Prehabilitation domains
Evidence for prehab
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
What is patient blood management (PBM)?
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
Definition of anaemia and causes for anaemia
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
Signs and symptoms of iron deficiency
Biochemical markers for iron deficiency vs anaemia of chronic inflammation
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
PREVENTT trial
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
Options to improve anaemia preop
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)
Premedication options and doses for kids?
Midazolam - oral 0.5mg/kg up to 20mg
Ketamine - oral or IM 2mg/kg
Clonidine - 4mcg/kg
Dexmeditomidine - 2-4mcg/kg IN
Advantages and disadvantages of premeds
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
Risk factors for PONV
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
Definitions for minimal, moderate and deep sedation
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
Requirements for moderate sedation
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
Delirium definition and causes for delirium
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
What is postoperative neurocognitive disorder?
Ways to reduce POCD?
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
Relief trial findings
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)
Why is CVP a poor indicator for fluid status / responsiveness to fluids?
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)
Uses for CVP (as it is no good for fluid status)
Alpha stat vs pH stat in DHCA for aortic arch surgery
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
Risk factors for AAGA (accidental awareness under GA)
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
Four important trials for awareness prevention under GA
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
What particular times did AAGA occur during the anaesthetic?
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
Treatment of PTSD following AAGA
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
Components of the Brice Questionaire
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)
Effects of cannabis perioperatively
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
Cocaine use effects on anaesthesia
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