place venous cannula into femoral vein and run it up the IVC, this will suck out venous blood into the ECMO machine - Then need a return cannula - usually into the right IJ and directed towards the atrio-caval junction - Femoral cannula pumps deoxygenated venous blood via negative pressure derived from a pump - then flows into oxygenator - membrane which oxygenates blood and removes CO2. Sweep gas applied at 1-10L/min which had air and O2. flow rate mainly determines extent of CO2 removal - Then returns to return cannula under positive pressure as oxygenated blood --> into PA through pulmonary circulation --> into aortic arch / systemic circulation - Can achieve flow rates of 3-6L/min depending on cannula size. Pulastile blood flow due to heart still functioning. Main use is for respiratory failure - also has bubble detector, O2 saturation detectors, flow detectors and warming VA ECMO difference is return cannula is into arterial system. Most commonly femoral artery (due to access). Can be into aortic arch directly but requires sternotomy. - Provides mechanical support for heart as driving pressure pumps oxygenated blood through systemic circulation, effectively replacing function of heart - Can achieve higher flow rates due to non-collapsable nature of arterial system. Non-pulsatile flow though
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Advantages and disadvantages of ECMO
VV ECMO ADVANTAGES - provides oxygenation while maintaining pulsatile flow through cardiac function. Oxygenated blood reaches coronary ostia, aortic arch and is delivered to heart and brain. Also normal blood flow through pulmonary circulation - May have benefit in severe ARDS. PaO2/FiO2 <100mmHg. Oxygenation and ability to provide lung protective ventilation - CESAR trial in 200 showed survival and major disability improvement at 6 months using ECMO. But 93% of ECMO patients had lung protective ventilation and only 70% of control did --> may just demonstrate lung protective ventilation improves outcomes - EOLIA (early initiation of ECMO) - no mortality improvement for severe ARDS - Some meta-analysis has demosntrated slight improvement of 60 day mortality with ECMO (Lancet 2019) DISADVANTAGES - No cardiac support - Reverse gas exchange in lungs possible - Re-circulation effect where drainage cannula sucks out oxygenated blood. Oxygenated blood not actually reaching PA VA ECMO ADVANTAGES - Cardiac support via high pressure, non pulsatile flow into systemic circulation - Can get better systemic PaO2 than VV ECMO - Better flow rates due to return into non-collapsible arterial vessel - If central VA ECMO, good aortic arch PaO2 DISADVANTAGES - Relative lung reduced O2 tension. If recover of heart function, can get pumping of deoxygenated blood from pulmonary circulation into aortic arch --> differential saturation effect (Harlequin syndrome) - Central VA ECMO needs sternotomy - High rates of bleeding (50%) due to femoral access + anticoagulation needed Both ECMO - Highly specialised, requires ECMO team to cannulate and manage patient - Bleeding at cannulation site (most common complications). Need ACT 180-200s (small amount of heparin 50-100U/kg) - Tension PTX, tamponade, tricuspid valve injury with long wires - Air embolism - Systemic thrombosis, VTE risk 10-40%. Circuit thrombosis relatively rare due to systemic anticoagulation and heparin coating tubing - systemic vasodilation due to systemic inflammatory reaction of ECMO
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Risks of IJ central venous access
Anatomical related - Carotid puncture / haematoma / dilation / line insertion / stroke - Bleeding, haematoma. Haemothorax - Pneumothorax - Chylothorax (left IJ) - Vagal nerve injury - Sympathetic chain injury (Horner's) - Thyroid injur - Trachea injury Insertion related - Infection - line associated sepsis - Arrythmia - VAE
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ANZICS (Aus Nz Intensive Care Society) guidelines for maintenance and insertion of CVL
Consider antibiotic or antimicrobial central lines if high rates CLABSI at instituion despite good care, if likely present >7 days. Reviewed daily for signs of infection, ongoing need, patency, catheter position CVLs replaced within 24 hours if not inserted with strict asepsis Re-wiring only recommended in few circumstances (high risk of bleeding, no alternative sites, line in <72 hours and no signs infection). If doing, send tip of old CVL for culture Hand hygeine and wipe lumen with alcohol + chlorhex before accessing Dressings changed every 7 days
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Colour and size for EZ IO cannula
Red = 15mm Blue = 25mm (standard size for most adults) Yellow = 45mm (more for obese adults or if humerus to be used) IO cannula has a proximal line on it at 5mm. When inserting and contact down to bone, need to ensure at least the black line is visible (as needs to go in at least 5mm into bone marrow through cortex)
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Advantages and disadvantages of PICC over CVL
ADV - Less likely PTX, carotid puncture, vagus nerve injury, haemothorax, chylothorax, sympathetic plexus injury - Less CLABSI - often can stay in for 6-8 weeks compared to 1-2 weeks for non-tunneled IJV CVL - Often nurses or anaesthesia assistants trained in insertion, can be done without doctors - time and cost efficient - Can put through same medications include vasopressors, TPN, chemotherapy - Appropriate for outpatients - More comfortable than IJVs and femoral lines. Well tolerated by children DISADV - High thrombosis rates - Not easily inserted in emergencies, easier to insert a CVL - Usually less lumens available - Lumens generally smaller than CVL - less useful for volume resus. Some CVLs have larger bore lumens - Requires US (although US is highly recommended by most due to reduced risk compared to landmark CVL insertion) - CVLs can be wired for sheath insertion / PAC insertion if needed
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Uses for a PAC
Cardiac output monitoring - can be intermittent or continuous. For guiding inotropes, vasopressors Monitoring RA / RV / PA / PCWPs, using to guide treatments Mixed venous blood sampling Core temp monitoring Infusions Common surgeries / conditions: mixed valves + CABG, mixed shock states, RV failure, or large fluid shifts (liver transplant)
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Colour of the different ports on a PAC?
Yellow = distal port. at 0cm (remember this as yellow the whole way along the PAC) Blue = proximal port. at 30cm. Approach RA / CVP lumen. Used for proximal injection of saline White = infusion port. at 31cm (white is the same colour you'd attach standard infusions to on a CVL) Red = balloon. 1.5ml balloon with a lock attached Other connections = thermistor (red and white), continuous cardiac monitoring lines
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Direct and indirect measaurements from a PAC
Direct - Core temp - Cardiac output - SvO2 - RA / RV / PA / PCWP pressures - Mixed venous gas samples Indirect - Stroke volume = CO / HR - SVR = (MAP - CVP) / CO = Ohms law - Cardiac index = CO / BSA - PVR = (mPAP - PCWP) / CO - PAPi = Pulmonary artery pulastility index = (sys PAP - diaPAP) / RA pressure. <1.85 indicates failing RV
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Complications of a PA cath?
On top of usual CVL things: PA rupture - 0.2% but 30-70% are fatal. Use maximum of 1.5ml air in ballon Pulmonary infarction - if balloon left up high risk of bleeding due to sheath being much larger
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Reasons for inaccuracies when injecting saline for CO monitoring in PAC?
- TR - Need to do 3x attempts. All same volume and temp of saline and given at same rate - Intracardial shunts (left to right or right to left, both will affect results) - Malpositioned PAC - not in zone 3 West zone - VV ECMO, VA ECMO - High infusion rates at proximal port
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Evidence for PACs?
PACMAN trial - non blinded, not randomised, prospective study. ICU physcian decided patient should have PAC (n=1000). No mortality benefit or deficit. 10% of PACs had complications, most common was haematoma. Non-cardiac patients Patient selection is likely key - don't put in everyone just those likely to benefit (high risk due to pHTN, RV failure, mixed shock patients) Multiple large observational studies demonstrated survival benefit with a PAC (one USA observational study had 85,000 PACs and n= 930,000). But no RCTs have been done that demonstrate survival benefit
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Basic TEG parameters and normal values (and ROTEM equivalents)
R time = start of test to start of clotting. Normal = 4-8 mins. - Measure of coagulation factors. So prolonged if anticoagulation, lack of clotting factors. Shortened in DIC type 1 - Treat with FFP, beriplex or reversal agent (e.g. protamine) - ROTEM equivalent = CT = Clot Timing K time = time to clot initiation until 20mm amplitude. Normal 1-3mins Alpha angle. In TEG it is angle at end of R time and K time. Normal = 55-78 degrees - Measure of rate of clot formation. Reduced mainly if lack of fibrinogen, to lesser extents anticoagulation and platelets - Treat with cryprecipitate or fibrinogen concentrate - Called the same thing in ROTEM. but it is angle at tangent at end of CT MA = maximum amplitude. Normal 50-69mm - Mainly product of platelet function and fibrinogen. Reduced if platelet dysfunction or thrombocytopenia (but not antiplateelt drugs due to additives) - Treat with platelet transfusion - = MCF = maximum clot firmness in ROTEM Ly30% = decrease in amplitude 30 mins after MA for TEG - Normal 0-8% - ROTEM it is called Li30% (lysis index) but it is measured from CT end to 30 mins after - Treat with TXA
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Different reagents used in TEG?
Rapid TEG = kaolin + tissue factor. Activation of both intrinsic (kaolin) and extrinsic (TF) pathways. Skips the R time part so get results faster hTEG = heparinase + kaolin. Compared to normal TEG to see effects of heparin and whether to give protamine or not FLEV-TEG = functional fibrinogen TEG. Tissue factor + Abciximab. Platelet inhibition, clot only reflects fibrin formation. Compare MA of FLEV-TEG to normal TEG to see contribution of platelets alone TEGPM = platelet mapping. Uses light aggregometry. Will get less aggregation if antiplatelet or thrombocytopenia
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ROTEM different testing performed
INTEM = standard intrinsic pathway activation. Uses ellagic acid. Same as standard TEG EXTEM = extrinsic pathway activation with tissue factor. Faster to activate. Similar to rapid TEG FIBTEM = tissue factor + cytochalasin D (platelet inhibition). Same as FLEV-TEG (functional fibrinogen test). Compare INTEM and FIBTEM to see effects of platelets HEPTEM = heparinase + ellagic acid. Same as hTEG. Compare INTEM and HEPTEM to determine difference in clotting due to heparin (and whether protamine useful) APTEM = aprotinin, tissue factor. Inhibits fibrinolysis (aprotinin is similar to TXA). compare EXTEM and APTEM to detect hyperfibrinolysis within 20 mins. (and whether TXA useful)
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Advantages and limitations of thromboeleastic testing
ADV: - Provides rapid coagulation information, point of care testing. Use in theatre and for guiding transfusion. Most pertient information available in 10 mins - More representative of true in vivo clotting mechanisms rather than more artificial intrinsic and extrinsic pathways - Parameters allow for guidelines for aiding interpretation. Guiding products to be given to treat coagulopathy - Provide patient with more targetted transfusion. 2017 meta-analysis found reduced RBCs, platelets and FFP. Mainly in cardiac surgery. Also a reduction in mortality (although low quality evidence for this). 5x decrease in platelet transfusion, less RBCs in liver transplant + 7 day mortality improved (but no overall mortality benefit in long term) DISADV: - Test done at 37c, does not account for hypothermia coagulopathy - calcium also added. So wont see effects of hypocalcaemia or citrate - Still takes 20-30 mins for some parameters. May be significantly changed since the test was run - Requires training to run - Expensive to purchase machine and cartridges - Requires expertise to interpret without a local guideline. May need haematologist or transfusion-experienced anaesthetist if unsure - No endothelial wall present so won't detect effects from VWB factor deficits - Antiplatelet effects are overcome by activation of phospholipase C pathway (overcoming ADP and COX1 pathway inhibition)
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Considerations for antibiotic prophylaxis
Giving an antibiotic to patient without infection to reduce risk of post-op infections. Should be part of WHO time out and discussed at team brief beginning of day - surgical type. ?Clean vs contaminated. ?prosthesis to be inserted - Commensual bacteria to be covered - Drug resistant organisms e.g. MRSA. Local guideline should be developed. Screening for MRSA / VRE - Narrow spectrum as possible to reduce c diff - Allergy status, cross reactivity - Bleeding - may need redosing - Renal function (e.g if eGFR <30ml/hr then push out cephaz to 6 hourly dosing) - timing - before KTS. If long infusion needed (vanc) should be completed before knife to skin - comorbidities - if higher risk for infection (poor control diabetics, mechanical heart valves, immunosupressed) --> more likely to give
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Gustilo-Anderson classification for open fractures
Grade 1 = open fracture with wound <1cm, not contaminated. - Give cefazolin Grade 2 = wound 1-10cm, without contamination or vascular injury - add gram negative cover. Augment or gent Grade 3 = wound >10cm, contamination in wound, complex comminuted fracture. - Add gram negative and anaerobic cover. Cefazolin, gentamicin and metronidazole
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Risk factors for infective endocarditis When to give prophylaxis?
-HOCM - Valve replacements - Acquired valve disease (stenosis, regurgitation, rheumatic heart disease) - Previous IE - Structural heart disease (except simple ASD, VSD) European society of cardiology and American Heart Association suggest only high risk patients should get IE prophylaxis - If contaminated / infected surgery + high risk for IE, give antibiotic coverage for infected surgery + IE coverage (ideally in same drug e.g. Augmentin) - If risk of IE and for dental surgery - discuss with patient. Most likely will give antibiotics. Strep viridins most common bacteria. Give 2g amoxicillin IV (or 600mg clindamycin if beta lactam allergy) NICE guidelines suggest only prophylaxis in those high risk getting GI, GU surgery with suspected infection.
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DREAMS trial for dexamethasone?
RCT for open and laparoscopic bowel surgery. Decreased PONV for 72 hours, early feeding and no increased risk of SSI (or any other complications)
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PADDI trial for dexamethasone
= non inferiority RCT for non-cardiac surgery in n=8000 patients, surgery >2 hours - 13% patients were diabetics. No increased risks of SSI, anastamotic leak. Transient increase in BGLs (on average 1.3mmol/L). Not other complications - improved post op fatigue, faster time to discharge, improved recovery scores
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Surgeries which dexamethasone has evidence for analgesia in?
Airway Tonsillectomy Spine Knees and hip arthroplasty Tonsillectomy
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When to dose reduce paracetamol?
Age - under 1 month IV dosing reduced to 7.5-10mg/kg up to 4x per day. Under 28 weeks, should be avoided - weight adjusted in children (15mg/kg up to 4 times per day) Low body weight in adults - if under 50kg --> max 3g / day Hepatic dysfunction (e.g. cirrhosis with raised bilirubin) - 2g / day. Avoid if fulminant liver failure Anorexia, cachexia, malnutrition - consider 3g/ day (reduced glutathione stores) Alcohol excess - consider 3g/day maximum. Induction of CYP2E1 --> increased production of NAPQI Paracetamol toxicity / overdose - avoided
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Paracetamol toxicity mechanism
Paracetamol predominately cleared by phase 2 metabolism - 70% glucuronidation, 20% sulfation, 1% into AM404. Non toxic metabolites - 10% cleared by phase 1 CYP2E1 into NAPQI = hepatocellular toxic. Usually rapidly cleared by conjugation with glutathione - If paracetamol excess --> shunting of more paracetamol into phase 1 metabolism so more NAPQI production + overwhelming of glutathione stores --> hepatocellular toxicity - NAPQI hepatotoxic by formation of ROS and oxidative stress on liver proteins. Causes centrilobular necrosis - 10% will get acute tubular necrosis of kidneys too
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Management of paracetamol toxicity
- Stop paracetamol delivery - ABCs, resus as required - consideration to be given to other drugs that may have been taken simultaneously if intention OD (TCAs, SSRIs common) - attempt history including timing of OD, dose amount, concurrent drugs / alcohol, SR formulation? - Activated charcoal if within 2 hours - may be role of gastroscopy if bezor suspected (hundred of pills taken) - Bloods including VBG, LFTs, renal function, coags - Rumack-Mathews nomogram. timing of OD and plasma paracetamol level - treat with NAC if above line at 4 hours post ingestion (NAC hydrolysed to cysteine, precursor aminoacid to glutathione --> promotes NAPQI clearance) - Discussion with liver transplant service early - use modified King's College Criteria. If any of the following: Acidiosis (pH <7.3), encephalopathy, lactate >3 after fluid resus, Cr >300uMol/L, INR >6 - O'grady classification. Acidaemia, AKI, encephalopathy or INR >6 = poor prognosis - Psych review - ICU admission possibly
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Main differences between Schnider and Eleveld TCI models
Development - Schnider based on 24 patients, age 25-81 years old, published in 2003 - Eleveld based on pooled data from 30 PK studies and 5 PD studies, >1000 patients. Ages 0.5 - 88 with weights 0.68kg-166kg. >15,000 blood samples. Modelling - Schnider - uses height, sex, weight and age as inputs. Uses James equation for lean body mass (inaccurate over BMI 40). 11 variables in model. Fixed central volume of 4.27L means loading dose generally small. Clearance is age adjusted (unlike Marsh) - eleveld - uses height, sex, weight, age and whether opioids in use. Uses allometric scaling for clearance calculation, based on weight (allometry = non-linear scaling). Uses 18 parameters for calculation. All rate constants and volumes are adjusted to weight Advantages - Schnider. Smaller bolus dose with same selected target concentration as Eleveld --> may be better for more haemodynamically stable inductions where less concern about rapid onset. Existed for >20 years, more familiar for many anaesthetists + more comfortable if handing over. - Eleveld. Paediatrics. Extremes of body weight, more validated data for these groups. Larger bolus dose --> more rapid onset, may be useful for LMA insertion where generally need larger bolus for insertion. Could be used as part of modified rapid sequence (infuse rate 1200ml/hr so maximum rate is 20ml/min) for handsfree induction. Maintenance rate generally reduced for Eleveld (could theoretically increase awareness but also increases speed to wake up especially for longer cases) Disadvantages - Schnider - smaller bolus for induction can increase time taken for LOC. Can be overcome by increasing target concentration (but risk not turning down after induction --> hypotension). Paediatrics. Extremes of body weight (low body weight and obesity). Higher maintenance rates may mean needing to downtitrate cet for longer cases - Eleveld - larger bolus dose - higher chance of haemodynamic instability with induction (but can see what the pre-programmed dose of propofol for induction will be and adjust target cet if concerned) - Both. Neither has been validated in acutely unwell patients
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Options for paeds TIVA
Eleveld - From 6 months and older. Weight from 700g - Can target effect site or plasma conc Paedsfuser - Ages 1-16. Weight 5-61kg - Only plasma conc target Kataria - Ages 3 or older. Weight 15-61kg - Also only plasma con target McFarlan model - Induction 2.5mg/kg - 15mg/kg/hr for 15 mins - then each 15 mins decrease by 2mg/kg/hour until 10mg/kg/hr and keep at this for maintenance
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How to do a spont breathing gas induction --> TIVA anaesthetic for an open airway procedure in a child
-Gas them off as usual, secure IV access. Monitoring on if not able to do beforehand -Volatile off - HFNP on, 2L/kg/min flow. 100% O2 - Propofol TCI on first. Start 1mcg/ml cet, increase to 3mcg/ml in small increments. Keep spont breathing - Then remi TCI. Start 1ng/ml and up titrate to 2ng/ml or RR of 10 (somewhere around 0.1-0.2mcg/kg/min - Laryngoscopy --> LA to cords - Surgeon to start
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Quality assurance and quality improvement things to know
PG58 = QA / QI professional document QA = organised process that assess and evaluates services to ensure maintenance of desired level of safety and quality QI = iterative process to continuously improve quality and safety Triple aims of QA - Imrpoved efficiency with current resources - Improved quality, safety and health outcomes for individuals - Improved health and equity for populations Quality management cycle: - Planning (design of project. Methods for data collection. Question to be answered) - Implementation (collection of data and analysis. Implement changes) - Review (monitoring any changes made and impact of changes) - Setting standards (write standards into guidelines) SQUIRE 2.0 = Standard for Quality Improvements Reporting Excellence = way to do QA project
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Ethics approval and informed consent for new research
Ethics approval required for any studies involving humans - Most institutions will have HREC = Human research ethics commitee - Need to create research proposal, risks and benefits to participants, benefits to wider society, declare COIs. Written application. - Need to demonstrate data collection and storage, safety concerns - Reporting of any adverse effects should go to HREC during study Informed consent for any research - Whether treatment or possibility of placebo. If placebo, will they get access to treatment after study? - risks of harms / benefits - Data collection, storage, confidentiality
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Definitions for standard deviation, standard error
Standard deviation = measure of distribution of data around its mean. Requires normally distributed data - 1SD = 68% of data within the mean. 1.967 SD = 95% of data - Larger the SD, more widely distributed the data is from the mean Standard error = SD / square root(n) - Standard deviation of the sampling distribution. Sampling distribution is the mean generated from repeat sampling from the same population - Used for confidence intervals usually. CI = +/- 1.96 SE
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Definition of error, bias, power, type 1 and type 2 error
Error = any factor that causes a difference in an observed value and the true value. - Combination of imprecision (random error, variability due to chance) and bias (systematic error due to flaw in study design Type 1 errors (alpha errors) = incorrectly rejecting the null hypothesis. Saying there is a difference when there isn't. Type 2 errors (beta errors) = incorrectly accepting the null hypothesis. Saying there isn't a difference but there truly is. Where p >0.05 but there is actually a true difference between groups Reducing error requires a small enough p value (0.05 or less usually) and large enough sample size to account for variation Power = likelihood of detecting a difference if it exists. Should do power calculation before commencing study. Power = (1-beta) x 100%, where beta = probability of type 2 error
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Types of bias
Selection bias (where selected population no representative) - recruitment bias (lots of exclusion criteria) - attrition bias (people of certain characteristic drop op) Information bias (errors in data collection) - Misclassification bias (classifying someone as non-smoker based on electronic record) - Recall bias (when interviewing patient - difficulty with recall) - Interview bias (interviewer asking differently based on control or not. Reduce with blinding) Diagnostic bias (treating patient differently if know they're on treatment) Performance bias (patient behaving differently as think they're getting treatment) Publication bias
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Ways to minimise study bias
Minimise exclusion criteria (reduce attrition bias) Randomisation (reduce selection bias, confounding) Double blinding (reduces interviewer bias (interviewing patient differently based on if they had treatment or not), diagnostic bias (different treatment based on control or not), performance bias (effects of placebo, nocebo) Intention to treat analysis - all those randomised are included in analysis, even if drop op. Reduces attrition bias Publish research despite negative or positive findings - reduce publication bias Peer review - scrutiny of research methods, likelihood of bias Discussion of study limitations - self reflection. Further research
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Steps for performing a systematic review and meta analysis
Systematic review and meta-analysis completed using PRISMA methodology = preferred reporting items for systematic reviews and meta analysis. Usually displayed in flow diagram format Systematic review = thorough, comprehensive, explicit method of interrogating medical literature. Involves: - Asking an answerable question - Identifying and using databases of medical publications - Selecting titles / abstracts / papers based on inclusion / exclusion criteria - Abstracting data into standardised form Once systematic review done, can then do meta analysis = quantitative formal study design using multiple studies to systematically dervice conclusions. Data typically displayed in forest plot. ADV - More precise estimate of effect of a treatment or disease. May be able to find differences even if conflicting studies. Reduces imprecision by effectively increasing sample population - Cheaper and less resources than doing a whole study with the same population size - Herterogeniety between studies may be a good thing for generalisability DISAD - Requires high quality systematic review - not including or excluding appropriate papers. follow PRISMA methodology and publish this with peer review of the study - Risk of publication bias (only positive studies being published) - can use funnel plot to demonstrate this effect - A well conducted RCT of the same population would likely be superior - Variability and heterogeniety within the different studies included could diminish an effect
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Definition of human factors Causes for human error
Human factors = any factors related to interaction with humans, acknowledgement of fallability of humans and non-technical skills that can lead to potential adverse events Causes: fatigue, stress, task overload, poor interpersonal communication, flawed decision making, biases, lack of leadership In NAP4 for airways, 70% of events were identified where they had human factors contribute Reason paper form 1990 - Swiss cheese model. Lining up of both active and latent factors --> adverse event
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ANTS framework for non-technical skills
Anaesthetist Non Technical Skills = ANTS STTD Situational awareness - absorbing and processing of information, anticipation of next steps Team work - communication style (closed loop), leadership, flat hierachy, shared mental model Task management - preparing, prioritising and utilising resources Decision making - weighing up options, risks and benefits, visual and cognitive aids
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Process of root cause analysis
RCA = structured analysis of system errors focusing on basis for why an adverse event or near miss may have occurred. Focusing on both latent and active errors (swiss cheese model). Goal is not for punative purposes. Aim to answer: What happened? Why did it happen? How can be prevent it happening again? Flow diagram developed from incident report. Sequence of events leading to adverse event - each event is then broken down into who, what, where, when, why and how questions to be further investigated Serious adverse event team then each further question by reviewing medical records, equipment and interviewing staff and patients - When interviewing, make sure psychosocial support for person and reassure not for punative purposes Cause and effect flow chart then developed. "5 whys" to determine root cause for each contribution to adverse event - Should focus on systems and processes factors, rather than individuals - decide on area of review to implement improvement Complete findings report. Summary, key findings. Submit to CMO - Can then let family know of findings and areas identified for improvement. CMO in charge of implementing review, further investigations or recommendations for implementation Formulate action plan
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CREATE acronym for creating guidelines or procuring equipment
Clinical problem identified Review of literature - cost benefit. Also standards from regulatory bodies Expert group convening - all stake holders Approval through governence - submit business proposal to HoD Training and implementation - training / education. Pilot roll out. Final roll out Evaluation - patient safety, Q+A
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Four phases of clinical drug development
Phase 1 - 20 or so healthy individuals usually. Find major adverse reactions. Safety. Tolerability. Pharmacokinetics Phase 2 - efficacy in humans and dose finding. Usually 100s of people with condition. Proof drug works in humans + find dose to treat Phase 3 - 1000s, confirm drug efficacy. find less common adverse events. Randomised, double blind studies here Phase 4 - post marketing surveillence. 10,000s. Large scale, observational data. Real world efficacy
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Legality of consent process
In Australia, consent is establish in common law In NZ, it is detailed in the Health and Disability Services Consumers Rights (the code). Informed consent is a legal requirement for any medical treatment Also laid out in PS26 = ANZCAs professional statement on informed consent Three main elements are: 1) informed 2) capacity to make decision and 3) must be voluntary. (4th = documentation)
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What to do if suspect colleauge to be impaired from opioids?
PG48 = ANZCA document on the matter Substance use disorder = chronic disease of brain, mediated by reward centres leading to compulsive substance use and self control. Not a loss of morality Priorities are: - Protection of patient - Protection of the staff member - high risk for suicide (if found to be using drugs on site --> emergency. Need to ensure safety ++. Get security. Person must not leave hospital. Need urgent intervention) - Initial reporting - must be done in confidential manner, avoid rumour or gossip. Can be reported by anyone. If you suspect a colleague is impaired and you do nothing - you are complicit - Investigation - must be thorough, prompt. Remove any doubt. Must be done by small team, done in confidential manner - Prepare for intervention- appropriate setting, time, people. Evidence compiled. Have trusted support person with staff member until meeting - Intervention - lay out evidence. Wait for rebuttal. Expect denial. Have treatment option organised (rehab) - Reassure staff member that they will be supported, many people can return to work once treatment done - Mandatory reporting - ANZCA, medical council - Follow up with supports - Return to work scheme- laid out in ANZCA PG48. May have conditions by medical council (e.g. drug testing). Initially 1:1 supervision for 6 months then stepdown to 1:2. Start with 2 days per week at a single facility. Tea breaks with supervisor. No bags in theatre. toilet breaks in main area. Limited security access
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Signs of substance misuse in a colleague
Direct evidence - seeing person directly injecting substance through a needle or cannula into body Everything else is circumstantial (but some have more weighting than others) Major - Obvious impairment, toxication or bizarre behaviour at work - IV track marks - Syringes, pills, vials on person, locker, at home or in car - Obvious discrepancies in signing out controlled drugs - Inconsistent record keeping - Tremors / withdrawal symptoms - Consistent pattern of patients being in severe pain, despite recorded high doses of opioids given intraop Circumstantial - Volunteering for more on call - Using more sick leave - Social withdrawal - Long sleeve clothing (in summer) - Moving hospitals frequently - Being at work when not on duty - Blood spots on clothing - Making more accidents or mistakes than the average anaesthetist - Deterioration of personal relationships / nutrition / personal hygeine - Mood swings - Loss of libido
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Causes of stress specific to anaesthetists Headings for how to mitigate stress
PG 43 = professional document on stress / fatigue management Causes - Critical incidents, mistakes at work, death in theatre - Long hours, on call, nights - Isolation from colleagues - Complaints, legal proceedings - Exams - Approaching retirement - Job applications Headings: - Work - Home - Health
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Effects of fatigue on clinical practice
PG 43 = ANZCA document on fatigue management Being awake 17 hours = 0.05% blood alcohol. 24 hours = 0.1% 4am is the wosrt time of the day for fatigue Technical skills - more errors, mistakes, longer time to perform tasks, worse fine motor skills Cognition - less able rationalise, reason, make complex decisions (which are often needed in anaesthesia) Alertness - diminished Empathy - gone Non-technical skills - impaired communication, team work, ability to lead How to reduce effects: - Personal level Planning - organise life so less likely to have fatigue Awareness - of signs of fatigue or in colleauges Risk mitigation - 60-90 min naps before nights. 15-30 min nap during night shift, eating proper meals, sleeping as soon as shift finishes, avoid caffiene, controlled exposure to lights (especially blue light) - Long term risk mitigation Diet, exercise Annual leave Breaks at work - Hospital level risk mitigation Area for sleep Only life or limb after 10pm Maximum hours in a shift Cover for anaesthetists Forward rotating shifts Safe commuting options
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Definitions of asepsis, disinfection and sterilisation
Asepsis = prevention of contamination of a body surface with pathogens Disinfection = thermal or chemical means to destroy micro organisms / pathogens Sterilisation = destruction of micro organisms / pathogens including spores
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Risk of blood borne virus transmission with needlestick if patient carrier
HIV - 0.3% HBV 1-5% if surface antigen +ve, 20-30% if HVeAg +ve HCV - 10%
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Advantages and disadvantages of povidone iodine 10%
Advantages - Broad spectrum - covers bacterial, viruses, fungi and spores. Works by oxidising microorganism proteins, lipids of cell membranes. Povidine = carrier molecule, has 1% free iodine - Not toxic to cornea - used in eye proceedures - Less neurotoxic than chlorhex - Non flammable Disadvantages - Inferior to chlorhex + alcohol in studies on CVLs. More colonisation of epidural catheters with bacteria too - Takes 2-3 mins to start working, slow onset - Doesn't linger around as long as chlorhex - active 4 hours or so - hypersensitivity - although anaphylaxis is rare compared to chlorhex - Stains everything
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Advantages and disadvantages of 70% isopropyl alcohol + chlorhexidine
Advantages - Broad spectrum microbial cover - although not sporacidal. Chlorhex +ve charge, disrupts -ve charged cell wall. Alcohol causes denaturation of proteins and damages cell walls too. - Faster onset than iodine - within seconds - due to alcohol - Superior for CVLs, epidurals compared to iodine. Recommended by ANZCA and ASRA - High affinity for stratum corneum - binds here to provide antimicrobial cover for up to 24 hours DISAD: - Flammable - need to wait to dry before ignition source - Not sporicidal - Neurotoxic (use 0.5% chlorhex for neuraxial / regional and wait til dry) - Corneal toxicity, ototoxicity - hypersensitivity - emerging increasing rates of anaphylaxis (10% of anaphylaxis in NAP6)
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Sip til send
ANZCA statement in PG07 appendix 1 - fasting guidelines: - Emerging practice with no current evidence to suggest increased risk of aspiration. May be useful to prevent prolonged fasting Improved fluid intake and reduced fasting times prior to anaesthesia - which tend to well exceed recommended fasting times (ANZCA PG07 specifically states prolonged fasting in children should be avoided). Some centres without STS, mean fasting time >7 hours - Less haemodynamic instability, less PONV, more compliant children STS relatively simple - clear cut when patient's can and can't drink More than 50 centres in Aus / NZ have adopted STS MARS study = current in progress study, 250,000 patients aim. Comparing aspiration risk Studies thus far have not demonstrated increased pulmonary aspiration risk. EUROFAST study (=prospective, multi centre, paediatrics. n=300,000) included 35,000 patients with STS (rates of 1.18:10,000) --> no statistical difference between groups for regurg, admission to ICU Clear fluids may promote increased gastric emptying Also, if clear fluids - may be at less risk if regurg occurs. More likely to dilute gastric juices --> higher pH --> less likely chemical pneumonitis
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Benefits of breastfeeding
Infant - Better immunity - IgA - Less NEC - Less adult diabetes - Better hydration - Less asthma - Bonding with mother Maternal - Bonding with child - Less postnatal depression - Less mastitis - Might reduce breast Ca, ovarian Ca
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Benefits and timing for quitting smoking
Day 1 - improved COHb levels, reduced sympathetic stimulating from nicotine. May have better tissue O2 delivery 3 weeks - improved wound healing demonstrated 4 weeks - statistically significant improvement in surgical outcomes - morbidity, mortality 6-8 weeks - improved lung function testing, reduced sputum production 6 months - improved immune function, back close to baseline 10-15 years - return to baseline CVS / stroke risk Annual smoking quitting rates about 2%. But higher for people around surgery - unique opportunity to quit
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AAAA model for smoking cessation
Ask, Advise, Assist, Arrange Ask about it Advise using motivational interviewing Assist - provide NRT, non-pharm measures Arrange follow up, quit services
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Pharmacological measures for quitting smoking And other things
NRT - patches, lozenges, gum, vaping. Most evidence for NRT for quitting success Nortriptyline - may be as effective or more effective than NRT clonidine Varenicline (champix) = partial nicotine agonist. Bad for depression Bupoprion (=dopamine and NA reuptake inhibitor). Good for depression. But seizures 1:1000 Quitlines - increase quitting changes by 25-50% over 12 month period Smoking cessation more common perioperatively - unique opportunity for cessation: ask, advise, assist, arrange
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Requriements for day stay surgery
Outlined in PG15 = ANZCA document on day stay surgery Patient factors - ASA 1 or 2s. Or medically stably 3s and 4s - Comorbidities optimised, stable - GCS 15, able to manage post op cares at home - Adult at home with them that is sensible + able to drive - If paeds, needs to be over 46 weeks post last menstrual dates (if term) or 54 weeks (if pre term) (risk of apnoea) - If paeds, need 2 adults for car ride home. 1 to drive, 1 to monitor child - Pain manageable with oral medications, eating and drinking, mobilising - Access to phone, transport and not too far from medical assistance - OSA screening + optimised + other comorbidities optimised - SAMBA guidelines Surgical factors - Airway surgery, airway bleeding less likely to be appropriate - Surgery with high chances of ileus, pain, post op nausea, bleeding - If uncertain, can place first on list and see how they respond in PACU Anaesthesia factors - GA vs sedation vs neuraxial vs regional all appropriate - consider prilocaine if neuraxial --> less urinary retention - Analgesia, PONV prophylaxis - Multi modal analgesia to reduce opioids --> less nausea, constipation, urinary retention, better analgesia - Monitor in PACU - if concerns, admission
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SAMBA guidelines for OSA and day stay surgery
SAMBA = Society for AMBulatory Anaesthesia = USA based Decision pathway based on if diagnosis of OSA or suspected. Then how well OSA is managed + other comorbidities. Also relevant are anaesthesia and surgical factors (e.g. analgesia requirements) Confirmed OSA diagnosis - Appropriate for day stay surgery if compliant on CPAP, can use CPAP at home (not airway surgery), minimal opioids during surgery / in PACU, comorbidities are well controlled, won't require opioids at home - Also dependent on surgical complications, and recovery in PACU - if apnoeas here --> admit Suspected OSA but no formal diagnosis (e.g. STOPBANG 5 or more) - Similar criteria to above - minimal opioids intraop, comorbidities well controlled, uneventful stay in PACU, no opioids required for discharge. May be suitable - If doesn't meet above criteria, not suitable. E.g. comorbidities not well controlled, apnoeas in PACU. May benefit from referral to resp for sleep study. Regional and neuraxial anaesthesia are good options for these patients
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Minimum monitoring requirements for ANY anaesthetic (GA, regional or sedation)
As per PG 18 Ventilation - must be continuously measured. Direct or indirectly Oxygenation - oximeter. And need to be able to assess colour Circulation - BP and HR. Minimum BP checks are Q10mins. BP could be A line or NIBP. Hr could be ECG or pulse oxi ECGs are mandatory if GA or major regional O2 analysis mandatory for any patient with breathing circuit attached Vent alarm if vent used Capnography if GA. Needs to be available for sedation Volatile analyser - if GA Temp monitoring - available if GA. Should be core. Monitoring if using warming devices Other: PNS, EEG, CO monitoring, TOE, cerebral oximetry
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Summary of PG40 - Healthcare industry relationships
Any association should be with wider community benefit as the primary goal Open declaration of any benefits - material or financial - should be made (conflicts of interest) For educational meetings - agenda should be under primary control of meeting organising committee. Industry involvement should be minor - No meeting or single session under primary industry control - Promotional materials should be labelled - Any industry involvement must be declared - More scrutiny will be applied to fellows and trainees if attending meeting with single industry company - Fellows and trainees are not ANZCA representatives and cannot speak for ANZCAs position without permission - Funding / flights / accommodation must be stated for any presentation For research: - Contract written up with 3rd party for funding (univerity, hospital) - Investigator must be able to publish research no matter findings - Usual ethics, consent processes - If prize, must be selected by an independent board If any concerns, circumstances, advice from ANZCA CEO or delegate
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Return to practice guideline
PG50 = ANZCA document on this Relevant to SMOs only, not trainees. Recommended if > 1 year from clinical practice (may be due to extended parental leave, rehab, return from retirement, illness) - If absence due to regulatory enforcement, ANZCA might have to endorse a return to work policy. But regulator has final say for registration - May need written confirmation from treating doctor that person can return to work Should be individualised - starting point is 4 weeks (1 month) per year of absence - Stage 1: before starting clinical practice need to do ACLS, CICO if not within 3 years. also CPD plan. And sort out work conditions (hours, on call, specialties to cover, trainee supervision) - Stage 2: 1:1 supervision. Duration depends on situation. Structured assessment with peer review - Stage 3: beyond 1:1 supervision, discussion of cases with peer support. Practice evaluation. CPD. Log book - Stage 4: Once satisfactory return to work, superviser will submit form to ANZCA
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Minimum dantrolene requirements in a facility?
As per PG55 = minimum requirements for safe facilitites. Based on MHANZ - 9 vials (180mg) within 5 minutes of any location that may use sux or volatile anaesthesia - Addition 180mg should be available Q15 minutely up to 720mg (=36 vials) at 50 minutes
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Definitions of culture, cultural safety and cultural competence
Culture = (as defined by UNESCO), whole complex of distinct spiritual, material, intellectual and emotional features of a societal group. Includes values, beliefs, traditions, fundamental rights and modes of life - May include cultures within ethnicities, but also LGBTQIA+, migrants, refugees Cultural competance (as defined by MCNZ) - awareness of cultural diversity, ability to function effectively and respectfully working with and treating those with different cultural backgrounds - set of behaviours, attitudes, polices that allow professionals / agencies / organisations to work effectively in cross cultural situations Cultural safety (also from MCNZ) - extensiof of cultural competence. Self reflection and insight into inherent power differentials between provider and patietns - Definied through perspective of patient's experience - Acknowledgement of own biases, attitudes, assumptions, prejudices - Cultural safety in healthcare includes diverse workforce
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Principles underpinning cultural competence and safety
PS 62 = ANZCA document on cultural safety / competence Respect and understanding - acknowledging beliefs and values and how this might influence health - Doctors responsibility to explore these - Doctors recommended to seek out professional development Culturally tailored communication - ensure interpreter. May want cukturally appropriate advocate - Use of pronouns Patient centred practice - do not make assumptions based on cultural group - Patient autonomy is key - Trauma informed care = recognition of prior trauma and prevention re-traumatisation e.g. in marginalised groups Partnership - Good working relationships between health system and culture - Diversity in health care work force
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Summary of PG 64 = environmental sustainability
Sustainability = reduce impact of healthcare on both environment, as well as economically ANZCA states commitment to lowering impact of health system in climate change - Health system accounts for approx 5-7% of national carbon emmissions Climate change will also worsen health for future generations, particularly affecting those from migrant or lower socioeconomic status - Aim to reduce waste, less air pollution Sustainability also associated with reduced costs financially Options include: - TIVA. Or low flows + no N2O / des if volatile - Reusable equipment. Cradle to grave analysis - Reducing flights - Recycling - Hospital guidelines, policies - Reducing energy costs - Research - Advocacy
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Most common tooth to injure during anaesthesia?
Left, maxilliary central incisor (top, front, left tooth)
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Risk factors for eye injury under anaesthesia
Relatively rare for complete vision loss, 1:120,000. But 1:1000 for cardiac surgery. 96% of cases are prone cases >6 hours Surgical - Prone position, particularly spine surgery - Cardiac surgery - High blood loss - Prolonged surgery. >6 hours - Surgery to head and neck Patient factors - Pre existing diabetes - Elderly (or any age >50) - Obesity - Smokers - Polycythaemia - Smokers - HTN
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Types of eye injury under anaesthesia
Corneal abrasion - most common form of eye injury (50%) under GA. Direct trauma to cornea - Prevent with eye tapes (not lube). Decompress stomach with NG if prolonged trendelenburg position - Most heal without intervention. Diagnosis with fluoroscein Central retinal artery occlusion (CRAO) - Most commonly unilateral, painless. Either from direct pressure on eye (causing ischaemia due to lack of perfusion through retinal artery) or from embolic phenomena - Embolic CRAO most common post cardiac surgery - Cherry red spot on fundoscopy + pale retina - Main prevention is avoiding eye pressure and checking eyes frequently - Treatment includes vasodilators, potentially steroids or thrombolysis. Prognosis generally poor Ischaemic optic neuropathy (ION) - Most common form of eye injury under GA causing visual loss. commonly bilateral and presenting 1-2 days post op. Afferent pupil defect, non-reactive pupils - due to raised IOP, reduced perfusion pression or high CVP (Starling resistor) - Posterior ION most common. Associated with spine surgery. Optic discs normal initially. Then get optic atrophy over weeks to months. Ischaemia posterior to optic disc, supplied by pial vessels - Anterior ION more common after cardiac and more commonly embolic in nature. Optic disc haemorrhages with onset of symptoms. Ischaemia to anterior optic disc which is supplied by ciliary arteries - Prevent by avoiding pressure on eyes, defending MAP and avoiding high CVP - Prognosis generally poor. AION better than PION. May treat with steroids, acetazolamide Stroke (as cause for visual loss but not really an eye injury)
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Mechanisms for nerve injury under anaesthesia?
- Direct trauma - may be surgical, or related to regional anaesthesia. Stretch. Transection - Compression (e.g. tourniquet) - Ischaemia - tourniquet, hypoxia, hypotension - Neurotoxic substances (chlorhexidine)
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Common nerve injuries following positioning
Risk factors: - Patient: elderly, obese, low BMI, diabetes, pre-existing neurology, risks for compartment syndrome, alcohol excess - Surgical: tourniquet, prolonged surgery, lithotomy, surgery near nerve - Anaesthesia: nerve blocks, intraop hypotension, NIBP, GA with paralysis Most common are: ulnar (.3-0.5% of anaesthetics), common peroneal and brachial plexus Ulnar (C8, T1). - Avoid by avoiding extension of elbow if pronated, elbow flexion <90 degrees, no NIBP over cubital tunnel, padding cubital tunnel, avoiding hypotension - 50% heal by self, 50% will persist at 2 years - Sensory = 5th digit and 4th digit medial aspect + ventral palm - Motor: adductor pollicus (Froments sign - hold paper between thumb and index finger with thumb straight. Pull on paper. If +ve, thumb will bend = ulnar injury), flexor carpi ulnaris, hypothenar muscles, interossei muscles (abduction and adduction of fingers) - If doing nerve conduction, test the other ulnar nerve too Common peroneal (L4-S2). From sciatic nerve. runs into lateral compartment of lower leg then splits into deep and superficial branches - 1:5000 GAs in lithotomy. Legs in stirrups put pressure on head of fibula - motor - foot drop (tib ant weakness from deep peroneal nerve), foot eversion weakness (peroneal longus / brevis in lateral compartment = superficial peroneal nerve). - Sensory - parasthesia of lateral lower leg and dorsum of foot - Avoid by reducing pressure on fibula. If >3 hours surgery, have 15 mins break from legs up Brachial plexus - Risk = 1:2000. Shoulder abduction >90 degrees, head rotation or lateral neck flexion away from brachial plexus - Inferior trunk most at risk from shoulder abduction or head rotation - Superior and middle trunks more at risk from external compression on shoulder (shoulder braces in trendelnburg) For all, reassurance to patient - most heal by self Referral neuro. for nerve conduction studies, MRI Neuropathic analgesia if pain / parasthesia an issue
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Prolonged operation considerations
Airway - ETT. Check cuff pressures. Avoid N2O. - consdier changing to LMA end of case - No bite block til end Breathing - Lung protective ventilation, PEEP - avoid atelectasis - Intermittent recruitment manouvers - Lowest FiO2 possible - HME filter + circle - humidification + warming. Low flows Circulation - MAP for kidney, other vital organ perfusion - consider arterial line - NIBP only as required - SCDs, TEDs - May have higher bleeding risk - ensure large bore cannula, group + screen - consider CVL for reliable access for long duration (especially if poor access to arms during case, or running TIVA). Or at least 2x IV - fluid balance - euvolaemia. Goal directed via PPV. Urine output >0.5ml/kg/hour Disability - Consider EEG, avoid excessive depth of anaesthesia - only reparalyse if needed - Use short acting agents. consider volatile --> finish on TIVA. Or remi + propofol (facilitate faster wake up) - analgesia will also need to cover aches / pains from long time in position Exposure - Warming, monitor temp. Normothermia - Padding all pressure points, eyes, nerve injury prone areas. c spine neural. Move sats probe around to different fingers. Check Q1hrly all pressure points - Moving limbs during case - IDC Other - Antibiotic prophylaxis - re dosing Staff - Breaks, handover Post op - Monitor for nerve injury, eye injury - VTE prophylaxis. aim to mobilise ASAP - ? destination. Rarely surgery may go into another day (and patient kept intubated into ICU)
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Respiratory and CVS effects of prone positioning
Resp - May have better V/Q matching in prone compared to supine. Due to less gravitational variation in ventilation and perfusion. Less compression of the dorsum of the lungs by the heart / mediastinum --> more 1:1 V/Q --> may improve oxygenation - Prone positioning shown to be effective in those with moderate - severe ARDS - Can have worse ventilation if chest wall compression or abdomen compression. Need abdomen free and not excessive chest wall pressure so lungs can freely expand - risk of airway dislodgement and secretions loosening tape - consider tying tube and glyco for secretions. CVS - Aortocaval compression from abdomen comrpession possible. Especially with obesity. Ensure abdomen free. Have plan to flip supine if loss of cardiac output or MAP drop
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Pneumoperitoneum insufflation rates and pressures
Initially CO2 at 4-6l/min to achieve 10-20mmHg. Then maintenance with 200-400ml/min. - Often start at 15mmHg to get ports in. Then down to 12mmHg
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FASTHUGS BID
Feeding Analgesia Sedation Thromboprophylaxis Head up Ulcer prophylaxis Glucose Spontaneous ventilation Bowel care Indwelling lines / catheters De-escalation
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Advantages and disadvantages of enteral vs parenteral feeding in ICU?
Enteral ADV - Lower cost - More simple - Less infective complications compared to TPN - Provision of food to gut associated lymphatic tissue (GALT) provides mucosal immunity. Not achieved in TPN DISADV - Aspiration risk - give PPI + prokinetic - Over feeding, gastric distention --> may worsen ventilation - NG tubes can cause harm (e.g. epistaxis, base of skull fractures) Parenteral ADV - does not rely on intact gut. Ileus - ICU patients often have CVLs anyway, not an added risk DISADV - More complex to start, requires dietician - Infection risks with CVL - Pancreatitis from lipid load - Refeeding syndrome - could be given through peripheral line but generally only up to 50% metabolic requirements
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Feeding calculations in ICU
There are >200 formulae for determining parenteral and enteral nutrition. British association for parenteral / enteral nutrition recommendations: - Determine BMR using Schofield equations - Adjust for stress (+10% for long bone fracture, +25-50% if multi trauma or sepsis) - Add activity + diet induced thermogenesis factor (+25% if mobilising) Get dietician to do this
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RASS in ICU?
Richmond Agitation Sedation Score (RASS). 10 point system. +4 = combative ... +1 = restless 0 = alert, oriented, at rest -1 = drowsy -2 = light sedation ... -5 = GA Tend to target -1 - -2 in ICU. May target -5 in neuro trauma or if invasive procedure or seizures. Sedation reduces BMR Need to consider options for sedation. Sedation causes harms too. Propofol, opioids, dexmed, benzos, ketamine Long term remifentanil for 9 days, 100% of patients demonstrated withdrawal...
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Pharmacokinetic and physiological effects of critical illness
Absorption - decreased GI absorption, often need IV formulation Distribution - loss of lean mass and fat mass. Decrease Vd drugs. Loss of protein --> decreased PPB Metabolism - impaired hepatic function, hepatic blood flow Excretion - kidney impairment, may be on RRT PD - hyperkalaemia from sux. Increased foetal nACHRs Physiological Resp - tracheal stenosis, aspiration, ARDS CVS MSK - poor muscle tone, chronic back pains. Pressure injuries. Neuro - Cognitive impairment - can last months Psychosocial - PTSD, appetite loss, sexual dysfunction, depression, chronic fatigue
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Advantages and disadvantages of muscle relaxants in ICU?
Advantages: - Facilitate intubation - Aid with ventilator dyssynchrony. May be used in severe ARDS to allow for lung protective ventilation - Reduce coughing / straining --> raised ICPs in neuro trauma - Facilitate invasive procedures - TOE, EVD, LP, bronchoscopy - Facilitate positioning - prone - Facilitate transporting - Prevent hyperthermia in refractory seizures Disadvantages: - Worsens critical polymyoneuropathy - not spont ventilating - Increases time on ventilator - increased risk VAP, mortality - Increases length of stay --> increased risk pressure injuries, VTE - Can't do neuromonitoring - may mask neurological deterioration or improvement - Allergy / anaphylaxis - Prevents engagement in physio - Hyperkalaemia from sux - Accumulation due to less predictable pharmacokinetics (atracurium preferred for long term use as undergoes hoffman degradation)
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Prevention of infection in the ICU
- Negative pressure rooms - Antimicrobial covered CVLs - Deescalation of CVLs / other indwelling lines and drains - Minimising time on ventilator - hand hygeine, PPE (standard precautions) - ID input, antibiotic stewardship - isolation of patients with MDROs - Prophylaxis for immunocompromised patients - cotrimoxazole, azithromycin, posaconazole for AIDS patients - Selective decontamination of digestive tract (SDD) - decolonising of GIT tract, reduces MAP, reduces mortality, reduces LOS in ICU (NNT = 18). But increased antibiotic resistance so controversial
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Indications for renal replacement therapy? (RRT)
All below - not ammenable / refractory to medical management. Hyperkalaemia Metabolic acidosis Fluid overload Uraemia Drugs that are dialysable (aspirin, lithium, ethylene, methanol, vancomycin) Other: sodium >160mmol/L - Sepsis (controversial - thought it might remove cytokines)
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Types of dialysis and risks / benefits of each, in the ICU
Can be either intermittent or continuous. Intermittent = haemodialysis, peritoneal dialysis or SLEDD -Haemodialysis = classic type. Can be via dialysis line or fistula. Can dialyse in 3-4 hours but effective. Readily available in most hospitals. But hypotension is a risk (not ideal in ICU) - Peritoneal dialysis. Use of dialysate bags to remove solutes, fluids. Cheap, effective for early stages of renal failure. Not used in ICU as can only remove small amount of solute + need peritoneal dialysis catheter --> risk of peritonitis. Peritoneal fluid may worsen ventilation mechanics - SLEDD (=slow low efficiency daily dialysis). Takes 6-12 hours (overnight usually). Good haemodynamic stability compared to haemodialysis but less stable than CRRT. Doesn't need anticoagulation. Uses conventional dialysis machines. 8x cheaper than CRRT. Solute removal is equivalent to CRRT. SHARF study (2010) - no difference in mortality for CRRT vs intermittent dialysis Continuous -CRRT = continuous RRT. Less hypotension than SLEDD. Most common type = CVVHDF = continuous veno-venous haemodiafiltration = roller pump circulates blood past haemofilter and another pump circulates ultrafiltrate in counter current mechanism. Usually citrate rather than heparin
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Complications of dialysis
From dialysing - hypotension, hypovolaemia, electrolyte abnormalities, air emoblism, removal of dialysable drugs (e.g. dabigatran),altered drug PK From line insertion - usual CVL risks of infection, bleeding, PTX, haematoma, haemothorax, arrythmia etc From anticoagulation - heparin (HITTS), citrate (toxicity)
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Principles of cardiac arrest from hypothermia
Brain is relatively protected due to hypothermia - coldest surviving patient was child that fell into winter sea. 13c core temp Remove wet / cold clothing and replace with warm blankets Start CPR (as long as not frozen solid). Continue until 35c Defib won't be possible until >28c No resus drugs until patient 30c (impaired metabolism). Then once 30c, give adrenaline every 4th cycle (half the rate) Warming - if arrest, need to warm rapidly. If VA ECMO available, consider this. Unclear optimal warming rate. ECMO can achieve >10c per hour but this could be suboptimal for brain - Monitor core temp with oesophageal probe - Options include forced air warmers, warm blankets, radiant heaters, ECMO, pulmonary lavage with warmed fluids, warmed IV fluids, warm theater Likely to get arrythmogenic >28c. Cover open wounds - high infection rate
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Definition of sepsis, septic shock
Sepsis = life threatening emergency leading to organ dysfunction caused by excess / dysregulated host response to pathogen infection Septic shock = shock from sepsis. Inadequate O2 or metabolic substrate delivery to meet tissue demands. Sepsis with end organ damage (MAP <65mmHg, AKI, altered GCS, resp failure, coagulopathy etc)
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qSOFA score for sepsis
Tachypnoea (RR >22) Hypotension (sys <100mmHg) Altered GCS (<15)
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Fluids in sepsis based on surviving sepsis guidelines (2021)
If hypotension, 30ml/kg over 3 hours. Or if lactate >4mmol/L - balanced crystalloid rather than saline recommended. But PLUS and BASIC trials showed no difference mortality for saline over other balanced solutions - Avoid colloids initially. ALBIOS trial did not find mortality benefit using 20% albumin + crystalloid. - Avoid gelatins / starches - Rivers trial = 2001 NEJM trial. EGDT (early goal directed therapy). Protocol included 500ml IV boluses until CVP >8mmHg, vasopressors until MAP >65mmHg, ScvO2 >70% (either got transfusion or dobutamine if Hct normal). Trial showed improved mortality (30 vs 46%). Controversial as lead author had trademarked "EGDT" and was paid consultant for ScvO2 device PROCESS trial (2014). RCt of 1200 patients. One group had EGDT (based on rivers trial) vs standard care vs relaxed protocolised care. No difference in 60 day mortality ARISE = NZ and AUS version. RCT 2014, n=1600. EGDT vs usual care. No difference in mortality or any secondary outcome should use dynamic measures to guide fluid therapy - over static measures or physical exam. Includes SV, PPV, SVV, stroke volume, dynamic leg raise with CO monitoring, declining lactate. - does not include HR, BP, CVP or cap refill
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What order of vasopressors to start for person with sepsis?
1) Noradrenaline - always first. Strong evidence of benefit over dopamine, moderate over vasopressin. Some evidence over adrenaline. Peripheral vasopressors should be started instead of waiting for CVL 2) Vasopressin (somewhere around norad levels of 0.25-0.5mcg/kg/min). VANISH trial showed catecholamine sparing effect of vasopressin. But not improved mortality or RRT 3) Adrenaline 4) Consider dobutamine (if septic shock + cardiac dysfunction). Methylene blue (1-2mg/kg). Hydroxycobalamin (all of these ones have no real evidence)
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When to start antibiotics in sepsis?
If high likelihood of sepsis, or septic shock, give within 1 hour If possible sepsis, without shock, time limited course of investigation. If concern persists, should give IV antibiotics within 3 hours of first recognition
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PROSEVA trial in ICU for ARDS?
If moderate - severe ARDS (PaO2 / FiO2 of <200mmHg) --> mortality benefit for prone ventilation (mortality 16% vs 30%, NNT = 6) Another meta-analysis confirmed mortality benefit (NNT = 11). Prone for >12 hours per day
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When to start corticosteroids in sepsis?
Norad at >0.25mcg/kg/min for 4 hours - ADRENAL and APROACCHSS studies. Increased resolution of shock, reduced vasopressor-free days, reduced ICU LOS, less time on ventilator. BUT increased muscle weakness. No mortality benefit Dose of 50mg hydrocortisone Q6Hrly for 5-7 days (or until discharge from ICU) Might work by suppressing cytokine release. Or by supplementing relative adrenal insufficiency from sepsis
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Uses for cardiac output monitoring
- Goal directed fluid therapy. See whether CO improves with fluid administration. Titration of fluids, inotropes and vasopressors - Differentiation in mixed shock states (e.g. sepsis and cardiogenic shock) - complex, high risk surgery with large fluid shifts (e.g. liver transplant)
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Types of CO monitoring?
Divide into invasive, semi invasive and non-invasive Invasive - Thermodilution (with PAC). Uses stewart Hamilton equation. CO inversely proportional to AUC. ADV: Can be done continously. Accurate. Saline = non toxic. Good agreement with Fick principle (= gold standard). DISAD: need PAC (risks with this), not accurate in TR / itnracardiac shunts. Not shown to improve mortality (PACMAN trial) Semi invasive - PiCCO = pulse contour analysis. Need arterial line at minimum (but best to have CVL for external calibration = thermodilution technique where saline injected into CVL and detected at a proximal arterial line (brachial or femoral)). Can be internally calibrated based on demogaphics AUC during systolic ejection (pressure over time) --> proportional to SV. to convert the AUC (pressure over time) to flow (=volume over time), need to know arterial impedence (which is obtained from either external validation or internal validation) ADV: less invasive than PAC, reasonably comparable to PAC for CO monitoring DISAD: still invasive, any alterations to arterial impedence (e.g. vascular tone from norad) will require re-calibration. Not valid if IABP, significant AR or aortic abnormalities - LiDCO = similar thing but uses lithium dose via CVL and detected at arterial line for external validation - OPTIMISE (2014) and OPTIMISE II (2024) both did not find mortality benefit for using semi-invasive CO monitoring in major abdo surgery - TOE Doppler US Non-invasive - Doppler US. Use doppler to determine velocity-time integral (VTI = AUC of the velocity time graph) through the LVOT = stroke distance - Then can determine area of LVOT by measuring the diametere (and multiply by pi) - Area x stroke distance = stroke volume - Then multiply SV by HR to get cardiac output
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Pulse pressure variation (PPV) and stroke volume variation (SVV)
SVV = (SV maximum - SV minimum) / SV mean PVV = (Pulse pressure max - pulse pressure min) / pulse pressure mean PPV is a surrogate for SVV, as PP on arterial waveform directly correlates to SV Variation in SV with respiration is due to changes in intrathoracic pressure. With IPPV, there is increase in intrathoracic pressure with inspiration. Causes decreased VR to right side, but increased VR to left heart. Causes increase in LV stroke volume. IPPV also causes reduction in LV afterload In expiration during IPPV, the reduction of RA VR (that occured during inspiration) --> decreased LV preload --> decreased SV (it is the opposite in spontaenous ventillation. And recall, in tamponade you get a bigger drop in inspiration "pulsus paradoxus") SVV (and PPV) is not a measure of preload. It is a measure of cardiac output and the cardiac output's responsiveness to preload. If SVV >13%, it indicates there is a large variation of CO due to changes in preload. It is more likely that if increase preload (e.g. give fluids), the CO will increase Conversely, if SVV <10%, then there is little change in SV with changing preload from respiration. It is more likely the cardiaac myocytes are on the flat portion of the Frank-Starling curve and extra preload is unlikely to improve CO. Typically, if both preload (PPV) and vasopressors have been optimised, and CO is still low, it iss an indicator to start inotropes SVV is part of PiCCO, LiDCO, Pulse Contour Analysis, FloTrac. But can just plug in an arterial line and use PPV Conditions necessary for SVV or PPV to be accurate: - IPPV - ideally paralysed with no spontaneous ventilation - TV 8ml/kg - minimal or low PEEP - normal lung compliance (inaccurate in ARDS) - Closed chest - sinus rhythm (not AF) Evidence: -Marik et al (2009). Meta-analysis of 29 studies. n=800. PPV highly predictive of fluid responsiveness in IPPV ICu patients (AUC = 0.94). threshold of 13% gave best balance of sensitivity and specificity. In comparison, from same paper CVP had AUC of 0.55 - One meta-analysis of IPPV under GA using PPV. AUC of 0.77 - but some included low TV patients and open chest, which are inaccurate.
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What is a VAD and how does it work?
Ventricular assist device. LVAD for LV, RVAD for RV. Can get biventricular ones too. HeartMate 3 = most common LVAD. Impella = temporary VAD that can be palced percutaneously through femoral artery. Sits across aortic valve Small tube like device that sucks blood from heart and pumps into aorta (LVAD) or PA (RVAD). Reduced venctricle work, decreases afterload and augments coronary perfusion. Can be transcutaenous or implanted. Pump has between 2,000 - 10,000 RPM. Can get CO anywhere between 3-10L/min Usually patients are anticoagulated (e.g. warfain, aspirin)
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Indications, contraindications and complications of ventricular assist devices?
Indications - Low CO states (e.g. HF with reduced LVEF, ischaemic heart disease) while bridging to definitive treatment (heart transplant, PCI, CABG) which is resistant to medical therapy - Bridging until decision making - Bridging until recovery of native cardiac function (e.g. myocardial stunning after cardiac contusion or CPB) Contraindications - Coagulopathy - Sepsis - Stroke - Mechanical cardiac valves - Severe valvular regurg (especially aortic) Complications - Bleeding - Infection - Haemolysis - Coagulopathy - Stroke
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Anaesthesia management of a patient with a VAD for non-cardiac surgery
High risk, 5-10% mortality in 30 days Preop - Should discuss with VAD coordinator at local VAD centre. If elective surgery, it should be done there. Or minor emergency that can survive the transfer. Or local cardiac anaesthetist - Determine type of VAD (LV, RV, biventricular), model (?HeartMate 3), indication (heart failure, IHD ?awaiting heart transplant), last echo, anticoagulation (often warfarin and aspirin), flow rates and settings, complications form VAD (haemolysis, infection, bleeding, thrombosis, stroke) - cease warfarin (may need reversal) and commence heparin infusion preop - Hb, renal function, coags, G+S Intraop - Ideally with VAD expert in the theatre, monitoring device and able to titrate flow rates. Or constant discussion with VAD coordinator if unable. Cardiac anaesthetist if able. - Non pulsatile flow - pulse ox and NIBP likely ineffective. Can use arterial line (MAP and sats) and cerebral oximetry (rCvO2). Alternative BP measurement is Doppler - If able to do regional, do this - goals of GA: maintain preload (prevent suction events), prevent spikes in afterload and reduce rise in PVR. Ketamine or etomidate reasonable options - Strict asepsis, surgical antibiotic prophylaxis - MAP goals - maintain at 60-80mmHg Post op - consider ICU or transfer to VAD centre - Extubate - Heparin infusion when able
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Differences between cardiac arrest in a post-cardiac patient and a general patient cardiac arrest?
- Survival is better. Only 0.8% of post cardiac patients will arrest in ICU. But 50% survival to discharge - Almost all are witnessed. Diagnosis can be rapidly ascertained (as continous arterial waveform and ECG monitoring) - Causes are different -tamponade, VF or major haemorrhage - Reopening of chest is the final common pathway for all presentations - 10 days is the cut off where best not to open chest (due to adhesions) - Drugs are different (adrenaline in smaller doses. Amiodarone immediately if VF / VT)
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Three pathways for a post-cardiac surgery patient in cardiac arrest (for VT/VF, asystole and PEA)
VT / VF: 3 x stacked shocks. 200J if external defib. 20J if internal. (1st shock has 78% success rate. 3rd it is 14%) - if unsuccessful - BLS + 300mg IV amiodarone via CVL - if still unsuccessful, continue BLS and perform open sternotomy. Shock every 2 mins until check is open if still VT / VF Asytole (or severe bradycardia) - attempt to pace at 80BPM if pacing wires. Dual chamber, asynchronous pacing, maximum current - If still unsuccessful, consider external pacing. Start BLS --> sternotomy PEA - sart BLS immediately. If paced, turn off pacing and see if underlying VF (if VF, 3x stacked shocks then amiodarone as above). - If unsuccessful --> sternotomy Other - Consider tension pneumothorax as possible cause for arrest (auscultate both lungs, lung US) - Turn IABP to pressure sensing (not ECG) - Routinely, should not give adrenaline. If giving should be in small increments (e.g. 50mcg). Will need adrenaline if anaphylaxis as cause. Hypertension may cause new anastamosis to blow off and cause catastrophic haemorrhage, certain death - external compressions lower priority as potential could cause injury to anastamoses. But case reports suggest this risk is low. aim for systolic of 60mmHg. If unable to achieve, more likely to be tamponade as cause and need chest opening Sternotomy - 3 person job - roles pre-defined before each shift - if done within 10 mins, survival of 50%. If more than 10 mins, survival 10% - Chest opener and 2x chest compressers - Once gowned / gloved (no hand washing - don gloves with hands in sleeves), stop CPR, remove sternotomy dressing, squirt on iodine, place sterile drape, commence CPR with gowned personal - Cut down to wires. Cut wires - Suck out clot. Place in sternal retractors - Once chest open can then: Suction out more clot / tamponade, clamp any bleeding vessels, internal cardiac massage, internal defib) - then needs to go to theatre post arrest Internal massage gives double cardiac output rate to external (1.3L/min/BSA). Use two handed technique - left han on top. Compress apex --> base in clapping motion
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Winter's formula for expected PaCO2 with a metabolic acidosis?
PaCO2 = (1.5x HCO3) + 8
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Boston rules for metabolic compensation of a respiratory acidosis
Acute resp acidosis. 1mmol/L of HCO3 increase for every 10mmHg PacO2 Chronic resp acidosis. 4mmol/L of HCO3 increase for every 10mmHg PaCO2
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Boston rules for respiratory alkalosis and expected metabolic compensation
Acute resp alkalosis. 2mmol/L HCO3 decrease for every 10mmHg PaCO2 decrease Chronic resp alkalosis. 5mmol/L HCO3 decrease for every 10mmHg PaCO2
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Calculation of anion gap
(Na + K) - (HCO3 + Cl). Normal = 12-16mmol/L or Na - (HCO3 + Cl). Normal = 8-12mmol/L Most of anion gap is due to albumin. And PO4-. If higher, then likely another anion contributing to acidosis
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Causes of NAGMA and HAGMA What is the delta ratio?
HAGMA = LTKR = lactate, toxins, ketones and renal. Toxins = methanol, ethelene glycol, toluene, carbon monoxide, salicylate) NAGMA = ABCD = Addisons, Bicarb loss (GI or renal aka renal tubular acidosis), chloride, diuretics (acetazolamide) Delta ratio is used to determine if just a HAGMA. Or a HAGMA with a NAGMA also present
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What is ARDS? Pathophysiology?
Acute respiratory distress syndrome - more severe form of acute lung injury. High mortality rate (worse if elderly, comorbid, high APACHE II score, acidosis or immunosuppression) Definition (Berlin criteria) - Predisposing acute onset (may be direct e.g. trauma, toxin inhalation, aspiration) or indirect (AFE, PE, sepsis, DIC, CPB, liver failure, TRALI) - Hypoxia. Need at least 5cmH2O for diagnosis. Based on PaO2 / fiO2 ratio ( e.g. PaO2 of 80mmHg and FiO2 0.5 --> 160mmHg = moderate ARDS) Mild = 200-300mmHg = 27% chance mortality Moderate = 100-200 Severe <100mmHg, 45% chance mortality - Bilateral lung infiltrates on CXR, not from CHF - Normal LVEDP or PCWP (not cardiogenic in origin) Pathophys - systemic inflammation mediators activate neutrophils, macrophages --> release leukotrienes, proteases, free radical formation --> endothelial damage, increased alveoli permeability --> exudate + pulmonary fibrosis - Impaired compliance, poor V/Q matching, atelectasis, shunting
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Management of ARDS
Mainly based on ARDSnet ARMA (2000) paper Goals are: suppport ventilation, oxygenation, treat underlying cause and minimise further injury to the lungs while providing time for supportive healing Mechanical ventilation strategy: - Lower TV 6ml/kg resulted in less mortality than higher TV. Less over distention and cytokine release - Moderate PEEP 8-14cmH2O. Sliding scale for PEEP up to 24cmH2O in ARDSnet trial - Peak pressures <30cmH2O, plateau <20cmH2O - Permissive hypercapnia Fluids - typically conservative. FACTT trial determined restrictive fluids reduced LOS (but not mortality). Target slightly negative fluid balance or euvolaemia Prone - Do for >12 hours if indicated - consider if PaO2/FiO2 <150mmHg with FiO2 >60%. Based on PROSEVA trial. Mortality 33-->16%, improved ventillator free days. Patients were proned for 16 hours per day until improvement - contraindications include: c spine instability, femur / other long bone instability, cardiac unstable rhythms, refractory hypotension, inability to deeply sedate patient, raised ICP, open abdomen, late pregnancy Treat underlying cause (e.g. sepsis with IV antibiotics) Steroids - DEXA-ARDS trial (2020) found mortality benefit and helped wean from ventilator in moderate-severe ARDS. 20mg dex for 5 days then 10mg for 5 days. All cause mortality from 36% --> 21% - Useful for sepsis too (e.g. surviving sepsis guidelines if norad >0.25mcg/kg/min for >4hours) VV ECMO - CESAR trial demonstrated benefit for severe ARDS (but there were differences in groups for lung protective ventilation too) - EOILA trial - didn't show mortality benefit in early ECMO - Meta-analysis of both these trials showed slight benefit in severe ARDS at 60 days for mortality (Lancet 2019) APRV (Airway pressure release Ventilation) - Only small RCT trials to date, no mortality benefit seen but demonstrated less time on ventilator and reduced time to extubation
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Summarise APRV
Airway pressure release ventilation "open lung" ventilation. Combines long periods of high continous pressures (almost continous CPAP) with very short drops (dumping breaths, which facilitate CO2 ventilation - Provides high mean airway pressures without high plateau pressures --> recruitment of lungs without barotrauma. Aim to recruit and improve oxygenation (mainly in ARDS) - Trial it in severe ARDS (PaO2/FiO2 <100mmHg). But only after prone trial (as this has more evidence e.g. PROSEVA trial) Setup: FiO2 100% which can often be reduced) P-high = highest pressure applied to system (set to current plateau pressure). T-high = time in seconds spent at high pressure (5s) P-low = lowest pressure (typically 0). T-Low = time at P-Low, often short (0.5s), intrathoracic pressure never reaches atmospheric pressure - Then can reduce sedation, stop NDMRs and allow for spont ventilation - If hypoxia despite above, increase fiO2 or increase T-High Well tolerated, patient can spont ventilate most the time. Less need for paralysis Contraindicated in COPD or severe asthma as risk of gas trapping. Also can cause hypotension due to increase intrathoracic pressures Evidence is lacking as of yet. No mortality benefit. Small RCTs have demonstrated less time on ventilator and faster times for extubation. One study in pigs found improved mucosal appearances using APRV compared to traditional ARDSnet ventilation
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Pathophysiology of ventillator associated pneumonia
= pneumonia in patient undergoing mechanical ventilation for the last 48 hours. Mortality risk 13%. - bypassing usual immune system barries with endotracheal tube (humidification and sputum clearance) - Immunosuppresion due to being in ICU (transfusion, critical illness) - Exposure to MDROs - Microaspiration If <48 hours since starting, more likely community pathogens (strep pneumoniae) If >48 hours, could be community or hospital acquired (staph aureus / MRSA, pseudomonas, klebsiella, enterobacter, acinetobacter)
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Prevention of VAP Management
Minimise time on ventilator - only intubate when needed - Wean off sedation and NDMRs as soon as possible - Treating underlying cause (sepsis, ARDS) to get off ventilator Reducing aspiration risk - Avoid unnecessary PPIs (which increase VAP risk due to increase gastric pH) - Head up 35degrees - Oral hygeine - Cuff pressures kept at 25cmH2O - Minimise over gastric feeding ICU systems - PPE - Hand hygeine - ID rounds Prevent immunosuppression - Transfuse only when needed (TRIC suggested Hb target 70g/L) Management: - Antibiotics - Tazocin at Waikato (mero if beta lactam allergy) - Bronchopulmonary lavage for micro / culture - Get off ventilator
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Complications from tracheostomies
More than 50% of NAP 4 airway events in ICU were related to traches. 90% in first week of insertion Early complications - Bleeding - Displacement - False passage - Obstruction - subcut emphysema - Pneumothorax Late complications - Infection (VAP, sepsis, pneumonia) - Trachael erosion (innominate artery, oesophageal, cutaenous fistulae) - Ulceration - Trachael stenosis (usually at level of cuff) - delayed healing
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Management of a tracheostomy emergency (e.g. can't ventilate)
Most common emergencies are bleeding, obstruction and dislodement. guideline from NTSP = National Tracheostomy Safety Project in UK - Should always be a tracheostomy box in ICU for emergency. Should have fresh inner cannula, suction catheters, airway algorithm for trache, tracheal dilators - Above each bed for trache patients (and laryngectomy) should be previous intubation grade (/ if they are intubatable), trache type - Massive haemorrhage in 72 hours often innominate artery-trachea fistula (90% mortality) --> hyperinflate trache cuff to see if that tamponades it. Get ENT and vascular in immediately 1) Check if breathing or not. If not, check for pulse. If not --> CPR - If breathing, give O2 via trache and mouth 2) Assess trache patency. Remove inner cannula and then use suction catheter. If passes easily, then liekly patent. Suction airway - if unable to pass catheter, deflate cuff and see if this improves ventilation (check capnography, feel for air movement). If it does, then likely partial obstruction - If sats okay, get bronchoscope and look down trache 3) if no improvement, remove trache (as dislodged or obstructed). could get airway patency at this stage 4) With trache out and patient still struggling, need to figure out alternative oxygenation - Standard oral manoeuvres - BMV, LMA, OPA (need to cover trache stoma with gloved hand or gauze for this) - Stoma ventilation with paeds BMV or classic 3 LMA covering stoma 5) If still unsuccessful, prepare for oral intubation. May be difficult or impossible - VAFI is a good technique if 2 people. Need to get ETT passed stoma (direct bevel posteriorly) 6) Last ditch efforts - re-intubation through stoma. Use bronchoscope / bougie and size 6 ETT
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Indications and complications of hyperbaric O2
Hyperbaric O2 is PO2 >1atm, therefore increasing dissolved O2 in blood and hopefully delivery to tissues Indications: - Air or gas embolism - Carbon monoxide poisoning - Soft tissue infections / gangrene / refractory osteomyelitis - improves time to healing, angiogensis and reduces rates of amputations - Decompression sickness - Radiation tissue damage - Crush injuries, compartment syndrome and acute peripheral ischaemia - Compromised skin flaps and grafts Complications - CNS - anxiety, seizures, visual field defects - Resp - atelectasis, endothelial damage and APO (free radical formation) - Other - FIRE!
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Advantages and disadvantages of NIV in the ICU
ADV - Avoid intubation (therefore no VAP, NDMRs, CICO, dental injury, critical illness myoneuropathy) - FIO2 up to 100%. Suitbale for most moderate-severe causes of hypoxaemia. Can also be used for preoxygenation before intubation - CPAP - reduce atelectasis, good for LV (less preload and afterload) in failure - BiPAP - reduced work of breathing, improved ventilation - Better tolerated than intubation - no need for sedation. Can assess neuro. Better comfort. PAtient can communicate. Less delirium or PTSD - Useful in particular circumstances - OSA, CHF, COPD DISADV - Might delay inevitable intubation. 30-50% patients started on NIV will need intubations. May make intubation more challenging as closer to hypoxaemic arrest (physiologically difficult airway) - Intubation more definitive therapy - No aspiration protection - Requires cooperative patient - Requires spontaneous ventilation - Rquries mask to fit - less effective if bears, morbid obesity, abnormal anatomy - Contraindicated if recent airway surgery, facial trauma, pneumothorax or pneumomediastinum
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Types of ICP monitors in ICU and risks
Risks of ICP monitoring - malplacement - haemorrhage - infection - obstruction -malfunction EVD = external ventricular drain = gold standard for ICP monitoring - inserted via right sided burrhole. connected to saline manometer or pressure transducer - Can be used to remove CSF. Can set heigh of EVD to remove CSF if ICP over certain pressure (reference pressure height always foremen of Muro) - Can rarely be used to give drugs (antibiotics in ventriculitis) - 1-5% infection risk - HArd to place in collapsed ventricle Intraparenchymal monitor - Sensor in parenchyma via small burrhole. Resistance within sensor is refelcted as voltage change - Almost as accurate as EVD, useful for when ventricles non-accessible - Less haemorrhage or infection risk than EVD - only measure localised pressure, may not be indicative of global pressure - Cant be recalibrated once inserted - subject to drift - Cant drain CSF Subdural pressure transducer - Dura pierced, hllow device wills with CSF and tubing transmits presure to transducer - Least invasive, lowest infection and haemorrhage rates - Least accurate for ICP monitoring - Cant measure ICPs - May occlude with debris
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Causes of delirium in ICU
DELIRIUMS Drugs Electrolyes Lack of drugs (withdrawl) Intracranial pathology Reduced sensory input (glasses, hearing aids) Infection Urinary obstruction / constipation Myocardial disease Sleep disturbances
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Prevention and treatment of delirium in the ICU
Prevention - Early mobilisation - Reduce sedation - Nutritional support - Minimise drains / lines - Give visual aids / hearing aids - Infection control, reducing chances of acquired infection - EArly operation (e.g. hip fractures) Treatment: Non-pharma - Reassurance, reorientation - single room, dedicated nurse - Family members - Minimise noise and lights - Investigate and treat underlying cause - Day- night circadian rhythm with lights Pharmacological - Antipsychotics (halopreidol, quetiapine) - Benzo (only really if PD or lewy body dementia) - DExmed (may reduce duration of delirium) - Propofol
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LP indicative of a bacterial infection
High white cell count (100-50,000) with predominate neutrophils, low glucose (<0.4), high protein (>1.0), high ICP TB meningitis more lymphocytes than neutrophils. With even higher protein and lower glucose fungal meningitis - very high ICPs, mainly lymphocytes. Raised protein. Low-normal glucose
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Treatment / management for meningitis
Most common bacteria are strep pneumo, nisseria meningiditis, listeria, haemophilus influenzae Usual ABCs, blood cultures, CT head and LP Antibiotics - 2g IV ceftriaxone - add vanc if gram +Ve cocci resembling strep - Add amoxicillin if suspecting listeria (CLL, pregnangy, immunosuppression) Steroids - Benefit if given with or before antibiotics. 10mg IV Q6Hrly dex for 4 days. Benefit only if known or suspected strep pneumo and GCS 8-11 Anticonvulsants if seizure Public health notification Prophylaxis for close associates / medical staff in close contact (e.g. intubation) - Rifampicin if haemophilus influenzae - Ciprofloxacin if neisseria meningitides
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Treatment for encephalitis
Most commonly a viral cause e.g. HSV1. high mortality rates Do CT and MRI brain before LP. LP for HSV, VZV, anti-NMDAR, anti VGKC PCR Acyclovir 10mg/kg Q8hrly Steroids AEDs consult neuro
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Summary of ANZCA PS52 - Requirements for Safe transfer for critcally ill patients
Critically ill patients have minimal physiological reserve - any further insult can lead to demise Pretransport - Assess + optimise patient for transport - Planning of transport with communciation between senior staff (referral and receving teams) - Equipment + medications - Skilled transport team - doctor + nurse - Central coordination hub for communication - Handover effectively - Documentation of patient's notes, treatment to date, investigations Transport - Level of care should be at same level as referring hospital and prepare patient for admission to receiving service - Suitable PPE (including ear protection for helo) - Equipment for any eventuality - airway, circulation, drugs including extras - CPAP / BIPAP better than HFNO as uses less O2 - Handover end of transport
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Comparison of road vs air transport
- Cost: Air much more expensive - Range: air can be 100s-1000s of kms (plane >helo). Road more practically limited to 200km or so - Speed: air much faster once in air. But can require multiple stops (e.g. getting to airfield). Road has traffic issues - Weather: Air much more influenced by this. Decision to fly is pilots. Road may be limited by flooding / road damage - Comfort: motion sickness an issue for both. Windy roads or air turbulence - Emergencies en route: easier to deal with in ambulance. Helo may have to land in field - Altitude effects: air may have rapid expansion of PTX (Boyles law) - Equipment: Air equipment needs to be weight rated, visible alarms as cant hear them - Weight limiting: Air need to know weight of patient and staff and equipment. Some helos are limited to 140kg patients. Parent of paeds patient may not get on helo - Safety: helos are more dangerous, crashes more likely to be fatal