General Flashcards
Myasthenia gravis are sensitive to depolarising NMB
MG resistant to suxamethonium (double dose)
TNF is associated with
Cytokine
Poor outcome
Extradural space may contain
Fat Spinal nerve roots Lymphatic Connective tissue Batsons plexus Spinal arteries Epidural venous plexus
ECT current
30-45 Up to 100j
Autonomic response to ECT
Initial parasympathetic response ie bradycardia hypotension sometimes asystole
Followed by sympathetic response hypertension and tachycardia
Compliance greater under static or dynamic conditions
Static
Static is periods when no gas flow. Dynamic is when there is flow ie active respiration…. need to overcome airway resistance so dynamic compliance will be less.
Complain when greater with water or air
Water (liquid) - more pressure needed to distend lung with air than liquid
Compliance is greatest at FRC or TLC
FRC
TLC is top of pressure volume curve so little compliance
Acclimatisation to altitude includes what changes
Increased 23dpg
Compensated respiratory alkalosis (I.e loss of hco3)
Increased blood viscosity
Increased diffusing capacity co2
Cardiac output initially increases but settles once acclimatised
Where does sympathetic outflow arise
T1-L2 (sympathetic chain runs parallel to spinal column)
Where does parasympathetic outflow arise
Cranial sacral
Which cranial never have parasympathetic nuclei
III, VII, IX, X
Where is larynx located
Anterior neck, level c4-c6
Narrowest part of larynx adults vs infants
Adults glottis
Infants cricoid
Recurrent laryngeal nerve innervates what intrinsic muscles
All except cricothyroid
Sensory inner action larynx
Superior laryngeal never above cords
Recurrent laryngeal nerve below cords
How does adrenaline effect glucose levels
Adrenaline causes hyperglycemia
a receptors Stimulation inhibit insulin secretion, stimulate gycogenolysis and glycolysis
B receptors stimulation results in glycogen secretion in pancreas, increased ACTH, and increased lipomas is
Do thiazides cause hyperglycemia
Yes possibly by insulin resistance
Lumbar plexus roots
L1-4 sometimes with t12 and l5 input
Lumbar plexus nerves
Femoral Obturator Ilioinguinal Iliofemoral Lateral cutaneous Genitofemoral
Tributaries of internal jugular vein
Medical school lets fun people in
Middle thyroid Superior thyroid Lingual Facial Pharyngeal Inferior petrosal
Major haemorrhage definitions
Loss of all blood volume in 24 hours (5liters or 70ml/kg in adults)
Loss of half circulating volume in 3 hours
Loss of 150ml/min
Genetics of malignant hyperthermia
Malignant hyperthermia is autosomal dominant
Error in RyR1 (Ryanodine receptor) on chromosome 19
Early signs of MH
Increase in co2
Increase in heart rate and oxygen consumption
Late sign is high temp
Mortality of MH
5% with introduction of dantrolene
What is cause of renal failure in ALF
Acute tubular necrosis
Association of chronic pain with
depression
Anxiety
Depression 30-40%
Anxiety 25%
What opiods can you do skin prick testing in
Fentanyl and remifentanil
Morphine codeine and diamorphine have significant direct mast cell degranulation without Ige so skin prick testing not appropriate
Mast cell tryptase measurements and why
Measure at time, 3hours and 24 hours
Mast cell tryptase is spontaneously released so need to see serial and rise and fall in anaphylaxis for confirmed diagnosis
What apart from anaphylaxis can cause raised mast cell tryptase
Typtase may be raised in mastocytosis, aml, myelodysplastic syndromes
What effect do volatiles have on venous admixture
Venous admixture is the lowering of arterial po2 from ideal level due to shunt. Volatiles impair HPV therefore increase venous admixture
Where is bilirubin produced
Bilirubin is produced in reticuloendothelial system in the spleen, bone marrow and hepatic kipper cells
Bilirubin is produced by macrophages by reduction of biliverdin
How is bilirubin transported to the liver
Bilirubin is bound to albumin as its insoluble
Conjugation makes bilirubin soluble
What is the concentration of intralipid
20%
What is the dose of intralipid on initial dose
1.5ml/kg
What is ongoing treatment with intralipid in LAST
Infusion intralipid 15ml/kg/hr
Two repeat boluses 1.5ml/kg (5 minutes between)
Increase infusion to 30ml/kg/hr (at 5 mins)
If CV stability not restored or deteriorates
Maximum dose of intralipid
12ml/kg
How does plasma site vary from effect site
Plasma site
Effect site has extra contant keo is effectively a 4th compartment but with negotiable volume
Time delay in equilibration between plasma and effect site as takes into account keo
In effect site need to overshoot CP then reduce to allow cp and Ce to equilibrate
Keo calculated by complex pharmacological modelling
Discuss marsh model for TCI
Marsh is based on weight
Safest to use in Cp as uses very large bolus in ce initially
Best for young people
Discuss Schneider model TCI
Snider uses age and lean weight (sex adjusted)
Always use in Ce
Beneficial in elderly
Smaller bolus doses
How can you minimise awareness in TIVA
Concurrent use of remifentanil Depth of anaesthesia monitoring ie BIS One way valves Anti Syphon valves Adequate equipment training Avoid muscle relaxant Alarms on pump ie. low high pressure, battery
Define aspiration
Inhalation of material below true cords
Commonly quoted 25ml and ph less than 7.2 comes from studies on monkeys extrapolated to humans
Kidneys cardiac output
25%
Kidneys glomerular filtrate volume
180l day
70 percent reabsorbed by pct
Renal perfusion ml/min/100g
Cortex 500, outer medulla 100, inner 20
Cortex least metabolically active so is a luxury blood supply in excess of requirement
Medullais very metabolically active, oxygen requirement is tight and is at risk of ischaemic injury
What matching required for cadeveric renal donors
Size, blood group and MHC complex
Side effects of ciclosporin
Ciclosporin causes hypertension, tremor, reduced egfr, encephalopathy
Why was glycine used for TURP
Doesn’t conduct electricity
TURP syndrome glycine level over 60mmol/l
TURP how high doe you need block
T9
Sickle cell genetics
Autosomal recessive most of the time
Trait carries some protective properties but phenotypically normal
Carried on chromosome 11
Abnormal B globin chain forms HbS which precipitated out of solution when deoxygenated
Heterozygotes 30% hbs (some protective from p.falciparum)
Homozygotes 100% hbs
Genetics of thalassemia
Group of heridatory anaemia causes by ineffective a or B chain formation.
Heterozygotes mild anaemia
Homozygotes severe
May be compensatory extramedullary haematopoesis
Diagnosis sickle cell
Sickledex but cannot distinguish between sickle trait and sickle cell
Blood film
Haemaglobin electrophoresis
Presentations of sickle cell
A/b - dypnoea, haemoptysis, chest pain (pulmonary infractions) - acute chest syndrome
Functional asplenism hypertrophy of other lymphoid tissue and osa
C- cardiomegaly due to anaemia or CCF, pulmonary heart failure
d- increase Tia and stroke, microvascualr changes in eye
E- automfarction pf spleen, pigment gallstones
f- renal failure
H- marrow hyperplasia frontal bossing and maxilla
Acute decreases in hb by infection induced myelosuppresion (ie parvovirus)
Bone marrow failure
Treatment sickle cell
Patient education re hydration, exercise, alcohol
Vaccinations
Folic acid
Hydroxyurea (increases fetal hb)
Acute
Analgesia
Rehydration
Remember acute abdomen differential is sickle cell
Sickle cell requiring op considerations
Pre op tests assessing organ dysfunction
Rehydrated
Hb and transfusion
Avoid adrenaline in Local
Positioning to avoid venous stasis
Tourniquets must be justified
Analgesia
Thalasseemia pre op considerations
Consider if could have sickle cell too
Haematocrit
Splenomegaly and thrombocytopenia
Facial changes and frontal bossing
Drugs with potential anti carcinogenic effects
Regional (directly from reduced sympathetic stress response or via reducing opiod consumption)
LA (possible direct immunomodulatory effect)
Propofol TIVA (as abolishes ischaemic reconditioning, increases apoptosis and decrease invasion migration and proliferation, more preserved NK function)
NSAIDS (reducing prostaglandin effects which is pro progression of neoplasia via IL6 IL4 ….. cox2 is higher in some cancers )
Drugs with potential pro carcinogenic effects
Inhalation agents ( promote tumour GF including HIF and IGF, reduction of NK cells.... overall promote tumour growth, invasiveness, migration) Opiods (some reduction via reduced stress response) (some evidence that reducing doses may reduce angiogenesis and a cancer recurrence) Steroids (immunosuppressant reduces NK cells and other T cell subtypes) so,e studies refute thus
Surgical indications for TIVA
Cancer surgery Tubeless ent or thoracic surgery Neurosurgery Surgery requiring neuromuscular monitoring ie scoliosis Day case surgery Non theatre environment
Patent indications TIVA
MH PONV Long QT Patient choice NM issues ie MG Anticipated difficult intubation or extubation
Checklist TCI systems
Only dedicated TCI pumps
Trained in use of pump and model
Pumps serviced last 12m
Ensure pumps plugged into mains
Ensure batteries are charged
Ensure drug dilutions correct and entered into pump
Ensure correct syringe type and mounted correctly
Ensure pump programmed for drug it is programmed for
Ensure high and low pressure alarms set
Ensure correct patient details entered
Consider if targets set are appropriate for asa and age
What is plan b if pumps fail
Recommendations to prevent technical problems with TIVA
Secure cannula
TCI system checklist
Keep cannula visible
Only use dedicated two way tap set includes anti siphon valves, non return on IV fluids, minimal dead’s peace
Only use Leur lock syringes when admin drugs
Don’t label remi until drug is in
Flush Tuva drug from dead space of three way way before connection and flush out at end
Potential problems with tiva
Awareness
Morbid obesity - marsh model will result in overdosing, snider based on LBW and once Bmi reaches a critical level the infusion rate is insufficiently corrected and may result in large bolus. Minto above certain bmi reduced bolus and inadequate analgesia
Analgesia and hyperalgesia
Propofol related infusion syndrome (metabolic acidosis with cardiac dysfunction plus possible rhabdo, hyper triglyceride, renal failure)
Nap 1
Supervisory role of consultant anaesthetists
Nap 2
Place of M&M meetings
Nap 3
Complications of central neuroaxial block in the uk
Nap 4
Major complications of airway management in the uk
Nap5
Accidental awareness during GA
Nap 6
Perioperstuve anaphylaxis
Nap7
Perioperative cardiac arrest
Why choice of agents in tiva
Remi and propofol synergistic effect
Short CSHT
Predictable pharmacological profile
When does propofol reach steady state concentration
20 hours
When all 3 compartments reach steady state concentration,
TCI matches elimination (k10)
Key components of TCI
User interface
Microprocessor
Infusion pump (up to 1200ml/hr)
Visual and audible safety systems and alarms
Calculates bolus dose required
Calculations repeated every 10s and infusion rate adjusted until Cpt
Diffusion to brain is exponential with first order rate constant keo
Marsh model fixed variable parameters and parameter determined by
Marsh model fixed rate constant
Variable v123
Parameter determined by weight
Schneider model fixed variable parameter and determined by parameter
Fixed in Schneider v1 v3 k13 and k31
Variable in Schneider V2
Parameter determined by age, weight, lean body mass
Minto model fixed and variable parameters and parameter determined by
Minto model v3 fixed
V1 v2 and rate constants variable
Model determined by weight and lean body mass
Stress response to surgery two broad categories
Neuroendocrine metabolic response
Inflammatory immune response
Surgery with largest stress response
Major open vascular and abdominal
Joint replacement cardiac on CPB
Describe neuroendocrine metabolic stress response to surgery
Sympathetic nervous system
- PVN nucleus detects changes ie hypotension
- impulses from site injury via limbic system
- PVN fibres into posterior pituitary and control anterior pituitary functions
- adrenaline secreted directly in response to hypothalmic activation and this increases sympathetic response
- heart rate and vascular sm time increased
- mobilised cho and fat stores
- glyogenolysis and lipolysis = hyperglycemia
- increased coag
Endocrine
- increased CRH stimulates HPA
- Increased ACTH which increases cortisol secretion in zone fasciculata
- uktradian pulsation increase
- chronic activation hpa leads to dysfunction with surgery - age and fragility risk factors and can get pre existing dysfunction ie in anxiety and depression.
- GH increases hepatic glycogenolysis leading to hyperglycemia
- increased in ADH, increased prolactin, reduced testosterone, thyroxine and t3
Metabolic response
Hyper metabolism and hylercatabolism
Glucose from all sources, and insulin ins inhibited and insulin resistance
Renin activates which eventually leads to increased aldosterone- retention of salt and water
Describe inflammatory immune stress response to surgery
Innate and cell mediated immunity
Macrophages, NK cells move into wounds and cause inflammatory mediators
Cytokines include ILS TNF interferons and cytokines
Early inflam cytokines IL6 TNFa IL8
Anti inflammatory il4il10
Acute phase response is increase in serum proteins stir by cytokines esp IL6
Ie crp, d dimmer, macroglobulins
IL6 and CrP can be linked to magnitude of surgical stress
Ways to modulate stress response to surgery
IV vs volatiles - volatiles may inhibit endocrine responses but other propofol lowest proteolytic effect
Benzodiazepine - inhibit cortisol at level HPA
A2 agonists - inhibit surgical stress response
Opiods - reduce acth and GH. Morphine fentanyl remi have immimo modulators role
Regional - blocks HPa axis response via afferent
Surgical techniques - minimally invasive surgery techniques, duration and extent surgery
Eras programmes
Early nutrition
Early mobilisation
Glucocorticoids and surgical stress response
Varied literature
Reduced CRP and IL6
Reduced post op ventilation, hyperthermia, infection and ,engage of stay
Caution in diabetes s
Define gbs and name subtypes
Guillian barre is and acute inflammatory polyneuropathy (ascending )
Types are Acute inflammatory demyelination polyradiculopathy Miller fisher variant Acute motor axonal neuropathy Acute motor sensory axonal neuropathy
GBS signs
Motor difficulty / paralysis Loss deep tension reflexes Paraesthesia without sensory loss Muscle wasting Urinary retention Ptosis Autonomic Speech problems Respiratory distress
Investigations in gbs
Nerve conduction studies
LP
LTFS
Spirometers (vc less than 15ml/kg indication for intubation)
Also consider serology, stool culture, HIV, spinal MRI
Anti ganglioside antibodies
Treatment GBS
Ventilator support 25% - facial bulbar laryngeal weakness -inability to clear secretions - resp and diaphragm muscle weakness - pulmonary infections Often nocturnal decompensation Regular VC and constant oximetry
Physio therapy Psychology Immmunoglobulin Plasmapheresis Nutrition Analgesia
Not steroids
Outcome GBS mortality 10%
Indications intubation in GBS
V1c less than 20
max inspiratory pressure of less than 30
Max exp pressure of more than 40
Decreased more than 30% of above
One MET
One met Represents the oxygen consumption of an adult at rest (approx 3.5ml kg min)
A person should be able to perform more than 4 mets which is equivalent of climbing one flight of stairs
Contraindications to CPET
Absolute contraindications to cpet Acute MI Unstable angina Uncontrolled arrhythmias Syncope Active endocarditis Myocarditis or pericarditis Severe AS Suspected dissecting aneurysm Uncontrolled asthma Room seats less than 85% Resp failure
Relative Left main condo art stenosis Moderate stenosis valve Severe hypertension sbp 200 dbp 120 HOCM Pulmonary hypertension Advanced or complicated pregnancy Electrolyte disorders
CPET timings
3 mins baseline
1-3mins unloaded
Increasing resistance
Full monitoring for ten mins cessation of exercise
CPET measurements
Work in watts Metabolic gas exchange ie vo2 and vco2 Respiratory exchange ratio Anaerobic threshold Hr 12 lead ecg Nibp Oxygen pulse (vo2/hr) Ve Vt Rr Spo2 Ventilator equivalents for oxygen
Computer software calculated expected for height age weight sex
9 panel plot
Graphical representation of CPET is called 9 panel plot
235 cardiovascular
147 ventilation
689 Ventilation perfusion
Vo2 max
As work rate 8ncreases exercise muscle requires more oxygen to generate adequate levels of ATP
Increase in oxygen consumption met by increasing CO
Vo2 = co x arterial venous oxygen difference
Co therefore increases linearly with vo2 as does the av difference until a peak oxygens extraction reached
Vo2 max is the maximum o2 consumption of the body (attainable by athletes)
Vo2 peak is the peak o2 consumption when test is not completed ie age fragility deconditioned
Anaerobic threshold
With imcreasing exercise oxygen demand exceeds supply and atp is generated anaerobically
Produces lactic acid- buffered with hco3- produces co2
Sudden increase of vco2 more than vo2 and rer becomes more than 1
AT usually reached about half way through test
Doesn’t vary with patient motivation or age
Safe AT and VO2 peak for surgery
At 11ml/kg/min
Vo2 peak 30
Functional walk test
6minute walk test (500-600m, says hr and Borg scale of dyspnoea and leg fatigue)
Incremental shuttle test (speed increases every minute - failure to reach come in next tone or exhaustion terminates test)
Both correlate well with peak vo2
Innervation of knee
Hilton’s law Femoral Obturator Common and recurrent perineal Tibial
The femoral nerve via its Soph branch and to vastus supplies suprpatella recess, patellar periosteum, anterior medial and anteriolateral joint capsule
Tibial never supplies medial lateral posterior joint capsule, infrapatellar fat pad, tibial periosteum
CPN supplies anteriolateral capsule
Recurrent peroneal - tibfib joint
Obturator - posteriormedial capsule
Cutaneous innervation anterior femoral
Independent predictors severe post op pain knee arthoplasty
Young age
Pre op pain
Depression
Cause of pain in knee surgery
Prostaglandins and bradykinin realised at site of injury
Nociecotive fibres travel STT (nmda receptors)
Prep knee surgery
Joint school
Preemptive analgesia nsaids good evidence, gabapentin unclear
RA for knee arthoplasty
Regional associated with reduction in post op complications including dot pulmonary embolism blood transfusion respiratory depression
Spinal (plus femoral nerve block and sciatic block)
Epidural
Femoral nerve block
Adductor canal block (contains saph nerve and posterior obturator nerve medial knee only)
Local infiltration analgesia
Novel techniques
I pack block (infiltration between popliteal artery and capsule of posterior knee)
Nerve to vastus lateralis
Adjuncts in knee surgery
Dexamethasone reduces acute phase reactants such as CRP and IL6
Avoid knee haematoma with TXA
Post op pain management knee surgery
Multimodal PCA Continuous LA infusion ie elastomeric Gabapentin? Cryocuff
Types of cognitive impairment after surgery
Preexisting or progression of existing neurocognitive disorder
Mild NCD- noticeable decline in cognitive function but maintains independence
Major NCD - impairs daily living
Acute onset of delirium (less than 7 days post operative)
Delayed neurocognitive recovery (first 30 days)
Post operative cognitive dysfunction (within a year)
Cognitive domains evaluated in NCD
Learning and memory (learn and recall new infor) Language Perceptual motor Social cognition Complex attention Executive function (planning) Delirium
Delirium
Fluctuating changes in attention, consciousness and cognitive f7nctuin within hours or days of event
Hypo or hyperactive
Post operative cognitive dysfunction
Describes a decline in cognitive ability from baseline that starts in the days after surgery.
May be in one or more cognitive domain
Timeframe remains undefined but can be detected after 7 days - transient effects after surgery are multi factorial and so can’t really test or attribute to POCD until this time
Can effect any age but more profound sequelae in elderly
Tools to diagnose POCD
Mmse not great as doesn’t detect subtle changes
Addie brookes cognitive examination
Montreal cognitive assessment tool
Needs to be dynamic and pre operative too
Cause of POCD
Unclear
? Neuronal death neuroinflammation and micro emboli
? Anticholinergic pathways
Patient Risk factors POCD
Age Lower education level History of cerebrovascular accident Preoperative mild cognitive impairment Cognitive dysfunction at discharge
Anaesthetic risk factors for POCD
Ga vs ra - suggestion is ra benefit but no evidence Propofol better than sevo EEG or BIS may reduce risk No association with abnormal physiology ie hypoxia Dexmed protective Ketamine may be protective Steroids no effect NSAIDs may be protective
Other risk factors include Long anaesthetic time Post op infection Multiple surgeries Respiratory complications
Drug reactions A to E
A is acute B is bizarre ie idiosyncratic C is chronic D is delayed ie cardiomyopathy secondary to chemo ten years later E is end of treatment Ie withdrawal
Sickle cell genetics
Sickle cell inherited haemoglobinopathy
Mutation on chromosome 11
Results in glutamate for valine at position 6 on beta chain
Physiological factors promoting sickling in sickle cell disease
Hypoxia Hypothermia Pain Dehydration Infection
Sickle dex test Reagent and limitations
Reagan’s is sodium metabisulphate
Test doesn’t differentiate between trait and disease
Parameters for exchange transfusion in sickle cell
Hb 10
Hb a more than 70%
Hb s more than 30%
Long term complications of sickle cell
Vasoocllusive sequels ie ulcers Haemolytic anaemia Functional asplenism Cardiomegaly Chronic pain Bone marrow failure Hypertrophic of lymphoid tissue
Cystic fibrosis genetics
Autosomal recessive
Single gene mutation on chromosome 7
1 in 2500
Results in failure to transport chloride ions across the cell membrane resulting in vscid mucus that can’t be cleared by cilia
Respiratory pathogens in CF
Pseudomonas spp
Staph aureus
Haemophilus influenzae
Burkholderia cepacia
Non respiratory manifestations of CF
Malabsorption
Diabetes
Infertility
Nasal polyps
Preooptimise CF
Pre optimise CF Physio Nutrition Mucolytics and nebulisers Protective isolation Prophylactic antibiotics
Tailor GA for CF
Consider carefully re intubation - do you need suction facilitaton of ETT Lung protective strategies Good analgesia deep breathing Opiate sparing Ensure adequate reversal
Mechanism of action of antiemetics
Dex Ondansetron Metoclopramide Cyclizine Droperidol Aprepitant Scopolamine Midazolam
Dex is steroid Ondansetron 5ht3 antagonist Cyclizine histamine 1 antangonist Metaclopramide dopamine antagonist Droperidol dopamine antagonist Apprepitant neurokinin antagonist Scopolamine anticholinergic Midazolam benzo
Adult PONV scoring system
Apfel
Provoc in children
Causes of secondar6 hypertension
Phaeo Conns syndrome Renal artery stenosis Endocrine disorder ie Cushing hypo and hyperthyroidism PCKD Diabetic nephropathy Cv causes like coactation
End organ effects hypertension
Cardiac LVH
Renal ESRF
Optahlmic hypertensive retinopathy
Neuro cva hypertensive encephalopathy
Aagbi guidance for BP for elective surgery
Primary care BP less than 160/100
Secondary care ie pre op less than 180/110
Hypertensive treatment algorithm step1 - over 55 or afrocaribean
Calcium channel blocker
Hypertension treatment algorithm under 55 or diabetes
Ace I
Second line treatment hypertension
Ace I or calcium channel whatever not on yet
Thiazides diuretic
Third line hypertension
ACD all 3
4th line hypertension
Seen in tertiary care
Spiro or a blocker
Perioperative complications hypertension
Labilecardiovascular Relative hypovolemia Exaggerated response to press or Post operative cognitive dysfunction Cardiovascular events ie mi
Define carcinoid syndrome
Carcinoid is a syndrome caused by release of serotonin histamine bradykinin prostaglandins by a slow growin* neuro endocrine tumour
What is serotonin
Monoamine neurotransmitter
Signs and symptoms of carcinoid
Symptoms flushing sob diarrhoea nausea
Signs bronchospasm sweating hypertension
Treatment carcinoid
Symptom control with serotonin receptors antangknists ie ondansetron
Somatostatin analogues ie octreotide
Surgical excision tumour
What pharm agents can manipulate serotonin
SSRIS
MAOI
Antiemetics
Sumatriptan
What are phaechromocytomas and what diseases are they associated with
Functionally active tumours secreting catecholamines (adrenaline, noradrenaline) mainly located in adrenals
Associated with MEN 2 VHL NF1
Clinical features phaeo
Hypertension Tachycardia Headaches Palpitations Sweating Ischaemia End organ damage
Preoperative assessment phaeo
Check end organ damage ie LVH BP control Control of arrhythmias Volume status Glycemic control Electrolytes
Pre op treatments phaeo
Alpha block ie phenyoxybenzamine
B block ie propranolol
Sometimes calcium channel antagonists
Intraoperative goals
Avoid hypertension ie arterial line, phentolamine, gtn
Prevent tachyarrythmias ie remifentanil esmolol
Hypotension post tumour removal fluids and vasopressors
Post op complications phaeo
Significant hypotension
Persistent hypertension
Hypoglycaemia
Hypoadrenalism
Cardiovascular features of autonomic neuropathy
Postural hypotension
Bradycardia
Resting tachycardia
Prolonged qtc
Respiratory features of autonomic neuropathy
Blunted chemoreceptors response to hypoxia
Post operative hypoventation
GI effects of autonomic neuropathy
Gastroparesis
Diarrhoea or constipation
Endocrine effects of autonomic neuropathy
Abnormal thermoregulation
Common causes of autonomic neuropathy
Diabetes Gillian barre Alcohol Drug induced ie chemo Nutritional ie b12 Autoimmune
Anaesthetic considerations perioperatively autonomic neuropathy
Lability BP
Reflux
Abnormal temp control
Atelectasis and blunted response to hypoxia
Positives of low flow anaesthesia
Cost
Environment
Humidification
Negatives of low flow anaesthesia
Exhausts soda lime quickly can mean rebreathe get Potential for hypoxic mixture Accumulation toxic intermediates Less real time effects Doesn’t compensate for leaks
Anaesthetic machine check
Self inflating bag present
Automatic manufacturers machine self check
Power supply - plugged in switched on battery
Supplies and suction- tug test, cylinder, hypoxic guard flow meters, flush, suction
Breathing system- 2 bag test, vaporisers, soda lime, common gas outlet
Ventilator - working
Scavenging - working
Monitors - working
Airway equipment
Recorded in patients notes
2 bag test
Attach a test lung to patients end
Fresh gas flow 5lmin, ventilate, check unidirectional valves and system patent. Check apl by squeezing both bags
Turn on ventilator, turn off fgf
One each vaporiser in turn and make sure no loss in system
Benefits HFNO2
Warmed humidified — secretion clearance
PEEP — prevention atelectasis and recruitment
High gas flow —oxygen reservoir, co2 washout
Indications HFNO2
Type 1 resp failure Awake fibreoptic intubation Apnoeic ventilation THRIVE Tubeless surgery Extubation Unable to tolerate FM High secretion load
Contraindications to HFNO2
Any contraindications to PEEP Basal skull fracture Epistaxis Recent neurosurgery Facial injury Agitation Patient refusal
Guidelines re pain fractured nof
Pain assessed on admission, 30 mins after analgesia and hourly until pain controlled then routinely throughout admission
Analgesia to allow for investigations and nursing care
Paracetamol 6 hourly
Avoid nsaids
Nerve block in ED and at some of surgery
Causes of falls that may impact on anaesthesia
Postural hypotension Arrhythmias Infection Abnormal electrolytes Cognitive dysfunction Valvular heart disease
Transfusion triggers in hip surgery
Less than 9
Less than10 if ischaemia heart disease
Reasons for delay fractured nof
Have to be correctable
Ie k less than 2.8 or more than 6 Na less than 120 or more than 150 Hb less than 8 Reversible coagulaopathy Uncontrolled diabetes Untreated heart failure Chest infection with sepsis
Risk factors for BCIS
Age
Male sex
Diuretics
Cardiopulmonary disease
Should consider uncenented prosthesis
Surgical role to reduce risk bcis
Tell anaesthetist when BC Wash and dry femeoral cabal Lavage clean and deep suction Retrograde cement Don’t use extra pressure
Anaesthesia role BCIS
Hydrated before
Vigilance when surgeon states cementing
Aim map within 20%
Vasopressors and fluid
GI and renal causes low magnesium
Diahhorea
Reduced dietary intake
Renal losses
Pharma causes low magnesium
Diuretics
Ace I
Chemotherapy
Patient factors associated low magnesium
Age Type 2 diabetes Alcohol dependence Coeliac Crohns
Cardiovascular effects low magnesium
Arrhythmias
High SVR
Neuro effects low magnesium
Seizures
Myoclonus
Non obs uses magnesium
Asthma Arrhythmias Pain SAH Phaeos Tetanus
Management magnesium toxicity
Calcium gucomate 10% over 10mins
Mechanism magnesium
Magnesium displaces calcium in synaptic endings reducing neuro transmitter transmission
Nmda antagonist
Magnesium blocks calcium = vasolidayikn of sm
What is myotonic dystrophy
Multisystem
Progressive muscle weakness and myotonia
Autosomal dominant
Perioperative concerns myotonic dystrophy
Consent and capacity Avoiding nm blockade Bulbar weakness Reflux OSA Diabetes Cardiomyopathy Arrhythmias
Pre op assessment myotonic dystrophy
Functional assessment ECG ECHO Glucose and diabetes management Pacemaker
Intraoperative management MD
RSI with rocurinium Short acting agents ie remifentanil Opiate sparing Full reversal but care TOF Pacemaker management Glucose momitoring Invasive monitoring ie arterial line Early extubation Hdu care
Never event
Adverse safety incident that is serious largely preventable and of concern to public and Heath. Are providers
Examples of never events in anaesthesia and icu
Wrong site block Wrong strength midazolam IV admin of epidural medication Misplaced NG Miselevtion potassium solution Overdosed insulin due to abbreviations Unintentional connection of patient to flow meter
Suspended currently oesophageal intubation
Risk factors OSA
Male Smoker Obesity Age over 50 Neck circ over 40 Alcohol Pregnancy Neuro muscular disease
AHI levels
Apnoea or hyponoease more than ten seconds, more than 5 times in an hour
More than 5 mild
More than 15 moderate
More than 30 severe
Stop bang
Snoring
Tired
Observed
Pressure ie hypertension
Bmi
Age over 50
Neck over 40
Gender male
Over 3 high risk
Medical consequences OSA
Hypertension Tachy Brady arrhythmia MI Pulmonary hypertension Simon CCF Mortality Endocrine ie glucose tolerance Raised cortisol and acth Dyslipidemia
Management OSA
Prehabilitation, if severe and elective consider referral for sleep studies and 3 months CPAP prior
Difficult intubation
Regional where possible
Short acting agents
Opiate sparing analgesia
Extubation safe place awake
CPAP for recovery
Does patient need HDU
Steroid 2020 guidelines for primary adrenal failure
100mg hydrocortisone on induction then immediately start 200mg over 24 hours
Start enteral feeding ASAP and change to double dose of normal steroid for 48 hours (up to a week)
This is the case for all surgery including regional and IVF egg retrieval.
Bowel procedures IV fluids and 100mg hydrocortisone
Dex is not ok for primary as no mineralocorticoid action
Steroids 2020 guidelines for those on steroids
Steroids of more than 5 mg over 4 weeks duration
100mg hydrocortisone at induction then 200mg over 24 hours
Major intermediate labour and and c section
Resume enteral at normal dose if uncomplicated Otherwise double
Alternative dex 6-8mg will give cover for 24 hours (not for labour)
2mg/kg in children then infusion based on weight
Steroid conversion
100mh hydrocortisone = 20mg pred = 1mg dex
2020 hip fracture mamagement main guidance
Anaesthesia integral to MDT Appropriately experiences anaesthetist and surgeon Facilitate surgery with 36 hours Agreed standards for hospital Involvement in pathways
Hip fracture guidance re analgesia
Assessed for single shot in Ed then theatre if more than 6 hours
Femoral or FIB
USS may help
Continuous has nit been assessed
Hip fracture guidance
Assessment scoring devices
Nottingham rip fracture score (National hip database tool) Frailty score 4 AT (NH risk)
Hip fracture guidance 2020
Reasons for delay
Na less than 120 more than 150 K less than 2.8 more than 6 Uncontrolled arrhythmia more than 120 Hb less than 8 Uncontrolled diabetes Uncontrolled left ventricular failure Chest infection with sepsis Reversible coagulopathy
Transfusion triggers in hip fractures
Hb less than 9
Hb less than 10 if ischaemia heart disease or not mobilised on first day
Post op pulmonary complications
Pulmonary abnormalities that lead to identifiable disease or dysfunction
Atelectasis Pneumonia Respiratory failure Pleural effusion Pneumothorax Aspiration pneumonitis
Patient risk factors for post op pulmonary complications
Age over 60 ASA 2 Functional dependence OSA (obesity actually isn’t risk factor in its,ef) Smoking Alcohol Pulmonary hypertension CCF COPD Albumin less than 30 Hb less than 100 Sats less than 90
Anaesthesia risk factors for post op complications
Ga
Use nmb
Surgical risk factors for post op pulmonary complications
More than 3 hours
Thoracic abdominal head and neck vascular
Emergency surgery
Strategies to reduce risk post op pulmonary complications
Pre op
Smoking cessation
Resp disease optimised
Inspiratory muscle training
Intraoperative Lung protective ventilation Minimally invasive surgery Avoid NG where possible Short acting NMB Neurocial Goal directed fluid
Post op Early mobilisation Effective analgesia Lung expansion techniques Physio
Diagnosis in myasthenia gravis
Clinical fatigue biliary
Anti achR and TFTs first
Anti musk
Anti LRP4
Neurophysiology - reduction in compound motor action potentials on repetitive stimulation
CT MRI
NOT EDROPHUM TEST
Mamagement myasthenia
Symptomatic ie pyridostigmine
Immune suppression
Plasmapheresis or IVig
Thymectomy
Assesment MG
Preoperative optimal control Bulbar symptoms, previous crisis Consider prep IVg or pex if severe Keep meds going Extra steroids if on
Investigations inc FVC
Consider and discuss post op ventilation (risk factors, long disease bulbar symptoms, high doses pyridostigmine, vital capacity less than 2, high antibody titres)
Intraoperative Short acting Regional where possible Careful upper limb blocks and neuro axial as don’t want to lose accessory muscles or phrenic Short acting agents TIVA is good If need paralysis 1/10 roc and Suggamadex Sv for short, iPpv for long Emergence tof more than 0.95
Drugs to avoid in myasethenia
Aminoglycosides B blockers Iodine contrast Magnesium Macrolides Statin
Myasthenia crisis
Severe resp or bulbar weakness that requires intubation
Vc less than 20ml per kg
Ch9linergic crisis
Rare, precipated by anticholinesterases ie neostigmine with pyridostimine
Bradycardia hypotension lacrimation sweating vomiting
Pregnancy and MG
Optimise before conception
Epidural great
Care spinal if severe resp involvement or bulbar disease
Transient MG in neonate
Preeclampsia care with drugs
Use methylpred or hydralazine
Caution with magnesium
Treatment acute adrenal insufficiency
Steroids 100mg the ph 200mg over 24 hours
Cautious spresus as may have had excess fluids
Do a random cortisol and when stable can consider short synacthen if borderline
Treatment of thyroid storm
Propylthiouravil or carbimazole Steroids B blockers for symptomatic relief Caution with fluids Temperature control
Plus or minus
Plasma exchange
Dialysis
Emergency thryoidectomy
Management myoxedema coma
Often in women with low consciousness level and signs hypothyroidism
Tsh up, t3 t4 down ck up glucose down
Sinus bradycardia
Treat giving thyroxine
IV t3
Mechanical ventilation
Consider steroids
Management pituitary apoplexy
Test all anterior pituitary hormones
Trigger hypertension drugs trauma
Can mimic sah so need CT or mri
Steroid replacement before thyroxine
Presentation DI
High volumes urine over 3 l day
Dehydrated
Hypernatremia
Urine dilute so not many osm ie l3ss than 300
Plasma concentration ie many osm ie more than 300
Cranial vs neprhogenic vs pregnancy placenta related (vassopressinase)
Acute hypercalcemia causes
Primary hyperparathyroidism and malignancy
Other bit d toxicity, thyroxicosis, lithium, tpn
Signs of acute hypercalcemia
Above 3
Weakness fatigue abdominal pain thirst polyuria vomiting stones
Above 3.5 arrthymias
Management hypercalcemia
Parathyroid
Fluids
Bisphosphinates
Dialysis
Urgent parathyroidectimy
Cell salvage principles
Specific suction
Washing swabs IV saline in clean area
Processed via cebtrifuge
Separated in fixed or variable bowl
Washed in sodium chloride
Reinfused within 6 hours, flush lin3s before drugs ie paracetamol causes red cells to clump
Consider filters ie leukocyte depleting filters in cancer or malignancy
Positives cell salvage
Reduced requirement allogenjc blood Superior oxygen delivery Plasma explosion Transfusion triggers irrelevant Moral option in some groups
? Reduced morbidity and length of stay
Negatives cell salvage
Labour intensive
High costs
Reinfused hypotension
Time to process
Contraindications to cell salvage
Refusal
Sickle cell
Care with suction Antibiotics not licences jv Iodine Chlorhexidine Topics, clotting agents Fibrin glue Orthopaedic unset cement
Iron deficiency
Ferritin less than 30
Or
Ferritin less than 100 with raised crp or tsats less than 20%
Preoperative target haemoglobin
130 men and women (who says 120 women)
How to replace iron
Oral iron if more than 6-8 weeks
(Delay if non urgent)
Low dose
Repeat test 4 weeks prior to surgery
IV iron if doesn’t respond, side effects or less than 6 weeks
Iron deficiency without anaemia
May benefit from iron and should consider investigating cause
What is hepcidin
Hepcidin regulates iron
Inhibits iron being released by cells into circulation and may prevent absorption
Hepcidin increased by High iron levels (hence why use low dose oral iron or may have counteract effect on hepcidin) Infection Inflammation Cancer
Hepcidin reduced by
Low stores
Anaemia
Hypoxia
Goals anaesthesia laparotomy
Rapid secure of airway
Management of fluid and haemodynamic support
Protective lung ventilation
Analgesia a
Post operative care
RAG indicators NELA
CT report before surgery
Risk death documented
Timing theatre appropriate
Consultant surgeon and anaesthetist when NELA more than 5%
Icu if risk of death more than 10%
Care by older person specialist over age 75
National laparotomy pathway quality improvement care bundle (NLP QuIC)
Early assessment and resuscitation Early antibiotics Early scan and surgery Goal directed therapy Icu all patients
Frailty
Frailty is a state of increased vulnerability to poor resolution (not being able to recover) homeostasis after a stressor
Frailty scores
Edmonton frailty score
Clinical frailty scale
TEG
Point of care testing
360 micro blood into 2 heated cups. The cups have wire place in
Cups rotate 4degree 45 for ten seconds each direction
Increasing clot strength measured by torsion on wire
Kaolin to activate clotting
Different Reagants to take heparin out, test plate tests etc
R time 4-8 minutes is time for initiation until 2mm amplitude and is influenced by clotting factors
K 1-4 mins 2 to 20mm clot kinetics
A angle 47 to 74 degrees build up of fibrin and cross linking
MA maximum amplitude max clot strength - platelets and fibrinogen
CY30 and 60 clot stability
Rotem
Rotem is point of care testing
300micro blood in corvette,
Heated 37 degrees
Pin and ball immersed, and rotates (corvette stays stationary)
Activated by tissue factor or contact factors
Patient blood management aims
Clinical concept main aim to avoid unnecessary blood transfusions
Pillars of patient blood management
)optimiseRed cell mass and erythropoiesis
2) minimise blood loss
3) manage post op anaemia
Nice blood transfusion guidelines (all products)
Fe before and after
TXA
Cell salvage
Red blood cells 70-90gl post transfusion
Single transfusion only
Platetekts less than 10 and single
FFP only if bleeding and abnormal coagulation tests
PCC warfarin and bleeding or head injury
Cryo if fibrinogen less than 1, 2 pools
Safety
Consent and information
Phaeo pre op
BP co tool and success
Volume status
End organ damage
Other syndromes ie calcium?
Pre surgical treatment phaeo
Phenoxybenzamine 10mg long acting irreversible
B1 selective blockade
May consider specific a 1 antagonists ie doxazocin
Tests for phaeo
Urinary vma and metenephrine
Carcinoid
Enterochromaffin cells
Secrete serotonin Bradykinin histamine neurokinin dopamine prostaglandins
Originate from embryonic divisions of gut but can be bronchus to rectum and liver
Carcinoid symptoms if met or in liver
Symptoms of carcinoid
Flushing Diarrhoea Lacrimagiom Wheezing Hypo and hypertension
Diagnosis carcinoid
Urinary 5 Hiaa
Ct
Anaesthetic management carcinoid
Consider as a multi system disease
Dehydration anaemia electrolytes
CV history ie heart failure
Hormone release resulting in hypo and hypertension
Treatment of carcinoid pre theatre
OCTREOTIDE (syndpnethetic somatostatin which reduced growth horomone and serotonin)
Can give further 50 mic boluses Intraoperative if issues
Carcinoid Intraoperative mamagement
Epidural
Avoid BP variation
Avoid morphine and atracurium where possible due to histamine release
Invasive cardiac monitoring
Liver resection keep CVP low to prevent venous bleeding
Phenyleprhine dpvasopressor of choice
Hdu 48 hours post op
